ALS Manual 2013

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Acknowledgement is made of all those who contributed to the development of this current edition of
the WBHS-FCC Advanced Life Support Manual.

Thank you to the Advance Life Support Instructor Team, Members of the Resuscitation Committee
and Medical Education Unit of the Wide Bay Health Service - Fraser Coast Campus for their
continued support.

Manual reviewed Nov 2009 by Jules Bennet
Clinical Educator- Advanced Cardiac Life Support
Medical Education Unit, WBHSD-FCC

Reviewed: August 2011
Reviewed March 2012 Pauline Alderding & Margaret Cassidy
Reviewed February 2013 Pauline Alderding
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Participant Information 5
Process for Medical ALS 10
Cardiac Arrest Management Processes 12
Basic Life Support 24
Summary of Changes to BLS 33
New Initiatives in Post Resuscitation Care 38
Rhythm Interpretation 41
Defibrillation 80
Elective Cardioversion 87
Pacing 90
Drugs Used in Cardiac Arrest 93
Algorithms 103
Airway 110
Leadership 120
Additional Resources 123
Appendices 124
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Participant Information
Adult Advanced Cardiac Life Support Course

Congratulations, you have been offered a place in the Wide Bay Health Service District Fraser
Coast Campus Adult Advanced Cardiac Life Support Course. Listed below is information pertaining to
the administration of the course.

Prerequisite Current IV Cannulation & Venipuncture competency (nurses only)
A demonstration of Basic Life Support (BLS) principles will be provided at the
commencement of the program. Following this demonstration all participants
will be assessed on BLS. You must successfully complete this skill check to
continue participation in the ALS course.

Pre reading It is essential that you familiarise yourself with the information provided in Wide
Bay Hospital and Health Service Fraser Coast Campus Advanced Cardiac
Life Support manual prior to attending the course. The focus of the ALS course
is on the practical application of the material covered within this manual.
Please note: not all assessable material will be discussed during the training
session.

You are welcome to attend as an observer during a full day course however
you will not be permitted to participate in assessment processes. Registration is
necessary as an observer. ALS training schedules are displayed within the
clinical units. You are welcome to attend the whole day or just a specific
session.

To Enrol:

Complete course registration form available from ERC at either campus

When completed and signed by line manager, send to
FC-ERC-registration@health.qld.gov.au
Or fax to 4122 8255

Program Description

Full day Program 8 hours
Theory & practical instruction as well as assessment
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Fast Track Program 4hr (on request only)
Annual Recertification Process - Assessment only
The course is aimed at senior clinicians, or those who have attended the
WBHHS-FCC ALS program previously and feel confident with both the practical
& theoretical components of ALS.
.

Time 0800 1630 Full Day *Please be 10 mins early*

If for some reason you are sick or unable to attend it is your responsibility to notify the
Education & Research Collaborative on 4122 8210 ASAP.

Venue Sessions will be held in the Education and Research Collaborative,
Maryborough Hospital.

Catering Is not provided

Assessment You will be required to complete a written exam as well as participate in a
number of clinical scenarios as part of the assessment process. Algorithms
have been included as an appendix in this manual.

To achieve ALS certification you must achieve at least 80% overall on the
written exam.

Whilst you will participate in a number of scenarios you will be assessed as
team leader on two occasions. You must receive 100% of the mandatory
criteria in these practical assessments. You will have time to practice in the
team leader role prior to assessments taking place.

Feedback will be given during these practice scenarios.

On completion of each assessment scenario feedback will be given. You are
encouraged to identify the aspects you feel you excelled in and areas for
improvement.

If a participant fails to achieve the specific assessment
requirements, they will be classified as unable to achieve
course requirements. Further study and reassessment will be
necessary as described below.

Resits If the participant does not meet the requirements of the program, the participant
may in consultation with the Clinical Educator ACLS attempt to resit the exam
/ practical assessment within one month of attending the full day/ fast track
program.

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Participants who fail to achieve competency in the practical scenarios can
either register to resit the practical assessment at the next Full day or Fast
Track session.

Participants who fail to achieve competency in the theoretical exam are able to
resit the components of the exam that they incorrectly answered at the next full
day or fast track session. There is no need to book in to resit the theoretical
exam, just attend at the appropriate time. One resit will be offered.

If you do not achieve competency in both practical and theoretical components,
you will be required to resit the whole course.

Certificates On completion of the course requirements you will receive a certificate
indicating successful completion of the Wide Bay Health Service - Fraser Coast
Campus Adult Advanced Life Support Course.

Appeals notice If you wish to appeal a decision regarding your competency assessment/s,
please discuss your concerns with the Clinical Educator Advanced Cardiac
Life Support.

Course Evaluation On completion of the course participants are encouraged to evaluate the
course on a variety of issues. This anonymous feedback will contribute to
improving the ACLS program.

Recertification On successful completion of the ACLS course, Registered Nurses will be
endorsed to practice ALS as per the Wide Bay Health Service - Fraser Coast
Campus Policy COFC 3.2.4 ALS1v3

Annual recertification is required to maintain competence and be covered by
the policy.

Cost The course is provided free of charge for all staff of the Wide Bay Health
Service District - Fraser Coast Campus.

Portability The knowledge of this program is completely portable within Australia as all the
information provided is in accordance with the Australian and New Zealand
Resuscitation Councils (ARC) and the International Liaison Committee on
Resuscitation (ILCOR).

ACRRM 20 POINTS

We are in the process of seeking ACCCN / ARC certification for our ACLS
program. The program has been developed in accordance with ARC curriculum
guidelines.

CPD 10 POINTS

Relevant policies Advanced Life Support Authorisation for Registered Nurses to
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Practise policy COFC 3.2.4 ALS1v3
Transfer of the Acute Patient policy # 362
Use of Adult Manual & Semi Automatic Defibrillator Policy # 014
Drugs for critical care areas policy # 769
Withholding and Withdrawing Life Sustaining Measures Policy # QH-POL-
005:2010
Laryngeal mask Airway Use by Medical Officers and Advanced Life Support
Competent Registered Nurses COFC 3.2.4 LM1v1
Procedure for Prescribing & Administration of IV Potassium Chloride Procedure
# WBHHS- PRO-4:001v3P

An ALS Advanced mannequin is utilised during the practical scenarios. These mannequins have the
following features.
Respiration
Rise and fall of chest when breathing (unilateral rise and
fall when intubated)
Obstructed airway
Tongue oedema
ETT intubation capable
Carotid, brachial & radial pulses
Surgical cricothyrotomy
Rhythm interpretation
Defibrillation
Measurement of NIBP
Cannulation
Subcutaneous & IM injections
Heart sounds
Lung sounds
Tension pneumothorax decompression
ICC insertion
Speaking voice

Gloves are to be worn at all times when handling the mannequin.

Any queries regarding course content, assessment processes etc please contact

Clinical Educator Advanced Cardiac Life Support
Education & Research Collaborative
Wide Bay Health Service Fraser Coast Campus
Maryborough Hospital
Phone: 07 41228943 / 0407356811
Email: FC-ERC-Adult-ALS@health.qld.gov.au

Process for Annual ALS Competency
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CE ACLS liaises with NUMS, MEO, CCE, ED Educator regarding attendance.
Staff are rostered to attend a full day training session.
Staff can collect memory sticks containing Manual and all other relevant information from the
Administration officer (ERC, HBH/MBH) at any time, or the information will be emailed to you prior to
the course date in which you are enrolled
Staff will be booked to attend once a registration form has been completed & confirmation emailed.

Staff attend full day program
Examination and practical assessment undertaken
Examination results and level of competency discussed with participant

Feedback is given to appropriate management
(NUM, MEO, CCE & ED Educator)
Regarding level of competency
& commitment to process

If deemed not yet competent, MEO / NUM / Educators to discuss results with staff member
Formulate a training plan & negotiate an opportunity for reassessment

Competency level formally documented as part of term review
& performance appraisal process

Results are entered onto databases
CE - ACLS provides report to NUM, MEO, and Educators monthly
Executive quarterly
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%
CE ACLS liaises with MEO and individual medical staff regarding attendance.
Medical staff to consult with own roster co-ordinator to arrange date to attend Full day or Half day
training session.
Staff can collect memory sticks containing Manual and all other relevant information from the
Administrative officer (ERC, HBH) at any time, or the information will be emailed to you prior to the
course date in which you are enrolled
Staff will be booked to attend once a registration form has been completed & confirmation emailed.
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Staff attend full day program
Examination and practical assessment undertaken
Examination results and level of competency discussed with participant

If deemed not yet competent, MEO/Educators to discuss results with staff member
Formulate a training plan & negotiate an opportunity for reassessment

Results are entered onto databases
CE - ACLS provides report to MEO, and Educators monthly
Executive quarterly
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QUEENSLAND HEALTH
WIDE BAY HEALTH SERVICE
FRASER COAST CAMPUS
POLICY & PROCEDURE MANUAL

2004v1
Section: 2
Document No: 172

ADVANCED LIFE SUPPORT AUTHORISATION FOR REGISTERED NURSES TO PRACTICE

DESCRIPTION: N/A

TARGET AUDIENCE: Nursing Staff

PURPOSE:
To provide patients in cardiac arrest or with a life threatening dysrhythmia, with appropriate and timely
resuscitation. To support Advanced Life Support (ALS) Registered Nurses to deliver appropriate and
timely resuscitation to patients in cardiac arrest or with life threatening dysrhythmias.

EXPECTED OUTCOME:
Cardiopulmonary resuscitation of patients with life threatening dysrhythmias or in cardiac arrest can
be provided immediately by appropriately skilled Registered Nurses.

To provide the minimum standards of education, training and annual certification of Registered
Nurses to ensure that registered nurses who perform defibrillation and administer First Line
emergency drugs are competent to do so.

POLICY

Advanced Life Support (ALS) is Basic Life Support (BLS) with the addition of invasive techniques e.g.
defibrillation, advanced airway management, intravenous access and drug therapy.

Authority for Registered Nurses to Practice Advanced Cardiac Life Support is only given under the
following conditions:
1. They must be a permanent staff member
2. They must have successfully completed an approved ACLS program including Fraser Coast
Health Service ALS Full Day, Fast Track Course, or ACCCN/ARC accredited course. Staff from
other hospitals who possess current QLD Health ALS qualifications and certification will be
considered competent within the Wide Bay Health Service - Fraser Coast Campus District.
3. They must be issued with a certificate of authorisation. This certificate must be signed by the
Clinical Educator Advanced Cardiac Life Support to validate successful completion of the
course and associated prerequisites.
4. The authorisation will be valid for one (1) year. Re-endorsement recredentialling must be
completed through the Clinical Educator Advanced Cardiac life Support before this time or
endorsement will no longer be valid. If more than two years have lapsed, staff must complete the
whole ALS course.
5. Current IV cannulation certification is a prerequisite for attendance at ALS courses and
recertification.
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Additional Information

The above requirements should be taken as a minimum standard for endorsement to practice. It
is strongly recommended that each individual practitioner supplement this by adding regular skill
practice and scenario challenges to their individual education initiatives.
Competency assessment within the district may only be performed by accredited WBHS-FCC
Assessors. The Clinical Educator- Advanced Cardiac Life Support shall keep records pertaining
to ALS Assessors and assessments.
ALS is a mandatory competency for all nursing staff working in ICU & ED, and all medical staff.

Procedure

Registered Nurses who hold current Wide Bay Health Service District- Fraser Coast Campus ALS
certification will initiate the following when attending a patient with a life threatening dysrhythmia or
cardiac arrest.
1. Coordinate and direct the stabilisation of airway, breathing and circulation as per Australian
Resuscitation Council (ARC) guidelines including post resuscitation management as per ARC
Policy statements 11.2 Dec 2010

2. Initiate manual defibrillation and administer first line emergency drugs as per Australian
Resuscitation Council (ARC) policy statement 11.5 Dec 2010 and Wide Bay Hospital and Health
Service - Fraser Coast Campus ALS protocols see attachments A & B.
First line emergency drugs are ADRENALINE, ATROPINE, and AMIODARONE.

3. If IV/IO access cannot be attained, endotracheal administration of some medications is
possible, although absorption is variable. Medical staff must insert the endotracheal tube.
Adrenaline, Atropine Lignocaine and Naloxone may be given via endotracheal tube.

4. Continue resuscitation as per ARC algorithm and WBHHS-FCC policy until medical orders
regarding further treatment is obtained. (per Australian Resuscitation Council (ARC) guidelines
policy statement 8.0 Dec 2010 &10.5 Jul 2012)

5. An ALS certified nurse cannot make the decision to not resuscitate a patient but valid Not for
Resuscitation orders and Advanced Health Directives should be followed.

6. An ALS certified nurses are not authorized to:
Perform manual defibrillation on children
Order/administer electrolytes without a written or verbal order from a medical practitioner
Order/administer Adenosine without a written or verbal order from a medical practitioner
Perform cardioversion
Initiate external pacing
Insert an endotracheal tube
Insert a laryngeal mask unless assessed and deemed competent within WHHS - FCC

7. Follow-up care of the resuscitated patient must also follow Australian Resuscitation guidelines.

Failure to adhere to the policy will be viewed as a serious misconduct and will be dealt
with accordingly.
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Attachment (A)

Drug Administration by ALS Certified Nursing Staff WBHHS-FCC
Guide ONLY, Please refer to Standing Orders for Nurses!

Drug ALS RN Indication for use Dose

Adrenaline

Ventricular Fibrillation
/Pulseless Ventricular
Tachycardia after initial
defibrillation have failed.
Asystole
Pulseless Electrical
Activity
Bradycardia

1mg repeated every 4
minutes during CPR

0.1mg repeated every 4
minutes

Atropine

Severe bradycardia

Bolus of at least 500 mcg
every 4 minutes repeated
to a maximum of 3 mg
over the entire resus

Amiodarone

Failure of defibrillation &
adrenaline to revert
Tachycardia
Prophylaxis of recurrent
ventricular fibrillation or
ventricular tachycardia

In Emergency bolus of
300mg diluted in 20mL5 %
glucose over 2 minutes
A further 150mg diluted in
20 mL5% glucose over 2
minutes

Prophylactically bolus
300mg in 50 mL
5% glucose over minimum
20 minutes
2
nd
Dose - An additional
150mg bolus if required 5
minutes after first dose

Lignocaine

Note:
Lignocaine is only
administered if the
pt is unable to
tolerate
Amiodarone or
requires ETT
administration.

Failure of defibrillation &
adrenaline to revert
Tachycardia
Prophylaxis of recurrent
ventricular fibrillation or
ventricular tachycardia

Bolus 1 mg/kg

Bolus 1mg/kg over 1-2
mins

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Wide Bay Health Service - Fraser Coast Campus
Cardiac Arrest Management Processes

%
ARC Guidelines

ARC Guidelines are reviewed every four years. New guidelines were released in
December 2010. You can access the ARC website through any computer with
internet access.

Cardiac Arrest Response Team

The cardiac arrest response team is made up of the following staff members:

ICU PHO
Emergency Response Team Nurse (only HBH)
Wards persons x2
Medical PHO (during office hrs MBH)
Nurse Manager

If the patient is a paediatric patient, the paediatric team and the CEPALS must be
called immediately. They will not automatically respond.

HBH has a Medical Emergency Team 24/7 who respond to emergency calls
from all areas of the hospital

Documentation

Accurate documentation of the arrest is essential. It is the Team Leaders
responsibility to ensure this documentation is completed appropriately.

At the completion of the arrest all drugs must be ordered and signed.

The arrest record can be used for all situations covered by the algorithms e.g. Arrest
and pre arrest rhythms.

A photocopy of this record MUST be forwarded to the CEACLS

A copy of the arrest record is included in the appendix. Take the time to familiarise
yourself with the document and ensure that in an emergency you are aware of
appropriate and correct documentation.

Auditing

All cardiac arrests that occur within the Health Service are audited by the CE-ACLS
this information is reported to the WBHHS-FCC Resuscitation Committee on a
monthly basis. This information is used to guide future education sessions and to
assist in identification of process problems e.g. pager problems, etc.

Feedback process

The CEACLS aims to meet with the Team Leader following the arrest to provide
support, give feedback and discuss any problems that they may have encountered.
Team Leaders are encouraged to keep a copy of the arrest record to assist with this
debrief process.
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Laminated algorithms are available on all cardiac arrest trolleys. These can be
placed on the patient during the arrest. This will ensure that all staff present will be
clear as to which algorithm is being followed and can anticipate the next step.

Emergency Trolley Location

AEDs are located in the gym and Yaralla Place Grevillia Ward

MBH Restocking of Trollies (After Hours)
From MBH ED
1. ED
2. Clinics
3. Ward one
4. Ward Two
5. Ward Three
6. Mental Health
7. Training Trolley ERC
8. OT
9. Renal

HBH
10. ED ward Restocking of Trollies (After Hours)
11. ED Resus From HBH ICU
12. X-ray
13. Training Room ED
14. ICU
15. OT
16. Surgical
17. MGW 20. Renal
18. Medical 21.Oncology
19. Paediatrics 22.Clinics
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Specific Paediatric Trolleys
HBH ED, MBH ED, PAEDS, ICU, OT, ERC MBH.
Paediatric packs in MH & HBH Clinics and Renal Units

Adult Trolley Drawers

Medications
Circulation
Fluids
Airway
Paediatric Airway Packs

Audit against ARC Standards

The CE-ACLS performs an audit against ARC Standards on an annual basis.
The results of this audit guide the priorities for the resuscitation committee for
the following year.

Mock Arrests action plan & schedule

Mock arrests are held on a monthly basis in alternate sites. Approximately 3-4 arrest
are held on the one day using the same algorithm, the idea of this is to allow staff to
build on and consolidate their learning, as feedback is given after each mock
scenario. Dates for mock arrests are available through ERC.

Process problems identified during these mock scenarios are added to an action
plan and discussed monthly at the Resuscitation Committee.

5 quick questions

Once a month the CE ACLS will visit the wards and ask random staff members 5
questions related to ALS processes. This is part of an inter-ward competition (prizes
are awarded).

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Skills

Basic CPR
Healthcare
workers

Advanced
CPR

Level Two
ALS

Medical Staff
Staff
AINs
ENs
EENs
Ward Nurses
RNs, CNs, NUMs
in ED & ICU and
Nurse Managers
All medical
staff
Hours of
training
Annually
2hrs as part of
Core
Competency
Minimum of
2hrs as part of
Core
Competency
8 hours 8 hours
CPR
Mid Chest
30: 2
30 : 2
Paed 15::2
30 : 2
Paed 15::2
30 : 2
Paed 15::2
Drugs
able to order &
administered
Nil Nil
Adrenaline
Atropine
Amiodarone
Lignocaine
All arrest drugs
including
electrolytes
Defibrillator
Competency
Nil SAED
Manual for
Adults
Manual
Adults & Paeds
Pacing and
Cardioversion
Rhythm
Interpretation
Nil Nil All rhythms All rhythms
Assessment Practical BLS
Practical BLS
Assist with
intubations
SAED
Written Exam
2 prac scenarios
SAED
External Pacing
Written Exam
2 prac scenarios
SAED
External Pacing

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Prevention of in-hospital cardiac arrest

%
Fewer than 20% of patients suffering an in hospital arrest will survive to go home.
Most survivors have a witnessed and monitored VF arrest, primarily myocardial
ischaemia as the cause and receive immediate defibrillation.

Cardiac arrest in unmonitored wards is usually not a sudden unpredictable event nor
is it primarily caused by primary cardiac disease. These patients often have a slow
deterioration, involving hypoxia, hypotension, which is unnoticed by staff or is
recognised but poorly treated.

The ARC standards recommend an early warning system for the early identification
and management of acute medical emergencies. We are currently using the MEWS
system and have introduced the ADDS tool.

Causes of Cardiac Arrest

%
The last ARC guidelines place greater emphasis on identifying and treating the
possible cause of cardiac arrest. It is essential that a good history / handover are
obtained to assist you to identify the cause.
%
Treatable causes of cardiac arrest - 4 Hs & 4 Ts

1. Hypoxemia
2. Hypovolemia
3. Hypo/Hyperkalemia & metabolic disturbances
4. Hypo/ Hyperthermia
5. Tension Pneumothorax
6. Tamponade
7. Toxins Drugs, envenomation
8. Thrombus PE, MI

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Management of Causes - Pre Arrest

Hypoxemia

Hx shortness of breath, anaphylaxis, known asthmatic, COAD
Administer high flow O
2
/ assist with ventilation
Intubate & ventilate as required
Treat specific cause eg nebulised / IV Ventolin

Hypovolemia

Hx hypotension, trauma, surgery etc
Treat specific cause - rapid infusion warmed fluids, gelofusion, blood,
dopamine
Stop bleeding pressure, OT,
Administer O
2

Hypo/Hyperkalemia & metabolic disturbances

Hypokalemia K
+
<3.6 mmol/l
Hx excessive fluid loss, weakness, constipation, muscle necrosis
(<2.5mmols/l)
paralysis (<2.0mmols/l)
Check urgent electrolytes
ECG look for key indicators eg ST depression, wide PR interval, U wave
RX administer IV K
+

Hyperkalemia K
+
>4.5 mmol/l Metabolic Disturbances
Hx impaired renal excretion- renal failure
Rapid / excessive administration of IV K
+
ECG look for key indicators eg tall, peaked T waves (=7 mmol/L),No P
waves, wide QRS ( = 5 mmol/L)
Rx- insulin / glucose infusion 10 u Actrapid + 50mL50 % glucose, loop
diuretics, dialysis

Hypermagnesemia

Hx impaired renal excretion - renal failure
supplements laxatives, enemas
2-3 mmol/L lethargy, decreased deep tendon reflexes
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3-5 mmol/L somnolence, absent deep tendon reflexes, hypotension,
bradycardia,
5mmol/L paralysis ,heart block
ECG look for key indicators eg tall, peaked T waves (=7mmols/L),No P
waves, wide QRS ( = 5 mmol/L)
Rx- exchange transfusion, dialysis

Hypomagnesaemia

History poor intake, vomiting, diarrhoea, laxatives, alcoholic, loop diuretics,
hypocalcaemia
Weakness, anorexia, Trousseau sign, Chvostek sign, seizure
ECG look for key indicators eg increased PR, progressive widening QRS,
loss of T
Rx - IV

Hypo/ Hyperthermia

Hypothermia T<35 degrees Celsius
History exposure, prolonged submersion
Small body weight, alcohol intake, elderly
Cool to touch, tachycardia then progressive bradycardia, tachypnea then
hypoventilation, shivering - diminished shivering - no motion
Central rewarm - fluids, warmed O
2
, Bair hugger

Hyperthermia
History extreme exertion, heat waves, elderly, uses of antidepressants,
illicit drug use, anaesthetic
Warm to touch, dry skin
Rx Cool, IV fluids, treat cause

Tension Pneumothorax

History trauma, mechanical ventilation - respiratory distress, altered level of
consciousness, decreased perfusion, high peak pressures; hyperresonance
to percussion, no breath sounds affected side, tracheal deviation, and
subcutaneous emphysema.
Needle decompression large bore cannula inserted 2nd intercostal space
mid clavicular line

Tamponade (cardiac)

The accumulation of fluid in the pericardial space in a quantity sufficient to
cause serious obstruction to the inflow of blood to the ventricles. The quantity
of fluid necessary to produce this critical state may be as small as 200 mls
when the fluid develops rapidly or >2000 mls in slowly developing effusions
when the pericardium has had the opportunity to stretch and adapt to an
increasing volume
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History blunt chest trauma, idiopathic pericarditis, pericardial effusion
secondary to renal failure, myocardial infarction Becks triad - istant heart
sounds, ecreased arterial pressure, istended neck veins reduction in
amplitude of the QRS complexes, and electrical alternans of the P, QRS, or T
waves

Toxins Drugs, Envenomation

History drug use, bite, stings
Administer antivenom / antidote as indicated.
Envenomation pathway
Thrombosis

Consider all possible types of emboli, including PE, MI, air embolism, fat
embolism and amniotic embolism
PE - Hx DVT, recent surgery, chest pain,positive D- dimmer/MI chest pain,
cardiac history, sob, diabetic, increased troponin, ECG changes
Rx - thrombolytics
%

Basic Management - Pre arrest

Administer specific interventions appropriate to likely cause

Apply O
2

Monitoring /? attach pads rather than monitoring leads

ECG

Gain history/review chart/check previous pathology

Insert 2 large bore IV cannulas

Urgent pathology electrolytes, troponin, U + E, etc

Consider IV fluids

Check / discuss NFR status

Alert staff early / bring arrest trolley to bedside

Prepare & check equipment
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Types of Resuscitation:

1. Basic Life Support (BLS)

D Danger
R Response
S Send for help, note the time and apply Personal
Protective Equipment
Activate Red button alarms, 333, 0-000, yell.
A Airway Assessment and Management
B Breathing Assessment
C Chest Compressions
D Defibrillation

2. Advanced Life Support (ALS)

BLS + Invasive procedures and drugs.

Signs & Symptoms of Cardiac Arrest

Not responding/moving
Not breathing/Not breathing normally

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Basic Life Support

The participant is required to
Assess,
(AIR) Interventions - perform
Reassess before moving onto the next action
Key principals of basic life support
1. Avoid hyperventilation
2. Avoid delays to CPR
3. Early defibrillation

DANGER: Check for Danger and Address if evident Eg. Snakes, fluids, bystanders, cords etc
RESPONSE : 3 Ts Talk, Touch & Trapezius
Talk to the patient, call their name
Touch the patients arm
Trapezius muscle - squeeze

SEND FOR HELP: Pull buzzer from the wall (In Maryborough)
Yell loudly & clearly

Press the emergency buzzer
Dial 333 in areas not serviced by emergency
buzzers
Dial 0-000 in Yarralla Place, Community Mental Health, Mental Health Unit and Oral Health Vans etc
Note the time
PPE - collects mask for mask to mouth resuscitation, and gloves.
AIRWAY: Assessment, Intervention & Reassessment
* In an unconscious patient care of the airway takes precedence over any injury including possible
C Spine (ARC Guidelines 4 and 9.1.6)
Assessment : Look in mouth for foreign bodies, vomitus, blood etc
Access for abnormal airway noises such as stridor, snoring, gurgling etc
Intervention: Roll over if foreign body, fluids present. Open mouth and turn slightly
downwards to allow gravity drainage.
2 Finger sweep of mouth with your gloved hand if indicated to clear foreign matter
Suction ensuring tip is not inserted past the back teeth
Remove foreign body with Magills forceps
Dentures : remove only if ill fitting and causing obstruction
Open airway using airway manoeuvre - 3 options include head tilt, chin lift or
jaw thrust

Backward head tilt, one hand is placed on the forehead or the top of the head. The other hand is used to
provide jaw support / chin lift. The head is tilted backwards (NOT the neck) Avoid excessive force and
hyperextension of the neck.

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BREATHING: Assessment, Intervention and Reassessment

Assessment:: LOOK< LISTEN and FEELfor normal breathing
Look for rise and fall of the chest
Listen for expired air
Feel for air on your cheek, hand on chest to feel for chest expansion

Intervention: If the victim is unresponsive and not breathing normally, after the airway has been cleared,
commence chest compressions

Reassessment: Look, Listen and Feel during ventilations, if the chest does not rise, possible causes are
Obstruction in the airway (inadequate airway manoeuvres, foreign body obstruction)
Insufficient air being blown into lungs
Inadequate seal around mouth or nose

Note: WBHHS does not support mouth to mouth or mouth to shield ventilation
The following airway adjuncts must be used Pocket mask or Bag valve mask

Mouth to Mask
Position yourself at the victims head facing his feet, and apply mask firmly over nose and mouth to achieve
an effective seal. Use both hands to maintain an open airway and to hold mask in place

Ventilate with Bag Valve Mask if available
Fill reservoir bag prior to use
15 litres of oxygen
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COMPRESSIONS: Assessment; Intervention & Reassessment
Assessment Signs of cardiac arrest Not responding or moving
Not breathing or not breathing normally
Intervention Commence compressions
Position mid nipple line
Ratio 30 Compressions: 2 Breaths pausing to give breaths
Depth 1/3 chest wall
Rate 100 compressions/ minute
Place victim on firm surface
Minimise interruptions
Reassessment: Swap CPR providers every 2 minutes
Do not perform recovery checks
Continue compressions until patient protests
Continue for up to 2 minutes following return rhythm compatible with life, then
check pulse
! If no pocket mask or bag valve mask available, it is reasonable to commence
chest compressions only
! Ensure space is allowed for quick change of CPR providers without interruption
to CPR
Assessment and Management of Circulation
Studies show that checking for a pulse is not a reliable indicator of cardiac function, even in
trained personnel.
The rescuer should also assess for other signs of poor perfusion such as colour capillary refill etc
If the patient is in respiratory arrest only, continue with ventilation at 12 breaths/ minute
If the patient is unconscious, not breathing and shows signs of poor perfusion,
commence cardiopulmonary resuscitation immediately.
This provides a small but critical blood flow
to the heart and brain.
It increases the likelihood of defibrillator shocks terminating VF.

Defibrillation and compressions are the two most important aspects of resuscitation
In the first few minutes after successful defibrillation, the rhythm may be slow and ineffective.
Chest compressions may be needed until adequate cardiac function returns ( up to 2 minutes)
CHEST COMPRESSION TECHNIQUE
Site: Mid nipple line
Do not waste time by using the calliper method to measure, as it delays CPR
COMPRESSION METHOD
There is insufficient evidence to support a specific hand position for chest compressions during CPR
in adults

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1. Lock the elbows into position and ensure arms are straightened
2. Position your shoulders directly over your hands, so that each thrust is in a downward direction
3. Depress the sternum 1/3 of the chest cavity, the force ids determined by compressions that
generate a palpable or carotid pulse.

COMPRESSION RATE
Adult & Paeds Single rescuer 100 compressions per minute
Two rescuers 100 compressions per minute

CORRECT COMPRESSION TO INFLATION RATES

Adult 30 Compressions : 2 Inflations

The CPR provider must now pause compressions to allow the breath to be delivered.The rescuer
performing external cardiac compression should count out loud, so that the second rescuer will know
when to deliver the inflation i.e. 25; 26; 27; 28; 29; 30
CPR providers need to rotate every 2 minutes to prevent fatigue and deterioration in quality and rate of
compressions.
The optimal time to change CPR providers in a shockable rhythm, is during defibrillation.
The CPR provider needs to pay full attention to ahieving full compression depth and to alow equal
amount of time for the chest to recoil.

NOTE: Compression ratio of 30:2; (which equates to 100 compressions & 8 breaths per minute),
is only applied until a definitive airway is insitu. After this time, compressions are performed
continuously at approximately 100 per minute and breaths are given at 6 10 breaths per
minute
It is therefore appropriate to intubate early, as long as this can be achieved without unnecessary delay
to CPR
Laryngoscopy should be performed without stopping chest compressions. A brief pause may be
required as the tube passes throughj the cords.

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Attempts to secure the airway should not interrupt CPR for more than 20 seconds.

RECOVERY CHECKS

Evidence has demonstrated that interruption of chest compressions is associated with poorer return of
spontaneous circulation and lower survival rates. On stopping chest compressions the coronary flow
decreases substantially, on resuming chest compressions, several compressions are necessary before
coronary flow recovers to its previous level.

Rescuers should minimise the use of recovery checks, the rhythm should now be checked every 2 mins prior
to defibrillating.

If an organised rhythm is seen during a 2 min period of CPR, do not interrupt chest compressions to palpate
a pulse unless the patient shows signs of life suggesting return of spontaneous circulation.

In most cases BLS is commenced before entering the ALS algorithm, however if defibrillation is immediately
available then applying an SAED or manual defibrillating takes precedence. ARC guideline 11.2.

CPR in the prone position is a reasonable alternative for intubated patients who cannot be placed in the
supine position.

Bystander CPR doubles or triples chance of survival for witnessed cardiac arrest.

Animal studies have shown that chest compression are only as effective as combined ventilation &
compression in the first few minutes after a non asphyxial arrest If CPR provider not willing to do mouth to
mouth, and a mask it not immediately available.

ADVANCED AIRWAY - ADVANCED CPR & ALS only
Measure & inserts Guedels or nasopharyngeal airway
Correct use of Bag- Valve Mask (appropriate mask sizes, fill reservoir bag, correct rate and depth of
bagging, 15 l oxygen.)
Prepare equipment required for intubation
ADDITIONAL CONSIDERATIONS
Removes bed head, pulley bar and obstructions
Discuss recovery management
Assembles intravenous equipment / insert if qualified
Demonstrate how to prepare minijets
Records and verbalise drugs, timing and events
Relative support /notification
Debrief team

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Summary of Changes to Basic Life Support

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For ease of teaching there is now a variation between processes for non healthcare
worker (lay rescuer) and healthcare worker.

The term Rescue Breathing replaces EAR Expired Air Resuscitation

Lay rescuer

Rationale for
Difference /changes
Advanced Life
Support

Signs of Arrest

Not breathing
properly
Not responding
Not moving

In out of hospital arrest
lay rescuers delayed starting
CPR because unsure or pt had
agonal resps (40 %)

Fear compressions will cause
harm No scientific evidence
To suggest this is accurate.

Nil respirations
Unconscious
Nil Pulse
No signs of life

Breathing

No rescue breaths
2 breaths:30
compressions
If no airway device
continuous CPR

Decreased from 2 full breathes
Interruptions to CPR must be
minimised. Even if victim takes
occasional gasps, CPR should
start with compressions.
Performing chest
compressions alone is
reasonable for trained
individuals if they are incapable
of delivering airway and
breathing manoeuvres to
cardiac arrest victims

No rescue breaths
2 breaths:30
compressions
6 - 10 breathes when
intubated.
If no airway device
continuous CPR

Pauses for
breathing

Pause to allow breath
to be given

No change

No pause required if
intubated. therefore less
interruption to
CPR

Compression
ratio

30 : 2 for everyone
no matter how many
rescuers

Ease of teaching
Prevent hyperventilation
Less interruption to
compressions

30 : 2 for adults
15 :2 for paediatrics
3 :1 for neonates

Compression
position

Nipple Line

Ease of teaching
Easy to remember

Nipple line

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Compression
Cycles

No longer relevant 30:2 100 bpm 2 min cycles

Compression
Depth

1/3 chest wall Approximately 5cm in adults

Recovery
checks

No pulse checks
Only stop if patient
protests

Pulse seen as unreliable
indicator of cardiac output
Difficult for lay person to
palpate carotid pulse
Causes interruption to
CPR
Fear compressions will
cause harm No scientific
evidence to suggest this is
accurate

Check rhythm prior to
defibrillation. If rhythm
compatible with life, check
pulse and continue
compressions for up to 2
mins or until patient
protests.

Defibrillation

SAED 1 shock
200J

One shock every 2
mins thereafter as
prompted by SAED.

Time delay in recharging &
analysing in automatic
machines.
Poor technique delivering
quick successive shocks
causing interruption to
CPR
Witness the blood hasnt
had time to pool in the
ventricle, therefore the
shock will be more
effective

SAED 1 shock 200J
Manual Defib

1 shock every 2 mins
thereafter

Joules

SAED
manufacturers
setting may vary
between machines

No evidence to suggest
Escalating joules improves
benefits.
More shocks = more damage
to myocardium

SAED 200j default
Manual 200j biphasic

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Resuscitation in late pregnancy

Problems can arise as a result of anatomical and physiological changes that
occur during pregnancy.

There can be an increased risk of aspiration of the gastric contents into the
lungs due to increased intraabdominal pressure and decreased gastric
motility.

Problems can also arise in decreased venous return due to pressure on the
abdominal and iliac vessels and there can also be decreased circulation to
the foetus.

Providing an obvious pelvic tilt to the left by placing padding under the
right buttock, or manually holding the uterus towards the patients left
side, can correct these problems. The shoulders should be flat against
the bed.

CPR It may be difficult to observe the rise and fall of the chest in late
pregnancy. CPR should be provided from the left side.

Ventilation of the pregnant woman is more difficult because the enlarged
uterus restricts chest expansion.

NOTE: Failure to achieve successful CPR is an indication for urgent
Caesarean section which should be performed as soon as possible
when medical personnel with appropriate expertise and equipment
are available. The ideal time is within 5 mins from the onset of the
arrest.

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Post Resuscitation Care

Basic management following a cardiac arrest for all patients include included:

1. Apply high flow oxygen

2. Patient positioning No single position has shown to be perfect for all victims.
Left lateral position is the preferred method.

3. ECG, constant monitoring

4. ICU, retrieval as appropriate

5. Check IV sites for patency

6. Take blood to ascertain electrolyte levels

7. Assess for possible complications

8. Document on Post Resuscitation Care Plan.

9. Maintain BGL 4 -10 mmol

10. Induced hypothermia

11. K+ 4-4.5 mmol

12. Maintain normocarbia

13. Debrief team

14. Continue antiarrhythmics as an infusion if used during resuscitation.

Summary Post Resuscitation Interventions
Airway Secure and clear ETT/Guedels, suction prn, chest x-ray
Breathing Assess depth ,rate, colour, ABGs
Circulation Consider volume expansion, Inotrope
Defibrillation Available at bedside until pt admitted to ICU
External Pacing Transcutaneous if required
Family Support
Explain events to family ,allow visit, arrange chaplain,
social worker
Group Support
Team leader to debrief group, Evaluate performance &
recommend individual follow up
Hospital documentation
Ensure summary record of events, interventions
&outcomes are documented
Instruments
All instruments & equipment should be cleaned &
replaced, ready for use

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Complications of CPR

Cerebral complications can occur if cardiopulmonary resuscitation and oxygenation
is not commenced in time. After 4 - 6 minutes permanent damage is usually evident.

Cerebral oedema, CVA

Rib fractures may be unavoidable in the elderly

Injury to sternum, costal cartilage, flail chest, lung damage, hemothorax,
contusions etc

If one hand is placed on the Xiphisternum during compressions, it may
break off, lacerating the liver

Renal failure

Metabolic imbalance

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New Initiatives in Post Resuscitation Care

Control of Arterial Carbon Dioxide

Hypocarbia should be avoided after cardiac arrest as it causes cerebral
vasoconstriction and decreased cerebral blood flow. There is no data to support the
targeting of specific PaCo2 after cardiac arrest but normocarbia is recommended,
but not less than 35 mmHg.

Blood Glucose Control

There is strong association between high blood glucose after resuscitation and poor
neurological outcomes. Blood glucose levels should be monitored post cardiac
arrest, treatment should be initiated in patients to avoid hyperglycaemia or
hypoglycaemia and maintain level between (4-10 mmol)

Prophylactic Anti arrhythmic

Hemodynamic instability is common after cardiac arrest and manifests as
hypotension, and arrhythmias. This dysfunction is usually transient and often
reverses in 24-48 hours. The post resuscitation period is associated with marked
increase in plasma cytokine concentrations, manifesting as sepsis like syndrome and
multiple organ dysfunction.

Continue an infusion of an anti arrhythmic drug that was used to successfully restore
a stable rhythm during resuscitation.

Induced Hypothermia

A period of hyperthermia is common in the first 48hrs after arrest. The risk of poor
neurological outcome increases for each degree the body temp > 37. Mild
therapeutic hypothermia is thought to suppress many of the chemical reactions
associated with reperfusion injury. This includes free radical production, excitatory
amino acid release and calcium shifts.

It is recommended for unconscious patients with return of spontaneous circulation
after cardiac arrest when the initial rhythm was VF should be cooled to 32- 34
degrees as soon as possible and continue for 12 - 24hours. A rapid infusion of
30mL/kg of saline at 4 degree Celsius can decrease core temperature of
approximately 1.5 degree Celsius. This may require use of muscle relaxants to
prevent shivering, EEG monitoring should be utilised to detect seizures.

ARC and the Resuscitation Committee support the use of the application of cold
blankets to achieve this lower body temperature.

Coagulation Control
There are no studies evaluating the role of anticoagulation alone to improve outcome
after return of spontaneous circulation. Anticoagulation may be indicated for
myocardial infarction or pulmonary embolism.
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Note: Thrombolytics should be considered in adult patients with cardiac
arrest with proven or suspected PE as successful resuscitation following
administration has occurred after initial failure of standard CPR techniques.
Four clinical studies have shown that there is no increase in bleeding
complications with fibrinolytic use during CPR for non traumatic cardiac arrest

Seizure control

Seizures occur in 5 15 % of adult patients with return of spontaneous circulation
and in approximately 40 % of those that remain comatose. Seizures can increase
oxygen requirements of the brain, therefore any seizures post cardiac arrest should
be treated promptly. Prophylactic anticonvulsants should be prescribed as
necessary.

Potassium levels

Immediately after an arrest there is typically a period of hyperkalemia. Subsequent
endogenous catecholamine release promotes intracellular transportation of
potassium causing hypokalemia. Hypokalemia can predispose the heart to
ventricular arrhythmias. Administer potassium to maintain serum potassium
concentrations between 4.0 - 4.5 mmol.

Post Resuscitation Care Plan

A Post Resuscitation Care plan has been developed to guide staff response in the
Post resuscitation period. This is located on the back page of the Cardiac Arrest
record. A copy of this has been included in the appendix.

All patients who have suffered a cardiac arrest MUST be admitted to the ICU/CCU
Unit post arrest or transferred to a tertiary facility. Admission to the Medical Unit on
telemetry is unacceptable.

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Workplace Health & Safety
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The following Workplace Health and Safety issues need to be considered during an
arrest situation:

1. Use of PPE Gloves, Gowns, goggles, infection control issues

2. Use of pocket mask/BVM. NO mouth to mouth

3. Manual handling CPR, moving patients. Slide sheets are located on the
cardiac arrest trolleys and evacuation pods are located throughout the ward
areas

4. Safety with defibrillation

5. Aggressive Behaviour Management

6. Safety with sharps

Professional, Ethical & Legal Issues

Please refer to relevant WBHS-FCC policies eg Guidelines for withholding
and documentation of adult & neonatal resuscitation Policy # 250

Legislative requirements such as Coroners act, Nursing scope of practice
etc.

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Cardiac conduction systems
Waveforms

Sinus Rhythm
Sinus Tachycardia
Sinus Bradycardia
Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardia

Junctional Rhythm
Heart blocks

Idioventricular
Ventricular Tachycardia
Torsades De Pointes
Asystole
Pulseless Electrical Activity
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Basic Cardiac Anatomy
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Cardiac Conduction System

The normal electrical contraction in the heart allows the impulse that is generated by
the Sinoatrial node of the heart to be propagated to (and stimulate) the myocardium.
The myocardium contracts after stimulation. It is an organised stimulation of the
myocardium that allows efficient contraction of the heart, thereby allowing blood to
be pumped throughout the body.

The heart is made up of two types of cardiac tissue

1. Ordinary myocardium (atrial & ventricular)

2. Specialised cardiac conduction system which includes:

Sinoatrial,
Anterior, middle and posterior internodal tracts
Atrioventricular node
Bundle of His
Right & left bundle branches
Purkinje fibres

The specialist cells are capable of depolarising spontaneously which enable them to
work as cardiac pacemakers.

The inherent spontaneous rate of depolarisation is progressively slower from the SA
node down to the purkinje fibres. The normal rate of spontaneous depolarisation in
the SA node is 60 - 100 bpm, which is faster than other cardiac pacemakers;
therefore it is the dominant pacemaker.

The activity of the other pacemaker cells is not recognised until the SA rate falls
below those of the other pacemakers cells. The inherent rate at the AV junction is
40 - 60 bpm and decreases to 20 - 40bpm in the ventricles.

The Sinoatrial Node

The sinoatrial (SA) node contracts generating nerve impulses throughout the
heart wall. This causes both atria to contract.
Located in the upper wall of the right atrium

The Atrioventricular Node

The atrioventricular (AV) node lies on the right side of the partition that
divides the atria ,near the bottom of the (R) atria
When the impulse from the SA node reaches the AV node they are delayed
for about a 10th of a second. This allows the atria to contract and empty their
contents first.

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The AV Bundle conduction

The impulses are then sent down the atrioventricular bundle. This bundle of
fibres branches off into two bundles and the impulses are carried down the
centre of the heart to the left & right ventricles.

Purkinje Fibres

At the base of the heart the atrioventricular bundles start to divide further into
purkinje fibre. When the impulses reach these fibres they trigger the muscle
fibres in the ventricle to contract.

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Measurement

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The Horizontal axis represents time. The vertical axis represents amplitude or
voltage
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Waveforms
(Understanding the P-QRS- T waveform)

Normal P wave

Represents atrial depolarisation. It reflects the passage of the electrical impulse
through the myocardial muscle of the atria.

Normal P waves should be gently rounded, It is often pointed in atrial ectopics
and biphasic or m shaped (called p mitral) in mitral valve disease, where there is
left atrial enlargement.

Duration 0.04- 0.10 seconds.

Voltage of 1- 2.5mm. Lung disease that has caused right atrial enlargement can
cause elevation.

Should have a polarity consistent with the normal atrial axis and the site of the
external electrode being recorded.

One P wave should precede each QRS.

The relationship between P wave and the QRS should be consistent on the
rhythm strip.

The rate of the P wave is 60 -100 per minute in adults and 100-180 per minute
(often slightly irregular in children).

The P wave should be regular in adults.

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The P R Interval

According to Mangean B 1990 p 3:27 an interval is defined as one waveform and
one segment such as the P wave and PR segment in the PR interval, in this case.
Although it is often observed, any depression or elevation above the isoelectric line
may reflect atrial myocardial injury.

Characteristics of the P- R interval

Duration varies according to different text from 0.10 seconds or 0.12 seconds
to less than 0.20 seconds.

PR intervals less than 0.10 0.12 seconds indicates an accessory pathway
such as Wolff- Parkinson White Syndrome where delta waves are
observed. Greater than 0.20 seconds indicates a heart block.

The PR interval should be the same for each beat on the rhythm strip.

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The QRS Complex

The Q, R and S waves represent ventricular depolarisation; these are
grouped together and termed the QRS complex.

The letter Q wave describes an initial downward deflection from the
isoelectric line.

The letter R wave is an upward deflection from the isoelectric line.

The letter S wave is a downward deflection from the isoelectric line, which
must follow an R or r wave.

One, two or three of these components may be present depending on which
lead you are viewing.

Characteristics of QRS complexes

Duration 0.05 - 0.12 seconds, some books (0.05 - 0.11).

Waveforms should be rigid straight lines, due to the velocity of conduction.
Wider slurred complexes tend to indicate extensive pathology, as discussed
above, such as Bundle Branch Blocks.

Where a QRS complex begins with a q wave, the q wave should be no
more than 1/3 of the R wave, otherwise this abnormality may indicate a
pathological Q wave, often warning of transmural infarction.

The voltage of the QRS complex also depends on whether you are observing
a limb or chest lead. Generally the QRS should not exceed 10 mm in the
limb leads and 20 mm in the chest leads.

Increased voltage indicates ventricular hypertrophy or reduced transthoracic
resistance, while reduced voltage can indicate pericardial effusion or
tamponade.

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ST Segment

During the ST segment the ventricles are refractory or unable to be restimulated by
an electrical impulse. Although you can feel a pulse during this segment, this is
because the calcium influx in this phase keeps myocardial cells in a state of
refractoriness, and calcium provides cellular contractile filaments with a stimulus
that promotes contraction (Mangan, B 1990)

Characteristics of the ST segment

Peak ST segment can indicate ischaemia
The ST segment should not deviate above or below the isoelectric line; at this
stage there is normally no net movement of ions across the cell membrane
(Calcium ions are only slowly influxing).
If the cell membrane integrity is compromised, resulting in loss of selective
permeability. The ST segment will deviate from the isoelectric line, such as in
injury, ischaemia, infarction or inflammation.

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Sinus Rhythm

Sinus rhythm represents the normal electrical activity of the heart. The sino-atrial
node is the pacemaker initiating impulses at the normal rate which is approx 60 -
100bpm. These impulses follow normal electrical pathways, within usual time
frames.

Identifying features

Rate 60 -100 beats per minute
P waves Normal
QRS Normal
Conduction The entire conduction from the SA node to the ventricles is
Normal
Rhythm Regular
Impulse Originates from the SA node.

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Sinus Tachycardia

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Rate > 100 beats per minute
P waves Normal
QRS Normal
Conduction The entire conduction from the SA node to the ventricles is
Normal
Rhythm Regular
Impulse Originates from the SA node.

The SA node usually is the normal pacemaker in the heart and initiates impulses at
60 100 beats per minute. In sinus tachycardia the normal waveform exists
however the rate is above 100 bpm, and is usually due to sympathetic stimulation.
Sinus tachycardia is normal in infants. In congestive cardiac failure, the reduced
stroke volume is compensated by an increased rate in the heart.

Causes of Sinus tachycardia include:

Fever
Anxiety
Physical activity
Congestive cardiac failure
PE
Infection
Thyrotoxicosis
Pain
Coughing
Drugs eg adrenaline
Caffeine ingestion
Blood loss
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Signs & Symptoms

The patient is usually asymptomatic, but may feel palpitations, dyspnoea, or
angina. The P waves may be indistinguishable (falling on a T). A 12 lead ECG is
required.

Risk

Any increase in heart rate increases oxygen consumption and demand. This may
result in left ventricular failure, myocardial ischaemia, or extension of a myocardial
infarction. The length of diastole is reduced with any tachycardia. As this is the time
that the coronary arteries fill, there will be less blood flow to the overworked
myocardium.

Treatment

If the patient is haemodynamically compromised depending on patient presentation,
treatment could include beta blockers eg metoprolol 5mg or calcium channel blocker
e.g. verapamil

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Sinus Bradycardia


Rate Usually 40 - 60 beats per minute, may be slower

P waves Normal

QRS Normal

Conduction Conduction from the SA node to the ventricles is normal

Rhythm Each P wave is followed by a normal QRS

Impulse Originates in the SA node

Causes of Sinus bradycardia

Sinus bradycardia is common in the first few hours after an MI.

The rate is below the 60, and this is usually due to vagal dominance from
parasympathetic stimulation. This is common when patients are vomiting,
being suctioned, feel cold or may be induced by drugs such as morphine.

Although bradycardia may be caused by ischaemia, it may also be present in
the healthy heart eg athletes.

Signs & Symptoms

If the heart is too slow and the cardiac output is reduced, the patient may
complain of syncope, hypotension, angina or present with cardiac
failure.

Risk

A faster pacemaker such as a ventricular focus may take over.
The reduced cardiac output impairs or reduces cerebral and coronary blood
flow.
Sinus bradycardia is occasionally a warning of potentially serious rhythm
such as atrioventricular blocks or asystole.
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Management

The patient is usually only treated if they are symptomatic or having escaped
ventricular ectopics. Oxygen should be given.

The main treatment is Atropine as it blocks the effects of the vagal
stimulation on the SA node, thereby increasing the heart rate.
The bradyarrhythmia algorithm should be followed for all slow rates
Drugs such as Digoxin, beta-blockers etc should be stopped.

All monitor alarms limits must be set at least 40bpm. Monitor BP as it is an important
indicator of perfusion in bradycardia.

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Atrial Fibrillation

Atrial fibrillation occurs when numerous sites in the atria fire
spontaneously as a result organised spread of depolarisation can no longer
take place.

Small sections of the atrial muscle are individually activated which results in
quivering of the atrial muscle without effective contraction.


Rate Atrial > 350 min unable to count
Ventricle 100-180 /min uncontrolled
< 100 controlled

Rhythm Irregularly irregular

P waves absent, replaced by fine fibrillatory waves

PR interval Indiscernable

QRS 0.06 -0.10 seconds

T wave Indiscernable

The QRS is usually normal because the pathway through the ventricles is
unchanged once the impulse leaves the AV node. The AV node acts as a filter to
protect the ventricles from the 350 600 sporadic atrial impulses that occur each
minute.

When atrial muscle surrounding the AV node is in a refractory state, impulses
generated in the other areas of the atria are unable to reach the AV node. This is
why there is a wide variation in the R- R interval in AF.
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Causes of Atrial Fibrillation

Infection and Fever Valvular heart disease
Pulmonary embolus chronic heart failure
Thyrotoxicosis Hypertension
Pericarditis Diabetes
Acute MI Increased age
Drugs & alcohol

Treatment for Atrial Fibrillation

The aim is reduced the ventricular response rate to below 100 beats per minute
by drugs, cardioversion or a combination of both.

Drug therapy includes Digoxin, Verapamil, Amiodarone, Magnesium sulphate
and anticoagulants.

Synchronised cardioversion is the treatment of the choice for the patient
with a low cardiac output, hypotension or a newly diagnosed AF.

If possible anticoagulants should be commenced prior to cardioversion due
to the risk of producing emboli. The conversion of sinus rhythm will cause
forceful atrial contraction to resume abruptly. If the thrombus forms in the
atria the resumption of the contractions can result in systemic emboli.

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Atrial Flutter

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Rate Atrial 280/beats per min
Ventricular 60 beats per min

Rhythm Atrial irregular
Ventricular regular

P waves Classic saw toothed appearance

PR Interval Not measurable

QRS 0.08 seconds

T wave Unidentifiable

Atrial flutter is represented by a saw tooth atrial activity with normal QRS
complexes. The mechanism is thought to be re-entry within the atria and possibly
increased automaticity. It is often associated with second degree heart block and the
AV node fails to allow conductions of all the impulses to the ventricles, resulting in a
slower ventricular rate.

The clinical significance of atrial flutter is determined by the number of conducted
impulses 2:1 or 4:1

Signs & Symptoms

If the ventricular rate is < 40 or >150 beats per min cardiac output may be
compromised due to reduced ventricular filling time. This may result in Angina,
CCF, pulmonary oedema, hypotension and syncope.

Causes of Atrial Flutter

Almost always associated with some form of heart disease

- Ischaemic heart disease

- Cardiac failure (leading to atrial distension)
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- Valve disease

- Pulmonary embolus
Atrial Flutter may be encountered in conditions such as:

Severe mitral valve disease COAD
Hypothyroidism Systemic arterial hypoxia
Pericardial disease Acute Myocardial Infarction

Management

The aim is reduced the ventricular response rate to below 100 beats per minute
by drugs, cardioversion or a combination of both.

Drug therapy includes Diltiazem, Digoxin, Verapamil, Amiodarone,
Magnesium sulphate.

Synchronised cardioversion is the treatment of the choice for the patient with a
low cardiac output and hypotension in a newly diagnosed atrial flutter. Cardioversion
is successful with 90% of cases requiring <25-50 joules.

Atrial activity is organised so there is a low risk of thrombus formation.

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Supraventricular Tachycardia

This basically refers to a tachycardia which has its focus above the ventricles, but
not in the SA node. Therefore the focus may be in the atrium such as paroxysmal
atrial tachycardia or atrial flutter with a 1:1 block, or foci may be in the junctional area
such paroxysmal junctional tachycardia. The paroxysms may last a few seconds to
several hours.


Rate 140 -220 per minute

Rhythm Regular

P waves usually upright in atrial tachycardia and may be inverted in
Leads II, I and AVF on 12 lead ECG if it a junctional rhythm.
Often they are not visible without a 12 lead ECG.

PR interval May be shorter with a junctional tachycardia than an atrial
tachycardia.

QRS Normal, missing in beats

Causes

Digoxin toxicity

Acute MI

Rheumatic heart disease

Drugs

Risks

Leads to myocardial ischaemia / angina, dyspnea

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Management

Commonly a vagal manoeuvre is tried such as Valsalva manoeuvre, or
coughing. This has shown to be effective in up to episodes of paroxysmal
SVT

Pharmacological treatment is Adenosine as first line treatment. Second line
drugs calcium channel blocker eg verapamil 2.5-5mg IV over 2 mins,
amiodarone 300mg over 10 -60 mins followed by infusion 900mg over 24 hr.

Compromised patients or those who do not respond rapidly to commonly
used drug therapy, cardioversion is an alternative.

Hints to help you differentiated between SVT & sinus tachycardia

a. SVT has a paroxysmal onset without signs of illness;

b. SVT the rate is usually faster

c. SVT responds to vagal manoeuvres and drugs such as Adenosine.

d. The heart rate in SVT is usually constant where in sinus tachycardia
the rate will vary e.g. a patient in pain who is given analgesia will see
the rate of sinus tachycardia decrease.

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Junctional Rhythm

The AV junction replaces SA node as pacemaker if for any reason the SA node fails
to initiate impulses or discharges too slowly. Junctional rhythm may be transient and
only last a few beats after which the SA node regains control.


Rate Slow 40 - 60 beats per minute

Rhythm Regular

P waves Occur before, within or after the QRS complex, may or may not
be visible if buried within the QRS complex

PR interval Shortened if P wave precedes the QRS (<0.12sec)

QRS Normal

Causes of Junctional rhythm

Excessive vagal activity

Ischaemic damage to SA node

Digoxin or quinidine toxicity

Management

Follow the Bradyarrhythmia pathway

Atropine 500 mcg is sometimes successful in increasing the discharge rate
of the SA node allowing it to regain control.

Pacing may be required if the rate compromises the circulation.

Withdraw Digitalis if it is the causative agent.

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Heart Blocks

Impulses from the SA node travel via internodal tracts to the AV node, down the
Bundle of His, the right and left bundle branches to the purkinje network, and
terminate in the myocardial cells.

A Heart block indicates a delay in conduction between the SA node and the
Bundles of His.

1st Heart Block

Identifying Features

Rate Usually normal
Rhythm Regular
P waves Normal
PR interval Greater than 0.2 seconds and
remains constant
QRS Normal

Signs & Symptoms

A first degree heart block produces no signs or symptoms or physical findings other
than the first heart sounds (S1) become softer. It can only be diagnosed by an ECG.

Management

Usually no treatment is required; unless the patient is compromised or has a slow
rate. The bradyarrhythmia algorithm should be used in this case.
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2ndHeart Blocks

Some of the impulses are blocked and do not reach the ventricles. The P waves are
not always followed by a QRS complex. There are 2 types of second degree heart
blocks.

Mobitz Type 1 Wenckebach


Rate Normal to slow, rarely rapid
Rhythm Atrial regular
Ventricular regularly irregular
P waves Present normal shape, not every P is followed by a QRS
PR interval Progressive lengthening until P wave not conducted through to
Ventricles
QRS Normal configuration
T waves occasionally abnormal due to buried or non conducted P wave

Mobitz Type 1 is characterised by progressive lengthening of the PR intervals
preceding the blocked beat. Conduction through the AV node becomes more difficult
with each successive impulse until finally an atrial impulse is completely blocked in
the AV node and the QRS fails to appear.

Signs & Symptoms

The arrhythmia produces few if any symptoms, unless the rate is < 50 bpm. The
patient is usually unaware of the presence of this conduction disorder. Diagnosis
requires a 12 lead ECG.

Management

Follow the bradyarrhythmia pathway if the patient is compromised.

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Mobitz Type 2


Rate Atrial usually normal
Ventricular normal to slower than atrial rate depending on
degree of block

Rhythm Atrial rhythm regular
Ventricular rhythm regular or irregular

P waves Normal, P waves more numerous than QRS complexes ratios
may occur e.g. 2:1, 3:1 etc

PR interval Normal or prolonged. Remains constant

QRS Usually widened

An arrhythmia in which a complete block of conduction of electrical impulses in one
bundle branch, and an intermittent block in the other. This produces an AV block
characterised by regular or irregular absent QRS complexes, commonly producing
an AV conduction ratio of 4:3, 3:2 or 2:1 and a bundle branch block.

Signs & Symptoms

Symptoms are related to the ventricular rate. With rates > 50 bpm, angina,
dyspnoea, or cerebral insufficiency may be experienced.

Diagnosis requires an ECG.

Causes

Often associated with an anterior septal MI and chronic fibrotic disease of
conduction system.

Digoxin, Amiodarone.

Risks
A very serious disorder of conduction often progressing to a third degree AV
block and even ventricular asystole.
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Management

Temporary transvenous pacing is indicated because of the ever present threat of
sudden complete heart block or ventricular standstill.

Emergency treatment should follow the bradyarrhythmia algorithm pathways.
Digoxin and antiarrhythmics should be discontinued.

3
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or Complete Heart Block


Rate Atrial usually normal and regular
Ventricular usually slow i.e. < 40; less than atrial

Rhythm Regular both atrial and ventricular

P waves Normal, disassociated with QRS

PR interval Inconsistent

QRS Usually widened

Complete absence of conduction of the electrical impulses through the AV
node, Bundle of His or bundle branches. It is characterised by independent
beating of the atria and the ventricles.

Signs & Symptoms

Heart rate remains constant and does not fluctuate with activity
Signs of cerebral ischaemia, ranging from confusion, light-headedness to
syncope and seizures
Left ventricular failure is usually present, as is hypotension

Causes

Results from ischaemia of the AV node associated with an acute MI,
increased vagal tone, acute myocarditis, digoxin toxicity, over beta blockage,
or an electrolyte imbalance. It can also be caused by chronic degenerative
changes in the bundle branches.
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Risks

The ventricular pacemaker is not reliable and may cease abruptly causing
ventricular standstill or be replace by a faster pacemaker in the ventricle i.e.
VT/VF

Management

Follow the bradyarrhythmia pathway.
In broad complex bradyarrythmias such as 3
rd
degree heart block atropine
will not work as the atria & ventricles are beating independently of each other
Temporary pacing with the view to insertion of a permanent pacemaker.

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Idioventricular Rhythm

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Rate < 40 bpm

Rhythm Can be regular or irregular

P waves Absent

Pr interval Not measurable

QRS Wide, >0.12 seconds, often bizarre

Causes

This is a safety mechanism when all potential pacemakers fail to discharge,
or when a block prevents supraventricular impulses from reaching the
ventricles.

Signs & Symptoms

The slow rate and loss of atrial kick cause decreased cardiac output leading
to hypotension syncope, vertigo, confusion.

Management

Follow the bradyarrhythmia pathway
In broad complex bradyarrythmias such as idioventricular atropine will not
work as the atria & ventricles are beating independently of each other
A pacemaker may be required
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NOTE: Do not give anti-arrhythmics this will cause
Asystole.

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Ventricular Tachycardia

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Rate Atrial variable
Ventricular 110 -250

Rhythm Usually regular

P waves Absent

PR interval Indeterminable

QRS Wide and bizarre >0.12 seconds

ST segments Often obscured

T waves Opposite polarity to the QRS complex

This is an arrhythmia which originates in an ectopic pacemaker in the ventricles, with
a rate between 110 250 bpm. The QRS complexes are abnormally wide and
bizarre. Rhythm is usually regular but may be slightly irregular.

This arrhythmia exists if 3 or more consecutive premature ventricular contractions
are present and the rate is 110 or greater. This may occur in paroxysms known as
non sustained, or persist for long periods sustained VT.

Ventricular Tachycardia is referred to as a precursor to Ventricular Fibrillation.

Causes

This arrhythmia is rare in normal hearts, but may occur as a complication of the
following;

Myocardial infarction /administration of thrombolysis
Ischaemic heart disease/congestive heart failure
Hypoxia
Cardiomyopathy
Mitral valve prolapse
Hypokalemia/ hypomagnesaemia
Digoxin toxicity
Insertion of indwelling cardiac lines.
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Risks

In VT, the atria do not regularly contract and empty before each ventricular
contraction, therefore filling of the ventricles during the last part of diastole is
impeded. This results in reduction in cardiac output. This often compounds an
already low cardiac output as seen in diseased hearts. From this it is evident that VT
is a life threatening arrhythmia and must be treated immediately.

Management

Management is governed by the hemodynamic and conscious state of the patient
(treat the patient not the monitor).

If the patient has a pulse, follow the Conscious Symptomatic VT algorithm.

If the patient is pulseless follow the VT /VF algorithm

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Rate Atrial indeterminable, ventricular indeterminable

Rhythm Irregular

P waves Absent

PR interval Indeterminable

QRS Indeterminable, no uniformity, chaotic

T waves Indeterminable

ST segments Indeterminable

This is one of the most common causes of cardiac arrest (40% of sudden cardiac
arrests) and is an arrhythmia arising from numerous ectopic pacemakers in the
ventricles firing at once characterised by rapid abnormal ventricular fibrillation
waves and no QRS complexes.

There are no coordinated ventricular beats and the ventricles contract about
300 - 500 times a minute, it is unsynchronised and uncoordinated.

The amplitude and waveform of VF deteriorates as high energy phosphate stores in
the myocardium decrease. This process can be slowed, or even reversed by
effective BLS. (ARC guideline 11.2)

Causes

A premature ventricular contraction can initiate VF, this occurs when PVC occurs
during the vulnerable period of ventricular repolarisation i.e. R on T phenomenon,
this occurs when the electrical stability of the heart is altered by ischaemia or
infarction. VF is common after the onset of myocardial infarction, but may also be
due to:

Electrocution
Drug intoxication
Trauma
Hypothermia (core temp below 30 degrees)
Other causes as for VT
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Risks

Cardiac output ceases the moment ventricular fibrillation occurs, patient feels faint
and within seconds becomes unconscious, apnoeic, and may have a seizure.
Ventricular fibrillation is life threatening and must be treated immediately.

Management

Follow the VF algorithm

Cardiopulmonary resuscitation should be commenced immediately and
defibrillations occur as soon as possible.

NOTE: ECG artefact/interference may be produced by loose, dry or broken leads.
Patient movement or muscle tremor may resemble VF. Treat the patient not
the monitor, rapid assessment of the patient is required.

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Torsades De Pointes


Rate Atrial indeterminable
Ventricular 150 -250

Rhythm Irregular

P waves Indeterminable

QRS Polymorphic, changing in amplitude and undulating about the
baseline

QRS duration Wide and bizarre

ST segments Obscured

T waves Difficult to interpret

The QT interval is long prior to the commencement of Torsades De Pointes

This rhythm is another form of VT, characterised by QRS complexes that gradually
change back and forth from one shape and direction to another. Torsades De
Pointes means twisting of the points.

Occurrences are frequent and often in short episode of less than 90 seconds.

Causes

Any situation that prolongs the QT interval, especially in the setting of an
acute MI.
Drugs Lignocaine, Amiodarone, Sotalol, Erythromycin and Tricyclic
Antidepressants.
Electrolyte disturbances hypokalaemia, hypomagnesaemia, hypocalcaemia
Management

Follow VT/VT algorithm
Conscious consider cardioversion early
Give Magnesium early

Note: Lignocaine is contra indicated as it prolongs the QT interval and
exacerbates AV blocks
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Asystole


There is no electrical activity happening in the heart. Usually appears as a
straight line on the monitor however it can appear as a wave across the screen.

Causes

Ventricular contraction depends on adequate ventricular stimulation. If
impulses fail to reach the ventricles or impulse formation ceases asystole
occurs.

You may find asystole divided into primary or secondary standstill.

- Primary standstill is when impulses originating from the SA node are
blocked and the ventricle are totally dependent on an inherent ventricular
pacemaker, which stops discharging, leaving no source for electrical
stimulation.

- Secondary ventricular standstill is caused by hypoxia which depresses
conduction, impulse formation and myocardial responsiveness to
stimulation.

Signs & Symptoms

Circulation stops, there is no heart beat, peripheral pulse or blood pressure. The
patient is unconscious and if prolonged, the pupils will dilate and death will occur
within minutes.

Risk

This is the most dangerous of all arrhythmias. Successful resuscitation is
unlikely once the rhythm has deteriorated to asystole.

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Management

Follow the Asystole algorithm
It is imperative to check for compression artefact on the monitor
screen, change the lead selection to view from different leads, and
increase the size.
Fine VF that is difficult to distinguish from asystole will not be shocked
successfully into a perfusing rhythm. Continuing good quality CPR may
improve amplitude and frequency of the VF and improve chances of
successful defibrillation to a perfusing rhythm.
Whenever a diagnosis of asystole is made, check the ECG carefully for the
presence of P waves as this may respond to cardiac pacing. There is no
benefit in attempting to pace a true asystole.
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Pulseless Electrical Activity


There is coordinated electrical activity on the monitor, but no mechanical activity
and therefore no cardiac output i.e. the patient is unconscious, not breathing,
without a pulse. These patientss often have some mechanical myocardial
contraction, but are too weak to produce a detectible pulse.

Survival is unlikely unless a reversible cause can be found and treated effectively.

This is the most common arrest rhythm in in-hospital cardiac arrests.

Causes

The 8 main reversible causes referred to as 4 Hs and 4 Ts are of particular
importance when identifying the cause of PEA. To assist you in identifying the
possible causes, more often than not the rhythm may fit the following -

Fast Rate with narrow QRS complex = the cause is due to something
not affecting the heart muscle eg. Pulmonary embolism

Fast Rate with wide QRS complex = the cause is something that is
affecting the heart muscle itself eg. Myocardial Infarction, Tension
Pneumothorax etc

Slow Rate with wide QRS complex = the cause is usually due to toxins
of some sort

Management

Rhythm identification in this instance is unnecessary!!! The way to
determine a PEA is through a matter of elimination: the rhythm is not a
VF, VT, Asystole or Torsades and the patient has had a cardiac arrest.
The rhythm in a PEA is always organised not chaotic eg VF

Follow the Asystole /PEA algorithm: CPR and Adrenaline are the primary
management strategies.

It is imperative that you find and treat the underlying cause of PEA, as
several of the causes will result in no cardiac output from compressions.
Therefore CPR is not providing circulation to the brain cells, resulting in
cellular death.
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1. Identify the above rhythm

...............................................

2. From which part of the heart does this impulse initiate?

...............................................

3. What are the key features of this rhythm?

...............................................

...............................................

...............................................


.................................................


...............................................

...............................................
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...............................................


...............................................

...............................................

...............................................

8. This rhythm is a type of

...............................................

...............................................


...............................................


...............................................

...............................................

...............................................
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Page 76 of 135


...............................................


...............................................

...............................................

..


...............................................


...............................................

...............................................

...............................................

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...............................................

16. From which part of the heart does this impulse initiate?

...............................................


...............................................

...............................................

...............................................

Identify the above rhythm

...............................................


...............................................

...............................................

...............................................

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................................................


...............................................

...............................................

...............................................

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Page 79 of 135

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Page 80 of 135

Precordial Thump

A precordial thump is a single sharp blow delivered by the rescuers fist to the mid
sternum of the victims chest. The clenched fist is held approx 25-30cm above the
sternum of the victim. The fist is brought down sharply so the side (ulna) makes
contact with the midsternum of the victims chest.

Indications Within 15 seconds
Witnessed, monitored arrest (ICU, ED)
Where the rhythm is VF/VT (pulseless)
When a defibrillator is not immediately available

Precordial thumps are not encouraged if a defibrillator would be close at hand.

Possible complications of a precordial thump include:

1. Rhythm acceleration of VT
2. Conversion of VT and bradycardic rhythm to VF
3. Complete heart block
4. Asystole

Therefore should only be delivered to a pulseless victim whose cardiac rhythm is
monitored.

The likelihood of conversion reduces with time
The conversion rate is higher for a pulseless VT than VF

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Defibrillation

Defibrillation takes priority over drugs & CPR in the management of VF and
pulseless VT
Rapid defibrillation remains the major determinate of survival in cardiac arrest
due to VF.
Each minute that defibrillation is delayed decreases chances of reversion by
10 -15 %
The underlying principle of defibrillation is that a high intensity charge
depolarises the entire myocardium allowing the normal pacemaker to
resume control of the rhythm.
Because bone is not a good conductor of electricity the pads/paddles
should not be placed over the sternum
((
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Defibrillation Electrode Placement

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Page 82 of 135

Defibrillation Electrode Placement

Correct electrode position optimised the amount of current flowing
through the ventricles

Biphasic Defibrillators

Deliver current that flows in a positive direction for a specific duration before
reversing and flowing in a negative direction for the remaining millisecond of
the charge.
Standard setting: 200joules for adults
Lower energy biphasic shocks cause less myocardial injury and subsequent
post resuscitation myocardial dysfunction thus potentially improving likelihood
of survival.
The Lifepaks used within the WBHSD-FCC are all Biphasic defibrillators

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Safety Precautions

Prior to defibrillating ensure that:

No one is touching the patient
No one is giving IV injections
Do a 360 degree safety check
Say step back in a clear voice
Ensure there is nothing between the defibrillation pads eg leads, necklaces
Ensure no one is standing in water or fluid
The Bag-Valve Mask should be covered and taken 1.5 metres away from the
patient
Look at monitor prior to discharge to ensure the patient is still in a shockable
rhythm

Remember

Ensure pads are placed correctly on patient
Ensure the chest wall is free of blood/fluid
Dont shock over GTN patches they can cause a small explosion, wipe after
removal
Avoid implantable pacemakers /defibrillators
Remove jewellery
Avoid ECG electrodes
You should not need to shave the chest as the current pads will adhere to all
chests regardless to ensure good contact.

It has been suggested that the most frequent mistakes made when defibrillating are poor
contact with chest wall and incorrect positioning of pads.

The Lifepak 12 pads last for up to 50 shocks without needing to be changed.

Waveform Analysis

%
VF waveform analysis has the potential to improve the timing and effectiveness of
defibrillation attempts. This technique is advancing rapidly but is not yet available to
assist rescuers.

Retrospective analysis of VF waveform in clinical and animal studies and theoretical
models suggest that it is possible to predict with varying reliability the success of
defibrillation from the fibrillation waveform.
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SAED (Semi Automatic External Defibrillator)

Characteristics of the SAED machine

The machine can be set to manual or advisory mode. WBHSD: All ICU & ED
machines default to manual, all others to advisory mode.
In advisory mode the machine utilises algorithm based internal software to
diagnose shockable rhythms and deliver a shock. The machine verbally
instructs staff what to do, when to shock etc. most Lifepak 12 machines in the
ward area are automatically set to advisory mode.
Manual mode can also be used, by pressing the analysis button. This allows
you complete control of the machine. This mode is much quicker for
experienced staff to use as they do not have to wait for the machine to go
through the analysis process, thereby allowing shocks in quick succession.
In the advisory mode the machine is configured to only provide one
shock.
The SAED can only diagnose and treat asystole and VF > 180 beats/min
All machines default to 200 joules except Paeds which defaults to 50 joules.

Always assess for signs of life
Whilst the machine is in diagnostic mode, do not touch the patient. Do not
perform CPR between shocks as the machine cannot diagnose the artefact
and will default to no-shock mode.

Dumping the load

If the SAED charges to its preset joules and the patients condition changes and the charged
joules are not to be delivered, press the black button in the centre of the round dial (on the
bottom right hand of the machine) as this will dump the load.

If the charge is not used in 30 45 seconds the machine will automatically disperse
the electricity.

Lifepak 12 Pads

There are two sizes of pads used with the Lifepak 12

1. Infant up to 15kg - Paediatric pads
These are placed in the anterior / posterior position.
2. Adult pads

o For children above 15kg, the adult pads are used but placed in the
anterior posterior position.

o In adults these are placed in the usual Right upper chest and below
Left lower armpit

o The pads have placement indicators on them to guide you
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The same pads can be used to monitor, defibrillate and external pace

You can :
Monitor for 24 hrs,
Defibrillate x 50 shocks
Pace for 8 hours with one set of pads.

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!
Cardioversion

Cardioversion refers to the use of electrical energy to revert a cardiac rhythm other
than pulseless ventricular tachycardia or ventricular fibrillation.

The difference between cardioversion and defibrillation is that in cardioversion the
electrical energy (shock) is synchronized to land on the R wave of the ECG. This is
to avoid the T wave (ventricular repolarisation) which can induce VT.

Indications

1. VT with a pulse
2. SVT
3. Atrial Flutter
4. Atrial Fibrillation when present for < 6 months

Urgent cardioversion is required for the listed arrhythmias where hypotension,
systemic hypoperfusion, congestive cardiac failure or myocardial ischaemia are
present.

Anti arrhythmic drugs are slower in effect and less reliable than electrical
cardioversion in converting a tachycardia to sinus rhythm, therefore drugs are
reserved for stable patients without adverse signs and elective cardioversion is
usually the preferred treatment for the unstable patients displaying adverse signs.

Contraindications

1. Sinus tachycardia
2. Sick sinus syndrome
3. Left atrial enlargement
4. Recent vascular surgery sinus rhythm is not usually maintained if restored
electrically, if rhythm is tolerated , cardioversion is withheld for 10 -14 days
5. Atrial fibrillation
a. Which has been present for more than 6 months as it
is unlikely to revert and there is an added risk of
embolic showers.
b. Which is associated with the following as they are
unlikely to revert
Thyrotoxicosis
Severe l ventricular dysfunction
Cardiomyopathy
Myocarditis
Pericarditis
Left atrial enlargement
c. Slow AF in the absence of drugs
d. If previous cardioversions have resulted in the return of
AF despite adequate drug therapy.
NOTE: When performing a cardioversion, it is essential that the same safety
procedures are adhered to as if you were defibrillating.
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Cardioversion Procedure

MO explains procedure and obtains consent
Nil by mouth for at least 6 hours prior to procedure unless emergency
cardioversion is required
IV cannula inserted
Pathology Blood for electrolytes (hyper/hypokalemia, hypocalcaemia,
Hypomagnesemia)
Full blood count (anaemia can cause arrhythmias)
ABG
Coagulation screen
Consider anticoagulation, as cardioversion of AF can cause thromboembolic
effects. This should be administered for minimum of 48 hours prior to the
procedure if possible
Record vitals
Baseline ECG and post cardioversion ECG
Continuous cardiac monitoring is required during procedure
Pre oxygenate via BVM 15 litres
Select synchronise mode on defibrillator
Give sedation
Have emergency equipment and drugs ready
Minimal current is used
Post cardioversion care regular observation, monitoring, give anti-
arrhythmic as needed

Energy Setting

The usual range of joules for defibrillation in a cardiac arrest is 200 joules in a
biphasic machine, & 360 joules using a monophasic machine.

For cardioversion this range will alter depending on the type of arrhythmia.

Suggested energy levels for cardioversion are as follows

VT with Pulse 50J, 100J, 150
VT with irregular form and rate 50J, 100J, 150
Atrial fibrillation 50J, 100J, 150
Atrial Flutter 50j, 100j, 200j,
SVT (unresponsive to medication) 50j, 100j, 200j,

Cardioversion in the presence of digoxin toxicity is to be avoided!! Cardioversion in
the presence of therapeutic digoxin levels is now thought to be safe.

%
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Non Invasive Pacing

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The purpose of the cardiac pacemaker is to provide an artificial electrical
stimulus to the heart muscle when either the impulse initiation or intrinsic
conduction system is defective.
Primarily used for emergency treatment of symptomatic bradyarrhythmia,
unresponsive to pharmacological intervention.
The electrical current is passed from an external pulse generator via cable to
adhesive electrodes thru the chest wall to the heart.
NOTE: The pads deliver the energy; the patient must have monitoring
electrodes on as well.
There are 2 different modes of transcutaneous pacing Demand and Non
demand
Pad placement is anterior posterior positioning.

Demand Pacing

The pacemaker delivers an impulse only when required or on demand. The
pacemaker searches for intrinsic cardiac activity if it does not detect or sense a beat
within a designated interval it will deliver a paced impulse.

All lifepaks in the district default to demand pacing.

Non Demand Pacing

Delivers electrical stimulus, at the selected pacing rate, regardless of the patients
cardiac activity. This mode is more likely to be used for patient transfer.

Procedure

External pacing via the Lifepak

1. The procedure should be explained to the patient.
2. Apply the pads preferably in the anterior posterior position
(Pads last approximately 8hrs)
3. Sedation commenced
4. Obtain baseline observations & ECG
5. The rate is selected first, normally 60 - 80bpm
6. The ma (amplitude) is selected next, start with lower Ma & increase gradually
until electrical capture is achieved
7. Check that mechanical capture is present by performing regular pulse checks
+ BP

8. Continue sedation and check patient comfort
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External pacing should not continue past 24hrs.

Care must be taken to monitor the patients response to external pacing eg capture
is maintained. Sometimes ma needs to be increased to keep capture. Care must be
given when ma required maintaining capture reaches in excess of 120ma.

Not all Lifepaks have the capacity to pace. Machines with pacing capabilities
are located in the Emergency departments, IC/CCU, OT and Mental Health.

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Drugs used in Cardiac Arrests

Whilst the listed drugs have theoretical benefits in selected situations, no medication
has been shown to improve long term survival in humans after cardiac arrest.
Priorities are defibrillation with external cardiac compressions (oxygenation and
ventilation together).

If there are no peripheral veins, an IO should be inserted. If a central line/PICC is
available it should be used.

Administration of IV/IO medication in a cardiac arrest situation is always followed by
a 30 mL flush. It is easier to hang a bag of saline rather than having to draw up
30mLin a syringe each time.

Avoid glucose which is redistributed away from the intravascular space rapidly and
causes hyperglycaemia, which may worsen neurological outcome after cardiac
arrest.

All resuscitation trolleys in the Wide Bay Health Service - Fraser Coast Campus are
equipped with emergency drugs, the following drugs are in the top drawer of every
trolley.

Mini jets

Atropine, 1mg
Adrnaline 1mg

Ampoules

Adrenaline 1:1000
Magnesium 10 mmol
Amiodarone 150mg in 3mL/ 500mLbag 5% glucose

Note: These drugs needs to be drawn up from an ampoule and so therefore will
take a few minutes to prepare.

Pre packed

Potassium 10mmols in 100mLof saline

Minijets usage

1. Flip yellow caps off both ends
2. Place both parts together and twist until you feel resistance
3. Administer

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Administration of Drugs via Intraosseous

If IV access cannot be obtained, intraosseous access is a safe and effective method
for administration of resuscitation drugs, laboratory evaluation and is attainable in all
age groups.

If pathology is taken from Intra-osseous make sure this is written on the pathology
form.

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http://www.youtube.com/watch?v=7aCkJDgXdFA&feature=related
EZI IO insertion
8 Sites
Proximal Humerus
Preferred site for
adults
Optimal si te for high
flow and quick drug
uptake
Awake, responsi ve
patients
Less painful
Distal Femur
Under 6 years
Proximal Tibia
Unresponsi ve
Unfamiliarity with
other sites
Unable to
landmark
Distal Tibia
Larger patient
Unable to access other
sites
Site selection
Dependent upon:
No previous IO in 48 hours
Absence of
contraindications
Accessibility
Ability to secure & monitor
After insertion, check
Firmly seated needle
Flash of blood
No leaking around site
No sign of extravasations'
Secure using EZ Stabilizer
Use EZ Connector
EZ-IO wrist band placed

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Administration of Drugs via ETT

ETT administration is acceptable if both IV and IO access cannot be obtained.

Procedure

1. Suction the airway if possible
2. Insert a clean suction catheter beyond the tip of the ETT and instil the
medication via the catheter
3. Administer THREE times the IV Dosage, diluted to 10 mL in water
(evidence suggest better drug absorption takes place when diluted with water
rather than saline)
4. Followed by at least two vigorous ventilations to disperse the drug.
5. Ensure eye and mucous membrane protection when opening airway for
instillation of drugs.

Drugs able to be administered down the ETT

Adrenaline
Lignocaine
Atropine
Naloxone

Lignocaine is the only anti arrhythmic that can be administered via the ETT.
This route cannot be used if a laryngeal mask is insitu!
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First Line Drugs used in a Cardiac Arrest

DRUG

LIST TWO
INDICATIONS FOR
USE

IV DOSE

ETT DOSE

MECHANISM OF ACTION

LIST TWO UNDESIRED EFFECTS

Adrenaline

Asystole
VF/VT arrest
PEA
Second line drug in
bradycardia

1 mg bolus every 4
mins in an arrest

0.1 mg as second
line drug in
bradycardia

Infusion
1 -20 mcg/min

3 mg bolus diluted
in 10 mLH0

Every 4 minutes in
arrest

Alpha & beta stimulant
causing vasoconstriction,
therefore improving
myocardial & cerebral blood
flow facilitates defibrillation

Increased A-V conduction,
Increased contractility
Increased automaticity initiate
cardiac rhythm

Increases ventricular irritability
converts fine VF to coarse

Bronchodilation

Necrosis if extravasation occurs (give via
central line ASAP)

Tachycardia, tachyarrythmias

Severe hypertension after resuscitation

Agitation

Do not mix with sodium bicarbonate it
inactivates it

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DRUG

LIST TWO
INDICATIONS FOR
USE

IV DOSE

ETT DOSE

MECHANISM OF ACTION

LIST TWO UNDESIRED EFFECTS

Atropine

Symptomatic
bradycardia

0.5mg every
4 mins
(maximum of
3mg)

1.5 mg bolus
diluted in 10mLH2O

Parasympathetic antagonist
that blocks action of vagus
nerve on the heart

Anticholinergic

Allows SNS to increase HR
&BP

Increased A-V conduction

Dry mouth

Urinary retention

Tachycardia ,hypotension

Excitement /delirium

Hyperthermia in large doses

Raises intraocular pressure in pt with
glaucoma. Treat with pilocarpine eye
drops if necessary

Dilated pupils

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Second Line Drugs used in a Cardiac Arrest

DRUG

INDICATIONS
FOR USE

IV DOSE

ETT DOSE

MECHANISM OF ACTION

ADVERSE EFFECTS
!
Amiodarone

Class III
antiarrhythmic

VT with pulse

In VF/VT arrest
when no response
to defibrillation &
adrenaline

300mg bolus
(5mg/kg )
in 20mL5%
glucose
over 2 mins
(in arrest)

Same dose
Dilute 50mL
Over 20 mins
Conscious
VT/SVT

repeat
dose (150mg)

maintenance
infusion 10-15mg
/kg/day

NOT able to be
given by ETT

Antiarrhythmic complex
pharmacokinetic

Effects sodium ,potassium &
calcium channels

Blocks alpha & beta adrenergic
blocking properties

Bradycardia / heart block

Hypotension

Phlebitis/ pain at IV site(should be given
through central line ASAP)

Us Non PVC infusion sets

Dilute in glucose 5 % only

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DRUG

INDICATIONS
FOR USE

IV DOSE

ETT DOSE

MECHANISM OF ACTION

ADVERSE EFFECTS

Lignocaine

VT with pulse

In VF/VT arrest
when no response
to defibrillation &
adrenaline

1mg/kg

3mg /kg

Antiarrhythmic complex
pharmacokinetic

Membrane stabilising agent inhibits
the fast inward sodium movement
and thus decreases the rate of
depolarisation, particularly in
ischemic tissue. Class 1 b anti arr
thymic

Respiratory depression

Hypotension, bradycardia, heart block,
asystole

Drowsiness, confusion, twitching

Blurred vision

Numbness

Slurred speech

NOTE: Lignocaine is now only recommended when Amiodarone is unavailable, or ETT administration of an
antiarrhythmic is required.

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Electrolytes
Electrolyte High Levels Low Levels Use Administration Adverse Effects

Potassium

Essential for membrane
stability

P waves K+ >8
flattened / no P waves
PR - prolonged
QRS K+ > 10 widened
ST depression
T waves - tall
symmetrical
AV blocks

PACs & PVCs

ST depression
T waves flat, broad
U waves appear

Cardiac arrest with

Hypokalemia

Digoxin toxicity

Hypomagnesaemia

Persistent VF/VT low K+

Fast bolus infusion of
5 mmol over 2 mins

(50mLof prepacked
10 mmol in 100mLbag )

Note : 10mmol ampoules
are available in ED/ICU only

Necrosis if
extravasates

Excess=bradycardia
& hypotension

Magnesium

Essential for membrane
stability
Hypomagnesaemia
causes cardiac
hyperexcitability
particularly in presence
of hypokalemia &
digoxin

Bradycardia
PR interval - prolonged

QRS widened

T waves - tall

AV blocks & PVCs

PR interval - prolonged
QT interval prolonged
(" risk of Torsades)
QRS widened
ST depression
T waves inversion flat
broad
U waves appear
PVCs

Torsades de Pointes

Hypomagnesaemia

Hypokalemia

Digoxin toxicity

In VF/VT when no
response to defib &
adrenaline

5mmol over 2 mins

repeat x1

then 20mmol over
4 hours if required

Bradycardia
Respiratory muscle
weakness Dilute &
give slowly
Dont mix with calcium

Calcium Chloride

5 mL over 2 mins

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Electrolyte Use Administration Adverse Effects
%
Sodium
Bicarbonate

Alkalising agent

!

Cardiac arrest with

Hyperkalemia

Documented severe
metabolic acidosis

Protracted arrest (more
than 15 min)

overdose of tricyclic
antidepressants

1mmol/kg
over 2 mins

further administration guided by
ABGs

Risk of alkalosis, hypernatremia and
hyper osmolality

Acidosis may worsen when CO2 is
liberated from NaHCO3 and freely
enters the cells

Sodium bicarbonate and adrenaline (or
calcium) when mixed may inactivate
each other, precipitate and block the IV
line

Note: All electrolytes are to be diluted into at least 20 mL of saline, for ease of administration

ABG analysis is an inaccurate measure of the magnitude of tissue necrosis in arrest situation

!
Use Dosage Adverse Effects

ADENOSINE

Note: WBHSD-FCC policy
states that ALS
Nurses are NOT
authorised to order
/ administer
Adenosine without
a written or verbal
order from a
Medical Officer

SVT

Atrial tachycardia

To differentiate diagnosis
in broad complex
tachycardia

6mg, then 12 mg,12mg
rapid bolus in large vein with a
three way tap, with a 30 mL flush
simultaneously

Flush feeling / impending doom

ventricular standstill /asystole

dyspnoea

chest pain

contraindicated in asthma/wheezing
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The algorithm below is produced by the Australian Resuscitation Committee.
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WBHSD-FCC algorithms have been produced in line with ARC Guidelines to support the WBHSD-FCC
ALS policy for nurses.

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Page 104 of 135
!
$/*25,7+0)259) $/*25,7+0)259) $/*25,7+0)259) $/*25,7+0)259)
38/6(/(66 38/6(/(66 38/6(/(66 38/6(/(66
977256$'(6 977256$'(6 977256$'(6 977256$'(6
977256$'(6 977256$'(6 977256$'(6 977256$'(6
BLS until defibrillator attached
6'#&$*789*:
Ventilate 100% O2
Defibrillate 200j 2 mins CPR
IV access & pathology
Intubate (<20secs) 6-10 bpm
Defibrillate 200j 2 mins CPR
IV Adrenaline 1mg every 4 mins
Defibrillate 200j every 2 mins
then 2 mins CPR
IV Amiodarone 300mg
in 20mls of 5% Glucose over
2 mins
;&20*<*!%,'#*='"),
>?@*?!A
Continuou s CPR
for 2 mins post
resus
or till pt protests
Check rhythm every
2 mins prior to
defibrillating.
On completion of infusion
IV Amiodarone 150mg in
20mls of 5% Glucose over 2mins
Note- Pt to have only 1200mg of
Amiodarone in total in 24hrs
!
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Page 105 of 135
!
$/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25
&216&,28697 &216&,28697 &216&,28697 &216&,28697
Valsalva Manoeuvre
High flow O2
IV/IO access & pathology
Severely compromised?
IV Amiodarone 300mg
in 50 mls of 5% Glucose over
20 mins
On completion of infusion
IV Amiodarone 150mg in 50mls of
5% Glucose over 20mins
Note- Pt to have only 1200mg of
Amiodarone in 24hrs
If the patient
becomes
unstable
Synchronised Cardioversion
;&20*<*!%,'#*='"),
>?@*?!A
NO YES
Signs of Compromise
Hypotension < 90 SBP
Heart failure
Chest pain
Dizziness
ALOC
!
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Page 106 of 135
!
$/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25
$6<672/(3($ $6<672/(3($ $6<672/(3($ $6<672/(3($
BLS - attach defibrillator
6'#&$*789*:
Ventilate 100% O2
IV/IO access & pathology
Intubate (<20secs) 6-10 bpm
!"#$%& '()
IV Adrenaline 1mg every 4 mins
!"#$%& '()
check rhythm,
response, breathing
;&20*<*!%,'#*='"),
>?@*?!A
Continuous CPR for
2 mins post resus
or till pt protests
Consider
electrolytes
!
!
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Page 107 of 135
$/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25
%5$'<$55<7+0,$6 %5$'<$55<7+0,$6 %5$'<$55<7+0,$6 %5$'<$55<7+0,$6
Any SLOW rhythm when:
1. HR <40bpm
2. BP <90 systolic
3. Ventricular arrhythmia
4. Heart failure
5. Chest pain
6. ALOC
High flow O2 therapy
IV Atropine 500mcg
If no immediate clinical effect,
follow with
IV Adrenaline 0.1mg
*)+,+-."./+&+"0123&"-%0"04&+&"+5+16 7"#$%8
NOTE- Max Atropine 3mg throughout entire resus
High risk rhythm
Fails to respond to
drugs
External Pacing
;&20*<*!%,'#*='"),
>?@*?!A

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Page 108 of 135

$/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25 $/*25,7+0)25697 697 697 697
If no response If no response If no response If no response
IV Am|odarone 300mg |n 50m|s of IV Am|odarone 300mg |n 50m|s of IV Am|odarone 300mg |n 50m|s of IV Am|odarone 300mg |n 50m|s of
5% G|ucose over 20m|ns 5% G|ucose over 20m|ns 5% G|ucose over 20m|ns 5% G|ucose over 20m|ns
OR OR OR OR
Verapam|| 5mg s|ow IV Verapam|| 5mg s|ow IV Verapam|| 5mg s|ow IV Verapam|| 5mg s|ow IV
IV Adenos|ne 6mg IV Adenos|ne 6mg IV Adenos|ne 6mg IV Adenos|ne 6mg
Rap|d Bo|us w|th f|ush Rap|d Bo|us w|th f|ush Rap|d Bo|us w|th f|ush Rap|d Bo|us w|th f|ush
If no response If no response If no response If no response
If no response then further If no response then further If no response then further If no response then further
Valsalva Manoeuvre
High flow O2
NO
Severely compromised?
YES
If the patient
becomes
unstable
Synchronised Cardioversion
Signs of Compromise
Hypotension < 90 SBP
Heart failure
Chest pain
Dizziness
ALOC
;&20*<*!%,'#*='"),
>?@*?!A

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Page 109 of 135

"19'34!!

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Page 110 of 135

!
Basic Airway Management

!
Insertion of Oropharyngeal Airway Guedels

Determine the patients mouth width and length, measure the airway from the corner of the
patients mouth to the ear lobe.

Insertion of a Guedels airway that is too large can obstruct respirations while one that is too small
will not hold the tongue in appropriate position.

Average size for adults Female size 3
Male size 4

The airway is now placed in the mouth facing the side of the mouth and then turned over to rest
on top of the tongue, rather than the old way in which it was placed facing towards the roof of the
mouth and then twisted.

Insertion of Nasopharyngeal Airway

Determine the patients size, nasal structure, sex, age, check by measuring airway from nasal
opening to the ear lobe.

Small (size 5-6mm) for under 45kg with a small bone structure
Medium (size 7-8mm) for under 70kg with a small bone structure
Large (size 9-10mm) for more than 70kg

General rule about the size of the persons little finger.

Nasopharyngeal airways are contraindicated in patients who have had injuries to the nose,
predisposition to epistaxis, suspected fractured based of skull, or who have prolonged clotting
times.

Oxygen is an essential part of cardiopulmonary resuscitation and emergency cardiac care. Oxygen
should always be delivered at high flow rates to ensure adequate ventilation using 100% O2.

Modest changes in oxygen tension (or PaO2) produce large haemoglobin saturation changes in patients
who are on the steep portion of the oxyhaemoglobin saturation curve. Oxygen administration elevates
oxygen tension, increases arterial content and improves tissue oxygenation.

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Page 111 of 135

Oxygen Delivery Systems

The following table summarises the non invasive O2 delivery systems, flow rates, percentage of oxygen
delivered and features of each device.

%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
%
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Page 112 of 135
%
%
%
%
%
%
%
%
%
%
%
%
%
!
!
!
!
!
NOTE:- Nasal prong O2 flow rate is not more than 4lpm & when using the non- rebreather mask,
the flow rate should not be less than 10lpm minimum

Bag Valve Mask

Oxygen should be set to 15 Litres per min

The reservoir bag must be filled prior to use, otherwise only 48% oxygen is being delivered rather
than 100%. This can be done by placing your hand over the mask to allow the bag to fill up.

Oxygen cylinders

Ensure dial is on the number not between numbers or only 5 L/min delivered.

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Page 113 of 135

Cricoid Pressure

Aim

The aim of the application of cricoid pressure is to:

Prevent the regurgitation of gastric contents during induction and intubation.

It is also to provide a better view of the cords for the person performing the intubation.

Provide pressure in an upwards, backwards movement.

This is achieved by the application of pressure over the cricoid cartilage which occludes the lumen of the
oesophagus until the respiratory tree is isolated by an endotracheal tube.

The cricoid cartilage is located inferiorly to the thyroid cartilage and superiorly to the trachea. The
pressure is applied with thumb and forefinger as the patient loses eyelid reflex during induction. This
pressure is maintained throughout the induction and intubation process.

There are several points to note from the ARC policy statement:

Cricoid pressure should not be applied at any time the victim is making active vomiting attempts.
With the build up of a high positive pressure if you maintain the cricoid pressure there is a risk that
the victim will rupture their oesophagus.
Cricoid pressure is maintained until advised to release it by the MO intubating. You must ask
before releasing the pressure.

It is imperative to check for correct tube placement as soon as possible following intubation. If there are
concerns about its position, e.g. oesophageal intubation, it should be removed and bag-valve mask
ventilation continued until a further attempt is made.

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Endotracheal Intubation

%
Benefits

The major benefits of endotracheal intubation are that the patient is being ventilated with 100% oxygen
directly into the lungs and the cuff provides protection for the lungs from gastric contents. This procedure
provides a much safer and more effective method of ventilating a patient during cardiac arrest.

Size

When preparing for intubation the appropriate size ETT should be selected. The ET tube is sized
according to the internal diameter.

Usual adult sizes female 7- 8 mm Male 8 - 9 mm

To inflate the cuff most ETT require approximately 10mL of air. Inflate until you can no longer hear
gurgling then add an addition 1mL.

Assessing placement of Endotracheal Intubation

Listen for air entry
Look for bilateral rise and fall of the chest
Misting in ET tube
Increased oxygen saturations
Measure ETCO2 levels
Check chest x-ray
%
%
Complications of Endotracheal Intubation include

1. Tracheal damage
2. Dental injuries
3. Vocal cord trauma
4. Improper tube placement
5. Hypoxia
6. Laryngeal oedema
7. Increased airway resistance if the tube is too small relative to anatomical airway or to minute
ventilation

Laryngeal Masks

LMAs are commonly used in pre and post anaesthetic care.

Mechanical Ventilation may be used in the initial management of a cardiac arrest
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Page 115 of 135

Sequence of Intubation

1. Equipment selection

Correct size ETT tube - Adult Male - 8 - 9mm
- Adult Female - 7 - 8mm
10mLSyringe
Tape
Laryngoscope
Bag-Valve-Mask equipment
O2 & suction
Introducer
Stethoscope

2. Equipment preparation

Ensure cuff can be inflated / deflated

Ensure suction is on and accessible
Laryngoscope blade is working
Other equipment is easily accessible
Positioning of patient is appropriate

3. Patient positioning head of bed off, remove pillows if requested
4. Applying cricoid pressure when asked and release when asked to
5. Monitoring of observations
6. Securing of ET tube, - there are various methods of securing ET tube.
This will be demonstrated during training sessions
7. Documentation ensure the recorder knows the size of the ETT tube, cm at teeth and how
much air is instilled into the cuff, number of attempts etc.

8. Post assessment of ET tube placement.

The patients chest should be auscultated to ensure equal and effective air entry.
Later the patient can be x-rayed to view proper placement
Observe your patients saturation's, colour etc

In an arrest situation if the patients airway is well maintained with a guedels and BVM intubation does
not need to be done immediately but can be performed later in the resuscitation.
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Page 116 of 135

RECOGNITION OF UPPER AIRWAY OBSTRUCTION

Airway obstruction may be partial or complete and may present in the conscious or the unconscious
victim. Some typical causes of airway obstruction may include, but are not limited to:

Relaxation of the airway muscles due to unconsciousness

Inhaled foreign body

Trauma to the airway

Anaphylactic reaction

The signs and symptoms of obstruction will depend on the cause and severity of the condition. Airway
obstruction may be gradual or sudden in onset and lead to complete obstruction within a few seconds.
Consequently the victim should be observed continually.

In the conscious victim who has inhaled a foreign body, for example, there may be extreme anxiety,
agitation, gasping sounds, coughing or loss of voice. This may progress to the universal choking sign
(clutching the neck with the thumb and fingers).

MANAGEMENT OF FOREIGN BODY AIRWAY OBSTRUCTION (CHOKING)
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Page 117 of 135

A Foreign Body Airway Obstruction (FBAO) is a life-threatening emergency. Chest thrusts and back
blows, effective for relieving FBAO in conscious adults and children > 1 year of age, although injuries
have been reported with the abdominal thrust {LOE IV} {Class A; LOE IV}

Ineffective Cough (Severe Airway Obstruction)

In all cases of choking send for help red alarm button 333

Conscious Victim

Perform up to five sharp back blows with the heel of one hand in the middle of the back between the
shoulder blades. Check to see if each back blow has relieved the airway obstruction. The aim is to
relieve the obstruction with each blow rather than to give all five blows. An infant may be placed in a head
downwards position prior to delivering back blows, i.e. across the rescuers lap [Class A; LOE IV]

If back blows are unsuccessful the rescuer should perform 5 chest thrusts. Check to see if each chest
thrust has relieved the airway obstruction. The aim is to relieve the obstruction with each chest thrust
rather than to give all five chest thrusts. To perform chest thrusts identify the same compression point as
for CPR and give five chest thrusts. These are similar to chest compressions but sharper and delivered
at a slower rate. The infant should be placed in a head downwards supine position across the rescuers
thigh. Children and adults may be treated in the sitting or standing position [Class A; LOE IV]

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@)3*)9.716!
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!
!
!
!
!
!
!
!
!
!
!
!
!
!
!
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Page 120 of 135

Leadership

Dont Panic!!

The Team Leader is responsible for:

1. Allocating the roles
2. Directing and coordinating the resuscitation attempt
3. The safety of the resuscitation team at the cardiopulmonary arrest
4. Ending the resuscitation attempt when indicated, always in consultation with other resuscitation
team members and medical staff otherwise in charge of the patient.
5. Documenting (including audit forms) and for communication with relatives and other healthcare
professional involved in the patients management.
6. Encourage all team members to contribute
7. Organising resuscitation team debriefing.
8. Allocating a nurse to stay with family if they are present during the arrest

Take control of the situation

There should be one team leader
If you are unsure ask for help, it is better than saying nothing or doing the wrong thing.
Listen to the other staff, ask for consensus?

Allocate tasks to others. If possible, the team leaders should step back and provide overall direction.

Give directions in a clear, firm voice

Be assertive, not aggressive.
Dont assume, not all staff feel confident handling arrest situations.

Take a second to get your head clear

What rhythm are you in?
Which algorithm do you need to follow? place the algorithm on the patient
Dont be indecisive

Regularly assess the effectiveness of other staff performing EAR / CPR

Is the depth and rate and rhythm appropriate?
Are they communicating?
Does the person doing CPR need a break?
Give positive feedback and direction for improvement
Can you feel a carotid pulse during compressions?

What has caused the arrest?

Do you know the person? What is the history? Why are they in hospital?
Have any bloods been done? Could it be an electrolyte imbalance?

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Dont forget to document appropriately and send photocopy of arrest record to CE-ALS

Talk to the family and offer support

Debrief and discuss process with team members.

Reflective practice what areas could you have done better?

Think about your performance from different perspectives
How did you perform clinically, did you provide good leadership etc.
Was there anything that you were unsure about?
Identify and action training needs

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Page 122 of 135

Additional Resources

Websites

Qheps http://qheps.health.qld.gov.au
Australian Resuscitation Council www.resus.org.au
European Resuscitation Council https://www.erc.edu
American Heart Association http://www.americanheart.org
Advanced Paediatric Life Support http://www.apls.org.au

Gold Coast Emergency Department http://emergencyweb.net/login.php?u
Skills Development Centre http://www.sdc.qld.edu.au/

Texts

ARC Manual is located in each Clinical Unit

Advance Paediatric Life Support, Practical Approach 4
th
Edition (located in the ACLS
Clinical Educators Office, ERC Maryborough Hospital)

Neonatal Resus located in the Special Care Nursery and Medical Education Unit, Hervey Bay Hospital

QSEU Library

Audiovisual

Life Pak 12 video

BOC O2 CD

Other

Difficult Intubation Pathway G:\Clinical Departments\Advanced Cardiac Life Support

Self Directed Learning Package G:\GDriveMaryborough\Education\Training Packages\ Vascular
EZYIO Access

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Page 123 of 135

"66)%*1#).!!
!

Participant Program Outline Fast track - Adult ALS

Fast Track Course (by request only)

Sessions
0800 0815 Welcome , Health & Safety ,session objectives
0815 - 0900 BSL demonstration & assessments
0900 - 0930 SAED Demonstration & assessments
0930 10.00 Exam
10.00 - 10.15 Morning tea
10.15 -10.20 Exam feedback
10.20 12.00
Practical demonstration
Practice & Assessment clinical scenarios
Evaluation

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Page 124 of 135
!

ALS Certification Guidelines Clinical Scenarios

Two types of scenarios

Each participant must successfully complete one shockable and one non-shockable scenario to pass.
If a resit is required - it must be from the similar type of scenario.

All mandatory criteria must be achieved

First line drug administration
Defibrillation indications, procedure & safety
Rhythm recognition.
Workplace health & safety requirements
Leadership

Team members are not allowed to prompt the team leader.

The team leader must demonstrate appropriate leadership skills i.e. checking on other team
members, giving requests in clear firm voice etc.

During assessment - You will not be expected to work outside of your scope of practice eg nurses
must receive a verbal/written order before ordering/administering Adenosine. Please refer to the ALS
Policy regarding scope of practice.

If necessary, resits where possible will be held on the same day, time permitting. If time does not
permit you will be required to register to do your resit at a future training/ practice sessions. Feedback
will be provided to assist you with this process.

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Page 125 of 135

AUSTRALIAN RESUSCITATION COUNCIL

SUMMARY OF MAJOR CHANGES TO ADVANCED LIFE SUPPORT GUIDELINES

DECEMBER 2010
In December 2010 the New Zealand Resuscitation Council and Australian Resuscitation Council
published their combined and updated ALS guidelines. These revised evidence based guidelines
incorporate the published literature including the evidence evaluated as part of the international evidence
consensus process (published in October 2010).
The main changes in these guidelines are outlined below, grouped according to the relevant guideline.

Guideline 11.1: Introduction to Advanced Life Support
Increased emphasis on:

Monitoring the effectiveness of compressions, adequacy of ventilation and quality of CPR and timing of
defibrillation

The early detection and prevention of cardiac arrest in the pre-hospital and in-hospital settings

Guideline 11.1.1: CPR for ALS Providers

CPR to commence with chest compressions rather than ventilation

Use the combination of unresponsiveness and absent or abnormal breathing (because agonal gasps
may continue despite cardiac arrest) to identify cardiac arrest.

Depth of compression increased to > 5 cm (with insufficient evidence to recommend a specific upper
limit for chest compression depth), but still using a target of 1/3 of the Antero-Posterior chest diameter

Chest compression rate remains at approximately 100/min, but states that there is no evidence that a
compression rate over 120 / minute offers any advantage

Use of waveform capnography to confirm ETT placement, monitor quality of CPR, and to provide early
indication of ROSC

Simultaneous compressions and breaths are to be avoided

Ventilation during cardiac arrest with LMA may require 15:1 or 30:2 to deliver effective breaths

CPR prompt /feedback devices may be considered for clinical use as part of an overall strategy to
improve the quality of CPR. Instructors and rescuers should be made aware that a compressible support
surface (eg, mattress) may cause a feedback device to overestimate depth of compression.

When using a defibrillator in manual mode, it is safe to charge the defibrillator while chest compressions
continue in preparation for rhythm analysis and possible defibrillation
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Increased emphasis on:

High-quality chest compressions with minimal interruptions

Fallibility of pulse check even in the hands of clinicians

Guideline 11.2: Protocols for Adult Advanced Life Support (inc ALS Flowchart)

New co-badged ALS flow chart, designed to be easier to follow, and to increase the awareness of the
importance of post-resuscitation care.

Only single shocks are recommended (stacked shocks considered only in specific special
circumstances)

Continuing compressions during defibrillator charging to minimise interruptions

Adrenaline still recommended at same points in the arrest
o
Non-shockable rhythm: 1 mg immediately for non-shockable rhythms then every 35 min: alternate
cycles of CPR
o
Shockable rhythms (VF/VT): 1 mg after the second shock then every 35 min: alternate cycles of CPR.
o
Timing of drug administration now recommended being at the time of recommencement of CPR.

Amiodarone 300mg is still recommended after the third shock, but timing of drug administration now
recommended being at the time of recommencement of CPR.

Atropine is no longer recommended for routine use for cardiac arrests due to asystole or PEA.

Reiterated emphasis on:

Quality CPR with minimal interruptions to chest compressions

Monophasic defibrillation: to use 360 joules for all shocks

Biphasic defibrillation: to use 200 joules for all shocks unless clinical evidence of other energy level for a
specific device

Use of AEDs to facilitate early in-hospital defibrillation

Guideline 11.3: Precordial thump and fist pacing

The precordial thump is no longer recommended for VF

It may be considered for patients with monitored, pulseless ventricular tachycardia if a defibrillator is not
immediately available.

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Guideline 11.4: Electrical therapy for Adult Advanced Life Support

For defibrillation when using biphasic defibrillators, self-adhesive defibrillation pads are safe and
effective and offer advantages (eg. facilitating pacing, charging during compressions, safety [including
removing risk of fires]) over defibrillation paddles.

Single (non-stacked) shocks are recommended (as for 11.2 above).

CPR should be continued during charging of the defibrillator, and CPR should not be interrupted until
rhythm reanalysis is undertaken (as for 11.2 above)

Reiterated:

Monophasic defibrillation: to use 360 joules for all shocks (as for 11.2 above)

Biphasic defibrillation: to use 200 joules for all shocks unless clinical evidence of other energy level for a
specific device (as for 11.2 above)

Guideline 11.5: Medications in Adult Advanced Life Support

Drug administration via IV or intra-osseous route, with the endotracheal route de-emphasised.

Adrenaline and Amiodarone as for 11.2 above.

Other drugs not recommended for routine use, but may have value for other specific reversible causes.

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Guideline 11.5: Medications in Adult Advanced Life Support

Drug administration via IV or intra-osseous route, with the endotracheal route de-emphasised.

Adrenaline and Amiodarone as for 11.2 above.

Other drugs not recommended for routine use, but may have value for other specific reversible causes.

Guideline 11.6: Equipment and Techniques in Adult Advanced Life Support

Decreased emphasis on the role of early tracheal intubation.

A supraglottic airway device may be considered by healthcare professionals trained in its use as an
alternative to bag-mask ventilation during cardiopulmonary resuscitation, or for definitive airway
management during cardiac arrest and as a backup or rescue airway in a difficult or failed tracheal
intubation.

Waveform capnography is recommended to confirm and continuously monitor the position of a tracheal
tube in victims of cardiac arrest and it should be used in addition to clinical assessment (auscultation and
direct visualization is suggested). It is also recommended to confirm and continually monitor tracheal
tube placement, quality of CPR, and to provide early indication of ROSC.

Potential role of CPR prompt devices to monitor and improve quality of CPR (as for 11.1.1 above).

Increased role of investigations (including intra-arrest ultrasound) to assist in detection of potentially
reversible causes.

Routine use of pacing (fist and electrical) not recommended in asystolic cardiac arrest (apart from
special circumstances)

Guideline 11.7: Post Resuscitation Therapy in Adult Advanced Life Support

Recommendation for the introduction of a comprehensive post-resuscitation treatment protocol for the
management of patients after cardiac arrest.

Specific changes include:

Avoid hyperoxaemia after ROSC; titrate oxygen to SaO2 9498%

Primary percutaneous coronary intervention in appropriate patients with sustained ROSC (including
those comatose and cooled)

Glucose control to treat hyperglycaemia (> 10mmol/L) and avoid hypoglycaemia.

More emphasis on identifying underlying cause or associated injuries, and managing them accordingly

More acute awareness of the limitations of the traditional tools used for prognostication after cardiac
arrest (especially after therapeutic hypothermia)

Guideline 11.8: Therapeutic Hypothermia after Cardiac Arrest
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Page 129 of 135
Reiterated:

Recommendation for routine use of therapeutic hypothermia for comatose survivors of out-of-hospital
cardiac arrest due to ventricular fibrillation

Consideration of routine use of therapeutic hypothermia for comatose survivors of cardiac arrest of any
rhythm for in and out-of-hospital cardiac arrest irrespective of aetiology.

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SUMMARY OF MAJOR CHANGES TO BASIC LIFE SUPPORT
GUIDELINES
NOVEMBER 2010
GUIDELINE 2 - Priorities in an
Emergency

Focus changed to cover a range of emergency
situations not just cardiac arrest and includes collapsed and
injured victims.

GUIDELINE 3 - Unconsciousness
Focus now on the breathing unconscious victim (the
non breathing unconscious victim will now fall under
Guideline 8: CPR)

GUIDELINE 4 - Airway
Minor error in FBAO flowchart corrected

GUIDELINE 5 - Breathing
References to signs of life removed as these are
open to interpretation and feedback from member
organisations suggests that the term signs of life is
confusing.
Focus on unresponsive and not breathing normally as
the indicators for resuscitation.

GUIDELINE 6 - Compressions
References to signs of life removed as these are
open to interpretation and feedback from member
organisations suggests that the term signs of life is
confusing.
Focus on unresponsive and not breathing normally as
the indicators for resuscitation.
If unwilling / unable to perform rescue breathing, then
perform compression only CPR.
Pulse check downgraded for health care
professionals as it is an unreliable indicator of the need for
resuscitation.
New focus on maintenance of CPR quality including
recommendations to change rescuers every 2 minutes to
decrease rescuer fatigue and maintain depth and rate of
compressions.
New section on use of prompt devices in clinical use
as a part of an overall strategy to improve quality of CPR.

NEW GUIDELINE
GUIDELINE 7 - AED Use In BLS

This is a new guideline recognising the role of AEDs as part
of BLS in both out of hospital and in hospital environments.
Clear recommendations that training in AED use should be
part of BLS education.

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GUIDELINES
GUIDELINE 8 - CPR Changes as per airway, breathing, compressions and AED
guidelines
Increase emphasis on bystander CPR as life saving
intervention.
Compression: rescue breathing ratio remains at 30:2
Steps in resuscitation are now DRS ABCD
check for Danger
check for Response
S has been added for Send for help
A directs rescuers to open the Airway
B directs rescuers to check Breathing but no need to
deliver two rescue breaths
C directs rescuers to perform 30 Compressions to
victims who are unresponsive and not breathing normally,
followed by 2 breaths
D directs rescuers to attach an AED as soon as it is
available
The major change is that in the victim who is
unresponsive and not breathing normally, CPR commences
with chest compressions rather than rescue breaths.
If unwilling / unable to perform rescue breathing, then
perform compression only CPR.

BLS FLOWCHART
Highlights Send for help
Enables compression only CPR if unwilling / unable to
perform rescue breathing.
in victims who are unresponsive and not breathing
normally, CPR commences with chest compressions rather
than rescue breaths.

GUIDELINE 10.1 - CPR Training
Regardless of the recency of CPR training or re-
training, any attempt at resuscitation is better than no
attempt and should be encouraged
Duration of CPR courses has not been determined.
Prompt / feedback devices can be used in training as
an overall strategy to improve quality of CPR.
The optimal interval for retraining has not been
established, but need for refresher training for individuals
who are not performing resuscitation on a regular basis is
recognised.
Recommendation that individuals trained in CPR
should refresh their CPR skills at least annually (opposed
to undertake assessment annually).

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GUIDELINES
GUIDELINE 10.2 - CPR Instructor
Competencies
DELETE
GUIDELINE 10.3 - Cross Infection
Risks & Manikin Disinfection

No major changes

GUIDELINE 10.5 - Legal And
Ethical Issues

Is undergoing a major re-write

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