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Cambridge University Press

978-1-107-13163-7 — Core Topics in Cardiothoracic Critical Care


Edited by Kamen Valchanov , Nicola Jones , Charles W. Hogue
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Core Topics in Cardiothoracic


Critical Care

© in this web service Cambridge University Press www.cambridge.org


Cambridge University Press
978-1-107-13163-7 — Core Topics in Cardiothoracic Critical Care
Edited by Kamen Valchanov , Nicola Jones , Charles W. Hogue
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Core Topics in Cardiothoracic


Critical Care
Second Edition
Edited by
Kamen Valchanov
Papworth Hospital

Nicola Jones
Papworth Hospital

Charles W Hogue
Northwestern University in Chicago

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Contents
List of Contributors page ix
Foreword xv
Nick Fletcher
Preface to the Second Edition xvii
Link between Cardiothoracic Anaesthesia and
Intensive Care: Which Patients are Admitted
to Critical Care? xix
Andrew Klein
Scoring Systems and Prognosis xxiii
Allanah Barker and Sam Nashef
List of Abbreviations xxix

Section 1 – Diagnosis 9 Chest Drainage 70


Alia Noorani and Yasir Abu-Omar
1 History and Examination 1
Lachlan Miles and Joseph E Arrowsmith 10 Cardiac Pacing and Defibrillation 77
Sérgio Barra and Patrick Heck
2 Electrocardiography 7
David Begley 11 Arterial and Venous Catheterisation and
Invasive Monitoring 86
3 Echocardiography in the Cardiothoracic Stuart A Gillon, Nicholas A Barrett and
Intensive Care Unit 15 Christopher IS Meadows
Ghislaine Douflé and Andrew Roscoe
4 Coronary Angiography 22
Unni Krishnan and Stephen P Hoole Section 3 – Therapeutic Intervention
5 Bronchoscopy in the Cardiothoracic 12 Antibiotics in the Cardiothoracic Intensive
Intensive Care Unit 28 Care Unit 95
Sumit Chatterji and Pasupathy Sivasothy Oana Cole and Olly Allen
6 Microbiology Testing 38 13 Blood Products and Transfusion 107
A Ruth M Kappeler and Margaret I Gillham Martin Besser
7 Radiology for Cardiothoracic 14 Fluid Administration 116
Intensivists 44 Vasileios Zochios and Kamen Valchanov
Kristian H Mortensen, Peter A Barry and
Deepa Gopalan 15 Inotropes and Vasopressors 123
Gabriel Kleinman, Shahzad Shaefi and
Charles Shayan
Section 2 – Practical Procedures
16 Sedation and Analgesia 130
8 Airway Management in Cardiothoracic
Lachlan Miles and Barbora Parizkova
Intensive Care: Intubation and
Tracheostomy 59 17 Mechanical Ventilation 142
Martin John and Christiana Burt Anja Schneider and Erik Ortmann

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Contents

18 Renal Replacement Therapy 149 30 Systemic Hypertension in Cardiothoracic


Jonah Powell-Tuck, Matt Varrier and Marlies Critical Care 263
Ostermann Antonio Rubino and Susan Stevenson
19 Nutritional Support for Cardiac Surgery and 31 Pulmonary Hypertension in the
Intensive Care 157 Cardiothoracic Intensive Care Unit 272
Peter Faber Mark Toshner and Joanna Pepke-Zaba
20 Physiotherapy and Rehabilitation 164 32 The Infected Patient 278
Adam Baddeley and Allaina Eden Simon J Finney
33 Seizures 285
Ari Ercole and Lara Prisco
Section 4 – Advanced Organ Support
34 The Acute Abdomen in the Cardiac
21 Percutaneous Mechanical Circulatory
Intensive Care Unit 294
Support 173
Simon JA Buczacki and Justin Davies
Evgeny Pavlushkov and Marius Berman
35 Cardiothoracic Trauma 301
22 Ventricular Assist Devices (VAD) 180
Alia Noorani and Ravi J De Silva
Harikrishna M Doshi and Steven SL Tsui
36 The Bleeding Cardiac Surgical
23 Cardiac Extracorporeal Membrane
Patient 307
Oxygenation 193
Jerrold H Levy, Kamrouz Ghadimi and
Jason M Ali and David P Jenkins
Ian J Welsby
24 Respiratory Extracorporeal Membrane
Oxygenation in the Cardiothoracic Intensive
Care Unit 202 Section 6 – Perioperative Care:
Darryl Abrams and Daniel Brodie
The Patient Post Cardiac Surgery
37 Management after Coronary Artery
Section 5 – Acute Disorders Bypass Grafting Surgery 313
Sam Nashef and Paolo Bosco
25A Resuscitation after Adult Cardiac
Surgery 211 38 Intensive Care Unit Management
Jonathan H Mackay Following Valve Surgery 317
Yasir Abu-Omar and Shakil Farid
25B Out-of-Hospital Cardiac Arrest Patients
in the Cardiothoracic Intensive Care 39 Pulmonary Endarterectomy Patients in
Unit 220 Cardiothoracic Critical Care 324
Lisen Hockings and Sophia Fisher Choo Yen Ng
26 Airway Emergencies 231 40 Heart Transplantation 333
Tom P Sullivan and Guillermo Martinez Stephen J Pettit and Anna Kydd
27 Chest Pain as a Symptom on the 41 Lung Transplantation 340
Cardiothoracic Intensive Care Unit 241 JS Parmar
Will Davies
42 Aortic Surgical Patients in the Intensive
28 Acute Dyspnoea and Respiratory Care Unit 347
Failure 247 Pedro Catarino and Swetha Iyer
Ken Kuljit Parhar
43 Thoracic Surgical Patients 356
29 Shock in the Cardiothoracic Intensive Care J Irons and S Ghosh
Unit 256
Fabio Guarracino and Rubia Baldassarri

vi

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Contents

Section 7 – Disease Management 52 Difficult to Wean from Mechanical


Ventilation Patients in the Cardiothoracic
in the Cardiothoracic Intensive Care Intensive Care Unit 434
Unit: Incidence; Aetiology; Diagnosis; Michael G Davies

Prognosis; Treatment
44 Respiratory Disorders: Acute Respiratory Section 8 – Provision and Delivery of
Distress Syndrome 365 Cardiothoracic Intensive Care
Alastair Proudfoot and Charlotte Summers
53 Cardiothoracic Critical Care Nursing,
45 Cardiovascular Disorders: the Heart Failure Outreach and Follow-up 441
Patient in the Intensive Care Unit 372 Jo-anne Fowles
Anna Kydd and Jayan Parameshwar
54 Systems and Processes in Cardiothoracic
46 Neurological Aspects of Cardiac Surgery 380 Critical Care 445
Max S Damian James Moore and Alain Vuylsteke
47 Postoperative Delirium 392 55 Clinical Information Systems 449
Makeida B Koyi, Joseph G Hobelmann and Matthew Jones
Karin J Neufeld
56 Medical Law and Ethics in the Cardiothoracic
48 Haematological Disorders and Cardiothoracic Intensive Care Unit 456
Intensive Care 402 Oana Cole
Jerrold H Levy, Kamrouz Ghadimi and
Ian Welsby 57 Training in Cardiothoracic Intensive
Care 462
49 Pregnancy and Cardiovascular Disorders 408 Amy Needham and Chinmay Padvardthan
Kiran Salaunkey
50 Paediatric Cardiac Intensive Care 418
Ajay Desai, Lidia Casanueva and Duncan Macrae
Exercise Answers 467
51 Grown-up Congenital Heart Disease (GUCH)
Index 471
Patients in the Cardiothoracic Intensive Care
Unit 427
Colour plates are to be found between
Susanna Price and Niki Walker
pages 230 and 231.

vii

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Contributors

Darryl Abrams Peter A Barry


Department of Medicine, Columbia University Department of Surgery, Royal Marsden Hospital,
College of Physicians and Surgeons, New York, London, UK
NY, USA
David Begley
Yasir Abu-Omar Department of Cardiology, Papworth Hospital,
Department of Surgery, Papworth Hospital, Cambridge, UK
Cambridge, UK

Jason M Ali Marius Berman


Department of Surgery, Papworth Hospital, Department of Surgery, Papworth Hospital,
Cambridge, UK Cambridge, UK

Olly Allen Martin Besser
Department of Pathology, Papworth Hospital, Department of Pathology, Papworth Hospital,
Cambridge, UK Cambridge, UK

Joseph E Arrowsmith Paolo Bosco


Department of Anaesthesia and Intensive Care, Department of Surgery, Papworth Hospital,
Papworth Hospital, Cambridge, UK Cambridge, UK
Adam Baddeley
Department of Physiotherapy, Papworth Hospital, Daniel Brodie
Cambridge, UK Department of Medicine, Columbia University
College of Physicians and Surgeons, New York,
Rubia Baldassarri NY, USA
Department of Anaesthesia and Critical Care
Medicine, Azienda Ospedaliero Universitaria Pisana, Simon JA Buczacki
Pisa, Italy Department of Surgery, Addenbrooke’s Hospital,
Cambridge, UK
Allanah Barker
Department of Surgery, Papworth Hospital, Christiana Burt
Cambridge, UK Department of Anaesthesia and Intensive Care,
Papworth Hospital, Cambridge, UK
Sérgio Barra
Department of Cardiology, Papworth Hospital, Lidia Casanueva
Cambridge, UK Great Ormond Street Hospital, London, UK

Nicholas A Barrett Pedro Catarino


Department of Intensive Care, Guy’s and St Thomas’ Department of Surgery, Papworth Hospital,
NHS Foundation Trust, London, UK Cambridge, UK

ix

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Contributors

Sumit Chatterji Simon J Finney


Department of Medicine, Addenbrooke’s Hospital, Department of Intensive Care, Barts Heart Central,
Cambridge, UK St Bartholomew’s Hospital, London, UK

Oana Cole Sophia Fisher
Department of Anaesthesia and Intensive Care, Department of Anaesthesia, Flinders Medical Centre,
Papworth Hospital, Cambridge, UK Adelaide, South Australia, Australia

Max S Damian Jo-anne Fowles


Department of Neurology, Addenbrooke’s Hospital, Department of Anaesthesia and Intensive Care,
Cambridge, UK Papworth Hospital, Cambridge, UK

Kamrouz Ghadimi
Justin Davies
Department of Anesthesiology, Duke University
Department of Surgery, Addenbrooke’s Hospital,
Hospital, Durham, NC, USA
Cambridge, UK
S Ghosh
Michael G Davies Department of Anaesthesia and Intensive Care,
Department of Respiratory Medicine, Papworth Papworth Hospital, Cambridge, UK
Hospital, Cambridge, UK
Margaret I Gillham
Will Davies Department of Pathology, Papworth Hospital,
Department of Cardiology, Papworth Hospital, Cambridge, UK
Cambridge, UK
Stuart A Gillon
Ajay Desai Department of Intensive Care, Guy’s and St Thomas’
Department of Paediatric Intensive Care, Royal NHS Foundation Trust, London, UK
Brompton and Harefield NHS Foundation Trust,
London, UK Deepa Gopalan
Department of Radiology, Imperial College,
Harikrishna M Doshi London, UK
Department of Surgery, Papworth Hospital,
Cambridge, UK Fabio Guarracino
Department of Anaesthesia and Critical Care
Ghislaine Douflé Medicine, Azienda Ospedaliero Universitaria Pisana,
University Health Network, University of Toronto, Pisa, Italy
Toronto, Ontario, Canada
Patrick Heck
Allaina Eden Department of Cardiology, Papworth Hospital,
Department of Physiotherapy, Papworth Hospital, Cambridge, UK
Cambridge, UK
Joseph G Hobelmann
Ari Ercole Department of Psychiatry, Johns Hopkins
Department of Anaesthesia, Addenbrooke’s Hospital, University School of Medicine, Baltimore,
Cambridge, UK MD, USA

Peter Faber Lisen Hockings


Department of Anaesthesia, Aberdeen Royal Department of Intensive Care, The Alfred Hospital,
Infirmary, Aberdeen, UK Melbourne, Victoria, Australia

Shakil Farid Charles W Hogue


Department of Surgery, Papworth Hospital, Department of Anesthesiology, Northwestern
Cambridge, UK University Feinberg School of Medicine, Chicago, USA

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Contributors

Stephen P Hoole Jerrold H Levy


Department of Cardiology, Papworth Hospital, Department of Anesthesiology, Critical Care and
Cambridge, UK Surgery, Duke University School of Medicine,
Durham, NC, USA
J Irons
Department of Anaesthesia and Intensive Jonathan H Mackay
Care, Papworth Hospital, Cambridge, UK Department of Anaesthesia and Intensive Care,
Papworth Hospital, Cambridge, UK
Swetha Iyer
Department of Surgery, Papworth Hospital, Duncan Macrae
Cambridge, UK Department of Paediatric Intensive Care, Royal
Brompton and Harefield NHS Foundation Trust,
David P Jenkins London, UK
Department of Surgery, Papworth Hospital,
Cambridge, UK Guillermo Martinez
Department of Anaesthesia and Intensive Care,
Martin John Papworth Hospital, Cambridge, UK
Department of Anaesthesia and Intensive Care,
Papworth Hospital, Cambridge, UK Christopher IS Meadows
Department of Intensive Care, Guy’s and St Thomas’
Matthew Jones NHS Foundation Trust, London, UK
Judge Business School, University of Cambridge,
Cambridge, UK James Moore
Department of Anaesthesia and Intensive Care,
Nicola Jones Papworth Hospital, Cambridge, UK
Deptartment of Anesthesia and Intensive Care,
Papworth Hospital, Cambridge, UK Kristian H Mortensen
Department of Radiology, Great Ormond Street
A Ruth M Kappeler Hospital, London, UK
Department of Pathology, Papworth Hospital,
Cambridge, UK Lachlan Miles
Department of Anaesthesia and Intensive Care,
Andrew Klein Papworth Hospital, Cambridge, UK
Department of Anaesthesia and Intensive Care,
Papworth Hospital, Cambridge, UK Sam Nashef
Department of Surgery, Papworth Hospital,
Gabriel Kleinman Cambridge, UK
Department of Anesthesiology, Northwestern
Amy Needham
University, Chicago, IL, USA
Department of Anaesthesia and Intensive Care,
Makeida B Koyi Papworth Hospital, Cambridge, UK
Department of Psychiatry, Johns Hopkins Karin J Neufeld
University School of Medicine, Baltimore, Department of Psychiatry, Johns Hopkins University
MD, USA School of Medicine, Baltimore, MD, USA
Unni Krishnan Choo Yen Ng
Department of Cardiology, Papworth Hospital, Department of Surgery, Papworth Hospital,
Cambridge, UK Cambridge, UK

Anna Kydd Alia Noorani


Department of Transplantation, Papworth Hospital, Department of Surgery, Papworth Hospital,
Cambridge, UK Cambridge, UK

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Contributors

Erik Ortmann Alastair Proudfoot


Department of Anesthesia and Intensive Care, Department of Perioperative Medicine,
Kerckhoff-Klinic, Heart and Lung Centre, Bad St. Bartholomew’s Hospital, London, UK
Nauheim, Germany
Andrew Roscoe
Marlies Ostermann Department of Anaesthesia and Intensive Care,
Department of Intensive Care, Guy’s and St Thomas’ Papworth Hospital, Cambridge, UK
NHS Foundation Trust, London, UK
Antonio Rubino
Chinmay Padvardthan Department of Anaesthesia and Intensive Care,
Department of Anaesthesia and Intensive Care, Papworth Hospital, Cambridge, UK
Papworth Hospital, Cambridge, UK
Kiran Salaunkey
Jayan Parameshwar
Department of Anaesthesia and Intensive Care,
Department of Transplantation, Papworth Hospital,
Papworth Hospital, Cambridge, UK
Cambridge, UK
Ken Kuljit Parhar Anja Schneider
Department of Critical Care Medicine, University of Zentrum für Akute und Postakute Intensivmedizin
Calgary, Calgary, Alberta, Canada Kreisklinik Jugenheim, Seeheim-Jugenheim,
Germany
Barbora Parizkova
Department of Anaesthesia and Intensive Care, Shahzad Shaefi
Papworth Hospital, Cambridge, UK Department of Anesthesiology, Northwestern
University, Chicago, IL, USA
Js Parmar
Department of Transplantation, Papworth Hospital, Charles Shayan
Cambridge, UK Department of Anesthesiology, Northwestern
University, Chicago, IL, USA
Evgeny Pavlushkov
Department of Surgery, Papworth Hospital, Ravi J De Silva
Cambridge, UK Department of Surgery, Papworth Hospital,
Joanna Pepke-Zaba Cambridge, UK
Department of Respiratory Medicine, Papworth
Hospital, Cambridge, UK Pasupathy Sivasothy
Department of Medicine, Addenbrooke’s Hospital,
Stephen J Pettit Cambridge, UK
Department of Transplantation, Papworth Hospital,
Cambridge, UK Tom P Sullivan
Department of Anaesthesia and Intensive Care,
Jonah Powell-Tuck
Papworth Hospital, Cambridge, UK
Department of Intensive Care, Guy’s and St Thomas’
NHS Foundation Trust, London, UK Charlotte Summers
Susanna Price University of Cambridge School of Clinical
Department of Intensive Care, Royal Brompton and Medicine, Cambridge, UK
Harefield NHS Foundation Trust, London, UK
Susan Stevenson
Lara Prisco Department of Anaesthesia and Intensive Care,
Department of Anaesthesia, Addenbrooke’s Hospital, Papworth Hospital, Cambridge, UK
Cambridge, UK

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Contributors

Mark Toshner Alain Vuylsteke


Department of Respiratory Medicine, Papworth Department of Anaesthesia and Intensive Care,
Hospital, Cambridge, UK Papworth Hospital, Cambridge, UK

Steven SL Tsui Niki Walker


Department of Surgery, Papworth Hospital, Department of Intensive Care, Royal Brompton and
Cambridge, UK Harefield NHS Foundation Trust, London, UK

Kamen Valchanov Ian Welsby


Deptartment of Anesthesia and Intensive Care, Department of Anesthesiology, Duke University
Papworth Hospital, Cambridge, UK Hospital, Durham, NC, USA

Matt Varrier Vasileios Zochios


Department of Intensive Care, Guy’s and St Thomas’ Department of Anaesthesia and Intensive Care,
NHS Foundation Trust, London, UK Papworth Hospital, Cambridge, UK

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Foreword

I am very pleased to be able to provide a brief intro- up and, combined with a very eminent US academic,
duction to the owner, borrower or reader of this text. revisited, reorganised and rewritten the problems and
This book is an update of the successful 2008 Core solutions in this area of practice. Kamen Valchanov
Topics in Cardiothoracic Care text. When that book and Nicola Jones have taken over the authorship
was published, it was the first to provide a detailed from their mentors at the world leading Papworth
insight into the cardiothoracic critical care unit and Hospital and have produced a book that retains the
was widely read and appreciated. Since then other vision and wisdom of the original and added the
authors have produced texts that explore this fascin- significant advances in knowledge, technology and
ating area of practice, but none have quite replicated practice. A  significant positive change is the addi-
that originality and quality. . . until now! tion of Professor Charles Hogue of Johns-Hopkins,
Cardiac critical care evolved quite separately Baltimore and Northwestern University, Chicago for
from general intensive care. It essentially originated a North American perspective. Knowing them all, it
as a side room on the cardiac surgical ward in the is not in the least surprising that they have produced
1950s where the patient who struggled after cardiac a book of such scope and such high quality. The con-
surgery was ventilated and cared for by the cardiac tributing authors are all experts in their fields and are
anaesthetist and surgeon. Today we have large mul- drawn from a wide international base.
tidisciplinary teams in large technology dominated This book will prove invaluable to the critical care
purpose-built tertiary units. This has been a rapid nurse, the trainee anaesthetist, surgeon and intensiv-
and hugely successful evolution. Cardiothoracic criti- ist. It will also be of value to the new and established
cal care is now a full blooded and highly influential consultants who are involved with patients with car-
subspecialty in the ever expanding critical care field. diothoracic disease, which extends well beyond the
Indeed I firmly believe that where cardiac intensivists bounds of surgery now. I  feel proud to have been
tread today, general intensivists will follow tomorrow. invited to write this foreword and I am proud to fully
This evolution has been accompanied by a vast expan- recommend this work.
sion in research and regulation. No branch of medi-
cine is so scrutinised and yet so open to new thinking Nick Fletcher
and new solutions. The link between cardiothoracic Consultant in Cardiothoracic and Vascular Critical Care
anaesthesia and cardiothoracic critical care is vital in St George’s University Hospital, London UK
the joined up care of these complex patients, as is the
close link with all the related specialties such as the Past President of the Association for Cardiothoracic
surgeon, the cardiologist, the echocardiographer and Anaesthesia and Critical Care (UK)
so many more.
We are fortunate that the new generation of critical
care doctors and authors from Papworth have stepped

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Preface to the Second Edition

Why the second edition of Core Topics in Cardio- How do we practise in this specialty? We pro-
thoracic Critical Care? The first edition of Core Topics vide organ support to patients who have undergone
in Cardiothoracic Critical Care was published in 2008. cardiothoracic surgery or who have failing cardiac
It has been a great success, providing a comprehen- or respiratory function, with the hope that they will
sive text for the specialty and selling so many paper respond to treatment and survive. However, these
copies that Cambridge University Press had to reprint days with modern advances in life support technol-
the book to meet the demands of the market. The first ogy, such as extracorporeal membrane oxygenation,
editors Dr Alain Vuylsteke, Dr Andrew Klein, and Mr death is no longer a binary phenomenon. As guard-
Sam Nashef laid the foundation stone. However, a lot ians of this technology we must be ever mindful of
has happened in the world of medicine since 2008, our patients’ quality of life and the long-term outcome
not least in cardiothoracic critical care. Indeed prac- from our interventions. Importantly we must guard
tice has expanded so much that cardiothoracic critical against sustaining life at all costs and offer patients
care has been recognised as a separate sub-specialty and their loved ones, care which makes them happy,
by the Faculty of Intensive Care Medicine in the UK. or at least acts in their best interests.
Therefore, the current editors were tasked with pro- In 2018 a vast amount of evidence exists to guide
viding an updated version of this textbook, which will this practice. However, it can be challenging to apply
hopefully offer to the reader state-of-the-art informa- evidence from trials to the heterogeneous group of
tion on the current practice in cardiothoracic critical patients we treat in Cardiothoracic Critical Care each
care. with unique, rapidly changing derangements of car-
diorespiratory function. The world of evidence-based
A Few Notes from the Editors medicine is also riddled with problems of spurious
Different sources point to different events as the birth evidence, and an ever-increasing number of articles
of our specialty of intensive care medicine. Most describing scientific trials are being retracted by the
revolve around mechanical ventilation with some publishers. In the end among a myriad of scientific
believing intensive care started in Boston in 1912 when and less scientific articles, guidelines and protocols,
a girl suffering from poliomyelitis received mechani- based on expert opinion, the patient has to be sup-
cal ventilation. Others feel that it is the organised care ported through their critical illness and recovery
for polio victims in need of invasive ventilation that after surgery. In most cases good doctors, nurses and
laid the foundations of the specialty. It is probably a allied healthcare professionals use patient tailored
little easier to define the birth of cardiothoracic criti- approaches in their daily work to provide patients
cal care medicine as this was born when cardiac sur- with the best possible care. We hope that the following
geons needed to leave patients who had undergone text will offer ample and unbiased information to help
heroic operations in a place where they could recover. us work in the best interest of each individual patient.
Similarly to general intensive care medicine we do not
have a specific disease to treat, rather we have very Kamen Valchanov
sick patients with complex disorders of the cardio- Nicola Jones
respiratory system to care for. Charles W Hogue

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Link between Cardiothoracic Anaesthesia and Intensive


Care: Which Patients are Admitted to Critical Care?
Andrew Klein
Introduction cardiac surgery, admission to an ICU will be manda-
tory after anaesthesia. It is reasonable to expect their
Admission to an intensive care area is undertaken
condition to worsen following a period of cardiopul-
for the diagnosis, management and monitoring of
monary bypass, and preparations should be made for
patients with conditions that require close or con-
any necessary organ support, for example use of ino-
stant attention by a group of specially trained health
tropes or haemofiltration.
professionals. Critical care encompasses all areas that
Consideration must also be taken as to whether
provide level 2 and/or level 3 care as defined by the
the patient is appropriate for long-term management
Intensive Care Society document ‘Levels of Critical
on an ICU. An example of this might be a palliative
Care for Adult Patients, 2009’ (Table  1). All level 2
thoracic oncology patient undergoing a procedure for
and level 3 areas have higher staffing levels, special-
symptom relief; such a patient might be more appro-
ist monitoring and more advanced treatment options
priately placed in an HDU with a limit on the medical
available. Level 2 areas are commonly referred to as
interventions that would be appropriate. This manage-
High Dependency Units (HDUs), while level 3 areas
ment plan should be discussed and formulated with
are Intensive Care Units (ICUs), and we will make
the patient and relatives prior to the procedure itself.
this distinction in our text. In some hospitals, the two
are separated geographically, whilst in others they co-
exist in one area. Diagnostic and Surgical Related
It is extremely common for patients undergoing Factors
cardiothoracic interventions under anaesthesia to be A diagnostic model can be utilised in order to pro-
admitted to an ICU or HDU afterwards and this can vide guidelines for admission, which identifies spe-
often be a preplanned decision based on the poten- cific conditions and diseases where it is felt a higher
tial for the patient to become more critically unwell or level of care is always warranted. With respect to car-
unstable. However, given the current pressures placed diothoracic intensive care, the majority of such condi-
on the health service, in terms of both bed occupancy tions will fall under the umbrellas of the cardiac and/
and finances, each individual case should be con- or respiratory systems. However, it is also possible for
sidered and a decision made as to whether such an a patient to require admission on the basis of an addi-
admission will be necessary. These decisions can often tional diagnosis, such as sepsis or a neurological com-
be very difficult and must take into consideration a plication of surgery.
number of factors. All patients undergoing sternotomy will man-
date admission to either an ICU or cardiac recovery
Patient Related Factors environment after their procedure. The differentia-
A patient’s comorbidities, physiological reserve, prog- tion between the two is discussed below. A  number
nosis and wishes should all be taken into account of cardiothoracic surgical procedures will always
when planning their most appropriate postoperative warrant ICU admission, due to the complex nature
destination. Prioritisation of patients for critical care of the intervention and often long procedural times.
beds should highlight only those patients likely to gain Examples of these are repair of aortic dissection, or
from an increased level of care and thus not those that multiple valve procedures.
are either too well or too sick to benefit. The majority of patients undergoing thoracic
It is clear that for some high-risk patients, such as surgery will either be admitted to an HDU or dis-
those with known chronic organ failure undergoing charged back to the ward following a period of close

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Which Patients are Admitted to Critical Care?

Table 1 Levels of critical care

Level of Criteria for admission Examples


care
0 General ward • Requires hospitalisation but needs can be met Intraveous drug administration
through normal ward care Observations needed less than 4 hourly
1 Coronary care unit • Recently discharged from higher level care Minimal 4 hourly observations
• In need of additional monitoring/intervention, Continuous oxygen therapy, management of
clinical input or advice epidural, chest drain in situ
• Requiring critical care outreach service Risk of clinical deterioration, high early
support warning score
2 High dependency • Requiring preoperative optimisation Invasive monitoring to optimise fluid balance
unit • Requiring extended postoperative care Major elective surgery, emergency surgery in
• Stepping down to level 2 from level 3 care unstable patient
• Requiring single organ support Minimal hourly observations
• Requiring basic respiratory plus basic Non-invasive ventilation, single intravenous
cardiovascular support vasoactive drug
Continuous oxygen therapy and intra-aortic
balloon pump
3 Intensive care unit • Requiring advanced respiratory support alone Invasive mechanical ventilator support via
• Requiring a minimum of two organ systems endotracheal tube or tracheostomy
supported (except basic respiratory plus basic Acute renal replacement therapy and
cardiovascular – level 2, as above) vasoactive medication

monitoring in recovery after surgery. An HDU bed Admission to an ICU may also depend on the
may often be requested to ensure vigilance in the availability of a required specific treatment for an
immediate postoperative period, and also to allow individual patient. Some centres provide special-
optimisation of pain control. ised advanced organ support, such as extracorporeal
membrane oxygenation. Also, cardiothoracic surgery
Alternative Resources is a high-risk specialty fraught with potential compli-
Each individual institution will have slightly different cations, some of which might require transfer out to
facilities available for the care of their patients and an alternative centre, for example to access neurosur-
these must be taken into consideration when plan- gical intervention.
ning postprocedural care. Early goal-directed ther-
apy and utilisation of a ‘fast-track’ approach has been Time of Admission
adopted successfully in many cardiothoracic centres A well-organised cardiothoracic surgical centre
and this may allow lower risk patients to be admit- should incorporate a robust system of communica-
ted to a cardiac recovery area as a temporary meas- tion with both its ICU and HDU with respect to the
ure postoperatively, before being discharged back to daily admission requirements and bed availability.
a ‘stepdown’ unit or ward. For such systems to work The majority of patients undergoing anaesthesia will
and ensure safe patient care, there must be immedi- require elective admission and surgical activity will be
ate access to critical care and adequate numbers of planned according to such requirements.
trained nursing staff. This model has been proven to However, the ICU and HDU must also always take
be successful in some hospitals and can potentially into account the potential for unplanned emergency
improve patient flow. However, for many institutions admissions, either transferred in for surgical inter-
the safest option remains to admit all cardiac surgical vention, or due to unexpected complications intraop-
patients to the ICU postoperatively. The priority in eratively. Patients should be admitted to the required
such institutions is then to discharge out into a step- higher level of care before their condition reaches a
down unit as soon as possible after extubation and a point from which recovery may be extremely difficult.
period of stability. In reality, it is often much better practice to assume

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Which Patients are Admitted to Critical Care?

a bed will be needed for your patient, than be left in advances in providing ‘fast-track’ surgery, and cardiac
a situation where the availability is not there and the recovery units have become increasingly popular. In
patient is unstable. This could potentially lead to a addition, thoracic surgery does not always necessitate
worsened patient outcome, and may also put unnec- an HDU bed and often an adequate level of care can be
essary pressure on the relevant intensive care unit to provided on general wards with critical care outreach
discharge prematurely. support. Requirements for a higher level of care are by
no means well defined and clinical practice will con-
Conclusion tinue to evolve with time.
It is often assumed that all patients undergoing cardi- Given the current climate in the health care sys-
othoracic surgery will warrant admission to either an tem, with a constant pressure for beds and a drive to
ICU or HDU postoperatively and in many instances improve patient flow, it is extremely important that
that remains the case. Cardiothoracic anaesthesia is a each case undergoing cardiothoracic anaesthesia is
high-risk specialty and it is imperative that the post- considered individually and the safest care for that
operative care system in place in each institution is patient determined. Such planning will take into con-
safe and robust. sideration patient related factors, their diagnosis and
However, variety in admission indications and required surgery and the resources available in the
rates does exist. In recent years there have been institution.

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Scoring Systems and Prognosis


Allanah Barker and Sam Nashef

Crystal Balls • Helping to measure the performance of the


service by comparing actual and predicted
Knowing the likelihood of survival after cardiac
outcomes; and
surgery is useful for multiple reasons including for
weighing the potential risks versus benefits of sur- • Comparing the performance of different
gery. Further, accurate predicting of outcome allows institutions, surgeons and anaesthetists by
for comparison with the actual outcome and thus correcting for risk when outcomes are assessed.
insight into the overall performance of the cardiac Preoperative models take no account of what happens
surgical unit. Knowledge of who is likely to develop in the operating theatre and are therefore less use-
major morbidity also has an impact on the use of valu- ful in predicting which of a number of postoperative
able resources and may allow for sensible planning of patients with complications are likely to emerge intact
operating lists. In addition, some believe that being from the critical care unit.
able to predict mortality with some certitude may help There are probably more risk models in cardiac
clinicians to determine when further efforts are futile. surgery than in any other branch of medicine. Most
Unfortunately, the perfect predictor – a crystal ball to rely on a combination of risk factors, each of which
foresee the future – has not yet been fully developed. is given a numerical ‘weight’. Weights are added,
multiplied or otherwise mathematically processed to
Risk Models or Scoring Systems come up with a percentage figure to predict mortality
Scoring systems allow reasonable prediction of out- or survival. In additive models, the weights given to
come after cardiac surgery. Many models have been the risk factors are simply summed to give the pre-
devised to work out the likelihood of survival, and dicted risk. They are easy to use and can be calculated
these and others have also been shown to predict mentally or ‘on the back of an envelope’. They are less
major morbidity, long-term survival and resource use accurate than more sophisticated systems and have a
with some accuracy. Models can be broadly divided tendency to overscore slightly in low-risk patients and
into two groups: to underscore considerably in very high-risk patients.
Examples of such models are the Parsonnet (the pio-
• Preoperative models, applied before the operation,
neering heart surgery risk model) and the original
with no knowledge of intraoperative events; and
additive EuroSCORE for cardiac surgery overall.
• Postoperative models, applied immediately after
Other models deal specifically with cardiac surgi-
the operation on admission into the critical care
cal subsets, like coronary surgery and valve surgery.
unit, taking some account of what the operation
Sophisticated models use Bayesian analysis, logistic
did to the patient.
regression or even computer neural networks. They
do not allow easy bedside calculation, necessitating
Preoperative Models a computer for determining risk. They are, however,
These are most useful for more stable than additive models across the risk range
• Establishing the risk of surgery as an adjunct and slightly more accurate in exact risk prediction.
to surgical decision making (determining the Examples of such models are the Society of Thoracic
indication to operate on the basis of risk-to- Surgeons (STS) model, the logistic EuroSCORE and
benefit assessment); EuroSCORE II for overall cardiac surgery.
• Providing the patient with information, which is The widespread application of scoring systems
helpful in obtaining consent; in heart surgery has allowed robust performance

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Scoring Systems and Prognosis

measurement and probably contributed to the dra- Extent of Cardiac Disease


matic drop in cardiac surgical mortality seen in the
The severity of coronary disease is subjective and
last 15 years.
therefore not included in surgical risk scores. The
Syntax score allows for a measure of the severity of
Preoperative Model Risk Factors disease, but is time consuming and partly subjective.
Not surprisingly, several common risk factors are Left main stem disease may be associated with more
included in all models (age, gender and left ventricu- risk. Objective measures of cardiac disease include
lar (LV) function). Other risk factors are included in recent myocardial infarction (MI), unstable angina
some models but not in others, such as hypertension, and mechanical complications of MI such as acute
diabetes and obesity. Models also differ depending rupture of the mitral valve or ventricular septum.
on whether they deal with all cardiac surgeries or a
specific subset, such as coronary surgery or valvular Repeat Operation
surgery. They share many risk factors and it would
Previous cardiac surgery (or previous sternotomy)
be repetitive to list them all here, but the models are
increases difficulty of access and prolongs operative
easily accessible and there are interactive calcula-
time. These patients therefore carry an increased risk of
tors available online:  www.euroscore.org and http://
bleeding as well as possibly having more advanced dis-
riskcalc.sts.org/stswebriskcalc/. EuroSCORE II also
ease than those undergoing their first cardiac procedure.
offers a smartphone ‘app’ for use at the bedside.

Lung Disease
Age The presence of chronic pulmonary disease such as
There is an increased risk above the age of 60 years. chronic obstructive pulmonary disease (COPD) has a
large impact on how a patient is managed in anaes-
Gender thetic and ventilatory terms. After cardiac surgery,
Females have a higher operative mortality than patients with concurrent lung disease are more likely
males, possibly because of smaller coronary artery to require extended ventilation and to develop pul-
size, smaller blood volume predisposing to risks monary complications, such as chest infections. Lung
associated with perioperative anaemia and transfu- function is difficult to quantify with a single test and
sion, although the definitive reason for the difference severity is based partly on subjective judgements.
is unknown. However, chronic pulmonary disease is taken into
account in the EuroSCORE and STS.

Left Ventricular Function Renal Disease


As estimated by echocardiography or angiography, LV
Renal dysfunction, as evidenced by dependence on
function is a good measure of cardiac status, but deter-
dialysis, increases mortality by as much as 40%, but
mination can be operator dependent and it is difficult
the spectrum of renal failure is wide and difficult to
to produce an accurate and reproducible percentage
quantify. Creatinine levels are easy to measure, but are
ejection fraction. Thus, LV function is generally classi-
not always an accurate measure of true kidney func-
fied as ‘good’, ‘moderate’ or ‘poor’; EuroSCORE II has
tion. The original EuroSCORE uses grossly deranged
an additional category of ‘very poor’.
serum creatinine (>200 μmol/l) as a measure of sig-
nificant renal impairment. Other scores use dialysis
Type of Surgery dependence. The best measure is probably creatinine
General cardiac risk models take into account patients clearance (CC), and this now features in EuroSCORE
that undergo different surgeries  – the risk for coro- II, where the categories of renal dysfunction have
nary artery bypass graft (CABG) surgery is less than expanded into four:  normal function (CC > 85 ml/
for valve surgery, which in turn is less than that for minute), moderate (CC 50–85 ml/minute), severe
surgery of the thoracic aorta. Combined procedures (CC <50 ml/minute) and on dialysis (regardless of
like valve with CABG carry a higher risk than single CC). Interestingly, patients with severe dysfunction
procedures. but not on dialysis yet fare worst.

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Scoring Systems and Prognosis

Other Risk Factors Renal


These include peripheral vascular disease, neurologi- As preoperatively, the mainstay of renal function is
cal dysfunction, degree of urgency, diabetes, hyper- serum creatinine level as it is easily measured and a
tension and degree of pulmonary hypertension. In relatively inexpensive test; this variable can be used
addition, various scoring systems give weight to the to monitor changes in renal function and to compare
type of operation performed. current with preoperative function.

Postoperative Models Gastrointestinal/Hepatic
These models benefit from information that is only Both APACHE and SOFA use bilirubin levels as a
available after the completion of the operation, such as measure of liver function. APACHE is used more
the physiological parameters on admission to critical widely in general critical care units and includes
care. Many have been devised for critically ill patients many more variables, such as amylase, albumin (as a
outside the cardiac surgical specialty, but have been rough measure of nutritional status) and other liver
used and validated in cardiac surgery. The most well- function tests. The APACHE score also contains
known models are the Acute Physiology and Chronic variables to measure metabolic function and sep-
Health Evaluation (APACHE) and the Sequential tic status. These criteria are less relevant in cardiac
Organ Failure Assessment (SOFA) (Table  1). The surgery.
APACHE score is used on admission to critical care to
assess the risk of in-hospital death, whereas the SOFA
was developed to quantify the severity of a patient’s ill- Thoracic Surgery
ness using the degree of organ dysfunction at any one Risk modelling is not as developed in thoracic sur-
time. The BRiSc score is specifically aimed at predicting gery, although recently some attempts have been
patients likely to bleed excessively after heart surgery. made to produce models for predicting mortality
after lung resection. The most important risk fac-
tors associated with a poor outcome are age (older
Postoperative Model Risk Factors people do less well) and how much functioning
Postoperative risk scores look at each organ system lung remains long after the resection (the more, the
systematically and score according to derangement of better).
function. Basically, the more organ dysfunction, the
poorer the prognosis.
Learning Points
Respiratory • Many models help to predict the outcome of
Oxygenation and the requirement for ventilatory sup- cardiac surgery, and these can be applied before
port are used as measures of respiratory function. or after the operation.
• Preoperative models help in the decision
making, consent and assessment of clinical
Circulatory performance.
Most scores which are applied postoperatively use mean • Postoperative models can help to plan resource
arterial pressure as an easily measured and monitored use and provide information to relatives.
parameter. However, whereas APACHE concentrates
• Models devised specifically for mortality
on derangement of normal physiology, SOFA concen-
have also been found to be useful in predicting
trates on the need for (and level of) inotropic support.
major morbidity, resource use and long-term
outcomes.
Neurological • No amount of risk modelling can predict with
Trends are more useful than a snapshot at a particular certainty which patient will live and which
point in time, but the Glasgow Coma Scale is easily will die and they should be used as an adjunct
measured and provides an easily reproducible meas- rather than as a replacement for sound clinical
ure of neurological status. judgement.

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Scoring Systems and Prognosis

Table 1 Postoperative cardiac surgery risk assessment scores

Organ system SOFA APACHE


Respiratory Oxygenation (PaO2/FiO2) Respiratory rate non-ventilated
Respiratory support PaO2 with FiO2 1.0
PaCO2
Coagulation/haematological WCC WCC
Haematocrit
Platelet count
Prothrombin time
Circulatory Mean arterial pressure Mean arterial pressure
Dopamine dose Heart rate ventricular response
Adrenaline dose Central venous pressure
Norepinephrine dose Evidence of acute MI
Dobutamine use Arrhythmia
Serum lactate
Arterial pH
Neurological Glasgow Coma Scale Glasgow Coma Scale
Renal Creatinine Creatinine
Urine ouput/24 hour Urine output/24 hour
Blood urea nitrogen
Gastrointestinal/hepatic Bilirubin Amylase
Albumin
Bilirubin
Alkaline phosphatase
Liver enzymes
Anergy by skin testing
Septic Cerebrospinal fluid positive culture
Blood culture positive
Fungal culture positive
Rectal temperature
Metabolic Calcium level
Glucose
Sodium
Potassium
Bicarbonate
Serum osmolarity
Abbreviations: APACHE, Acute Physiology and Chronic Health Evaluation; FiO2, fraction of inspired oxygen; MI, myocardial infarction;
PaCO2, partial pressure of carbon dioxide in arterial blood; PaO2, partial pressure of oxygen in arterial blood; SOFA, Sequential Organ
Failure Assessment; WCC, white cell count.

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Scoring Systems and Prognosis

Nashef, SAM, Roques F, Sharples LD, et al. EuroSCORE


Further Reading II. European Journal of Cardio-Thoracic Surgery. 2012;
Arts D, de Keizer NF, Vroom MB, et al. Reliability and 41: 1–12.
accuracy of sequential organ failure assessment. Parsonnet V, Dean D, Bernstein AD. A method of uniform
Critical Care Medicine. 2005; 33: 1988–1993. stratification of risk for evaluating the results of
Knaus WA, Draper EA, Wagner DP, et al. APACHE II: a surgery in acquired adult heart disease. Circulation.
severity of disease classification system. Critical Care 1989; 79: 3–12.
Medicine. 1985; 13: 818–829. Vuylsteke A, Pagel C, Gerrard C, et al. The Papworth
Nashef S. The Naked Surgeon. The Power and Peril of Bleeding Risk Score: a stratification scheme for
Transparency in Medicine. London: Scribe, 2015. identifying cardiac surgery patients at risk of
Nashef SAM, Roques F, Michel PR, et al. European system excessive early postoperative bleeding. European
for cardiac operative risk evaluation (EuroSCORE). Journal of Cardio-Thoracic Surgery. 2011; 39:
European Journal of Cardio-Thoracic Surgery. 1999; 924–930.
16: 9–13.

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Abbreviations

AC  Assist-Control ventilation BLUE  Bedside Lung Ultrasound in


ACBT  Active Cycle of Breathing Technique Emergency
ACEI  Angiotensin Converting Enzyme BNP  B-type Natriuretic Peptide
Inhibitor BPF  Bronchopleural Fistula
ACLS  Advanced Cardiac Life Support BPS  Behavioural Pain Scale
ACT  Activated Clotting Time BTC  Bridge to Candidacy
AD  Advanced Directive BTS  British Thoracic Society
AEDs  Automated External Defibrillators BTT  Bridge to Transplant
AEG  Atrial Electrocardiogram BURP  Backwards, Upwards and Rightward
AEP  Auditory Evoked Potentials Pressure on the thyroid cartilage
AF  Atrial Fibrillation CABG  Coronary Artery Bypass Grafting
AFE  Amniotic Fluid Embolism CAM-ICU  Confusion Assessment Method for the
AKI  Acute Kidney Injury ICU
ALG  Anti-human Lymphocyte Globulin CAP  Community Acquired Pneumonia
ALS  Advanced Life Support CC  Creatinine Clearance
AMP  Adenosine Monophosphate CCA  Critical Care Area
APACHE  Acute Physiology and Chronic Health CCS  Canadian Cardiovascular Society
Evaluation ccTGA  Congenitally Corrected Transposition
APRV  Airway Pressure Release Ventilation of the Great Arteries
aPTT  Activated Partial Thromboplastin CCU  Coronary Care Unit
Time CDC  Centers for Disease Control
AR  Aortic Regurgitation cEEG  Continuous Electroencephalography
ARB  Angiotensin Receptor Blockers CF  Cystic Fibrosis
ARDS  Acute Respiratory Distress CHD  Congenital Heart Disease
Syndrome CHF  Congestive Heart Failure
ARF  Acute Respiratory Failure CICO  ‘Can’t Intubate, Can’t Oxygenate’
ASD  Atrial Septal Defect CIN  Contrast Induced Nephropathy
ATG  Anti-human Thymocyte Globulin CI  Cardiac Index
ATLS  Advanced Trauma Life Support CIS  Clinical Information Systems
AVNRT  Atrioventricular Node Re-entrant CK  Creatinine Kinase
Tachycardia CKD  Chronic Kidney Disease
AVSD  Atrioventricular Septal Defect CLABSI  Central Line Associated Bloodstream
BAL  Bronchoalveolar Lavage Infections
BALF  Bronchoalveolar Lavage Fluid CLAD  Chronic Lung Allograft Dysfunction
BIPAP  Biphasic or Bilevel Positive Airway CMR  Cardiac Magnetic Resonance
Pressure CMV  Continuous Mandatory Ventilation
BIPDs  Bilateral Independent PDs CMV  Cytomegalovirus
BIS  Bispectral Index CNI  Calcineurin Inhibitors
BiVAD  Bilateral Ventricular Assist Device CO  Cardiac Output
BLS  Basic Life Support

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Abbreviations

COAD  Chronic Obstructive Airways Disease, ELSO  Extracorporeal Life Support


same as COPD Organisation
COPD  Chronic Obstructive Pulmonary EMR  Electronic Medical Records
Disease ERP  Enhanced Recovery Programmes
CP  Constrictive Pericarditis ESBL  Extended Spectrum Beta-Lactamases
CPAP  Constant Positive Airway Pressure ESG  Endovascular stent graft
CPAx  Chelsea Critical Care Physical ETT  Endotracheal Tube
Assessment Tool EVLWI  Extravascular Lung Water Index
CPB  Cardiopulmonary Bypass EWMA  Exponentially Weighted Moving
CPE  Carbapenemase Producing Average
Enterobacteriaceae EWS  Early Warning Scores
CPOT  Critical Care Pain Observation Tool FAC  Fractional Area Change
CPP  Cerebral Perfusion Pressure FALLS  Fluid Administration Limited by Lung
CRP  C-Reactive Protein Sonography
CT  Computerised Tomography FAM  Functional Assessment Measure
CTCA  Computerised Tomography Coronary FB  Flexible Bronchoscopy
Angiogram FBC  Full Blood Count
CTEPH  Chronic Thromboembolic Pulmonary FDO2  Fraction of Oxygen Delivered
Hypertension FEV1  Forced Expiratory Volume for 1
CV  Stroke Volume second
CVC  Central Venous Catheter FFP  Fresh Frozen Plasma
CVD  Cardiovascular Disease FIM  Functional Independence Measure
CVP  Central Venous Pressure FIRDA  Frontal IRDA
CXR  Chest X-Ray FOUR  Full Outline of Unresponsiveness
DAG  1,2-Diacylglycerol FRC  Function of Residual Capacity
DBD  Donation after Brain Death FS  Fraction of Shortening
DBexs  Deep Breathing Exercises FVC  Forced Vital Capacity
DCD  Donation after Circulatory Death GBS  Guillain–Barré Syndrome
DD  Diastolic Dysfunction GCS  Glasgow Coma Score
DNAR  Do Not Attempt Resuscitation Order GEDVI  Global End-Diastolic Volume Index
DOLS  Deprivation of Liberty Safeguards GICS  Gastrointestinal Complication Score
DSI  Daily Sedation Interruption GPCR  G Protein Coupled Receptors
DT  Destination Therapy GUCH  Grown-Up Congenital Heart disease
DTI  Direct Thrombin Inhibitor HD  Haemodialysis
DVT  Deep Venous Thrombosis HDF  Haemodiafiltration
EACA  Epsilon Aminocaproic Acid HDU  High Dependency Unit
ECC  Emergency Cardiovascular Care HES  Hydroxyethil Starch
ECCO2R  Extracorporeal Carbon Dioxide HF  Haemofiltration
Removal HFV  High Frequency Ventilation
ECG  Electrocardiography HIT  Heparin Induced Thrombocytopenia
ECLS  Extracorporeal Life Support HIV  Human Immunodeficiency Virus
ECMO  Extracorporeal Membrane HLHS  Hypoplastic Left Heart Syndrome
Oxygenation HOCM  Hypertrophic Obstructive
ECPR  Extracorporeal Cardiopulmonary Cardiomyopathy
Resuscitation HSV  Herpes Simplex Virus
EDA  End-Diastolic Area HTEA  High Thoracic Epidural Analgesia
EEG  Electroencephalography IABP  Intra-aortic Balloon Pump
EF  Ejection Fraction ICD  Implantable
ELISA  Enzyme-Linked Immunosorbent Cardioverter-Defibrillators
Assay ICP  Intracranial Pressure

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Abbreviations

ICSD  Intensive Care Delirium Screening MDT  Multidisciplinary Team


Checklist MET  Medical Emergency Teams
ICU-AW  Intensive Care Unit Acquired MHI  Manual Hyperinflation
Weakness MI  Myocardial Infarction
IE  Infective Endocarditis MIC  Minimum Inhibitory Concentration
IJV  Internal Jugular Vein MMF  Mycophenolate Mofetil
IMCA  Independent Mental Capacity MMV  Mandatory Minute Ventilation
Advocate mPAP  Mean Pulmonary Arterial Pressure
IMV  Invasive Mechanical Ventilation MR  Mitral Regurgitation
INR  International Normalised Ratio MRSA  Methicillin Resistant Staphylococcus
INTERMACS Interagency Registry for Mechanically aureus
Assisted Circulatory Support MSE  Myoclonic Status Epilepticus
IPF  Idiopathic Pulmonary Fibrosis MSSA  Methicillin-Sensitive Staphylococcus
IR  Interventional Radiology aureus
IRDA  Intermittent Rhythmic Delta Activity mTOR  Mammalian Target of Rapamicin
IRV  Inversed Ratio Ventilation Inhibitors
IS  Incentive Spirometry MUST  Malnutrition Universal Screening Tool
ISHLT  International Society for Heart and MV  Mitral Valve
Lung Transplantation NAAT  Nucleic Acid-Based Amplification
ITBVI  Intrathoracic Blood Volume Index Technologies
IUGR  Intrauterine Growth Retardation NAP4  Fourth National Audit Project
IVC  Inferior Vena Cava NAVA Neurally Adjusted Ventilatory Assist
IVS  Interventricular Septum NCS  Non-convulsive Seizures
JET  Junctional Ectopic Tachycardia NCSE  Non-convulsive Status Epilepticus
LAD  Left Anterior Descending artery NHSBT  National Health Service Blood and
LAS  Lateral Amiotrophic Sclerosis Transfusion
LBBB  Left Bundle Branch Block NI  Narcotrend Index
LCx  Left Circumflex Artery NICE  National Institute for Clinical
LMA  Laryngeal Mask Airway Excellence
LMCA  Left Main Coronary Artery NIPPV  Non-invasive Positive Pressure
LMWH  Low Molecular Weight Heparin Ventilation
LTACH  Long-Term Acute Care Hospitals NIRS  Near Infrared Spectroscopy
LV  Left Ventricle NIV  Non-invasive Ventilation
LVAD  Left Ventricular Assist Device NMDA  N-Acetyl-D-Aspartate receptor
LVEDV  Left Ventricular End-Diastolic Volume NOAC  Newer Oral Anticoagulants
LVESV  Left Ventricular End-Systolic Volume NRS  Nutritional Risk Screening
LVOT  Left Ventricular Outflow Tract NVE  Native Valve Endocarditis
LVOTO  Left Ventricular Outflow Tract NYHA  New York Heart Association
Obstruction OD  Optical Density
LVSF  Left Ventricular Systolic Function OHCA  Out-of-Hospital Cardiac Arrest
MACE  Major Adverse Cardiac Events OIRDA  Occipital IRDA
MALDI Matrix Assisted Laser Desorption/ OpCAB  Off pump Coronary Artery Bypass
TOF MS Ionisation Time-of-Flight Mass PAC  Pulmonary Artery Catheter
Spectrometry PAH  Pulmonary Arterial Hypertension
MAO  Monoamine Oxydase PAP  Pulmonary Arterial Pressure
MAP  Mean Arterial Pressure PAWP  Pulmonary Arterial Wedge Pressure
MCCD  Mechanical Chest Compression PBM  Patient Blood Management
Devices PBW  Predicted Body Weight
MCFP  Mean Circulatory Filling Pressure PCAS  Post-Cardiac Arrest Syndrome
MDR  Multidrug Resistance PCI  Percutaneous Coronary Intervention

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Frontmatter
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xxxi

Abbreviations

PCP  Pneumocystis jirovecii Carinii ROTEM  Rotational Thromboelastometry


Pneumonia RRT  Renal Replacement Therapy
PCR  Polymerase Chain Reaction RV  Right Ventricle
PCT  Procalcitonin RVP  Right Ventricular Pressure
PCWP  Pulmonary Capillary Wedge Pressure RVAD  Right Ventricular Assist Device
PD  Peritoneal Dialysis RWMA  Regional Wall Motion Abnormalities
PDA  Posterior Descending Artery SACP  Selective Antegrade Cerebral
PDE  Phosphodiesterase Inhibitors Perfusion
PDR  Posterior Dominant Rhythm SAH  Subarachnoid Haemorrhage
PDs  Periodic Discharges SAM  Systolic Anterior Motion
PE  Pulmonary Embolism SAS  Sedation Agitation Scale
PEA  Pulmonary Endarterectomy SDD  Selective Digestive Decontamination
PEEP  Positive End Expiratory Pressure SE  Status Epilepticus
PF  Pulmonary Fibrosis SGA  Subjective Global Assessment
PF4  Platelet Factor 4 SIMV  Synchronised Intermittent Mandatory
PFIT  Physical Functional Intensive Care Ventilation
Test SLED  Slow Low-Efficiency Dialysis
PGD  Primary Graft Dysfunction SMR  Standardised Mortality Ratio
PH  Pulmonary Hypertension, same as SOFA  Sepsis Related Organ Failure
PAH Assessment
PKC  Protein Kinase C SR  Sarcoplasmic Reticulum
PLC  Phospholipase C SRA  Serotonin Release Assay
PPCs  Postoperative Pulmonary SSEP  Somatosensory Evoked Potentials
Complications SSRI  Selective Serotonin Reuptake Inhibitor
PPCI  Primary Percutaneous Coronary SVC  Superior Vena Cava
Intervention SVCS  Superior Vena Cava Syndrome
PPCM  Peripartum Cardiomyopathy SVR  Systemic Vascular Resistance
PPHN  Persistent Pulmonary Hypertension of TAA  Thoracic Aortic Aneurysm
the Newborn TAH  Total Artificial Heart
PPV  Pulse Pressure Variation TAPSE  Tricuspid Annular Plane Systolic
PRC  Post-resuscitation Care Excursion
PRES  Posterior Reversible Encephalopathy TAPVD  Total Anomalous Pulmonary Venous
Syndrome Drainage
PRVC  Pressure Regulated Volume TCPC  Total Cavopulmonary Connection
Controlled Ventilation TEG  Thromboelastography
PSI  Patient State Index TETS  Transcutaneous Energy Transfer
PT  Prothrombin Time Systems
PTE  Pulmonary Thromboendarterectomy, TEVAR  Thoracic Endovascular Aortic Repair
same as PEA TGA  Transposition of the Great Arteries
PTLD  Post-transplantation TnC  Troponin C
Lymphoproliferative Disorder TNF  Tumour Necrosis Factor
PVE  Prosthetic Valve Endocarditis TOE  Transoesophageal Echocardiography
PVR  Pulmonary Vascular Resistance TOF  Tetralogy of Fallot
RAP  Right Atrial Pressure TPG  Transpulmonary Gradient
RASS  Richmond Agitation Sedation Scale TR  Tricuspid Regurgitation
RBBB  Right Bundle Branch Block TRALI  Transfusion Related Lung Injury
RCM  Restrictive Cardiomyopathy TTE  Transthoracic Echocardiography or
RCT  Randomised Controlled Trial Thoracic Expansion Exercises as TTEs
ROC  Receiver Operating Characteristic TTM  Targeted Temperature Management
ROSC  Return of Spontaneous Circulation TXA  Tranexamic Acid

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Edited by Kamen Valchanov , Nicola Jones , Charles W. Hogue
Frontmatter
More Information
xxxi

Abbreviations

URR  Urea Reduction Ratio VT  Ventricular Tachycardia


VALI  Ventilator Associated Lung Injury VTI  Velocity-Time Integral
VAP  Ventilator Associated Pneumonia VTM  Viral Transport Media
VATS  Video Assisted Thoracic Surgery vWF  von Willebrand Factor
VF  Ventricular Fibrillation WCRS  Withdrawal of Cardiorespiratory
VHI  Ventilator Hyperinflation Supports
VRE  Vancomycin Resistant Enterococci WOB  Work of Breathing
VSD  Ventricular Septal Defect WPW  Wolff–Parkinson–White syndrome

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1

Section 1 Diagnosis

History and Examination


Chapter

1 Lachlan Miles and Joseph E Arrowsmith

The first rule of diagnosis, gentlemen!


Eyes: first and most; hands:  next and least; tongue:
History
not at all! The Conscious Patient
Sir Lancelot Spratt –​as played by James Robertson All available sources of information should be drawn
Justice upon to construct as detailed a history as possible.
In: Doctor in the House (1954, The J. Arthur Rank Where the patient is conscious and able to respond
Organisation) to direct questioning, this important primary source
of information should not be overlooked. Rather
than using ‘open’ questions and expecting them to
Introduction recount their entire current and past medical history
Patients may be admitted to the specialist cardio- in a concise fashion and in chronological order, it is
thoracic critical care unit from a variety of sources often easier to ask the patient to confirm previously
(Figure  1.1). In all elective admissions, and in the documented information and append newly acquired
majority of emergency admissions, a clinical his- information as necessary. When faced with an acutely
tory will already have been elicited and a physical unwell and possibly deteriorating patient, the skilled
examination performed  –​often more than once. intensivist needs to be able to quickly gather sufficient
Most patients will already have undergone exten- information to aid diagnosis and guide management.
sive investigation or therapeutic intervention, and Of particular importance is the patient’s understand-
the underlying diagnosis or diagnoses will have ing of their medical condition, their insight into treat-
been established. Despite this seemingly ideal situ- ment options and prognosis, and their expectations.
ation, the cardiothoracic intensivist should adopt an Corroborative history from family and carers is also
inquisitive attitude and use the so-​called ‘history and invaluable, especially in the setting of acute delirium
physical examination’ to confirm previous findings, or dementia, where the patient’s own account may be
assess disease progression and exclude new path- unreliable. This information should be solicited and
ology. Contrary to popular belief, this is often the documented whenever possible.
most efficient and effective means of predicting and Symptoms of cardiorespiratory disease (e.g.
detecting significant comorbid conditions. Clinical angina pectoris, dyspnoea, orthopnoea, syncope, pal-
investigations should therefore be considered an pitations, ankle swelling, etc.) (Table  1.2) should be
adjunct to, rather than a substitute for, basic medical actively sought, as should any recent progression in
assessment. symptom severity. Symptoms should be described in
In the critical care setting, particularly when a terms of their nature (using the patient’s own words),
patient is physiologically unstable or has reduced con- onset, duration, progression, modifying factors and
sciousness, the conventional stepwise approach to the associations. The impact of symptoms on functional
history and physical examination will usually require status should be documented using the New  York
modification (Table  1.1). Indeed it may have to be Heart Association (NYHA) classification and the
conducted during or after initial resuscitation. Canadian Cardiovascular Society (CCS) angina scale.

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Section 1: Diagnosis

Table 1.1  Modification of conventional history and physical for use in critical care

Conventional Critical care


History of presenting complaint Handover information
Past medical history Review of medical notes
Past surgical/​anaesthetic history Information from family members
Drug history, allergies, sensitivities
Recreational substance (mis)use
Educational level/​native language
History
Social/​employment history
Religious/​cultural beliefs
Family history
Systematic enquiry
Sensory impairments
Review of medical notes
Patient supine –​reclining at 45° Patient supine, lateral or prone
Cardiovascular ABC (Airway, Breathing, Circulation)
Respiratory Lines, tubes, drains and catheters
Physical Gastrointestinal Drug and fluid infusions
Genitourinary Ongoing physiological monitoring
Neurological Anatomical examination
Integument

Airway Intervention Operating Room Emergency


(Bronchoscopy) Suite Department

Critical
External Care High Dependency Unit
Community Unit /Stepdown Unit
Other hospital

Radiology Department Ward/Floor


(Coronary, structural,
electrophysiological)

Figure 1.1  Cardiothoracic critical care admission sources.

Enquiry into the patient’s past medical history respect to the unintubated patient who may require
should include coexisting conditions, previous hospital intervention during their stay, and the patient who is
admissions, surgical procedures and complications, already intubated who will require extubation before
prolonged hospitalisation and unplanned admissions discharge to the ward. Factors known to be associated
to a critical care unit. It is important to note the indi- with increased mortality and morbidity (e.g. con-
cation for any surgical procedure or therapeutic inter- gestive cardiac failure, peripheral vascular disease,
vention (e.g. splenectomy, permanent pacemaker, renal insufficiency, arterial hypertension, pulmonary
angioplasty), the outcome of the procedure and any hypertension, diabetes mellitus, chronic pulmonary
anaesthetic related morbidity. A  history of difficult disease, neurological disease and previous cardiovas-
tracheal intubation is of particular note, both with cular surgery) should be documented.

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Chapter 1: History and Examination

Table 1.2  Common symptoms associated with Where adherence to a particular cultural or reli-
cardiorespiratory conditions gious belief system (e.g. Jehovah’s Witnesses) has
Cardiovascular Respiratory the potential to influence any aspect of critical care
Syncope Recent overseas travel
management, this should be comprehensively docu-
mented. In some instances it may be appropriate to
Chest pain Fever and/​or rigors
explore and document a patient’s specific wishes in a
Fatigue or exercise Facial or sinus pain
number of hypothetical clinical scenarios, including
intolerance
limits of care. It is often preferable that limits of care
Exertional dyspnoea Chest pain
be discussed with the patient and family early on in the
Paroxysmal nocturnal Cough
critical care stay, rather than late in the course of the
dyspnoea
illness when the patient is in extremis. It is important
Orthopnoea Sputum production (volume,
that both the patient and the family have a realistic
time course, purulence)
understanding of what intensive care can offer, rather
Palpitations Haemoptysis
than relying on preconceived ideas.
Intermittent claudication or Dyspnoea
ischaemic rest pain
Stroke or transient Exercise intolerance
The Unconscious Patient
ischaemic attack The unconscious, critically unwell patient represents a
Cough or sputum History of bird keeping, special challenge for any clinician. From a cardiothor-
production asbestos exposure, or other acic point of view, such patients cover a wide range of
sources of occupational lung potential presentations, including, but not limited to
disease
the following:
Peripheral oedema
• A patient transferred from the operating theatre
or catheter laboratory following an invasive
procedure;
Where the patient has been admitted following a
diagnostic or therapeutic intervention (e.g. coronary • A patient admitted following out-​of-​hospital
angiography or angioplasty), a comprehensive medical cardiac arrest, via either the catheter laboratory or
and nursing ‘handover’ is essential. This is particularly the emergency department;
important when the patient has been brought to hospital • A patient requiring ongoing organ support
by emergency ambulance and taken directly to the angi- following an interventional cardiology or
ography suite. Similarly, when a patient is transferred bronchoscopic intervention; and
from another hospital for specialist cardiothoracic care • A ward patient who has physiologically
(e.g. surgical repair of acute type A  aortic dissection), deteriorated and requires more advanced
a formal handover of clinical information and docu- treatment modalities or resuscitation.
mentation is an absolute prerequisite for the transfer of When reviewing an obtunded patient the clinician
clinical responsibility and for safe ongoing care. In many is deprived of many of the usual visual and auditory
areas a formal handover document or aide memoire is clues that guide patient assessment, forcing the use of
used both to guide and to document the comprehensive alternative sources of information. Family members
handover of clinically relevant information. and carers are often the key source of information
It is essential to record current and recent pre- regarding recent symptoms, and it is often possible to
scription drug administration, including formula- establish the temporal course of the presenting com-
tion, dosage and route of administration. In addition, plaint with thorough questioning. In many respects,
the medication history should include drugs taken it is often possible to obtain a full history, provided
‘as required’, proprietary or ‘over-​the-​counter’ medi- that the right questions are asked, and an open mind
cines, complimentary or alternative therapies, and maintained.
recreational drugs. This latter category should include A thorough review of the medical record is also
alcohol and tobacco products. A  history of allergic invaluable when the patient is not able to speak for
or other idiosyncratic reaction to a specific drug (e.g. him or herself. Written correspondence from other
suxamethonium) or class of drugs (e.g. penicillins) clinicians (e.g. surgeons, cardiologists, respiratory
should be sought and documented. physicians, general practitioners) will answer many

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Section 1: Diagnosis

questions regarding the course of illness leading up The postoperative cardiac or thoracic surgical
to admission. Where questions remain unanswered patient will have a variable number of mediastinal and
regarding the previous clinical course, direct commu- pleural drains in situ. The volume of blood in these
nication with these sources is encouraged, not only to should be recorded so that an accurate estimation of
obtain further information, but as a matter of courtesy any ongoing blood loss can be made. An air leak may
regarding the condition of their patient. also be present when pleural drains are on suction, and
the magnitude and respiratory phase of this should be
Physical Examination judged. Where epicardial pacing wires are present,
their function should be confirmed. If in use, external
The Conscious Patient pacing should be converted from fixed rate mode to
Whilst a comprehensive physical examination is some- demand mode, with an appropriate backup rate.
times not possible given the limitations that reception
and resuscitation of the critically ill patient places on The Hands and Arms
assessment, a full physical examination should never- Examination of the hands reveals much about the
theless be attempted. There is also a frequent tempta- circulatory state of the patient. Cold and shut down
tion for the clinician to rely on the battery of monitors extremities with delayed capillary return may suggest
that an intensive care admission entails, especially a high degree of systemic vascular resistance, usually
during daily review of the patient, or to perform an because of hypovolaemia or low cardiac output state,
investigation rather than seek clinical findings. This is or alternatively, an acutely ischaemic limb. In con-
a fallacy, as even an abbreviated physical examination trast, warm peripheries suggest a normal or high car-
during a ward round may reveal a finding (e.g. bron- diac output state. Finger clubbing may be indicative of
chial breathing) that may take hours to manifest as chronic cardiorespiratory disease, notably congenital,
worsening hypoxia or increasing oxygen requirement, cyanotic heart disease, non-​small-​cell lung cancer and
permitting early investigation and intervention. suppurative lung conditions such as cystic fibrosis or
bronchiectasis.
General Inspection The peripheral pulses can give clues to the presence
This should initially be undertaken from the end of of significant valvulopathy (e.g. the ‘water hammer’
the bed, so as to better appreciate the overall Gestalt. pulse of severe aortic regurgitation) and regional per-
The initial focus should be on the patient. Central or fusion abnormalities, particularly in aortic dissection
peripheral cyanosis may be evident in the setting of (i.e. radioradial and radiofemoral delay). Inspection
hypoxaemia or shunting. The patient posture pro- of the palmar creases was popularised for the esti-
vides many important clues, especially when assessing mation of plasma haemoglobin concentration, but
respiratory effort. Pursed lip breathing to increase end-​ has subsequently proven to be unreliable. Rarely, the
expiratory pressure and a ‘tripod’ position with the immunological and embolic phenomena of infective
shoulders rotated forward and the hands on the lower endocarditis (Janeway lesions and Osler’s nodes) may
extremity to engage the accessory muscles are evidence be evident.
of respiratory distress. Attention should then be turned
to the various drug infusions being administered, the The Neck
relevant concentration, rate and route of administra- Neck examination in the critical care environment
tion. Peripheral and central venous access should be is often difficult, due to the presence of indwelling
noted and recorded including available lumens for jugular venous catheters. In the event that the neck
other medications and the size of each catheter if the is unencumbered, examination of the jugular venous
administration of volume is required. Invasive moni- waveform can be used to assess right atrial filling and
toring (e.g. arterial line, pulmonary artery catheter), compliance, atrioventricular dissociation (cannon a-​
circulatory support devices (intra-​ aortic balloon waves) and torrential tricuspid regurgitation (massive
pump, ventricular assist device and extracorporeal cv-​waves). These abnormalities are also visible on the
circuits) and renal replacement therapy should also be central venous waveform if invasive monitoring is
evaluated. An indwelling urinary catheter may be pre- present.
sent, and if so, the volume and concentration of urine If pericardial tamponade is suspected, an early
in the drainage bag should be noted. sign of compromise is an increase in right atrial

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Chapter 1: History and Examination

pressure on deep inspiration (Kussmaul’s sign). If the and dorsalis pedis pulses should be sought, particu-
patient’s trachea is not intubated, it is wise to conduct larly if the femoral vessels have been used for arterial
an airway assessment at this juncture if not already access. Whilst a rare event, acute lower limb ischaemia
performed. Auscultation of the carotid arteries may is a recognised complication of a wide range of inva-
reveal bruits consistent with turbulent flow if there is a sive devices, in particular peripheral venoarterial
substantial atheroma burden, or the referred murmur ECMO cannulae and the intra-​aortic balloon pump.
of aortic stenosis. It is important to note that even if a distal reperfu-
sion line is incorporated into an ECMO circuit, distal
The Praecordium pulses may be absent. However, the limb should feel
As for other parts of the body, and as alluded to in the warm and well perfused or, at the very least, similar to
starting quotation, examination of the chest should its counterpart.
follow the traditional route of observation, palpation, Deep venous thrombosis is a common compli-
percussion and auscultation. Ideally, both the anterior cation in many postoperative patients, and whilst
and posterior chest should be examined, as the lower at least half of these are completely asymptomatic,
lobes of the lung (particularly on the left) can take up the remainder may exhibit the classical signs of calf
much of the posterior aspect, preventing examination tenderness, swelling, distended superficial veins
of the other lobes if the anterior chest is not examined. and warmth. The traditional test for this condition,
The often high volume of ambient noise in the critical Homan’s sign (rapid passive dorsiflexion of the ankle
care environment may make ausculation challenging. with the aim of causing pain in the calf), is no longer
Subtle abnormalities may be missed, and seemingly recommended because of the risk of clot fragmenta-
positive findings may be misinterpreted. It is wise to tion and acute pulmonary embolism.
correlate findings not consistent with the overall con- Finally, the presence and extent of any peripheral
dition of the patient with appropriate investigation. oedema should be assessed. Oedema is, by definition,
Radiological investigation and bedside modalities an excess of interstitial fluid, and therefore must be the
such as ultrasound and transthoracic echocardiog- result of a derangement of the Starling forces across
raphy are valuable for this purpose. the microcirculation (increased capillary hydrostatic
pressure, decreased plasma colloid oncotic pressure,
The Abdomen increased capillary permeability or deranged lymph-
Initially, at least, the abdomen is rarely a focus in the atic drainage).
cardiothoracic critical care unit. Interest in this region
is limited largely to distension and the presence of
bowel sounds or the absence thereof. However, small The Unconscious Patient
or large bowel ischaemia is a not uncommon phenom- As for history, the physical examination of the uncon-
enon following cardiac surgery, as a result of a low scious individual is hindered by the lack of patient
cardiac output state, embolic phenomenon or use of participation. Nevertheless, such an examination
intra-​aortic balloon counterpulsation. A high index of should always be undertaken with the same care as
suspicion is required for this condition, particularly in if the patient were awake and fully conscious. The
the setting of an unexplained lactataemia and wors- presence of the mechanical ventilator at the bedside
ening acidosis, despite the presence of a seemingly increases the ambient noise level, further impairing
adequate cardiac output. The opportunity should be the ability of the clinician to auscultate. Heavy sed-
taken at this point to assess the back of the patient for ation or neuromuscular blockade naturally prevents
sacral oedema, as this is the most dependent point in patient movement, and simple tasks such as leaning
the semirecumbent patient, and is an important find- the patient forward to auscultate the chest are impos-
ing when assessing volume status. sible. Nevertheless, an attempt should be made, as
much valuable information can still be gained, par-
The Legs ticularly with respect to tissue perfusion.
An assessment of the legs completes the examination. As for physical examination in the conscious
Like the hands, the lower extremities reveal much patient, assessment of the unconscious patient should
about perfusion status, thus capillary refill and skin follow in the same stepwise fashion. Many of the same
temperature should be assessed. The posterior tibial clinical features may be found on careful inspection.

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Section 1: Diagnosis

Caution should be taken during joint manipulation and examination. Whilst cardiothoracic critical care
and palpation. The patient will not be able to report requires a different skill set to that of the emergency
discomfort or resist painful movements, and tissue department or ward, the temptation to forgo the basic
damage may result if the examiner is overly rough. diagnostic process must be resisted, as history and
Examination of the abdomen in the unconscious examination findings serve to clarify the clinical scen-
patient is considerably confounded, especially in the ario and highlight evolving problems that monitoring
setting of neuromuscular blockade. This is because the may not detect for some time. Furthermore, history
early features of gut ischaemia or peritonism will be and physical examination allow appropriate targeting
absent, partly because the patient is unable to report of investigations, minimising patient discomfort and
discomfort, but also because of a lack of abdominal unnecessary cost to the health system.
muscle tone. As a result, the early features of guard-
ing and tenderness to percussion (formerly tested as Learning Points
‘rebound tenderness’) are absent. Consequently,
• The cardiothoracic intensivist should adopt an
abdominal distension, free gas under the diaphragm
inquisitive approach to history and physical
and a rising lactate in the setting of apparently
examination so as to confirm previous findings,
adequate cardiac output may be the only features of
assess disease progression and exclude new
a major intra-​abdominal pathology. A  high index of
pathology.
suspicion must be maintained as a result.
Daily assessment of the unconscious patient • It can be challenging to elicit a history and
should also include a brief neurological examination. undertake a physical examination in the critically
Naturally, a full assessment of muscle power cannot ill patient and it may be necessary to modify the
be undertaken, but a brief examination for features of conventional stepwise approach.
an upper motor neurone lesion such as hypertonia, • Advanced monitoring modalities are prone to
hyperreflexia and clonus (in the absence of neuromus- artefact and incorrect interpretation and should
cular blockade) can be quickly and easily performed. not be seen as a substitute for a thorough history
As described in detail in Chapter  16, on sedation and physical examination.
and analgesia, the indications for deep sedation and • On admission/​discharge from cardiothoracic
neuromuscular blockade are becoming fewer as car- critical care a formal handover of clinical
diothoracic critical care evolves, and targeted sed- information is an absolute prerequisite for
ation and sedation breaks are increasingly de rigueur. continuity of care.
Conscious state can be graded with any number of • It may be necessary to explore and document
specialist sedation scores, which are beyond the scope a patient’s specific wishes in a number of
of this c­hapter  –​however, response to approach, hypothetical clinical scenarios so as to inform
voice and pain should be assessed. A  variety of dif- decision making should the patient deteriorate.
ferent techniques have been described to evaluate
response to painful stimulus. However, firm pressure Further Reading
over the superior orbital notch is usually the most Arrowsmith JE. Symptoms and signs of cardiac
unambiguous means of assessing global response, disease. In: Mackay JH, Arrowsmith JE (Eds).
as peripheral stimulation may not give an accurate Core Topics in Cardiac Anesthesia, 2nd Edition.
assessment of localisation if a hemiplegia is present. Cambridge: Cambridge University Press, 2012,
Likewise, withdrawal to stimulation, decerebrate and pp. 75–​80.
decorticate posturing can be difficult to assess when Campeau L. Grading of angina pectoris. Circulation. 1976;
the focus point is on the hand or foot. 54: 522–​523.
Criteria Committee of the New York Heart Association.
Conclusions Nomenclature and Criteria for Diagnosis of Diseases
of the Heart and Great Vessels, 9th Edition. Boston,
The presence of advanced monitoring modalities and MA: Little Brown & Co, 1994, pp. 253–​256.
ready access to bedside investigations, combined with Glynn M, Drake WM (Eds). Hutchison’s Clinical
difficult examination conditions, are all powerful moti- Methods: An Integrated Approach to Clinical Practice.
vators to de-​emphasise the traditional focus on history Oxford: Saunders, 2012.

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Section 1 Diagnosis

Electrocardiography
Chapter

2 David Begley

Introduction Precordial (Chest) Electrodes


Electrocardiography (ECG) has been the main heart Most errors occur in placement of the chest electrodes,
investigation method for most of the twentieth cen- especially V1 and V2, which may be placed too high.
tury and still plays a pivotal role in diagnostics. ECGs This can have a significant effect on the resultant ECG.
can provide a wealth of information about cardiac Correct anatomical positioning must be adhered to,
function and can often show early signs of systemic with the centre of the electrode aligned with the cor-
abnormalities as well. In order to accurately inter- rect location.
pret an ECG it is important to first ensure its correct • V1 (C1)  fourth intercostal space, right sternal
acquisition. The process involves recording small edge
electrical changes on the skin that occur as a result • V2 (C2)  fourth intercostal space, left sternal
of cardiac muscle depolarisation. Ten electrodes are edge
used to record the heart’s electrical activity in 12 dif-
• V3 (C3)  midway between V2 and V4
ferent orientations, which encompass the 12 ‘leads’ of
• V4 (C4)  fifth intercostal space, midclavicular
the ECG. It is important therefore to ensure that these
line
10 electrodes are consistently applied in order to
accurately assess for any abnormalities. In addition, • V5 (C5)  horizontal level with V4, anterior
account must be made of sources of interference. axillary line
• V6 (C6)  horizontal level with V4, midaxillary
line
Recording the ECG After placement of V1 and V2, V4 is located in the fifth
As posture may affect the appearance of the ECG it
intercostal space, midclavicular line. V3 is then placed
is preferably performed in the supine position where
directly in between V2 and V4. V5 and V6 are located at
practicable. Skin preparation is important to reduce
the same horizontal level as V4, perpendicular to the
artefacts and may include hair removal and/​or skin
midclavicular line.
cleansing.

Limb Electrodes Filter Settings and Calibration


Most filter settings are set by default but it is recom-
Moving the limb electrodes away from the distal
mended that the low frequency filter is set on or below
limbs may affect the ECG appearance and it is there-
0.05 Hz. This filter will account for respiration. If it is
fore preferable that these are placed just proximal to
set too high, it will distort the ST segment. This may
the wrists and ankles in order to produce consistent
also reduce the accuracy of detecting myocardial
results. Limb electrodes are often colour coded to aid
ischaemia based on ST segment shifts. The high filter
placement.
setting should be set on or above 100 Hz. This filter set-
• Right arm  (RA, red)   proximal to right wrist ting should account for the artefact created by muscle
• Left arm   (LA, yellow)    proximal to left wrist tremor. The mains filter (50 Hz) is normally set to ‘Off ’.
• Left leg   (LL, green)    proximal to left ankle A standard ECG has a voltage calibration of
• Right leg   (RL, black)    proximal to right ankle 10  mm/​mV and is recorded with a paper speed of

13:37:33 7
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Section 1: Diagnosis

25  mm/​s. This results in 10 second recording. Each –90°


small square is equal to 40 ms and each large square (5
small squares) is equal to 200 ms.

The 12 ‘Lead’ ECG
aVR –150° aVL –30°
The 12  ‘leads’ of an ECG correspond to 12 vec-
tors along which depolarisation of cardiac tissue is
recorded. Each is created by measuring the electrical
potential between two points. In each case one of the
±180° I 0°
ten electrodes is the positive pole. There are three
bipolar limb leads where another electrode is the
negative pole. The negative pole for the unipolar limb
leads and the precordial leads is a composite pole
(VW) called Wilson’s central terminus, which is cre-
ated by averaging the potential recorded by RA, LA
and LL electrodes: III +120° II +60°

VW = 1/​3 (RA + LA + LL). aVF +90°

The six limb leads view the heart in the coronal (ver- Figure 2.1  Hexaxial reference system.
tical) plane while the six precordial leads view the
heart in a perpendicular transverse (horizontal) plane. The vectors created by the bipolar and augmented limb
leads together form the hexaxial reference system (see
Bipolar Limb Leads Figure 2.1).
• Lead I is the potential difference between
LA and RA, Precordial Leads
I = LA –​ RA. For each of the precordial leads the positive pole
is the corresponding electrode and the negative pole
• Lead II is the potential difference between
is VW.
LL and RA,
II = LL –​ RA.
ECG Arrangement
• Lead III is the potential difference between A standard ECG records a 2.5 second tracing of each
LL and LA, lead arranged in a grid of four columns and three
III = LL –​ LA. rows. A marker depicts the change from one lead to
the next in each row and can be confused with part
Unipolar Augmented Limb Leads of the ECG. The first column contains leads I, II and
III, the second column aVR, aVL and aVF, the third
• Lead aVR is the potential difference between column V1, V2 and V3 and the final column contains
RA and Vw, leads V4, V5 and V6. A fourth row is often provided as
aVR = 3/​2 (RA –​ VW). a continuous tracing to aid determination of rhythm.
• Lead aVL is the potential difference between Although each lead records electrical activity of
LA and Vw , the heart from a different angle, contiguous leads are
associated with different anatomical regions.
aVL = 3/​2 (LA –​ VW).
• Inferior leads      II, III and aVF
• Lead aVF is the potential difference between • V3 and V4
Anterior leads       
LL and Vw , • Septal leads         
V1 and V2
aVF = 3/​2 (LL –​ VW). • Lateral leads     I, aVL, V5 and V6

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9

Chapter 2: Electrocardiography

Interpretation of the ECG of which are perfect. Most commonly used is the


Sokolow–​Lyon index:
Waves and Intervals • S wave in V1 + R wave in V5 or V6 (whichever
largest) > 3.5 mV.
P Wave
There is a large S wave in lead V1, which gradually
The P wave (see Figure 2.2) represents depolarisation becomes smaller (absent) by lead V6. Its presence or
of the right and left atria. In normal sinus rhythm, its absence is rarely of clinical significance.
origins are from the sinus node, which is normally
located posteriorly high in the right atrium. Therefore, J Point
the P wave is positive (upright) in all leads except aVR, The J point is the junction between the QRS complex
and can be positive or biphasic in V1. It typically has and the subsequent ST segment. Elevation or abnor-
duration <80 ms. malities of the J point are frequently seen and their
In right atrial enlargement, the P wave is tall significance is debated. Elevation of the J point is
and peaked, and is prolonged and bifid in left atrial observed in hypothermia.
enlargement.
ST Segment
PR Interval The ST segment is the section between the end of the
The PR interval is measured from the beginning of QRS complex (J point) and the T wave. It is typically
the P wave to the beginning of the QRS complex and isoelectric and represents the period of time when the
represents the time taken for atrial depolarisation ventricles remain depolarised prior to repolarisation. If
and conduction through the AV node. A normal PR the ST segment is down sloping or depressed, this may
interval varies between 120 and 200 ms. indicate myocardial ischaemia. ST segment elevation,
If the PR interval is shorter than 120 ms then taken as more than 1 mm, 80 ms following the J point,
conduction is bypassing the AV node (see Wolf–​ may indicate myocardial infarction but has a false posi-
Parkinson–​White syndrome). Prolongation of the PR tive rate between 15 and 20% (even slightly higher in
interval indicates 1° AV block. Depression of the short women). Abnormalities of the ST segment can also
isoelectric segment between the end of the P wave occur in pericarditis and left ventricular hypertrophy.
and the beginning of the QRS complex can indicate
pericarditis. T Wave
The T wave represents ventricular repolarisation. It
QRS Complex is typically positive in all leads except aVR and V1.
Q, R and S waves form the QRS complex, which rep- A  variety of situations can result in T wave abnor-
resents ventricular depolarisation. If the first deflec- malities, which are often non-​ specific. Myocardial
tion is negative it is termed the Q wave, otherwise an ischaemia and left ventricular hypertrophy can result
initial positive deflection is an R wave. A final nega- in T wave inversion. Metabolic abnormalities can also
tive deflection is the S wave. Normally the whole QRS manifest as T wave abnormalities.
complex is <120 ms in duration. Q waves represent
left to right depolarisation of the interventricular U Wave
septum and are typically seen in left sided leads (I, The U wave is poorly understood but may represent
aVL, V5 and V6). Small Q waves can be seen in most repolarisation of the interventricular septum or pap-
leads except V1, V2 and V3. illary muscles and therefore can be observed on the
Large Q waves are pathological if >40 ms wide, normal ECG, although their absence is not patho-
and >2  mm deep or >25% of the height of the QRS logical. Prominent U waves are observed in hypokal-
complex. This can represent myocardial infarction, aemia and hypothyroidism.
cardiomyopathy or electrode malposition.
If the QRS complex is particularly tall this may QT Interval
indicate left ventricular hypertrophy. A  number of The QT interval is measured from the beginning of
criteria have been developed to aid diagnosis, none the QRS complex to the end of the T wave. There are

13:37:33 9
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10

Section 1: Diagnosis

-QRS Width-

ST
-PR Interval- - -
Segment

T
P

-QT Interval-

Figure 2.2  PQRST intervals.

several issues regarding its measurement, not least the result of a genetic abnormality or due to a variety
determining where the T wave ends. The best lead of medications.
to measure the QT interval is lead V3 or II. Several
consecutive beats should be measured with the long-
est value taken. Prominent U waves are not normally
Rate and Rhythm
included in the calculation and the end of the T wave Heart Rate
is then assumed to be where the downslope of the T The heart rate is most accurately obtained by dividing
wave would cross the isoelectric line. If depolarisation the cycle length (RR interval) into 60,000. However,
is prolonged, the difference between the measured this is more easily achieved by dividing the number
QRS complex and 120 ms should be subtracted from of large squares on a standard ECG between succes-
the measured QT interval. sive QRS complexes into 300. These formulae work
Because of the close relationship of the QT interval well provided the rhythm is regular. However, if the
and heart rate (the QT shortens with increasing heart rhythm is irregular then we can take advantage of
rate), a correction factor must be applied. Although the fact that the ECG is recorded over 10 seconds.
many methods have been developed to calculate a cor- Counting the number of QRS complexes across the
rected QT (QTc), the one most widely used is Bazett’s ECG and multiplying by 6 will give an estimate of the
formula: heart rate.
QTc = QT / √RR interval.
Rhythm
The RR interval is measured in seconds such that at a The presence of P waves on their own does not indi-
heart rate of 60 bpm the RR interval is 1, and QTc = QT. cate sinus rhythm. It is important to ensure that their
The QTc is typically less than 440 ms. Gender, how- morphology (as discussed earlier) is consistent with an
ever, also has an effect on QTc and therefore a value of origin from the sinus node. A disparate morphology
less than 460 ms is acceptable for women. might indicate an ectopic atrial origin and prompt
An abnormally prolonged QTc can predispose to closer scrutiny. If the P wave is not clear on the surface
malignant ventricular arrhythmias. A long QT can be ECG then, post cardiac surgery, the temporary atrial

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11

Chapter 2: Electrocardiography

Lead I +ve

Lead II –ve

aVL Left Axis aVL


aVR aVR
Deviation
Lead I +ve

I I

Normal
Axis

III II III II
aVF aVF
Lead II +ve

Lead II –ve
(aVF –ve)
Lead I –ve

aVR aVL aVR Indeterminate aVL


Axis

I I

Right Axis
Deviation

Lead I –ve

III II III II
aVF Lead II +ve aVF
(aVF +ve)

Figure 2.3  Mean frontal axis.

pacemaker wires can be used to create an atrial elec- block). A  normal QRS axis is usually between −30°
trocardiogram (AEG). This is recorded by connect- and +90°.
ing the atrial pacing wires to the left and right arm The mean frontal axis provides a mean electrical
leads, or to one of the precordial chest leads, and may ventricular depolarisation vector in two dimensions
be useful in differentiating various tachy and brady only. The QRS transition provides an indication of the
arrhythmias. ventricular depolarisation in the third dimension (z
axis). The QRS transition is determined from the pre-
Axis and QRS Transition cordial leads. The QRS complex in lead V1 is usually
negative and gradually becomes more positive through
The mean frontal axis (Figure 2.3) of the heart pro-
V6. The transition zone is where the QRS changes from
vides an average electrical axis (vector) of ventricular
being predominantly negative to being predominantly
depolarisation. Any deviation from a normal axis may
positive. This usually occurs at V3 or V4.
indicate pathology. This may be in the form of struc-
tural abnormalities (i.e. increased muscle mass –​left
ventricular hypertrophy or loss of muscle mass –​fol- Calculating the QRS Axis
lowing myocardial infarction) or electrical abnormal- To estimate the QRS axis we focus solely on the limb
ities (i.e. accessory AV connections or bundle branch leads (not V1–​V6) and use the fact that depolarisation

13:37:33 11
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12

Section 1: Diagnosis

towards any lead will provide a positive deflection in left anterior fascicle results in left axis deviation and
that lead. less marked widening of the QRS complex. This is
If lead I is positive, the axis must lie between −90° called left anterior hemiblock (LAHB). A qR com-
and +90°. If lead II is negative, then the axis is between plex is observed in lateral leads I  and aVL, and rS
−30° and −240°. Together the axis must be between pattern in the inferior leads II, III and aVF. Due to
−30° and −90°. This is left axis deviation. its broad nature and dual blood supply, left posterior
If lead I  is negative, the axis must lie between hemiblock (LPHB) is much less common. It is charac-
−90° and −270°. If lead aVF is positive, the axis must terised by right axis deviation, a rS complex in lateral
be between 0° and 180°. Together the axis must be leads and qR complex in inferior leads.
between −90° and 180°. This is right axis deviation.
If lead I  is negative and lead aVF is negative, AV Block
then the axis lies between −90° and 180°. This is an When conduction between the atria and ventricles
indeterminate axis. is impaired, AV block is said to be present. If the PR
interval is prolonged beyond 200 ms but each P wave
Arrhythmias remains associated with a single QRS complex, 1° AV
block is present.
Conduction Abnormalities Progressive beat-​to-​beat prolongation of the PR
interval with the final beat not conducting to the
Bundle Branch Block ventricles is Mobitz 1 2° AV block (Wenckebach
Electrical impulses transmitted through the AV node phenomenon). However, if the PR interval remains
and bundle of His are conducted to the ventricular unchanged prior to loss of conduction to the ventri-
myocytes via the left and right bundles. cles then Mobitz 2 2° AV block is present.
The right bundle remains sheathed in connective When there is complete dissociation between
tissue within the septum until it reaches the base of the atrial and ventricular depolarisation (i.e. no associ-
papillary muscle when it divides into multiple fibres ation between P waves and QRS complexes) 3° AV
connecting with the Purkinje fibres. The left bundle block is present.
however divides immediately into anterior and pos-
terior fascicles supplying Purkinje fibres within the Tachyarrhythmias
left ventricle.
Supraventricular Arrhythmias
Right bundle branch block (RBBB) occurs when Atrial flutter: Atrial flutter refers to any macro re-​
there is loss of conduction through the right bundle entrant rhythm within the atria. Typical atrial flutter
branch. The left ventricle is excited normally by the is a right atrial rhythm where depolarisation occurs
left bundle branch but the right ventricle is depolar- continuously, usually in a counterclockwise fashion,
ised via conduction through the myocardium from around the tricuspid valve. The AV node will conduct
the left ventricle. As a result, ventricular depolarisa- at a variable rate depending on other factors such as
tion is prolonged and there is an extra deflection indi- concomitant medication etc. The resultant ECG dem-
cated by rapid left ventricular depolarisation followed onstrates a continuously cycling baseline between QRS
by slower right ventricular depolarisation. A QRS dur- complexes. These ‘flutter’ waves have a slow phase and
ation >100 ms indicates incomplete block and a dur- a fast phase, are negative in the inferior leads, positive
ation >120 ms indicates complete block. A  terminal in lead V1 and isoelectric in lead I  which is perpen-
R wave is observed in lead V1 (rsRʹ) and a slurred S dicular to the re-​entrant circuit.
wave in leads I and V6. The T wave should be deflected
opposite the terminal deflection of the QRS complex. Atrial fibrillation (AF): Although theories regarding
Right bundle branch block can be observed in normal the exact mechanisms responsible for atrial fibrilla-
individuals without cardiac disease. tion abound, it is still poorly understood. In essence,
however, there are multiple re-​entrant circuits and
Left bundle branch block (LBBB) is demonstrated by wavelets that are constantly colliding and interrupt-
a QRS >120 ms, a QS or rS complex in lead V1 and a ing each other. The AV node is continuously receiving
notched R wave in lead V6. Involvement of only the impulse, which again will be conducted at a variable

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13

Chapter 2: Electrocardiography

rate. The ECG will demonstrate a chaotic baseline, be assessed and treated promptly within current
constantly changing in frequency and amplitude. guidelines. Distinguishing between ventricular
tachycardia and supraventricular tachycardia with
AV node re-​entrant tachycardia (AVNRT): The AV aberrant ventricular depolarisation can be difficult.
node receives multiple inputs within the transition Clearly dissociated P waves, fusion beats (partial ven-
zone around the compact AV node. These inputs may tricular depolarisation over the AV node) and cap-
have different properties with regards to conduction ture beats (complete ventricular depolarisation over
velocities and refractory periods. This discordance the AV node) are all good indicators of VT but are
can result in a re-​entrant rhythm between the different frequently absent. Other features, which are sug-
connections. The ECG depicts a regular narrow com- gestive of VT are:
plex tachycardia with no discernable P waves as both
atria and ventricles are depolarised simultaneously. • Absence of typical LBBB or RBBB
• Indeterminate axis
AV re-​ entrant tachycardia (AVRT): Additional • Very broad QRS >160 ms
accessory electrical connections between the atria • Positive/​negative concordance
and ventricles can result in pre-​excitation. The rela- • R wave > Rʹ in V1.
tively quick conduction over the accessory connec-
tion results in the ventricle beginning to depolarise
from an area other than those directly supplied by
Learning Points
the bundle branches. This ventricular depolarisation • Accurate electrode placement is essential to ECG
is fused with depolarisation from the normal conduc- interpretation.
tion system as signals catch up through the AV node. • Care should be taken to examine all leads when
The slurred onset of the resultant QRS complex is making measurements.
termed a ‘delta’ wave and represents pre-​excitation. • QRS axis and transition can be used together
Under certain circumstances, impulse can con- to indicate underlying ventricular
tinuously cycle between the AV node and accessory abnormalities.
connection. If the AV node is the anterograde limb of • Narrow complex tachycardias can often be
the circuit, the resultant arrhythmia is orthodromic distinguished by their ECG features.
AVRT. Rarely, the accessory connection is the antero- • Broad complex tachycardias should be considered
grade limb and the resultant arrhythmia is antidromic to be ventricular tachycardia until proved
AVRT. The ECG of orthodromic AVRT will show a otherwise.
narrow complex tachycardia (no pre-​excitation evi-
dent) with inverted P wave discernible shortly after Further Reading
the QRS complex. Antidromic AVRT will show a
Bazett HC. An analysis of the time-​relations of
maximally pre-​excited QRS complex. electrocardiograms. Heart. 1920; 7: 353–​370.
Subjects with pre-​excitation and symptoms that
Eldridge J, Richley D. Recording a standard 12-​lead
may be related to it (palpitations, breathlessness, electrocardiogram. An Approved Methodology by
presyncope and syncope) are said to have Wolff–​ the Society for Cardiological Science & Technology
Parkinson–​White syndrome (WPW). (SCST), 2014.
Sokolow M, Lyon TP. The ventricular complex in left
Ventricular Arrhythmias ventricular hypertrophy as obtained by unipolar
A broad complex tachycardia is ventricular tachy- precordial and limb leads. American Heart Journal.
cardia (VT) until proved otherwise. Patients should 1949; 37: 161–​186.

MCQs
1. Electrode V2 is positioned at the following position: (c) Left sternal edge, 3rd intercostal space
(a) Right sternal edge, 3rd intercostal space (d) Left sternal edge, 4th intercostal space
(b) Right sternal edge, 4th intercostal space (e) Left sternal edge, 5th intercostal space

13:37:33 13
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14

Section 1: Diagnosis

2. The QTc attempts to correct the QT interval to a heart 4. A gradual beat-​to-​beat lengthening of the PR interval
rate of: followed by a dropped beat is known as:
(a) 50 (a) 1° AV block
(b) 55 (b) Mobitz 1 2° AV block
(c) 60 (c) Mobitz 2 2° AV block
(d) 70 (d) Complete AV block
(e) 75 (e) Normal
3. A normal QRS axis lies between: 5. An ECG with a continuously cycling regular baseline
(a) −90° and +90° between QRS complexes is likely to be showing:

(b) −30° and +90° (a) Atrial flutter

(c) −30° and +120° (b) Atrial fibrillation

(d) 0° and +90° (c) AVNRT

(e) 0° and +120° (d) Orthodromic AVRT


(e) Antidromic AVRT

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

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15

Section 1 Diagnosis

Echocardiography in the Cardiothoracic


Chapter

3 Intensive Care Unit
Ghislaine Douflé and Andrew Roscoe

Introduction PLAX PSAX


Since its introduction into the intensive care environ-
ment in the early 1980s, echocardiography has been
recognised as an invaluable tool. Transthoracic echo-
cardiography (TTE) provides a non-​invasive, portable
imaging modality, which allows for rapid diagnosis
and cardiovascular monitoring in the critically ill.
Transoesophageal echocardiography (TOE) produces
A4C SC
better resolution images and is often utilised as an
adjunct, or when TTE image quality is inadequate.
Focused echocardiography provides a goal
directed ultrasound examination to address specific
diagnostic and monitoring questions.

Indications for Echocardiography


Figure 3.1  Basic focused transthoracic echocardiography views.
In the critically ill patient echocardiography has been PLAX, parasternal long-​axis; PSAX, parasternal short-​axis; A4C, apical
shown to provide supplemental information to phys- four-​chamber; SC, subcostal.
ical examination and other monitoring modalities. It
may be performed for diagnostic reasons, as a haemo-
dynamic monitor, to assess volaemic status, or for development of skills to obtain adequate ultrasound
procedural guidance. images, but also the knowledge to interpret the find-
ings and the experience to request a comprehensive
Focused Scanning study when indicated. Consequently, training and
accreditation programmes are now established to
A focused TTE evaluation comprises four views of the
ensure competency and focused echo is a skill to be
heart: parasternal long-​axis and short-​axis, apical four-​
possessed by all critical care physicians.
chamber and subcostal views (Figure 3.1). Each view
provides basic information on biventricular function,
volaemic status, valvular function, and the presence Left Ventricle
of pleural or pericardial collections. When integrated Left ventricular (LV) systolic function (LVSF) is fre-
with clinical examination and other haemodynamic quently altered in the critically ill, either as a cause
parameters, point-​of-​care echocardiography provides of decompensation, or as a consequence of critical
a bedside tool for diagnosis and monitoring of cardio- illness:  the incidence of LVSF in septic shock, for
vascular pathophysiology. Multiple focused cardiac example, may be as high as 60%.
scanning protocols are now in use across the globe Advances in perioperative management and myo-
(e.g. FICE, FEEL, FATE) and extended algorithms cardial protection have seen a reduction in the inci-
have been developed to allow basic assessment of dence of postcardiotomy cardiogenic shock, but it
valvular pathology and quantification of ventricular may still occur in up to 6% of cardiac surgical pro-
function. Focused scanning requires not only the cedures, and is associated with high mortality. Early

13:38:41
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16

Section 1: Diagnosis

Figure 3.2  TOE midoesophageal four-​chamber (a) and two-​chamber (b) views, showing biplane method (modified Simpson’s rule) to
derive left ventricular ejection fraction.

postoperative detection or exclusion of LV dysfunc- The modified Simpson rule involves tracing the LV
tion is paramount to initiate prompt and appropriate cavity in the four-​chamber and two-​chamber views
therapy. at end-​diastole and end-​systole to estimate LVEDV
Although some studies have reported good correl- and LVESV (Figure 3.2). Three-​dimensional echocar-
ation between qualitative and quantitative assessment, diography has also been shown to produce accurate
objective quantification of LVSF is recommended and and reproducible measures of LV volumes. EF is
allows for interobserver comparisons. calculated as:
Fractional shortening (FS), derived from M-​mode
linear measurements, is a quick and reproducible EF = (LVEDV –​ LVESV) /​ LVEDV.
measure of LVSF. However, it is only representative
of a single dimension, and in the presence of regional The presence of RWMA before and after cardiac
wall motion abnormalities (RWMA) may give an surgery is not uncommon, but the detection of new
inaccurate measure of global LVSF. defects warrants further investigation. After coronary
Ejection fraction (EF) is calculated from estimates artery bypass grafting (CABG) surgery, a new RWMA
of LV end-​diastolic volume (LVEDV) and end-​systolic suggests myocardial ischaemia or possibly infarction
volume (LVESV). EF derived from the FS, using the from multiple causes including a compromised cor-
Teichholz method, is limited by its assumptions of the onary artery bypass graft occlusion, coronary vaso-
geometric LV shape, and is no longer recommended. spasm, inadvertent left circumflex artery ligation

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17

Chapter 3: Echocardiography

during mitral valve (MV) surgery (presenting with In the presence of tricuspid regurgitation (TR), RV
LV lateral wall akinesia), coronary ostial compromise systolic pressure can be reliably estimated by applying
after aortic root surgery and others. The 17-​segment the simplified Bernoulli equation to the peak TR jet
LV model is typically used and each segment is scored velocity.
as follows: Due to its geometry, echocardiographic quan-
1 normokinesia, normal regional wall motion tification of RV systolic function is challenging.
2 hypokinesia, reduced regional wall motion Longitudinal measures of function, such as tricuspid
3 akinesia, no movement of one or more annular plane systolic excursion (TAPSE) and tissue
segments Doppler derived tricuspid lateral annular systolic vel-
4 dyskinesia, paradoxical movement of one or more ocity (Sʹ), provide excellent measures of RV function.
segments in relation to other LV areas. They are easily obtainable by TTE, but with TOE,
values can be underestimated due to linear malalign-
However, RWMA may occur in the absence of sig-
ment. Their use in the perioperative setting is less
nificant coronary artery disease:  postoperative epi-
robust:  opening of the pericardium is accompanied
cardial pacing induces abnormal motion of the
by a significant decline in TAPSE and Sʹ without
interventricular septum (IVS) and posterior LV;
an associated decrease in global RV function. This
stress induced (Takotsubo) cardiomyopathy clas-
makes preoperative and early postoperative com-
sically presents with apical akinesia and ballooning;
parisons unreliable. RV fractional area change (FAC)
the inferior and inferolateral LV walls are most often
provides an accurate measure of global RV function
affected in myocarditis.
(Figure 3.3), correlates with RVEF derived from mag-
The assessment of LV diastolic function should
netic resonance imaging and is an independent pre-
form an integral part of a routine examination, espe-
dictor of mortality. Global longitudinal strain and
cially in patients presenting with heart failure. In fact,
three-​dimensional imaging offer alternative measures
up to 50% of patients with CHF have isolated LV dia-
of RV performance.
stolic dysfunction (DD) in the presence of a normal
LVEF. In addition, LVDD may play an important role
in a subset of patients difficult to wean from mechan- Valvular Heart Disease
ical ventilation. In the early postoperative period, echocardiography is
Patients with dynamic LV outflow tract (LVOT) used to assess adequacy of valve repair, competence of
obstruction exhibit hypotension, a low cardiac index valve replacement, detection of significant paravalvu-
and high LV filling pressures, but deteriorate with ino- lar leaks, recognition of patient-​prosthesis mismatch,
tropic administration. Typically seen in hypertrophic and iatrogenic valve injury.
obstructive cardiomyopathy (HOCM) and post-​MV Valvulopathies responsible for acute deterior-
repair surgery, it may also occur in severe hypovol- ation can be postischaemic, infective and traumatic in
aemia. Echocardiography is indispensable in making origin. Acute myocardial infarction (MI) may be com-
the correct diagnosis, allowing expeditious treatment plicated by papillary muscle rupture and severe MR.
revision to vasopressor therapy, volume loading and Infective endocarditis (IE) is a life threatening condi-
cessation of inotropic support. Echocardiography tion. TOE is recommended in patients with high clin-
findings include the presence of a significant gradient ical suspicion of IE. It is essential to determine the size
in the LVOT, systolic anterior motion (SAM) of the and precise location of vegetations, extent of leaflet
MV and mitral regurgitation (MR). destruction and valvular dysfunction, the presence
of abscess cavities or fistulae, and dehiscence of pros-
Right Ventricle thetic valves (Figure 3.4). Echocardiography findings
are crucial in predicting embolic risk and establishing
Acute right ventricular (RV) failure after cardiac sur-
the timing of surgical intervention.
gery carries a poor prognosis. It occurs frequently after
heart transplantation and LV assist device (LVAD)
implantation. RV dysfunction is a well-​ recognised Pericardium
complication of acute respiratory distress syndrome Cardiac tamponade is a clinical diagnosis comprising
(ARDS) and RV-​protective ventilation strategies have haemodynamic instability associated with equalisa-
emerged to impact on RV function. tion of diastolic filling pressures and large respiratory

13:38:41
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18

Section 1: Diagnosis

Figure 3.3  TOE midoesophageal four-​chamber right ventricular views in end-​diastole (a) and end-​systole (b), used to calculate right
ventricular fractional area change.

Figure 3.4  TOE midoesophageal long axis view, showing Figure 3.5  TTE subcostal view, showing a large pericardial
vegetations (arrows) on the aortic valve (AV). LA, left atrium; LV, left effusion (arrows). LV, left ventricle; RV, right ventricle.
ventricle.

patients, echocardiography may be utilised to monitor


fluctuation in arterial pressure (pulsus paradoxus). the progression of a pericardial effusion.
After cardiac surgery, however, classic signs of cardiac Constrictive pericarditis (CP) results in impaired
tamponade are often mild and atypical presentations diastolic filling due to a rigid, non-​compliant peri-
are not uncommon. Localised pericardial collections cardium. Patients present with chest pain, dyspnoea
and thrombus formation may cause isolated left-​sided and peripheral oedema. Although usually idiopathic
compression, with normal right-​ sided pressures. in origin, it can occur post-​MI and postcardiac sur-
A  high index of suspicion is required postcardiac gery. It is important to differentiate it from restrictive
surgery and TTE or TOE often provides rapid con- cardiomyopathy (RCM).
firmation of diagnosis (Figure  3.5). Loculated and Echocardiographic features to distinguish CP from
posterior collections may necessitate TOE. In patients RCM include a hyperechogenic pericardium, dynamic
with significant pulmonary hypertension, RV diastolic changes in LV diastolic filling velocity with respiration
collapse may be absent. In haemodynamically stable and preservation of myocardial relaxation velocities.

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19

Chapter 3: Echocardiography

Aorta
Aortic dissection typically presents with chest pain
and symptomology overlaps that of acute MI, how-
ever, it may be asymptomatic perioperatively. Contrast
computed tomography (CT) and cardiac magnetic
resonance (CMR) usually confirms the diagnosis,
but TOE may assist in demonstrating complications,
including aortic regurgitation (AR), pericardial effu-
sion, pleural effusion and RWMA secondary to cor-
onary involvement of the dissection flap. In particular,
TOE examination of the mechanism of AR is essential
to determine the surgical plan.
In the haemodynamically unstable postoperative
patient, an echocardiographic study must include Figure 3.6  TOE midoesophageal bicaval view, showing thrombus
assessment of the aorta: the incidence of intraoperative (arrows) attached to a central venous catheter (CVC), in the right
iatrogenic type A dissection is approximately 0.2%. atrium (RA). LA, left atrium; SVC, superior vena cava.

Intracardiac Shunts (McConnell’s sign), peak TR jet velocity >2.7 m/​s and


Previously undiagnosed interatrial shunts may pre- pulmonary artery acceleration time <80 ms all sup-
sent with hypoxaemia or paradoxical emboli, particu- port the diagnosis of PE.
larly in patients subjected to increased positive airway
pressures. Right-​to-​left shunting via a persistent for- Cardiac Arrest
amen ovale is observed in up to 20% of patients with A focused TTE exam may be of value in the rapid
ARDS and refractory hypoxaemia. identification of reversible causes of cardiac arrest. To
Post-​MI cardiogenic shock may be precipitated by avoid interruptions in chest compressions, a subcostal
ventricular septal defect that often requires placement view is obtained during the 10-​second pulse check.
of an intra-​aortic balloon pump and urgent surgical Readily detectable reversible causes include hypovol-
correction. Echocardiographic examination must aemia, tamponade, tension pneumothorax, myocar-
exclude this rare but life threatening complication in dial ischaemia and signs of PE.
patients with haemodynamic instability after an MI
involving the interventricular septum.
Trauma
Chest wall trauma usually precludes the acquisi-
Intracardiac Masses tion of adequate TTE views. TOE, as the preferred
Cardioembolism accounts for 15–​30% of ischaemic modality, aids in the diagnosis of myocardial con-
strokes. Echocardiography represents the mainstay tusion, pericardial effusion, and valvular and aortic
in evaluation for left-​sided cardiac masses. In atrial injuries.
fibrillation, thrombus typically develops in the left
atrial appendage; thrombus also occurs in areas of
LV akinaesia or aneurysm, and on pacemaker wires
Haemodynamic Monitoring
Inferior vena cava (IVC) diameter and its respira-
or indwelling catheters in the right side of the heart
tory variation as a marker of fluid responsiveness has
(Figure 3.6). Other potential embolic sources include
been well characterised. Initially described in spon-
tumours and vegetations.
taneously breathing patients, its extension to the ven-
tilated population remains debatable. The effect of
Pulmonary Embolism positive pressure tidal volumes and pulmonary com-
Although CT remains the gold standard for the diag- pliance on IVC variability makes interpretation prob-
nosis of pulmonary embolism (PE), echocardiography lematic. Even with spontaneous ventilation, increased
may be of value for the patient too unstable to transfer work of breathing with the generation of extreme
to the radiology suite. RV dilatation, RV dysfunction negative intrathoracic pressures IVC collapsibility can

13:38:41
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20

Section 1: Diagnosis

be misleading. IVC collapsibility and distensibility • Comprehensive training is essential to ensure


indices have been developed to improve reliability in appropriate use.
determining fluid responsiveness. The superior vena • Objective quantification of ventricular function is
cava (SVC), an intrathoracic structure, offers a more recommended.
reliable parameter of fluid responsiveness in the venti- • Echocardiography has an increasing role to play
lated patient, but requires TOE for visualisation. in patients on ECLS.
LV end-​diastolic area (EDA) can be easily mea­
sured in short-​ axis views of the heart. Reduced
LVEDA is suggestive of hypovolaemia and may pre-
Further Reading
Charron C, Caille V, Jardin F, et al. Echocardiographic
dict fluid responsiveness. However, in the presence of measurement of fluid responsiveness. Current Opinion
RV failure, the LV will appear underfilled, and inspec- in Critical Care. 2006; 12: 249–​254.
tion of the LV in isolation may result in inappropriate
Chockalingam A, Mehra A, Dorairajan S, Dellsperger KC.
fluid administration. Measurement of LVOT velocity-​ Acute left ventricular dysfunction in the critically ill.
time integral (VTI) provides a surrogate for LV stroke Chest. 2010; 138: 198–​207.
volume. Respiratory variation in LVOT VTI has been Doufle G, Roscoe A, Billia F, et al. Echocardiography
used to guide fluid responsiveness and to calculate the for adult patients supported with extracorporeal
cardiac output. membrane oxygenation. Critical Care. 2015;
19: 326.
Procedural Guidance Douglas PS, Garcia MJ, Haines DE, et al. ACCF/​ASE/​AHA/​
ASNC/​HFSA/​HRS/​SCAI/​SCCM/​SCCT/​SCMR 2011
Ultrasound plays a pivotal role in the field of mech-
Appropriate use criteria for echocardiography. Journal
anical circulatory support. Intra-​aortic balloon pump of the American Society of Echocardiography. 2011;
insertion and positioning can be optimised by TOE, 24: 229–​267.
and immediate aortic complications readily detected. Expert Round Table on Echocardiography in ICU.
Echocardiography can be used to guide cannulation International consensus statement on training
of extracorporeal life support (ECLS), to manage standards for advanced critical care echocardiography.
patients on ECLS and to assess suitability for wean- Intensive Care Medicine. 2014; 40: 654–​666.
ing from support. Pericardiocentesis should be per- Krishnan S, Schmidt GA. Acute right ventricular
formed under echocardiography guidance. dysfunction: real-​time management with
echocardiography. Chest. 2015; 147: 835–​846.
Summary Lang RM, Badano LP, Mor-​Avi V, et al. Recommendations
for cardiac chamber quantification by
The role of echocardiography in the critical care echocardiography in adults: an update from the
setting is expanding. As with any monitoring tool, American Society of Echocardiography and the
physicians need to be aware of its limitations and European Association of Cardiovascular Imaging.
integrate the findings with the clinical context. Journal of the American Society of Echocardiography.
Comprehensive training, accreditation and mainten- 2015; 28: 1–​39.
ance of skills are essential to ensure appropriate use Vignon P. Ventricular diastolic abnormalities in the
and interpretation. critically ill. Current Opinion in Critical Care. 2013;
19: 242–​249.
Learning Points Walley PE, Walley KR, Goodgame B, et al. A practical
approach to goal-​directed echocardiography in the
• Echocardiography is pivotal in the evaluation of critical care setting. Critical Care. 2014; 18: 681.
the unstable patient. Zafiropoulos A, Asrress K, Redwood S, et al. Critical care
• Focused echo is a skill to be possessed by all echo rounds: Echo in cardiac arrest. Echo Research
critical care physicians. Practice. 2014; 1: D15–​D21.

13:38:41
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21

Chapter 3: Echocardiography

MCQs
True or False (c) Left ventricular outflow tract (LVOT) VTI variation
1. Regarding left ventricular systolic dysfunction: can be used to guide fluid administration

(a) The incidence in septic shock is up to 60% (d) Left ventricular end-​diastolic area (LVEDA) is
measured in the long-​axis views of the heart
(b) Occurs in 20% of patients after cardiac surgery
(e) Reduced LVEDA is suggestive of hypovolaemia
(c) Can be accurately quantified by fractional short-
ening in patients with regional wall motion 4. Features of left ventricular outflow tract (LVOT)
abnormalities obstruction include:

(d) Can be accurately quantified by modified Simpson’s (a) Systolic anterior motion of the anterior mitral valve
biplane method in patients with regional wall leaflet
motion abnormalities (b) Pressure gradient in the LVOT
(e) Septal wall akinesia after mitral valve surgery sug- (c) Worsening hypotension with adrenaline
gests injury to the left circumflex coronary artery administration
2. Tricuspid annular systolic plane excursion (TAPSE): (d) Mitral valve regurgitation
(a) Can easily be measured with transthoracic (e) Clinical improvement with administration of fluids
echocardiography and vasopressors
(b) Is a measure of the longitudinal function of the left 5. Cardiac tamponade:
ventricle
(a) Remains a clinical diagnosis
(c) A value >20 mm suggests right ventricular
(b) Can present with atypical features after cardiac
dysfunction
surgery
(d) Allows for calculation of the estimated right ven-
(c) Always presents with right ventricular diastolic
tricular systolic pressure
collapse
(e) Typically increases in value after pericardial
(d) Can be diagnosed by focused transthoracic
incision
echocardiography
3. Regarding fluid responsiveness:
(e) May be caused by a small loculated collection
(a) Inferior vena cava (IVC) collapsibility >50% always
indicates hypovolaemia
(b) Superior vena cava collapsibility index is a
more reliable parameter of fluid responsiveness
than IVC

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:38:41
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22

Section 1 Diagnosis

Coronary Angiography
Chapter

4 Unni Krishnan and Stephen P Hoole

Definition acute coronary syndromes including STEMI, heart


failure, sudden cardiac death, valvular heart disease,
Coronary angiography uses radio-​ opaque contrast
preoperative evaluation for non-cardiac surgery and
agent to delineate the anatomy of the coronary cir-
major organ transplantation. These are summarised
culation. This may be performed either invasively
in Table 4.1. A detailed report listing the appropriate
using specially designed intra-​ arterial catheters or
use criteria for coronary angiography was published
non-​invasively by computerised tomography (CT)
in 2012. Appropriate use of invasive coronary angiog-
imaging. This chapter will focus on invasive coronary
raphy to investigate stable angina is also discussed in
angiography and its role in current clinical practice.
section 1.5 of the NICE guidance on the management
of stable angina.
Historical Perspective
The Nobel Laureate Werner Forssmann is credited Preprocedural Assessment
with the first cardiac catheterisation in 1929 although
this was exclusively right heart catheterisation via the Route of Arterial Access
left antecubital vein. Various reports of non-​selective The latest available annual report of the British
coronary angiography in human subjects followed in Coronary Interventional Society indicates a steady
the 1940s and 1950s, culminating in the first selective increase in the use of radial access and a correspond-
(albeit serendipitous) coronary angiogram performed ing decline in femoral access for percutaneous cor-
in 1958 by Frank Mason Sones in his basement labora- onary intervention (PCI). Diagnostic angiography
tory at the Cleveland Clinic. Melvin P Judkins and has also followed a similar trend over the last decade.
Kurt Amplatz made significant modifications to the With multiple clinical trials suggesting a net reduction
technique in the 1960s. They designed catheters spe- in adverse clinical events with radial access for PCI,
cifically for selective coronary cannulation, develop- this trend is likely to continue.
ing J-​tipped guidewires that were introduced via the Assessment of the peripheral arterial supply is
catheter lumen, and popularised the Seldinger tech- important before deciding the route of access for inva-
nique of percutaneous arterial access via the femoral sive coronary angiography. Symptomatic lower limb
route. Eponymously named catheters designed by peripheral arterial disease, abdominal aortic aneu-
Judkins and Amplatz are still routinely used for cor- rysms with thrombus in situ or previous vascular sur-
onary angiography today. gery (peripheral arterial bypass and/​or grafts) may
preclude a femoral approach although femoral access
Indications can be gained if necessary through Gore-​Tex™ grafts.
Invasive coronary angiography remains the gold Increasingly, radial arterial access is utilised, as the
standard investigation for the assessment of cor- hand has a dual arterial blood supply. Confirmation
onary anatomy. The indications for coronary angi- of ulnar artery patency (and/​or radial artery patency
ography in the assessment of ischaemic heart disease in patients that have had this artery cannulated pre-
are described in detail in joint ESC, ACCF, ACC viously) is recommended by performing a modified
and AHA guidelines for the diagnosis and manage- Allen’s (or reverse Allen’s) test, plethysmography or
ment of patients with stable ischaemic heart disease, pulse oximetry.

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23

Chapter 4: Coronary Angiography

Table 4.1  Indications for invasive coronary angiography

Indicated Rationale
ACS (STEMI/​NSTEMI/​UA) High pretest probability of CAD and/​or symptoms despite two antianginal
Stable CAD medications and/​or a positive non-​invasive function test and/​or in cases
where revascularisation may improve prognosis
Prior to non-cardiac surgery
Pretransplant assessment
New diagnosis of heart failure To delineate coronary anatomy and rule out or confirm significant CAD
Survivor following sudden cardiac death/​ventricular
arrhythmia
Prior to heart value surgery If age >35 years or postmenopausal at any age
Not indicated
Preoperative evaluation ‘Routine’ angiography in the absence of clinical suspicion or where
Pretransplant non-​invasive tests indicate low pretest probability

Angiography of coronary artery bypass graft


conduits is traditionally performed from a fem-
Access Site Preparation
The area of skin around the access site (radial artery or
oral arterial access although the left radial artery is
femoral artery) may need to be prepared according to
also an appropriate route of access for left internal
standard aseptic surgical practice.
mammary grafts. In patients awaiting assessment
for haemodialysis, it is prudent to avoid radial access
as this is a commonly used site for arteriovenous Premedication
fistulae. An anxiolytic is useful in allaying anxiety and to avoid
spasm of the radial artery. This is usually achieved
by appropriately timed oral or parenteral benzodiaz-
History of Adverse Reaction/​Allergy epines after consent has been obtained.
Any prior history of allergy to contrast agents is an
important consideration. The onset and severity of
the reaction should be explored as well as the indi-
Prehydration
cation for invasive coronary angiography before Acute kidney injury is rare following diagnostic cor-
deciding whether further contrast exposure is jus- onary angiography, which typically uses <100 ml of
tified. Although a history of seafood allergy is often contrast agent. Contrast induced nephropathy (CIN)
documented, there is no evidence to suggest that this is a form of acute kidney injury following adminis-
increases the likelihood of adverse reaction to iodi- tration of an iodinated contrast agent and is usually
nated contrast media. The risk of a serious allergic reversible. A 25% rise in serum creatinine levels from
reaction is reported as 0.02–​0.5%. It is routine practice baseline at 48 hours after administration of the con-
to administer systemic steroids several hours before trast agent is often set as a threshold for diagnosis of
the procedure and antihistamines 1–​2 hours prior to CIN in clinical trials. International guidelines recom-
angiography in patients with a history of suspected or mend the use of isoosmolar contrast agents to reduce
confirmed adverse reactions. the risk of CIN. Prehydration with isotonic saline has
been shown to be effective in preventing CIN espe-
cially in women, diabetics and in those requiring high
Consent volumes of contrast agent (>250 ml). Trials comparing
Written informed consent by a competent operator intravenous saline versus bicarbonate prehydration
following discussion of potential complications is have failed to demonstrate any advantage of one
mandatory prior to the procedure (see Complications agent over the other. We recommend the use of 0.9%
section). saline for periprocedural hydration in patients at risk

13:40:34
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24

Section 1: Diagnosis

of CIN. Patients are encouraged to drink clear fluids The right and left coronary arteries arise from the
freely in the periprocedural period. A risk score based corresponding coronary sinuses immediately above
on eight clinical variables proposed by Mehran et al. the aortic valve. The right coronary artery runs in
more than a decade ago has been validated in a recent the right atrioventricular (AV) groove until the crux
study as a reliable tool in predicting the risk of CIN in (the anatomical intersection of the right and left AV
ACS patients undergoing coronary angiography. grooves and the posterior interventricular groove).
Along its course the RCA supplies the sinoatrial and
atrioventricular nodes, the right atrium and right ven-
Anticoagulation tricle and frequently the inferoposterior wall of the
A careful review of the indication for anticoagula- left ventricle as it enters the posterior interventricular
tion and the risk of thrombosis from interruption of groove as the posterior descending artery (PDA) in
anticoagulant therapy should be made in all cases. over 80% of cases. This is referred to as a right dom-
In an elective setting the anticoagulant is tempor- inant circulation.
arily suspended where possible, although coronary The left main coronary artery (LMCA) runs a
angiography may be performed via the radial route short course (usually 5–​10 mm) before bifurcating
in anticoagulated patients if necessary. Such cases into the left anterior descending artery (LAD) that
should be discussed with the operator and planned runs in the anterior interventricular groove and
on an individual patient basis. A  meta-​analysis of the left circumflex artery (LCx) which mirrors
studies that compared uninterrupted anticoagula- the course of the right coronary artery in the left
tion with interruption ± heparin bridging suggests AV groove. The LAD supplies most of the inter-
that coronary angiography may be safely performed ventricular septum through its septal perforating
by continuing warfarin therapy with a target INR of branches and the anterolateral wall of the left ven-
2.0–​2.5. tricle from two or more diagonal branches. Obtuse
marginal branches arise from the LCx and supply
Antiplatelet Agents the posterolateral LV myocardium. In 10% of cases
There is no reason to discontinue antiplatelet therapy the LCx continues as the PDA (left dominant cir-
prior to diagnostic angiography. In instances where culation) in the posterior interventricular groove,
angiography may proceed to PCI it is mandatory to while in the remaining 10% of cases both the RCA
treat the patient with loading doses of antiplatelets and the LCx provide branches to the posterior
according to local protocols. interventricular groove (codominant circulation).
Many of these preprocedural checks are confirmed Typical coronary angiographic images are repre-
with a World Health Organisation (WHO) surgical sented in Figure 4.1.
check list.
Haemostasis and Postprocedural
Coronary Angiography Care of Access Site
Manual compression may be employed to gain
Image Acquisition, Analysis and haemostasis at the site of arterial puncture. The radial
Interpretation artery is more superficial and readily compressed by
Invasive coronary angiography is an accurate imaging a band applied around the wrist. Femoral punctures
modality to delineate luminal anatomy although, can be compressed by a FemoStop device if manual
unlike non-​invasive CTCA, it cannot comment on the compression is not sufficient to achieve haemostasis.
arterial wall. Multiple views (projections) are acquired Intravascular or extravascular closure devices (such
by radiography by injecting iodinated contrast into as the AngioSeal™ or Proglide™ devices) are also
the coronary arteries whilst being mindful of mini- used routinely following femoral puncture and can
mising contrast and radiation exposure to the patient, help to achieve haemostasis earlier when compared
as a stenosis in the ‘lumenogram’ may be eccentric or to manual compression. The AngioSeal™ device
foreshortened and could otherwise be missed. This is was noted to be more expensive and resulted in a
especially true in bifurcation lesions. slight delay in the patient leaving the catheter suite,

13:40:34
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25

Chapter 4: Coronary Angiography

(a) (b)

(c) (d)

pre post
Figure 4.1  Diagnostic angiograms of (a) normal left coronary artery, (b) normal right coronary artery, (c) prepercutaneous and
postpercutaneous coronary intervention to left anterior descending artery and (d) a saphenous vein graft.

but facilitated early patient ambulation and caused of ‘patent’ haemostasis using specially designed com-
less patient discomfort compared to the FemoStop pression bands.
device.
Patency of the radial artery following angiography Compl ications
has been shown to be increased by the use of 5F versus These may occur during or after the procedure.
6F sheaths, administration of 5000 units of heparin Serious complications are rare with a reported cumu-
via the side port of the arterial sheath and a technique lative incidence of <0.5%.

13:40:34
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26

Section 1: Diagnosis

Major Adverse Cardiac Events (MACE) from skin rash to sudden unexplained haemodynamic
collapse during or after the procedure.
Death is rare after coronary angiography and has been
consistently noted to be around 0.1% in large regis-
tries, whilst the rate of myocardial infarction ranges Learning Points
from 0.06% to 0.17% depending on the location of • Invasive angiography is the gold standard test for
atherosclerotic disease. Emergency coronary artery delineation of coronary lumen anatomy.
bypass surgery is rarely indicated (<0.1%). Ischaemic • Written informed consent by a competent
stroke rates of 0.05–​0.1% have been reported and can operator following discussion of potential
arise from catheter manipulation in an atheroscler- complications is mandatory prior to the
otic ascending aorta, catheter related thrombosis and procedure.
embolism, air embolism or vessel dissection.
• Coronary angiography is an extremely safe
procedure in experienced hands with an overall
Access Site Complications complication rate of 0.1–​0.5%.
These occur more frequently following femoral • The use of radial arterial access for coronary
arterial access and include local haematoma (with or angiography has steadily increased and may
without retroperitoneal extension in 0.15%), pseudo­ confer a net clinical benefit by reducing the risk of
aneurysm, iatrogenic arteriovenous (AV) fistula and vascular complications.
rarely arterial thrombosis or embolisation. Sudden • Contrast induced nephropathy can be avoided by
haemodynamic collapse may be the first indicator of a appropriate prehydration and use of isoosmolar
retroperitoneal haematoma but this is often preceded contrast agents in high risk patients.
by persistent tachycardia with or without hypoten-
sion and flank pain. A  tender, pulsatile mass with a
systolic bruit is commonly noted in pseudoaneurysm Further Reading
while a continuous bruit may be audible in cases of Abellas-​Sequeiros RA, Raposeiras-​Roubin S, Abu-​Assi E,
AV fistula. Clinical suspicion should prompt urgent et al. Mehran contrast nephropathy risk score: Is it
Doppler ultrasound and/​or CT imaging to establish still useful 10 years later? Journal of Cardiology. 2015;
67: 262–​267.
the diagnosis. Urgent referral to a vascular surgical
unit is often indicated in such cases. Barbeau GR, Arsenault F, Dugas L, Simard S, Lariviere
MM. Evaluation of the ulnopalmar arterial arches with
Benign vasovagal episodes precipitated by femoral
pulse oximetry and plethysmography: comparison
sheath removal are reported in 5–​6% of patients, espe- with the Allen’s test in 1010 patients. American Heart
cially if the patient is dehydrated, but rapidly respond Journal. 2004; 147: 489–​493.
to intravenous fluid and atropine. Delaney A, Carter A, Fisher M. The prevention of
Local complications are less common follow- anaphylactoid reactions to iodinated radiological
ing radial access but include pseudoaneurysm and contrast media: a systematic review. BMC Medical
sterile granuloma caused by deposition and hyper- Imaging. 2006; 6: 2.
sensitivity reaction to the hydrophilic coating on the Fleisher LA, Fleischmann KE, Auerbach AD, et al. ACC/​
surface of radial sheaths. The more serious complica- AHA guideline on perioperative cardiovascular
tion of compartment syndrome caused by local tis- evaluation and management of patients undergoing
sue compression from a radial haematoma occurs in noncardiac surgery. Circulation. 2014; 130: 2215–​2245.
<0.01% of cases but can be limb threatening if not rap- Krone RJ, Johnson L, Noto T. Five year trends in cardiac
idly decompressed. It is heralded by the six Ps in the catheterization: a report from the Registry of the
affected limb:  pulseless, painful, pale, paraesthesia, Society for Cardiac Angiography and Interventions.
paralysis and perishing cold. Catheterization and Cardiovascular Diagnosis. 1996;
39: 31–​35.
NICE. Management of Stable Angina. NICE Guidelines CG
Contrast Complications 126. July 2011.
Complications related to the contrast agent include Patel MR, Bailey SR, Bonow RO, et al. ACCF/​SCAI/​AATS/​
CIN and allergic reaction to the iodinated compounds AHA/​ASE/​ASNC/​HFSA/​HRS/​SCCM/​SCCT/​SCMR/​
(discussed above). Allergic manifestations may range STS 2012 Appropriate use criteria for diagnostic

13:40:34
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27

Chapter 4: Coronary Angiography

catheterization. Journal of the American College of myth exposed. Journal of Emergency Medicine. 2010;
Cardiology. 2012; 59: 1995–​2027. 39: 701–​707.
Ryan TJ. The coronary angiogram and its seminal Valgimigli M, Gagnor A, Calabro P, et al. Radial versus
contributions to cardiovascular medicine over five femoral access in patients with acute coronary
decades. Circulation. 2002; 106: 752–​756. syndromes undergoing invasive management: a
Schabelman E, Witting M. The relationship of randomised multicentre trial. Lancet. 2015;
radiocontrast, iodine, and seafood allergies: a medical 385: 2465–​2476.

MCQs
1. Coronary angiography is indicated in the following 4. Which of the following is FALSE?
scenarios EXCEPT: (a) The circumflex artery may supply the proximal
(a) Prior to aortic valve surgery in a 48 year old male interventricular septum
with bicuspid aortic valve (b) The PDA usually arises from the RCA
(b) In a 56 year old male with exertional angina (c) Diagonal branches usually supply the posterolateral
(c) New onset heart failure with severe global LV LV myocardium
impairment on echocardiography (d) The SA nodal artery arises from the proximal RCA
(d) Prior to balloon mitral valvuloplasty in a 29 year (e) The AV nodal artery is usually the last branch
old female with mitral stenosis of the RCA before it enters the posterior
(e) Following out of hospital cardiac arrest and good interventricular groove
neurological recovery 5. A 55  year old man is recovering on ITU following a
2. Which of the following is most useful in reducing the witnessed cardiac arrest. New onset atrial fibrillation
risk of contrast induced nephropathy? is noted on the ECG and a bedside echocardiogram
(a) 0.45% saline by intravenous infusion suggests moderate–​ severe LV systolic impairment
with pronounced anteroseptal hypokinaesia. Further
(b) 0.9% saline prehydration is most useful at evaluation is planned with invasive coronary angiog-
preventing CN raphy. Which of the following is the most appropriate
(c) 10% sodium bicarbonate by intravenous infusion step before the procedure?
(d) Intravenous furosemide infusion at a rate of 20 mg/​ (a) Administer regular dose of diuretics
hour (b) Load with aspirin and clopidogrel orally
(e) Use of hyperosmolar contrast agents (c) Start loading dose of warfarin
3. The advantages of radial access for coronary angiog- (d) Administer intravenous prehydration with 1 l 0.9%
raphy include all except: saline over 2 hours
(a) Lower rate of access site bleeding (e) (b) and (d)
(b) Lower rate of bleeding requiring transfusion
(c) Early ambulation post procedure
(d) Shorter fluoroscopic screening time during
angiography
(e) Lower rate of pain and discomfort post procedure

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:40:34
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28

Section 1 Diagnosis

Bronchoscopy in the Cardiothoracic


Chapter

5 Intensive Care Unit
Sumit Chatterji and Pasupathy Sivasothy

Introduction In this chapter, the role of bronchoscopy in the


CICU, contraindications, preparation, procedural
In 1897 Gustav Killian, a German laryngologist, per-
considerations and potential complications will be
formed the first airway examination in a human, with
discussed.
a rigid oesophagoscope, to remove a piece of bone
lodged in a mainstem bronchus. The next milestone
occurred with Shigeto Ikeda in 1964 and the devel- Indications for Bronchoscopy
opment of the first flexible bronchoscope capable One can generally group the indications for bron-
of examining the airways down to subsegmental choscopy into diagnostic and therapeutic reasons,
bronchi. Flexible bronchoscopy (FB) has been used though there is often overlap. Examples of this include
clinically since 1966 and has largely replaced rigid haemoptysis, foreign body removal, central airway
bronchoscopy as the technique of choice for airway obstruction, tracheo-​oesophageal fistula and removal
examination and intervention. It can be of significant of proximal sputum plugs. Studies suggest 65% to 79%
help in the diagnosis and management of pulmonary of bronchoscopies performed in the ICU setting are
pathology in severely ill patients in the cardiothoracic conducted on patients being mechanically ventilated,
intensive care unit (CICU). Intensivists, interven- and of these 47% to 75% have a therapeutic indication.
tional pulmonologists and cardiothoracic surgeons In one review of bronchoscopies performed in critic-
are typical operators in this setting. Given its wide- ally ill patients on an ICU, 45% were performed to
spread use, it may be surprising that its role, efficacy remove bronchial secretions, 35% for collecting sam-
and safety in critically ill patients has largely been lim- ples from the lower respiratory tract, 7% for airway
ited in the published literature to small case series and assessment, 2% for haemoptysis, 0.5% for assisting
expert opinions. A few meta-​analyses have attempted difficult tracheal intubation and 0.5% for removing
to evaluate its role, particularly in the context of venti- foreign bodies.
lator acquired pneumonia. Indications for bronchoscopy in a CICU are sum-
Patients in a CICU are typically selected for pre- marised in Table 5.1.
dominantly cardiac or respiratory support, with over
40% on mechanical ventilation. Patients are varied and Orotracheal Intubation
include recipients of heart/​lung transplants, immuno-
compromised established transplant recipients, those Difficult Intubation
receiving anticoagulation or multiple antiplatelet FB can be useful to facilitate difficult endotracheal
agents, and those with chronic cardiac or respiratory intubations in patients with a Cormack–​Lehane score
disease. Polypharmacy is common, with the poten- of 3 or more, limited mobility of head and neck, cer-
tial for multiple drug interactions adding to issues vical spine fractures, or where severe coagulopathy
facing the bronchoscopist, which need to be carefully or excessive secretions might make intubation with
evaluated before deciding to proceed. Determining a layngoscope inadvisable. Despite its advantages in
the appropriateness of the procedure, then optimis- these situations, it is typically only used in a small
ing the patient and environment to ensure a safe and proportion (0.07–​3.4%) of patients in the ICU set-
effective intervention, depends on a multidisciplinary ting. The oral route is preferred as a larger diameter
approach with the physician/​ surgeon, intensivists, endotracheal tube (ETT) can be passed. Adult bron-
interventional pulmonologist and nurses all involved. choscopes have a diameter of approximately 6  mm,

13:41:59
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29

Chapter 5: Bronchoscopy

Table 5.1  Indications for bronchoscopy in a CICU ETT cuff is deflated and the bronchoscope/​new ETT
Primarily diagnostic passed through the vocal cords alongside the old ETT.
• Pneumonia (nosocomial, ventilator associated, The old ETT is then withdrawn and the new tube
immunocompromised host) adjusted accurately under direct vision prior to cuff
• Acute inhalational injury or burns inflation.
• Assessment for airway trauma (post blunt or penetrating
thoracic injury) Controlled Extubation
• Localised wheeze or stridor
• Diffuse or focal lung disease (infiltrates or mass lesions)
Patients with suspected upper airway obstruction are
• Assessment of bronchial stump or anastomosis ideal candidates for FB directed extubation. Examples
• Assessment of graft rejection (transbronchial lung biopsies) include bilateral vocal cord paralysis, tracheomalacia
Primarily therapeutic or tracheal stenosis due to causes such as multiple
• Airway management (difficult intubation, double lumen intubation attempts, prolonged intubation or airway
endotracheal tube placement, endotracheal tube injury. The bronchoscope is inserted into the ETT
replacement) just beyond the tip, the cuff deflated and the bron-
• Atelectasis (lobar or whole lung) due to proximal choscope/​ETT slowly removed en bloc. During with-
mucus plug
drawal, if there is endoscopic evidence of significant
• Airway foreign bodies
subglottic or glottic obstruction, the ETT can be safely
• Massive haemoptysis
• Strictures and stenoses (balloon dilatation and stents)
reinserted under direct vision.
• Central airway obstruction due to tumour (cryodebulking,
electrosurgery, laser)
• Tracheo-​oesophageal fistula (stenting)
Diagnosis of Respiratory Infection in
• Bronchopleural fistula (fibrin glue, endobronchial valve Ventilated Patients
insertion)
• Percutaneous dilational tracheostomy insertion Ventilator Associated Pneumonia (VAP)
Pneumonia is the most common infection in the
CICU. The overall incidence of VAP ranges from 9%
able to pass through a size 7.5 ETT or larger –​typical to 25% in the general ICU population, with rates up to
sizes used in adult patients. To prevent damage to the 70% in those with acute respiratory distress syndrome
bronchoscope, a bite block is advised. As four minutes (ARDS). The risk increases over the first 10 days and
or more must be allowed to accomplish intubation, can affect two thirds of patients who have been ven-
this technique is not recommended for apnoeic or tilated for more than 30 days. Mortality ranges from
near apnoeic patients. 35% to 90%. Bronchoscopically directed lavage, pro-
tected brushing and occasionally deep lung biopsies
Double Lumen Endotracheal Tubes (transbronchial lung biopsies) are often used to deter-
FB can be used to assist placement of a double lumen mine the cause of infection. Qualitative or quantita-
ETT used for differential ventilation or management tive (number of colony forming units, or number of
of massive haemoptysis. A thin 4 mm diameter bron- intracellular organisms) techniques can be used to
choscope can pass through a 35F double lumen tube; analyse the samples obtained. This results in a wide
the smallest size used in adults. range of reported sensitivities of bronchoscopic tech-
niques (51–​100%) with the overall impression that
Changing Endotracheal Tubes bronchial lavage and brushing are safe techniques
Occasionally an ETT may need to be changed due for microbiological diagnosis in ventilated patients.
to cuff leakage or to facilitate a bronchoscopic inter- However, well-​ conducted systematic reviews look-
vention. If endotracheal reintubation is expected to ing at bronchoscopic versus ‘non-​invasive’ techniques
be difficult, a flexible bronchoscope may be used to (tracheal suctioning, blind catheter brushing) in redu-
facilitate the exchange as an alternative to a bougie. cing mortality and ICU stay in clinically diagnosed
The stomach contents are aspirated via a nasogastric VAP patients have shown no statistically significant
tube, following which the new ETT is inserted over differences in mortality, duration on mechanical
the bronchoscope and inserted into the posterior ventilation, length of ICU stay or antibiotic change.
pharynx, whilst suctioning secretions. The existing The British Thoracic Society therefore recommends

13:41:59 29
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Section 1: Diagnosis

directed non-​invasive diagnostic strategies in prefer- • Failure to respond to chest physiotherapy and
ence to bronchoscopy in ventilated patients suspected other measures;
to have VAP. • Where physiotherapy or repositioning is not
feasible (e.g. thoracic trauma, spinal fractures)
Immunocompromised Patients • Patients with neuromuscular disorders and
Patients with solid organ transplants receiving impaired cough;
immunosuppressive medications in the CICU are at • Cystic fibrosis patients (copious inspissated
higher risk of developing opportunistic fungal infec- secretions);
tions, including Pneumocystis jirovecii, invasive asper- • Lung transplant patients with tenacious plug
gillosis, candidiasis, cryptococcus, bacterial infections composed of necrotic tissue and mucus.
and viral infections such as cytomegalovirus. In areas
of high prevalence in the UK, or in patients from
endemic areas worldwide (Sub-​Saharan Africa, Far Diagnosis and Management of
East, Southeast Asia, parts of Eastern Europe and Haemoptysis
South America), tuberculosis must also be excluded. Bronchoscopy in conjunction with CT can be useful to
Bronchoalveolar lavage (BAL) with 120–​200 ml of identify the endobronchial source of haemoptysis in
instilled 0.9% saline can be performed via the bron- intubated patients with persistent or excessive bleed-
choscope into an affected lobe. If diffuse changes are ing from the ETT. It is also typically employed (usually
present, bilateral BAL (preferentially of the upper through an ETT) for diagnosis and control of massive
lobes) appears to provide the highest sensitivity. BAL haemoptysis, defined as 400 ml in 24 hours, or 200
is reported to have sensitivity for P. jirovecii of 90–​98% ml in any one event. Through the bronchoscope, iced
and is considered the gold standard. Diagnostic sen- saline, fibrin precursors or topical adrenaline 1/​10,000
sitivity for pulmonary tuberculosis can be increased can be instilled to attempt haemostasis in a bleeding
from up to 30% based on microscopy alone to 86% segment. Alternatively, the bronchoscope can be used
with rapid PCR techniques, and is preferable to to facilitate the passage of specific endobronchial
transbronchial lung biopsies in the majority of ICU blockers (e.g. Cohen flexitip® or Arndt®) and a Fogarty
patients due to the potential risk of pneumothorax or or Swan-​Ganz catheter to occlude the bleeding lobe
bleeding. For patients with suspected invasive asper- or segment. Finally, an ETT can be directed broncho-
gillosis, BAL galactomannan testing has shown super- scopically into the normal lung to isolate the bleeding
iority to fungal staining and culture, with sensitivity of side and avoid spillover of blood, or help direct a dual
94% and specificity of 79% and should be considered lumen ETT to achieve the same effect. Where facilities
if available. and expertise exist, rigid bronchoscopy may be pref-
erable in cases of massive haemoptysis as it provides
Managing Lobar or Whole Lung Atelectasis a secure airway, large volume suction capability and
FB has been used in ventilated patients with lobar or easy access to the airways with endobronchial block-
whole lung atelectasis who have failed to respond to ing devices. All these measures attempt to secure the
treatments such as physiotherapy, nebulised saline, airway, ensure adequate oxygenation, prevent soiling
mucolytics or repositioning (including prone venti- of the normal lung and in some cases allow definitive
lation). In several small case series it has been shown airway intervention  –​or buy time for a surgical or
to be effective in immediate reversal of lobar atelec- interventional radiology solution.
tasis. Physiotherapy and conventional non-​invasive
measures are still recommended first line treat- Thoracic Trauma
ment with bronchoscopy reserved for the following Tracheobronchial injuries affect up to 2.8% of severe
situations: blunt chest trauma and accidental deaths. Sternal or
• Life threatening whole or near-​whole lung upper rib fractures can indicate significant blunt force
collapse; injury and likelihood of internal problems so bron-
• Lobar atelectasis due to proximal sputum plug choscopic examination is mandatory. Physical and
with a lack of visible air bronchograms on radiological signs include hypoxaemia, haemoptysis,
radiology; pneumothorax, surgical emphysema, haemothorax,

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Chapter 5: Bronchoscopy

pneumomediastinum, flail chest and the so-​ called atelectasis, ARDS, central airway obstruction, obesity,
‘falling lung sign’ on chest radiograph (pneumothorax hypotension), the effects of sedation and the pro-
with atelectatic lung collapsing away from the medias- cedure being undertaken (such as suctioning to clear
tinum) which is pathognomonic of rupture of a main- airway debris).
stem bronchus. All these factors need consideration prior to under-
taking FB, and in intubated patients particular atten-
Persistent Bronchopleural Fistula (BPF) tion needs to be paid to ensuring an adequate sized
airway and choosing an appropriately sized broncho-
The incidence of BPF after pulmonary resection var- scope for the task (a thinner scope may be safer but
ies between 4.5–​20% after pneumonectomy and 0.5% will have less suctioning capacity and may not allow
after lobectomy. Risk factors for this serious complica- passage of certain instruments such as a cryoprobe).
tion include right-​sided pneumonectomy, a long bron- Table  5.2 summarises the main physiological
chial stump, residual cancer at the bronchial margin, effects of bronchoscopy in intubated patients.
devascularisation of the bronchial stump, prolonged
ventilation and reintubation after resection. Many
patients may not be fit enough to have repeat sur-
Procedures Performed with
gery where intercostal drainage and sometimes pleu- Bronchoscopy
rodesis methods fail. The extent of the air leak may Flexible bronchoscopes typically have working chan-
prevent lung reinflation and delay ambulation, even nels 2.0–​3.2 mm in diameter, allowing varying suction
with Heimlich valves or portable suction devices (e.g. capacity or ability to pass specialised instruments to
Thopaz®, Medela Switzerland). Bronchoscopy can be perform interventions.
used in these patients to identify the predominant Additionally, linear endobronchial ultrasound
lobe/​segment causing the air leak (by employing an scopes available today (with approximate external
endobronchial occluding balloon), followed by inser- diameter 6.9  mm) can be used via larger ETTs to
tion of one-​way valves preventing airflow into that seg- facilitate transbronchial needle aspiration of medias-
ment. Examples of valves used for this purpose include tinal lymph nodes or masses.
Emphasys® (Pulmonx, Redwood, USA), Spiration Advanced bronchoscopic interventions are gener-
IBV® (Olympus Medical, Japan) or Watanabe spigots® ally the remit of the interventional pulmonologist or
(Novotech, France). These devices require consid- thoracic surgeon.
erable expertise to deploy accurately and are usually Procedures likely to be encountered in the CICU
inserted by interventional pulmonologists. are detailed in Table 5.3.

Physiological Effects of Bronchoscopy Contraindications to Bronchoscopy


In the non-​intubated adult patient, a standard 5.7 mm There are very few absolute contraindications to per-
diameter bronchoscope occupies only 10% of the forming FB. Among these are non-​cooperation or
cross-​sectional area of the trachea. Therefore, in spon- refusal by the awake patient, operator inexperience,
taneously breathing patients endotracheal pressures lack of suitable equipment and the inability to main-
generated are similar to those in patients without tain adequate oxygenation during the procedure.
bronchoscopy. The remainder are considered relative contrain-
In an intubated, ventilated patient, the effect is dications as they place the patient at risk of certain
quite different. The obstructive effect of the broncho- complications. FB in these settings should be weighed
scope is added to that of the ETT, with the potential to carefully against potential risks to the patient.
cause quite dramatic changes in respiratory mechan- Hypoxaemia defined as an inability to maintain SpO2
ics, gas exchange and haemodynamics. Indeed, a > 90% can predispose to arrhythmias through myocar-
5.7  mm bronchoscope occupies 40% of the cross-​ dial ischaemia and recent acute coronary syndromes
sectional area of a 9.0 mm inner diameter ETT, 51% of increase the risk of fatal myocardial ischaemia.
a 8.0 mm ETT and 66% of a 7.0 mm ETT. Relative contraindications include:
Complicating the effect of the bronchoscope on • Severe hypoxaemia with CPAP or FiO2 >0.5 to
the patient’s physiology are patient-​specific factors achieve a PaO2 >9.0 kPa;
including the underlying diagnosis (for example, • Acute coronary syndrome within 4 weeks;

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Section 1: Diagnosis

Table 5.2  Effect of bronchoscopy on respiratory physiology in the ventilated patient

Outcome Additional notes


Respiratory mechanics Increased VT reduction 200–​300 ml with suctioning
• PEEP (10–​15  cmH20, up to 35 cmH20) Main determinants of effect are ETT internal diameter,
• Peak inflation pressures (up to 80–​90 cmH20) bronchoscope external diameter and duration of
• FRC  (30%) suctioning
Cough can further exacerbate peak airway pressures
Reduced
risking barotrauma
• VT
Auto-​PEEP can develop leading to raised FRC, reduced
• FEV1 (40%, bronchospasm can exacerbate)
FEV1 and expiratory tidal volumes
• PEEP (with suction)
• FRC (with suction)
Gas exchange Increased Suction can reduce PaO2 by 40%. Mechanisms include
• PaCO2 (average 1 kPa) atelectasis, small airway collapse, reduced VT, reduced FRC
• PaO2 (in some cases with secretion clearance and increased V/​Q mismatch
or due to auto-​PEEP recruitment) Low FEV1, prior LTOT, raised BMI and significant
comorbidities are risk factors for an exaggerated response
Reduced
• PaO2 (average 2.5 kPa)
• SpO2 (>5% desaturation in over 65% cases)
• SpO2 falls below 90% in at least 20% cases
Haemodynamics Increased Sympathetic stimulation due to hypoxaemia, hypercapnia
• Heart  rate and mechanical irritation of the airways
• Mean arterial pressure Raised ICP potentially caused by a combination of
• Cardiac  output hypoxaemia, hypercapnia and cough with auto-​PEEP. Is
• Pulmonary artery pressure usually compensated by the raised mean arterial pressure
during the procedure
• Intracranial pressure (can increase >100%)
Reduced
• Mean arterial pressure (if significant
auto-​PEEP)

• Uncontrolled arrhythmia; coagulation parameters must be within safe limits. If


• Systolic blood pressure <90 mmHg despite on warfarin for a metallic heart valve, discuss with the
vasopressors; cardiologist and typically discontinue and cover with
• Uncontrolled bronchospasm; low molecular weight heparin (LMWH) until the INR
• Auto-​PEEP >15 cmH20; is below 1.5 (omitting the LMWH dose 24 hours prior
• Bleeding diathesis (thrombocytopenia <20–​ to bronchoscopy). For other indications, warfarin
50 × 109/​l, INR >1.5, clopidogrel, newer oral may be stopped or partially reversed with vitamin
anticoagulants (NOAC), chronic renal failure); K if a biopsy is planned. Clopidogrel should also be
• Severe pulmonary arterial hypertension; discontinued 7 days prior where possible as there is a
• Intracranial hypertension. significant risk of bleeding with biopsies. NOACs can
be stopped 48 hours prior. Review the list of relative
and absolute contraindications to consider whether
The Bronchoscopy Procedure the procedure can be safely deferred.

Preparation The Equipment


A working sterilised video bronchoscope of appro-
The Patient priate diameter and monitor/​stack is required. It can
Ensure the patient is correctly identified and consent be difficult to position the equipment around a bed
obtained if feasible. Radiology must be reviewed to space when there are other pieces of equipment in
identify the reason for the procedure and a target area the vicinity. The best position involves the operator
for sampling or intervention. The full blood count and on one side of the bed, facing the monitor/​stack on

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Chapter 5: Bronchoscopy

Table 5.3  Bronchoscopic procedures performed in the CICU

Procedure Basic or advanced Indications Requirements


Bronchial wash Basic Bronchial clearance and sampling Platelet count >20
Bronchoalveolar lavage Basic Cytological and microbiological Platelet count >20
sampling
Bronchial brush Basic Cytological and microbiological Platelet count >50
sampling INR <1.5
Bronchial biopsy Basic Histological and microbiological Platelet count >50
sampling INR <1.5
Foreign body extraction Basic/​Advanced Removal of airway foreign body Platelet count >50
INR <1.5
Working channel diameter >2.6 mm
(for larger forceps or retrieval baskets)
Transbronchial biopsy Advanced Histological and microbiological Platelet count >50
sampling INR <1.5
Cryotherapy Advanced Freezing/​extraction of Platelet count >50
endobronchial tissue or debris INR <1.5
Working channel diameter >2.6 mm
Diathermy Advanced Tissue debridement Platelet count >50
Haemostasis INR <1.5
Insulated scope
Avoid FiO2 >0.4 (risk of airway fire)
Care with pacemakers
Earth electrode pad
Balloon dilatation Advanced Intrinsic or mixed benign or Platelet count >50
malignant airway narrowing INR <1.5
Stenting Advanced Malignant or benign airway stenosis Platelet count >50
INR <1.5
Some operators prefer fluoroscopy
Endobronchial ultrasound Advanced Sampling mediastinal or hilar nodes/​ Platelet count >50
mass INR <1.5
Size 9.0 ETT if intubated
Endobronchial valves Advanced Persistent bronchopleural fistula Platelet count >50
INR <1.5
Working channel diameter >2.6 mm

the other side. If fluoroscopy is needed, the patient signs and electrocardiogram should be continuously
will need to be transferred onto a screening trolley, monitored during and after the procedure. Consider
which allows access to a ‘C arm’ imaging device. All end-​tidal CO2 monitoring in hypercapnic patients.
bronchoscopic accessories required for the procedure
should be assembled. For patients with an ETT (or Personnel and Skills
tracheostomy) being ventilated, a ‘swivel adaptor’ is Typically, in the CICU, a bronchoscopy requires the
connected between the tube and ventilator tubing bronchoscopist, an anaesthetist (to separately monitor
to allow bronchoscope access without losing venti- sedation and ventilation parameters), a nurse assisting
lation pressure (see Figure  5.1). For those not being the bronchoscopist and a further nurse to control the
invasively ventilated, ensure an appropriate mode of position of the ETT/​tracheostomy or provide general
delivery of ventilation or oxygen is established (e.g. a support for the procedure. The bronchoscopist and
Venturi mask, CPAP or non-​invasive ventilation full their nursing assistant should have the requisite com-
face mask, laryngeal mask airway). The patient’s vital petency to perform the intended procedures and be

13:41:59 33
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Section 1: Diagnosis

(a) (b)

Figure 5.1  Bronchoscopy swivel catheter mount. (a) Close up image of the bronchoscope entering the catheter mount via a self-​sealing soft
rubber ring. This allows for reduced air leakage during bronchoscopy of an invasively ventilated patient. (b) Bronchoscope entering the catheter
mount and passing via the endotracheal tube (ET). To ensure smooth passage down the ET tube, lubricant is applied to the outside of the
bronchoscope. (A black and white version of this figure will appear in some formats. For the colour version, please refer to the plate section.)

familiar with the equipment and devices used. They demonstrated this can be an effective option
must also be able to deal efficiently with potential in patients in respiratory failure with PaO2/​
complications. FiO2 <300 and can be well tolerated by patients.
A full face mask or hood can be used with the
Precautions bronchoscope accessing the mask through a
All staff should wear personal protective equipment. swivel adaptor attached to the front of the mask
At the very least gloves, an apron, face mask and eye (see Figure 5.2).
shield. For patients with potentially transmissable dis-
eases through aerosolisation, an FFP3 or respirator With General Anaesthesia
face mask should be used and local infectious disease
• Laryngeal mask airway. This can be useful for
control guidance sought where needed.
complex procedures (e.g. airway debridement,
The bronchoscope should be lubricated with
stenting) where the bronchoscope is withdrawn
sterile gel to facilitate easy passage and reduce the risk
and reinserted repeatedly.
of damage.
• ETT. Most patients in the CICU will be
Ventilation and Oxygenation Options mechanically ventilated by ETT. The internal
Adequate ventilation during bronchoscopy aims to diameter of the ETT should be at least 2 mm
achieve a consistent SpO2 >90% with patient comfort larger than the external diameter of the
and normal haemodynamics. If the procedure is likely bronchoscope to permit effective ventilation
to be complex and prolonged, or have significant risk and prevent scope damage. The ETT should
of airway compromise, invasive ventilation or a laryn- also be withdrawn as necessary to allow the
geal mask airway should be considered –​or in some bronchoscope easy access to both main bronchi.
cases rigid broncoscopy in theatre. If invasively venti- • Tracheostomy. The internal diameter of the tube
lated, the patient is preoxygenated with FiO2 1.0 start- (usually quoted as the internal diameter of the
ing 10 minutes preprocedure. outer tube if an inner tube is also present) must
be 2 mm greater than the external diameter of
the scope. A standard adult bronchoscope with
With Conscious Sedation external diameter 5.5–​6.2 mm should safely fit
• Self-​ventilating with oxygen delivered by nasal in a size 8–​10 tracheostomy tube. The inner tube
cannulae or a face mask (Venturi or Hudson). should be removed if present and the 15 mm
• Self-​ventilating on CPAP or non-​invasive connector attached to a swivel adaptor. Special
ventilation (NIV) with oxygen. Studies have care should be taken during scope withdrawal

13:41:59
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Chapter 5: Bronchoscopy

(a) (b)

Figure 5.2  Bronchoscopy during non-​invasive ventilation using modified full face masks (a) via the oral approach using a bite block and
(b) via the nasal approach. (A black and white version of this figure will appear in some formats. For the colour version, please refer to the
plate section.)

to prevent tube displacement or shearing of the patients, lung transplant recipients, renal or hepatic
scope on the distal end of the tracheostomy tube. disease, malnutrition, platelet dysfunction or those
Fenestrated tubes can pose particular risks in this with acquired coagulopathies.
regard. Other risks include pneumothorax (7–​15% with
lung biopsies), significant cardiac arrhythmia (3–​
The Procedure 5%), oxygen desaturation, which may persist for sev-
eral hours postprocedure (especially in patients with
In spontaneously breathing patients on oxygen, or
ARDS), bronchospasm and haemodynamic instability.
CPAP/​ NIV, the upper airway is anaesthetised with
Postbronchoscopy fever occurs in 5–​16% of patients
lidocaine spray and the nostrils with lidocaine gel.
due to release of inflammatory mediators a few hours
Care must be taken with lidocaine dosing in the eld-
after the procedure and is self-​limiting. Finally, one
erly and those with cardiac, hepatic or renal impair-
must also be aware of the effect of medications used
ment. Although up to 15.4 mg/​ kg has been used
during the procedure. Lidocaine toxicity may present
without adverse effects, mild forms of lidocaine toxicity
with tremulousness, shivering, dizziness and progress
have also been reported with doses above 9.6 mg/​kg.
to sedation, unconsciousness, and convulsions fol-
The British Thoracic Society recommends a dose not
lowed by cardiorespiratory collapse. Blood concen-
exceeding 8.2 mg/​kg ideal body weight. Effective cough
trations after topical application may be 30% of that
suppression can be associated with total lidocaine dose
obtained by rapid intravenous administration. In the
<160 mg and the aim should be to use the lowest dose
ventilated patient, early features may not be clinically
to achieve the desired effect. The dose used must always
apparent and therefore care must be exercised with
be documented. The transnasal approach is contrain-
dosing and the operator vigilant for signs of toxicity.
dicated in patients with coagulopathy due to the risk of
epistaxis. The oral approach requires a mouth guard to
prevent biting of the bronchoscope. A summary of the
process in ventilated patients is given in Table 5.4. Learning Points
• Flexible bronchoscopes typically have an external
Complications of Bronchoscopy diameter 5.5–​6.2 mm with working channel 2.0–​
Reported complications of FB in the ICU are less 3.2 mm. Be familiar with local equipment. Some
than 10% with a mortality rate 0.01–​0.05%. Death instruments require a larger working channel.
from bleeding ranges from 0.03% to 0.05% and is • The inner diameter of an ETT must be at least
usually confined to those undergoing biopsy (typ- 2 mm larger than the external diameter of the
ically transbronchial lung biopsy) procedures. The bronchoscope. Replace the ETT or use a smaller
risk of bleeding is increased in immunocompromised bronchoscope if necessary.

13:41:59 35
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Section 1: Diagnosis

Table 5.4  Summary of the bronchoscopy process in ventilated patients

1 Ensure ETT/​tracheostomy internal diameter >2 mm larger than diameter of bronchoscope. Change if needed, or consider using a
thin/​paediatric scope if necessary.
2 Attach a swivel adaptor to the 15 mm connector.
3 Increase sedation and consider opiate antitussive or muscle relaxants.
4 FiO2 increased to 1.0 starting 10 minutes prior to procedure. Unless life-​saving, postpone bronchoscopy if SpO2 remains <90%.
5 Mandatory ventilation mode used. Volume control may result in unacceptably high peak airway pressures. Pressure controlled
modes require an increase in peak pressure setting.
6 Aim for tidal volume (TV) 6–​8 ml/​kg ideal body weight.
7 PEEP stopped or reduced by 50% during the procedure.
8 Lubricate the scope well with sterile gel and insert through the swivel adaptor into the airway. An assistant should hold the ETT
throughout the procedure.
9 Instill 2 ml aliquots of 1–​2% lidocaine to trachea, carina, right and left bronchial tree.
10 Use suction sparingly and no more than 3 seconds each time.
11 If using diathermy or laser in the airway, ensure the FiO2 is < 0.4 to minimise the risk of airway fire.
12 Monitor blood pressure, pulse, electrocardiography, oximetry, end-​tidal CO2, sedation, VT and peak airway pressures throughout
the procedure.
13 If oxygenation cannot be maintained, or there is haemodynamic instability, the procedure must be terminated and the patient
stabilised.
14 Check the position of the ETT at the end of the procedure.
15 Wean FiO2 and reinstate preprocedure ventilation parameters after the procedure.
16 A chest X-​ray after bronchoscopy is important to exclude complications including pneumothorax and to assess the result of an
intervention.

• Physiological effects are variable but generally British Thoracic Society Interventional Bronchoscopy
include increased PEEP, FRC and airway Guideline Group. British Thoracic Society
pressures, with reduction in SpO2, VT and FEV1. guideline for advanced diagnostic and therapeutic
flexible bronchoscopy in adults. Thorax. 2011; 66:
Parameters need continuous monitoring and
1–​21.
ventilation settings adjusted where appropriate.
Chen A, Kollef MH. Bronchoscopy in the intensive care
• Unless for life-​saving intent, bronchoscopy
unit. In: Wang K-​P, Mehta AC, Turner JF (Eds).
must not be performed where SpO2 cannot be Flexible Bronchoscopy, 3rd Edition. Oxford: Wiley-​
maintained >90% with FiO2 1.0. Blackwell, 2012. doi:10.1002/​9781444346428.ch24
• Be alert to signs of local anaesthetic toxicity. Du Rand IA, Blaikley J, Booton R, et al. British Thoracic
Use the lowest effective dose and no more than Society guideline for diagnostic flexible bronchoscopy
8.2 mg/​kg ideal body weight. Document the in adults. Thorax. 2013; 68: 1–​44. doi:10.1136/​
dose used. thoraxjnl-​2013–​203618
Estella A. Bronchoscopy in mechanically ventilated
Further Reading patients. In: Haranath SP (Ed). Global Perspectives on
Bronchoscopy. InTech, 2012. http: //cdn.intechopen.
Antonelli M, Conti G, Rocco M, et al. Noninvasive
com/pdfs/37333/In Tech-Bronchoscopy-in_
positive-​pressure ventilation versus conventional
mechanically_ventilated_patients.pdf.
oxygen supplementation in hypoxemic patients
undergoing diagnostic fiberoptic bronchoscopy. Chest. Khalil A, Soussan M, Mangiapan G, et al. Utility of
2002; 121: 1149–​1154. high-​resolution chest CT scan in the emergency
management of haemoptysis in the intensive care
Bion JF, Barrett H; CoBaTrICE Collaboration, European unit: severity, localization and aetiology. British Journal
Society of Intensive Care Medicine. Development of Radiology. 2007; 80: 21–​25.
of core competencies or an international training
programme in intensive care medicine. Intensive Care. Kreider ME, Lipson DA. Bronchoscopy for atelectasis in
2006; 32: 1371–​1383. the ICU. Chest. 2003; 124: 344–​350.

13:41:59
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Chapter 5: Bronchoscopy

Krell WS. Pulmonary diagnostic procedures in the Raoof S, Mehrishi S, Prakash UB. Role of bronchoscopy in
critically ill. Critical Care Clinics. 1988; 4: 393–​407. modern medical intensive care unit. Clinics in Chest
Lindholm C, Ollmann B, Snyder J, Millen E, Grenvik Medicine. 2001; 22: 241–​261.
A. Cardiorespiratory effects of flexible fiberoptic Toma TP, Kon OM, Oldfield W, et al. Reduction of
bronchoscopy in critically ill patients. Chest. 1978; persistent air leak with endoscopic valve implants.
74: 362–​367. Thorax. 2007; 62: 830–​833.
Olopade CS, Prakash UBS. Bronchoscopy in the
critical care unit. Mayo Clinic Proceedings. 1989;
64: 1255–​1263.

MCQs
1. Which of the following is true during bronchoscopy in (d) Paediatric bronchoscope
a ventilated patient? (e) Rigid bronchoscope
(a) Tidal volume is reduced 4. When undertaking a bronchoscopy via a tracheos-
(b) PEEP is reduced during suctioning tomy which one of the following is correct?
(c) PaO2 can rise in some scenarios (a) The tracheostomy tube should have an internal
(d) Mean arterial pressure can be reduced diameter >2 mm compared to the bronchoscope

(e) All of the above (b) The inner tube should remain in situ

2. Which of the following is NOT a relative contraindica- (c) No additional considerations are needed if the tube
tion for bronchoscopy? is fenestrated

(a) Tachyarrhythmia (d) Additional sedation is routinely required in add-


ition to topical local anaesthetic
(b) PEEP >15 cmH2O
(e) A swivel adaptor is not required in this setting
(c) Aspirin
5. Which of the following cannot be done directly via the
(d) INR >1.5 or platelets <20 × 109/​l working channel of the flexible bronchoscope?
(e) Intracranial hypertension (a) Bronchial biopsy
3. Which of the following will fit down a double lumen (b) Endobronchial valve placement for bronchopleural
endotracheal tube? fistula
(a) Linear EBUS (endobronchial ultrasound) scope (c) Cryotherapy
(b) Standard bronchoscope with outer diameter (d) Bronchial stent placement
of 5.7 mm
(e) Foreign body extraction
(c) Interventional bronchoscope with outer diameter
of 6.2 mm

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:41:59 37
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38

Section 1 Diagnosis

Microbiology Testing
Chapter

6 A Ruth M Kappeler and Margaret I Gillham

Introduction enable appropriate sampling of patients and as short a


time as possible to sample processing whether the unit
Infections in cardiothoracic intensive care units are
has an on-​site or off-​site laboratory. There should be
common, either as the primary presenting illness as in
24 hour access to the laboratory for handling urgent
the case of infective endocarditis or severe respiratory
samples and for viewing results. Furthermore, round-​
failure, or as a secondary complication of cardiothor-
the-​clock accessibility to infection specialists is crucial
acic procedures. Moreover, infectious complications
to ensuring correct test selection, timely reporting,
are known to impact on morbidity and mortality.
interpretation of microbiology results, infection con-
The sites of infection encountered include surgical
trol and antimicrobial advice.
site infections (including organ space), device related
infections (prosthetic valve endocarditis, ventricular
assist device infections), bloodstream infections, line Ordering of Tests
related infections, respiratory tract, gastrointestinal Most hospitals use an electronic ordering system for
tract and urinary tract infections. pathology requests, including those for microbiology.
The time taken to identify microorganisms in clin- Testing protocols can be set up to ensure that the appro-
ical samples can have an impact in the management priate range of tests is ordered for different clinical
of patients with sepsis. Best practice in collection and scenarios. For example, patients admitted with severe
timely processing of microbiological samples is essen- respiratory failure for ECMO will require extensive
tial, not only to ensure optimal antimicrobial manage- testing on admission to critical care (see Table 6.1 for
ment and thereby outcome, but also to ensure optimal guidance on test selection for this scenario) whereas
infection control management of patients within car- patients admitted for elective cardiac surgery, who
diothoracic units. The ability to culture organisms from have no complications, will only require preoperative
clinical samples is affected by type and quality of the spe- screening samples. Electronic ordering systems can be
cimen, prior antibiotic therapy, transportation, storage set up as specimen or sample type based. It is important
conditions of samples and time to sample processing. to ensure from the outset that the way the system is con-
Emerging technologies are enabling faster identification figured not only allows ease of ordering for the clinical
and quantification of pathogens, resulting in more rapid user but also includes a degree of demand management
diagnostics. This has the potential not only to affect to reduce inappropriate testing. Electronic test order-
patient outcome but also to ensure better antimicrobial ing also allows the development of testing sets whereby
stewardship by enabling targeted antimicrobial therapy a standard protocol for microbiology testing can be
and avoidance of unnecessary antimicrobial use which agreed according to the patient’s circumstances, and the
can lead to adverse effects for patients and encourage same testing strategy can be followed each time. This
development of resistance in bacteria. It is necessary can be beneficial in cases of severe respiratory failure
to perform a systematic physical examination before on ECMO where an infective cause is suspected or for
requesting diagnostic tests as this will enable test selec- patients who develop postoperative sepsis.
tion and avoid unnecessary sampling.
The importance of microbiological diagnostics to Correct Sampling Procedures
cardiothoracic units cannot be underestimated and General principles apply to collection of all micro-
units need to ensure that processes are in place to biology samples. They should be collected at the correct

13:43:27
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39

Chapter 6: Microbiology Testing

Table 6.1  Suggested testing set for patients with severe that the correct procedures are followed so that sam-
respiratory failure requiring ECMO ples are transported safely and in a timely manner to
Baseline tests the laboratory. Samples requiring immediate atten-
Sample Organism tion for processing should be notified to the labora-
tory in advance and identified as urgent. All samples
Blood Human immunodeficiency
(HIV) virus should be transported with completed information
Herpes simplex virus (HSV) IgG identifying the patient, time and date collected, tests
and PCR required and antibiotic history. This may be in bar
Cytomegalovirus (CMV) IgG and PCR code format or with a physical request form. Samples
N. meningitidis PCR with risk of infection should be identified by the clin-
Pneumococcal PCR ical user and visible to the laboratory handling the
Mycoplasma and chlamydia sample. Where possible, samples should be collected
serology
prior to antibiotic therapy but this should not lead
Blood cultures
to delays in managing the patient or administering
Bronchoalveolar lavage Respiratory virus PCR
antibiotics.
CMV, HSV, adenovirus PCR
Hand hygiene should be performed before and
Pneumocystis jirovecii PCR
Galactomannan
after specimen collection. Personal protective equip-
Legionella culture and PCR ment (gloves, waterproof apron) is required during
Mycoplasma pneumoniae PCR specimen collection when contact with bodily flu-
Chlamydophila pneumoniae PCR ids is anticipated. Masks may be required for collec-
Smear and culture for tion of respiratory samples, for example with sputum
Mycobacterium tuberculosis induction.
Fungal culture Blood cultures are taken when bacteraemia is sus-
Routine culture pected and should be taken via a dedicated venepunc-
Nose and throat viral Respiratory virus PCR ture, peripherally, rather than through an existing
swab Consider pernasal swab for pertussis line. Where endocarditis or device related infection
Urine sample Culture is suspected, up to three sets can be taken at separate
Legionella antigen times over a 24 hour period. However, it is the actual
Pneumococcal antigen
volume of blood that is important, therefore inocu-
lating one bottle with the correct volume of blood is of
Additional tests
greater value than sharing the blood volume between
Risk factor/​clinical Organisms to consider multiple bottles. Local procedures should be followed
feature when taking blood cultures to minimise the risk of
Immunocompromised Cryptococcus contamination with skin flora. When using vacuum
Exposure to rodents or Leptospirosis blood taking systems, care should be taken that blood
contaminated fresh water Hantavirus cultures are inoculated first before filling other blood
Rash Varicella zoster virus tubes. This is to prevent the possibility of bacterial
HSV contamination from blood tubes entering the blood
Measles culture bottles, resulting in a ‘pseudobacteraemia’
Toxic shock Staphylococcus aureus and assigned to the patient.
Streptococcus pyogenes Stool samples should only be sent for micro-
Travel MERS, avian influenza, malaria biology testing when an infective cause is suspected
Animal contact Anthrax, Coxiella for patients with diarrhoea. The Bristol stool scale
can be used to identify diarrhoea stools where types
5–​7 indicate diarrhoea. Clostridium difficile should be
time, using the correct technique, the correct volume considered as a cause of hospital acquired infective
and in the correct specimen containers. Lids must be diarrhoea in cardiothoracic centres and requested as a
tightened securely as leakage may mean specimen specific test. Laboratory testing should follow national
rejection, and clinicians and laboratories must ensure testing guidelines to ensure optimal diagnosis. In the

13:43:27
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40

Section 1: Diagnosis

UK this amounts to a combination of tests looking for time as possible to sample processing. Microscopy per-
presence of the C. difficile organism and the presence formed on arrival in the laboratory can provide essen-
of toxin. tial information on the presence of organisms and can
Care should be taken when obtaining respiratory aid antimicrobial management. In patients who have
samples that sputum is collected rather than saliva. had previous cardiac surgery and who develop a deep
Physiotherapists can help with obtaining a good infection or endocarditis where no pathogen is identi-
quality respiratory sample. Any respiratory sample fied, mycobacterial infection should be considered.
obtained in a trap should be transported in a leak-​
proof CE marked specimen container. Lower respira- Screening for Resistant Organisms
tory tract samples can be obtained by directed or
Screening for methicillin resistant Staphylococcus
non-​directed BAL. Respiratory samples in particular
aureus (MRSA) prior to cardiac surgery and on
must reach the laboratory in a timely manner and
admission to hospital is standard practice in UK
should be processed within 2–​3 hours to maximise the
hospitals. Persons carrying MRSA will be offered
chance of culturing respiratory tract organisms.
decolonisation treatment prior to surgery, where
Wound swabs are best obtained after first cleansing
time allows. Some centres also screen for methicillin
the wound. This reduces the risk of contamination of the
sensitive Staphylococcus aureus (MSSA) and offer
sample with therapeutic agents that may be contained
decolonisation prior to cardiac surgery or insertion
within the dressing material. Dry swabs should be mois-
of ventricular assist devices (VAD). Screening for
tened with sterile water (or saline) or transport media.
other resistant organisms is carried out ­ according
Where possible the whole wound should be swabbed
to local and national recommendations but may
using a zigzag movement while rotating the swab.
include vancomycin resistant enterococci (VRE), car-
Fluid from vesicular lesions can be aspirated or
bapenemase producing Enterobacteriaceae (CPE),
swabs used to collect the vesicular fluid and inocu-
multidrug resistant (MDR) Acinetobacter spp.,
lated into viral transport media (VTM).
Enterobacteriaceae producing extended spectrum β-​
Urine samples are collected as a midstream sample
lactamases (ESBL) or AmpC β-​lactamases. The fre-
after first cleaning the urethral meatus with soap and
quency and nature of who is screened depends on
water or saline. Disinfectants should be avoided as
local resistance patterns, carriage rates, and healthcare
they can irritate the urethral mucosa. However, the
associated infection rates within the local setting and
vast majority of patients in ICU will have a urinary
those of referring hospitals. It is important to note that
catheter in situ. Catheter specimens of urine should
any screening programme should be monitored on a
only be taken where urosepsis is suspected. The cor-
regular basis and action taken when carriage or clin-
rect local procedure should be followed and urine
ical infection rates exceed those expected for a local
sampled through the catheter sampling port.
unit. The implementation of an enhanced screening
If urine samples cannot be examined within 2
programme also depends on what action can be taken
hours then they should be refrigerated until they can
if patients are found to be positive. This may involve
be processed by the laboratory. Urine samples held at
commencement of specific infection control precau-
room temperature will allow overgrowth of bacteria,
tions and/​or alteration in prophylactic regimens for
affecting the result. The addition of boric acid to urine
surgery, VAD insertion or transplantation to ensure
containers will preserve the urine sample for longer
that the antibiotic cover at the time of surgery covers
where transport delays exist.
the resistant organism. One very important factor in
being able to action positive screening results within
Surgical Samples critical care units is the availability of side rooms.
Any samples obtained at the time of surgery should be
placed into a sterile pot for onward transportation to the Microscopy and Culture
laboratory. Samples may include native or prosthetic Microscopy and culture of samples continues to be
heart valves, sternal wound biopsies or samples of pus the mainstay of microbial diagnostics. Microscopy
or fluid. These surgical samples are precious, unrepeat- is a quick, useful test indicating the presence of
able specimens and should be notified to the labora- organisms from normally sterile sites, for example
tory ahead of the sample arriving to ensure as short a blood, pericardial fluid or surgical samples, and

13:43:27
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Chapter 6: Microbiology Testing

also for determining smear positivity in the case of for example aminoglycosides and glycopeptides.
Mycobacterium tuberculosis. Microscopy is less useful Pharmacokinetics and dynamics of various antimi-
at determining the presence of pathogens in samples crobials vary in vivo, for poorly understood reasons,
from non-​sterile sites, i.e. the respiratory tract. Urine in many cardiothoracic critical care patients. This is
microscopy can aid in the differentiation between especially true in patients on ECMO where maximum
infection or contamination of the sample by the pres- licensed drug dosing regimens may need to be used
ence of significant numbers of pus cells. Microscopy in drugs with a wide therapeutic window. The alter-
of urine samples is not helpful in catheterised nation of PK/​PD is poorly understood in this set of
patients. Culture of the sample is more informative patients but drugs may be sequestered or broken down
than microscopy to enable organism identification as a result of the ECMO circuit. Dosing regimens may
and sensitivity testing. However, this takes time and need to be adjusted based on levels informed by thera-
is influenced by transport times, storage conditions peutic drug monitoring.
and prior antibiotic use. Culture results from non-​
sterile sites require a degree of interpretation, taking New Technologies
into account the expected normal flora from the spe-
Speed is an essential factor in the diagnosis of sepsis
cific site. Furthermore, there are some organisms that
and in other acute organ dysfunction states, i.e. severe
by their very nature are difficult to culture, or cannot
respiratory failure, where the appropriate manage-
be cultured or present a danger to laboratory staff.
ment of infection affects outcome. One of the issues is
Thereby other methods of organism identification
that the diagnosis of sepsis can be difficult as clinical
are used.
signs can overlap with other non-​infectious systemic
inflammatory states and blood culture results may
Antibiotic Susceptibility Testing take days to complete. New technologies being devel-
Performing antimicrobial sensitivity testing is another oped and introduced into clinical laboratories have
important function of the microbiology laboratory. the potential to speed up microbial diagnosis within
The aim is to inform antimicrobial treatment deci- cardiothoracic units.
sions and detect antimicrobial resistance. Sensitivity
testing requires live organisms and is performed using
a variety of testing methods. Manual disc diffusion Molecular Testing
assays are the mainstay of antimicrobial testing for The development of polymerase chain reaction
most organisms in UK laboratories, alongside gra- (PCR) and other nucleic acid-​based amplification
dient diffusion methods (including E-​tests). Disc test- technologies (NAATs) over the last 20  years has
ing provides a qualitative measurement, recording the helped to address some of the downsides of culture.
organism as sensitive, intermediate or resistant. More The introduction of such molecular techniques into
qualitative methods that provide a more accurate min- routine clinical microbiology laboratories has revo-
imum inhibitory concentration (MIC) are required lutionised microbial diagnostics. These techniques
for organisms that give borderline results with disc are now used as the primary diagnostic method
diffusion methods or where a more accurate measure for HIV, hepatitis viruses and respiratory viruses.
is required, for example in management of endocar- Amplifying and detecting microbial and genetic
ditis. In addition to manual methods, there are auto- sequences within a prepared clinical sample improves
mated methods commercially available. speed, sensitivity and specificity of microbial testing
and is not so affected by specimen transport times
or prior antibiotic use. The range of organisms that
Therapeutic Drug Monitoring for molecular tests are routinely used for has expanded
Antimicrobials from HIV, hepatitis viruses and respiratory viruses
This is another important function traditionally into bacterial, fungal, parasitic and atypical agents.
carried out in microbiology laboratories but now These techniques are not only used for the diagnosis
often performed in blood science laboratories. Drug of infectious disease but also in the detection of
monitoring is important in drugs with a narrow drug resistant genes. These methods, with the devel-
therapeutic window where it is important to ensure opment of nanotechnology, are also now used for
maximum drug dosing with minimum risk of toxicity, point-​of-​care testing.

13:43:27
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Section 1: Diagnosis

Sequencing organisms detected from non-​sterile sites require a


degree of interpretation of the result to consider when
Several sequence based methods have been used to
the organism is a pathogen, when it is normally found
identify microorganisms directly from clinical samples
at that site or when it represents contamination of the
including blood cultures, biopsies and heart valves.
sample. The diagnosis of infection in these circum-
The cost of these tests is high compared with conven-
stances needs to be taken into consideration with the
tional diagnostic methods and they are best used on
clinical picture, inflammatory markers, presence of
samples from normally sterile sites. However, ampli-
fever and localising signs. If the organism is repeatedly
fication and sequencing of 16S rRNA present within
isolated and pus cells are seen on microscopy, the evi-
heart valve samples where no organism has been cul-
dence points to the likelihood of the organism being
tured has changed microbial diagnostics in culture-​
pathogenic.
negative endocarditis. Amplification and sequencing
of 18S rRNA is also of value in the identification of
fungal pathogens from samples from normally sterile Liaison with Medical Microbiologists
sites, for example pleural fluid, lung biopsy. These Close liaison on a regular basis between clinical teams
techniques are being researched and developed for and infection specialists is essential to optimise infec-
use in samples from other sites, including the lower tion prevention, diagnosis and management of car-
respiratory tract. diothoracic patients. Such specialist input will not
only optimise appropriate use of antibiotics and infec-
Mass Spectrometry tion control management, but will also assist with
Matrix-​assisted laser desorption/​ionisation time-​of-​ specimen requesting, provision of laboratory services,
flight mass spectrometry (MALDI TOF MS) is being appropriate use of technologies, and rapid interpret-
used currently for the routine identification of bac- ation and communication of critical results.
terial colonies from positive cultures. Although it
requires culture of the organism and sensitivity testing Learning Points
by conventional means, it provides rapid turnaround • Infections in cardiothoracic intensive care units
of pathogen identification with a minimal amount are common and antimicrobial drugs are used
of labour compared with traditional identification widely and sometimes unnecessarily.
methods. • Correct diagnosis of infections requires careful
physical examination of patients as well as
Microarrays appropriate microbiology testing.
This ‘test-​all’ approach allows identification of a large • New technologies being developed and
panel of microbial pathogens from a single sample on introduced into clinical laboratories have the
a single test card within one test run. Cards can be potential to speed up microbial diagnosis within
developed to cover a whole range of relevant patho- cardiothoracic units.
gens based on a syndromic approach. This may prove • Close liaison on a regular basis between clinical
useful in the infection diagnosis of patients with severe teams and infection specialists is essential.
respiratory failure requiring ECMO. The cost of this • Such specialist input will not only optimise
test is comparable to the combined cost of running the appropriate use of antibiotics and infection
PCR tests individually by conventional means, but has control management, but will also assist with
potential clinical benefit in terms of ease of request- specimen requesting, provision of laboratory
ing, sampling and turnaround times. services, appropriate use of technologies, and rapid
interpretation and communication of critical results.
Interpretation of Results
The finding of an organism from a normally sterile site Further Reading
is usually diagnostic of infection with that pathogen. Caliendo AM, Gilbert DN, Ginocchio CC, et al. Better
Some organisms are only ever present when causing tests, better care: improved diagnostics for infectious
an infection, therefore their detection implies infec- diseases. Clinical Infectious Diseases. 2013; 57(Suppl 3):
tion, for example, Mycobacterium tuberculosis. Other S139–​S170.

13:43:27
.008
43

Chapter 6: Microbiology Testing

Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis Schweizer ML, Chiang HY, Septimus E, et al. Association
campaign: international guidelines for management of of a bundled intervention with surgical site infections
severe sepsis and septic shock. Intensive Care Medicine. among patients undergoing cardiac, hip or knee
2013; 39: 165–​288. surgery. Journal of the American Medical Association.
Kohler P, Kuster SP, Bloemberg G, et al. Healthcare-​ 2015; 313: 2162–​2171.
associated prosthetic heart valve, aortic vascular graft, Tsai D, Lipman J, Roberts JA. Pharmacokinetic/​
and disseminated Mycobacterium chimaera infections pharmacodynamic considerations for the optimization
subsequent to open heart surgery. European Heart of antimicrobial delivery in the critcally ill. Current
Journal. 2015; 36: 2745–​2753. Opinion in Critical Care. 2015; 21: 412–​420.
Liesenfeld O, Lehman L, Hunfeld KP, et al. Molecular Vondracek MI, Sartipy U, Aufwerber E, et al. 16S rDNA
diagnosis of sepsis: new aspects and recent sequencing of valve tissue improves microbiological
developments. European Journal of Microbiology and diagnosis in surgically treated patients with infective
Immunology. 2014; 4: 1–​25. endocarditis. Journal of Infection. 2011; 62: 472–​478.
Robich MP, Sabik JF, Houghtaling PL, et al. Prolonged Wolk DM, Dunne(Jr) WM. New technologies in clinical
effect of postoperative infectious complications on microbiology. Journal of Clinical Microbiology. 2011;
survival after cardiac surgery. Annals of Thoracic 49(suppl 9): S62–​S67.
Surgery. 2015; 99: 1591–​1599.

MCQs
True or False 3. Sequencing techniques are best used for samples from
1. Microscopy has been superseded as a method used in normally sterile sites.
bacteriology laboratories. 4. The length of time a sample takes to get to the labora-
2. Molecular testing can only be used for organism tory does not affect the ability to culture pathogens.
identification and not for detection of antimicrobial 5. Finding an organism in a sample always indicates an
resistance. infection.

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:43:27
.008
44

Section 1 Diagnosis

Radiology for Cardiothoracic Intensivists


Chapter

7 Kristian H Mortensen, Peter A Barry and Deepa Gopalan

Introduction rarely attainable; (c) Distribution of fluid and air in the


pleural space is altered, where a pneumothorax will
Diagnostic imaging of patients in the cardiothoracic
locate to the anterior pleural space and pleural effusions
intensive care unit (ICU) can pose unique challenges.
settle posteriorly on supine CXR, albeit loculations may
Where possible, the patient should be imaged in situ
limit the free movement of pleural collections particu-
using mobile chest X-​ ray (CXR) and ultrasound,
larly. This may happen when there is longstanding
including transthoracic (TTE) and transoesophageal
pleural disease, prior malignancy or previous surgical
echocardiography (TOE), unless computed tomog-
intervention, and ultrasound or CT will often be pref-
raphy (CT) is specifically required. An outline of the
erable; (d) Forward slumping may obscure apical pul-
advantages and limitations of each imaging modality
monary disease or pneumothorax; (e)  Rotation  –​as
is followed by presentation of the optimal use and
judged by medial clavicles not being equidistant from
escalation of imaging to diagnose specific cardio-
the midline relative to the spinous processes  –​may
respiratory conditions in the context of this highly
mimic mediastinal disease; and (f)  Artefacts such as
specialised setting.
skin folds, hair braids, asymmetrical soft tissues, moni-
toring leads and other radio-​opaque equipment over-
Cardiothoracic Imaging Modalities lying the field of interest, may degrade the diagnostic
quality and should be minimised prior to imaging.
Chest X-​ray
Chest X-​ray (CXR) has a high diagnostic accuracy Ultrasound
for the assessment of the position of lines, tubes and Bedside thoracic ultrasound is predominantly used
drains. When compared with this area and imaging of for assessment of pleural effusions, and to confirm
the lungs and pleural spaces, the accuracy of CXR is CXR findings. Ultrasound may give clues to the nature
less impressive for cardiovascular disease, and hence of a pleural effusion, and has an important role in
CXR should never delay other definitive cardiovas- image-​guided thoracic interventions. In experienced
cular imaging in the ICU patient. In established car- hands, ultrasound can also assess for pneumothorax,
diorespiratory disease, serial CXR has an additional but emphysematous lung has the potential to cause
role in the investigation of evolving respiratory misdiagnosis and ultrasound is of limited practical
compromise or non-​response to treatment. Despite use. Extensive subcutaneous emphysema and severe
ease of use, daily routine bedside CXR is no longer obesity may limit adequate visualisation of the pleural
encouraged because this does not appear to improve spaces. Echocardiography is invaluable in the assess-
outcomes in ICU patients compared with a directed ment of cardiac valves and chamber function as well
approach. as any pericardial disease, and has been dealt with in a
In the majority of ICU patients, the CXR is acquired dedicated chapter (see Chapter 3).
bedside with the patient in the semi-​erect or supine pos-
ition. This has several effects: (a) This gives an antero-
posterior (AP) projection, with apparent enlargement Computed Tomography
of cardiac and mediastinal structures compared to the Thoracic CT is of immense value in the assessment
posteroanterior (PA) projection obtained in the ambu- of the ICU patient, particularly when CXR find-
latory setting; (b)  An optimal full-​inspiratory view is ings are equivocal or if complex disease processes

13:44:45
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45

Chapter 7: Radiology for Cardiothoracic Intensivists

are suspected. CT adds valuable information to CXR Acute Aortic Syndrome


findings in up to 70%, changing management in 22%. Aortic dissection, intramural haematoma and pene-
The cross-​sectional nature of CT allows more detailed trating ulcer together comprise acute aortic syndrome
interrogation of disease processes and can also provide (Figure  7.1), which is classically encountered in
image guidance for interventions. CT has a particular patients with systemic hypertension or those with pre-
role when cardiac and great vessel disease such as disposing factors such as connective tissue disease.
pulmonary embolus (PE) and acute aortic syndrome However, it can also occur in healthy vessels as a con-
are suspected, but is also a key diagnostic tool for the sequence of iatrogenic injury following intra-​arterial
diagnosis of postoperative thoracic collections, pleural catheterisation and intra-​aortic balloon pump inser-
or pulmonary sepsis, malignancy, complications of tion. Potentially devastating consequences of aortic
mechanical ventilation, concurrent pulmonary path- dissection include extension into the aortic annulus
ologies, and in the assessment of life support device leading to severe aortic regurgitation, rupture into the
related complications. The diagnostic yield of CT must pericardium causing cardiac tamponade or multiorgan
be weighed against the risks of transporting the ICU ischaemia (coronary, cerebral, spinal, and visceral).
patient to the imaging department. Potentially nephro- CXR has limited value in diagnosing acute aortic
toxic intravenous iodinated contrast medium should syndrome, with a sensitivity of 64% and a specificity
be used with caution, and where potential benefit out- of 86%. Typical features are useful when present, such
weighs risk, attention to pre-​emptive renal protection as upper mediastinal widening, double aortic con-
and coordination of the timing of contrast admin- trast and discrepancy between the diameters of the
istration with haemodialysis are helpful. Radiation ascending and descending aorta, displacement of the
constraints are less of an issue in this setting, however trachea and of the left main bronchus, ill definition of
repeated CT imaging should be monitored. the aortopulmonary window, left apical cap, pleural
effusion, haemothorax and widening of the left para-
Imaging for Cardiac Emergencies vertebral sulcus, but their absence cannot exclude
the diagnosis. The CXR may be completely normal
Chest Pain in 11–​15%. Echocardiography has immense value in
unstable patients as it is portable, quick and can even
Chest pain in the ICU requires urgent appraisal. The
be used in theatres to facilitate diagnosis. The aortic
differential diagnosis is varied, ranging from life
root, valve and proximal ascending aorta can all be
threatening emergencies to more benign conditions.
assessed with relative ease using echocardiography,
A clue to the aetiology can be gained by focused his-
which also has the ability to document ancillary find-
tory, physical examination and electrocardiogram,
ings such as impairment of ventricular function and
with imaging playing a smaller role.
haemopericardium. A  major limitation of the trans­
thoracic approach, TTE, is the inability to clearly
Acute Coronary Syndrome visualise beyond the proximal ascending aorta. The
A minority of patients, particularly elderly and females transoesophageal approach, TOE, has a much higher
with risk factors for atherosclerosis such as hyperten- sensitivity of up to 98% for detecting entry tear sites,
sion, chronic renal disease or previous cerebrovascular coronary and great vessel involvement and differential
events, may sustain an acute myocardial infarction flow characteristics in the false lumen. TOE, however,
while being hospitalised for another reason. The first requires sedation and also cannot image the entire
step in its management is expeditious recognition to thoracic aorta.
optimise myocardial salvage and reduce mortality by a Multidetector CT has sensitivity and specificity of
prompt attempt of reperfusion therapy. Non-​invasive almost 100%. The high negative predictive value in
imaging such as ECG-​gated cardiac CT is not recom- combination with rapid image acquisition and wide
mended as it will not only delay consideration for availability has made CT the investigation of choice in
primary percutaneous coronary intervention (PCI) an acute setting. Triple rule out is a new concept that
or fibrinolysis but also often will be non-​diagnostic, can be used in the same study to evaluate the aorta, cor-
particularly in patients with cardiogenic shock, heart onary arteries and pulmonary vasculature. It requires
failure or ventricular tachyarrhythmia. ECG-​gating and should ideally be performed using a

13:44:45 45
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46

Section 1: Diagnosis

Figure 7.1  Acute aortic syndrome. Top panel, far left and middle images: ECG-​gated CT in a 65 year old male with acute type A aortic
dissection. The aortic root is dilated (black star) with a dissection flap (block black arrow) that extends into neck vessels (thin white arrow)
and the ostium of the left main stem coronary artery (middle image, block white arrow). Top panel, far right image: rupture of descending
thoracic aneurysm with high attenuation blood (white star) around the aorta. Bottom panel: different CT findings of acute aortic syndrome
in different patients. Intramural haematoma with a rim of high attenuation material on the unenhanced CT (far left image); aneurysmal
descending aorta with a dissection flap (middle image, thin black arrow); small penetrating ulcer in the descending thoracic aorta (far right
image, notched arrow).

scanner with 64 slice or higher detector number. The attenuation material representing the incompletely
need for simultaneous opacification of pulmonary and sheared media (cobweb sign) and a wedge of haema-
systemic circulation can be particularly challenging toma (beak sign) that forms to create a space for the
in haemodynamically unstable patients and in some development of the false lumen. Occasionally, circum-
circumstances it is better to do one focused exam- ferential dissection can be complicated by intimo-​
ination rather than an all-​in-​one approach. Initial intimal intussusception (windsock sign). Secondary
unenhanced data are useful to demonstrate crescentic features of aortic dissection include displacement of
foci of high attenuation in the aortic wall due to intra- intimal calcification, delayed enhancement or throm-
mural haematoma or a thrombosed false lumen. On a bosis of the false lumen and complications such as medi-
contrast-​enhanced examination, the classical feature astinal and pericardial haematoma and compromise
of dissection is an intimal flap that separates the true from coronary, neck vessel, mesenteric, renal and
lumen that is contiguous with the undissected vessel peripheral vascular involvement. Penetrating ulcers
from the false lumen. The false lumen generally has a are shown as focal crater-​like pouching of the aortic
larger cross-​sectional area, thin linear strands of low wall with irregular edges in the presence of extensive

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Chapter 7: Radiology for Cardiothoracic Intensivists

Figure 7.2  Pulmonary oedema and acute respiratory distress syndrome with pneumothorax. Far left image: CXR with pulmonary
oedema in a 60 year old male in the aftermath of acute myocardial infarction. Note the intra-​aortic balloon pump (block white arrow) and
Swan–​Ganz catheter (thin arrow). Middle image: CXR of a 45 year old male with acute respiratory distress syndrome on extracorporeal
membrane oxygenation (black block arrow). There is a supine, right-​sided pneumothorax (white star) with deepened costophrenic sulcus
and contralateral mediastinal shift suggestive of tension pneumothorax. Far right image: axial CT thorax in a different patient with acute
respiratory distress syndrome. Note the gravitational, dependent consolidation in the posterior lung segments with diffuse ground-​glass
opacification and fibrosis. There is a left pneumothorax (white star) and surgical emphysema (black arrow head).

aortic atheroma, which is most common in the middle (<12  mmHg); (b)  early oedema (12–​ 15  mmHg)
and distal thirds of the thoracic aorta. with vascular engorgement and peribronchovascu-
CT is the imaging modality of choice for sus- lar cuffing; (c)  interstitial oedema (15–​25  mmHg)
pected rupture. A  peripheral hyperattenuation with progressive blurring of the pulmonary vessels
crescent within the thrombus of an aneurysm on with engorgement of peribronchovascular spaces,
an unenhanced CT is a sign of acute or impending Kerley lines and subpleural effusions; and (d) alveolar
rupture, as is the close apposition of the posterior oedema (> 25  mmHg) with nodular or acinar areas
aortic wall to the spine (draped aorta sign). Rupture of increased opacity that evolve into frank consolida-
into mediastinal, pericardial or pleural spaces tion. CXR can detect the majority of these changes
gives rise to high attenuation haematoma in the and is often adequate, particularly when the mor-
respective anatomical space. Fistulous communica- phological findings are complemented by haemo-
tion with the tracheobronchial tree or oesophagus dynamic data. CT is reserved for cases where there is
is a recognised complication. CT may not show the a need to distinguish hydrostatic oedema from other
communication, but development of haemoptysis/​ causes. The combination of upper lobe predominant
haematemesis and new onset of pulmonary haem- ground-​glass opacification with a central distribution
orrhage/​ consolidation should raise the clinical and central airspace consolidation favours hydro-
suspicion. static oedema. Conversely, ARDS classically gives
rise to a gravitational anteroposterior density gra-
Pulmonary Oedema dient within the lung due to dense consolidation in
Pulmonary oedema may be hydrostatic as seen in car- the dependent region and normal or hyperexpanded
diac disease, renal failure or overhydration. Alterna­ lung in the non-​dependent regions, which merge into
tively, it may be non-​cardiogenic due to increased a background of diffuse ground-​glass opacification.
permeability oedema as encountered in acute Additionally, ARDS persists for days to weeks, does
respiratory distress syndrome (ARDS) (Figure  7.2). not respond to diuretic therapy and may progress to a
Differentiating cardiogenic and non-​cardiogenic pul- reticular pattern due to secondary fibrosis.
monary oedema is arduous, and most optimally would
require measurement of pulmonary capillary wedge Cardiogenic Shock
pressure. Image findings in hydrostatic pulmonary Cardiogenic shock is characterised by systemic hypoten-
oedema depend on the degree of elevation of the pul- sion and tissue hypoxia secondary to decreased cardiac
monary capillary wedge pressure: (a) no abnormality output. Diagnostic evaluation should be carried out in

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Section 1: Diagnosis

conjunction with resuscitative efforts. Ultrasonography Right Ventricular Failure


and TTE are essential bedside imaging modalities, The aetiology varies from worsening of compensated
which allow rapid assessment of multiple organ systems right ventricular failure, frequently seen in chronic
including cardiac chambers for biventricular function, left-​sided heart or pre-​existing lung disease such as
proximal aorta for aortic dissection, pleural and peri- emphysema, to acute right ventricular failure in mas-
cardial spaces for effusions, and the abdominal cavity sive pulmonary embolus, right-​ sided myocardial
for peritoneal fluid and organ appearances. A  port- infarction, ARDS or sepsis (Figure  7.4). Pulmonary
able CXR is useful for the exclusion of pneumothorax, artery catheterisation provides reliable and con-
whilst targeted imaging such as thoracic CT should be tinuous monitoring of haemodynamic parameters
considered in patients in whom the aetiology of the cir- whilst echocardiography allows for bedside evaluation
culatory failure remains unclear despite initial bedside of cardiac function although estimates of RV systolic
imaging. Coronary angiography should not be delayed and pulmonary artery pressure can be inaccurate in
in patients with suspected myocardial infarction who patients with chronic lung disease and those under-
might be candidates for revascularisation. going IPPV. CXR is of limited value and can dem-
onstrate generic features such as cardiomegaly and
Pericardial Tamponade
proximal pulmonary artery dilatation. It can be useful
Tamponade can occur due to collection of fluid, for tracking of lung parenchymal changes like atelec-
blood, pus, air or soft tissue within the pericardial tasis or consolidation and pleural effusions, and for
space (Figure  7.3). Although challenging, it is fore- the assessment of lines, tubes and drains. CT can be
most a clinical diagnosis and must be considered in all more useful in detailing this pathology.
patients with unexplained cardiogenic shock or pulse-
less electric activity. TTE is the most appropriate ini- Pulmonary Embolus
tial imaging modality as it facilitates assessment of the CT pulmonary angiography is the imaging modality
haemodynamic impact and may guide diagnostic and of choice in suspected PE. With optimisation of
therapeutic pericardiocentesis. Progressively enlar- contrast enhancement (Hounsfield unit >200 in the
ging cardiac silhouette resulting in a globular feature- main pulmonary artery) and minimisation of motion
less water-​bottle appearance is a characteristic feature artefact, the high spatial resolution of modern CT
on serial CXRs. However, tamponade due to pneu- scanners allows for the detection of emboli down to
mopericardium can cause reduction in the size of the 2–​3 mm. Acute emboli can occlude the entire lumen,
cardiac silhouette with sharp outlining of the pericar- or form central filling defects surrounded by a rim
dium by radiolucent air. CT is not routinely indicated of contrast, causing the ‘polo mint’ sign on images
for the diagnosis and should be reserved for cases perpendicular to the long axis of a vessel and ‘railway
where there is diagnostic uncertainty. The attenuation track’ sign on longitudinal images. When periph-
value of the collection on a precontrast scan can give eral, thrombi form an acute angle to the vessel wall
a clue to its nature, with haemopericardium typically as opposed to chronic thrombus that is eccentric with
being of higher attenuation than simple fluid. Imaging obtuse angle to the fibrosed arterial wall. The pres-
features such as compression of the cardiac chambers ence of stenosis, intravascular webs, bronchial collat-
and coronary sinus, straightening of the right heart erals and mosaic perfusion patterns implies chronic
border, interventricular septal bowing, distension of thromboembolic disease. Peripheral wedge-​ shaped
the systemic veins and reflux of contrast medium into areas of hyperattenuation representing infarcts can
the azygos vein may be seen even on non-​ECG gated be seen in acute as well as chronic thromboembolic
CT. Although the addition of gating will improve disease. Obstruction of more than 30% of the pul-
the anatomical and functional delineation, the need monary circulation can raise the pulmonary vascular
for prompt treatment should override any poten- resistance sufficiently to produce significant pul-
tial delays in image acquisition. Percutaneous drain- monary hypertension. CT signs of RV strain include a
age should be performed using image guidance, and right-​to-​left ventricular diameter ratio >1.0, leftwards
echocardiography, fluoroscopy or CT have all been septal bowing, abrupt increase in size of the azygos
shown to be successful, with the relative use of each vein, widening of the vascular pedicle, and reflux of
technique much depending on the institutional and contrast medium into a distended inferior vena cava
individual preferences. and hepatic veins.

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Chapter 7: Radiology for Cardiothoracic Intensivists

Figure 7.3  Pericardial tamponade. Top panel: pneumopericardium (left image, black arrows) and globular cardiac silhouette secondary to
pericardial effusion (right image) on CXR. Lower panel: pericardial collections on CT. Haematoma (left image, black star) with compression
of the underlying cardiac chambers, and ventricular assist device catheters in situ. Circumferential pericardial thickening and enhancement
(right image, block white arrow) secondary to a purulent collection (white star) with an enhancing left pleural collection (thin white arrow).

Complications of Cardiac Surgery tamponade and left ventricular outflow tract obstruc-
The use of cardiopulmonary bypass during cardiac sur- tion are some potential culprits. In addition to haemo-
gery results in a distinct group of postoperative com- dynamic assessment and ECG, TTE is often the most
plications. Unexplained hypotension, tachycardia and useful initial imaging modality. CXR excludes non-​
pulmonary oedema should raise the suspicion of post- cardiac complications such as pneumothorax, haemo-
surgical cardiac dysfunction. Coronary artery graft thorax, pneumonia, atelectasis, pleural effusions and
occlusion, prosthetic valve malfunction, pericardial diaphragmatic injury, and malposition of lines and

13:44:45 49
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Section 1: Diagnosis

RV

Figure 7.4  Right ventricular failure. Top panel: massive, acute pulmonary emboli (block white arrows) with right ventricular (RV)
enlargement alongside interventricular septal bowing (thin white arrow) and a pulmonary infarction (notched arrow). Bottom panel: catheter
angiography with thrombolysis for acute pulmonary embolus (left image, white arrow) and another patient with idiopathic pulmonary
arterial hypertension with right-​sided cardiac chamber dilatation and right ventricular hypertrophy (right image). The latter patient had
acute decompensation with development of pneumonia in the right lower lobe complicated by formation of segmental pulmonary artery
pseudo-​aneurysm (right image, black block arrow).

tubes. Neurological complications such as ischaemic be used with caution. Some abdominal conditions
cardiovascular insults or intracranial haemorrhage such as cholecystitis can be diagnosed by ultrasound,
will often require an unenhanced CT for confirmation. whilst persistent elevation of inflammatory markers
Bowel ischaemia can be precipitated by atheroembo- and metabolic disturbances that require exclusion of
lism, intracardiac thrombus, atrial fibrillation, acute intra-​abdominal sepsis will require a CT for more
aortic syndrome and tissue hypoperfusion. Arterial comprehensive assessment.
and portal venous phase CT of the abdomen and
pelvis is often needed but since up to 30% of patients Respiratory Emergencies
who have undergone cardiac surgery can suffer from CXR is the first line imaging modality, in the setting of
acute renal injury, iodinated contrast medium should both de novo and persistent or worsening oxygenation

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Chapter 7: Radiology for Cardiothoracic Intensivists

levels. CT offers superior accuracy for the underlying emphysema hinders the ability to diagnose under-
cause, but serial bedside radiography may in many lying pneumothorax.
instances be sufficient.

Pleural Effusion
Desaturation Associated with Pleural Fluid in the pleural space is exceedingly common in
Abnormalities the critically ill, and may be a transudate, exudate,
pus, blood or chyle. Blunting of the costophrenic
Pneumothorax angles is a sine qua non on the erect or semi-​erect
Pneumothoraces are common in the ICU but their CXR, and there may be associated volume loss of the
recognition is lacking with up to 30% missed on adjacent lung. When the effusion accumulates in the
CXR. Even small pneumothoraces are important subpulmonary space, the findings include: (a) a seem-
because they may rapidly become clinically sig- ingly elevated hemidiaphragm with a lateral shift of
nificant during positive pressure ventilation. The the diaphragmatic apex and blunted costophrenic
volume of the pneumothorax dictates the associated angle; and (b) increased density below the diaphragm
pulmonary changes, which range from small areas with no bronchovascular markings and a gastric air
of atelectasis to extensive collapse. Imaging of ten- bubble that is situated well below the apparent dia-
sion pneumothorax, with ensuing circulatory com- phragm. On supine CXR, the costophrenic angle may
promise, must not delay emergency decompression. not be blunted but there may be: (a) a hazy ‘veil-​like’
If CXR has been obtained, signs of tension include opacity, with bronchovascular markings visible, due
extensive lucency of the hemithorax with contralat- to dependent layering of the fluid in the paraverte-
eral mediastinal shift and ipsilateral diaphragmatic bral gutters and posterior pleural space; and (b)  an
flattening. apical cap (when this is most dependent) and fis-
Stereotypical CXR signs of pneumothorax include sural thickening. The presence of gas locules and
a medial position of the visceral pleural line, with loculations should raise the possibility of empyema
absent bronchovascular markings lateral to this line. (Figure  7.5). CT better characterises the complex
The air typically collects at the apex when erect or pleural collection, depicting pleural thickening,
semi-​erect but the movement of air may be impeded enhancement and separation in empyema, and can
by loculations. The supine CXR is more challen- differentiate hypodense fluid and pus from hyper-
ging, with signs of pneumothorax including the fol- dense blood, especially important after recent sur-
lowing:  (a) a deep, sometimes tongue-​like, lateral gery or trauma. The need for sampling is governed by
costophrenic sulcus; (b)  sharp demarcation of the clinical presentation.
diaphragm or cardiomediastinal silhouette; (c)  gas On the erect CXR, blunting of a lateral costo-
outlining the costophrenic or cardiophrenic sulci; phrenic angle can be seen with as little as 200 ml but
and (d) hyperlucent right upper quadrant. Skinfolds may be absent with as much as 500 ml. The semi-​
can be mistaken for a pneumothorax, but should erect CXR is less sensitive to pleural fluid and may
be differentiated by noting continuation of the line miss even moderate effusions. Bedside ultrasound
beyond the thoracic cavity and the presence of vas- is very useful with the pleural fluid demarcated by
cular markings beyond the apparent line. Previous either the echogenic visceral pleura or by lung that
imaging may show the presence of a bulla in emphy- may be hyperechoic when there is atelectasis, collapse
sematous patients. A  lateral decubitus, horizontal or consolidation. The fluid can have internal echoes,
shoot-​through or expiratory CXR may help clarify layering and septations depending on its nature and
the presence of a suspected pneumothorax when duration. Even though some guidance can be taken
there is doubt. However, the sensitivity of CT and its from ultrasound appearances (e.g. most transudates
ability to assess the underlying cause make it the diag- are without internal echoes), ultrasound appear-
nostic modality of choice in these situations. CT is ances should not be taken as specific to the nature of
also more sensitive to pneumomediastinum, which in the fluid. Ultrasound can also aid sampling of pleural
the ventilated patient may be due to barotrauma, and fluid and drain insertion, improving the safety of
CT may be preferred when extensive subcutaneous these procedures.

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Section 1: Diagnosis

Figure 7.5  Empyema, lung abscess and sepsis. Top panel: CXR and CT demonstrate a loculated left pleural collection with (right image,
white star) locules of free air secondary to empyema (right image, thin white arrow). Bottom panel: CXR of a cavitating lung abscess (left
image, block black arrow) and left lower lobe collapse with a tiny effusion in an immunocompromised patient. Another profoundly septic
patient with recent aortic valve replacement has sternal dehiscence due to osteomyelitis shown on CT (right image, block white arrow).
(A black and white version of this figure will appear in some formats. For the colour version, please refer to the plate section.)

Desaturation Associated with Pulmonary involvement. Volume loss is the most common find-
ing on CXR in the ICU setting, often present as sub-
Abnormality segmental linear atelectasis in the dependent lower
lobes, and resolves spontaneously. CXR findings in
Atelectasis and Collapse
collapse and atelectasis will depend on the extent of
Atelectasis and collapse represent pulmonary volume volume loss but classically are those of increased opa-
loss, with the latter implying more extensive, lobar city with (a) loss of contour of the diaphragm, heart

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Chapter 7: Radiology for Cardiothoracic Intensivists

or mediastinum, (b) shift of pulmonary fissures, hilar more patchy involvement but also limited to a lobe;
points, mediastinal structures or hemidiaphragm, and (c)  interstitial pneumonia, with initially more
(c)  bronchovascular crowding or (d)  hyperinflation linear opacities that can have a nodular appearance.
of non-​affected lung. With smaller atelectasis, for Appearances similar to infective consolidation can
example due to scarring or a patchy area of insuffi- appear with fluid, blood, aspirate or tissue filling the
cient surfactant with alveolar collapse, a linear opa- alveoli, and correlation with markers of sepsis and
city with little volume loss is more typical. clinical presentation are essential. Classically, the
The distinction between obstructive atelectasis, consolidation caused by pneumonia will take days to
due to endobronchial obstruction or compression, improve whereas for instance that due to pulmonary
and passive atelectasis, caused by external compres- oedema resolves within hours.
sion of alveoli, is important. In the ventilated patient, In many cases of pneumonia there will be predis-
endobronchial obstruction from mucus plugging posing lung disease, with an acute or chronic insult
is a common cause of acute segmental atelectasis or causing hypoxia. It can be extremely helpful to com-
lobar collapse, which responds well to endobronchial pare with prior CXRs and to look for underlying
intervention. Other causes of obstructive atelectasis pathology within areas of non-​consolidated lung.
include aspiration, inhaled foreign body, blood clots, Common associations of acute pneumonic exac-
endotracheal tube malposition and bronchial neo- erbations on chronic lung disease include emphy-
plasm. Passive atelectasis or collapse when air is forced sema, bronchiectasis and interstitial lung disease,
out of the alveoli will necessitate therapeutic measures which in the majority of cases will be recognised
addressing the underlying cause. Air bronchograms by CT or CXR. Disease progression can be rapid,
favour an obstructive over a passive process and indi- and early CT can help diagnose occult disease in
cate higher likelihood of successful inflation following patients with persistent sepsis of unknown origin,
bronchoscopy. The differentiation from pneumonia with as many as 40% of CXRs in immunocom-
may be difficult, especially on the supine CXR where promised patients not demonstrating pneumonic
volume loss is more difficult to assess. Here CT may consolidation. CT also has an important role when
help by showing relatively reduced enhancement in there is a suspicion of pneumonia related compli-
infective consolidation. cations such as cavitation, empyema, abscess for-
mation or bronchopleural fistulation. Mediastinal
Pneumonia collections are also a differential diagnosis in septic
Pneumonia is common in the ICU with aspiration patients, especially in the postoperative patient,
and mechanical ventilation contributing as risk fac- and CT should be utilised when findings are incon-
tors. The radiographic diagnosis of pneumonia can sistent with pneumonia.
be particularly challenging in the ventilated patient,
with as many as 62% with clinical diagnosis of pneu- Aspiration
monia not recognised from CXR. Consolidation is Risk factors include intubation, impaired cough
the key radiographic finding, occurring when the or gag reflex, sedation and enteric tube feeding.
airspaces have become filled with inflammatory Aspiration in the recumbent position most com-
material. The vessels are obscured and air broncho- monly affects the upper lobes (posterior segment)
grams appear due to increased visibility of large and lower lobes (superior segment). A rapid onset of
airways. The increased density of the involved lung ill-​defined areas of ground-​glass opacity, consolida-
leads to effacement of the contours of the struc- tion or nodularity represents acute airway plugging
tures that it abuts (the diaphragm, mediastinum and and surrounding inflammatory response, and can
heart), which aids in localising consolidation to spe- be seen on CXR and CT. The imaging findings often
cific lobes. In addition, a straight line indicates con- increase over the initial 24–​48 hours and diminish
solidation limited by a fissure. Pleural effusions are thereafter. Progression or persistence indicates the
common ancillary findings, and in the septic patient development of complications. CT may depict the
the possibility of empyema must always be consid- dependent changes in more detail but its main role
ered. Pneumonic consolidation may take the form is demonstration of suspected cavitation and abscess
of: (a) lobar pneumonia, classically with diffuse con- formation, which are increased in patients who
solidation of a lobe; (b)  bronchopneumonia, with aspirate non-​sterile stomach contents.

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Section 1: Diagnosis

Acute Respiratory Distress Syndrome 24–​ 48 hours whereafter they start to resolve over
ARDS is a severe form of acute lung injury, where the following 7–​10  days. Classically, contusions are
increased capillary permeability causes influx of fluid ill-​defined patchy areas of ground-​glass opacity and
and protein into the interstitium and alveoli. ARDS consolidation that do not adhere to the bronchopul-
may be caused by a whole range of both intratho- monary segmental anatomy and often have subpleural
racic or extrathoracic disease. The radiological diag- sparing. If resolution within the expected timeframe
nosis of ARDS is, in the appropriate clinical context, does not occur, then compounding diseases such as
made based on bilateral pulmonary opacities in the pneumonitis from fat embolism, aspiration, ARDS
absence of heart failure. In its classical form, ARDS and pneumonia need to be entertained. Lacerations
follows a triphasic pattern: (a) exudative phase (day 1–​ are areas where the lung parenchyma has lost its
7), with an initially normal CXR followed by patchy, integrity, which may appear as focal abnormalities on
symmetrical bilateral consolidation; (b)  proliferative imaging that may be filled with air or blood (pneuma-
phase (day 7–​14), when the initial changes persist but tocele or haematoceles, respectively). In the patient
may take on a more coarse and linear pattern; and with deteriorating oxygenation after initial stabilisa-
(c) fibrotic phase (>15 days), when the changes begin tion, undiagnosed haemothorax or pneumothorax
to resolve and may completely resolve or leave the will need to be excluded using bedside CXR initially.
lungs fibrotic. In the exudative phase, appearances are Tracheobronchial tears and bronchopleural fistulation
similar to pulmonary oedema but ARDS is indicated (BPF) are often difficult to detect on initial imaging,
when there is a more peripheral and dependent distri- and should be suspected with worsening pneumo-
bution with a lack of response to diuretics. In addition, thorax, pneumomediastinum or pleural effusions.
the patient with ARDS without prior cardiac disease Most BPFs are, however, not traumatic but result from
will have normal cardiac size with absence of upper surgical intervention (pneumonectomy) or necrotis-
lobe diversion, septal lines and pleural effusions. CT ing pneumonia, with other causes including neo-
may aid the characterisation of ARDS, showing an plasia and radiotherapy. Radiological findings of BPF
anterior-​posterior gradient, heterogeneous mixture include a drop in the air-​fluid level exceeding 2  cm
of ground-​glass opacity and consolidation, and bron- during the postoperative period or the reappearance
chial dilation within affected areas. Decreased lung of an air-​fluid level in a patient who has undergone
compliance increases the risk of complications of pneumonectomy (Figure 7.6).
the required positive pressure ventilation, including Postoperative lung torsion (Figure 7.7) can cause
pneumothorax, interstitial emphysema and pneumo- rapid clinical deterioration and is due to rotation of
mediastinum. This may be surveyed with serial CXRs a lobe or the whole lung around the hilar structures
but when there is extensive disease, pneumothoraces resulting in compromise of the airways, vasculature
may be extremely difficult to diagnose without the and the lymphatic drainage. Rapid opacification of the
use of CT. lung or unusual position of a collapsed lobe on a radio-
graph should raise the suspicion. CT is often required
Desaturation Associated with Trauma and Surgery prior to lung salvage and demonstrates obliteration
of the proximal pulmonary artery and accompanying
CT diagnoses 20% more injuries than CXR, in par-
bronchus with poorly enhancing consolidation,
ticular pulmonary contusions, aortic injuries and
ground-​glass attenuation, interlobular septal thicken-
osseous trauma. Many CXR-​detected injuries are also
ing and intralobular linear attenuation with bulging
upgraded in severity by CT. Nevertheless, bedside
of the neofissure. Traumatic phrenic nerve injury and
CXR maintains an important role for the immediate
diaphragmatic rupture may be concealed by positive
diagnosis of large pneumothoraces, flail chest, and
pressure ventilation and may also need fluoroscopy or
malpositioned lines and tubes.
CT for confirmation.
Pulmonary contusions are areas of alveolar haem-
orrhage that occur in intact lung parenchyma, and are
most commonly seen in blunt trauma when tearing-​ Conclusion
shearing forces have been applied. Contusions may The highly specialised setting of the cardiothoracic
become apparent any time from the time of injury intensive care unit demands detailed knowledge of
until 6 hours after, and can progress during the initial the natural history and treatment complications of

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Chapter 7: Radiology for Cardiothoracic Intensivists

Figure 7.6  Bronchopleural fistula and abdominal ischaemia. Top panel: CXR performed on day 19 (left image) and day 23 (right image)
after left pneumonectomy with the drop in the air-​fluid level highly suspicious for bronchopleural fistula; this would require CT confirmation.
Bottom panel: elderly patient with septic shock and an intra-​aortic balloon pump (left image, notched arrow) in the distal descending
thoracic aorta. There is multiorgan ischaemia as evidenced by heterogeneous liver attenuation (right image, white star), thickened stomach
with intramural gas (right image, thin white arrows). Also note small bowel dilatation on the CT scout view (left image).

particular disease processes. The timely recognition of


specific imaging findings necessitates close collabor-
Learning Points
ation between specialised radiologists and clinicians. • Systematic CXR evaluation is essential taking into
Serial imaging must, where available, be reviewed in account the positioning of the patient and mode
light of ever changing clinical circumstances. In cer- of acquisition at the time of imaging.
tain life threatening emergencies, lack of imaging • CXR should be undertaken to help answer a
should not delay prompt intervention. specific clinical question; routine CXR, as a part

13:44:45 55
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Section 1: Diagnosis

Figure 7.7  Pulmonary torsion.


Thoracic CT on mediastinal (left image) and lung (right image) windows in a patient with severe deterioration 2 days following right
lobectomy. There is tapered obliteration of the proximal pulmonary artery and accompanying bronchus with poorly enhancing
consolidation (left image, white star), diffuse ground-​glass attenuation (right image) and interlobular septal thickening (right image, thin
black arrow), which are all features in keeping with ischaemia and oedema due to lobar torsion.

of the daily assessment of patients in the intensive Ayres J, Gleeson F. Imaging of the pleura. Seminars
care unit, does not improve outcomes. in Respiratory and Critical Care Medicine. 2010;
• Review of previous CXRs provides important 31: 674–​688.
diagnostic clues to the nature of thoracic disease Bentz MR, Primack SL. Intensive care unit imaging. Clinics
and helps identify causes for acute clinical in Chest Medicine. 2015; 36: 219–​234, viii.
deteriorations by demonstrating the evolution Eisenhuber E, Schaefer-​Prokop CM, Prosch H, Schima
over time. W. Bedside chest radiography. Respiratory Care. 2012;
57: 427–​443.
• Bedside echocardiography should be the first
line imaging for assessment of cardiac function, Franquet T, Gimenez A, Roson N, et al. Aspiration
diseases: findings, pitfalls, and differential diagnosis.
cardiac valves and the pericardium.
Radiographics. 2000; 20: 673–​685.
• CT should be reserved as a problem-​solving tool,
McMahon MA, Squirrell CA. Multidetector CT of aortic
to be used only when the diagnosis is unclear
dissection: a pictorial review. Radiographics. 2010;
even after careful review of portable imaging. 30: 445–​460.
Oikonomou A, Prassopoulos P. CT imaging of blunt chest
Further Reading trauma. Insights into Imaging. 2011; 2: 281–​295.
Amorosa JK, Bramwit MP, Mohammed TL, et al. ACR Sheard S, Rao P, Devaraj A. Imaging of acute respiratory
appropriateness criteria routine chest radiographs in distress syndrome. Respiratory Care. 2012; 57: 607–​612.
intensive care unit patients. Journal of the American Trotman-​Dickenson B. Radiology in the intensive care
College of Radiology. 2013; 10: 170–​174. unit (Part I). Journal of Intensive Care Medicine. 2003;
18: 198–​210.

MCQs
1. Signs of right lower lobe collapse on CXR include: (c) High position of the left hilum
(a) Inability to see the line of the right hemidiaphragm (d) Decreased transradiance of the right upper lobe
(b) Inability to see the line of the right heart border (e) High position of the right horizontal fissure

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Chapter 7: Radiology for Cardiothoracic Intensivists

2. Alveolar opacities in hydrostatic pulmonary oedema 4. CT pulmonary angiographic features of acute PE


are seen on CXR: include:
(a) With a pulmonary capillary wedge pressure (a) Central vascular filling defect
<25 mmHg (b) Eccentric vascular thrombus
(b) Immediately with an increase in intracapillary (c) Intravascular webs
pressure
(d) Pulmonary stenosis
(c) Prior to the development of pleural effusions
(e) Thrombus forms obtuse angle with the vessel wall
(d) After blurring of the pulmonary vasculature
5. Echocardiographic indicators of haemodynamic com-
(e) with a distinctive appearance from ARDS promise secondary to pericardial tamponade include:
3. A peripheral crescent of high attenuation in the aortic (a) Inspiratory collapse of right-​sided chambers
wall in unenhanced CT is seen with the following:
(b) Early-​systolic right ventricular inversion
(a) Penetrating ulcer
(c) Rightward septal shift
(b) Intramural haematoma
(d) Reciprocal respiratory variation on Doppler
(c) Aortic aneurysm less than 6 cm transvalvular flow
(d) Atherosclerotic plaque (e) Increase in inferior vena caval diameter during
(e) Aortic aneurysm greater than 6 cm inspiration

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:44:45 57
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Section 2 Practical Procedures

Airway Management in Cardiothoracic


Chapter

8 Intensive Care: Intubation and


Tracheostomy
Martin John and Christiana Burt

The ability to safely secure and manage a definitive Patients who are breathing unsupported or receiv-
airway on the cardiothoracic intensive care unit is an ing non-​invasive ventilation may require intubation
essential and challenging skill. Patients are frequently for a number of reasons (Table 8.1).
haemodynamically compromised with reduced car-
diorespiratory reserve, resulting in poor tolerance of Airway Assessment
suboptimal ventilation.
When planning any intubation, it is important to per-
Important airway competencies within cardiotho-
form an initial airway assessment to gauge whether
racic intensive care include endotracheal intubation
there may be any potential difficulties with facemask
and tracheostomy forming techniques, as well as a
ventilation or laryngoscopy. A  key finding from the
good working knowledge of how to rescue the airway
4th National Audit Project on major airway events in
should initial attempts fail.
the UK found that poor airway assessment contrib-
uted to poor airway outcomes. The degree of harm
Tracheal Intubation from airway incidents was also found to be highest in
The presence of a cuffed tube within the trachea repre- intensive care patients.
sents a secure airway, providing protection from aspi- Recognised predictors of difficult intubation are
ration and facilitating positive pressure ventilation. listed in Table  8.2. An absence of these signs how-
Endotracheal tubes are made from polyvinyl chloride ever does not guarantee straightforward airway
and are sized based on their internal diameter in mil- management.
limetres. Since the internal diameter is inversely pro-
portional to airflow resistance, it is appropriate to use Performing Endotracheal Intubation
the largest size that can be easily accommodated (usu-
The intubating environment on the intensive care unit
ally 8–​9 mm for males and 7–​8 mm for females).
can be very different from that of the elective operat-
Many patients following cardiac surgery already
ing room. Critically ill patients have less physiologi-
have an endotracheal tube in place when admitted
cal reserve and often require intubation urgently to
to the critical care unit. In these patients a period of
address cardiorespiratory collapse. They may not be
haemodynamic stability may be required before prep-
fasted and often experience delayed gastric emptying,
arations are made for discontinuation of sedation and
so a rapid sequence induction with cricoid pressure is
extubation. It is important to document the endotra-
often performed.
cheal tube position, laryngoscopic grade and whether
there were any difficulties with facemask ventilation
and/​or intubation following induction. Preparation
In contrast, the postoperative management of Prior to intubation, it is necessary to prepare the
patients following thoracic surgery tends to focus on patient, drugs, equipment and intubating team. Roles
early extubation and the avoidance of positive pres- should be applied to appropriately skilled personnel
sure mechanical ventilation where possible. This is and a backup plan for a failed intubation should be
to avoid positive pressure stress on suture and staple in place. Essential equipment required for emergency
sites, which may increase the risk of postoperative intubation, along with rescue equipment in case of
complications including persistent air leaks. difficulty, should be immediately available in the

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Section 2: Practical Procedures

Table 8.1  Indications for tracheal intubation on the critical Equipment


care unit
Basic airway equipment includes: a self-​inflating bag,
Hypoxia gum-​elastic bougie, oropharyngeal airway, function-
Hypercarbia ing laryngoscope (with a spare in case of failure) and
Reduced conscious level at least two options of appropriately sized endotra-
Increased work of breathing cheal tubes. A  supraglottic airway device (laryngeal
Cardiac arrest mask airway, LMA) should also be present in case
Airway obstruction of intubation difficulty, in order to assist with rescue
To facilitate transfer
oxygenation. A  suitable device for emergency crico-
thyrotomy should also be available in case of failure to
intubate or oxygenate.
Table 8.2  Predictors of difficult intubation It is necessary to be able to tilt the patient’s bed
in a head-​down position in case of regurgitation dur-
Receding chin
ing airway manipulation and to have working suction
Short neck
available. It is also prudent to ensure the ventilator
Thick neck to be used after intubation is fully operational and
Limited neck extension/​flexion attached to a reliable oxygen source.
Long upper incisors Occasionally it may be necessary to site a double-​
Prominent overbite lumen endotracheal tube rather than a single-​lumen
Inability to extend mandibular incisors anterior to the maxillary tube, either to facilitate protection of one lung from
incisors soiling by secretions or blood from the other lung, or
Less than 3 cm interincisor distance to enable differential ventilation of the lungs. Double-​
High arched palate lumen tube placement requires additional experience
Less than 3 finger breadth thyromental distance and specific training.
Mallampati score greater than II
Non-​compliant mandibular space
Drugs
Adapted from American Society of Anesthesiologists Task Force
Rapid sequence induction involves the administra-
on Management of the Difficult Airway (2013). tion of a predetermined dose of intravenous induc-
tion agent followed immediately by a neuromuscular
blocking drug to achieve rapid loss of consciousness
intensive care unit and moved to the patient’s bed- and optimal intubating conditions with minimal
space. A ‘difficult airway’ trolley containing basic and patient apnoea time.
advanced equipment is an ideal way to organise this. The haemodynamic side effects of the common
induction agents at dosages used in anaesthetic prac-
Patient tice are such that their administration in critically
Critically ill patients requiring intubation should have ill patients can cause catastrophic cardiovascular
standard monitoring (non-​invasive blood pressure, collapse. To reduce the amount of induction agent
electrocardiography, pulse oximetry) and working needed, operators often coadminister opioids and
intravenous access as a minimum. Capnography to benzodiazepines. Despite coinduction, vasopressors
confirm correct tube position after intubation should are still frequently needed following induction and
be immediately available. should be immediately available.
Head position should be gently manipulated (if it Suxamethonium has been the traditional neuro-
is safe to do so) into the ‘sniffing the morning air posi- muscular blocking agent used to achieve paralysis due
tion’ which includes a mild amount of cervical flex- to its speed of onset and offset. Rocuronium is now an
ion (a pillow is usually necessary behind the head to alternative option, since the recently developed sug-
provide this) and mild atlanto-​occipital extension in ammadex allows immediate block reversal in case of
order to optimise direct laryngoscopic view. In obese emergency.
patients extra pillows may be necessary behind the The choice of drugs used should be tailored to the
shoulders in order to allow atlanto-​occipital extension. individual critical care patient based on an assessment

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Chapter 8: Airway Management: Intubation and Tracheostomy

Table 8.3  Commonly used intubating drugs preoxygenation, cricoid pressure, anaesthetic induc-


tion, paralysis, laryngoscopy and confirmed endotra-
Drug Comments
cheal intubation.
Thiopentone Fastest speed of onset
Cardiovascular suppression Preoxygenation
Potential harm from extravasation Preoxygenation describes the process of replac-
Propofol Rapid speed of onset ing nitrogen with oxygen in the functional residual
Suppresses laryngeal reflexes capacity (FRC) of the lungs to maximise oxygen
Cardiovascular suppression stores. This allows for a longer apnoeic time to
Ketamine Slower onset time
secure the airway before desaturation occurs, and
should be performed where possible. Effective
Cardiovascular stability
preoxygenation is performed by encouraging the
Bronchodilation
patient to take tidal volume breaths of 100% oxygen
Etomidate Rapid speed of onset through a tight fitting mask (to prevent entrainment
Cardiovascular stability of air) at flows above 10 l (to minimise rebreathing)
Possible adrenal suppression for 3–​5 minutes. Since FRC is lower in the supine
Midazolam Slower onset time position, adopting a head-​up position can improve
Prolonged duration of action oxygen storage capacity. An expired oxygen concen-
Reduces anaesthetic dose requirements tration of 90% signifies effective preoxygenation.
Opioids Unreliable amnesic These ideal conditions for preoxygenation are not
always possible, particularly in patients requiring
Limits sympathetic response to intubation
intubation for respiratory failure who are deterio-
Reduces anaesthetic dose requirements
rating despite non-​invasive respiratory support, or
Suxamethonium Rapid onset and offset of paralysis
who are not able to cooperate with instructions. In
Hyperkalaemia these patients a careful attempt at preoxygenation
Risk of malignant hyperthermia can often be made, but care must be taken not to
Rocuronium Rapid onset of neuromuscular block cause stomach inflation, which increases the risk of
Rapid reversal with sugammadex regurgitation and aspiration.

Cricoid
of aspiration risk, physiological reserve and indication Cricoid pressure is a manoeuvre intended to reduce
for intubation (Table 8.3). the risk of aspiration during induction. The circum-
ferential cricoid cartilage is the most inferior laryngeal
Team structure and can be pressed against the body of the
Clear roles matched to the skillset within the team fifth cervical vertebrae to compress the oesophageal
need to be allocated prior to induction. The team lumen. The thumb and index finger are placed either
leader is responsible for the overall running of the side of the cartilage and a posterior force of 10 N is
intubating process and ideally should not be per- applied before induction, which is increased to 30 N
forming any other tasks. The first intubator performs following loss of consciousness. The assistant applying
preoxygenation, laryngoscopy and intubation, with a cricoid pressure needs to be experienced since incor-
second intubator on standby in case of failure. One rect technique can result in airway obstruction and a
team member is responsible for administering drugs poor view on laryngoscopy.
and another should be competent at performing cri-
coid pressure. Laryngoscopy
Laryngoscopy is most commonly performed with a
curved Macintosh laryngoscope blade (sizes 3–​5) to
Endotracheal Intubation: Sequence allow visualisation of the glottis and enable intuba-
of Events tion under direct vision. The laryngoscope is held in
The salient sequence of events during an uncompli- the left hand and the blade is inserted into the oral
cated tracheal intubation on the intensive care unit is cavity to the right side of the midline, which allows

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Section 2: Practical Procedures

Table 8.4  Cormack and Lehane classification of The endotracheal tube should be sited to roughly
laryngoscopy view 2  cm above the carina. Once capnography has con-
Grade 1 Full view of vocal cords/​glottis firmed placement within the patient’s airway, clinical
Grade 2 Only posterior commissure/​arytenoid cartilages examination can be used to avoid endobronchial intu-
visible bation, but in difficult cases or where there is doubt,
Grade 3 Only epiglottis visible fibreoptic bronchoscopy can be used to ensure opti-
Grade 4 No glottic structure visible mal placement above the carina. Too far in and flex-
ion of the patient’s neck may cause contact with the
carina causing irritation and bronchospasm or right
distraction of the tongue to the left. The tip is then main bronchial intubation. If the tube is not advanced
slowly advanced over the base of the tongue and into far enough into the trachea, extension of the neck can
the valecula, where an anterior vector force is applied lead to inadvertent extubation.
to remove the tongue from the line of sight. The
laryngeal view is graded according to the Cormack
and Lehane classification (Table 8.4). Poor views can
Difficult Intubation
often be improved by external laryngeal manipulation A difficult intubation is defined as an inability to
(BURP; backwards, upwards and rightward pressure secure the airway with an endotracheal tube follow-
on the thyroid cartilage) or a reduction in cricoid ing three attempts, and occurs more commonly in
pressure. With grade 3 and 4 views, the glottic aper- critically ill patients. Repeated intubation attempts
ture is not visualised and advanced airway equipment (more than three) can lead to airway oedema or bleed-
such as videolaryngoscopes and fibreoptic scopes may ing, which will worsen visualisation with subsequent
be required to aid intubation. attempts. Expert help needs to be sought early, and
the priority is to oxygenate via bag-​mask ventilation
Confirming Correct Positioning aided by airway manoeuvres (jaw thrust, head tilt–​
chin lift) and adjuncts (oropharyngeal, nasopharyn-
It is crucial to confirm that the endotracheal tube is in
geal airways), or ventilation via a supraglottic device.
the trachea as opposed to the oesophagus following
Management should follow local and national proto-
intubation. The most reliable test confirming correct
cols (see Further Reading).
positioning is six successive carbon dioxide traces on
If ventilation and oxygenation are satisfactory, a
the capnograph with a value for end-​tidal carbon diox-
definitive airway is required by another technique.
ide (EtCO2) that corresponds to that expected for the
Allowing the patient to wake up (recommended in the
patient. The absence of CO2 on the capnograph trace
elective setting) is unlikely to be an appropriate option
should prompt immediate suspicion of incorrect tube
in the critically ill patient.
position, with direct laryngoscopy or fibreoptic bron-
Advanced airway options available to secure a
choscopy to resite the tube into the trachea. Failure to
definitive airway in the ‘can’t intubate, can ventilate’
recognise oesophageal intubation will result in severe
scenario include the following.
hypoxia within minutes followed by cardiac arrest and
death. Clinical signs such as chest wall movement and 1. Videolaryngoscopy There are a number of
breath sounds on auscultation, and misting within the videolaryngoscopes available to aid intubation. All
tube, as well as appropriate compliance of the inflat- contain a distal light source and camera to allow
ing bag are of value, but can all occur and give false indirect visualisation of the glottis on a screen.
reassurance with oesophageal intubation. Extra care is These devices obviate the need for a direct line of
needed to confirm correct tube placement in patients sight in order to intubate.
in cardiac arrest undergoing CPR, or patients who are 2. Asleep fibreoptic intubation A fibrescope preloaded
on venoarterial extracorporeal membrane oxygena- with an endotracheal tube can be passed either
tion (VA ECMO) support since the value for EtCO2 orally or nasally under direct vision into the
on the capnograph trace will be lower than normal trachea.
despite a correctly sited endotracheal tube (reduced 3. Intubation through the existing laryngeal
pulmonary blood flow). If the value for EtCO2 is <2 mask airway An Aintree catheter (hollow bougie)
kPa, extra steps should be taken to ensure that tube can be loaded on to a fibrescope and the whole
placement is correct. unit passed through the lumen of the ventilating

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Chapter 8: Airway Management: Intubation and Tracheostomy

laryngeal mask airway and into the trachea under scalpel incision through the cricothyroid
direct vision. Upon removal of the fibrescope, an membrane. Caudal traction on the membrane
endotracheal tube can then be passed over the can then be applied from a tracheal hook to allow
Aintree catheter. intubation with a size 6 mm ID cuffed tracheal or
4. Intubating laryngeal mask airway The intubating tracheostomy tube.
laryngeal mask airway is specifically designed to
allow an endotracheal tube to blindly pass through Managing the Intubated Patient
its lumen into the trachea.
Attention to the endotracheal tube needs to be main-
5. Tracheostomy Tracheostomies are usually tained following intubation in order to prevent airway
performed electively on intubated patients. related morbidity. Continuous waveform capnog-
However in the difficult intubation scenario in raphy should be used for every intubated patient to
the critically ill, there may be a case for direct ensure correct tube positioning and allow surveil-
tracheostomy formation whilst ventilating with a lance against tube migration. Endobronchial intuba-
laryngeal mask airway. tion should be monitored for using auscultation, and
chest X-​ray. Checking the cuff pressure regularly is
Failed Ventilation important since excessive pressures can cause tracheal
Failure of ventilation is defined as the inability to mucosal damage, whereas an inadequate pressure
maintain oxygen saturations above 90% (if initially can lead to microaspirates and ineffective ventila-
above this value) whilst administering 100% oxygen tion. Cuff pressures between 20 and 30  cmH2O are
using a facemask or laryngeal mask airway. recommended.
Failed ventilation with increasing hypoxaemia in To reduce the risk of inadvertent extubation, judi-
the setting of a difficult intubation, the ‘can’t intubate, cious use of sedation is required as well as care when
can’t oxygenate’ scenario, is a rare but life threatening moving patients.
emergency. The immediate priority is to achieve oxy-
genation and since the upper airway route has failed,
an invasive approach via the cricothyroid membrane Extubation
is recommended. The cricothyroid membrane lies Tracheal extubation is the process of removing the
inferior to the vocal cords, is relatively avascular and endotracheal tube to allow the patient to protect and
can normally be easily located below the thyroid carti- maintain their own airway. To increase the likelihood
lage and above the cricoid cartilage. of a successful extubation on the intensive care unit, a
There are three types of cricothyroidotomy number of criteria firstly need to be met:
approach: 1. Indication for intubation has been corrected,
1. Small cannula devices (2–​3 mm ID) Kink resistant 2. Haemodynamic stability,
cannulae can be directed caudally into the trachea 3. Adequate ability to cough and clear secretions,
and their position confirmed by aspirating air 4. Neurologically appropriate,
freely. The resistance through these narrow 5. Adequate oxygenation without requiring high
devices is large, so a high pressure (2–​4 bar) levels of PEEP/​FiO2,
oxygen source is needed to oxygenate. Some 6. Fully rewarmed (i.e. after cardiac surgery),
degree of upper airway patency is required to 7. Minimal chest drain output.
allow passive exhalation. This limits their use A spontaneous breathing trial can then be performed
beyond short-​term rescue oxygenation. using a T-​piece or low-​level pressure support and
2. Large-​bore devices (>4 mm ID) These devices are low PEEP to determine the likelihood of extubation
inserted using either the Seldinger or cannula-​ success.
over-​needle technique. The larger diameter A backup reintubation plan should always be part
accommodates a 15 mm standard breathing of the extubation strategy as it may be more difficult
circuit, which allows the patient to be effectively than the original intubation. Tracheal extubation in
low pressure ventilated. the presence of a known difficult airway can be per-
3. Surgical cricothyroidotomy (>6 mm ID) The formed over an airway exchange catheter, which may
surgical approach involves making a horizontal be tolerated for up to 72 hours.

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Section 2: Practical Procedures

To perform an extubation in an uncomplicated Other indications for tracheostomy include failure


airway, the patient should be given 100% oxygen for of protective airway reflexes, management of excessive
at least 3 minutes and the nasogastric tube (if pre- secretions and relief of upper airway obstruction.
sent) should be suctioned. Gentle positive pressure
should be applied followed by cuff deflation and con-
trolled tube removal. Patients may initially be extu-
Tracheostomy Tubes
bated onto a facemask and Waters circuit with 100% Tracheostomy tubes are made from either polyvinyl
oxygen in order to assess adequacy of spontaneous chloride, silicone or metal, and are available in a vari-
ventilation. ety of shapes and sizes. When sizing tracheostomy
tubes, important dimensions to consider include the
diameter (inner and outer), length (proximal and dis-
Tracheostomy tal) and curvature.
Tracheostomy refers to the creation of a stoma at The optimal tracheostomy tube size provides
the skin surface, which is in continuity with the tra- the maximum internal diameter to facilitate airflow,
chea. This procedure is commonly performed on the whilst confining the outer diameter to roughly three
cardiothoracic intensive care unit and involves the quarters of the tracheal lumen. This minimises resist-
insertion of a tracheostomy tube usually between the ance across the tube and also allows adequate air-
second and third tracheal rings. Despite being one of flow around the tube during weaning and attempted
the oldest airway interventions, controversy still exists phonation.
regarding the optimal timing, insertion technique and Since the trachea is essentially straight, the tip
type of tracheostomy tube to use. of an inappropriately long and curved tracheostomy
tube can traumatise the anterior tracheal wall, whilst
Advantages shorter tubes can abut posteriorly. To avoid these
Tracheostomy tubes offer a number of practical and problems, angled tracheostomy tubes have a straight
clinical advantages over oral endotracheal tubes when portion designed to lie more anatomically within the
managing the critically ill. trachea.
Tracheostomy tube length is also an important
1. The work of breathing is reduced since the
consideration since patients with large necks often
dead-​space and airflow resistance is less than for
need a longer proximal portion, whereas patients with
equivalent sized endotracheal tubes.
tracheal pathology (tracheomalacia) may need extra
2. Suctioning the tracheobronchial tree in patients
distal length to bypass disease.
with a high secretion burden is easier.
Two different sizing systems exist, which can
3. Tracheostomy tubes are well tolerated, which often
cause confusion since one is based on the length (and
allows the sedation and associated adverse effects
taper) of the outer tube, whilst the other refers to the
to be reduced.
internal diameter. As a reference for the clinician and
4. Mouth hygiene is easier to maintain and to avoid sizing errors, the diameters and distinguish-
phonation as well as swallowing is possible. ing features of tracheostomy tubes are marked on the
5. Complications associated with prolonged flange.
translaryngeal intubation such as vocal cord
damage and laryngeal ulceration are avoided. Cuffed and Uncuffed Tubes
In the intensive care setting, most patients will initially
Indications require a cuffed tracheostomy tube to facilitate positive
The most common indication for tracheostomy in pressure ventilation and protect against aspiration. To
the intensive care setting is to facilitate prolonged reduce the risk of tracheal mucosal ischaemia and
mechanical ventilation and weaning. Recent esti- subsequent stenosis, a high volume/​low pressure cuff
mates suggest that approximately 5% of patients inflated to a pressure of no more than 20–​25 cmH2O
following cardiac surgery require mechanical ven- is recommended. Uncuffed tracheostomy tubes allow
tilation for at least 7 days due to perioperative com- for airway clearance but do not protect from aspira-
plications, often on a background of underlying tion, so are usually reserved for patients with adequate
respiratory disease. bulbar function who are unable to clear secretions.

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Chapter 8: Airway Management: Intubation and Tracheostomy

Single and Double Cannula Tubes Percutaneous Tracheostomy


Tracheostomy tubes can be stand-​ alone single Patients are in the supine position and often have a
lumen devices or contain an accompanying inner bolster placed between their shoulders to allow ade-
cannula (double cannula tubes). Double cannula quate neck extension and exposure. Preprocedural
tubes are inherently safer since in the event of ultrasound scanning of the neck is now increasingly
obstruction the inner cannula can be removed com- being used to assess the anterior neck landmarks.
pletely and independently from the outer lumen Sedation needs to be increased to anaesthetic levels
to manage the blockage. For this reason, and to and paralysis should be given. It is important to venti-
facilitate cleaning, it is often the preferred choice late with 100% oxygen.
of tube for patients discharged to a stepdown unit Capnography to confirm correct tube position-
or ward. Many intensive care units now use double ing is mandatory and bronchoscopy through the
cannulas from the outset. It is however important tracheal tube to guide tracheostomy placement is
to appreciate that the addition of an inner cannula recommended. In order to accommodate the tra-
reduces the functional internal diameter of the tra- cheostomy tube, the endotracheal tube needs to be
cheostomy tube, which increases airflow resistance withdrawn under bronchoscopic guidance so the tip
and the work of breathing. Furthermore, in some lies at the level of the cricoid cartilage prior to nee-
designs, attachment to the ventilator is only possi- dle puncture.
ble when the inner tube and its associated 15  mm All percutaneous tracheostomy tube placements
connector is in place. are based on the Seldinger technique, with initial
needle aspiration and guidewire insertion midway
Fenestrated and Non-​fenestrated Tubes between the cricoid cartilage and sternal notch. This
Fenestrated tracheostomy tubes have single or multi- usually correlates to the space between the second and
ple openings located posteriorly and above the cuff. third tracheal rings. Tract dilatation and tracheos-
Following cuff deflation during spontaneous ven- tomy railroading can be performed using single step
tilation, the fenestrations encourage maximal air- or sequential dilators, balloon inflation, forceps dila-
flow through the larynx to allow phonation and an tation, or by the retrograde translaryngeal approach.
assessment of native airway patency in preparation
for decannulation. Fenestrated tracheostomy tubes Surgical Tracheostomy
are often used in conjunction with one-​way speak- This procedure is often performed in an operating
ing valves. These valves cap the tracheostomy tube room under general anaesthesia. A  vertical inci-
and allow inspiration but close on expiration, which sion below the cricoid cartilage is usually made and
directs airflow through the larynx when the patient following blunt dissection down, the strap muscles
exhales. Non-​fenestrated inner tubes should be used and thyroid isthmus are retracted to expose the tra-
if positive pressure ventilation is required to avoid chea for tracheostomy placement. Open-​ended stay
air leaks. sutures can be sited either side of the tracheal stoma
to facilitate postoperative tube reinsertion in case of
Insertion Technique displacement.
Tracheostomies can be performed as open surgical
procedures, most commonly in the operating theatre Timing
or percutaneously at the bedside. Controversy exists as to when the optimal time is to
Both procedures carry low complication rates in perform tracheostomy placement. The benefit of a
experienced hands and individual unit practice is tracheostomy over prolonged translaryngeal intuba-
largely determined by resource and local preference. tion needs to be balanced against the likelihood of
The percutaneous approach is logistically easier the patient needing extended ventilation and the risks
and proponents suggest that peristomal bleeding associated with the procedure.
and infection rates are lower. Surgical tracheosto- The largest randomised controlled trial to date
mies, however, are more appropriate in patients (Tracman) found no benefit in performing early
with difficult neck anatomy and in the emergency tracheostomies within 4  days, and suggested delay-
scenario. ing this procedure until day 10 of translaryngeal

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Section 2: Practical Procedures

ventilation. The initial tracheostomy tube is usually Prior to allowing oral feeding, patients need to be able
cuffed, non-​fenestrated and may be either single or to tolerate cuff deflation and should have passed a
double cannula in design. It is recommended that bedside swallowing assessment by a speech therapist.
the first routine tube change should not be per-
formed within 4  days after a surgical tracheostomy Weaning and Decannulation
and 7–​10 days after a percutaneous one to allow the There is no clear consensus on the optimal trache-
stoma and tract to be established first. The decision to ostomy weaning protocol and different units vary in
change the tracheostomy tube should be multidisci- their practice. The overriding theme is to gradually
plinary, based on the weaning, swallowing and venti- reduce ventilatory support and encourage normal air-
latory needs of the patient. For the first tube change flow patterns in the upper airways to such an extent
or if there are anticipated difficulties, the exchange is that the patient can manage without the tracheostomy
usually performed over a guide such as a gum-​elastic tube. This involves increasing periods of cuff defla-
bougie, exchange catheter or suction tubing. With tion, changing to smaller diameter and fenestrated
well-​established tracts a guide is not usually needed. tubes, and using speaking valves or caps. A  success-
During all tube exchanges, however, there needs to be ful wean requires patient commitment and regular
the necessary equipment and personnel available to multidisciplinary input from nurses, physiotherapists,
manage failure. speech therapist, intensivists and surgeons.
Decannulation should occur as soon as the trache-
Tracheostomy Management ostomy tube is no longer required and it is safe to do
A large proportion of adverse airway events on the so. This occurs at the end of a successful wean, with
intensive care unit involve tracheostomies and can be multidisciplinary team agreement and when core
fatal. To minimise the risk of accidental decannulation criteria have been met (Table  8.5). It is advisable to
or migration, the tracheostomy tube should be safely decannulate during the morning when the patient is
secured with sutures or an approved tracheostomy fasted and can be observed during the day with equip-
tube holder. Sedation should be used judiciously and ment and expertise to manage any complications to
care taken upon patient rolling and moving. In case hand.
of accidental tracheostomy dislodgement or removal,
the safest approach is oral reintubation of the trachea Summary
to stabilise the situation. The establishment and maintenance of a patent airway
Humidified air should be given in order to prevent with ventilation to the lungs is a critically important
the formation of excessively viscous secretions, which first step in the management of a patient on the car-
can obstruct the tube. Heat and moisture exchangers diothoracic intensive care unit. Capnography is an
can be used for this purpose in patients who are either essential adjunct for any patient receiving artificial
self-​ventilating or needing ventilator support. To help
manage especially thick secretions, heated water baths
may be needed. Intermittent suctioning and physi- Table 8.5  Patient decannulation criteria
otherapy at intervals dependent on patient secretion
Able to maintain and protect their own airway
burden is also beneficial. The management of sus-
Adequate respiratory function, free from ventilator support
pected dislodgement should follow guidance from the
National Tracheostomy Safety Project (Figure 8.1 and Haemodynamically stable
Chapter 26 Airway Emergencies). Absence of fever or active infection
Consistently alert
Swallowing Strong cough

Swallowing allows early establishment of oral feed- Competent swallow


ing and contributes to the psychological well being Clinically stable
of patients with tracheostomy tubes. However, these No forthcoming procedures requiring anaesthesia (within
patients are at risk of aspiration since the tube and 7–​10  days)
cuff can impede normal laryngeal movements during Adapted from the National Tracheostomy Patient Safety
swallowing as well as cause oesophageal compression. Manual 2013.

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Emergency tracheostomy management – Patent upper airway

Call for airway expert help


Look, listen & feel at the mouth and tracheostomy
A Mapleson C system (e.g. ‘Waters circuit’) may help assessment if available
Use waveform capnography when available: exhaled carbon dioxide indicates a patent or partially patent airway

No Is the patient breathing? Yes

Call Resuscitation Team Apply high flow oxygen to BOTH


CPR if no pulse/signs of life the face and the tracheostomy

Assess tracheostomy patency

Remove speaking valve or cap (if present)


Remove inner tube
Some inner tubes need re-inserting to connect to breathing circuits

The tracheostomy tube is patent


Can you pass a suction catheter? Yes Perform tracheal suction
Consider partial obstruction
No Ventilate (via tracheostomy) if
not breathing
Deflate the cuff (if present) Continue ABCDE assessment
Look, listen & feel at the mouth and tracheostomy
Use waveform capnography or Mapleson C if available

Tracheostomy tube partially


Yes obstructed or displaced
Is the patient stable or improving? Continue ABCDE assessment

No
REMOVE THE TRACHEOSTOMY TUBE
Look, listen & feel at the mouth and tracheostomy. Ensure oxygen re-applied to face and stoma
Use waveform capnography or Mapleson C if available

Call Resuscitation team No Yes Continue ABCDE


Is the patient breathing?
CPR if no pulse/signs of life assessment

Primary emergency oxygenation Secondary emergency oxygenation

Standard ORAL airway manoeuvres Attempt ORAL intubation


Cover the stoma (swabs/hand). Use: Prepare for difficult intubation
Bag-valve-mask Uncut tube, advanced beyond stoma
Oral or nasal airway adjuncts
Supraglottic airway device e.g. LMA

Attempt intubation of STOMA


Small tracheostomy tube/6.0 cuffed ETT
Tracheostomy STOMA ventilation
Consider Aintree catheter and fibreoptic
Paediatric face mask applied to stoma ‘scope/Bougie/Airway exchange catheter
LMA applied to stoma

National Tracheostomy Safety Project. Review date 1/4/14. Feedback & resources at www. tracheostomy.org.uk

Figure 8.1  Emergency tracheostomy management. Reproduced from McGrath et al. Anaesthesia. 2012; 67: 1025–1041, with permission
from the Association of Anaesthetists of Great Britain & Ireland/​Blackwell Publishing Ltd. (A black and white version of this figure will appear
in some formats. For the colour version, please refer to the plate section.)
13:49:14
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68

Section 2: Practical Procedures

ventilatory support via an endotracheal tube or tra-


cheostomy tube. Extra care must be taken not to miss
Further Reading
tube dislodgement in the setting of reduced CO2 deliv- American Society of Anesthesiologists Task Force on
Management of the Difficult Airway. Practice
ery to the lungs, i.e. in cardiac arrest, or in VA-​ECMO
Guidelines for Management of the Difficult
support. Anticoagulation can increase the risk of Airway: An Updated Report. Anesthesiology. 2013;
bleeding into the airway following manipulation, and 118: 1–​20.
extra care is required in these patients. Cook TM, Woodall N, Frerk C; 4th National Audit Project
of The Royal College of Anaesthetists and the Difficult
Learning Points Airway Society. Major complications of airway
• Equipment for emergency intubation should management in the United Kingdom. Report and
findings March 2011. Available from: www.rcoa.ac.uk/​
be immediately available in the cardiothoracic document-​store/​nap4-​full-​report
critical care unit alongside equipment for
Difficult Airway Society UK Guidelines. 2015. Available
management of the difficult airway.
from: www.das.uk.com/​guidelines/​downloads.html
• Extra care is needed to avoid airway bleeding in
McGrath BA, Bates L, Atkinson D, et al. Multidisciplinary
patients receiving anticoagulation.
guidelines for the management of tracheostomy and
• Oesophageal intubation may be difficult to laryngectomy airway emergencies. Anaesthesia. 2012;
diagnose in the presence of low pulmonary blood 67: 1025–​1041.
flow: use direct assessment via laryngoscopy or Young D, Harrison DA, Cuthbertson BH, et al. Effect
fibreoptic bronchoscopy in case of doubt. of early vs late tracheostomy placement on survival
• Management of the difficult airway should follow in patients receiving mechanical ventilation. The
local and national guidance. Tracman randomized trial. Journal of the American
• Safe airway management requires Medical Association. 2013; 309: 2121–​2129.
multidisciplinary input.

MCQs
Please identify whether the below statements are true or (c) Decannulation can occur as soon as the patient is
false. weaned from positive pressure ventilation

1. Difficult intubation management in the cardiotho- (d) The tube with deflated cuff should be a tight fit in
racic critical care unit should involve: the trachea so that no air can escape around it

(a) At least five attempts at intubation before help 3. Endotracheal intubation:


is called (a) Requires specific training under supervision by an
(b) A logical approach guided by local and national expert in airway management
protocols (b) Should always be performed by an anaesthetist
(c) Preparation of the patient, equipment, drugs and (c) Should always have waveform capnography avail-
team if time allows able continuously to aid with assessment of tube
(d) Administration of the same doses of induction position
agents as in an elective setting (d) Requires chest X-​ray to exclude oesophageal
(e) Clear communication of team roles intubation

2. Regarding tracheostomy: (e) Can be more difficult to perform in the critically ill
patient
(a) A fenestrated inner tube should be used with posi-
tive pressure ventilation 4. Cardiothoracic patients may experience airway com-
plications due to:
(b) Tracheostomy should be performed routinely after
4 days of endotracheal intubation (a) Presence of anticoagulation

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Chapter 8: Airway Management: Intubation and Tracheostomy

(b) Low pulmonary blood flow reducing the level of 5. Predictors of difficult intubation include:
expected end-​tidal carbon dioxide (a) Limited neck extension
(c) Airway oedema secondary to critical illness (b) Prominent overbite
(d) Cerebrovascular accident following surgery (c) Short legs
(e) Prolonged endotracheal intubation (d) Marfan’s syndrome
(e) Mallampati score of I

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:49:14
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70

Section 2 Practical Procedures

Chest Drainage
Chapter

9 Alia Noorani and Yasir Abu-​Omar

Introduction Table 9.1  Common indications for chest drainage

The pleural space is a thin, fluid filled space between Traumatic haemothorax
the visceral and parietal pleura. In a healthy 70  kg Large spontaneous or traumatic pneumothorax
individual, this space contains a few millilitres of Benign or malignant pleural effusion
serous pleural fluid, the function of which is to allow Chylothorax
the pleurae to slide easily over the lungs during ven- Following cardiac or thoracic surgery
tilation. The presence of air or fluid (pus, blood, chyle
or excessive pleural fluid) impedes the normal func-
tion of the lungs, and depending on the symptoms and Figure 9.1a shows a chest radiograph of a patient
signs affecting the patient, will require chest drainage. with a large pneumothorax following cardiac surgery,
Usually, the pressure in the pleural space is less and Figure  9.1b shows the same patient post chest
than atmospheric. This negative pressure helps main- drain insertion. Figure 9.2a shows a chest radiograph
tain partial lung expansion and the magnitude of of a patient with a left pleural effusion and Figure 9.2b
negativity changes during the respiratory cycle. In shows the same patient post drain insertion.
inspiration the pressure is approximately −8  cmH2O
and in expiration this falls to −4 cmH20. A breach of Technique
the pleural cavity leads to development of a positive The emergency insertion of a large bore chest drain for
pressure in this space either equal to or more than the relief of a tension pneumothorax is well described
atmospheric pressure, leading to a pneumothorax. in the Advanced Trauma Life Support guidelines and
there are many published step-​by-​step descriptions of
History the procedure.
The earliest known reference to chest drainage dates The British Thoracic Society guidelines for the
back to the fifth century Hippocratic texts. Here con- insertion of chest drains were originally developed in
servative management of empyemas is described 2003 and subsequently updated in 2010. These guide-
using plants and herbs, and open drainage for per- lines were in effect aimed at training and guiding phy-
sistent infections is well documented including the sicians to safely perform this procedure. Figure  9.3
surgical technique for doing this. Hippocrates gave shows the BTS guidelines as an algorithm.
detailed descriptions of using a scalpel to cut between
the ribs, evacuating pus and leaving a hollow tube in Anatomical Landmarks
for 2 weeks. The BTS describes the triangle of safety within which
Since this, other physicians have described the chest drains should be placed (Figure 9.4). This trian-
technique including the leading French physician sur- gle is the area bounded by the anterior border of latis-
geon Guy de Chauliac in 1395. The first description of simus dorsi and the lateral edge of pectoralis major
a closed chest drainage system was by Hewett in 1876. with the base formed by a line superior to the horizon-
tal line of the nipple.
Indications The advantages of this position are to minimise
The indications for chest drain insertion are to remove potential damage to underlying nerve and vascular
fluid, air or both from the pleural space. Table  9.1 structures such as the long thoracic nerve and the lat-
shows the common indications for chest drainage. eral thoracic artery. Additionally, placement in this

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71

Chapter 9: Chest Drainage

Figure 9.1  (a) Radiograph of a patient with a large right pneumothorax (black arrows). (b) The same patient with a right sided chest drain in
situ (white arrow) and reinflation of the right lung.

Figure 9.2  (a) Chest radiograph of a patient with a large right pleural effusion (black arrows) and (b) resolution of the effusion with the
insertion of a right sided chest drain (black arrows).

area may prevent excessive breast or muscle tissue premedication prior to the procedure can include
dissection, reducing the risk of scarring. The pres- midazolam or an opioid. Caution with these drugs
ence of a loculated effusion may require a more pos- should be exercised in patients with underlying res-
terior drain placement but this should be undertaken piratory disease.
under the supervision of a specialist or under image Patients with abnormal coagulation or platelet
guidance. Posteriorly placed drains are more likely to defects should have these corrected before an elective
cause discomfort. drain insertion, and for those on warfarin the INR
should be allowed to reach 1.5 or below if possible.
Preinsertion Preparation
All patients requiring a chest drain should be con- Patient Positioning
sented for the procedure (unless unable to do so The ideal position for drain insertion is with the
due to their clinical status) and this consent should patient upright or at a 45° angle, with the arm on the
be recorded in the clinical notes. Appropriate affected side abducted and externally rotated and

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Section 2: Practical Procedures

Insertion of Chest Drain

Pneumothorax or pleural fluid requiring drainage

Does this need to be done YES


as an emergency? Insert drain
(e.g. tension)
NO

Consider pleural aspiration to relieve


YES Does the patient have YES symptoms and delay a drain insertion
Is it outside of normal
significant respiratory until working hours and when appropriate
working hours?
compromise? expertise and/or supervision is available

NO NO
Requirements for Insertion
Delay procedure
Prepare patient for chest drainage of Chest Drain
until working hours
Written consent
Clean area to perform procedure
Is the drain required for Insert drain Competent operator or supervisor
fluid? NO Nursing staff familiar with drain management

YES
Equipment Required for Chest Drain
Insertion
Is the operator Seek senior
experienced? help 1% lidocaine
NO
Alcohol based skin cleanser x2 coats
YES Sterile drapes, gown, gloves
Needles, syringes, gauze swabs
Scalpel, suture (0 or 1–0 silk)
Insert drain.
Chest tube kit
Ultrasound guidance
Closed system drain (including water) and tubing
strongly recommended.
Dressing
Clamp

Figure 9.3  British Thoracic Society algorithm for the insertion of chest drains.

placed behind the patient’s head. This exposes the


axillary area.
Prior to insertion it is imperative to undertake a
clinical examination to confirm the presence of pleu-
ral fluid or pneumothorax and to confirm the side of
the pathology on a recent chest radiograph. The only
exception is in the case of a tension pneumothorax
where clinical signs alone are sufficient.
The increasing use of thoracic ultrasonogra-
phy to identify the presence of an effusion is highly
recommended.

Procedure
1. Once the patient is positioned appropriately, the
triangle of safety is prepped with antiseptic and
draped. The entire procedure must be carried out
Figure 9.4  The triangle of safety. Anteriorly the lateral border of
pectoralis major, laterally the anterior border of latissimus dorsi and in an aseptic manner to avoid infection ascending
inferiorly a line superior to the fourth nipple. into the thoracic cavity. The rates of empyema

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Chapter 9: Chest Drainage

following chest drain insertion after trauma skin incision just above and parallel to the ribs is
are approximately 3% and lead to significant made. This incision should be similar in size to the
morbidity. One study has identified no infections diameter of tube being inserted and the operator’s
in a group of 80 patients requiring a chest drain index finger.
for trauma carried out in an aseptic manner. 5. Much debate has been had about the size of the
2. The procedure equipment is usually available chest tubes used. General recommendations are
sterile and prepacked in most hospitals. Chest to use a large bore tube in the setting of trauma
tubes are made of clear plastic and are available in or acute haemothorax, to facilitate drainage
a variety of sizes (diameters) based on the French and monitor on-​going losses (28–​30F). Smaller
scale (multiples of 4, e.g. 12F, 16F, 20F, up to 36F). drains are more comfortable and can be used for
These drains have multiple side holes to allow pneumothoraces. Blunt dissection into the pleural
effective drainage and have a radio-​opaque marker cavity, skirting the upper border of the ribs to
strip to help identification on chest radiography. avoid injury to the neurovascular bundle, should
Trocars are occasionally present within chest be performed, with a finger sweep manoeuvre into
drains but the routine use of these is not the pleural space, in particular with larger drains,
recommended as they can cause undue visceral to avoid injury to the lung parenchyma and other
damage. thoracic organs.
6. Once a chest drain is inserted into the
The kit should contain:
pleural cavity it should be connected to an
• Sterile drapes underwater seal and secured to the skin. A chest
• 1% lidocaine (in a dose of up to 2 mg/kg) radiograph should be requested to assess the
• 20 ml syringe position.
• Green and yellow needles (21–​25 gauge)
• Sterile skin preparation solution Underwater Seals
(chlorhexidene) All chest drains should be connected to a single flow
• Scalpel drainage system which can comprise an underwater
• Curved instrument such as a Roberts’s clamp seal bottle or a flutter valve. The purpose of such a
or Spencer Wells system is to maintain a negative intrapleural pressure
• Chest drain (sizes vary, usually 28F and larger and although there are different methods of achiev-
for effusions and smaller for pneumothorax) ing this, in a traditional underwater seal, a tube is
• Skin suture (nylon or silk) placed at a depth of 3 cm with a side vent that allows
• Chest drain tubing the escape of air. Often a suction system is required
• Chest drain bottle primed with sterile water to maintain a negative pressure. The newer thoracic
(underwater seal) drainage systems such as the Thopaz (Medela, IL) are
• Dressing to cover drain insertion site. compact devices that allow for patient mobility, with-
out restriction.
3. Next, local anaesthesia is infiltrated using a
small gauge needle and by raising a dermal bleb.
Lidocaine in a safe dose (up to 2 mg/kg) or an Contraindications
alternative local anaesthetic is used. The next There are no contraindications to chest drain inser-
step is to freely aspirate either air in the case of tion in a clinically urgent scenario. For non-​urgent
pneumothorax or fluid in the case of an effusion cases, however, if a patient is anticoagulated, the INR
to confirm the pathology. If neither can be done, a should be less than 1.5. Any other clotting abnormali-
chest drain should not be inserted without further ties should also be corrected.
image guidance. Studies have shown that image
guided placement of drains has a low complication Nursing Care
rate of pneumothorax at 3% and a successful The aftercare of chest drains is extremely important.
insertion rate of over 70%. Patients should be managed on a ward where staff
4. Once a successful aspirate has been obtained are experienced in the routine care of chest drains.
and the local anaesthetic deemed successful, a A  daily record of the volume of drainage, the type

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Section 2: Practical Procedures

of fluid drained and the presence or absence of an


air leak and swing should be clearly documented to
Drain Malposition
Malpositioning of drains is the commonest complica-
facilitate decision making with regards to the timing
tion of chest drain insertion and understandably this
of drain removal. Additionally, drains should rou-
is commoner in the emergency setting than the elec-
tinely be inspected for non-​function as heralded by
tive setting where the speed of the procedure can lead
lack of fluctuation of fluid within the tube with res-
to injury. Intraparenchymal positioning of drains can
piration or coughing. Non-​function may be due to
occur in the presence of pleural adhesions. Chest wall
kinking, debris or malposition. Tension pneumotho-
placement has been reported to occur in up to 18%
rax is a serious complication within the context of an
of cases and can be diagnosed with a lack of swinging
on-​going air leak and a blocked drain. Due care with
in the drain tubing and bottle. Drains placed too far
adequate fixation of the drain and subsequent patient
into the chest cavity can result in perforation of other
education are important to avoid inadvertent chest
intrathoracic organs such as the heart, major vessels,
drain dislodgement.
nerves, and oesophagus as well as the diaphragm.
Abdominal placement of drains can occur when the
Removal of Drains insertion point is lower than the base of the triangle of
Chest drains should be removed once the clinical indi- safety. Injury to the liver, spleen, stomach and bowel
cation for their use has been fulfilled. For pneumotho- have all been reported.
races this is when the lung has reinflated on the chest
radiograph and when the drain has stopped bubbling.
For pleural effusions this depends on the pathology
Nerve Injuries
that prompted drain insertion and the volume of Horner’s syndrome has been reported due to direct
fluid drained. An empyema will require a prolonged pressure of the tip of the chest tube on the sympathetic
period of drainage compared to a postoperative drain chain in the medial portion of the apex of the thoracic
inserted in a cardiac patient. cavity. Phrenic nerve injury can cause diaphragmatic
Chest drain removal is a two-​person job whereby paralysis and severe cases may require plication.
both professionals are trained in the procedure. Injury to the long thoracic nerve of Bell during inser-
One removes the drain while the patient performs tion too far laterally in the triangle of safety can lead
a Valsalva or during expiration. The assistant then to winging of the scapula. Ulnar neuropathy due to
pulls the purse string present and ties it to close the injury of the posterior cord of the brachial plexus has
insertion site. also been reported.

Complications Heart
Chest drainage is a fairly common procedure but Inadvertent injury to the heart is a potentially fatal
it is not without risk. The NPSA reported over 2000 complication of chest drain insertion. Injuries to all
patient safety incidents relating to chest drains chambers have been reported and the continued
between January 2005 and March 2008. Of these there drainage of fresh blood should raise the suspicion of
were 12 deaths and 15 cases of severe harm associated this injury. Urgent surgical intervention is required.
with chest drains between January 2005 and March
2008. The main reasons for these incidents were Intercostal Vessels
deemed to be: Injury to the intercostal vessels can lead to significant
• Inadequate level of supervision, training or haemorrhage. Knowledge of intercostal bundle anat-
operator experience, omy and the technique of dissecting above a rib are
• Incorrect site of insertion and poor patient essential to avoid this complication.
positioning,
• Inadequate preprocedure imaging, Re-​expansion Pulmonary Oedema
• Excessive insertion of the dilator when using a This is an uncommon but potentially fatal complica-
Seldinger technique. tion following chest drain insertion for pleural effu-
Details of some complications are given below. sion or pneumothorax. Mortality rates of up to 20%

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Chapter 9: Chest Drainage

have been reported. The aetiology of re-​expansion in up to 8% of cases. Cases of infection are higher for
pulmonary oedema is unclear and it can affect the emergency insertions of drains than for elective proce-
ipsilateral, contralateral or both lungs. It is thought dures. Routine antibiotics are not indicated, except in
that increased endothelial permeability and loss of trauma cases where gross contamination is expected.
alveolar integrity are the main factors leading to
exudation of proteinaceous fluid. Rapid drainage Summary
of large volumes of pleural fluid resulting in sudden Chest drain insertion is a vital part of the management
re-​expansion may be a contributing factor as can re-​ of the trauma, cardiothoracic surgical and chest medical
expansion of a lung which has been collapsed for sev- patient. It should be undertaken by experienced opera-
eral days. Clinical findings can be quite profound with tors to avoid significant injury to other intrathoracic or
the patient developing symptoms and signs within 2 intra-​abdominal structures leading to morbidity and
hours following chest drainage and lung re-​expansion. mortality. Routine aftercare should be undertaken by
Signs include tachypnoea, tachycardia and central experienced staff who can monitor the functionality of
cyanosis. Chest radiography may show ground glass the drain and observe closely for complications.
appearance. Close cardiorespiratory monitoring with
symptomatic support is key to survival.
Further Reading
Oesophageal Perforation Adegboye VO, Falade A, Osinusi K, Obajimi MO.
Reexpansion pulmonary oedema as a complication
This is a rare complication following chest drain inser- of pleural drainage. Nigerian Postgraduate Medical
tion. The drainage of enteric contents should raise the Journal. 2002; 9: 214–​220.
suspicion of an injury and contrast imaging will con- Havelock T, Teoh R, Laws D, Gleeson F. Pleural procedures
firm the diagnosis. and thoracic ultrasound: British Thoracic Society
Pleural Disease Guideline 2010. Thorax. 2010;
Chylothorax 65(Suppl 2): 61–​76.

Injury to the thoracic duct can lead to the development of Hewett FC. Thoracentesis: the plan of continuous
aspiration. British Medical Journal. 1876; 1: 317.
chylothorax. Appropriate investigations include medium
chain triglycerides levels, which directly enter the portal Kesieme EB, Dongo A, Ezemba N, et al. Tube
thoracostomy: complications and its management.
system, thereby avoiding the lymphatic system.
Pulmonary Medicine. 2012; 256878.
Lamont T, Surkitt-​Parr M, Scarpello J, et al. Insertion of
Infection chest drains: summary of a safety report from the
Ascending infection leading to empyema is a serious National Patient Safety Agency. British Medical Journal.
complication following chest drainage and can occur 2009; 339: b4923.

MCQs
1. Indications for insertion of a chest drain include: (b) Lateral border of serratius anterior, medial border
(a) Pneumothorax of latissimus dorsi and superiorly the nipple

(b) Chylothorax (c) Medial border of pectoralis minor, lateral border of


pectoralis major and the sixth costal interspace
(c) Empyema
(d) None of the above
(d) Haemothorax
3. The commonest complication of chest drain insertion is:
(e) All of the above
(a) Malposition
2. The boundaries of the triangle of safety are:
(b) Bleeding
(a) Anterior border of latissimus dorsi, lateral border
of pectoralis major and inferiorly a line superior to (c) Infection
the nipple (d) Tension pneumothorax

13:50:40 75
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Section 2: Practical Procedures

4. The purpose of an underwater seal is to: minutes. You are asked to see her because she is in
(a) Maintain a positive intrapleural pressure respiratory distress with tachypnoea, tachycardia and
mild cyanosis. The most likely cause for this is:
(b) To allow drainage of pleural contents
(a) Tension pneumothorax
(c) To prevent infection
(b) Haemothorax
(d) To maintain a negative intrapleural pressure
(c) Re-​expansion pulmonary oedema
5. A 65 year old female had a right chest drain inserted
for a large pleural effusion 2 hours ago. She drained (d) Bronchopleural fistula
3 litres of serosanguinous fluid within the first 45 (e) Cardiac herniation

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:50:40
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77

Section 2 Practical Procedures

Cardiac Pacing and Defibrillation


Chapter

10 Sérgio Barra and Patrick Heck

Introduction and these parameters will also influence the urgency


and type of treatment required.
Patients admitted to a cardiothoracic critical care unit
In addition, patients in the cardiothoracic CCU
(CCU) are at increased risk for cardiac arrhythmias
may have previously implanted cardiac electronic
and severe conduction disturbances, which represent
devices such as standard pacemakers, cardiac resyn-
an important cause of morbidity and can be poten-
chronisation therapy (CRT) devices and implantable
tially life threatening. Sustained arrhythmias may
cardioverter-​defibrillators (ICD). Although implanta-
occur in up to 20% of critically ill patients admitted
tion, follow-​up and troubleshooting of these devices
to the CCU. Atrial fibrillation (AF) and ventricular
should be in the domain of a trained cardiologist, it
tachycardia (VT) represent the majority of tachyar-
is imperative that intensive care physicians are famil-
rhythmias, while conduction disturbances with severe
iar with the patients’ underlying cardiac diagnoses,
bradycardia can account for up to 20%.
the reason for the device implant, the basics of the
These events may represent the primary reason
current cardiac electronic device technology and
for admission, but are often the result of a series of
the most frequent issues relevant in the context of a
insults commonly seen in the context of a CCU, such
cardiothoracic CCU.
as hypoxia, myocardial ischaemia, infection, sepsis,
The purpose of this chapter is to discuss the role
adrenergic hyperactivity, QT interval prolongation
of pacing and defibrillation in patients admitted to a
and electrolyte imbalance. Additional causes or trig-
cardiothoracic CCU and the most frequently encoun-
gers include cardiac surgery, mechanical ventilation,
tered issues involving pacemakers and ICDs.
mechanical irritation from central venous catheters,
inotropic and vasopressor agents and drugs known to
prolong the QT interval. Pacing in the Cardiothoracic Critical
The presence of significant structural heart dis-
ease, chronic obstructive pulmonary disease or other
Care Unit
The most common indication for pacing, either tempo-
significant extracardiac comorbidities, systemic
rary or permanent, is bradycardia. Bradyarrhythmias
inflammatory response syndrome, sepsis, high cen-
are relatively common in patients admitted to the
tral venous pressure and low arterial oxygen tension
CCU following cardiac surgery. In most cases, these
are known predictors of a higher arrhythmic risk.
events are temporary and due to sick sinus syndrome,
However, it is often not possible to predict or prevent
slow AF or atrioventricular (AV) block.
the occurrence of severe arrhythmias or conduction
disturbances and therefore a prompt diagnosis and
treatment are required. Causes of Bradycardia
Management includes the correction of a known The most common cause of bradycardia in the cardio-
trigger as well as treatment directed at the arrhyth- thoracic CCU is postoperative heart block. Up to 8%
mia itself (such as antiarrhythmic drugs, pacing, car- of patients undergoing aortic valve replacement were
dioversion or defibrillation). The impact of a certain shown to require permanent pacemaker implantation.
arrhythmia depends on the patient’s underlying car- Local oedema may prolong conduction times, but direct
diac and respiratory function and the characteristics injury to the conduction system during removal of
of the arrhythmia itself (rate, duration, irregularity), penetrating calcium or insertion of deep stiches placed

13:52:42 77
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Section 2: Practical Procedures

during valve surgery are the main cause. Postoperative The cost of prolonged occupation of intensive
complete AV block is seen in approximately 4% of care beds and prolonged hospital stay, as well as the
patients undergoing mitral valve replacement and ring increased morbidity, reduced mobilisation, comfort
annuloplasty, although any degree of AV block may be and safety associated with prolonged temporary pac-
seen in nearly 25%. Damage to the AV nodal artery ing should be weighed against the cost and risks of
may play a role in these cases. Proximal left ante- unnecessary pacemaker implantation in patients who
rior descending artery and septal artery disease have would otherwise demonstrate a full recovery.
also been shown to increase risk of postoperative AV
block. Predictors of need for permanent pacemaker Basic Pacemaker Functioning
implantation include older age, female sex, greater
A detailed review of pacemaker function is beyond
preoperative end-​systolic diameter and left ventricu-
the scope of this chapter, but certain considerations
lar septum hypertrophy, pre-​existing conduction sys-
regarding basic pacemaker types and function are
tem disease, severe annular calcification, prolonged
worth mentioning. In its simplest form a pacing sys-
total perfusion time, re-​do operations and history of
tem delivers regular electrical impulses to the heart at
renal dysfunction, hypertension and bicuspid aortic
a programmed rate. The minimum energy required to
valve. Predictive models have been developed for the
be delivered by the pacing system in order to achieve
prediction of perioperative need for permanent pace-
electrical capture is called the pacing threshold. Most
maker implantation.
modern pacing systems are designed to also look
for intrinsic electrical activity first, before pacing, in
When to Pace order to minimise any unnecessary pacing but also to
prevent delivery of a ventricular pacing stimulus on a
Acutely, the decision to pace is based on the haemody-
T wave, which can be dangerous and trigger arrhyth-
namic impact caused by the underlying bradycardia,
mias. To do this the pacing system has to be able to
rather than the specific rhythm disturbance per se.
sense intrinsic electrical activity.
When pacing is required, it may be temporary or per-
manent. Temporary pacing options include surgically
implanted epicardial pacing wires, transvenous pacing Pacing Mode
leads implanted fluoroscopically or using floatation
Whether permanent implanted systems or tempo-
balloons or, in emergency situations, transcutane-
rary external pacing boxes, all pacing systems have
ous pacing via external defibrillator pads. Decisions
different pacing modes that dictate their function.
on permanent pacemaker implantation are based on
The North American and British Group (NBG) pace-
whether the bradycardia is expected to resolve or not.
maker code is a three-​to five-​letter code designed to
The American College of Cardiology/​American
describe pacemaker mode.
Heart Association guidelines recommend perma-
nent pacemaker implantation for patients with post- • Th
​ e first letter designates the chamber paced: A
operative third-​ degree or advanced second-​ degree stands for atrium, V for ventricle, D for both
AV block that is not expected to resolve, although the (dual), O if the pacemaker has been deactivated.
timing for implant is left to the physician’s discretion. • The second letter designates the chamber sensed
Most authors recommend pacemaker implantation (A, V, D, O): O represents asynchronous pacing
5–​7  days after the operation if conduction distur- without sensing.
bances persist, especially in patients in whom these • The third letter describes the pacemaker’s
disturbances are unlikely to recover, namely those at response to a sensed signal: I (inhibition) means
advanced age, with pre-​existing conduction system the pacemaker discharge is inhibited by a sensed
disease and submitted to valve surgery. Recovery is signal; T (trigger) means the pacemaker discharge
common in patients with sick sinus syndrome, but is actually triggered by a sensed signal; D (dual)
unlikely in the case of complete heart block. Predictors means both inhibition and triggering responses
of long-​term pacemaker dependency are complete are available (for example, in a DDD pacemaker,
AV block as the indication, bypass time longer than an atrial sensed signal will inhibit atrial pacing
105–​120 minutes, preoperative history of syncope and but trigger ventricular pacing after a prespecified
body mass index ≥28.5 kg/​m2. delay).

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Table 10.1  Pacemaker modes of potential applicability to patients in the cardiothoracic critical care unit

MODE Applicability
AOO and VOO • Asynchronous pacing without any sensing
• Useful during surgery or when a patient is exposed to external sources of noise (such as diathermy)
• AOO should only be selected if the underlying condition is sick sinus syndrome, but with normal AV conduction
VVI • Ventricular demand pacing
• This is the most common mode used for patients with severe bradycardia
• Spontaneous ventricular activity is sensed and therefore there is a low risk of R-​on-​T phenomenon with
subsequent ventricular arrhythmias
• There is also a low risk of pacemaker mediated tachycardia
• The lack of AV synchrony may reduce cardiac output
DDD • Pacing and sensing in both chambers with AV synchrony
• Optimal pacing mode in patients with sick sinus syndrome or AV block
• The response to DDD pacing depends on the underlying rhythm
• There is a small risk of pacemaker mediated tachycardia
DDI • Sensing occurs in both chambers, but a sensed atrial signal does not trigger ventricular pacing
• Tracking of rapid atrial rates (in patients with atrial fibrillation, atrial flutter or atrial tachycardia) will not occur
• Pacemaker mediated tachycardia is not possible in this mode

• Position four refers to the rate-​response algorithm Biventricular pacemakers (also referred to as
and is only relevant for permanent systems. Rate-​ CRT) deserve special mention. These devices are
response means the pacemaker will be able to indicated in patients who may not actually have any
increase its pacing rate in response to increasing bradycardia, but have a LV ejection fraction ≤35%,
physiological needs. This is possible due to the QRS duration ≥120 ms and heart failure symptoms,
incorporation of either activity sensors with especially in the presence of left bundle branch block.
vibration detectors or minute-​ventilation CRT can improve cardiac output, haemodynamics,
sensors. heart failure symptoms, functional capacity and qual-
• ​Position five is used to indicate whether multisite ity of life in appropriately selected patients. It is there-
pacing is present. fore reasonable to expect that a patient on the CCU
who already has a CRT device in situ has advanced
A three-​letter code is adequate to describe emer-
heart failure, and maintaining correct device function
gency temporary pacing and most forms of perma-
in these patients is even more critical.
nent pacing in the context of a cardiothoracic CCU.
Table 10.1 gives examples of pacemaker modes, which
the CCU physician should be familiar with. Although Implantable Cardioverter Defibrillators
the VVI mode is potentially applicable to all cases of ICDs are seeing more widespread use within cardi-
bradycardia, it should be kept in mind that the lack ology and are therefore likely to be seen in patients
of AV synchrony may reduce cardiac output by up to on the cardiothoracic CCU. They are implanted in
25%, which is particularly relevant in patients with patients at high risk of life-​ threatening ventricu-
structural heart disease. A DDD mode, where possi- lar arrhythmias, most commonly due to structural
ble, will ensure appropriate AV synchrony. heart disease such as ischaemic or dilated cardiomyo­
pathies. All ICDs have pacemaker functions in addi-
tion to their defibrillator function. Accordingly, they
Pacemaker Type can be single, dual or biventricular systems.
Permanent pacemakers can be single chamber (usu- Figure  10.1a illustrates a simple single chamber
ally right ventricle), dual chamber (right atrium and pacemaker with a solitary lead in the right ventricle.
right ventricle) or biventricular systems. The choice of Figure  10.1b shows a more complex CRT-​D device
system is decided based upon underlying cardiac con- with leads in the right atrium, right ventricle and in
ditions and indication for the device, and will be made a branch of the coronary sinus (for left ventricular
by an appropriately trained cardiologist. pacing).

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(a) (b)

Figure 10.1  Single chamber pacemaker (a) and cardiac resynchronisation therapy defibrillator (b). (a) White arrow, right ventricular lead
placed in the interventricular septum. (b) Black arrow, right atrial lead placed in the right atrial appendage; grey arrow, single-​coil ICD lead
placed in the right ventricular apex; white arrow, left ventricular lead placed in a branch of the coronary sinus; black arrow, high-​energy
device.

Pacing Related Complications Pacemaker–​Patient–​Environment


Pacing related complications can either be as a con- Interactions and Special
sequence of the implant procedure itself or due
to abnormal or unexpected pacemaker function. Considerations
Although intensive care physicians do not implant or Certain precautions should be taken when perform-
program pacemakers, it is important to be aware of ing specific procedures or manoeuvres in patients
potential environmental factors that may impact on carrying cardiac electronic devices and this list is by
pacemaker function and possible acute complications no means exhaustive:
related with the temporary or permanent pacing sys- • When externally defibrillating a patient with a
tem implantation. pacemaker the external electrodes should not
be placed close to the pacemaker, the minimal
Implant Complications effective energy should be used and the device
With any transvenous system, permanent or tempo- must be checked afterwards.
rary, the following acute implant related complications • Certain situations may cause a temporary rise
may occur:  myocardial perforation with pericardial in pacing threshold and thereby impair device
effusion and tamponade, pneumothorax, haemotho- function, including electrolyte disturbance and
rax, lead displacement or acute infection. immediately after CPR.
• Subclavian puncture should be avoided
Other Complications ipsilateral to implanted devices when inserting
Other potential issues involving patients with pace- a central venous line due to the risk of lead
makers include the precautions needed when per- insulation tear.
forming direct current cardioversion or defibrillation, • Pulmonary artery catheters should also be
the applicability and utility of magnet application, the avoided, if possible, in patients with recent
possibility of electromagnetic interference and appar- device implantations due to the risk of lead
ent or real system malfunction with failure to pace, displacement.
failure to capture, failure to sense or increasing pacing • Atrial pacing spikes might be misinterpreted as
threshold. QRS complexes by intra-​aortic balloon pumps

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Table 10.2  Troubleshooting issues encountered in patients with pacemakers

Causes Manifestations Troubleshooting


Failure of • ​Battery depletion Absence of pacing spikes, with • Perform chest X-​ray to exclude lead
output • Component failure or without magnet application fracture
• Total lead fracture Asystole or bradycardia, • Pacemaker interrogation will reveal
• Loose connections between depending on the patient’s battery voltage depletion if true
generator and lead underlying rhythm output failure is due to battery
• Oversensing end-​of-​life or very high or infinite
impedance in the presence of lead
fracture
• Replace lead or generator if needed
• Reduce sensitivity if oversensing is
the cause of pacing inhibition
Failure to • Increase in pacing threshold above Presence of pacing spikes • Reprogram energy output (increase
capture programmed value without subsequent myocardial voltage output or pulse duration)
• Defective pacing leads (partial capture (shown by the absence • Pacemaker interrogation will reveal
fracture or insulation breach; the of an electrogram) high impedance in the presence of
latter may be caused by central Higher than normal amplitude lead fracture or low impedance if
venous catheter placement through of pacing spikes if insulation insulation failure
subclavian route) failure • Perform chest X-​ray to exclude lead
• Battery depletion Asystole or bradycardia, displacement
• Lead displacement depending on the patient’s • Replace lead if needed
• Severe hyperglycaemia, underlying rhythm • Correct electrolyte and metabolic
hyperkalaemia, acidosis and alkalosis disturbances
Rapid pacing • Oversensing of the atrial channel Rapid ventricular paced • Adjust sensitivity to prevent
(due to partial lead fracture or rhythm –​there is ‘tracking’ of oversensing
electromagnetic interference) the atrial sensed events • Program pacemaker to VVI or DDI
• Underlying atrial tachyarrhythmia mode to prevent tracking of atrial
with tracking of p waves to the tachyarrhythmia
programmed upper rate limit

and interfere with triggering. Using arterial of sensing. When lack of pacing or lack of capture
waveform is an alternative. are detected, all connections should be immediately
• The use of electrocautery can cause interference checked, the ventricular output set to maximum and
with both pacing and ICD systems. In the generator programmed into asynchronous mode.
pacemakers it might result in inappropriate Lack of capture is usually the result of lead displace-
inhibition of pacing as the device misinterprets ment or threshold rise.
the electrical interference as intrinsic rhythm. Whilst there are many similarities to the approach
In ICDs it may result in the delivery of shock taken with troubleshooting a permanent pacing sys-
therapy as the high frequency noise from tem, it is a more complex device and often will require
electrocautery may be interpreted as a tachycardia the assistance of a physician familiar with pacemak-
requiring treatment. ers. Pacing and sensing problems can originate in the
generator, the pacing leads, the lead–​ myocardium
interface or the patient. Table 10.2 lists the most fre-
Troubleshooting Pacing and ICD quent troubleshooting issues encountered in patients
Systems with pacemakers, their most frequent causes and rec-
Temporary pacing, either with epicardially or trans- ommendations to overcome the problem. Figure 10.2
venously placed leads, is often needed following car- illustrates ECGs of different pacemaker malfunctions.
diac surgery. Problems associated with temporary Most of the considerations made for pacemaker
pacing include the displacement of the lead, myo- troubleshooting are equally valid in patients with ICDs.
cardial perforation, which may lead to tamponade, Other important occurrences in these patients include
increasing pacing threshold, lack of capture and lack the delivery of inappropriate ICD shocks, ICD storms or

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(a) (b)

(c)

Figure 10.2  Pacemaker troubleshooting. (a) Failure to output (absence of pacing spikes causing a 3 second pause). (b) Failure to capture
(4th and 5th pacing spikes are not followed by ventricular electrograms). (c) Undersensing (all but the first pacing spike are delivered
inappropriately due to undersensing of electrical signals). (A black and white version of this figure will appear in some formats. For the colour
version, please refer to the plate section.)

ineffective ICD therapies in patients with true life-​threat-


ening ventricular arrhythmias. As ICD systems are even
Cardioversion and Defibrillation in the
more complex than pacing systems, specialist input is Cardiothoracic Intensive Care Unit
invariably required in troubleshooting these devices. Defibrillation and cardioversion are occasionally
required in the CCU. Any atrial or ventricular tach-
Pacemaker and ICD ‘Magnet’ Mode yarrhythmia causing severe haemodynamic compro-
mise may need to be immediately dealt with using
Intensive care physicians should also be familiar with
electrical cardioversion and local advanced life sup-
the typical response of pacemakers and ICDs to mag-
port guidelines should be followed. Unsynchronised
net application but this should generally only be used
high energy shocks should be used to treat ventricular
when appropriate reprogramming of the device to the
fibrillation or very fast polymorphic VT, whereas syn-
desired function is not possible. Magnet modes can
chronised shocks should be used for cardioverting AF
vary between manufacturers and can permanently
and haemodynamically stable VT. Defibrillators deliv-
alter device function. Some new devices allow for pro-
ering biphasic waveforms should be preferably used.
gramming to ‘off ’ function.
Electrical cardioversion is very effective in the
A magnet placed over a pacemaker, but not an ICD,
treatment of tachyarrhythmias, but it should be
will usually make it pace in an asynchronous mode
borne in mind that unless the underlying cause of the
at a fixed heart rate. This is useful to protect pace-
arrhythmia is identified and treated, such as ischae-
maker dependent patients during diathermy or other
mia or electrolyte disturbance, there is a high prob-
sources of electromagnetic interference. However, not
ability of the arrhythmia recurring.
all pacemakers switch to a continuous asynchronous
mode when a magnet is applied, as the response to
magnet application may vary across models. Special Considerations for
Magnet application over an ICD will prevent the
device from sensing and delivering any therapies,
Defibrillation or Cardioversion
which is useful in patients having inappropriate ICD • Electrical cardioversion is contraindicated in
shocks or ICD storms or when electrocautery is being patients with known digitalis toxicity, not only
used. However, different ICD models may respond due to the lower efficacy in this context, but
differently, if at all, and in some cases therapies may also because junctional or paroxysmal atrial
be turned off completely until the magnet is removed tachycardia and even VF may occur within a few
and then reapplied. minutes of cardioversion.

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Chapter 10: Cardiac Pacing and Defibrillation

• Ipsilateral pneumothorax can increase pre-​existing conduction system disease or history


defibrillation threshold in patients with an ICD of syncope and submitted to valve surgery.
and may result in unsuccessful defibrillation by • With any transvenous pacing system, intensive
the device. care physicians should be aware not only of any
• Patients with atrial fibrillation lasting for longer potential periprocedural complications, but also
than 24 to 48 hours and without appropriate issues such as the precautions required when
anticoagulation are at risk of stroke following performing direct current cardioversion, the
cardioversion and therefore this should not be utility of magnet application, electromagnetic
performed without previously excluding left atrial interference and apparent or real system
appendage thrombus with a transoesophageal malfunction with failure to pace, capture or sense
echocardiogram, unless there is significant and increasing pacing threshold.
haemodynamic compromise. Consideration • Appropriate management of an electrical storm
of anticoagulation should be made following includes the correction of the underlying cause,
cardioversion even in the absence of clots, the use of intravenous amiodarone or beta-​
as the thromboembolic risk is higher in the blockers and reprogramming the ICD if the
postcardioversion period. arrhythmia is well tolerated. Magnet application
• When external cardioversion fails, potential may be useful to prevent subsequent therapies,
solutions include applying additional pressure while deep sedation or general anaesthesia may
to the paddles during the shock, changing the in some cases provide complete, albeit temporary,
electrodes to an anteroposterior orientation or control.
administering intravenous antiarrhythmics such • Electrical cardioversion is very effective in
as amiodarone (for both atrial and ventricular the treatment of tachyarrhythmias, but unless
arrhythmias) or ibutilide (for atrial fibrillation), the underlying cause of the arrhythmia is
which lower the energy required to restore sinus identified and treated there is a high probability
rhythm. of recurrence. When cardioversion fails,
applying additional pressure to the paddles
Conclusions during the shock, changing the electrodes to an
Cardiac arrhythmias and conduction disturbances are anteroposterior orientation or administering
frequent in the context of a cardiothoracic critical care intravenous antiarrhythmics which lower the
unit. Furthermore, an increasing number of patients energy required to restore sinus rhythm may be
with cardiac electronic devices are currently admitted useful.
to these units. It is imperative that the intensive care
physician is aware of the basic function of pacemak-
ers and implantable cardioverter-​defibrillators, pos-
Further Reading
sible complications associated with the use of these Berdajs D, Schurr UP, Wagner A, et al. Incidence and
pathophysiology of atrioventricular block following
devices, the most frequent troubleshooting issues and mitral valve replacement and ring annuloplasty.
the diagnostic and therapeutic options that pacemak- European Journal of Cardiothoracic Surgery. 2008;
ers and ICDs may offer to critical patients. 34: 55–​61.
Dawkins S, Hobson AR, Kalra PR, et al. Permanent
Learning Points pacemaker implantation after isolated aortic valve
replacement: incidence, indications, and predictors.
• In patients admitted to the cardiothoracic CCU
Annals of Thoracic Surgery. 2008; 85: 108–​112.
and presenting with bradycardia, the decision
El-​Chami MF, Sawaya FJ, Kilgo P, et al. Ventricular
to pace is based on the haemodynamic impact
arrhythmia after cardiac surgery: incidence, predictors,
caused by the underlying bradycardia, rather than and outcomes. Journal of the American College of
the specific rhythm disturbance per se. Cardiology. 2012; 60: 2664–​2671.
• Recovery of severe conduction disturbances is Epstein AE, Di Marco JP, Ellenbogen KA, et al. ACC/​
common in patients with sick sinus syndrome, AHA/​HRS 2008 Guidelines for Device-​Based Therapy
but unlikely in the case of complete heart block, of Cardiac Rhythm Abnormalities: a report of the
especially in patients at advanced age, with American College of Cardiology/​American Heart

13:52:42 83
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84

Section 2: Practical Procedures

Association Task Force on Practice Guidelines Merin O, Ilan M, Oren A, et al. Permanent pacemaker
(Writing Committee to Revise the ACC/​AHA/​NASPE implantation following cardiac surgery: indications
2002 Guideline) Journal of the American College of and long-​term follow-​up. Pacing and Clinical
Cardiology. 2008; 51: e1–​62. Electrophysiology. 2009; 32: 7–​12.
Erdogan HB, Kayalar N, Ardal H, et al. Risk factors for Mosseri M, Meir G, Lotan C, et al. Coronary pathology
requirement of permanent pacemaker implantation predicts conduction disturbances after coronary artery
after aortic valve replacement. Journal of Cardiac bypass grafting. Annals of Thoracic Surgery. 1991;
Surgery. 2006; 21: 211–​215. 51: 248–​252.
Glikson M, Dearani JA, Hyberger LK, et al. Indications, Nardi P, Pellegrino A, Scafuri A, et al. Permanent
effectiveness, and long-​term dependency in permanent pacemaker implantation after isolated aortic valve
pacing after cardiac surgery. American Journal of replacement: incidence, risk factors and surgical
Cardiology. 1997; 80: 1309–​1313. technical aspects. Journal of Cardiovascular Medicine
Gordon RS, Ivanov J, Cohen G, Ralph-​Edwards (Hagerstown). 2010; 11: 14–​19.
AL. Permanent cardiac pacing after a cardiac Onalan O, Crystal A, Lashevsky I, et al. Determinants of
operation: predicting the use of permanent pacemaker dependency after coronary and/​or mitral
pacemakers. Annals of Thoracic Surgery. 1998; or aortic valve surgery with long-​term follow-​up.
66: 1698–​1704. American Journal of Cardiology. 2008; 101: 203–​208.
Knotzer H, Mayr A, Ulmer H, Lederer W. Reinelt P, Karth GD, Geppert A, Heinz G. Incidence and
Tachyarrhythmias in a surgical intensive care unit: a type of cardiac arrhythmias in critically ill patients: a
case-​controlled epidemiologic study. Intensive Care single center experience in a medical-​cardiological
Medicine. 2000; 26: 908–​914. ICU. Intensive Care Medicine. 2001; 27: 1466–​1473.
Liu Q, Kong AL, Chen R, et al. Propofol and Trappe H-​J, Brandts B, Weismueller P. Arrhythmias in the
arrhythmias: two sides of the coin. Acta intensive care patient. Current Opinion in Critical Care.
Pharmacologica Sinica. 2011; 32: 817–​823. 2003; 9: 345–​355.

MCQs
1. In patients admitted to the cardiothoracic CCU fol- 3. In patients admitted to the cardiothoracic CCU and
lowing cardiac surgery, which features predict the presenting with a fast atrial arrhythmia, which acute
need for pacing in the event of significant bradycardia? measure should not be taken?
(a) Valve surgery rather than coronary (a) Direct current cardioversion in the case of severe
revascularisation haemodynamic compromise
(b) Advanced age (b) Unsynchronised direct current cardioversion
(c) History of syncope (c) Correction of any electrolyte disturbance
(d) Previous left bundle branch block (d) Administration of an appropriate antiarrhythmic
(e) All of the above medication, such as amiodarone, in the first hours
of well-​tolerated atrial fibrillation
2. In patients admitted to the cardiothoracic CCU fol-
lowing cardiac surgery and with temporary pacing (e) Correction of underlying heart failure, myocardial
systems showing failure to capture, which underlying ischaemia, bleeding or anaemia
mechanisms should be considered? 4. A patient is day 1 post cardiac surgery and pac-
(a) Increase of the pacing threshold above ing dependent with epicardial temporary pacing
programmed value wires. Brief periods of asystole are seen on the moni-
tor. Which of the following measures should not be
(b) Lead displacement considered?
(c) Loose connections (a) Retesting the pacing threshold and increasing out-
(d) Hyperkalaemia, acidosis or alkalosis put if required
(e) All of the above

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Chapter 10: Cardiac Pacing and Defibrillation

(b) Checking the connectors of the pacing wires and (a) The atrium will be paced by the device
pacing box when needed
(c) Placement of transcutaneous pacing pads in case (b) The pacemaker will provide adequate AV
of need synchrony
(d) Increasing the sensitivity of the pacing system to (c) The pacemaker will prevent the heart from going
detect any intrinsic rhythm slower than 60 beats per minute
(e) Replacing the batteries in the pacing box (d) The pacemaker will be unaffected by the use of
5. A patient has a permanent pacemaker in situ in VVI electrocautery
mode and a lower heart rate limit of 60 beats per min- (e) The pacemaker will increase the patient’s heart rate
ute and is functioning normally. Which of the follow- beyond 60 beats per minute with exercise
ing statements is correct?

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

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Section 2 Practical Procedures

Arterial and Venous Catheterisation and


Chapter

11 Invasive Monitoring
Stuart A Gillon, Nicholas A Barrett and Christopher IS Meadows

Principles of Vascular Access Table 11.1  Factors defining vascular catheters

Vascular catheters are ubiquitous to cardiothoracic Type of vessel: arterial, venous; peripheral, central
critical care. They may be defined or described on the Site of insertion: jugular, femoral, central, etc.
basis of numerous factors (Table  11.1). For the pur- Duration of access: short term, medium term, long term
poses of this chapter, vascular access relates to cath- Pathway from skin to vessel: tunnelled, non-​tunnelled
eters within the arterial or central venous system. Length: short, mid, long
Additional features: number of lumens, antibiotic, antiseptic or
heparin impregnated
Insertion
Vascular catheter insertion within the critical care
unit is almost universally by the Seldinger technique:
a needle is inserted into the target vessel (or a tribu- Pressure Monitoring
tary of the target vessel); a guide wire is passed into
the vessel; one or more dilators are passed over the
Transducers
guide wire to create a tract through the skin and soft A transducer converts mechanical energy (hydrostatic
tissues; and the catheter is advanced over the guide pressure within the vascular system) into an electri-
wire, into the vessel. cal signal; the hydrostatic pressure within the cath-
Traditionally, the target vessel was sought using a eter is quantified and displayed as both a value and a
combination of anatomical landmarks and palpation. waveform.
The increasing availability of point-​of-​care ultrasound A continuous column of fluid maintains con-
technology within the critical care environment has tact between the transducer and the vascular sys-
led to a gradual move towards real-​time ultrasound tem. Changes in pressure are transmitted down the
guided vascular access. The use of ultrasound for vas- column of fluid, leading to distortion of the trans-
cular access has been demonstrated to increase suc- ducer membrane. The membrane contains a strain
cess and reduce complications and is now considered gauge:  distortion of the membrane stretches a wire,
a standard of care by the National Institute of Clinical altering its resistance. The wire is integrated into a
Excellence. Wheatstone bridge, which allows accurate determina-
Position may be confirmed by ensuring free aspi- tion of changes in resistance. The change in resistance
ration of blood, by transduction of pressure (thereby equates to change in pressure and this is displayed on
confirming arterial or venous placement), by meas- the monitor.
urement of the oxygen content of aspirated blood A valve within the transducer system permits
(suggestive of arterial or venous placement) or by flow of 3–​4 ml of saline per hour through the arterial
imaging (either X-​ray or ultrasound). line, to maintain line patency. Some units heparinise
the saline flush on the basis that this may reduce the
risk of intracatheter thrombus formation. The use of
Complications heparin, however, exposes the patient to heparin (and
The complications associated with line placement, associated reactions) and may interfere with the accu-
and potential strategies to minimise risk are listed in racy of coagulation samples drawn from the line if the
Table 11.2. flush fluid is incompletely removed prior to sampling.

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Chapter 11: Arterial and Venous Catheterisation

Table 11.2  Complications related to central venous catheter placement and strategies to reduce risk
Immediate Damage to adjacent structure (e.g. Ultrasound guidance, experienced operator (particularly in the presence of
arterial puncture, pneumothorax) anatomical abnormalities)
Air embolism Head-​down position in jugular and subclavian approaches
Bleeding Correction of coagulopathy prior to insertion
Late Infection Introduction of CVC insertion ‘bundles’, full barrier precautions during insertion,
use of antibiotic impregnated catheters, use of antimicrobial impregnated patches
over the insertion site, avoidance of the femoral vein as an insertion site, removal
of catheters when no longer required
Thrombosis Avoidance of femoral insertion, use of heparin impregnated catheters, early
removal

Systematic review of studies examining the efficacy of is unaffected. Whilst pressure measurement systems
heparinised saline in this context found no convinc- are produced with material and dimensions most
ing evidence of improved catheter patency. suited to optimal damping, over-​damping and under-​
damping may occur.
Resonance and Damping
Every material has a natural frequency: the frequency Zeroing
at which it freely resonates. If a material is exposed Accurate measurement of physiological pressure
to a frequency close to its natural frequency it will requires the transducer to be ‘zeroed’ to atmospheric
resonate, or oscillate, at its maximum amplitude. This pressure (a system pressure of zero equates to atmos-
physical phenomenon is of significance to pressure pheric pressure, as physiological pressures are described
monitoring systems as, if the frequency of one of the as relative to atmospheric pressure). Calibration
components of the measured pressure wave is close to involves opening the pressure system to air, and refer-
the natural frequency, the excessive oscillation gener- encing this pressure to zero on the system. Transducers
ated will distort the measured pressure. are prone to baseline drift and therefore this process
In order to avoid this phenomenon, the natural should be undertaken several times per day.
frequency of a pressure monitoring system must be The height of the transducer relative to the patient
several orders of magnitude greater than the compo- is also important. By convention, the transducer
nent frequencies of the waveform being measured. should be at the same height above the floor as the
Using longer tubing, of wider diameter and using a left atrium of the patient. A transducer placed above
low density fluid within the tubing, will increase the or below the height of the atrium will lead to under-​
natural frequency of a system. reading and over-​reading of pressure respectively.
Damping describes the dissipation of energy in a
resonant, oscillating system. A  pressure monitoring
system may be over-​damped by tubing, which is of
Arterial Catheters
excessive length, insufficient diameter, or made from There are three major indications for placement of an
highly compliant material. Additionally, kinks, clots arterial catheter.
or air bubbles within the system will contribute to 1. Haemodynamic instability (either current or
damping. expected) in which beat to beat measurement
The optimal system strikes a balance between of arterial pressure allows close monitoring of
resonance and damping. A  system with excessive haemodynamic state and safe titration of inotropic
resonance will tend to over-​measure peak (systolic) and vasoactive drugs.
pressures and under-​measure trough (diastolic) pres- 2. Need for frequent arterial blood sampling (e.g.
sures; mean pressure should be unaffected. Such sys- respiratory failure or severe, persistent metabolic
tems are described as under-​damped. In contrast, a disturbance).
system with excessive damping and insufficient reso- 3. Non-​pulsatile flow (for example in cardiac bypass
nance (damped system) will under-​measure peak and or venoarterial ECMO) as there is no alternative
over-​measure trough pressures; again mean pressure method of measuring systemic pressures.

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Section 2: Practical Procedures

Arterial catheters may be inserted into: Pulse Pressure Variation


• Peripheral arteries (e.g. most commonly radial,
• The intrathoracic pressure varies throughout
also ulnar, brachial, dorsalis pedis);
the respiratory cycle; this alters the loading
• Central arteries (e.g. most commonly femoral,
conditions of the heart and results in variation
also axillary).
in stroke volume and pulse pressure between
The arterial pressure in peripheral arteries differs inspiration and expiration.
from that in central arteries. • The magnitude of this variation is greater
• A decrease in arterial compliance with increasing on the steep portion of the Frank–​Starling
distance from the heart leads to a higher systolic curve (where a patient is likely to increase
and lower diastolic pressure measurement in cardiac output in response to fluid) than on
peripheral compared with central arteries; the the flat portion (with less likelihood of fluid
mean pressure should be comparable. responsiveness).
• The tone of peripheral arteries will demonstrate • Meta-​analysis of studies relating to pulse
a more significant response to temperature and pressure variation (PPV) (and the closely
vasoactive medications than central arteries; related stroke volume variation) suggests that
measurement of peripheral arterial pressure variation of >13% is strongly predictive of fluid
could therefore be a poor reflection of the central responsiveness.
arterial pressure perfusing vital organs. • The studies relating to PPV were however largely
• These differences between central and peripheral conducted in highly controlled environments,
pressure are more pronounced in the elderly and in deeply sedated patients, with no spontaneous
in those with vascular disease. ventilation; analysis of the intensive care
population shows that few patients are
Information Derived from the Arterial comparable to the subjects of the initial studies;
Waveform the practical application of PPV in the clinical
setting therefore has significant limitations.
• Pulse rate
• Systolic blood pressure
• Diastolic blood pressure Central Venous Catheters
• Mean blood pressure A central venous catheter (CVC) is a vascular catheter
• The shape of the arterial waveform is determined with a tip sitting in the central venous system. These
by numerous factors: may be short catheters (15–​20  cm) inserted into a
○ The stroke volume, central vein (femoral, jugular or subclavian) or longer
○ Left ventricular contractility, catheters inserted into a peripheral vein and advanced
○ Capacitance of the central arterial tree (the to the central circulation (peripherally inserted cen-
ability to distend and accommodate ejected tral catheter, PICC).
blood), Indications for CVC placement include the
○ Peripheral resistance (the rate at which blood following.
dissipates from the central arteries into • Administration of drugs which may only be
peripheral circulation). safely delivered directly into a central vein
• The dichrotic notch is the positive deflection in (e.g. amiodarone, noradrenaline, concentrated
the downstroke of the arterial waveform, which potassium, cytotoxic agents, total parenteral
represents closure of the aortic valve: nutrition).
○ Typically occurs at one third into the pressure • Measurement of central venous pressure
wave descent when aortic pressure (AoP) (CVP) or central venous oxygen saturation
exceeds left ventricular pressure (LVP); (ScvO2).
○ If peripheral resistance is reduced (e.g. sepsis), • To facilitate a procedure which requires access
AoP > LVP later in the cycle and the dicrotic to the central venous circulation (e.g. renal
notch shifts down the curve. replacement therapy, pulmonary artery catheter

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Chapter 11: Arterial and Venous Catheterisation

a not least because it is impossible to test in an intact


c
human circulation. It remains therefore primarily a
theoretical construct.
One key practical product of Guyton’s work has
v however arisen:  the use of the RAP (in the form of
x CVP) in the clinical optimisation of cardiac output.
y
Guyton considered RAP to be an independent deter-
minant of SV (and therefore cardiac output). He pro-
Figure 11.1  CVP trace: a atrial contraction; c closure of tricuspid posed RAP and SV to have a similar relationship to
valve; x atrial relaxation; v ventricular contraction; y opening of the
tricuspid valve. that between end-​diastolic volume and SV reported
by Starling. Given its ease of measurement, CVP was
thus widely integrated into clinical practice as a meas-
flotation, temporary pacing wire insertion, ure of left ventricular preload.
extracorporeal membrane oxygenation). The intervening six decades have witnessed sig-
• If peripheral venous access proves impossible. nificant technological advances in terms of haemody-
namic monitoring. Yet the use of CVP as a marker of
left ventricular preload persists. The Surviving Sepsis
Central Venous Pressure Trace Campaign, for example, recommends a CVP of 8–​
The central venous pressure (CVP) trace is outlined 12 mmHg as a target for volume resuscitation in the
in Figure 11.1. shocked septic patient.
The clinical utility of CVP in the assessment of
Central Pressures preload is however questionable. Manipulation of
The CVP, when measured in the superior vena cava preload in the shocked patient is undertaken with a
(SVC) equates to right atrial pressure (RAP). The view to optimising cardiac output; any assessment of
significance of CVP in terms of the global haemody- preload is therefore beneficial only if it reliably iden-
namic state is complex and its role in management of tifies those patients in whom increase in preload
the haemodynamic state is controversial. (by fluid administration) is likely to increase car-
At the end of the nineteenth century, Otto Frank diac output. In clinical trials, the CVP has consist-
and Ernest Starling described the relationship between ently been shown to be a poor determinant of fluid
myocardial stretch and stroke volume and demon- responsiveness. As such, there are calls from some
strated an increase in cardiac output in response to quarters for the CVP as a marker of preload to be
increasing preload. This so-​ called Frank–​ Starling abandoned.
mechanism became a cornerstone of cardiovascu-
lar physiology and remains an important concept in Pulmonary Artery Catheter
haemodynamic management.
Some 50 years after this original work, Arthur History
Guyton built upon the Frank–​ Starling concept. The pulmonary artery catheter (PAC) evolved dur-
Guyton concluded, on the basis of a series of animal ing the twentieth century as a means of measuring
models, that venous return (Vr) was the key deter- pressure and flow within the pulmonary vasculature.
minant of cardiac output. According to the Guyton Ronald Bradley of St Thomas’ Hospital, London, first
model, Vr is determined by three factors:  the mean described the placement of a catheter in the pulmo-
circulatory filling pressure (MCFP) (generated by the nary circulation of humans in the 1950s. This origi-
elastic properties of the vasculature and the hydro- nal catheter was, however, difficult to site. Harold
static force exerted by volume within the vessels, the Swan (an alumnus of St Thomas’ Medical School) and
so-​called stressed volume); RAP (against which the his colleague William Ganz (Cedars-​Sinai Medical
MCFP must drive); and the venous resistance (which Center, Los Angeles) adapted Bradley’s design by
may be altered by changes in regional blood flow to adding a flotation balloon, thereby enhancing ease
organ vascular beds). The accuracy of this complex of insertion. The names of Swan and Ganz have since
model remains the subject of significant debate, become eponymous with the PAC.

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Section 2: Practical Procedures

Components 40

• A typical adult PAC is 110 cm in length and 7–​8 F Right Right Pulmonary Pulmonary artery
atrium ventricle artery wedge
in diameter; distance markers are found every
10 cm to guide insertion. 30

• It is made of radio-​opaque polyvinyl chloride.

Pressure (mmHg)
• There are typically four lumens, the most distal
is located at the tip and used for measuring 20
pulmonary pressures; the most proximal is
located around 30 cm from the tip, measures RAP
and serves as the route of injection of cold saline
for cardiac output measurement. 10

• A thermistor is located close to the tip for the


purposes of cardiac output and core temperature
measurement. 0
• A balloon, 1–​1.5 ml in volume, is located close
Figure 11.2  Pulmonary artery catheter waveform as it is ‘floated’
to the tip of the catheter; this is inflated for the through the heart into pulmonary circulation.
purposes of flotation into the pulmonary artery,
and measurement of the pulmonary artery wedge
pressure.
smooth motion; the passage of the catheter from
Indications atrium to ventricle to pulmonary artery may be
tracked by:
Indications for insertion of the PAC include:
○ The changing pressure waveform
• Cardiac output monitoring;
(Figure 11.2), the most common approach;
• Measurement of right heart pressures, pulmonary
○ Fluoroscopy;
artery pressure, and left atrial pressure;
○ Transoesophageal echocardiography.
• Measurement of central venous oxygen saturation
(ScvO2) and mixed venous oxygen saturation
(SvO2). Pulmonary Artery Measurements
The PAC allows measurement of pressure and flow
within the pulmonary vasculature. Table 11.3 outlines
Insertion of the Pulmonary Artery direct and indirect variables, which may be obtained
Catheter from the PAC.
• The procedure is undertaken using an aseptic
technique; all lumens of the catheter are flushed; Cardiac Output Monitoring
the distal port is connected to a pressure The PAC measures cardiac output by means of ther-
transducer. modilution. A known volume of cold saline is rapidly
• An insertion sheath is placed using a Seldinger injected into the proximal, RA, port. The resultant
technique into a central vein (right internal change in temperature of blood is measured by the
jugular and left subclavian provide the most thermistor at the tip of the PAC and a washout curve
direct route for the flotation catheter). is generated. Blood flow, which equates to cardiac
• The PAC is introduced via the sheath; once the tip output, is inversely proportional to the rate of tem-
is sitting within the vena cava or right atrium, the perature change; flow is quantified by means of the
balloon is inflated and the catheter advanced in a Stewart–​Hamilton equation:

k(core temperature − indicator temperature)


volume of indiicator
CO =
Change in blood temperature

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Chapter 11: Arterial and Venous Catheterisation

Table 11.3  Direct and indirect variables obtained from the pulmonary artery catheter

Variable Equation Normal values


Direct measurements Right atrial pressure (RAP) 2–​6  mmHg
Right ventricular pressures (RVP) systolic 20–​30 mmHg
diastolic 0–​5 mmHg
Pulmonary artery pressures (PAP) systolic 20–​30 mmHg
diastolic 8–​12 mmHg
mean 10–​20 mmHg
Pulmonary artery wedge pressure (PAWP) 4–​12  mmHg
Cardiac output (CO) 4–​8 l/​min
Derived variables Cardiac index (CI) CO 2.5–​4 l/​min
BSA
Systemic vascular resistance (SVR) MAP − RAP 800–​1200 dyne s/​cm5
CO
Pulmonary vascular resistance (PVR) mPAP − PAWP 37–​250 dyne s/​cm5
CO
DO2 CO ( SpO2 × Hb × 1.34) + (0.003PaO2 )

VO2 10 (CaO2 − CvO2 ) × CO

where k is a constant. The appropriateness of the randomised control


The traditional means of cardiac output monitor- trial as a means of testing a monitoring tool is however
ing via the PAC relies upon intermittent bolus stud- questionable, since the utility of the PAC is dependent
ies and cannot therefore provide continuous cardiac upon clinician ability to correctly interpret the results.
output monitoring. Variants of the PAC are now avail- Therefore, whilst there have been calls to remove the
able which have a heating element in the region of the PAC from clinical practice based upon the results of
proximal injection port. This element intermittently the above named trials, the PAC proponents remain,
heats the passing blood, allowing regular washout particularly amongst those clinicians managing com-
curves to be created and near-​continuous cardiac out- plex cardiac patients.
put to be calculated.
Transpulmonary Dilution and Pulse
Evidence Basis Contour Analysis
The PAWP may be used in a similar manner to the CVP,
as a static marker of preload. However, like the CVP, the PiCCO
PAWP has been demonstrated to be a poor predictor of
• The PiCCO system utilises a modified arterial
fluid responsiveness and has therefore, in many centres,
line to provide advanced cardiovascular
been replaced by other, dynamic assessments.
monitoring.
The impact of PAC monitoring upon outcome has
• The PiCCO arterial line is inserted in a central
been tested in randomised control trials in the gen-
artery (usually femoral, alternatively axillary).
eral intensive care population (PACMAN study), in
• The PiCCO connects to a transducer, providing
patients admitted with acute respiratory distress syn-
standard arterial line information.
drome (ARDSnet group), in high risk cardiac surgical
patients and those with severe heart failure (ESCAPE • A thermistor, at the tip of the PiCCO line,
study). No study demonstrated improved outcomes allows performance of transpulmonary
with the additional information provided by the PAC thermodilution.
and there was an increased incidence of adverse, cath- ○ 15 ml of cold saline is injected into a
eter related, events. central line placed in the internal jugular or

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Section 2: Practical Procedures

subclavian vein; a sensor placed in the CVC muscle relaxants (which cross react with the
port monitors the timing of injection and the molecular sensor).
temperature of the injectate. ○ The lithium injectate does not require a CVC;
○ The cold injectate crosses the pulmonary a peripheral cannula will suffice.
circulation and enters the systemic ○ LiDCO does not provide the volumetric
circulation; the resultant change in blood measurements offered by the PiCCO.
temperature is monitored by the PiCCO
thermistor; a temperature washout
curve –​similar to that generated by a Non-​calibrated Systems
PAC –​is used to determine cardiac In addition to the PiCCO and LiDCO, several non-​
output. calibrated systems are available. Like the continu-
○ PiCCO transpulmonary thermodilution also ous cardiac output monitoring offered by calibrated
provides volumetric data. counterparts, these non-​ calibrated systems utilise
■ Global end diastolic volume (index) waveform analysis to determine stroke volume and
(GEDVI) (650–​1000 ml/​m2), volume of subsequently cardiac output. They may offer stroke
blood within the cardiac chambers at end-​ volume variation (as described in the arterial wave-
diastole; indicative of preload. Typically form section). The lack of calibration has called the
indexed to body surface area. accuracy of these systems into question and compari-
■ Intrathoracic blood volume (index) son to calibrated systems demonstrates a discrepancy
(ITBVI) (800–​1000 ml/​m2), volume of between measured cardiac output.
blood within the chest, derived from
thermodilution technique; indicative of
preload.
Learning Points
• Vascular access is a common undertaking in
■ Extravascular lung water (index)
critical care; the use of insertion bundles and real-​
(EVLWI) (3–​7 ml/​m2), volume of
time ultrasound appears to reduce the incidence
water lying within the lung
of complications.
parenchyma, a marker of pulmonary
• Central venous pressure appears to be a poor
oedema.
predictor of fluid responsiveness in clinical
• Following calibration using the described
practice, it may however offer information
thermodilution technique, the PiCCO
regarding the venous system not obtainable by
system uses mathematical analysis of the
other means.
pulse waveform to provide continuous
• The pulmonary artery catheter offers a means of
measurement of stroke volume (and therefore
measuring pulmonary pressures, cardiac output
cardiac output).
and a surrogate of left atrial pressure; its use has
not however been demonstrated to change patient
LiDCO outcomes.
• The LiDCO, like the PiCCO, utilises a • Transpulmonary thermodilution and pulse
transpulmonary dilutional technique to contour analysis techniques are more commonly
determine cardiac output. There are however a employed means of measuring cardiac output
number of differences. than the pulmonary artery catheter; performance
○ The LiDCO utilises a standard arterial line, in trials is comparable to the pulmonary artery
in any artery; the LiDCO system is attached catheter.
externally to the arterial line. • Dynamic markers of cardiovascular performance,
○ Lithium is used for the dilution technique, such as pulse pressure analysis, may be more
rather than cold saline; the dependence accurate in determining volume status than
upon lithium makes the LiDCO unreliable traditional static parameters; whether this
in those patients on therapeutic lithium or accuracy is maintained in the complex critical
who have recently received non-​depolarising care population is not clear.

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Chapter 11: Arterial and Venous Catheterisation

Further Reading McGee DC, Gould MK. Preventing complications of


central venous catheterization. New England Journal of
Binanay C, Califf R, Hasselblad V, et al. Evaluation study Medicine. 2003; 348: 1123–​1133.
of congestive heart failure and pulmonary artery Pronovost P, Needham D, Berenholtz S, et al. An
catheterization effectiveness: the ESCAPE trial. intervention to decrease catheter-​related bloodstream
Journal of the American Medical Association. 2005; infections in the ICU. New England Journal of
294: 1625–​1633. Medicine. 2006; 355: 2725–​2732.
Guyton AC. Determination of cardiac output by equating Sakka S, Kozieras J, Thuemer O, van Hout N. Measurement
venous return curves with cardiac response curves. of cardiac output: a comparison between
Physiological Reviews. 1955: 35: 123–​129. transpulmonary thermodilution and uncalibrated
Harvey S, Harrison DA, Singer M, et al. Assessment of the pulse contour analysis. British Journal of Anaesthesia.
clinical effectiveness of pulmonary artery catheters 2007; 99: 337–​342.
in management of patients in intensive care (PAC-​ Sandham JD, Hull RD, Brant RF, et al. A randomized,
Man): a randomised controlled trial. Lancet. 2005; controlled trial of the use of pulmonary-​artery
366: 472–​477. catheters in high-​risk surgical patients. New England
Marik PE, Cavallazzi R. Does the central venous pressure Journal of Medicine. 2003; 348: 5–​14.
predict fluid responsiveness? An updated meta-​ Wheeler A, Bernard G, Thompson B, et al. Pulmonary-​
analysis and a plea for some common sense. Critical artery versus central
Care Medicine. 2013; 41: 1774–​1781. venous catheter to guide treatment of acute lung
Marik PE, Lemson J. Fluid responsiveness: an evolution injury. New England Journal of Medicine. 2006;
of our understanding. British Journal of Anaesthesia. 354: 2213–​2224.
2014; 112: 617–​620.

MCQs
1. What degree of pulse pressure variation is suggestive (d) Antimicrobial impregnated patch over
of fluid responsiveness? insertion site
(a) >5% (e) Introduction of an insertion ‘bundle’ into the
department
(b) <5%
4. At which point in the cardiac cycle does the dichrotic
(c) >13% notch occur?
(d) <13% (a) End systole
(e) >100% (b) Mid systole
2. Which of the following parameters is derived from (c) End diastole
pulmonary artery catheter measurements? (d) Mid diastole
(a) Cardiac output (e) None of the above
(b) Systolic pulmonary artery pressure 5. Which of the following pulmonary artery catheter
(c) Pulmonary artery wedge pressure measurements is most in keeping with a patient with
cardiogenic shock secondary to an anterior myocar-
(d) Pulmonary vascular resistance dial infarction?
(e) Right atrial pressure (a) Cardiac index 1.6 l/​min/​m2; pulmonary artery
3. Which of the following is NOT associated with wedge pressure 22 mmHg; mean pulmonary
decreased incidence of central line associated artery pressure 27 mmHg; central venous oxygen
infection? saturation 44%
(a) Full barrier precautions at time of insertion (b) Cardiac index 1.6 l/​min/​m2; pulmonary artery
wedge pressure 4 mmHg; mean pulmonary
(b) Early removal of central line artery pressure 10 mmHg; central venous oxygen
(c) Insertion into the femoral vein saturation 44%

13:54:58 93
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Section 2: Practical Procedures

(c) Cardiac index 4.6 l/​min/​m2; pulmonary artery artery pressure 14 mmHg; central venous oxygen
wedge pressure 8 mmHg; mean pulmonary saturation 64%
artery pressure 12 mmHg; central venous oxygen (e) Cardiac index 2.2 l/​min/​m2; pulmonary artery
saturation 84% wedge pressure 12 mmHg; mean pulmonary
(d) Cardiac index 2.6 l/​min/​m2; pulmonary artery artery pressure 36 mmHg; central venous oxygen
wedge pressure 9 mmHg; mean pulmonary saturation 64%

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

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Section 3 Therapeutic Intervention

Antibiotics in the Cardiothoracic Intensive


Chapter

12 Care Unit
Oana Cole and Olly Allen

The modern era of antibiotics starts with the dis- the median length of stay and the hospital mortal-
covery of penicillin by Alexander Fleming in 1928. ity were significantly higher in the inappropriate
Since then, antibiotics have transformed the face of antibiotic group.
modern medicine and enabled major advances in An example of an algorithm for presumptive anti-
the treatment of patients. So much so that antibiotics biotic therapy for pneumonia in a critically ill patient
could partially be credited for the staggering increase is presented in Figure 12.2.
in the general population’s life expectancy from Critically ill patients have multiple risk factors
around 60 years old in the UK in the 1920s, accord- for serious and life-​threatening infections. Exposure
ing to the Office for National Statistics, to 81  years to antibiotics and other treatments which eradicate
old in 2015. and modify the commensal flora, compromised host
Critical care is a young specialty whose evolution defences due to nutritional deficiencies, critical illness,
has largely been shaped by the evolution of antimicro- compromised integument (intravascular devices, per-
bial therapy. It can be argued that the only treatment cutaneous interventions and devices) and disruption
we can offer our patients is antimicrobials, the rest –​ of cellular and humoral immunity as in the transplant
vasoactive medications, mechanical ventilation, diu- patients lead to a high susceptibility to sepsis. In the
retics and so on –​are merely supportive measures. context of severe infections, Table 12.1 highlights the
The aim of this chapter is to present the aspects most prevalent microorganisms in Western world
of antimicrobial therapy most pertaining to a cardio- critical care patients.
thoracic critical care context. Data are presented as
valid in 2016. We do not assume to give an exhaust-
ive representation of the myriad of issues faced by the Antibiotic Administration in the
modern intensivist, but to offer a brief update of the Critically Ill Patient
most important issues we are currently confronting. In the last few years there has been a focus on the most
appropriate way of administering and dosing antibi-
‘Appropriate’ Antibiotic Therapy otics in intensive care. This has been triggered by a
There is no universal recipe for which antibiotics better understanding of the critical illness pathophysi-
should be used first in a critically ill patient. As shown ology, as well as the emergence of new technologies
in Figure  12.1, the choice is individualised for the that alter the pharmacodynamics and pharmacokin-
patient, unit, hospital and geographical area. Most etics of drugs in this patient population (Figure 12.3).
clinicians, when faced with a patient with a severe Time dependent antimicrobials (fT>MIC) include
infection or septic shock, would choose to start with beta-​lactams, glycopeptides, macrolides and linezolid.
a broad spectrum antibiotic or combination and nar- Their concentrations have to be well above the mini-
row down as pathogens and their susceptibilities are mum inhibitory concentration (MIC) for the pathogen
identified. for at least 40% of the interval between doses in order
The comparative effects of appropriate and to achieve their therapeutic targets. There is a grow-
inappropriate antibiotic therapy are well illustrated ing body of research concerning the administration of
in a recent retrospective study by Neinaber et  al. beta-​lactams as a continuous or prolonged infusion so
conducted over 6  years in a single institution in the that the optimum concentration is achieved for sus-
USA. In this study, the risk of nosocomial infections, tained periods of time.

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Section 3: Therapeutic Intervention

ANTIBIOTIC
CHOICE

LABORATORY-
EMPIRICAL
GUIDED

Consultation
Individual case Efficacy in Cost-benefit Susceptibility
Policy/protocol with
advice clinical studies ratio report
microbiologist

Known
Evidence based
Clinical Knowledge of sensitivity and
on hospital and
suspicion likely cause resistance of
national trends
local flora

Figure 12.1  Flow chart for choice of antibiotic.

No Follow CAP
guidelines

Concern for
No Vancomycin
HCAP?
PLUS
antipseudomonal
Yes beta-lactam
OR
carbapenem +/–
vancomycin

Currently
mechanically
Vancomycin
ventilated?
PLUS
antipseudomonal
No beta-lactam
OR
carbapenem +/–
vancomycin

concern for
Yes HAP or VAP
MDRs? Carbapenem OR
antipseudomonal
beta-lactam PLUS
+/– vancomycin
(or linezolid) PLUS
Yes aminoglycoside
OR
antipseudomonal
fluoroquinolone
PLUS
vancomycin

Figure 12.2  Presumptive antibiotic therapy for pneumonia in the ICU. HCAP Health Care Associated Pneumonia; HAP hospital acquired
pneumonia.

Concentration dependent antimicrobials (fCmax/​ The antibiotic concentrations in the target tissues
MIC) include aminoglycosides, fluoroquinolones, are influenced by the pharmacokinetic changes in the
metronidazole, echinocandins, polyenes and dapto- critically ill patient.
mycin. These antibiotics need to be administered in 1. Volume of distribution, Vd –​increased for
doses which achieve target concentrations well above hydrophilic drugs due to increased total body
8–​9 times MIC of the pathogen. water; unchanged for lipophilic drugs.

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Chapter 12: Antibiotics

Table 12.1  Most prevalent organisms in Western world critical care patients

Diagnosis Potential pathogens Initial therapy Alternative therapy


Catheter-​related blood S. aureus, coagulase-​ Flucloxacillin Vancomycin
stream infections negative staphylococci, Vancomycin Linezolid
Gram-​negative  rods Tazocin Ciprofloxacin
Candida spp. Fluconazole Echinocandins
Infectious endocarditis Streptococci, Amoxicillin Flucloxacillin –​ MSSA
S. aureus, Enterococci Flucloxacillin Vancomycin –​ MRSA
Vancomycin Gentamicin if Enterococci
± gentamicin Rifampicin if prosthetic valve
± rifampicin
Pneumonia, including VAP Gram-​negative rods, Piperacillin-​tazobactam Carbapenems
Haemophilus, S. pneumoniae Ciprofloxacin
Penicillins
Sepsis/​bacteraemia S. aureus, Gram-​negative rods Piperacillin-​tazobactam Fluoroquinolone
Candida spp. Flucoxacillin Vancomycin
Aspergillus Vancomycin Echinocandins
Fluconazole Amphotericin B
Voriconazole Echinocandins

Figure 12.3  The kill characteristics of antibiotics.


Modified from Tsai et al. (2015).
f Cmax/MIC
E.g. aminoglycosides
Drug concentration

fAUC0–24:MIC
E.g. glycopeptides

4x MIC

MIC

Time
f T>MIC
f T>4XMIC E.g. β-lactams

2. Clearance and elimination –​may change elimination half-​time and the risk of toxicity and
according to the renal and hepatic blood flows drug accumulation.
and function; severely deranged in septic shock; 5. Tissue penetration –​can be variable due to
drug clearance and elimination also dependent on microcirculatory dysfunction.
whether renal replacement therapy is instituted.
3. Decreased albumin levels –​the volume of Special Case –​Antibiotics and
distribution and clearance of protein-​bound drugs Extracorporeal Circuits
increase, decreasing their efficacy. The pharmacokinetics of antibiotics in patients on
4. End-​organ dysfunction –​cardiac dysfunction extracorporeal circuits is a growing area of research.
in the context of septic shock increases the The volume and distribution and clearance of drugs

13:57:49 97
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Section 3: Therapeutic Intervention

24 Figure 12.4  Meropenem concentration


during ECMO run with two different dosing
regimens.
20
Meropenem concentration (mg/l)

16

12

Target concentration (8 mg/l)


8

0
0 4 8 12
Time (h)

Standard dosing (1g/8 h) High-dose infusion (6.5 g/24 h)

is altered and these are compounded by the added includes transcatheter implanted valves and
potential for sequestration in the circuit. The import- homografts.
ance of understanding the pharmacology and chan- 2. Patients with previous IE; they also have a higher
ging the doses and intervals of administration of risk of infectious complications than patients with
antimicrobials is colossal, since subtherapeutic doses a first episode of IE.
are associated with worse outcomes. 3. Patients with untreated cyanotic congenital
An example is provided in Figure  12.4, which heart disease (CHD) or with prosthetic baffles
shows the effect of two dosing regimens of merope- or conduits as part of palliative management;
nem, as described by Shekar et al. (2013). the European Society of Cardiology (ESC)
Unfortunately, data are very limited to be able to guidelines 2015 recommend that patients with
generalise these results for all antimicrobials. What is definitive repair of CHD with prosthetic material
certain, though, so far, is that ‘one size does not fit all’ should only receive antibiotic prophylaxis for the
when it comes to drug dosing in patients on extracor- first 6 months, while endothelialisation of the
poreal circuits. If feasible, drug levels should be moni- prosthetic material occurs.
tored in this category of patients in order to establish
Diagnosis of infective endocarditis is based on the
the appropriate therapeutic regime.
modified Duke criteria and the ESC 2015 guidelines,
as shown in Table 12.2.
Endocarditis and Intracardiac Device Successful treatment of IE involves primarily
Infection pathogen eradication. Surgical treatment and the
treatment of complications are beyond the scope of
Infective endocarditis (IE) is a deadly disease. Despite
this chapter. With respect to antimicrobials in IE,
major improvements in diagnosis and treatment, IE
there are currently the following recommendations,
remains associated with high morbidity and mortal-
according to the British Society of Antimicrobial
ity. IE patients admitted to critical care are among the
Chemotherapy, 2012 guidelines.
sickest the intensivist will have to deal with.
The following categories of patients have the high- 1. Initial empirical treatment of native valve
est risk to acquire IE, as well as a poorer prognosis of endocarditis (NVE) depends on the clinical
the disease: presentation.
1. Patients with a prosthetic valve or with prosthetic (i) NVE indolent presentation: amoxicillin +
material used for valve repair; this category gentamicin.

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Chapter 12: Antibiotics

Table 12.2  Diagnosis of infective endocarditis

Definite IE
Pathological criteria •  Positive blood cultures for IE
• Microorganisms identified on histological analysis of vegetation or embolic material
•  Vegetation or embolic material identified by histology
Clinical criteria •  2 major criteria
•  1 major criterion and 3 minor criteria
•  5 minor criteria
Possible IE
•  1 major criterion and 1 minor criterion
•  3 minor criteria
Unlikely/​rejected IE
•  Firm alternative diagnosis
•  Resolution of symptoms with antibiotic treatment ≤4 days
•  No histological evidence of IE

Major and minor criteria of IE (ESC, 2015)


Major criteria
Blood cultures positive
Typical IE microorganisms from 2 separate cultures
Viridans streptococci, Streptococcus gallolyticus (Streptococcus bovis), HACEK group, Staphylococcus aureus; or
Community acquired enterococci in the absence of a primary focus; or
Microorganisms consistent with IE from persistently positive blood cultures:
≥2 positive blood culture drawn >12 hours apart; or
All 3 or a majority of ≥4 separate blood cultures (with first and last sample drawn >1 hour apart); or
Single positive blood culture for Coxiella burnetii or phase I IgG antibody titre >1:800
Imaging positive for IE
Echocardiogram positive for IE
Vegetation
Abscess, pseudoaneurysm or intracardiac fistula
Valvular perforation or aneurysm
New partial dehiscence of prosthetic valve
Abnormal activity around the site of prosthetic valvular implantation detected by radiolabelled WBC SPECT/​C T
Definite paravalvular lesions by cardiac CT
Minor criteria
Predisposition –​heart condition or intravenous drug administration
Temperature >38 °C
Vascular phenomena: major arterial emboli, septic pulmonary infarcts, intracranial haemorrhage, conjunctival
haemorrhages and Janeway’s lesions
Immunological phenomena –​glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor
Microbiological evidence –​positive blood culture but does not meet the major criteria above or serological
evidence of active infection with a microorganism consistent with IE

(ii) NVE severe sepsis: vancomycin + gentamicin. 3. Antibiotic treatment of IE due to oral streptococci
(iii) NVE severe sepsis + risk of MDR: and Streptococcus bovis group depends on
vancomycin + meropenem. minimum inhibitory concentration, MIC (usual
2. Prosthetic valve endocarditis (PVE): vancomycin course is 4 weeks for NVE and 6 weeks for PVE).
+ gentamicin + rifampicin; this applies to all PVE (i) Penicillin-​susceptible strains, non-​penicillin
irrespective of time. allergic patients:

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Section 3: Therapeutic Intervention

(a) Benzylpenicillin, or (iii) Multiresistance to beta-​lactams,


(b) Amoxicillin, or aminoglycosides and vancomycin:
(c) Ceftriaxone. (a) Daptomycin and ampicillin,
(ii) Penicillin-​susceptible strains, penicillin-​ (b) Linezolid,
allergic patients: Vancomycin BD. (c) Vancomycin, if beta-​lactam resistance
(iii) Strains relatively resistant to penicillin but vancomycin susceptibility detected.
(higher MIC required), non-​penicillin We must stress that these are only guidelines, and
allergic patients: that individual hospitals in different regions may have
(a) Benzylpenicillin, double the dose different antibiotic policies, depending on the local
for penicillin-​susceptible strains and ecology.
gentamicin, or
(b) Amoxicillin, double the dose for
penicillin-​susceptible strains and
Catheter Related Bloodstream
gentamicin, or Infections
(c) Ceftriaxone and gentamicin. The definition of catheter related bloodstream infec-
(iv) Strains relatively resistant to penicillin tions, also known as central line associated blood-
(higher MIC required), penicillin- stream infections (CLABSI), is bacteraemia or
​allergic patients: Vancomycin and fungaemia in a patient with an intravascular catheter,
gentamicin. sepsis and at least one positive blood culture taken
4. Antibiotic treatment of IE due to Staphylococcus from a peripheral vein, in the absence of another
spp., for NVE: apparent source except for the catheter. In add-
(i) Methicillin-​susceptible Staphylococcus spp., ition, there should be evidence that the catheter was
non-​penicillin-​allergic patients: infected based on quantitative or semi-​quantitative
methods. Another diagnostic method for CLABSI is
Flucloxacillin. differential time to positivity –​blood cultures taken
(ii) Methicillin-​susceptible Staphylococcus from the central line presumed to be infected may
aureus, alternative strategy: turn positive at least 2 hours before blood cultures
Vancomycin or daptomycin. taken simultaneously from a peripheral vein. This is
(iii) Penicillin-​allergic patients or methicillin-​ due to the almost three-​fold increase in the micro-
resistant Staphylococcus spp.: organism load of an infected catheter compared to
(a) Vancomycin for 4–​6 weeks, intravenous blood.
administration, Prevention of CLABSI relies on several measures,
(b) Daptomycin for 4–​6 weeks, intravenous as follows:
administration. 1. Choice of insertion site –​femoral lines should
5. Antibiotic treatment of IE due to Enterococcus be a last resort; they should be changed as soon
spp.: as possible, within a maximum time frame of
(i) Beta-​lactam and gentamicin-​susceptible 48 hours.
strains: 2. Insertion techniques –​experienced personnel,
(a) Amoxicillin and gentamicin for 4 avoidance of haematoma formation around the
weeks for NVE or 6 weeks for PVE, insertion site.
(b) Ampicillin with ceftriaxone for 4 3. Adoption of a care bundle; the Matching Michigan
weeks for NVE or 6 weeks for PVE, for campaign has shown that CLABSI decreased by
E. faecalis, more than 60% over 2 years in ICUs in England
(c) Vancomycin and gentamicin for 6 after introduction of a care bundle.
weeks if penicillin allergy known or 4. Antibiotic-​coated central venous catheters have
suspected. been proposed and adopted with success across
(ii) Gentamicin-​resistant species –​ replace intensive care units worldwide. The catheters are
gentamicin with streptomycin, if susceptible impregnated with minocycline-​rifampicin and
to the latter. are effective in inhibiting the development of

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Chapter 12: Antibiotics

Table 12.3  Systemic treatment of CLABSI –​a possible guide

Pathogen First line antibiotic Alternative treatment


Coagulase-​negative staphylococci
Methicillin-​sensitive Flucloxacillin mecA gene negative Vancomycin
Methicillin-​resistant Vancomycin Daptomycin or linezolid
S. aureus
MSSA Flucloxacillin Vancomycin
MRSA Vancomycin Daptomycin or linezolid
Enterobacteriaceae
ESBL  –​ve Piperacillin/​tazobactam Ciprofloxacin or aztreonam
ESBL +ve Carbapenem Ciprofloxacin
Pseudomonas Carbapenem or piperacillin-​tazobactam Ciprofloxacin or aztreonam
May consider the addition of an aminoglycoside
Candida spp. Echinocandins or fluconazole Amphotericin
Candida glabrata Echinocandins or fluconazole at higher Amphotericin
doses if susceptible strains

Table 12.4  Retrospective analysis of all VAD patients from the Mayo Clinic between 2005 and 2011

Infection type Cases per 100 patient-​years of LVAD support (95% CI)
All 32.8 (26.7–​39.9)
Endocarditis 1.6 (0.5–​3.8)
Pump and/​or cannula infection 4.9 (2.7–​8.0)
Bloodstream infection
VAD related 7.5 (4.7–​11.2)
Non-​VAD related 6.8 (4.2–​10.4)
CLABSI related 3.3 (1.6–​6)
CLABSI associated 1.6 (0.5–​3.8)
Pocket infection 2.3 (0.9–​4.7)
Driveline infection 15 (10.9–​20)
Permanent pacemaker/​CRT-​D infection 1.6 (0.5–​3.8)
Mediastinitis, VAD related 2 (0.7–​4.2)

biofilm of both Gram-​negative and Gram-​positive a percutaneous drive-​line, which has been termed
bacteria, with the exception of P. aeruginosa and the ‘Achilles’ heel’ of these devices. The most recent
Candida spp. INTERMACS report (March 2016)  has shown that
major infections in MCSD are the third highest cause
Table  12.3 shows possible systemic treatment for
of death with an overall death toll of 9% (June 2006 to
CLABSI.
March 2016), surpassed only by neurological dysfunc-
tion and multiorgan failure.
Mechanical Circulatory Support Device The results of a retrospective analysis of all VAD
(MCSD) Infections patients from the Mayo Clinic between 2005 and 2011
Infections in MCSD patients are difficult to treat are shown in Table 12.4.
and have been associated with poor prognosis and The salient points of international standards for
poor quality of life. Ventricular assist devices differ the management of MCSD infections as valid in June
from other cardiac devices by the fact that they have 2016 are presented below.

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Section 3: Therapeutic Intervention

1. Bacterial infections: infections in intensive care is increasing due to the


(a) Gram-​positive cocci are the most prevalent increasing complexity of medical and surgical ICU
pathogens, followed by Gram-​negative rods. patients, the presence of medium-​and long-​ term
(b) Nosocomial pathogens –​ Pseudomonas, devices, such as ECMO and VAD cannulae, and the
Serratia and Enterobacter –​account for use of broad spectrum antibiotics.
the second most common cause after Although all species of yeasts can be encoun-
Staphylococcus spp. tered, Candida and Aspergillus spp. are by far the
(c) The duration of antimicrobial treatment is not most prevalent in cardiothoracic ICU patients, so we
clearly established; most centres recommend will refer to treatment for these two pathogens in the
courses of at least 2 weeks for superficial discussion below.
driveline infections and at least 4 weeks for 1. Candida spp:
deep-​seated infections.
(a) The 2012 European guidelines recommend
(d) Due to the wide variety of possible scenarios, that fungicidal agents –​echinocandins or
there are currently no international guidelines lipid-​based polyenes –​be used for the initial
on the treatment of bacterial infections treatment of invasive Candida infection; once
associated with MCSD. The antibiotic agents the species of Candida and the sensitivities are
should be administered after consultation with identified, treatment can be de-​escalated to
the local microbiology department, infectious azoles for susceptible strains.
diseases specialist and the transplant or heart
(b) Polyenes are preferred to other classes for the
failure specialist teams.
treatment of deep-​seated infections, such as
2. Fungal infections:
mediastinitis or endocarditis.
(a) The prevalence of fungal infections has
2. Aspergillus:
increased over the years.
(b) Most fungal infections are caused by (a) Caspofungin is the only echinocandin
Candida spp., with a few other case reports of approved for the treatment of invasive
Aspergillus spp. and other yeasts. aspergillosis; however, it is an inferior choice
to voriconazole and amphotericin.
(c) No evidence has demonstrated that the
routine use of antifungal prophylaxis (b) Voriconazole is recommended as first line
decreases the rate of fungal infections in agent for aspergillosis; notably, it interacts
MCSD patients; however, preimplantation with tacrolimus and cyclosporine by
prophylaxis should be considered in high-​risk interfering with the hepatic metabolism
patients. pathways; the therapeutic levels of the
immunosuppressants should be monitored
(d) Candida spp. pump or cannula infection
and higher doses may be required.
should be treated with 8–​12 weeks of
amphotericin, echinocandin intravenously or (c) Lipid-​based polyenes (amphotericin B)
high dose fluconazole if susceptible Candida are recommended as second line therapy
strains. for aspergillosis, where voriconazole is
contraindicated.
(e) Deep-​seated pocket or driveline infection
should be treated with 8–​12 weeks of
echinocandin or amphotericin intravenously Antibiotic Resistance and the
followed by prolonged suppressive oral Development of New Agents
therapy. The last decade has seen worrying levels of increased
(f) Superficial driveline infections should be antimicrobial resistance, prompting the Centre for
treated with 2 weeks of azole therapy. Disease Control in the USA and similar organisations
worldwide to declare the current situation an emer-
Antifungals in the ICU gency. The Review of Antimicrobial Resistance has
Fungal infections are associated with high morbidity recently published a report outlining the problem and
and mortality in the critically ill patient and lead to proposing several strategies of tackling the issue of the
very high healthcare costs. The prevalence of fungal increase in antimicrobial resistance.

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Chapter 12: Antibiotics

Table 12.5  Microorganisms showing resistance In Spain, a country with a high prevalence of


Urgent threats C. difficile multidrug resistant organisms (MDR), a recently
Carbapenem-​resistant implemented ‘zero resistance’ programme recom-
Enterobacteriaceae (CRE) mends that antimicrobials against MDR should only
Serious threats Multidrug-​resistant Acinetobacter spp. be administered in patients with septic shock and a
Fluconazole-​resistant Candida spp. high risk of MDR based on risk factors or knowledge
Extended spectrum beta-​lactamase-​ of local ecology.
producing Enterobacteriaceae (ESBL) The following are risk factors for carriage of
Multidrug-​resistant Pseudomonas MDR.
Carbapenemase-​producing
Pseudomonas 1. Hospital admission for more than 5 days in the
Methicillin-​resistant S. aureus (MRSA) last 3 months.
Concerning threats Vancomycin-​resistant S. aureus (VRSA) 2. Institutionalised patients (prison, healthcare,
social centre).
3. Known previous colonisation or infection with
Which are the microorganisms causing these MDR.
issues and where are they most likely to be 4. Antibiotic course of at least a week in the previous
encountered? month, especially with one or more of the
The Centre for Disease Control has published a list following:
of the current microorganism resistance threats. We (a) Third or fourth generation cephalosporins;
present the ones most likely to be encountered in a (b) Fluoroquinolones;
cardiothoracic critical care unit in Table 12.5. (c) Carbapenems.
There have been volumes written on how to best 5. End-​stage renal disease or renal-​replacement
tackle the emergence of these infections in the ICU. therapy.
The key message from organisations all over the world 6. Comorbid conditions associated with colonisation
is to implement antibiotic stewardship programmes or infection with MDR, such as:
and improve the education of the ‘jobbing’ intensiv-
ists in the pharmacology of antimicrobials. (a) Cystic fibrosis;
Antimicrobial stewardship is a bundle of inter- (b) Bronchiectasis;
ventions designed to optimise and measure the (c) Chronic skin ulcers.
appropriate use of antimicrobials based on pharma- Even though these risk factors were highlighted in
codynamics and pharmacokinetic data available, the context of the Spanish healthcare system, they are
local ecology and patient and unit characteristics. internationally recognisable as the situations which
A  well-​run stewardship programme is a two-​stage should alert most clinicians to the possibility of the
process. patient being colonised by or having an infection with
Stage 1: a MDR pathogen.
(a) Identification of patients with infection; The arsenal available to combat these infections is,
(b) Empirical antibiotics according to local policy as explained earlier, getting more and more limited.
and microbiological advice; Commonly used antibiotics to treat potential MDRs
(c) Optimised dosing according are complemented by some new preparations and
to pharmacokinetics(PK)/​ combinations. Table 12.6 lists some of the most com-
pharmacodynamics(PD). monly available.

Stage 2: Learning Points
(a) Review within 72 hours with laboratory • The most common approach to empirical
results and clinical progress; antibiotic treatment in severe infections
(b) Switch to narrow spectrum antibiotics (if in the critically ill is to ‘start broad and
broad spectrum antibiotics started initially); narrow down’.
(c) Stop antibiotics if the pathology is unlikely to • Consider the most likely source of sepsis when
be infection. deciding which antibiotics to start.

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Table 12.6  Most commonly available new preparations against MDRs

Antibiotic Active against No activity Remarks


Colistin (polymyxin E) Acinetobacter spp. Serratia spp. • Emergent strains of
P. aeruginosa Providencia spp. colistin-​resistant  KPC
Enterobacteriaceae Burkholderia cepacia • Serious nephrotoxicity and
Most other Gram-​negative aerobic Gram-​positive and Gram-​ neurotoxicity
bacilli negative aerobic cocci
Gram-​positive aerobic bacilli
Anaerobes
Tigecycline MRSA P. aeruginosa Can be used for deep-​seated
VRE Proteus spp. infections, note poor lung
Carbapenemase-producing Providencia spp. penetration of this antibiotic
Enterobacteriaceae
Several ESBL strains
Carbapenems Most Enterobacteriaceae Strains of Gram-​positive Emerging strains of
MSSA cocci with reduced carbapenemase-​producing
P. aeruginosa penicillin sensitivity microorganisms (KPO)
ESBL
Anaerobes
Glycopeptides (vancomycin, Gram-​positive  cocci Gram-​negative bacteria
teicoplanin) Clostridium difficile
Daptomycin MDR Gram-​positive cocci, Gram-​negative bacteria Inactivated by alveolar
especially MRSA and VRSA surfactant –​ineffective in
VRE pneumonias
MSSA right-​sided endocarditis
Linezolid MRSA Gram-​negative bacteria • Reversible
VRSA thrombocytopenia
VRE • Interacts with SSRIs –​
Penicillin-​resistant S. pneumoniae serotonin syndrome
Fosfomycin S. aureus, including MRSA Some Pseudomonas and High potential for
Enterococcus spp. including VRE E. coli strains development of resistance
ESBL-​producing K. pneumoniae under prolonged therapy
and E. coli
Ceftolozane/​tazobactam Indications:
• Complicated  UTI
• Complicated intra-​abdominal
infections
• Complicated ventilator
associated pneumonia
Tedizolid MRSA Gram-​negative • Fewer side effects than
VRSA bacteria linezolid
VRE • More bactericidal activity
than linezolid
Avibactam ESBL
Carbapenemase-​producing
K. pneumoniae
Plazomicin Metallo-​beta-​lactamase-​ Phase 3 clinical trials
producing strains
MRSA
Echinocandins Fluconazole-​resistant Candida spp.
Aspergillus

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Chapter 12: Antibiotics

• The rate of discovery of new antibiotics is lower De Pascale G, Tumabarello M. Fungal infections in
than the rate of development of multidrug ICU: advances in treatment and diagnosis. Current
resistant strains in pathogens. Opinion in Critical Care. 2015; 21: 421–​429.
• In the current context of drug resistant Husain S, Sole A, Alexander BA, et al. The 2015
pathogens, antibiotic stewardship is a must. International Society for Heart and Lung
Transplantation Guidelines for the management
• In certain cases, be mindful of the of fungal infections in mechanical circulatory
pharmacokinetic and pharmacodynamics support and cardiothoracic organ transplant
changes which occur due to critical illness recipients: Executive summary. Journal of Heart and
pathophysiology. Lung Transplantation. 2016; 35: 261–​282.
Neinaber JJ, Kusne S, Riaz T, et al. Clinical manifestations
Further Reading and management of left ventricular assist device-​
associated infections. Clinical Infectious Diseases. 2013;
Bion J, Richardson A, Hibbert P, et al. ‘Matching 57: 1438–​1448.
Michigan’: a 2-​year stepped interventional programme Shekar K, Roberts JA, Ghassabian S, et al. Altered
to minimise central venous catheter–​blood stream antibiotic pharmacokinetics during extracorporeal
infections in intensive care units in England. British membrane oxygenation: cause for concern? Journal of
Medical Journal Quality and Safety. 2013; 22: 110–​123. Antimicrobial Chemotherapy. 2013; 68: 726–​727.
doi:10.1136/​bmjqs-​2012-​001325
Tsai D, Lipman J, Roberts JA. Pharmacokinetic/​
Coley CJ II, Miller MA. Ventilator-​Associated Pneumonia pharmacodynamics considerations for the
in Healthcare Associated Infections. Oxford: American optimisation of antimicrobial delivery in the critically
Infectious Disease Library OUP, 2013. ill. Current Opinion in Critical Care. 2015; 21: 412–​420.

MCQs
1. A 19  year old girl is admitted to the ICU following (a) Send the patient urgently to the regional cardiac
double lung transplant for cystic fibrosis. She was surgical centre and give a dose of intravenous
known to be previously colonised with multidrug flucloxacillin and gentamicin, with instruc-
resistant Pseudomonas. After initial satisfactory pro- tions to be continued for 6 weeks or until
gress, the patient develops severe pneumonia on day microbiological advice
3 postoperatively. Talking to the anaesthetist for the (b) Keep the patient in overnight, start a vasoconstric-
case, it was a difficult intubation with a small double tor to help increase the perfusion pressure to the
lumen tube and incomplete tracheobronchial toilet brain and start piperacillin/​tazobactam and gen-
may have been performed. Suspecting that this is pos- tamicin intravenously
sible contamination with the patient’s previous flora, (c) Send the patient urgently to the regional cardiac
choose which antibiotic you would consider starting. surgical centre and give a dose of intravenous
(a) Tigecycline vancomycin with gentamicin and rifampicin, with
(b) Linezolid instructions to be continued for 6 weeks or until
microbiological advice
(c) Piperacillin-​tazobactam ± gentamicin
(d) Intubate the patient prior to transfer and give fluids
(d) Vancomycin with ciprofloxacin to compensate for increased capillary permeability
(e) Colistin with sepsis; start a course of rifampicin
(e) Keep the patient in overnight, start a diuretic, give
2. A 57 year old male presents to the A&E department of
fluid boluses and a vasoconstrictor to maintain
a peripheral hospital with a history of 3 weeks of fever,
MAP > 65 mmHg; start vancomycin with cipro-
chills and malaise. In the last few hours, though, he is
floxacin and fluconazole
increasingly dyspnoeic and has started to cough pink,
frothy sputum. His medical history is unremarkable 3. An acceptable initial choice of antibiotics for presumed
apart from an aortic valve replacement for a stenotic ventilator associated pneumonia in a non-​penicillin-​
bicuspid aortic valve 3 years previously. The cardiol- allergic patient who is otherwise progressing well
ogy registrar does a ‘quick TTE’ and, despite the poor would be:
windows, detects free aortic regurgitation and a rock- (a) Meropenem
ing valve. What would you do next? (b) Piperacillin/​tazobactam

13:57:49 105
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Section 3: Therapeutic Intervention

(c) Nebulised colistin (c) Flucloxacillin, rifampicin and gentamicin and an


(d) Metronidazole and piperacillin/​tazobactam echinocandin for 6 weeks

(e) Levofloxacin (d) Amphotericin for 12 weeks, metronidazole and


ceftriaxone for 6 weeks
4. A 36 year old woman with a LVAD for postpartum car-
diomyopathy is referred to the parent cardiac centre (e) Linezolid and amphotericin for 12 weeks
with fever and chills. The device has been alarming 5. The risk of CLABSI is highest with:
increased power for the last 24 hours. She has a his- (a) Line insertion in an emergency
tory of frequent driveline infections with MSSA and
C. albicans. What is the choice of antibiotics if we pre- (b) Line insertion in a septic patient
sume that LVAD infection is a possible diagnosis? (c) Line insertion at a prior infected line site
(a) Echinocandin for 8–​12 weeks and vancomycin and (d) Multiple line insertions in the same vein
gentamicin for at least 6 weeks
(e) Long-​term catheter insertion in the radiology
(b) Rifampicin for 6 weeks and fluconazole for department
6–​8 weeks

Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

13:57:49
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Section 3 Therapeutic Intervention

Blood Products and Transfusion


Chapter

13 Martin Besser

Introduction To reduce the risk of transmission of infection, all


donors complete a health questionnaire prior to donation
Along with cardiothoracic operating departments,
to identify those that may be unsuitable. Any donations
cardiothoracic intensive care units are some of the
taken are then tested for a range of infections including
greatest consumers of blood products in the world; so
HIV 1 and 2, syphilis, HTLV1 and 2, hepatitis B and
for example UK cardiac surgical centres use approxi-
hepatitis C. As of April 2016, NHSBT also commenced
mately 10% of the national supply. Furthermore, use
screening for hepatitis E negative blood for transfusion
of blood products is currently on the increase due to
to some patients who are immunosuppressed due to
a combination of factors, including advancing patient
haematological malignancy or who are scheduled for or
age, increasing burden of comorbidities, expanding
have undergone solid organ or bone marrow transplan-
use of antiplatelet therapy and greater surgical com-
tation. Several initiatives are also in place to reduce the
plexity. Importantly, transfusion of blood products
risk of transmission of Variant Creutzfeldt-Jakob disease
is associated with increased morbidity and mortal-
including leukodepletion (1999) and the use of non-​UK
ity thus it is imperative to employ strategies such as
methylene blue treated plasma components or com-
patient blood management (PBM) to avoid unneces-
mercial solvent/detergent fresh frozen plasma (SD FFP)
sary transfusion and conserve precious resources.
treated pooled plasma for patients born after 1995.

Blood Products
More than 2  million donations are made each year Red Blood Cells
in the UK to National Health Service Blood and It has been shown that isovolaemic haemodilution of
Transfusion (NHSBT). From these donations, approx- normal volunteers and non-​anaemic patients is tol-
imately 2,000,000 units of red cells, 300,000 units of erated to a haemoglobin of 50 g/​l. Studies that have
platelets, 350,000 units of FFP and 126,000 units of assessed patients who refuse blood found that the
cryoprecipitate are prepared. The current commonly degree of preoperative anaemia affected the risk of
prescribed blood products in the UK are listed in death but did not have an effect on mortality. Hebert
Table 13.1. showed in a randomised controlled trial (TRICC) that
Blood components are not blood group specific a restrictive (70 g/​l) transfusion strategy was superior
due to pooling of donors in the production process. to a liberal (90 g/​l) one in ICU patients. However,
This means equilibration of interindividual varia- some doubt has been cast on this in the setting of
tion from donor to donor and the dilution of hazard- cardiothoracic surgery after a recent study reported
ous antibodies such as antineutrophil antibodies. It improved outcomes with a liberal strategy. In the
is important to note that some products have traces TITRe2 trial, patients undergoing elective cardiac
of heparin and may be potentially contraindicated surgery were randomised between 90 g/​l and 75 g/​l as
in heparin induced thrombocytopenia. Red cells are the transfusion threshold. Ischaemic cerebral events,
considered suitable in the UK for transfusion for up myocardial infarction, infection or acute renal failure
to 35 days post donation and are stored at 4 oC ±2 oC, within 3 months of surgery were non-​significantly dif-
FFP and cryoprecipitate are usable for up to 2  years ferent. This leads to transfusion rates of 92.7% versus
and are stored at −30 oC. Platelets have a shelf life of 53.4%. Strikingly, the mortality was different, 2.6%
7 days if stored at room temperature with agitation. versus 4.2%, in the two groups with a hazard ratio

14:04:16 107
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Section 3: Therapeutic Intervention

Table 13.1  Comparison of blood products and components currently in use in the UK


Commercial Protein Platelet Fibrinogen II V VII VIII vWF IX X
product

Blood Packed red cells Haemoglobin trace trace trace trace trace trace trace trace trace
components <40 g/​l

Platelets >240 × 109/​l trace trace trace trace trace trace trace trace

FFP >50 g/​l nil 0.9 g/​l variable variable variable >70 U variable variable variable
Cryoprecipitate nil >0.7 g/​pool variable variable variable 350 U/​pool variable variable variable
Methylene blue FFP >50 g/​l nil 0.7 g/​l variable variable variable 50 U variable variable variable
Methylene blue cryo nil 0.7 g/​pool variable variable variable 350 U/​pool variable variable variable
(80% of (80% of
untreated) untreated)
Blood products Fibrinogen concentrate Riastap ® Albumin nil 20 g/​l
Prothrombin complex Beriplex ® 6–​14 g/​l nil NA 20–​60** NA 10–​25** NA NA 20–​31*** 22–​60***

Octaplex ® 1.3–​4.1 g/​l nil NA 20–​76*** NA 18–​48** NA NA 50*** 36–​60***

SD FFP 45–​70 g/​l nil NA NA 31 NA 28 NA NA NA

*  Assumed to be 100% activity but donors will vary 70–​100%.


**  Prior to freezing.
***  Per ml reconstituted.
Beriplex ® and Riastap ® are trademarks of CSL Behring.
Octaplex ® is a ® trademark of Octapharma.

of 1.67 (1.00–​2.67) (p  =  0.045) favouring the higher an interesting alternative ADP-​inhibitor that allows
threshold. rapid platelet function recovery within a few hours
Accepted side effects of transfusion are infection, of stopping administration. Despite the recent devel-
immune reactions, volume overload, immune sup- opment of near patient platelet function testing,
pression, and red cell and HLA allo-​immunisation. the problem remains that the platelet function test-
General recommendations agree that a Hb of <70 g/​l ing becomes abnormal with reducing platelet count
is an indication for transfusion; however when the (around 75 × 109/​l for the Multiplate). Moreover, the
Hb is >70 g/​l the circumstances of the patient need to treatment of confirmed or assumed platelet dysfunc-
be taken into account and the risk/​balance of trans- tion is platelet transfusion. The British Commission
fusion assessed. In patients with a Hb of 80–​100 g/​l, for Standards in Haematology have published guid-
the transfusion decision should be individualised and ance for platelet transfusion. The evidence for the
generally a transfusion is not indicated with a Hb of use of platelet transfusion is marred by the impact of
>100 g/​l. However, these recommendations do not ongoing antiplatelet therapy on both the patient’s own
include patients with coronary artery disease. and transfused platelets. The general advice is to dis-
continue antiplatelet therapy where possible, taking
Platelets into account the time required to normalise platelet
We usually apply the threshold of platelets <100  × function. Platelet transfusion in patients requiring
109/​
l in the immediate postoperative setting. antiplatelet therapy may increase the risk of athero-
Controversies exist for patients with concomitant sclerotic complications while not positively affecting
antiplatelet therapy. Patients exposed to antiplatelet platelet function.
therapy take several days to recover normal platelet During the intensive care stay there is contro-
function:  clopidogrel (7  days), aspirin (7  days), tica- versy about the optimal platelet count for preventing
grelor (5  days) and prasugrel (7  days). Cangrelor is bleeding with a number of invasive procedures. The

14:04:16
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109

Chapter 13: Blood Products and Transfusion

XI XII XIII Protein C Protein S Antithrombin Heparin Red cell Blood White cell Clinically Donor Pathogen
stroma group contaminant important exposure inactivation or
specific subtypes reduction

trace trace trace trace trace trace No Yes Yes <5106/​unit washed, 1 Leukodepletion (UK)
CMV,
negative,
irradiated
trace trace trace trace trace trace No trace Yes <5106/​unit** pool, single 1 to 6 Leukodepletion (UK)
donor
apheresis,
HLA
matched
variable variable variable * variable * variable * variable * No trace** Yes <5106/​unit** 1 Leukodepletion (UK)
variable variable variable variable variable variable No trace** Yes <5106/​unit** 5 Leukodepletion (UK)
variable variable variable variable variable variable No trace** Yes <5106/​unit** 1 Methylene blue
variable variable variable variable variable variable No trace** Yes <5106/​unit** Methylene blue

No nil No No >20,000 Pasteurisation


NA NA 15–​45 12–​38​ Yes Yes nil No No >20,000 Filtration,
pasteurisation
NA 26–​62** 24–​64** NA Yes nil No No >20,000 Filtration,
pasteurisation
NA NA NA 50 NA No nil Yes No >20,000 Solvent detergent

insertion or removal of epidural catheters is con- In individual patients who develop thrombocyto-
sidered safe with platelet counts >(80–​100) × 109/​l. penia while on ECMO, a number of possible causes
The majority of procedures, such as line insertions such as drugs, mechanical factors or immune mecha-
or chest drain removals, are safe with platelet counts nisms have to be considered. Where there is an associ-
over 50  × 109/​l provided concomitant anticoagula- ated bleeding pattern this is important and the need
tion has been corrected or stopped. Our practice, for ongoing anticoagulation needs to be reviewed.
with the exception of epidurals and lumbar punc- Where reduced anticoagulation therapy can be com-
tures, is to transfuse platelets for counts <50 × 109/​l pensated with measures such as increasing the flow of
prior to intervention and to not transfuse platelets the ECMO circuit, this is likely to be more effective
for counts of >80 × 109/​l. Between 50 and 8​ 0 × 109/​l than a small increment in platelet count. Any trans-
we will reserve a unit of platelets for 8 hours for the fused platelets will be subjected to the same causes of
patient in case of excessive bleeding or if the clini- thrombocytopenia as the patient, and particularly in
cian requests these. moderate thrombocytopenia are unlikely to have a
In patients on ECMO the agreed platelet threshold prolonged effect.
is currently debated. We accept 100 × 109/​l in a bleed- We assume that a unit of platelets will contain a
ing patient but have had individual patients where we minimum of 250  × 109/​l per adult therapeutic dose.
tried to achieve higher platelet counts due to concom- In a healthy adult we assume a daily platelet produc-
itant intracranial bleeding with a continued need for tion of 10  × 109/​l. A  platelet transfusion is clinically
heparin anticoagulation. Others advocate thresholds most effective in a patient with thrombocytopenia.
as low as 20 × 109/​l. The coagulation system in adults The platelet recovery following a fixed dose infu-
and children is fundamentally different and therefore sion of platelets is highly variable and is dependent
it is not likely that the same threshold can be applied on the original reason for thrombocytopenia in the
for both groups of patients. patient. It is bound to be optimal in a patient with

14:04:16 109
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110

Section 3: Therapeutic Intervention

lack of production but far less satisfactory in a patient Ranucci et  al. recently reported a prospective,
with platelet destruction. There are a number of spe- randomised, blind study of 116 patients under-
cific cardiothoracic interventions that will reduce the going high risk cardiac surgery with an expected
platelet recovery in a given patient such as extracor- cardiopulmonary bypass duration of >90 minutes.
poreal membrane oxygenation (ECMO) and intra-​ Patients received fibrinogen concentrates after pro-
aortic balloon pump (IABP). tamine administration and prothrombin complex
Human platelet concentrates express very few concentrates (PCCs) if bleeding persisted. Patients
AB antigens and are suspended in less than 50 ml receiving fibrinogen had a significantly lower rate of
of plasma. For this reason ABO groups can be over- any allogeneic blood product transfusions, includ-
ridden in case of an emergency. Platelets do how- ing PRBCs and FFP. Postoperative bleeding was also
ever express HLA class I antigens, which can lead to reduced in the fibrinogen treated patients (median,
antibody formation causing platelet refractoriness 300 ml; interquartile range, 200 to 400 ml) com-
(defined as repeated platelet increments of <5 × 109/​l). pared with the control patients (median, 355 ml;
Red cells are more potent HLA type sensitisers than interquartile range, 250 to 600 ml). However, the
platelet transfusions and multiparous women are par- recently published REPLACE-​trial comparing the
ticularly at risk. The UK national blood service is able early aggressive use of fibrinogen concentrate in
to provide HLA class I typing and antibody screening patients undergoing aortic surgery with placebo, on
with a view to providing HLA selected/​matched plate- the background of a defined transfusion algorithm
lets. These products are considerably more expensive with platelets and FFP, did not demonstrate clinical
than standard platelets but may lead to better incre- benefit.
ment and thus overall reduction in platelet usage. All
HLA matched platelets must be irradiated. Fresh Frozen Plasma and Prothrombin
Complex Concentrate
Cryoprecipitate and Fibrinogen Concentrate Fresh frozen plasma may increase clotting factor
Fibrinogen is a critical haemostatic factor for the activity by up to 30% with administration of 15 ml/​
development of effective local clotting in all surgi- kg. The absolute increment depends on the baseline
cal patients, and in particular for the management factor activity in 40 ml/​kg of patient plasma and may
of perioperative bleeding in cardiac surgical patients. be considerably smaller if the clotting factor levels are
Normal fibrinogen levels are 200–​400 mg/​dl in the nearly normal. There may be considerable variation in
non-​parturient, but may be >400 mg/​dl during the the concentration of individual factors such as factor
third trimester of pregnancy. The optimal transfusion XI or IX between donors. In some congenital coagu-
threshold for fibrinogen replacement is unknown. lation factor deficiencies, it may therefore be advis-
There is no RCT evidence for the transfusion thresh- able to use pooled products to minimise these effects
old of 1 g/​dl but it has been accepted in clinical prac- between donors.
tice. More recently, higher thresholds for fibrinogen Prothrombin complex is a pooled plasma prod-
replacement have been advocated with thresholds of uct that contains factors II, VII, IX and X as well as
up to 2 g/​dl. The massive transfusion guidelines pub- Protein C and S. It is licensed for use in acquired defi-
lished by the BCSH advise use of a cut-​off of 1.5 g/​dl as ciency of the vitamin K dependent clotting factors.
the threshold, as do the NICE transfusion guidelines The most recent guidelines (2015) on the treatment of
of November 2015. massive haemorrhage explicitly advise against the use
An adult dose of cryoprecipitate (10 units or 2 of prothrombin complex in massive transfusion out-
pools) is equivalent to 2–​4 g of fibrinogen concentrate. side studies. The main advantage of using PCC over
Based on the relative content of fibrinogen per ml, FFP is the reduced volume and easier administration.
fibrinogen concentrate should be superior to cryopre- An FFP equivalent dose is 15 U/​kg, and there are pub-
cipitate in restoring low fibrinogen levels. However, lished dosing recommendations for warfarin reversal
cryoprecipitate also contains factors such as vWF based on baseline INR with up to 50 U/​kg. The avail-
and factor XIII which may be of therapeutic benefit. able PCCs also contain traces of heparin so are con-
Importantly, a therapeutic dose of 4 g of fibrinogen is traindicated for the reversal of warfarin in patients
four times as expensive as cryoprecipitate. with HIT.

14:04:16
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111

Chapter 13: Blood Products and Transfusion

Recombinant Activated Factor VIIa Platelets may also have been exposed to antiplatelet
agents in the immediate preoperative phase, which
Recombinant FVIIa is used off-​ label as a prohae-
will have reduced platelet activation further. High
mostatic agent for life threatening hemorrhage.
doses of unfractionated heparin inhibit the majority
Its mechanism of action is thought to be related to
of the serin proteases in an antithrombin dependent
binding with tissue factor (TF) expressed at the site
manner. If administered in high doses, the half-​life of
of vascular injury to locally produce thrombin and
heparin is prolonged, ranging between 30 and ​90 min-
amplify haemostatic activation. Controlled clinical
utes. Elimination is via renal and hepatic mechanisms
trials report the incidence of thrombotic complica-
in addition to poorly delineated pathways involving
tions among patients who received rFVIIa to be rela-
the macrophages and endothelial cells. Sequestration
tively low and similar to that among patients who
sites can be a source of heparin rebound, which is
received placebo. In the most recent cardiac surgi-
sometimes observed in patients who have received
cal study, patients bleeding postoperatively >200 ml/​
exceedingly high doses of heparin during CPB for
hour were randomised to placebo, 40 µg/​kg rFVIIa or
up to 12 hours. Tissue debris is aspirated by cardi-
80 µg/​kg rFVIIa. Primary endpoints were the number
otomy suckers from the surgical field and mixed with
of patients suffering critical serious adverse events.
the other blood and recirculated, adding a source of
Secondary endpoints included rates of reoperation,
extrinsic clotting factor activation.
blood loss and transfusions. Although more adverse
events occurred in the rFVIIa groups, they did not
reach statistical significance. However, after ran-
Diagnostic Testing
domisation, significantly fewer patients in the rFVIIa The majority of cardiac patients have postoperative
group underwent a reoperation because of bleeding or thrombocytopenia and the clotting factors, if meas-
needed allogeneic transfusions. ured, can be as low as 25–​50% of baseline immediately
after separating from CPB. A gradual recovery occurs
over the next 2–​4 days. No single laboratory test has
Bleeding and Coagulopathy been shown to be predictive of postoperative clinical
About 50% of cardiac surgical patients receive red bleeding and unselected correction of platelet count
cells, 30% of which also receive blood product com- or fibrinogen has had only disappointing results.
binations including platelets or plasma. Established
risk factors for transfusion include preoperative Preoperative Screening
anaemia, low body mass index, complexity and It is currently accepted practice to screen aPTT and
urgency of surgery. PT preoperatively along with full blood count (FBC).
The cell based model of haemostasis is complex The reason for screening PT and aPTT is an anachro-
and not easily reproducible in vitro (Figure  13.1). nism dating back to when warfarin and unfraction-
Haemostasis is initiated following tethering of plate- ated heparin were the main anticoagulants in use.
lets to a site of vascular injury through vWF and The FBC is more important than ever in that it allows
GPIb/​V/​IX. The platelet membrane undergoes activa- screening for preoperative anaemia or thrombocyto-
tion and mediators are released. Traces of tissue factor penia, which may be amenable to preoperative inter-
stabilise the factor VIIa, which in turn activates traces vention. Generally we accept platelet counts >90  ×
of IXa, Xa and thrombin. This sets off an autofeed- 109/​l, aPTT <38 s and PT <18 s, assuming the patient
back mechanism that propagates self-​activation and is not on anticoagulants. A bleeding score is more use-
results in fibrin polymerisation, followed by thrombin ful to identify patients with a potential undiagnosed
inactivation. bleeding disorder.
The effects of CPB on haemostasis are also com-
plex and multifactorial. During surgery the major- Blood Tests Used To Assess and Direct Treatment of Post
ity of the surgical field is bypassed by the circulating CPB Coagulopathy
blood; the patient’s blood is haemodiluted with crys- The majority of centres now use a combination of lab-
talloid and albumin. Hypothermia in combination oratory and point-​of-​care assays in combination with
with partial activation of the clotting cascade prolongs clinical assessment to guide transfusion of products
the clotting reaction further. Primary haemostasis is according to predefined algorithms (see Figure 13.2);
impaired by platelet consumption and degranulation. for further details see Chapter 36.

14:04:16 111
.015
112

HK
FXII
PK

FXIIf
FXIIa
K

FXI PL, FVIIIa, Ca


HK
intrinsic
PL, HK, Zn, Ca FXIa

extrinsic FIXa

FIX
PL, FVIIIa, Ca FXIII

.015
FVII FVIIa FXa FIIa

PL, TF, Ca FX FII FXIIIa


FI

14:04:16
Leucocyte
Fibrin Cross-linked Fibrin
tPA
PAF

RESTING

ADP

Complement
PG, TXA2, NO, 5HT, OR,
lysosome, IL-1, Histamine, NET
Endothelial Cell

FRAGMENTED NEWLY
ACTIVATED
FORMED

Figure 13.1  Cell based model of haemostasis. Contact activation occurs with activation of the four contact factors: K, PK, HK and XII. This leads to activation of the intrinsic pathway and activated
complement. Both the activation of the complement pathways and the formation of thrombin activate platelets and lead to platelet aggregation and fragmentation. Platelet activation, in turn,
activates endothelial cells and causes release of tPA platelet activation.
K kallikrein, PK prekallikrein, HK high-​molecular-​kininogen, F factor, a activated form, f fragmented form, PG prostaglandin, NO nitrous oxide, TXA2 thromboxane A2, OR oxygen radicals, 5HT
serotonin, IL1 interleukin 1, PAF platelet activating factor, tPA tissue plasminogen activator. (A black and white version of this figure will appear in some formats. For the colour version, please refer to
the plate section.)
113

Chapter 13: Blood Products and Transfusion

Admission to ICU

yes

Blood loss
no No therapy
> 3ml/kg/hr

no

50 mg of protamine yes ACT >110% of


baseline

no

2 pools of
cryoprecipitate Fibrinogen
yes
or 4 g fibrinogen <1.5 g/l
concentrate

no

Reassess patient 1 unit of platelets yes Platelets <100 ×


109/l

no

15 ml/kg of FFP yes Pt >25 s

no

aPTT >48 s
TT<25 s

no

aPTT >48 s
50 mg protamine yes
TT>25 s

no
Consider
tranexamic acid or
15U/kg of
DD AVP Patient on
prothrombin yes warfarin preop
complex

no

Figure 13.2  Part of the rationale for use of blood products is the use of preagreed transfusion algorithms to restore near normal haemostasis.

Laboratory Based Tests essential. Generally it is assumed that thrombocyto-


The conventional laboratory tests in use are the penia will respond clinically to platelet transfusions
PT/​INR, aPTT, Clauss fibrinogen and throm- up to 100 ×109/​l. PT >20 s and aPTT >48 s correct with
bin time. Others include anti-​Xa level. FBC is also FFP. These screening tests tend to become prolonged

14:04:16 113
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114

Section 3: Therapeutic Intervention

when the levels of some individual factors have


decreased to 40% or less.
Blood Conservation
PBM is an international initiative based on the
The main drawback of using laboratory based
Australian experience of using a multimodal approach
assays is the slower turnaround time, which may be as
to optimise red cell mass, minimise blood loss and
long as 40 minutes. Furthermore, these assays are sen-
harness the physiological tolerance of anaemia, so as
sitive to high heparin levels. Thrombin time allows the
to reduce the need for transfusion, improve patient
detection of heparin and interpretation of prolonged
outcomes and ensure that blood products are available
clotting tests in complex patients. It is more sensitive
for those patients that absolutely require transfusion.
to heparin than aPTT, and a TT value >25 s suggests
The UK Department of Health has published guide-
heparin contamination. In the context of recently dis-
lines which can be downloaded freely and encompass
continued warfarin therapy, mildly prolonged aPTT
a range of interventions beginning with rapid diagno-
and PT may hint at potentially correctable deficits in a
sis of preoperative anaemia and correction of revers-
patient with protracted bleeding. Dabigatran or arga-
ible causes when possible prior to surgery, the use of
troban may similarly potentially produce falsely low
cell salvage and adjuncts such as fibrin glue, along with
fibrinogen results.
targeted reversal of anticoagulants and algorithms to
Point-​of-​Care (POC) Testing correct coagulopathy, so as to minimise perioperative
blood loss, and use of a restrictive policy of diagnostic
POC testing is firmly establishing itself in the set-
testing to reduce the impact of repeated blood sam-
ting of cardiothoracic surgery. The benefit of these
pling on postoperative haemoglobin.
tests is the rapid turnaround and the ability to detect
hypofibrinogenaemia at the POC. The drawback is
the relative insensitivity to some of the more subtle Future Outlook: Anticoagulant
imbalances of coagulation such as warfarin or heparin Reversal with Beriplex, Idaricuzimab
therapy for which laboratory based assays have been
validated and have a long track record.
and Adexanet Alfa
The two dominant technologies are thrombo­ Four new oral anticoagulants have come on the market
elastography (TEG) and rotational thromboelasto­ over the past 5 years. While the adoption was slow ini-
metry (ROTEM). A third, the Sonoclot, was evaluated tially, now patients present for urgent or elective surgery
by NICE in 2014 but was not deemed suitable to be while on these drugs. There are set recommendations
used outside a clinical trial. All the viscoelastic assays by the manufacturers with regard to pausing treatment
benefit from a number of activator kits which usu- prior to surgery based on renal function and risk of sur-
ally include a PTT like reagent with kaolin or celite, gery. Tranexamic acid and correcting other correctable
a tissue factor based activator (EXTEM or fastTEG), factors like thrombocytopenia may also help.
a fibrinogen activator (functional fibrinogen, or Prothrombin complex has become the reversal
FIBTEM) and a heparinase containing Celite or kaolin agent of choice of the novel anticoagulants with doses
assay. Manufacturers are developing a cartridge based of 25–​50 IU/​kg (albeit not licensed). This has now
solution that allows the simultaneous assessment of been superseded for dabigatran by idaricuzimab, a
several of the assays at once in varying combinations monoclonal antibody for dabigatran. We are expect-
to improve reliability. ing that adexanet alfa (a dummy factor Xa molecule)
The TEG is able to assess platelet function in will receive a license in the near future for Xa inhibi-
addition to the above tests by making the reaction tors for specific reversal.
dependent on ADP platelet activation or arachidonic
acid based activation. Another potentially useful test Learning Points
is the Multiplate platelet function assay. This utilises • Blood products and components vary in their
electric impedance to detect platelet function/​aggre- indications, and internationally and randomised
gation in whole blood. Results are available in under control trials to determine their optimal use are
10 minutes but one of the problems with the test is the lacking.
interference from low platelet counts, which may be a • Recombinant products are only available for a
secondary reason for a lack of detectable platelet func- minority of indications such as congenital factor
tion perioperatively. VIII deficiency.

14:04:16
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115

Chapter 13: Blood Products and Transfusion

• Recombinant factor VIIa was inferior to best


conventional management in cardiothoracic
Further Reading
http://www.b-s-h.org.uk/guidelines/guidelines/
surgery. use-of-platelet-transfusions/
• Point-​of-​care testing has advantages over
www.nice.org.uk/​guidance/​ng24
laboratory testing of turnaround time and global
nature. Laboratory assays by comparison have a http://transfusion.com.au/transfusion_practice/
blood_conservation
defined advantage in their reproducibility and use
in transfusion algorithms. Weiskopf RB, Viele MK, Feiner J, et al. Human
cardiovascular and metabolic response to acute, severe
• Prothrombin complex has become the
isovolemic anemia. Journal of the American Medical
unlicensed reversal agent of choice for direct oral Association. 1998; 279(3): 217–​221.
anticoagulants (DOACs). Specific reversal agents
will probably be available in the near future.

MCQs
Which of the following statements is true? (d) There is no role for the aPTT and PT in postopera-
1. UK Plasma: tive quantification of coagulopathy
(a) Is being used to manufacture plasma derived sin- (e) DOAC should be reversed with activated pro-
gle factor concentrates where so far there is no thrombin concentrate
recombinant option 4. Blood products:
(b) Is no longer used (a) Red cells can be stored for up to 2 years
(c) Is used in patients born after 1.1.1996 only if (b) FAC sorted platelets can be ordered by the
treated with methylene blue NHSBT
(d) Is now only used for FFP, cryoprecipitate and (c) Platelets express class I HLA antigens
platelets
(d) Red cell transfused patients will not develop HLA
(e) Is pooled before use class I antibodies
2. Point-​of-​care testing: (e) Platelet increments should be performed 7 days
(a) Has been endorsed by NICE after cardiothoracic after administration
surgery 5. Transfusion associated risks:
(b) Is advocated for warfarin reversal (a) Greatest risk to the patient is viral transmission
(c) Leads to more restrictive cryoprecipitate or (b) Patients who refuse blood on grounds of lack of
fibrinogen use safety of the blood supply should be offered con-
(d) Increases the use of FFP comitant antiretrovirals
(e) Should not be performed intraoperatively (c) Patients who refuse blood should be offered autolo-
gous predeposit of blood
3. Laboratory based testing:
(d) Prothrombin complex is a recombinant product
(a) The thrombin time is sensitive to heparin overhang
(e) A liberal transfusion threshold >90 g/​l was superior
(b) The anti-​Xa levels may be falsely low in HIT to 75 g/​l in the T2 study
(c) Clauss fibrinogen is unaffected by thombin inhibi-
tors such as dabigatran

Exercise answers are available on p.468. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

14:04:16 115
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Section 3 Therapeutic Intervention

Fluid Administration
Chapter

14 Vasileios Zochios and Kamen Valchanov

Introduction intracellular (potassium) and extracellular (sodium)


ions. In addition, proteins and large molecules main-
Intravenous fluid administration is performed in crit-
tain the colloid distributions between intracellular,
ically ill patients to maintain fluid volume homeosta-
interstitial and intravascular spaces.
sis and to achieve many other goals. Intensivists and
The fate of any intravenous fluid given into the
perioperative physicians who care for the cardiotho-
vascular compartment depends on many factors
racic critically ill patient must appreciate that fluids
including the electrolyte and colloid (if any) compo-
are ‘drugs’ and therefore it is necesssary to understand
sitions, the patient’s intravascular volume status, the
their physiology and pharmacology. Appropriate fluid
total volume of fluid administered, and the integrity
resuscitation is often the first intervention for the
of endothelial glycocalyx. The endothelial glycoca-
haemodynamically unstable patient. There is ongoing
lyx modulates vascular permeability and inflamma-
debate regarding whether the fluid chosen for these
tion and according to the Starling model it is a key
patients should be a crystalloid solution (i.e. isotonic
determinant of fluid disposition. The primary forces
saline, Ringer’s lactate) or a colloid containing solu-
defining transcapillary fluid movement and the coun-
tion (i.e. albumin solution, hyperoncotic starch).
terbalancing process of fluid movement into the vas-
Large international surveys have shown that choice
cular space in a normal and damaged vasculature are
of fluid is mostly a matter of institutional preference
shown in Figure 14.1. It has been shown that CPB is
rather than due to specific procedural/​patient related
associated with loss of glycocalyx integrity and micro-
factors.
vascular dysfunction. Interestingly, significant shed-
ding of the glycocalyx also occurs during off-​CPB
Pathophysiology procedures. In critical illness, including post-​CPB/​
There are several determinants in assessing the need postoperative states, endothelial glycocalyx denuda-
for intravascular volume replacement in the context of tion causes high transcapillary movement of fluid
cardiac surgery: (i) blood loss, (ii) increasing vascular leading to tissue oedema and inadequate intravas-
capacitance as often occurs with patient rewarming, cular volume expansion after intravenous fluids are
(iii) third space fluid losses secondary to cardiopul- administered.
monary bypass (CPB) induced systemic inflamma-
tion, and (iv) increased cardiac preload requirements
in the setting of transient cardiac ischaemia –​reper- Fluids in the Cardiothoracic ICU
fusion injury, myocardial stunning and reduced ven-
tricular compliance. Colloids Versus Crystalloids
Total body water for the average 70 kg adult male is There is a lack of prospective data with special regard
about 45 l of which 30 l (65%) is intracellular and 15 l to ‘ideal’ fluid in the cardiac surgical patient popula-
(35%) is extracellular fluid. The extracellular space can tion. Colloid fluids would be expected to produce a
be subdivided into interstitial space (10l) and intravas- much larger volume expanding effect. Usual teaching
cular space (5 l). All three compartments also contain suggests that the colloid to crystalloid volume expan-
electrolytes, including ions and larger molecules. The sion efficacy is 1:3 (300% greater efficacy for colloids),
cellular membranes maintain potential differences whereas the colloid to crystalloid ratio for volume
via a complex differential concentration between expansion in adequately powered and well-​designed

14:08:11
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117

Chapter 14: Fluid Administration

Normal Vasculature Damaged Vasculature

Vascular Endothelium Vascular Endothelium

Glycocalyx Glycocalyx

πc Pc Capillary Flow πc Pc
Capillary lumen Capillary lumen

σ Kf σ Kf less glycocalyx

less tight
junctions

Interstitium Interstitium

πi Pi πi Pi

Jt Lymphatic Flow more oedema


formation

Figure 14.1  The opposing forces defining the steady state net flow of fluid from the capillary into the interstitial space are defined by the
hydrostatic pressure differences between the capillary lumen pressure (Pc) and interstitial pressure (Pi) as opposed by the filtration coefficient
(Kf) which itself is a function of the vascular endothelial cell integrity and the intraluminal glycocalyx. This net efflux of fluid out of the
capillary into the interstitium is blunted by an opposing oncotic pressure gradient moving fluid in the opposite direction because capillary
oncotic pressure (πc) is greater than interstitial oncotic pressure (πi). And like hydrostatic pressure dependent flow, oncotic dependent flow
is blunted by the reflection coefficient (σ), which like Kf is a function of the glycocalyx and vascular endothelial integrity. Under normal
conditions (left side), both Kf and σ are high, minimising fluid flux resulting in a slight loss of plasma into the interstitium which is removed by
lymphatic flow. However, if the vascular endothelium and glycocalyx are damaged (right side), oncotic pressure gradients play a minimal role
because a large amount of protein-​rich plasma translocates into the interstitial space, minimising the oncotic pressure gradient, whereas the
constant Pc promotes massive fluid loss and interstitial oedema.
Adapted from Lira and Pinsky (2014), permission to reproduce granted under SpringerOpen general terms.

randomised controlled trials (RCTs) was 1:1.2–​1:1.4 hypernatraemia, hyperchloraemia and acidosis. There
(approximately 30% greater efficacy for colloids). The was a black box warning from FDA for heat starch.
contents of solutes in colloid and crystalloid solutions In a 9 y​ ear multicentre open label trial (CRISTAL),
are presented in Tables 14.1 and 14.2. 2857 patients with hypovolaemic shock, due to any
It would stand to reason that early during elec- cause, were randomly assigned to fluid resuscitation
tive cardiac surgery colloid fluids may have a better with colloid or crystalloid. There was no difference
volume expansion effect than crystalloids as capillary in 28 day mortality or need for RRT between the two
pressures are likely to be normal and loading with arms. Patients treated with colloids had more mechan-
crystalloids would produce a dilutional effect on ical ventilation free days (13.5 versus 14.6  days) and
plasma oncotic pressure leading to tissue oedema and vasopressor therapy (15.2 versus 16.2 days), as well as a
a reduced volume expansion effect. lower 90 day mortality (31% versus 34%). However, the
Crystalloids are preferred over colloid contain- open label design and heterogeneity of fluids that were
ing solutions for the management of patients with compared between the groups limit confidence in the
severe hypovolaemia not due to bleeding. Saline solu- apparent benefit of colloid solutions in this population.
tions seem to be as effective as other crystalloid solu-
tions and colloid containing solutions, and are much Albumin
less expensive. It is recommended that hyperoncotic In theory, albumin has two possible advantages over
starch solutions are avoided as they increase the risk crystalloid solutions:  (i) more rapid plasma volume
of acute kidney injury, need for renal replacement expansion, since the colloid solution remains intravas-
therapy (RRT) and mortality. They may also lead to cularly (in contrast to saline, three quarters of which

14:08:11 117
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118

Table 14.1  Composition of currently available crystalloid solutions

Fluid/​solute Na+ K+ Cl− Ca2+ Mg2+ Osmolarity Lactate Gluconate Acetate Glucose
mEq/​l mEq/​l mEq/​l mEq/​l mEq/​l mOsm/​l mEq/​l mEq/​l mEq/​l g/​l
Plasma 142 4 103 5 3 290 2 —​ —​ 1
NaCl 0.9% 154 —​ 154 —​ —​ 230 —​ —​ —​ 50

.016
Dextrose 5%
NaCl 0.45% 77 —​ 77 —​ —​ 203 —​ —​ —​ 50
Dextrose 5%

14:08:11
NaCl 0.9% 154 —​ 154 —​ —​ 308 —​ —​ —​ —​
Lactated Ringer’s 130 4 109 3 —​ 273 28 —​ —​ —​
Dextrose 5% —​ —​ —​ —​ —​ 252 —​ —​ —​ 50
Plasmalyte 148 140 5 98 —​ 3 294 —​ 23 27 —​
Normasol 140 5 98 —​ 3 294 —​ 23 27 —​
119

Chapter 14: Fluid Administration

Table 14.2  Composition of currently available colloid solutions

Fluid/​solute Osmolarity pH Na+ K+ Ca2+ Cl−


mOsm/​l mEq/​l mEq/​l mEq/​l mEq/​l
Gelofusine 274 7.4 154 <0.4 <0.4 125
Hetastarch 308 4.0–​5.5 154 —​ —​ 154
Haemaccel 301 7.4 145 5 6.25 145
Pentastarch 326 5.0 154 —​ —​ 154
Albumin 4.5% 7.4 <160 <2 —​ 136

enters the interstitium) and (ii) lesser risk of pulmo- anything but ‘normal’ or ‘physiological’ as it is slightly
nary oedema, since dilutional hypoalbuminaemia will hypertonic and contains equal amounts of sodium and
not occur. Well-​designed RCTs and meta-​analyses have chloride making it hypernatraemic and very hyper-
failed to demonstrate benefits from the use of albumin. chloraemic relative to plasma. Administration of high
However, in some cardiothoracic intensive care units volume ‘normal’ saline will result in hypernatraemia,
albumin remains the colloid of choice for patients hyperchloraemic acidaemia leading to renal vasocon-
undergoing lung transplantation and pulmonary striction and reduction in renal blood flow. This has
endarterectomy when volume expansion is needed in led to suggestions that physiologically buffered fluids
the immediate postoperative period, in an attempt to with a chemical composition that approximates extra-
reduce the risk of early reperfusion lung injury. cellular fluid (e.g. Ringer’s lactate solution, Hartman’s
solution, Plasma-​lyte 148, Accusol) are used instead
Hydroxyethyl Starch (HES) of ‘isotonic’ saline for large volume resuscitation.
A recent RCT which enrolled healthy volunteers, and
Use of hyperoncotic starch solutions has been associ-
large observational series, have demonstrated that
ated with increased incidence of acute kidney injury
adverse effects associated with saline use were not evi-
(AKI) and high mortality in some studies. In a RCT,
dent when physiologically buffered fluids were used.
7000 patients were randomised to receive 6% HES
or normal saline for all fluid resuscitation until ICU
discharge. There was an increased incidence of AKI Hypertonic Solutions
requiring RRT in the HES group compared with the Hypertonic solutions typically used in cardiac sur-
saline group (5% versus 5.8%). Two meta-​analyses, gery include 2–​7% saline. They have been used in
one of which excluded seven trials that were retracted an attempt to minimise volume overload and prod-
due to scientific misconduct of one investigator, found uce cellular dehydration in the context of cerebral
that compared to conventional fluid resuscitation reg- oedema. The majority of the trials of hypertonic
imens, HES was associated with increased risk of mor- solutions have been in patients with traumatic brain
tality and need for RRT. HES associated AKI appears injury. The results cannot be extrapolated for the gen-
to be related to pinocytosis of metabolites into renal eral cardiac surgical population. However, cardiac
proximal tubular cells after glomerular filtration. HES surgical patients with cerebral oedema may bene-
has also been associated with increased risk of bleed- fit from hypertonic saline solutions on an individual
ing, which is probably due to impaired fibrin polymer- basis. Studies examining use of hypertonic solutions
isation and decreased factor VIII, vWF and XIII levels did not examine their effect on renal function and
and not associated with haemodilution. Given the fact reported a high incidence of hypernatraemia.
that the cardiac surgical patient population is at risk of
AKI and coagulopathy anyway, the use of HES in the Fluid Balance Management
setting of cardiac surgery is not recommended. Positive fluid balance has been associated with worse
outcomes in some but not all critically ill patient pop-
Crystalloids ulations. A  recent observational study that included
One of the most commonly used crystalloid solutions a large cohort of medical, surgical and cardiothoracic
is 0.9% sodium chloride or ‘normal’ saline, which is ICU patients showed that positive fluid balance at the

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Section 3: Therapeutic Intervention

time of ICU discharge was associated with increased result in impaired gas exchange, need for prolonged
risk of death, after adjusting for markers of illness mechanical ventilation, prolonged length of stay and
severity and chronic medical conditions, particularly high mortality.
in patients with underlying heart or kidney disease.
A secondary analysis of the FACTT trial demon-
strated that patients with ARDS who developed AKI Fluid Responsiveness
had a higher mortality (independent of a conservative In the cardiothoracic intensive care populations,
or liberal fluid administration strategy). This study reduced cardiac output is treated by correcting the
demonstrated some evidence of causality, as diuretic main determinants: heart rate, myocardial contractil-
use was associated with a protective effect, potentially ity, afterload and preload. When preload is reduced
due to its effect on fluid balance. When the diuretic and fluid replacement is needed then the strategy is
effect was adjusted for fluid balance, the protective usually to administer the minimum fluid required to
effect was attenuated, thus potentially suggesting that achieve optimising of cardiac output for the particu-
the modulation of fluid balance promoted the benefit. lar moment of time. Overenthusiastic fluid adminis-
Intravenous fluid administration is a common tration in the cardiac surgical population can lead to
intervention used for both the prevention and treat- increased preload (which is more difficult to treat),
ment of AKI. The pathogenesis of AKI in cardiac surgi- overstretching of myocardial fibres, pulmonary
cal patients is multifactorial, not only due to perturbed oedema and generalised oedema. However, on occa-
haemodynamics but also the result of direct cellular sions fluid administration in cardiothoracic criti-
injury as well as indirect injury from inflammation cally ill patients is required. In general this is guided
and microcirculatory changes. AKI with oliguria as by imaging of the heart and IVC or cardiac output
well as fluid resuscitation often results in accumula- monitors. Sometimes, a more pragmatic way of moni-
tion of excess total body fluid. This fluid accumulates toring fluid administration can be measuring fluid
in all tissues of the body, and through the interstitial responsiveness.
space, as well as remaining within the vascular space, The definition of fluid responsiveness varies
resulting in increased venous pressure. The presence according to the clinical or research setting. A recently
of oliguria is associated with a poor prognosis; how- proposed definition is ‘an increase in a physiologic
ever, it remains unclear whether this is due to severity parameter, preferably cardiac output, within 15 min-
of injury or due to fluid overload. Most studies to date utes superseding twice the error of the measuring
have been conducted in the general ICU population. technique after a 15-​minute administration of 6 ml
Similar findings have been reproduced in the cardiac kg–1 of crystalloids’. In the critical care setting, only
surgery population, as early administration of fluid 50% of haemodynamically unstable patients are ‘fluid-​
can lead to AKI. In a prospective observational cohort responders’ when the fluid bolus is given on ‘clinical
of 100 patients undergoing cardiac surgery, those grounds’. This emphasises that fluid loading is not
patients in the quartile receiving the highest volume always the correct therapy for a clinically hypoper-
of fluid suffered the highest degree of AKI. This study fused patient and that ‘non-​responders’ are exposed
was limited by the small number of patients included. to the risks of volume overload, systemic and pulmo-
It has been demonstrated that positive fluid bal- nary oedema and tissue hypoxia. In other words, fluid
ance in the first 3 postoperative days is associated with responsiveness is a measure of ‘preload dependence’
primary graft dysfunction after lung transplantation. or ‘preload reserve’ but not all ‘fluid-​responders’ nec-
Patients undergoing pulmonary endarterectomy con- essarily need volume loading.
stitute a unique patient population at risk of develop- Examples of clinical measures include static and
ment of ARDS due to high permeability lung injury. dynamic parameters. The static parameters (such as
Therefore restrictive fluid management strategies and central venous pressure) are described as having little
adequate diuresis in the first 48 hours (aiming for 2 l value; however, the dynamic parameters (stroke vol-
negative fluid balance) is of paramount importance. ume variation and pulse pressure variation, as meas-
Negative fluid balance should also be maintained dur- ured using a number of monitors) are shown to be
ing the first week after lung resection surgery. Fluids good physiological determinants of fluid responsive-
should be limited because lung resection decreases ness. Passive leg raise is an increasingly popular fluid
the pulmonary vascular bed and overhydration will responsiveness assessment tool. In patients receiving

14:08:11
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Chapter 14: Fluid Administration

mechanical circulatory support (extracorporeal life perfusion in healthy volunteers. Annals of Surgery.
support, ventricular assist devices, intra-​aortic bal- 2012; 256: 18–​24.
loon pump), transthoracic and transoesophageal Finfer S, Bellomo R, Boyce N, et al. A comparison of
echocardiography are invaluable diagnostic tools albumin and saline for fluid resuscitation in the
that can be utilised to assess fluid responsiveness and intensive care unit. New England Journal of Medicine.
intravascular volume status. 2004; 350: 2247–​2256.
Fulop T, Pathak MB, Schmidt DW, et al. Volume-​
Learning Points related weight gain and subsequent mortality in
acute renal failure patients treated with continuous
• Fluids are drugs. renal replacement therapy. ASAIO Journal. 2010;
• The integrity of the endothelial glycocalyx 56: 333–​337.
appears to have a major role in fluid exchange and Gheorghe C, Dadu R, Blot C, et al. Hyperchloremic
distribution. metabolic acidosis following resuscitation of shock.
• Starch solutions should be avoided during and Chest. 2010; 138: 1521.
after cardiothoracic surgery. Hahn RG. Volume kinetics for infusion fluids.
• Physiologically buffered fluids have some Anesthesiology. 2010; 113: 470–​481.
advantages including maintenance of renal Lee J, de Louw E, Niemi M, et al. Association between fluid
perfusion and avoidance of acid-​base balance and survival in critically ill patients. Journal of
Internal Medicine. 2015; 277: 468–​477.
imbalance.
• Bedside assessment of fluid responsiveness should Lira A, Pinsky MR. Choices in fluid type and volume
during resuscitation: impact on patient outcomes.
always precede fluid loading.
Annals of Intensive Care. 2014; 4: 38.

Further Reading Marik PE, Baram M, Vahid B. Does central venous pressure
predict fluid responsiveness? A systematic review of
Annane D, Siami S, Jaber S, et al. Effects of fluid the literature and the tale of seven mares. Chest. 2008;
resuscitation with colloids vs crystalloids on 134: 172–​178.
mortality in critically ill patients presenting with
Michard F, Teboul JL. Predicting fluid responsiveness in
hypovolemic shock: the CRISTAL randomized trial.
ICU patients: a critical analysis of the evidence. Chest.
Journal of the American Medical Association. 2013;
2002; 121: 2000–​2008.
310: 1809.
Morgan TJ. The meaning of acid-​base abnormalities
Banks DA, Pretorius GV, Kerr KM, et al. Pulmonary
in the intensive care unit: part III –​effects of fluid
endarterectomy: part I. Pathophysiology, clinical
administration. Critical Care. 2005; 9: 204.
manifestations, and diagnostic evaluation of chronic
thromboembolic pulmonary hypertension. Seminars Myburgh JA. Fluid resuscitation in acute medicine: what
in Cardiothoracic and Vascular Anesthesia. 2014; is the current situation? Journal of Internal Medicine.
18: 319–​330. 2015; 277: 58–​68.
Bouchard J, Soroko SB, Chertow GM, et al. Fluid Myburgh J, Cooper D, Finfer S, et al. Saline or albumin
accumulation, survival and recovery of kidney for fluid resuscitation in patients with traumatic
function in critically ill patients with acute kidney brain injury. New England Journal of Medicine. 2007;
injury. Kidney International. 2009; 6: 422–​427. 357: 874–​884.
Bruegger D, Rehm M, Abicht J, et al. Shedding of the Myburgh JA, Finfer S, Bellomo R, et al. Hydroxyethyl
endothelial glycocalyx during cardiac surgery: on-​ starch or saline for fluid resuscitation in intensive
pump versus off-​pump coronary artery bypass graft care. New England Journal of Medicine. 2012;
surgery. Journal of Thoracic and Cardiovascular 367: 1901–​1911.
Surgery. 2009; 138: 1445–​1447. O’Dell E, Tibby SM, Durward A, Murdoch IA.
Cherpanath TG, Aarts LP, Groeneveld JA, et al. Defining Hyperchloremia is the dominant cause of metabolic
fluid responsiveness: a guide to patient-​tailored acidosis in the postresuscitation phase of pediatric
volume titration. Journal of Cardiothoracic and meningococcal sepsis. Critical Care Medicine. 2007;
Vascular Anesthesia. 2014; 28: 745–​754. 35: 2390.
Chowdhury AH, Cox EF, Francis ST, et al. A randomized, Perel P, Roberts I. Colloids versus crystalloids for
controlled, double-​blind crossover study on the effects fluid resuscitation in critically ill patients.
of 2-​L infusions of 0.9% saline and Plasma-​lyte® 148 Cochrane Database of Systematic Reviews. 2012;
on renal blood flow velocity and renal cortical tissue 2012(6): CD000567.

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Section 3: Therapeutic Intervention

Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl Tollofsrud S, Noddeland H. Hypertonic saline and
starch 130/​0.42 versus Ringer’s acetate in severe sepsis. dextran after coronary artery surgery mobilises
New England Journal of Medicine. 2012; 367: 124. fluid excess and improves cardiorespiratory
Raghunathan K, McGee WT, Higgins T. Importance of functions. Acta Anaesthesiologica Scandinavica. 1998;
intravenous fluid dose and composition in surgical 42: 154–​161.
ICU patients. Current Opinion in Critical Care. 2012; Woodcock TE, Woodcock TM. Revised Starling equation
18: 350–​357. and the glycocalyx model of transvascular fluid
Shaw A, Raghunathan K. Fluid management in cardiac exchange: an improved paradigm for prescribing
surgery: colloid or crystalloid? Anesthesiology Clinics. intravenous fluid therapy. British Journal of
2013; 31: 269–​280. Anaesthesia. 2012; 108: 384–​394.

MCQs
1. The main determinant of fluid disposition after car- 4. Regarding physiologically balanced solutions:
diopulmonary bypass is: (a) They can cause hyperchloraemic metabolic acidosis
(a) Total volume of fluid given (b) Their use is associated with maintenance of renal
(b) Electrolyte composition blood flow

(c) Endothelial glycocalyx integrity (c) Administration of physiological solutions is an


acid-​base intervention
(d) The patient’s intravascular fluid status
(d) They are preferred to colloids in cardiac surgical
(e) Serum albumin level patients
2. Fluid responsiveness in the postoperative cardiac sur- (e) Their use is contraindicated in hypoalbuminaemic
gical patient is assessed by: patients
5. Regarding colloids in the cardiothoracic ICU:
(a) Increase in central venous pressure
(a) Their use has been associated with impairment of
(b) Increase in stroke volume
the blood-​brain barrier
(c) Increase in mean arterial pressure
(b) Starch solutions can cause acute kidney injury and
(d) Decrease in lactate levels should be avoided
(e) Increase in urine output (c) Albumin has a role in hypoalbuminaemic patients
3. Fluid overload in the cardiothoracic critically ill: with clinical tissue oedema

(a) Is associated with poor clinical outcomes (d) They are the fluid of choice to assess fluid
responsiveness
(b) Is associated with acute kidney injury
(e) The incidence of anaphylaxis relating to use of gela-
(c) Is associated with postoperative acute respiratory tin solutions is 0.04%
distress syndrome (ARDS)
(d) Is associated with prolonged mechanical ventilation
(e) Is associated with late graft dysfunction in lung
transplant recipients

Exercise answers are available on p.468. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

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Section 3 Therapeutic Intervention

Inotropes and Vasopressors


Chapter

15 Gabriel Kleinman, Shahzad Shaefi and Charles Shayan

Introduction (Figure 15.1). The end result is vascular smooth mus-


cle constriction. This leads to globally increased sys-
Ahlquist’s discovery in animal models of two distinct
temic vascular resistance (SVR). In the perioperative
types of adrenergic receptors in 1948 set the founda-
setting, A1r agonists are used to counter the decreased
tion for the modern day critical care use of inotropic
SVR seen with a variety of physiological and patho-
drugs. He named these receptors in relation to their
physiological processes. The A1r does not undergo
activity as activators (alpha) or blockers (beta). His
sensitisation, or internalisation, though at maximal
original work has been expanded exponentially by dis-
supratherapeutic agonist doses, it could produce
covery of subtypes of the originally identified recep-
organ ischaemia or substantially increase SVR, which
tors as well as many other discrete types of vasoactive
can be widely distributed in epicardial, renal, splanch-
receptors. Though it was uniquely postulated that
nic, cerebral and pulmonary vascular beds.
these vasoactive receptors respond only to sympathin
(epinephrine), we now know that these G protein cou-
pled receptors (GPCRs) are regulated by a variety of Beta Receptors
agonists and antagonists and play a key role in preva- B receptors (Br) are subtyped into B1, B2 and B3 vari-
lence of sympathetic nervous system activity. In the ants and regulate inotropy and chronotropy as well as
cardiac ICU, these vasoactive receptors are stimulated smooth muscle relaxation in various vascular beds.
with various natural and synthetic molecules, result- Their distribution is not uniform. Although B1r and
ing in augmented cardiac output (CO), chronotropy B2r are both present in myocardium, thoracic aorta
and mean arterial pressure (MAP), and in some and carotid artery, and epigastric and pulmonary
cases enhanced lusiotropy in the postsurgical cardiac artery, B1 is the predominant receptor subtype in the
setting. Norepinephrine, epinephrine, dopamine, myocardium. B1 agonism exerts its effect through the
dopexamine, dobutamine, milrinone, enoximone, Gs GPCR pathway. This interaction in cardiac cells
levosimendan and phenylephrine are the most com- leads to calcium induced calcium release from the
monly encountered vasoactive agents in the intensive myocardial sarcoplasmic reticulum, thereby allow-
care unit. We will review the current evidence for the ing increased actin-​ myosin cross linkages and an
use of inotropic agents in the perioperative care of car- enhanced chronotropic and inotropic state.
diac patients. In contrast to the action of beta agonists on car-
diac cells, in smooth muscle, B2r stimulation leads
Alpha-​1 Receptors to increased activity of cAMP dependent protein
kinase, increased phosphorylation and activation of
Furthering Ahlquist’s work, Piascik elucidated the
phospholamban, increased cellular calcium reuptake
mechanism of action of GPCRs. Upon agonist bind-
through the ryanodine receptors and, ultimately,
ing to the alpha-​1 receptor (A1r), Gq protein stimu-
vasodilation.
lates the phospholipase C (PLC) system, which in its
turn activates the 1,2-​diacylglycerol (DAG) protein
kinase C (PKC) pathway through hydrolysis. The con- Dobutamine
sequence of this enzymatic process is an increased Dobutamine is a synthetic Br (B1, B2) agonist,
release of calcium from the sarcoplasmic reticu- which entered clinical use in 1978 as a promising
lum (SR) and increased protein phosphorylation replacement for dopamine in the treatment of acute

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Section 3: Therapeutic Intervention

overall metabolic and objective parameters (O2 deliv-


ery and renal perfusion) between the two groups.
Thus, in patients with non-​ischaemic HF requiring
inotropic support, dobutamine may be the better
agent compared to epinephrine given the tendency
of epinephrine to aggravate lactic acidosis and, con-
versely, its lower effectiveness in an acidotic milieu.
Though dobutamine infusions are frequently used as
pharmacological therapy for bridge to cardiac trans-
plantation or for long-​term management of heart fail-
ure in patients not eligible for transplant, eosinophilic
hypersensitivity reactions have been reported. The
relationship between dobutamine and eosinophilia
appears to be related to dose of dobutamine and dura-
tion of treatment, eventually resulting in eosinophilic
myocarditis with unfortunate further decompensation
of the patient’s underlying cardiac disease. It is well
documented that chronic infusions of dobutamine are
Figure 15.1  β1 receptor: AC adenylyl cyclase, cAMP cyclic associated with higher risk for mortality.
adenosine monophosphate, PDE phosphodiesterase, PKA
phosphokinase A, SR sarcoplasmic reticulum, TnC troponin
C. Please refer to the text for detailed explanation.
Norepinephrine (NE)
The primary endogenous neurotransmitter in humans,
decompensated heart failure. It has a 3:1 B1:B2 ago-
norepinephrine, has a more profound effect at A1r than
nist activity and a trivial alpha-​1 effect. Dobutamine
at B1r and B2r at clinically relevant doses. Extensive
is used in clinical practice for the treatment of acute
research has been done focusing on the effects of NE
decompensated heart failure in a dose dependent
in the setting of sepsis, and in clinical practice it has
fashion, usually starting with an infusion of 2–​3 μg/​
a profound vasoconstrictive effect with less heart rate
kg/​min and rapidly uptitrated to a therapeutic dose of
variability when compared to dopamine and epineph-
7.5–​15 μg/​kg/​min. It increases CO, stroke volume and
rine. This finding, along with the decreased mortality
coronary perfusion with minimal pulmonary vascu-
associated with NE as compared to other vasoactive
lar effect. Furthermore it has moderate chronotropy
medications, makes it the gold standard choice in the
as it improves the atrioventricular (AV) conduction.
setting of septic shock. In the cardiac ICU it is used to
Tachycardia has been reported to be more signifi-
increase systolic and diastolic pressures and therefore
cant compared to use of milrinone, hence overall
coronary perfusion pressure, in a variety of vasoplegic
oxygen (O2) consumption may be increased with its
states, thus giving it a favourable cardiac profile com-
use. Dobutamine has a mean plasma half-​life of 2–​3
pared to dopamine and phenylephrine. It appears that
minutes titratable, though after a 72 hour infusion,
the overall effect of NE on CO is determined through
many patients become resistant to dobutamine, due
the interplay of systemic vascular resistance, heart rate
to tachyphylaxis, with resultant rebound hyperten-
and stroke volume variation (SVV). Patients with a
sion on discontinuation probably due to beta receptor
SVV greater than 8.4% are likely to increase their CO
downregulation and internalisation. Dobutamine has
in response to NE, while those with a SVV less than
been shown to increase myocardial oxygen consump-
8.4% are likely to decrease their cardiac output in the
tion, as well as malignant ventricular arrhythmias, at
same setting. Prolonged infusions of NE may have dir-
any dose. Even though dobutamine improves cardiac
ect toxic effects on cardiac myocytes, though this has
output, it has not been shown to optimise regional O2
only been demonstrated in animal models.
delivery to ischaemic vascular beds that need O2 the
most. A  recent randomised controlled trial compar-
ing norepinephrine-​ dobutamine to epinephrine in Epinephrine (Epi)
patients with acute non-​ischaemic cardiogenic shock Epinephrine has a dose dependent affinity for A1r,
requiring inotropic support found no difference in B1r and B2r. At low doses, it acts primarily on B1r,

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Chapter 15: Inotropes and Vasopressors

increasing chronotropy, inotropy and lusitropy. As the endothelium. These receptors couple to Gs which
dose is increased, a profound A1r effect is noted. Epi peripherally increases cAMP, causing vasodilation.
acts to increase coronary blood flow at low doses by At low dose infusions up to 3 μg/​kg/​min, dopamine
increasing the relative time the myocardium is in dias- stimulates DA1 predominantly and results in vaso-
tole. At higher doses, it acts by increasing diastolic and dilation by increasing the intracellular cAMP (and
therefore coronary perfusion pressure. Epi also acts therefore lowering calcium influx) at the level of vas-
to increase blood flow to the pulmonary vasculature cular endothelium in renal, mesenteric beds. In the
through alpha-​1 mediated pulmonary vasoconstric- kidneys, dopamine inhibits the NaCl cotransporter at
tion, and dilates bronchioles through B2 mediated the distal convoluted tubule causing diuresis. Despite
smooth muscle dilation. Levy et al. compared Epi to improving renal blood flow, dopamine has not been
combination norepinephrine-​ dobutamine in car- shown to improve glomerular filtration rate. At the
diogenic shock patients without acute coronary syn- level of myocardium DA1–​DA4 receptors are found
drome and found that although Epi is as effective as mainly in atria. At escalating doses (3–​10 μg/​kg/​min)
norepinephrine-​ dobutamine at achieving haemo- dopamine binds to these receptors as well as B1r and
dynamic goals, it was also associated with increased causes both chronotropy and inotropy, although it is
rates of lactic acidosis, tachycardia, arrhythmias and not quite clear whether these effects are indirect (via
worsened perfusion to gastric mucosa. Furthermore, presynaptic NE release) or by direct B1r stimulation.
use of Epi in treatment of myocardial depression and At doses higher than 10 μg/​kg/​min, dopamine binds
low cardiac output syndrome may be associated with to A1r causing peripheral vasoconstriction. A  trial
more adverse effects on the end-​organ function such comparing dopamine to NE in patients with diagnosis
as kidneys in the postoperative period. of shock found that among the subset of patients with
cardiogenic shock, the rate of death was significantly
Isoproterenol higher in the group treated with dopamine than in the
group treated with NE.
Isoproterenol is a purely synthetic B1 and B2 receptor
agonist at clinical doses. While the B1 effects in cardiac
cells lead to increased inotropic and chronotropic states,
the increased cAMP in smooth muscles of the respira-
Milrinone
While most of the vasoactive medications used in the
tory bronchioles and vasculature leads to bronchodila-
cardiac ICU directly exert their effects on GPCRs, mil-
tion with an increase in lung compliance and decrease
rinone, a bipyridine PDE-​3 inhibitor, utilises a novel
in SVR respectively. Isoproterenol is used in the EP
mechanism, and is therefore not subject to receptor
laboratory to induce AV nodal re-​entrant tachycardias,
phosphorylation, internalisation of deactivation, and
as well as to initiate Wolff–Parkinson–White (WPW)
thus does not demonstrate the need for therapeutic
syndrome re-​entry and to chemically pace patients in
dose escalation due to tachyphylaxis. Milrinone exerts
third degree heart block, a property that is very useful
its inotropic effect by inhibiting the conversion of
in heart transplants particularly at the time of separa-
cAMP to AMP, which causes smooth muscle relaxa-
tion from CPB. Experimentally, isoproterenol is used to
tion in peripheral vasodilation, while in cardiac cells
induce acute myocardial infarctions and HF due to the
increased cAMP causes increased lusitropy and inot-
myocardial ischaemia it induces during long infusions.
ropy (Figure 15.2). Due to its lack of receptor internal-
isation and downregulation, like direct B2r, milrinone
Dopamine can be used in a beta receptor depleted state, such
Dopamine is the immediate in vivo precursor to nor- as stage D heart failure awaiting heart transplant.
epinephrine. The actions of dopamine are mediated Milrinone has been shown to improve diastolic dys-
by five distinct GPCRs (D1–​ D5). These receptors function and increases flow in coronary artery bypass
are found in various densities on the surface of cells grafts after cardiopulmonary bypass, however this
in the nervous system, pulmonary artery, splanchnic effect is not demonstrable if milrinone is given prior
circulation and renal tubules. Dopamine-​1 receptors to initiation of cardiopulmonary bypass. On the other
(DA1) are found in the proximal convoluted tubules, hand if milrinone is administered in inhaled fashion
ascending loop of Henle and collecting ducts. DA2 prior to initiation of CPB it is beneficial in the first
receptors are mainly located in the renal vascular 24 hours postoperatively in cardiac patients with

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Section 3: Therapeutic Intervention

considered an inotrope. Animal studies initially dem-


onstrated that dopexamine may have immunomod-
ulatory effect (B2 interaction), notably decreased
lactataemia and cytokine release in animal models
of endotoxaemia. This effect has not been duplicated
in clinical observations. Dopexamine was compared
to dobutamine in a randomised double blind, cross-​
over fashion, in a paediatric population undergoing
cardiac surgery for non-​complex congenital correc-
tion, for separation from CPB and mitigating myocar-
dial stunning. Both agents had a similar increase in
CI. Obviously patients treated with dopexamine had
lower systemic vascular resistance (SVR).

Calcium Sensitisers
In normal cardiac cells, tropomyosin and troponin C
Figure 15.2  V1 receptor: DAG diacylglycerol, GDP guanosine (TnC) inhibit the binding of thick to thin filaments.
diphosphate, IP3 inositol triphosphate 3, PIP2 phosphatidylinositol
4,5-​biphosphate, PKC phosphokinase C, PLC phospholipase TnC, in the presence of calcium released from the
C. Please refer to the text for detailed explanation. sarcoplasmic reticulum, causes a conformational
change in the troponin-​tropomyosin complex, allow-
pulmonary hypertension. The clinical effect of long-​
ing extensive thick and thin filament interaction and
term administration of milrinone in ambulatory
thereby myocardial contraction (Figure  15.2). Once
patients was evaluated by Packer who found an exces-
calcium diffuses off its binding site on TnC, tropo-
sive mortality rate in the milrinone treated group.
myosin again returns to its resting position, block-
Milrinone home infusion may be an alternative in
ing the thick and thin filament contractile apparatus.
stage 1B patients awaiting OHT, although the pres-
Under typical physiological conditions, a large cardiac
ence of ICD is advisable given the possibility of ven-
contractile reserve exists. Experimental and in vivo
tricular tachycardia. Milrinone may also be combined
models have demonstrated that increasing calcium
with beta-​blockers in stage D heart failure, although
concentration in the sarcoplasmic reticulum leads to
large scale studies still need to be designed to evalu-
increased binding of TnC and, therefore, increased
ate outcomes in these patients. A 2012 meta-​analysis
heart rate and inotropic state. It was this contractile
of milrinone treatment in adult cardiac surgery sug-
reserve that led to the development of calcium sensi-
gests that milrinone is associated with a significantly
tising agents that either increase the affinity of TnC for
increased risk of dying when compared with other
calcium or act directly on the thick and thin filaments
drugs (mainly levosimendan). Even though OPTIME-​
to allow interaction with little endogenous calcium
CHF investigation showed that milrinone infusion in
required. Two drugs that act to increase the affinity
CHF exacerbation does not improve the mortality, it
of TnC for calcium are currently available outside the
demonstrated that it may have a positive impact on
USA, pimobendan and levosimendan.
renal functions when secondary outcomes were ana-
Pimobendan is an oral agent that exerts its ino-
lysed. However, the full extent of this effect would
tropic effect through calcium sensitising as well c-​
have to be evaluated further.
AMP dependent pathway. It has only been studied in
the EPOCH study in a randomised double blind fash-
Dopexamine ion, which demonstrated a non-​statistically significant
Dopexamine is a dopamine analogue that has activity decrease in sudden cardiac death, hospitalisation for
at DA1, DA2, B1r and B2r. It has more significant B2r HF, and death from HF in the pimobendan treatment
activity than B1r and hence, along with DA receptors, group. This study also found significantly decreased
activation leads to cerebral, coronary and renal vaso- adverse cardiac events in the treatment group.
dilation and increased perfusion. Despite its particu- Levosimendan, which has a similar mechanism
lar vasodilatory property, in certain vascular beds it is of action to pimobendan, has been shown not only to

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Chapter 15: Inotropes and Vasopressors

improve inotropy as well as lusitropy, but also to cause cardiovascular homeostasis. Vasopressin receptors
vasodilation by activating ATP dependent K chan- are GPCRs, and there are three subtypes of these
nels on the smooth muscles. Levosimendan has been receptors: V1 is found in vascular smooth muscles;
demonstrated to increase SV and CI by 28% and 39% liver, platelets and most peripheral tissues; V2 is only
respectively, while marginally increasing heart rate found in renal collecting ducts; and V3 is limited to
and meanwhile decreasing the left and right filling the anterior pituitary. Stimulation of the V1 receptor
pressures and systemic arterial pressures when com- leads to vasoconstriction through a mechanism simi-
pared to placebo in a double blind RCT. The LIDO lar to that of alpha-​1 receptor agonists, Gq activation
trial, which compared levosimendan to dobutamine, of PLC leading to calcium release from intracellular
demonstrated that levosimendan exerted superior stores (Figure 15.2). This vasoconstriction is apparent
haemodynamic effects and in secondary and post hoc when there is a severe dysregulation of sympathetic,
analyses was associated with a lower risk of death after renin-​angiotensin systems. Interestingly, vasopressin
31 and 180 days. In addition, the second Randomized has a vasodilatory effect in the cerebral, pulmonary
Multicenter Evaluation of Intravenous Levosimendan and coronary vascular bed at low doses while increas-
Efficacy (REVIVE II) study showed that patients ing the vascular tone in splanchnic, skeletal and cuta-
with ADHF who received levosimendan in addition neous circulations. Recent studies have shown that a
to standard therapy were more likely to show clini- deficiency in vasopressin exists in some shock states,
cal improvement and less likely to deteriorate than and numerous case studies and small trials show vas-
patients on standard therapy alone. However, there opressin increases arterial pressure in septic shock.
was no significant change in 90  day mortality and The largest randomised prospective controlled study
there were more adverse side effects (tachyarrhythmia was published in 2003 by Dunser and colleagues. In
and hypotension) in the levosimendan group. As the this study, 48 patients with catecholamine-​resistant
previous studies had only compared levosimendan to vasodilatory shock were prospectively randomised
placebo, the SURVIVE trial compared levosimendan to receive a combined infusion of vasopressin and
to dobutamine in a double blind RCT in patients norepinephrine or norepinephrine alone to main-
requiring inotropic support for ADHF and found that tain a MAP above 70 mmHg. The vasopressin group
despite an initial reduction in plasma B-​type natriu- showed a significant increase in MAP, cardiac index,
retic peptide level in patients in the levosimendan systemic vascular resistance index, and left ventricu-
group compared with patients in the dobutamine lar stroke work index as well as reduced norepineph-
group, levosimendan did not significantly reduce rine requirements and heart rates. Compared with the
all-​cause mortality at 180  days or affect any second- norepinephrine group, there was better preservation
ary clinical outcomes. Like milrinone, levosimendan of gut mucosal blood flow and a significantly lower
used in combination with a beta adrenergic antago- incidence of tachyarrhythmias. In survivors of cardiac
nist may have beneficial effects in patients with car- arrest, vasopressin levels have also been demonstrated
diogenic shock who exhibit tachycardia in response to to be higher than in those cardiac arrest patients who
inotropic agents. do not survive, a finding which led to the inclusion of
vasopressin in the ACLS algorithm.
Vasopressin
Pathophysiology of vasoplegia post cardiac surgery Phenylephrine
involves generation of interleukins, decreased endog- The principal alpha agonist used in clinical practice
enous vasopressin and increased production of NO is phenylephrine, which is a direct-​acting syntheti-
by endothelial cells. Vasopressin is a peptide synthe- cally derived alpha-​1 agonist. It exerts no beta effects
sised by the paraventricular and supraoptic nuclei due to its lack of a hydroxyl group at position 4 on
of the posterior hypothalamus and is released in the its benzene ring and it causes its vasoconstrictive
capillary bed of the posterior pituitary gland where effects through inhibition of cAMP production. In
there is no blood-​brain barrier. Its release is potently the perioperative period, it is used to rapidly increase
regulated by plasma osmolality and haemodynamic the mean arterial pressure and maintain forward flow
parameters such as decreased blood pressure produc- in patients with systolic outflow tract obstruction
ing hormones that are essential for osmotic as well as and single ventricle physiology. The rapid increase in

14:13:54 127
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128

Section 3: Therapeutic Intervention

MAP caused by phenylephrine can lead to a carotid


baroreceptor-​mediated bradycardia. At clinically rel-
Further Reading
Alhashemi JA. Treatment of cardiogenic shock with
evant doses, phenylephrine reduces CO and increases levosimendan in combination with β-​adrenergic
myocardial work, and oxygen requirements. Though antagonists. British Journal of Anaesthesia. 2005;
not definitive, this may be associated with myocardial 95: 648–​650. doi: 10.1093/​bja/​aei225
injury and significantly decreased coronary perfusion. Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh
In addition to its usefulness as both a bolus and infu- J. Low-​dose dopamine in patients with early renal
sion perioperative medication, phenylephrine has also dysfunction: a placebo-​controlled randomised trial.
been described in case reports to correct smooth mus- Australian and New Zealand Intensive Care Society
cle vascular tone in patients who coingest both PDE-​5 (ANZICS) Clinical Trials Group. Lancet. 2000;
inhibitors and nitrates. 356: 2139–​2143.
De Backer D, Biston P, Devriendt J, et al. Comparison
of dopamine and norepinephrine in the treatment
Methylene Blue of shock. New England Journal of Medicine. 2010;
Methylene blue, which is normally used as a cell dye 362: 779–​789.
and as a treatment for cyanide poisoning, when given Klein L, Massie BM, Leimberger JD, et al. Admission
as an intravenous bolus or infusion, binds to and or changes in renal function during hospitalization
inhibits guanylate cyclase, scavenges nitric oxide and for worsening heart failure predict postdischarge
inhibits synthesis of nitric oxide via iNOS. All three survival: results from the Outcomes of a Prospective
of these actions lead to decreased systemic levels of Trial of Intravenous Milrinone for Exacerbations
of Chronic Heart Failure (OPTIME-​CHF).
cGMP and NO, which act to synergistically mini-
Circulation: Heart Failure. 2008; 1: 25–​33.
mise the overall response to endogenous vasodila-
tors. Methylene blue has been used successfully for Laflamme M, Perrault LP, Carrier M, et al. Preliminary
experience with combined inhaled milrinone
the treatment of vasoplegic syndrome, for which fluid
and prostacyclin in cardiac surgical patients with
resuscitation and conventional vasopressors are inef- pulmonary hypertension. Journal of Cardiothoracic and
fective, as well as vasopressor resistant septic shock. Vascular Anesthesia. 2015; 29: 38–​45.
Two studies have specifically looked at the role of
Levy B, Perez P, Perny J, Thivilier C, Gerard A. Comparison
methylene blue in cardiac surgery patients at highest of norepinephrine-​dobutamine to epinephrine for
risk for developing vasoplegic syndromes (preopera- hemodynamics, lactate metabolism, and organ
tive ACE inhibitors, calcium channel blockers). When function variables in cardiogenic shock. A prospective,
administered in the preoperative period, the treated randomized pilot study. Critical Care Medicine. 2011;
patients had greater haemodynamic stability, less 39: 450–​455.
vasopressor requirements, less fluid administration, Majure DT, Greco T, Greco M, et al. Meta-​analysis of
fewer blood transfusions, and decreased intensive care randomized trials of effect of milrinone on mortality
unit and overall hospital stays. None of the patients in cardiac surgery: an update. Journal of Cardiothoracic
who received methylene blue developed vasoplegic and Vascular Anesthesia. 2013; 27: 220–​229.
syndrome, while 26% of the placebo patients did go Mebazaa A, Nieminen MS, Packer M, et al. Levosimendan
on to develop some degree of vasoplegic syndrome. vs dobutamine for patients with acute decompensated
The same haemodynamic stability and decreased heart failure: the SURVIVE Randomized Trial.
Journal of the American Medical Association. 2007;
ICU and hospital stay held true for patients that were
297: 1883–​1891.
given methylene blue after the development of vaso-
plegic syndrome. Though a rapid and effective treat- Movsesian M, Stehlik J, Vandeput F, Bristow MR.
Phosphodiesterase inhibition in heart failure. Heart
ment for vasoplegic syndrome, methylene blue is not
Failure Reviews. 2009; 14: 255–​263.
a completely benign drug. Severe renal impairment
is an absolute contraindication, as it is excreted pre- Nathan Coxford R, Lang E, Dowling S. Dopamine versus
norepinephrine in the treatment of shock. Canadian
dominantly by the kidney. Relative contraindications
Journal of Emergency Medicine. 2011; 13: 395–​397.
include G6PD deficiency and other oxidiser initiated
haemolytic anaemias. Methylene blue also inhib- Ozal E, Kuralay E, Yildirim V, et al. Preoperative methylene
blue administration in patients at high risk for
its MAO and must be used cautiously in patients on
vasoplegic syndrome during cardiac surgery. Annals of
SSRIs, who are at a higher risk for serotonin syndrome. Thoracic Surgery. 2005; 79: 1615–​1619.

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Chapter 15: Inotropes and Vasopressors

MCQs
1. A 45 year old male is presenting to CTICU for postop- (a) Milrinone
erative management after a heart transplant. His past (b) Dobutamine
medical history is significant for arrhythmogenic right
ventricular hypertrophy. His immediate postoperative (c) Epinephrine
vitals include a BP = 100/​70, HR = 65. (d) Dopamine
What inotropic agent would be MOST appropriate to
(e) Centre dependent
start at this point?
(a) Dopamine 4. A 55  year old patient s/​p MVR/​TVR/​AVR is present-
ing to CTICU. On admission the patient is on infusion
(b) Milrinone
of high dose milrinone, dobutamine and dopamine.
(c) Dobutamine Patient BP = 80/​40, HR = 100, CI = 2.1.
(d) Norepinephrine What agent would be the MOST useful to infuse at
this time?
(e) No need for inotropic agent
2. A 65 year patient with longstanding history of CAD is (a) Phenylephrine
presenting to CTICU for further postoperative manage- (b) Norepinephrine
ment. His preoperative systolic and diastolic functions
(c) Epinephrine
are severely reduced.
What would be the LEAST appropriate inotropic agent (d) Vasopressin
in this patient?
5. A 66  year old African American male is presenting
(a) Dopamine s/​p heart transplant (complicated intraoperative course),
(b) Milrinone with profound thrombocytopenia and high pyrexia. His
past medical history is significant for anxiety, severe
(c) Dobutamine depression and opioid abuse.
(d) Epinephrine Administration of all the following agents may contrib-
ute to his symptomology EXCEPT:
(e) Levisomendan
(a) Odansetron
3. A 75 year old patient with longstanding history of non-​
(b) Fluoxetine
ischaemic cardiomyopathy and chronic heart failure
(CHF), necessitating multiple hospitalisations and vol- (c) Trazadone
ume overload management in the past, is readmitted for (d) Methylene blue
acute exacerbation of his CHF.
What is the MOST desirable inotropic agent to use in (e) Methadone
this patient?

Exercise answers are available on p.468. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

14:13:54 129
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Section 3 Therapeutic Intervention

Sedation and Analgesia


Chapter

16 Lachlan Miles and Barbora Parizkova

Introduction target concentration will be immediately achieved and


maintained by the infusion without needing to wait
Analgesia and sedation are ubiquitous in the man-
the requisite 3–​5 half-​lives. If the loading dose yields
agement of the intubated ICU patient, and attitudes
a drug concentration more or less than the target con-
towards them have undergone a paradigm shift in
centration, it will still take 3–​5 half-​lives for steady
recent years. Where once the ICU was viewed as an
state to be reached, but the starting concentration will
extension of the operating room environment, the
be closer to the steady state concentration than if the
‘anaesthetic triad’ of deep sedation, potent analgesia
loading dose had not been given (Figure 16.2).
and neuromuscular blockade is now rarely indicated
beyond the doors of theatre.
The problems of delirium, agitation and pain are
Sedation
intrinsically connected. It is perhaps best to conceptu- Oversedation is an important cause of morbidity in
alise this ‘ICU triad’ as a three-​legged stool –​if any ‘leg’ the ICU. The initiation of a sedative or analgesic agent
is neglected, the stool cannot function as intended. should not be based on anticipated distress but rather
on that which is perceived by the clinical team at the
bedside.
Infusion Pharmacokinetics In the postcardiac surgery setting, sedation may be
The administration of sedative and analgesic medica- misused to mask a variety of problems without con-
tions in the ICU is frequently via intravenous infusion. sidering the underlying issue (particularly pain). With
When administering any drug via continuous a few exceptions (status epilepticus, raised intracra-
intravenous infusion, a steady state concentration will nial pressure and severe respiratory failure), it is rec-
eventually be achieved, as determined by the dose rate ognised that maintaining light levels of sedation leads
and the clearance of the drug. to improved clinical outcomes (i.e. shorter duration
The time taken for an infusion to reach this steady of mechanical ventilation, decreased length of ICU
state is determined by the half-​life of the drug (the stay). Whilst lighter levels of sedation lead to a more
time taken for the plasma concentration of the drug to pronounced physiological stress response, this has not
decrease by 50%). It takes 3–​5 half-​lives for a drug to been linked to an increased incidence of myocardial
reach steady state. ischaemia.
For agents with a prolonged half-​life, an increase Consequently, it is vital to identify the underlying
in the infusion rate is an inefficient means of achieving cause of any distress, rather than resorting to seda-
desired depth of sedation within a short timeframe. tion in the first instance. Anxiety, pain, delirium and
Increasing the infusion rate to a level such that the tar- residual neuromuscular paralysis are amongst the
get concentration is achieved quickly will result in a most common causes in the intensive care setting.
relative overdose if the infusion is allowed to continue A  common underlying cause of anxiety amongst
at that rate (Figure 16.1). this population is patient-​ventilator dys-​synchrony,
To achieve the target concentration of a drug whilst and the adjustment of ventilator settings (despite
maintaining a continuous infusion at a safe dose rate, acceptable blood gas values) may negate the need for
a loading dose is used. sedation.
If the loading dose is sufficient to achieve the tar- Non-​pharmacological strategies are equally impor-
get concentration for a given infusion rate, then the tant. Whilst attention must be paid to addressing the

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Chapter 16: Sedation and Analgesia

4.5
Drug concentration (mgl–1)

3.5

2.5

2
A

1.5

B
1

0.5

Time (hours)
2 4 6 8 10 12 14 16

Figure 16.1  The effects of increasing the rate of infusion to achieve a rapid clinical effect with a hypothetical drug with a half-​life of
approximately 4 hours. An increase in the infusion rate (from a steady state of 0.5 mg l−1) is performed. The desired clinical effect is achieved
relatively rapidly, within 15 minutes (at a blood concentration of 1 mg l−1). However, due to the prolonged half-​life of the drug, the blood
concentration steadily rises over the next 16 hours, a situation which, if left unchecked, will result in a steady state blood concentration
nine-​fold that of the original level, with potentially deleterious effects.

cause of agitation and distress, frequent reassurance • Bispectral index (BIS);


and communication is equally important. Regular • State entropy (SE);
family visits, preservation of regular sleep-​wake cycles • Auditory evoked potentials (AEP);
and cognitive-​behavioural therapies (music therapy, • Narcotrend index (NI);
relaxation therapy) where available should also be • Patient state index (PSI).
incorporated into patient care.
Whilst these have some use in patients who cannot
be clinically assessed (i.e. patients receiving neuro-
Monitoring Sedation muscular blockade), or in whom monitoring of EEG
A variety of different structured, subjective seda- is particularly important (i.e. non-​convulsive status
tion assessment scores have been proposed. Of these, epilepticus), it is generally recognised that they are
the Richmond Agitation-​ Sedation Scale (RASS) inferior to subjective scoring systems in the non-​
(Table 16.1) and the Sedation-​Agitation Scale (SAS) paralysed, non-​comatose patient.
(Table  16.2) are the most psychometrically reliable
(particularly in terms of inter-​ rater variability) in Planning Sedation
measuring the quality and depth of sedation in adult As previously mentioned, lighter levels of sedation
ICU patients. In direct comparisons, neither of these lead to improved patient outcomes when combined
measures is clearly superior. with effective analgesia. This has led to the advent of
A variety of different devices have been evaluated protocolised sedative-​analgesic strategies, whereby
for the objective measurement of cerebral function in the bedside clinician titrates sedation to a set of prede-
the sedated ICU patient. These include: fined goals, guided by routine, structured, subjective

14:31:24 31
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Section 3: Therapeutic Intervention

Table 16.1  The Richmond Agitation-​Sedation Scale (RASS)

Score Classification Description


4 Combative Overly combative or violent; immediate danger to staff
3 Very agitated Pulls on or removes tube(s) or catheter(s) or has aggressive behaviour towards staff
2 Agitated Frequent non-​purposeful movement or patient-​ventilator dys-​synchrony
1 Restless Anxious or apprehensive but movements not aggressive or vigorous
0 Alert and calm
−1 Drowsy Not fully alert but has sustained (more than 10 seconds) awakening with eye contact to voice
−2 Light sedation Briefly (less than 10 seconds) awakens with eye contact to voice
−3 Moderate sedation Any movement (but no eye contact) to voice
−4 Deep sedation No response to voice, but movement to physical stimulation
−5 Unarousable No response to voice or physical stimulation

8
Drug concentration (mgl–1)

B
4

Time (hours)
2 4 6 8 10 12 14 16

Figure 16.2  This graph demonstrates the effects of a loading dose for a hypothetical drug with a half-​life of approximately 4 hours. Curve
A demonstrates the effect of no loading dose, and the target steady state of 4 mg l−1 is reached after 4 half-​lives. Curve B shows the effect
of a perfectly calculated loading dose –​the target steady state is reached immediately, and maintained by the infusion. Curve C shows the
effect of a partial loading dose. The starting concentration is higher, but it still takes 4 half-​lives until steady state is reached. Finally, curve
D shows the effect of an excessive load. The starting concentration is extremely high, and takes 4 half-​lives to fall to the target steady state
concentration. Drug concentration in mg l−1. (A black and white version of this figure will appear in some formats. For the colour version,
please refer to the plate section.)

assessments. The ability to undertake such intensive period to allow comprehensive, formal assessment
monitoring is dependent on bedside staffing and of underlying neurological function. The use of this
training, but it is effective in orientating practice technique in isolation has met with controversy in the
towards sedation minimisation. literature. If a unit is already practising sedation mini-
Another strategy is the use of daily sedation inter- misation and/​or protocolised sedation, the use of DSI
ruption (DSI). This involves ceasing sedation for a offers little benefit.
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Chapter 16: Sedation and Analgesia

Table 16.2  The Sedation-​Agitation Scale

Score Classification Description


7 Dangerous agitation Pulls at endotracheal tube, tries to remove catheter, climbs over bed rail, strikes at staff, thrashes
side to side
6 Very agitated Does not calm despite frequent verbal reminding of limits, requires physical restraints, bites
endotracheal tube
5 Agitated Frequent non-​purposeful movement or patient-​ventilator dys-​synchrony
4 Calm and cooperative Is calm, awakens easily, follows commands
3 Sedated Is difficult to arouse, awakens to verbal stimuli or gentle shaking but drifts off again, follows
simple commands
2 Very sedated Arouses to physical stimuli but does not communicate or follow commands, may move
spontaneously
1 Unarousable Has minimal or no response to noxious stimuli, does not communicate or follow commands

Despite years of use, the common agents used for side effect profile, with respiratory depression and
sedation (propofol and benzodiazepines) in the ICU systemic hypotension being the major manifestations.
have only recently been assessed by large, randomised These are often seen when benzodiazepines are used
controlled trials, many of which have significant limi- in combination with other sedating agents. All ben-
tations. This renewed interest came about as a result zodiazepines undergo extensive hepatic metabolism
of the introduction of dexmedetomidine. Sodium by cytochrome P450 enzymes, particularly CYP3A4
thiopentone and the other barbiturates are rarely used and CPY2C19. This leads to prolonged action in
outside of neurosurgical intensive care. They will not low cardiac output states due to diminished hepatic
be discussed in this chapter. extraction.
In general, the choice of sedative agent is
driven by: Midazolam
1. The specific clinical circumstances and sedation Midazolam is possibly the most popular of the ben-
goals for the individual patient including zodiazepines, with a relatively short median half-​life
haemodynamic compromise and end-​organ of 6.6 hours. It rapidly equilibrates across the blood-​
impairment; brain barrier, with duration of action of approxi-
2. The pharmacokinetic profile of the agent, mately 30 minutes after a bolus dose. Accumulation
including half-​life, context sensitive half-​time, in the setting of prolonged infusion is a common
metabolism and active metabolites, clearance and problem, especially in the elderly or in renal and
side-​effects; and hepatic failure. Metabolised by CYP3A4 to the equi-
3. Pharmacoeconomic factors and overall cost. potent active metabolite α-​hydroxy-​midazolam, it
competes with other drugs (particularly fentanyl) for
Benzodiazepines elimination.
These agents act at the α/​γ subunit of the GABAA
receptor to produce sedative effects, mostly by enhanc- Diazepam
ing neurotransmitter binding. They exhibit anxiolytic No longer used as an infusion in the ICU setting as it
and skeletal muscle relaxant properties, although their binds to PVC, diazepam has an elimination half-​time
sedative-​hypnotic effects are not as pronounced as roughly ~20-​fold that of midazolam (20–​50 hours),
those of some other classes of agent. Cheap and read- leading to gross prolongation of effect relative to other
ily available, there is some evidence that protracted sedatives. This issue is further compounded by its
use can lead to prolongation of mechanical ventila- multiple active metabolites, including desmethyldi-
tion and length of ICU stay, resulting in diminished azepam, n-​methyloxazepam and oxazepam. It cannot
popularity especially when sedation is required for be removed by dialysis and is extremely irritant when
more than 96 hours. They all demonstrate a similar extravasated.

14:31:24 33
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Section 3: Therapeutic Intervention

Lorazepam metabolic acidosis, hypertriglyceridaemia, arrhyth-


mia and escalating vasopressor and inotrope require-
More potent than midazolam or diazepam, lorazepam
ments. The risk of PRIS is increased by high infusion
is less lipid soluble, with a slower onset of effect fol-
rates (>70 μg kg−1 min−1) over prolonged periods, but
lowing a bolus dose. Uncommonly used in the ICU
it has been reported with low dose infusion. The inci-
setting relative to midazolam, the major advantage of
dence of PRIS has been estimated to be as high as 1%.
lorazepam is the lack of active metabolites, theoret-
The syndrome is difficult to diagnose as these patients
ically leading to more rapid offset when the drug is
frequently have multiple aetiologies for clinical insta-
ceased, although the elimination half-​life is still 8–​15
bility. Management involves early recognition and
hours. The clinical effects and duration of action are
cessation of the infusion, followed by supportive care.
still prolonged by hepatic dysfunction. Parenteral
This may not be sufficient to arrest its progress, and
formulations of lorazepam contain propylene glycol,
consequently, PRIS has a mortality of 33% in some
which has toxic effects. Thought initially to only occur
series.
with very high doses, it has been seen with cumulative
doses as low as 1 mg kg−1 day−1, manifesting as renal
dysfunction and metabolic acidosis. Both of these α2-​Adrenoceptor Agonists
occur frequently in the postcardiac surgical patient, Frequently used as second line agents, the α2-​agonists
and hence propylene glycol toxicity may be over- act on spinal and supraspinal α2-​adrenoceptors
looked as a cause. to accelerate the reuptake of adrenaline and nor-
adrenaline into the presynaptic nerve terminal, thus
Propofol mitigating their excitatory effects. This produces a
different quality of sedation to the more traditional
Propofol is an intravenous sedative that has a number
agents, typified by a more arousable state, with less
of useful properties for use in the ICU. It demonstrates
respiratory depression, as well as demonstrating anal-
sedative, hypnotic, anxiolytic, amnestic and anticon-
gesic (and hence opioid-​sparing) effects. These agents
vulsant effects, but is not an analgesic. Whilst acting
are rapidly finding a role in the management of the
as a GABAA agonist, it also acts at a number of other
ICU patient with delirium, both intubated and extu-
receptors in the CNS, such as glycine, nicotinic and
bated. However, despite the absence of respiratory
muscarinic cholinergic receptors.
depression, these agents have been known to cause
As a sedative, propofol is characterised by a rela-
loss of oropharyngeal tone at higher doses, and hence
tively rapid offset of action. This is due to its high lipid
close monitoring of patients receiving them is still
solubility and redistribution away from the site of
required to detect airway obstruction. In keeping with
action, but also its unusual hepatic and extra-​hepatic
their site of action, the α2-​agonists have cardiovascular
clearance. This results in a short context sensitive
side effects, particularly hypotension and bradycardia.
halftime (despite a prolonged duration of infusion),
As a result, α2-​agonists are relatively contraindicated
allows for rapid changes in sedation depth and facili-
in patients with haemodynamic instability or rate
tates daily sedation interruptions.
dependent cardiac output.
Despite its many positive qualities, the use of
propofol is not without risk, particularly in the post-
cardiac surgery patient. Similar to other sedative Clonidine
agents, it causes dose dependent respiratory depres- Despite its relatively unfavourable pharmacokinetics
sion, and hypotension due to systemic vasodilation. (with an elimination half-​life of 8 hours), clonidine
These changes are more pronounced in the patient can be administered as an intravenous infusion for
with pre-​existing circulatory instability. sedation in the ICU. The drug has an α2:α1 selectiv-
The propofol infusion syndrome (PRIS) is caused ity ratio of 200:1, and is classified as a partial agon-
by the inherent mitochondrial toxicity of the drug, ist by some as increasing doses lead to inevitable
and resembles the mitochondrial myopathies. The α1-​adrenoceptor stimulation. Because of the relatively
underlying pathophysiology is impaired entry of low α-​adrenoreceptor selectivity, a rise in blood pres-
long-​chain fatty acids, disruption of fatty acid oxida- sure due to α1 stimulation following a bolus dose is
tion and failure of the respiratory chain. Manifestation not uncommon, followed by a more sustained fall in
is uncommon, but presents with an unexplained blood pressure and heart rate. Rebound hypertension

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Chapter 16: Sedation and Analgesia

can be seen following sudden cessation of high dose theory, impairs weaning from mechanical ventilation,
infusion (>1.2 g day−1). and increases the risk of lower respiratory tract infec-
tion and deep venous thrombosis.
Dexmedetomidine In the long term, the experience of pain, and an
inability to communicate this, is a common source of
The D-​stereoisomer of medetomidine, this agent is a
psychological sequelae, even after physical recovery is
relatively recent addition to the ICU sedation arma-
complete. Those patients who have poorly controlled
mentarium, and is frequently used for the man-
pain during their ICU stay have a higher incidence of
agement of severe delirium. The drug has an α2:α1
post-​traumatic stress disorder, chronic pain and an
selectivity ratio of 1600:1, and is classified as a full ago-
overall poorer quality of life.
nist. Onset of action is within 15 minutes after starting
an infusion, with peak sedation reached at 60 minutes.
This may be hastened with the use of a loading dose, Monitoring Analgesia
albeit at a greater risk of haemodynamic instability. There has not been the same focus on analgesia moni-
The drug is rapidly redistributed and broken down by toring scales for the ICU patient as there has been
the liver to inactive metabolites, with an elimination on sedation scales in the literature. In many centres,
time of 2–​3 hours; however hepatic dysfunction can crude measures such as vital signs are still in use as the
prolong this. Some studies suggest dexmedetomidine primary means of assessing pain. Whilst such tools
offers decreased time to extubation and decreased may be occasionally of use in the more robust patient,
incidence of delirium relative to midazolam. the postcardiac surgical state is frequently typified by
The uptake of dexmedetomidine has been slow haemodynamic disturbance, meaning that the char-
relative to other agents. This is largely because of cost, acteristic nociceptive response of hypertension and
although the aforementioned benefits offered relative tachycardia may not be present despite the patient
to benzodiazepines may represent a cost saving when experiencing pain.
the drug is used routinely. Monitoring scales for analgesia do exist, and the
realisation that pain and agitation are potentially sep-
arate entities implies that clinical staff should employ
Analgesia separate rating scales and pharmacological strategies
The recognition that agitation and pain are separate in their management. In observational studies, the
entities in ICU patients has been incorporated into behavioural pain scale (BPS) (Table 16.3) and critical
recent clinical guidelines. This is an important dis- care pain observation tool (CPOT) (Table 16.4) score
tinction, as the intubated, sedated ICU patient may consistently well on psychometric evaluation. They
still have some awareness and recollection of their can be implemented quickly and have been shown to
experience, but no way of communicating unpleasant improve patient outcome when used routinely.
sensations to clinical staff. Most patients will experi-
ence pain as part of their ICU stay, whether this is due
to tracheal intubation, the postoperative state or pre-​
Planning Analgesia
existing conditions. This can have both short-​term A complete overview of all the factors in planning
and long-​term consequences. an effective analgesic strategy for a critically ill post-
In the short term, pain results in an acute stress operative patient is beyond the scope of this chapter.
response, with increases in circulating catechola- However, some general principles are worthy of dis-
mines, increasing cardiac afterload, heart rate and cussion when planning an analgesic regimen, and
contractility, all of which increase myocardial oxygen have been highlighted in recent consensus guidelines.
consumption. Tissue perfusion may be impaired due 1. A therapeutic plan and goal of analgesia should be
to peripheral vasoconstriction. The release of other established and communicated to care givers.
stress hormones such as glucocorticoids results in 2. Assessment of pain and response to therapy
a hypermetabolic response, with increased rates of should be performed regularly.
lipolysis and glycolysis being compounded by insu- 3. The level of pain reported by the patient is the
lin resistance and hyperglycaemia, with resultant standard for assessment but subjective observation
impaired wound healing. The presence of a catabolic and physiological indicators may be used when
state increases the risk of disuse myopathy, and, in the patient cannot communicate.

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Section 3: Therapeutic Intervention

Table 16.3  Behavioural pain scale, scores in the range 4–​12

Item Description Score


Facial expression Relaxed 1
Partially tightened (i.e. brow lowering) 2
Fully tightened (i.e. eyelid closing) 3
Grimacing 4
Upper limb movements No movement 1
Partially bent 2
Fully bent with finger flexion 3
Permanently retracted 4
Compliance with mechanical ventilation Tolerating movement 1
Coughing but tolerating ventilation for most of the time 2
Fighting ventilator 3
Unable to control ventilation 4

4. Sedation of critically ill patients should only be oxycodone), morphine has formed the mainstay of
commenced after providing adequate analgesia opioid therapy for decades. It has relatively low lipid
and treating reversible physiological causes. solubility, and hence the onset of effect following a
Needless to say, the involvement of a specialist acute bolus dose is between 15 and 3​ 0 minutes with peak
pain service for those patients with complex or diffi- effect at 45–​90 minutes. The drug is metabolised via
cult to treat pain is invaluable (see Figure 16.3). hepatic conjugation into morphine-​ 3-​
glucuronide
(a metabolite with known neurotoxic side effects),
morphine-​6-​glucuronide (an active metabolite con-
Opioid Analgesia siderably more potent than morphine) and normor-
Currently, opioids are recommended as the first line phine. These metabolites are then excreted unchanged
agents in the management of non-​neuropathic pain in the urine, and dose reduction is required in patients
in the critically ill. This is largely because of their rela- with renal and hepatic dysfunction.
tive efficacy and predictable side effect profile. The
analgesic effects of opioids are achieved through the
μ1-​receptor, which is found at a variety of spinal and Oxycodone
supraspinal locations. Indeed, pure μ1-​receptor stimu- Another phenanthrene similar to morphine, oxy-
lation provides excellent pain relief. However, there is codone is rarely used in the ICU setting due to the
more than one type of opioid receptor, and stimulation expense of the parenteral formulation. However, it
of the μ1-​receptor and these additional sites leads to the undergoes hepatic conjugation to inactive or weakly
characteristic acute side effects of respiratory depres- active metabolites, noroxycodone and oxymorphone,
sion, sedation, reduced gut motility and bradycardia, meaning that accumulation in renal failure is not as
and the longer term issues of tolerance, dependence pronounced.
and opioid induced hyperalgesia. Consequently, opi-
oids should always be prescribed with caution, and the Fentanyl
use of non-​opioid analgesia considered in all cases. All
Fentanyl is a potent phenylpiperadine, or synthetic
opioids exhibit similar analgesic efficacy and are asso-
opioid. It has onset of action within 3 minutes due to
ciated with similar outcomes (duration of intubation,
lipid solubility 700–​800 fold, and potency 100 fold,
length of stay) when titrated to similar endpoints.
compared with morphine. Consequently, bolus doses,
if not administered with caution, have a greater poten-
Morphine tial to cause sedation and respiratory depression.
Based around three benzene rings, and hence clas- In bolus doses, the duration of action (20 minutes)
sified as a phenanthrene (along with codeine and is limited by redistribution away from the effect site.

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Chapter 16: Sedation and Analgesia

Table 16.4  Critical care pain observation tool (CPOT), scores in the range 0–​8

Indicator Description Score


Facial expression No muscular tension observed Relaxed, neutral 0
Presence of frowning, brow lowering, orbit Tense 1
tightening and levator contraction
All of the above plus eyelids tightly closed Grimacing 2
Body movements Does not move at all Absence of movement 0
Slow, cautious movements, touching or Protection 1
rubbing the pain site, seeking attention through
movements
Pulling tube, attempting to sit up, moving limbs, Restlessness 2
thrashing, not following commands, striking at
staff, trying to climb out of bed
Muscle tension No resistance to passive movements Relaxed 0
Resistance to passive movements Tense, rigid 1
Strong resistance to passive movements, inability Very tense or rigid 2
to complete them
Compliance with the ventilator (if Alarms not activated, easy ventilation Tolerating ventilator or 0
intubated) movement
Alarms stop spontaneously Coughing but tolerating 1
Asynchrony; blocking ventilation, alarms Fighting ventilator 2
frequently activated
OR
Vocalisation (extubated patients) Talking in normal tone or no sound Talking in normal tone or no 0
sound
Sighing, moaning Sighing, moaning 1
Crying out, sobbing Crying out, sobbing 2

However, with a prolonged infusion, these periph- is desirable, or in those patients at high risk of exces-
eral sites (particularly adipose tissue) may become sive opioid accumulation. However, possibly due to
saturated, leading to a depot of drug and a marked its potency, remifentanil carries a high risk of opioid
increase in half-​life once these compartments equili- induced hyperalgesia, and many studies have sug-
brate with the plasma. Fentanyl is often recommended gested a higher incidence of chronic pain after using
in the setting of renal impairment due to the relative remifentanil in the operative setting, including in car-
lack of active metabolites. The accumulation of nor- diac surgery. This risk may also translate to the ICU.
fentanyl has, however, been reported, and is a poten-
tial cause of toxic delirium. Non-​opioid Analgesia
Whilst current guidelines recommend opioids as first
Remifentanil line therapy for the management of nociceptive pain
Remifentanil has been used in anaesthetic practice in the ICU, multiple other classes of analgesic agents
for a number of years. An extremely potent opioid, exist. These drugs are useful, for two reasons:
remifentanil has a unique metabolic pathway, being 1. Minimisation of opioid dose, and hence opioid
rapidly metabolised by plasma esterases. This lim- related side effects; and
its the redistribution of the drug to peripheral com- 2. Management of pain that is not responsive to
partments and keeps the half-​life of the drug at 4–​5 opioids.
minutes, regardless of the duration of the infusion. It is assumed that the mechanism of action and side
Consequently, it is ideal for those patients in whom effect profile of commonly used drugs such as para-
rapid weaning of sedation to assess neurological status cetamol and the non-​steroidal anti-​inflammatories are

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138

Anaesthetic and surgical handover from theatre


Actively rewarm if temperature < 36 ºC
Is patient at high risk of severe post-operative pain Optimise cardiac output
(i.e. opioid tolerant, history of substance abuse, history Assess chest tube drainage
of chronic pain)?

Yes No

Administer IV morphine bolus


Commence or continue (0.05–0.1 mg kg–1) unless
opioid infusion patient has already received
(fentanyl or morphine) up to 0.3 mg kg–1 of IV
morphine in the preceding 24
hours
Consider the possible causes for
Administer IV morphine altered level of consciousness
VAS ≤ 3?
bolus (0.05–0.1 mg kg–1) or agitation including inadequate
Stop sedation and assess
analgesia
level of sedation and
analgesia

.018
No Yes

Has patient received adequate Yes RASS 0–1? No


opioid loading (i.e. up to Switch to or maintain oral analgesic regimen:
No
0.3 mg kg–1 of IV morphine) First line: Paracetamol, 1g PO q6h
in the preceding 24 hours?
Second line: Slow release oral opioid BD +
immediate release oral opioid q2 - 4h PRN

14:31:24
Yes Third line: Tramadol PO 1–2 mg kg–1 q8h PRN

Consider alternate analgesic


strategies if appropriate:
Tramadol IV 1–2 mg kg–1
Whilst in ICU, every hour:
PCA opioid (if pain is opioid
responsive) Assess respiratory frequency
Ketamine 0.1 mg kg–1 ± infusion Assess VAS
Monitor analgesic requirements
(particularly opioids)
Monitor chest drain and urine output

Figure 16.3  This algorithm presumes that the patient returns to the ICU on some form of sedation (i.e. propofol, 1–​2 mg kg−1 hour−1, and has received some form of opioid loading in the
operating theatre (i.e. morphine bolus, morphine infusion, etc.), and that the patient is receiving regular paracetamol (1 g NG or intravenous q6h). Unless stated otherwise, all medications
should be dosed according to ideal body weight. It is valid only for management of pain in the ICU.
139

Chapter 16: Sedation and Analgesia

well understood, and hence they will not be discussed used in anaesthetic practice, although the use of such
here. However, there are other classes of drug that are a dose in the awake patient increases the risk of side
less commonly used that should be examined. effects. Rapid administration causes nausea and vom-
iting, and hence slow administration over 20 minutes
Ketamine is recommended.
A phencyclidine derivative, ketamine acts via block- In equianalgesic doses, tramadol is far less likely
ade of the n-​acetyl-​d-​aspartate (NMDA) receptor. It to cause respiratory depression than morphine.
effectively has two roles: Respiratory depression has only been observed in
patients with severe renal impairment. Tramadol also
1. Prevention and management of pain due to
has a reputation for provoking seizures. However,
‘central sensitisation’, particularly neuropathic
when given within the recommended dose limits,
pain, severe ‘acute’ pain and opioid resistant
tramadol does not increase seizures relative to other
pain; and
analgesic agents.
2. Reducing the overall dose of opioid required in a
Due to the enhancement of 5-​ HT release and
given pain situation.
inhibition of reuptake, tramadol is a theoretical
At relatively low doses of 0.1–​0.2 mg kg−1 hour−1, cause of serotonergic syndrome. In practice, this is
ketamine acts primarily as an analgesic. Bolus doses rare. Caution should be exercised when prescribing
of 0.1–​0.25 mg kg−1 can be used as a loading dose or tramadol in the elderly, in patients with renal impair-
as rescue therapy. Beyond this infusion rate, adverse ment, and with concurrent high doses of serotonergic
effects begin to emerge with relatively little incremen- medications, particularly selective serotonin reuptake
tal analgesic benefit. Vivid dreams and hallucinations inhibitors, noradrenaline-​serotonin reuptake inhibi-
are often limiting factors in its use. These effects are tors and monoamine oxidase inhibitors. Note that
entirely dose dependent, and a cessation of the infu- drugs that block the effect of serotonin (particularly
sion will reliably eliminate neurocognitive phenom- the 5-​HT3 receptor blockers such as ondansetron) will
ena within the drug half-​life of 1–​2 hours. The drug is diminish the analgesic efficacy of tramadol.
metabolised to norketamine, an active metabolite that
is renally excreted. Regional Analgesia
At high bolus doses (1–​2 mg kg−1), ketamine can First described in 1984, high thoracic epidural anal-
be used to induce anaesthesia. It is often popular in gesia (HTEA) in cardiac surgery has found sporadic
trauma situations as it affords a degree of haemody- acceptance. Proponents argue that the diminished
namic stability relative to other agents by increasing catecholamine release and central neuraxial block-
the peripheral effects of circulating catecholamines. ade attenuates the sympathetic response to the sur-
However, in a state of maximal sympathetic tone, ket- gical insult, leading to a diminished inflammatory
amine cannot increase these effects further, and may response, superior analgesia and earlier postopera-
act as a negative inotrope. Ketamine also preserves tive extubation. It is also argued that the postulated
respiratory drive, although the airway may be compro- risk of epidural haematoma with cardiopulmonary
mised by increased muscle tone and hypersalivation. bypass has not eventuated, provided the epidural is
placed sufficiently in advance of systemic heparini-
Tramadol sation. Depending on the preference of surgeon and
A cyclohexanol derivative, tramadol has a triphasic anaesthetist, patients having cardiac surgery may
mechanism of action. Given intravenously, tramadol occasionally arrive in the intensive care unit with
inhibits the reuptake of noradrenaline and serotonin an epidural catheter in situ, delivering a mixture of
(5-​HT), enhancing the action of the descending nox- local anaesthetic and opioid according to local pref-
ious inhibitory control system. In addition, one of its erence. Serious complications of epidural analgesia,
metabolites (M1 or O-​desmethyltramadol) is a weak such as epidural haematoma or abscess, will often
opioid agonist. This opioid effect is enhanced with oral manifest with lower limb neurological signs. Hence,
administration due to hepatic first-​pass metabolism. sedation should be titrated to allow continuous
Intravenously, tramadol is administered as a bolus assessment of lower limb motor function as the con-
dose of 1–​2 mg kg−1 (based on ideal body weight) every sequences of late detection of such a complication are
6 hours. A loading dose of 3 mg kg−1 is occasionally catastrophic.

14:31:24 39
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Section 3: Therapeutic Intervention

A well-​ functioning, high thoracic epidural will The association with prolonged weakness has been the
inevitably cause a degree of sympathetic blockade, biggest factor in the decline in popularity of neuro-
which may manifest as hypotension. This can nor- muscular blockade. This phenomenon may be more
mally be managed with judicious intravascular vol- common when aminoglycoside antibiotics or cor-
ume replacement; however, particularly in patients ticosteroids are administered concurrently, because
unable to tolerate further fluid therapy, vasopressors of their interaction at the neuromuscular junction.
may be required. Clinicians may be tempted to stop Spontaneous muscle breakdown during total muscle
the epidural as part of managing hypotension. It is inactivity has also been postulated.
worth noting that the prolonged half-​life of the local In practice, neuromuscular blockade can be a
anaesthetic agents commonly used in epidural anal- useful, albeit last line, clinical tool. This is especially
gesia (ropivacaine, bupivacaine and levo-​bupivacaine) true in the presence of significant, persistent hypoxia.
means that the benefit of such an action will not be Neuromuscular blockade in this scenario reduces
reaped for some hours, and that it is often best to initi- VO2, and hence reduces tissue perfusion requirements
ate a more definitive plan from the outset whilst con- in skeletal muscle. Patient synchronisation with the
tinuing the epidural. ventilator is also improved.
Regional analgesia is practised commonly in tho- The choice of drug for neuromuscular blockade
racic surgery, where a continuous infusion of local is often clinician dependent; however, the benzyliso-
anaesthetic provides excellent analgesia of the sur- quinoliums (atracurium and cisatracurium) are often
gical site, and minimises the use of oral or intrave- preferred as they undergo organ independent metab-
nous opioid, with the associated risk of respiratory olism. Rather than undergoing hepatic modifica-
depression. For unilateral thoracic surgery where the tion, these drugs are hydrolysed by plasma esterases,
pleura has not been breached adjacent to the verte- or undergo Hoffman elimination. This is a pH and
bral column, many authors advocate a paravertebral temperature dependent process that is prolonged by
block, arguing that the quality of analgesia provided hypothermia and acidosis. The breakdown products
is just as good, with a lower incidence of common of this process (in particular laudanosine) can be neu-
side effects such as hypotension, urinary retention, rotoxic, but at doses well in excess of those encoun-
nausea and vomiting. tered clinically.

Neuromuscular Blockade Further Reading


In the new era of ‘daily sedation interruptions’ and Barr J, Fraser GL, Puntillo K, et al. Clinical practice
‘sedation minimisation’ , the indications for neuro- guidelines for the management of pain, agitation and
delirium in adult patients in the intensive care unit.
muscular blockade (beyond short-​term paralysis for
Critical Care Medicine. 2013; 41: 264–​306.
invasive procedures such as intubation, bronchoscopy,
Macintyre PE, Scott DA, Schug SA, et al. (Eds). Acute
etc.) in the ICU are limited. Effectively, they can be
pain management in intensive care. Acute Pain
summarised into three categories: Management: Scientific Evidence, 3rd Edition.
1. Facilitation of invasive modes of ventilation, when Melbourne: Australian and New Zealand College of
they are not tolerated by an adequately sedated Anaesthetists and Faculty of Pain Medicine, 2010,
Section 9.8, pp. 286–​289.
patient.
2. Open chest: surgical bleeding or indwelling Reade MC, Finfer S. Sedation and delirium in the intensive
care unit. New England Journal of Medicine. 2014;
vascular cannulae may necessitate the patient’s
370: 444–​454.
chest being left open for a short time and the
Shehabi Y, Bellomo R, Mehta S, et al. Intensive care
patient being kept completely still.
sedation: the past, present and future. Critical Care.
3. Raised intracranial pressure or status epilepticus. 2013; 17: 322–​329.

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Chapter 16: Sedation and Analgesia

MCQs
1. Which of the following represents the ‘ICU triad’ of (d) Diminished haemodynamic perturbation
sedatoanalgesia? (e) Decreased myocardial oxygen demand
(a) Pain, neuromuscular blockade, sedation 4. Which of the following is the superior modality for
(b) Analgesia, sedation, delirium the monitoring of sedation in the standard cardiotho-
(c) Delirium, agitation, pain racic ICU patient?

(d) Agitation, sedation, pain (a) Bi​spectral index

(e) Analgesia, neuromuscular blockade, sedation (b) Auditory evoked potentials

2. Which of the following determines the time taken for (c) Multichannel electroencephalography
an intravenous infusion of a drug to reach steady state? (d) Richmond agitation-​sedation scale
(a) Half-​life (e) Glasgow coma score
(b) Clearance 5. Poorly controlled postoperative pain in the ICU set-
(c) Dose rate ting leads to an increased long-​term incidence of
which of the following:
(d) Lipid solubility
(a) Major depressive disorder
(e) Molecular weight
(b) Post-​traumatic stress disorder
3. Which of the following statements is NOT true? In
general, lighter levels of sedation lead to: (c) Complex regional pain syndrome

(a) Shorter duration of mechanical ventilation (d) Drug induced psychosis

(b) Decreased ICU length of stay (e) Improved quality of life

(c) Increased patient-​ventilator dys-synchrony

Exercise answers are available on p.468. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ

14:31:24 41
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Section 3 Therapeutic Intervention

Mechanical Ventilation
Chapter

17 Anja Schneider and Erik Ortmann

Introduction Limiting Phase
Most patients admitted to the cardiothoracic criti- The limiting variable defines the length or size of
cal care unit will require a form of mechanical ven- inspiratory gas flow. It can also be set to a certain pres-
tilation at some point during their journey. However, sure, volume, flow or time. The type of waveform pro-
the spectrum of indications is wide and ranges from duced for pressure, flow and volume defines a breath
patients on a ‘fast-​track’ concept, who are only being delivery. Depending on the chosen limiting vari-
ventilated for a very short period of time directly after able the ventilation pattern may be one of the three
surgery, to very complex patients with severe cardio- following types:
vascular and respiratory failure due to their under-
lying disease or the impact of major cardiothoracic Volume controlled: A constant volume and constant
surgery. Therefore a sound knowledge of the various flow waveform; the pressure waveform will vary
techniques of invasive and non-​invasive mechanical depending on lung characteristics.
ventilatory support is essential to develop the appro- Pressure controlled: The pressure waveform has a
priate strategy for the individual patient and their preselected specific pattern but volume and flow
current clinical state. will vary depending on lung characteristics.

Technical Aspects Time controlled: Pressure, volume and flow


The basic principle of modern intensive care ventila- waveforms all vary depending on lung
tors is a positive pressure gradient, which creates gas characteristics.
flow into the lungs during inspiration. Expiration is
usually passive due to fall of the pressure gradient to Cycling Phase
an expiratory level (PEEP). The gas flow is delivered The cycling variable starts the expiration phase by end-
either invasively through an endotracheal tube or a ing inspiratory gas flow. This may also be pressure,
tracheostomy cannula, or non-​invasively via a tight volume, flow or time. For example the ventilator may
fitting facemask or similar device. cycle to the expiratory phase after a certain time (i.e.
Traditionally ventilation modes have been preset frequency for mandatory ventilation), when the
described as either volume or pressure controlled. pressure reaches a certain set maximum during inspi-
Modern ventilators however provide a variety of dif- ration, or cycle to the expiratory phase when flow falls
ferent sophisticated modes, some of which combine to a set level (commonly 5 l/​min) or percentage (com-
characteristics of both, and are controlled by the so-​ monly 25%) of peak flow (patient trigger).
called ‘phase variables’ triggering, limiting and cycling. By combining various settings to the different
phase variables, modern ventilators can create a large
Triggering Phase number of ventilation patterns, which can be further
The triggering variable sets the start of inspiratory gas individualised to specific clinical situations. These are
flow and can be time, pressure, flow or volume. Thus all based on three types of breath:
the trigger can be controlled by the ventilator, the A mandatory breath is one in which the ventilator
patient, or a combination of both. When time is the does all the work of breathing and controls the
trigger variable, the breath is considered mandatory. transition between phases of the breath.

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Chapter 17: Mechanical Ventilation

An assisted breath is one where the patient begins no patient effort is detected during a set time
or ‘triggers’ inspiration but the ventilator window, a mandatory inspiration can be triggered
controls the inspiratory phase and the cycling of (time trigger) to guarantee a certain ventilation
inspiration to expiration. frequency.
A spontaneous breath is one in which the patient Respirator triggered: A mandatory breath is
controls the transition between all breathing triggered by set parameters such as inspiratory
phases. time, frequency and I:E (inspiration:expiration)
ratio. The timing is obligatory and the patient has
Ventilation Modes no influence.
Nomenclature of modes of ventilation has become
confusingly complex, with different names being used Expiration
for similar modes by different manufacturers. We want The variable that ends inspiratory gas flow can be
to review the most common terms and explain the either flow or time:
technical principles of the different ventilator modes