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Clinical Examination and

Applied Medicine
Clinical Examination and
Applied Medicine
Pulmonology Series

Volume II

Mushtaq Haroon

MOMENTUM PRESS, LLC, NEW YORK


Clinical Examination and Applied Medicine: Pulmonology Series,­Volume II

Copyright © Momentum Press, LLC, 2020.

All rights reserved. No part of this publication may be reproduced,


stored in a retrieval system, or transmitted in any form or by any
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except for brief quotations, not to exceed 400 words, without the prior
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First published in 2020 by


Momentum Press, LLC
222 East 46th Street, New York, NY 10017
www.momentumpress.net

ISBN-13: 978-1-94944-947-1 (paperback)


ISBN-13: 978-1-94944-948-8 (e-book)

Momentum Press Health Education ­Collection

Cover and interior design by Exeter Premedia Services Private Ltd.,


Chennai, India

First edition: 2020

10 9 8 7 6 5 4 3 2 1

Printed in the United States of America.


This book is dedicated to my loving wife, Romana.
My daughters Sundus, Saima, and Anum.
Abstract
This is the second in the series of books dealing simultaneously with exam-
ination technique with detailed pathophysiological principles, ­differential
diagnosis, and clinical interpretation, along with correlated and applied
medicine about the common diseases. A medical student or a postgraduate
doctor studying for higher exam will learn to take a good history, examine
the patient, and find relevant applied medical knowledge, which is needed
for assessment of the patient. It should also serve as an invaluable collec-
tion of facts to get through undergraduate or ­postgraduate examination.
This book attempts to answer pertinent questions such as how and
why about clinical examination while providing relevant information
needed for a thorough bedside assessment. It is hoped that the book will
not only serve to make a correct diagnosis by examination, but also give
relevant differential diagnosis, and localize the disease and, hopefully,
define its cause. The book intends to fill this gap and inspire the reader to
gain confidence not only in the performance of the examination, but also
to answer most bedside queries and problems. It will hopefully serve as an
indispensable resource for preparation of undergraduate and p ­ ostgraduate
viva and bedside short and long case examination.
Volume II of this book includes a section on common pulmonary
investigations, blood gases, pulmonary functions, and radiology. A wealth
of diagrams and figures along with brief clinical notes has been included
to stimulate understanding and learning. As a further stimulus for learn-
ing, a picture test with MCQ and a short applied medical note have been
added. The book is not a replacement for standard textbook on the sub-
ject, but it is hoped that it would help mastering relevant knowledge and
clinical skills to diagnose and assess the patient’s problem at the bedside
and also prepare for undergraduate and postgraduate examination.

Keywords
history taking; respiratory examination; pulmonary clinical examination;
bedside assessment; pulmonary diseases; chest diseases; lung diseases;
­pulmonology images; COPD; asthma; X-ray chest; pulmonary func-
tions; ABG; pulmonary investigations; pulmonary infections; chest dis-
eases; interstitial lung disease; tuberculosis; pulmonary embolism; pleural
­diseases; lung tumor; obstructive airway disease; restrictive airway disease
Contents
Forewordxiii
Prefacexv
Acknowledgmentsxvii

TopicsPage
Section I 1
Pulmonary Investigations 1
Arterial Blood Gases (ABG) 4
Normal Values for ABG 5
Summary of Acid-Base Disturbances 6
Blood Gas Values and Nomenclature 7
Academia and Alkalemia 7
Metabolic and Respiratory Compensation 7
Simple Acid-Base Disturbance and Compensation 8
Examples of Mixed Acid-base Disturbances 8
Respiratory Acidosis 8
Respiratory Alkalosis 9
Metabolic Acidosis 11
Metabolic Alkalosis 12
Hypoxemia in Relation to the A-a Gradient 13
Pulmonary Function Tests (PFTs) 13
Common Indication of PFT 14
Types of PFTs 14
Utility of PFTs 15
FEV115
Obstructive disorders 16
Restrictive disorders 16
Walking test 17
Pulmonary diffusion capacity 17
Causes of Reduced TLco18
Causes of Increased TLco18
x Contents

Respiratory Failure 18
Section II 21
Radiology Section 21
Normal X-ray chest 21
Sequence of Examination 21
Classification of Opacities 23
Classification of Cavities 23
Causes of Pulmonary Cavitation 23
Simple cavity 23
Classification of Linear Shadows 24
Pulmonary nodules 24
Causes of Pulmonary Nodules 25
Evidence of Benign Nature 26
Evidence of Malignant Nature 26
Honeycombing26
Diffuse Miliary Pattern 27
Some Important X-rays 27
Acute chest syndrome 27
Acute respiratory distress syndrome (ARDS) 28
Aortic aneurysm 29
Aspergillosis30
Azygos lobe 31
Behcet’s disease 31
Bilateral infiltrates 31
Bronchiectasis33
Bronchogenic carcinoma 33
Bronchogenic cyst 34
Bronchopneumonia35
Cardiomegaly35
Cavitary lesions 36
Collapsed lung 38
Diaphragmatic pathologies 38
Emphysema39
Gas Under the Diaphragm 41
Heart failure 42
Hilar shadows 43
Contents xi

Hydatid disease 44
Lung abscess 44
Mediastinal lymphadenopathy 45
Mesothilioma46
Miliary shadowing 47
Pericardial effusion 48
Pleural effusion 49
Unilateral50
Subpulmonic50
Massive52
Pneumonia52
Pneumothorax53
Hydropneumothorax54
Tension pneumothorax 55
Pulmonary alveolar microlithiasis 55
Causes of Pulmonary Calcification 55
Pulmonary edema 56
Bedside chest ultrasound 56
Pulmonary embolism 58
Pulmonary hemorrhage 59
Causes of Diffuse Alveolar Hemorrhage 59
Pulmonary fibrosis 59
Pulmonary nodules 61
Retrosternal goiter 63
Sarcoidosis63
Silicosis65
Tuberculosis66
Latent tuberculosis 67
Section III 69
Picture Quiz, MCQs, with Applied Medicine 69
Acanthosis nigricans 69
Achalasia72
Ankylosing spondylitis 74
Digital clubbing 76
COPD79
Hypoxia and cyanosis 83
xii Contents

Guillain-Barré syndrome 86
Interstitial lung disease 89
Lambert-Eaton myasthenic syndrome 91
Lung abscess 94
Miliary tuberculosis 97
Pulmonary nodules 100
Pancoast tumor and Horner’s syndrome 103
Pectus excavatum 106
Pericardial disease 108
Pleural effusion 111
Pneumococcal pneumonia 114
Pneumonia117
Pott’s disease 121
Pulmonary hypertension 123
Pulmonary nodules 126
Pulmonary sarcoidosis 129
Pulmonary tuberculosis 132
Rheumatoid Lung 136
SLE139
Supraclavicular Lymphadenopathy 141
SVC Obstruction 144
Thoracic outlet syndrome 146
Tracheal Stenosis 149
Tuberculous Lymphadenitis 151

List of Contributors 153


About the Author 155
Index157
Foreword
Medicine is expanding at such rapid pace in our times that it is difficult
to keep up with the latest developments. The author has made every effort
to update the contents while keeping them as concise and pertinent as
possible. Examination skills are described along with applied background
knowledge needed to evaluate the patient with a note on management in
Volume I. Pathophysiological principals are explained along with differ-
ential diagnosis. In Volume II, radiology with MCQs and picture test and
applied notes on different respiratory disease are given to help acquire and
retain knowledge. Both volumes complement each other to prepare for
undergraduate and postgraduate examinations.
Preface
The pulmonology series of clinical examination and applied medicine
is the second in the series of books dealing with examination tech-
niques, pathophysiological principles, and clinical interpretation, besides
­delivering ample details of applied medicine about the common diseases.
A medical student or a postgraduate doctor studying for higher exam will
find relevant applied medical knowledge that is needed for assessment of
the patient. It should also serve as an invaluable collection of facts to get
through undergraduate or postgraduate examination.
History-taking and clinical examination form the foundation of diag-
nosis and pave the way for the correct management. Clinical examination
is an essential prerequisite for a medical student entering the clinical side
of his or her undergraduate career. It can haunt him or her at all stages of
his or her undergraduate and postgraduate life. It forms the basis of his
clinical practice during the professional career.
Pathophysiological principles of examination, where relevant, are
explained for a sound understanding. Once the pathophysiological basis
of signs and symptoms is understood, it can be applied to a variety of
clinical situations in different patients. The process then becomes one
of deduction, application of principle, and logical outcome that is the
foundation and cornerstone of knowledge. This book attempts to answer
pertinent questions such as how and why about clinical examination
and bedside medicine. Further, interpretation of the physical finding
is important. It is not enough to know that there is a lesion, but it is
important to localize it and find a possible cause. The investigations and
treatment plan then depend on proper differential diagnosis. The book
intends to fill this gap and provide some food for thought and inspire the
reader to gain confidence not only in the performance of the examina-
tion, but to answer most bedside queries and problems. It will hopefully
serve as an indispensable resource for preparation of undergraduate and
postgraduate viva and bedside short and long case examination.
This new edition has been thoroughly revised and updated, which
includes a wealth of X-ray along with CT and MRI scans. A wealth of
xvi Preface

diagrams, figures, and photos has also been included to stimulate under-
standing and learning. As a further stimulus for learning, picture test and
MCQs with brief notes have been added.
The book is not a replacement for standard textbook on the subject,
but it is hoped that it would help the objective of transferring relevant
clinical knowledge with the arsenal to solve bedside problems of patients
efficiently and appear in undergraduate and postgraduate examination.
Dr. Mushtaq Haroon
MBBS (Pb); MCPS (Pak); MRCP (UK)
FRCP (London)
Acknowledgments
I am ever grateful to the Lord almighty, Allah Subhana wa Taala, for
granting me the knowledge and strength to reproduce what I have
learned through my teachers, colleagues, and students of Allama Iqbal
Medical College, Lahore; King Edward Medical University, Lahore; and
­Quaid-i-Azam Medical College, Bahawalpur. I have found a conducive
and friendly environment at the Pakistan Kidney and Liver Institute,
Lahore, where I am presently working. The task would never have been
possible without the blessings of the Lord Almighty.
Section I

Pulmonary Investigations
The choice of investigations always depends on the differential diagnosis
and is tailored to the patient’s need. One must seriously question the
need of an investigation if it is not going to help in the diagnosis, assist
in ­prognosis, or follow-up or alter the management. Therefore, always
consider the cost and the need.

1. Routine investigations like complete blood examination, urinalysis,


electrolytes, and so on.
2. X-ray of the chest in different views (PA, AP, lateral or decubitus)
is the baseline test used in symptomatic cases or as screening test,
especially in TB endemic areas.
3. Sputum examination for microscopy, culture, and cytology forms
the basis for the diagnosis for respiratory infections and choosing the
correct antibiotic and also detecting cancer cells, mycobacteria, fungi
in the sputum. Hemosiderin-laden macrophages may be seen in dif-
fuse alveolar hemorrhage and Charcot–Leyden crystals in ­allergic
asthma (associated with eosinophilia).
4. Nucleic acid amplification (NAA) using polymerase chain reac-
tion (PCR) to detect mycobacterium tuberculosis (MTB) has now
become standard. The Xpert MTB/RIF test not only detects MTB,
but rifampicin-resistant strains as well (it needs 131 bacilli/ml
compared to direct smear that needs 10,000 bacilli/ml). PCR
testing is also useful for diagnosis of pneumococcal pneumonia,
H1N1, MERS CoV, SARS, influenza and parainfluenza infection,
mycoplasma, legionella, bartonella, pneumocystis, aspergillosis,
­
­pertussis, respiratory syncytial virus, and so on.
5. Pulmonary function tests include a battery of tests, including PEFR,
FEV1, FVC, FEV1/FVC, lung volumes, flow volume curves, air-
way resistance, and gas transfer. They are used to assess shortness
2 Clinical Examination and Applied Medicine

of breath and can differentiate obstructive from restrictive airway


diseases. They are also used to follow the progression of disease or
effect of therapy.
6. Pulse oximetry provides noninvasive continuous monitoring of oxy-
gen saturation.
7. Blood gas analysis provides valuable information regarding acid and
base disorders besides giving PaO2, PaCO2, pH, and HCO3 values.
8. Allergic skin testing, Mantoux test and Kveim test.
9. D-dimer to detect disseminated intravascular coagulation for pul-
monary embolism (and a negative test indicative against the diagno-
sis of pulmonary embolism).
10. Provocation tests for bronchial hypersensitivity are done for detect-
ing hyper-reactive airway disease and bronchial asthma. A 20 percent
decline in FEV1 is considered a positive test.
11. Immunological tests as required.
12. Specific tests and serology.
13. Thoracic ultrasound is best used to diagnose and help aspirate small
pleural effusions or pleural lesions.
14. Thoracic CT scan.
15. Magnetic resonance imaging (less valuable than CT scan in assessing
lung parenchyma). It is good for assessing apex lung tumors, paraspi-
nal masses, mediastinum, and chest wall lesions. It may also be done
when CT scan cannot be done in renal failure or for the detection of
arteriovenous malformations or pulmonary sequestration.
16. Positron emission tomography can help differentiate benign from
malignant lesions (malignant lesions take up much more glucose). PET
scan can successfully pick up involved lymph nodes and metastasis.
17. Bronchoscopy is commonly indicated for assessment of suspected
lung nodule or tumor, persistent cough, or hemoptysis. It may also
be indicated in atelectasis, diffuse lung diseases, and lung infections.
Therapeutically, it can be used in atelectasis with retained secretions,
removal of foreign bodies, dilatation of airway stenosis, and obstruc-
tive lesions (laser therapy or stent). Bronchoscopy is also valuable in
the staging of lung cancer.
18. Ventilation perfusion lung scans (V/Q scan) is usually done for sus-
pected pulmonary embolism.
Pulmonary Investigations 3

19. Pulmonary angiography with CT (CT angiography) is done pri-


marily to detect pulmonary embolism or sometimes to detect
­arteriovenous fistula and malformations.
20. Bronchial angiogram is performed for massive pulmonary hemor-
rhage with hemoptysis to stop bleeding via embolotherapy.
21. Bronchial aspirate or lavage is done with about 100 ml of sterile
­normal saline into the involved segment and aspirated back for
cytology, chemical analysis, and cultures. Normally, more than
­
90 percent cells are macrophages and less than 10 percent lympho-
cytes with no or less than 1 percent polymorphs. BAL is useful in the
diagnosis of alveolar proteinosis, pulmonary Langerhans cell granu-
lomatosis, lymphangitic pulmonary metastasis, and in immunocom-
promised patients, including AIDS.
22. Pleural tap can be diagnostic or therapeutic. The fluid is usually sent
for biochemical analysis (protein, LDH), hematology (total WBC
and differential counts), histopathology (cytology for malignant
cells), microbiology (gram stain and AFB stain and culture both
­aerobic and anaerobic, including MBTB).
23. Pleural biopsy is useful if the pleural fluid examination is not
­diagnostic. It can detect TB in up to 80 percent cases and m
­ alignancy
in up to 60 percent cases if done under good expertise.
24. Lymph node biopsy is done not only to detect TB or lymphoma,
but metastatic disease or other diseases associated with generalized
lymphadenopathy.
25. Lung scan (gallium) is used to detect inflammation or cancer in the
body (radiation exposure less than CT scan). A gallium scan of the
lung may be used for the diagnosis of sarcoidosis and some respira-
tory infection or tumors. A technetium-99m scan is sometimes done
for detecting diffuse pulmonary calcification seen rarely in chron-
ically hemodialysed patients.
26. Lung biopsy may be percutaneous, transbronchial, via thoracos-
copy, or open (during thoracotomy). Bronchoscopic lung biopsy can
provide a diagnostic yield of up to 80 to 90 percent in sarcoidosis,
eosinophilic pneumonitis, hypersensitivity pneumonitis, infections,
lymphangitic carcinomatosis, drug-induced lung disease, pulmo-
nary Langerhans cell granulomatosis, lymphangioleiomyomatosis,
4 Clinical Examination and Applied Medicine

­ ulmonary alveolar proteinosis. Special staining techniques are used


p
for diagnosis under specific circumstances.
27. Mediastinoscopy, mediastinotomy, and at times, thoracoscopy may
be required.
28. Video-assisted thoracoscopy (VATS) and lung biopsy.
29. Nitric oxide in the expired air is indicative of airway inflammation
and is increased in asthma.
30. Pulmonary diffusion capacity.
31. Exercise test with six-minute walking is done to assess the amount of
disability and monitor the effect of therapy.
32. Cardiorespiratory assessment to assess heart or lung disease and fitness.

Arterial Blood Gas (ABG)


Blood gas analysis forms an integral part of investigations of a critically
ill patient. The ratio of acids and bases in the body determines the pH.
This is kept constant at around 7.4 because of a balance of bicarbonate
and carbonic acid kept in a ratio of 20:1. Any alteration in the pH is due
to the changes in the acids or bases that the body tries to compensate to
bring the pH back toward normal. This is called compensation, which
may be partial or complete, and occurs over time.
A normal person has a PaO2 usually more than 97 mmHg and sat-
uration greater than 95 percent. It is more important to note the trend
rather than a single reading of falling PaO2 or saturation or rising PaCO2.
Measuring the PaO2 and SaO2 will provide values of the alveolar-arte-
rial gradient (A-a gradient), partial pressure of arterial oxygen/fraction
of inspired oxygenation ratio (PaO2/FiO2), and oxygen delivery (DO2).
Hypoxemia is a decrease in PaO2 (saturation < 90 percent with a resul-
tant PaO2 < 60 mmHg), while hypoxia is a decrease in tissue oxygenation.
A rise in temperatures, acidic pH, higher concentration of 2,3-diphos-
phoglycerate reduces hemoglobin oxygen saturation, despite adequate
PaO2 due to shift of oxygen dissociation curve to the right (hemoglobin
has a decreased affinity for oxygen).
Arterial blood gas (ABG) measures PaO2, PaCO2, pH, SaO2, and
HCO3 concentration in the arterial blood. ABG is ordered to determine
Pulmonary Investigations 5

the presence of acidosis (metabolic or respiratory) or alkalosis (meta-


bolic or respiratory) or mixed problems. It is used not only to assess the
adequacy of a ventilated patient or a patient on BiPAP, but the need to

Normal Values for ABG


Values Arterial Venous
pH 7.35 to 7.45 Lower by 0.03–0.04
PaCO2 35–45 mmHg (4.7 to 6.0 kPa) Higher by 3–8 mmHg
HCO3 21–27 mEq/L Higher by 1–2 mEq/L or normal
pO2 80–100 mmHg Lower
O2 saturation 95–100 percent Lower

put the patient on BiPAP or ventilator support. A quick look at the pH,
PaCO2, and HCO3 will give good information about the acid base status.
ABG is normally done from the radial, brachial, or femoral artery. The
most dreaded complication of arterial puncture is ischemia distal to the
puncture site. Therefore, a proper evaluation of the site must be performed
before the procedure. After any arterial puncture, the site must be pressed
for more than five minutes. If an arterial sample cannot be obtained from
the radial (severe peripheral vascular disease, active R ­ aynaud’s syndrome,
local infection, or other pathology) site, an alternative source may be
attempted or a venous sample taken. The procedure may be relatively con-
traindicated in severe coagulopathy (INR > 3 or APTT > 100 or platelet <
30,000 cmm) or when streptokinase has just been used.
In acute conditions, the pH correspondingly changes but in chronic
cases, there is respiratory or renal compensation resulting in minimal
change in pH (Figure 1). Any change in the pH primarily due to change in
bicarbonate is called metabolic, where the kidneys are usually responsible.
If a patient has low bicarbonate (metabolic acidosis), with time in chronic
cases, there is respiratory compensation by hyperventilation and lowering
of the pCO2. On the other hand, a patient with high bicarbonate (meta-
bolic alkalosis) with time in chronic cases will have respiratory compensa-
tion by hypoventilation, thus raising the pCO2. In acute metabolic acidosis
or alkalosis, there is more shift in the pH, while in the chronic condition,
the shift is less because it is associated with variable degree of compensation.
6 Clinical Examination and Applied Medicine

Compensatory mechanism of
acid base balance

CO2 HCO3

Changes are rapid Changes are slower


Usually in minutes pH 7.4 usually 8–24 hours

Figure 1  Acid–base balance and compensatory mechanisms A change


in pH associated with change in HCO3 is associated with CO2
compensation in the same direction and vice versa

Similarly, any change in the pH due to PaCO2 is called respiratory,


where the lungs are primarily involved. Therefore, one can get r­ espiratory
acidosis (high PaCO2 associated with hypoventilation), which, in chronic
cases, is associated with compensatory accumulation of HCO3 by the
­kidneys. On the other hand, respiratory alkalosis (low PaCO2 associated
with hyperventilation) in chronic cases is associated with excretion of
HCO3, which becomes low to compensate for the alkalosis. ­Bicarbonate
changes the pH in the same direction, while pCO2 changes it in the
opposite direction. The respiratory compensation usually occurs within
hours, but the renal compensation takes several days.
When looking at the result of the ABG, the questions to ask are:

• Is the primary disorder respiratory or metabolic?


• What is the pH (acidic or alkalotic)?
• What is the pCO2 (high or low), and what is the HCO3
(high or low).
• Then decide whether the compensation is partial of complete.

Summary of Acid–Base Disturbances


The pH may be normal, acidic (less than 7.35) or alkaline (higher than 7.45).
Any change in HCO3 consistent with the pH will point to a metabolic cause.
Any change in PaCO2 consistent with the pH will point to a respiratory cause.
When HCO3 is primarily responsible for the change in pH, pCO2 acts to compensate.
When pCO2 is primarily responsible for the change in pH, HCO3 acts to compensate.
If the compensation is partial, the pH is partially corrected, but does not return into the
normal range. In uncompensated acid–base disturbance, CO2 or HCO3 is in the normal
range, while in the compensated acid–base disturbance, the pH is within the normal range.
Pulmonary Investigations 7

Blood Gas Values and Nomenclature


Value Ø (Decrease) ≠ (Increase)
pH Acidosis (< 7.35) Alkalosis (> 7.45)
CO2 Alkalosis (< 35mmHg) Acidosis (> 45mmHg)
pO2 (dissolved oxygen) Hypoxemia O2 therapy
HCO3 Acidosis (<21mEq/L) Alkalosis (> 28mEq/L)
O2 saturation Hypoxemia (< 95 percent) Not applicable
Base excess (BE) Acidosis (< –2) Alkalosis (> +2)
Anion gap Low ratio (< 10) High ratio (> 15)
Bases are Hb, Cl , PO4, SO4, and albumin. Provide info about the degree of metabolic

component.
Anion gap determines the source of acidosis from positive and negative ions.

Anion gap is calculated by (Na + K – {Cl + HCO3}) and is normally 10–15 mEq/L.

Academia is defined as a state of low blood pH < 7.35, while acidosis


describes the processes leading to academia. It may be due to fall in serum
bicarbonate (metabolic acidosis) or rise in PCO2 (respiratory acidosis).
Compensation (partial or complete) by the body is via metabolic alkalosis
(high HCO3) in the first instance and respiratory alkalosis (low PCO2)
in the second. Alkalemia is associated with an arterial pH above 7.45,
while alkalosis describes the processes leading to alkalemia. It may be due
to rise in serum bicarbonate (metabolic alkalosis) or fall in PCO2 (respi-
ratory alkalosis). Compensation (partial or complete) by the body is via
metabolic acidosis (low HCO3) in the first instance or respiratory acidosis
(high PCO2) in the second.
Mixed acid–base disorders can be best diagnosed from the history of
underlying disorder, disproportionate change in pH, keeping in view the

Metabolic and Respiratory Compensation


For metabolic acidosis and alkalosis.
Calculate the expected PaCO2 in metabolic acidosis [= 1.5 × HCO3 + 8 ± 2].
Calculate the expected PaCO2 in metabolic alkalosis [= 0.7 × (HCO3 – 24) + 40 ± 2].
For respiratory acidosis and alkalosis.
In respiratory acidosis, for every rise of 10 mmHg pCO2 above 40 mmHg, HCO3 will rise
by 1 (in acute cases) and 3.5 (in chronic cases where it will be reflected after a few days).
In respiratory alkalosis, for every fall of 10 mmHg in pCO2 below 40, HCO3 will fall by
2 mEq/L in acute cases and 4 or 5 mEq/L in chronic cases.
8 Clinical Examination and Applied Medicine

compensatory respiratory or renal responses and from the values of elec-


trolytes and calculating the anion ion gap. In an example of a patient
with excessive vomiting, there is loss of acid from the stomach and a met-
abolic alkalosis. If there is associated hypoperfusion from low BP, lactic
acid accumulates causing HCO3 to fall below normal, and resulting in
academia.

Simple Acid–Base Disturbance and Compensation


Primary Compensation
Disorder pH change response
Metabolic acidosis ↓Ø ↓ØHCO3 ↓ØpCO2
Metabolic alkalosis ↑≠ ↑≠HCO3 ↑≠pCO2
Respiratory acidosis ↓Ø ≠pCO2 ↑≠HCO3
Respiratory ­alkalosis ↑≠ ØpCO2 ↓ØHCO3

Examples of Mixed Acid–base disturbances


Disorder pH HCO3 pCO2 pO2
Respiratory acidosis + metabolic acidosis 6.85 15(30) 90 50
Respiratory acidosis + metabolic alkalosis 7.3 45(30) 90 50
Metabolic acidosis + respiratory alkalosis 7.3 6 12(22) 100
Metabolic alkalosis + respiratory alkalosis 7.75 40 25(43) 100

Respiratory acidosis occurs with alveolar hypoventilation causing hyper-


capnia (increased PaCO2 > 45 mmHg). About 15,000 mmol of CO2 is
produced daily at rest, and this combines with water to form carbonic acid
(H2CO3). In acute respiratory acidosis, the rise in PaCO2 is responsible
for the reduction in pH (pH < 7.35) while serum HCO3 is near normal.
In chronic respiratory acidosis, the pH is normal or near-normal in spite
of a rise in PaCO2 due to compensation with increase in serum HCO3.

Causes of Respiratory Acidosis


1. Depression of central nervous system: sedatives, obesity, hypoventilation, stroke,
encephalitis, hypothyroidism, hypothermia, and so on
2. Peripheral nervous system abnormalities: spinal injuries, poliomyelitis, Guillain–Barre
syndrome, myasthenia, muscular dystrophy, transverse myelitis, tetanus, tick paralysis,
Lambert–Eaton syndrome, acute intermittent porphyria and phrenic nerve involve-
ment, and chest wall deformities
3. Respiratory muscle problems:
Pulmonary Investigations 9

4. Upper airway problems: vocal cord and epiglottis problems, foreign body aspiration
5. Lung problems: severe pulmonary embolism and pulmonary vascular disease

Note that problems with mechanical ventilation may lead to hyper-


capnia, but gas exchange abnormalities alone are relatively uncommon
causes of hypercapnia.

Clinical Features of Respiratory Acidosis


Slow onset of mild to moderate hypercapnia may be symptom-free.
Anxiety leading to delirium.
Dyspnea and day-time hypersomnolence.
Headache confusion, obtunded, and drowsy.
Signs may be those of underlying disease for example Chronic Obstructive Pulmonary
Disease (COPD).
Cyanosis is present if there is accompanied hypoxia.
Asterixis, myoclonus, and seizure.
Intracranial pressure may be raised.

In respiratory acidosis, the expected HCO3 compensation = 24 +


pCO2 – 40 × 1/10 in acute cases (there is increase in HCO3, 1 mEq for
every 10 mmHg increase in pCO2 above 40).
Respiratory alkalosis occurs with alveolar hyperventilation causing
hypocapnia (decrease in PaCO2). In acute respiratory alkalosis, the fall in
PaCO2 (<35 mmHg or 4.7 kPa) is responsible for a rise in pH, which is
appropriately alkalemic (> 7.45). In chronic respiratory alkalosis, PaCO2
is low (< 35 mmHg or 4.7 kPa), but the pH level is at or close to normal
due to compensatory decrease in HCO3.

Causes of Respiratory Alkalosis


Anxiety, panic, and psychosis
Fever and pain
In certain medical conditions, the respiratory rate is high and may cause respiratory
alkalosis, as sometimes, in pulmonary embolism, heart failure, pneumonia, pneumo-
thorax, interstitial lung disease, chronic liver disease, stroke, meningitis, high altitude,
right-to-left shunts, pregnancy, hyperthyroidism
Hyperventilation syndrome
10 Clinical Examination and Applied Medicine

It may also sometimes be seen in any medical condition that increases


alveolar ventilation like, and aspirin overdose or mechanical ventilation.

Features and Clinical Diagnosis of Alkalosis


Confusion (can progress to stupor or coma).
Lightheadedness, dizziness, or syncope from cerebral vasoconstriction.
Symptoms of hypocalcemia (e.g., jitteriness, perioral tingling, muscle twitching or
spasms and carpopedal spasm, and tetany (Chvostek sign, Trousseau sign).
Hypokalemia and hypophosphatemia secondary to increased intracellular shifts of these
ions. This may be associated with weakness, myalgia, polyuria, and cardiac arrhythmias.
Nausea, vomiting, and diarrhea may point to the cause (gastric acid loss, villous adenoma).
Volume depletion stimulates aldosterone secretion, which in turn increases sodium
reabsorption in the collecting duct and increases hydrogen ion and potassium secretion.
Urine chloride is low after discontinuation of diuretic therapy, while it is high during
active diuretic use.
History of drug use may point to the cause (e.g., loop or thiazide diuretics; licorice,
tobacco chewing, carbenoxolone, fludrocortisone, glucocorticoids).
Milk-alkali syndrome (ingestion of antacids like magnesium hydroxide or calcium car-
bonate) is associated with hypercalcemia, renal insufficiency, and metabolic alkalosis.
History of hypertension associated with features of hypokalemia, and metabolic alkalosis
may be seen in Conn’s syndrome.
History of hypertension, diabetes with weight gain, and Cushingoid features may be seen
in Cushing’s syndrome in which there may be metabolic alkalosis.
History of surgery may point to ileostomy.
Patients with cystic fibrosis may develop hypochloremic alkalosis.
Chloride-resistant hypokalemic alkalosis (urine chloride > 20 mEq/L) with hypotension
or normotension is a feature of Bartter syndrome.
Citrate may be given during hemodialysis for anticoagulation, with blood transfusion,
and during plasmaphoresis and may cause metabolic alkalosis. With heparin anticoagu-
lation, this may be avoided.
Hypoalbuminemia may be associated with metabolic alkalosis, and a decrease in plasma
albumin of 1 g/dL is associated with an increase in plasma bicarbonate of 3.4 mEq/L.

Respiratory alkalosis is typically managed by treating the underlying


cause (e.g., reassurance, anxiolytic, pain control) and using maneuvers to
reduce alveolar ventilation (e.g., sedation, reduce respiratory rate, and tidal
volume when on mechanical ventilation). Chloride-responsive a­ lkalosis is
associated with loss of gastric secretions, ingestion of large doses of non-
absorbable antacids, and use of thiazide or loop diuretics. In ­respiratory
alkalosis, the expected HCO3 compensation = 24 – 40-pCO2/10 × 2
Pulmonary Investigations 11

in acute cases (there is decrease in HCO3, 2 mEq for every 10 mmHg


increase in pCO2 below 40). In chronic cases, it is 24 – 40-pCO2/10 × 5
(there is decrease in HCO3, 5 mEq for every 10 mmHg increase in pCO2
below 40).
Metabolic acidosis occurs due to accumulation of acids (lactic acid,
ketoacids, alcohol associated, methanol or various glycol ingestion, ­citric
acid, sulfuric acid) due to failure of normal utilization or renal acid
excretion (Types 1 and 2 renal tubular acidosis and CKD with tubular
­dysfunction) or loss of HCO3 (severe diarrhea, ureteric diversion, Type 2
renal tubular acidosis), resulting in fall in the pH. In acute conditions,
the pH is low with low HCO3 and near normal PaCO2. In chronic
­conditions, HCO3 is low with near-normal pH and low PaCO2 (hyper-
ventilation), which acts as a compensating mechanism. PaCO2 usually
falls by 1 to 1.3 mmHg for every 1 mEq/L fall in serum HCO3‒. If the
decrease in PaCO2 is less than the expected change, then primary respira-
tory acidosis also is present.

Causes of Metabolic Acidosis


Increase acid production (diabetic ketoacidosis, cardiac arrest, lactic acidosis, starvation,
alcohol, methanol, ethylene glycol, aspirin ingestion)
Decrease acid excretion (CKD and tubular dysfunction, Types 1 and 4 renal tubular
acidosis)
Loss of bicarbonate (diarrhea, carbonic anhydrase inhibitors, ureteric diversion, Type 2
renal tubular acidosis)

Metabolic acidosis may be initially recognized by finding a low serum


bicarbonate, usually less than 15 mEq/L (milder decrease also seen in
respiratory alkalosis as a compensatory response). The pH and PCO2 are
also low. Next, calculate the anion gap (normal is 10–12 mEq/L) and
the osmolar gap. The anion gap decreases by 2.5 mEq for every 1 g/dL
decrease in serum albumin. Ethylene glycol, methanol poisoning, and
acetone increase the AG and the osmolar gap. Salicylate level, ketones,
and lactic acid levels can be sent to the lab when suspected. If the anion
gap (AG) is not elevated, then a urinalysis with a urine pH on a fresh
urine sample should be obtained. The anion gap in the urine is calculated
from urinary Na+, K+, and Cl-. This helps to differentiate between GI and
renal losses of HCO3- in non-AG metabolic acidosis. The change in AG
12 Clinical Examination and Applied Medicine

(delta AG) helps in detecting the presence of a second acid–base disorder


in patients with an elevated AG.
A value less than 1 indicates that the drop in serum HCO3‒ is not
accompanied by a corresponding increase in the AG. This suggests the
presence of a mixed metabolic acidosis. A value greater than 1.6 indicates
that the drop in serum HCO3‒ is associated with a larger-than-expected
increase in the AG. This would indicate the presence of a mixed metabolic
acidosis and metabolic alkalosis. Measuring the transtubular potassium
gradient (TTKG) is useful in determining the etiology of hyperkalemia
or hypokalemia associated with metabolic acidosis.
In metabolic acidosis, a drop in HCO3 is compensated by a fall in
PCO2 up to a limit of 15 mmHg in a healthy person. Further drop in
HCO3 will lead to rapid decompensation. The expected CO2 compensa-
tion = 1.5 × (HCO3) + 8 (±2).

Features and Clinical Diagnosis of Acidosis


Hyperventilation with rapid and shallow breathing. Kussmaul breathing is more of an
increase in tidal volume, rather than the respiratory rate.
Headache, drowsiness, and confusion.
Fruity smell in the breath form ketoacidosis.
Palpitation, tachycardia, fatigue, and general weakness.
Urinary problems, anorexia, nausea and vomiting, pruritus, and anemia or a pericardial
rub may point to CKD.
In young children consider inherited causes.
Diarrhea may point to gastrointestinal cause of HCO3 loss.
History of diabetes, alcoholism, or starvation may point to ketoacidosis.
History of overdose may suggest salicylates.
Hypotension and peripheral hypoperfusion may be associated with lactic acidosis and
acute tubular necrosis.
Signs of chronic liver disease point to decompensated liver disease as the cause.
Renal stones may be associated with renal tubular acidosis.
Jaundice.

Metabolic alkalosis is associated with increase in serum bicarbonate


and corresponding increase in pH in acute conditions, but near-normal
pH in chronic cases due to respiratory compensation. Hypochloremic
alkalosis is caused by severe loss of chloride, for example, in prolonged
vomiting. Hypokalemic alkalosis is best seen with diuretic use and is
Pulmonary Investigations 13

caused by the kidneys’ response to hypokalemia. Hyperkalemic acidosis


results from the loss of sodium bicarbonate.

Causes of Metabolic Alkalosis


Gastric acid loss (vomiting or nasogastric suction)
Renal hydrogen loss (loop diuretics, Conn’s syndrome, Cushing’s syndrome, Liddle
syndrome, Bartter syndrome
Associated with severe hypokalemia (villous adenoma, laxative abuse)
Alkali administration (milk alkali syndrome, bicarbonate administration)
Massive transfusion

CO2 dissociation is quite like oxygen dissociation curve, and PCO2


is maintained normally between 35 and 45 mmHg. Hypercapnea occurs
predominantly due to hypoventilation, while hypocapnea is caused by
hyperventilation (commonly seen in pulmonary diseases like pulmonary
embolism and pulmonary edema, cardiac diseases like CCF, neurologi-
cal diseases like tumors, infections and raised intracranial pressure, met-
abolic acidosis, drugs like aspirin and progesterone, and hyperventilation
of ­anxiety). In metabolic alkalosis, the expected CO2 compensation =
0.7 × (HCO3) + 20 (±5).
A-a gradient is the difference between alveolar O2 (PAo2) and PaO2 or
arterial oxygen.

Hypoxemia in Relation to the A-a Gradient


Increased A-a
Low ventilation/perfusion (like COPD, asthma) Right to left shunt (pulmonary AV
malformations, Eisenmenger syndrome). Impaired diffusion capacity (can be with exer-
cise or in high altitudes).
Normal A-a
Hypoventilation (neuromuscular diseases, severe obesity, drugs, and exacerbation of
COPD. Low PiO2 (high altitude).

Pulmonary Function Tests (PFTs)


PFTs are utilized to identify the cause of dyspnea, quantify the disabil-
ity, monitoring disease progression, and document benefit from therapy.
The pattern of abnormality determines the type of disease (obstructive or
restrictive).
14 Clinical Examination and Applied Medicine

Common Indication of PFT


Chronic shortness of breath thought to be due to lung disease
Chronic cough or history of wheeze
Classifying dyspnea into obstructive or restrictive or mixed pattern
Checking reversibility of airway obstruction
COPD
Asthma and evaluation of bronchodilator therapy
Interstitial lung disease. Preoperative testing and assessment
Disability evaluation

There are various types of PFTs that can be ordered according to the
requirement.

Types of PFTs
Spirometry and pulse oximetry
Measurement of lung volumes
Diffusion capacity
Measurement of flow volume loops and maximum respiratory pressures
Exercise testing (e.g., six-minute walk)

Peak expiratory flow rate (PEFR) is the measure of the peak velocity
of air in the first 10 msec as the patient takes a very deep breath and blows
out as hard as possible into the PEFR meter. The measurement depends
on the caliber of the airways and patient cooperation (normal value is
about 4–6 liters/min).

PULMONARY FUNCTION TESTS


Inspiratory reserve volume (IRV)

Inspiratory capacity (IC)


Vital capacity (VC)
Total lung capacity (TLC)

Tidal volume (TV) FRC = ERV + RV


IC = IRV + VT
VC = IRV + VT + ERV
TLC = VC + RV

Residual volume (RV) Functional residual capacity (FRC)

Figure 2  Respiratory excursion during normal breathing, maximal


inspiration and expiration are shown along with common nomenclature
Pulmonary Investigations 15

• Tidal volume (TV) is the amount of air exchanged during


inspiration or expiration during normal breathing (Figure 2).
• Total lung capacity (TLC) is the volume of air contained in
the lungs after maximal inspiration. In adult males, it averages
about 6 liters (Figure 2).
• Vital capacity (VC) is the total amount of air that can be
expelled at TLC (it is about 70 percent of TLC) (Figure 2).
• Reserve volume (RV) is the remaining volume of air after expi-
ration for vital capacity and amounts to 30 percent of TLC.
It is also called end expiratory volume (Figure 2).
• Functional reserve capacity (FRC) is the lung volume at the
end of a normal expiration (Figure 2).
• Diffusion capacity measures the magnitude of the carbon
monoxide (TLco) transfer across the alveoli depending on
the volume of pulmonary capillary bed and matching of
­ventilation and perfusion.

Utility of PFTs
Decreased FEV1/FVC (< 70 percent) is seen in obstructive airway disease.
The ratio of FEV1/FVC (> 90 percent) is increased in restrictive airway diseases.
Increases in TLC and RV suggest hyperinflation (asthma or COPD).
Decreased TLC and VC suggest restrictive lung disease (fibrosis) or loss of lung volume.
Flow rates (FEV1 and PEFR) are diminished in COPD.
Diffusing capacity for carbon monoxide (DLCO) is low in emphysema, restrictive lung
diseases, pulmonary fibrosis, pneumonectomy, pulmonary hypertension, and recurrent
pulmonary emboli. A decrease in hemoglobin by 1 g diminishes DLCO by 7 percent.
DLCO is increased in the supine posture, after exercise, in polycythemia, in obesity, in
left-to-right shunt, and in some patients with asthma.
Maximal voluntary ventilation (MVV) tests airflow through major airways and muscle
strength.

FEV1 (forced expiratory volume in 1 second) and FVC (forced vital


capacity) are measured together using a spirometer. The patient is asked
to take the deepest possible inspiration, and then, expire into the instru-
ment as hard, quickly, and completely as possible. The amount of air
expelled in 1 second is FEV1, and the total amount expelled is FVC.
About 70 to 80 percent of the air is normally expelled as FEV1 (Figure 3),
but this is grossly reduced in case of airways obstruction. Therefore, the
16 Clinical Examination and Applied Medicine

ratio of FEV1/FVC is usually less than 65 percent in such cases (Figure 3).
In diseases that affect the lung parenchyma (restrictive airway diseases),
the airways are normal, the FEV1 is not reduced as much as FVC, the
ratio of FEV1/FVC is usually greater than 90 percent (Figure 3).

PULMONARY FUNCTION TESTS

FVC
FEV1
Normal FEV1/FVC
200 ratio = 80 Percent

Seconds 1 2 3

Restrictive airway Obstructive


disease ratio = >90 percent disease, ratio = <70 percent

FVC FV
FEV1
FEV1

sec. 1 2 3 sec. 1 2 3

Figure 3  A normal, restrictive, and obstructive pattern of curve form


a vitalograph

Obstructive disorders are associated with reduction in FEV1 and FEV1/


FVC values as seen in Figure 3. They are caused by increased resistance to
airflow due to luminal problems, bronchial wall abnormalities, or prob-
lems in recoil. Expiration is, therefore, prolonged, and air trapping occurs
with increase in lung volume. Air way obstruction when improved by
12 percent or more or by 200 mL by bronchodilator therapy is indica-
tive of reversibility and bronchial hyper-responsiveness classically seen in
asthma and some cases of COPD.
Provocative testing with methacholine (bronchial irritant) is used
to diagnose cases where the spirometry and lung volume studies are not
diagnostic and suspicion of asthma is high. A 20 percent drop in FEV1
from baseline with less than 1 mg/mL of inhaled methacholine is diag-
nostic of increased bronchial reactivity. The same test can be done with
exercise (achieving 80 percent of the predicted heart rate) and checking
for ≥ 15 percent drop in FEV1or FVC in exercise-induced bronchospasm.
Restrictive disorders are associated with reduced lung volume (TLC) to
less than 80 percent of the predicted value with a resultant reduction in
FEV1 and FEV1/FVC ratio is normal or increased.
Pulmonary Investigations 17

Restrictive Ventilator Defect


1. Stiff lung:
Diffuse pulmonary infiltration, fibrosis, and congestion
2. Replacement with non-ventilatory tissue:
Pneumonia and atelectasis
3. Compression of lung:
Large tumor, pleural effusion, pneumothorax, and cardiomegaly
4. Weakness/paralysis of respiratory muscles:
Poliomyelitis, phrenic nerve paralysis, and muscular dystrophy
5. Immobilization of pleura or chest wall:

Extensive pleural fibrosis, trauma, marked obesity, and thoracic


deformity
Walking test is an objective and reproducible method to test the func-
tional capacity of the patient. The patient is asked to walk the corridor
of known length, as many times as possible in a fixed time like 6 or 12
minutes. It is commonly used to assess benefit of therapy and to monitor
the course of the disease.
Pulmonary diffusing capacity (DLCO) is the same as the transfer factor
for carbon monoxide (TLCO) and determines the diffusion capacity of the
lung to carbon monoxide or assesses the gas exchange from inspired air to
the red blood cells. In diseases that affect the alveoli or microvascular struc-
tures (e.g., emphysema, interstitial lung disease, chronic pulmonary embo-
lism, and idiopathic pulmonary hypertension), it is reduced. Patients with
chronic bronchitis and asthma have normal DLCO or TLCO. A healthy
person has a value of 75 to 125 percent on an average, while DLCO below
45 percent predicted is seen in severe respiratory impairment. KCO is the
carbon monoxide transfer coefficient at the alveolar level (transfer factor
divided by the alveolar volume) and expressed in mmol/min/kPa/liter. An
overall decrease in the lung surface area decreases the TLCO, but not the
KCO, while in a diffuse disease like emphysema or severe interstitial fibro-
sis, both are reduced. When chest expansion is reduced as in Guillain–
Barre syndrome, myasthenia or chest wall diseases the TLCO is reduced,
but KCO may even be increased, thus differentiating extra-pulmonary
from intra-pulmonary causes of restrictive airway disease. Remember that
18 Clinical Examination and Applied Medicine

TLCO is calculated from KCO and VA (alveolar volume), and a low value
indicates a low KCO and or VA. Cardiac output, hemoglobin level, and
heavy smoking affect KCO directly, and thus, TLCO.

Causes of Reduced TLCO


Reduced capillaries
Emphysema
Pulmonary fibrosis
Pulmonary embolism
Primary pulmonary hypertension
Marked ventilation perfusion mismatch
Pneumonia
Pulmonary infiltration
Emphysema
Heavy smokers (high carboxyhemoglobin)
Severe anemia

Causes of Increased TLCO


Asthma
Alveolar hemorrhage
Polycythemia
Heart failure

Respiratory Failure
It is the inadequacy of the respiratory system to maintain blood gases and
is diagnosed by doing an ABG study. All such patients should also have
X-ray chest, ECG, pulmonary function tests, and sometimes, echocardio-
gram, but rarely require right heart catheterization.
It may be classified as Type I or hypoxemic, with PaO2 less than 60
mmHg and normal or low PaCO2, or Type II or hypercapnic with PaCO2
greater than 50 mmHg, which is usually associated with hypoxemia as
well. It can further be classified as acute (associated in minutes to hours
with severe metabolic derangements and symptomatic patient) or chronic
(associated over days or weeks with some compensation by the kidneys,
and therefore, milder metabolic changes and less symptomatic patient
who may also have polycythemia and cor pulmonale).
Pulmonary Investigations 19

Type I respiratory failure is more frequent and seen with any acute
pulmonary disease associated with dysfunctional alveoli (e.g., pneumonia
cardiogenic or non-cardiogenic pulmonary edema or ARDS, p ­ ulmonary
hemorrhage, high altitude, pulmonary embolism, atelectasis and pulmo-
nary fibrosis). There is hypoxemia (PaO2 usually less than 60mmHg) with
a normal or low PaCO2 and increased PA-aO2. There is ventilation and
perfusion mismatch or shunt.
In Type II respiratory failure, because CO2 is high, the pH is lowered
in acute conditions and compensated partially or fully by bicarbonate
accumulation in chronic cases. It is usually seen in conditions that effect
the chest wall, neuromuscular disease, drug overdose, and severe airway
disorders like COPD and severe asthma, upper airway obstruction, cen-
tral hypoventilation and obesity hypoventilation syndrome. The PaCO2
is greater than 45mmHg with accompanying hypoxemia and normal
PA-aO2. There is reduction in minute volume and or increased dead space
ventilation.
Type III respiratory failure is associated with perioperative respiratory
problems of increased atelectasis due to low functional residual capacity
(FRC) in the setting of abnormal abdominal wall mechanics. It may be
type I or type II. It is avoided by proper anesthetic or operative technique,
posture, incentive spirometry, proper analgesia and lowering the intra—
abdominal pressure.
Type IV respiratory failure is associated with intubated and ventilated
patients in shock.
Respiratory failure can also be acute, chronic or acute on chronic. On
examination one should look for clinical features of hypoxia and hyper-
carbia (see volume page 167). Investigations involve ABG, X-ray chest,
ECG, echocardiography, pulmonary functions, CT angiography, sleep
study as needed.
Index
A-a gradient, 13 Campylobacter jejuni infection,
ABG. See Arterial blood gas 86–87
Academia, 7 Cardiomegaly, 35
Acanthosis nigricans, 70 Cavitary lesions, 36–37
Achalasia, 72 Cavities, classification of, 23
Acidosis, 7 Central airway obstruction, 149
Acquired unilateral clubbing, 76 Chagas disease, 72
Acrocyanosis, 84 Chest, normal X-ray of, 21
Acute chest syndrome, 27–28 Chronic obstructive pulmonary
Acute respiratory distress syndrome disease (COPD), 78–81
(ARDS), 28–29 Clubbing, 76
Alkalemia, 7 Collapsed lung, 38
Alkalosis, 7 COPD. See Chronic obstructive
Ankylosing spondylitis, 74 pulmonary disease
Aortic aneurysm, 29–30 Cyanosis, 83–84
ARDS. See Acute respiratory distress
syndrome
Diaphragmatic pathologies, 38–39
Arterial blood gas (ABG)
Diffuse alveolar hemorrhage, 59
acid–base balance and
Diffuse military pattern, 27
compensatory mechanisms, 6
Diffusion capacity, 15
acute conditions, 5
metabolic acidosis, 11–12 Digital clubbing, 76–77
metabolic alkalosis, 12–13 DLCO. See Pulmonary diffusion
metabolic and respiratory capacity
compensation, 7 Dressler’s sign, 109
normal values for, 5
overview of, 4–5 Emphysema, 39–41
respiratory acidosis, 8–9
respiratory alkalosis, 9–11 FEV1. See Forced expiratory volume
Aspergillosis, 30 in 1 second
Axial spondyloarthritis, 74 Forced expiratory volume in 1 second
Azygos lobe, 31 (FEV1), 15
Forced vital capacity (FVC), 15
Beck’s triad, 109 FRC. See Functional reserve capacity
Bedside chest ultrasound, 56 Functional reserve capacity (FRC), 15
Behcet’s disease, 31 Funnel chest, 106
Bilateral infiltrates, 31 FVC. See Forced vital capacity
Bronchiectasis, 33
Bronchogenic carcinoma, 33–34 Gas under diaphragm, 41
Bronchogenic cysts, 34 GBS. See Guillain-Barré syndrome
Bronchopneumonia, 35 Gibbus, 121
158 Index

Guillain-Barré syndrome (GBS), 86 Obstructive disorders, 16


Opacities, classification of, 23
Haller index, 106
Heart failure, 42 Pancoast tumor, 103–104
Hilar convergence sign, 130 Panda sign, 130
Hilar shadows, 43–44 Peak expiratory flow rate (PEFR), 14
Hilum overlay’ sign, 130 Pectus excavatum, 106
Honeycombing, 26 Pectus severity index, 106
Horner’s syndrome, 103–104 PEFR. See Peak expiratory flow rate
Hydatid disease, 44 Pericardial disease, 108–109
Hydropneumothorax, 54 Pericardial effusions, 48–49
Hypoxemia, 13 Pericardial knock, 109
Hypoxia, 83 Pericardial rub, 108
Peripheral cyanosis, 83
ILD. See Interstitial lung disease PFTs. See Pulmonary function tests
Interstitial lung disease (ILD), 89 PH. See Pulmonary hypertension
PHO. See Primary hypertrophic
osteoarthropathy
Kussmaul’s sign, 108
Pleural effusion, 49–50, 111–112
Pneumococcal pneumonia, 113–115
Lambda sign, 130 Pneumonia, 52, 117–119
Lambert-Eaton myasthenic syndrome pneumococcal, 113–115
(LEMS), 91–92 Pneumothorax, 52–53
Latent tuberculosis, 67 Pott’s disease, 121
LEMS. See Lambert-Eaton Primary hypertrophic
myasthenic syndrome osteoarthropathy (PHO), 77
Linear shadows, classification of, 24 Pulmonary alveolar microlithiasis, 55
Lovibond angle, 76 Pulmonary calcification, 55–56
Lung abscess, 44–45, 94–95 Pulmonary cultivation, causes of, 23
Lupus, 139 Pulmonary diffusion capacity
(DLCO), 17
Massive pleural effusions, 52 Pulmonary edema, 56
Mediastinal lymphadenopathy, 45 Pulmonary embolism, 58–59
Mesotheliomas, 46–47 Pulmonary fibrosis, 59–61
Metabolic acidosis Pulmonary function tests (PFTs)
causes of, 11–12 causes of increased TLCO, 18
definition of, 11 causes of reduced TLCO, 18
features and clinical diagnosis of, 12 definition of, 13
Metabolic alkalosis forced expiratory volume in 1
causes of, 13 second, 15
definition of, 12–13 indication of, 14
Methemoglobinemia, 84 obstructive disorders, 16
Miliary pattern, differential diagnosis, pulmonary diffusion capacity, 17
48 restrictive disorders, 16
Miliary shadowing, 47–48 types of, 14
Miliary tuberculosis, 97–98 utility of, 15
Mixed acid–base disorders, 7–8 walking test, 17
Index 159

Pulmonary hemorrhage, 59 Sarcoidosis, 63–64


Pulmonary hypertension (PH), Secondary hypertrophic
123–124 osteoarthropathy, 77
Pulmonary investigations, 1–4 Silicosis, 65
Pulmonary nodules, 24, 61–62, Single-digit clubbing, 76
100–101, 125–127 Spondyloarthritis, 74
causes of, 25–26 Subpulmonic effusion, 50–52
Pulmonary sarcoidosis, 129–130 Superior vena cava (SVC) obstruction,
Pulmonary tuberculosis, 66, 144
132–134
Supraclavicular lymphadenopathy,
141–142
Radiology Systemic lupus international
benign nature evidence, 26 collaborating clinics (SLICC)
causes of pulmonary cultivation, 23
criteria, 137–138
causes of pulmonary nodules,
25–26
classification of cavities, 23 Tension pneumothorax, 55
classification of linear shadows, 24 Thoracic outlet syndrome (TOS),
classification of opacities, 23 146–147
diffuse military pattern, 27 Thyroid acropachy, 77
honeycombing, 26 Tidal volume (TV), 15
malignant nature evidence, 26 TLC. See Total lung capacity
normal X-ray of chest, 21 TLCO. See Transfer factor for carbon
pulmonary nodules, 24 monoxide
sequence of examination, 21–23 TOS. See Thoracic outlet syndrome;
Reserve volume (RV), 15 Tracheal stenosis
Respiratory acidosis Total lung capacity (TLC), 15
causes of, 8 Tracheal stenosis (TOS), 150
clinical features of, 9 Transfer factor for carbon monoxide
definition of, 8 (TLCO), 17
Respiratory alkalosis Tuberculosis lymphadenitis, 151
causes of, 9 TV. See Tidal volume
definition of, 9 Type I respiratory failure, 19
features and clinical diagnosis,
Type II respiratory failure, 19
10–11
Type III respiratory failure, 19
Respiratory failure, 18–19
Restrictive disorders, 16 Type IV respiratory failure, 19
Restrictive pulmonary disease, 74
Restrictive ventilator defect, 17–18 Unilateral pleural effusion, 50
Retrosternal goiter, 63
Rheumatoid lung, 136 VC. See Vital capacity
RV. See Reserve volume Vital capacity (VC), 15