Advanced life support training manual final 2017

Advanced Life Support Training Manual
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This guideline was developed by:
The ALS Subcommittee,
National Committee On Resuscitation Training
Ministry of Health Malaysia

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Second published in Malaysia in September 2017 by
Medical Development Division
Ministry of Health Malaysia
© The Ministry of Health Malaysia 2017 www.moh.gov.my
Institute for Medical Research Cataloging in Publication Data
A catalogue record for this book is available from the
Institute for Medical Research, Ministry of Health Malaysia
National Library of Malaysia Cataloging in Publication Data
A catalogue record for this book is available from the
National Library of Malaysia
MOH/P/PAK/347.17(GU)
ISBN 978-967-0769-85-1
All rights reserved: no part of this publication may
be reproduced, stored in a retrieval system, or
transmitted in any form or by any means,
electronic, mechanical, photocopying, recording,
or otherwise without the prior permission of the
Ministry of Health Malaysia.

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content
Foreword
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ii
Director General of Health Malaysia
Deputy Director General of Health (Medical)
Director Medical Development Division iii
Chapter 1-11
Chapter 1
Course Overview 1
Chapter 2
The Systematic Approach 3
The BLS Primary Survey 3
The ALS Secondary Survey 4
Chapter 3
Team Dynamics 6
Chapter 4
Airway Management & Ventilation 8
Overview of Airway Management 8
Oxygen Delivering Devices 9
(nasal cannula/simple face mask/venturi mask
/mask with O2 reservoir)
Non-invasive Airway Devices 12
(oropharyngealairway/nasopharyngealairway)
Manual Assist Ventilation 13
(mouth to mask ventilation/bag-mask ventilation)
Advanced Airway 15
(supra-glottic airways eg: LMA/ETT)
WaveformCapnography 25
Tracheobronchial Suctioning 27

Chapter 5
Defibrillation and Electrical Therapy 28
What is Defibrillation? 28
The Importance of Early Defibrillation 28
Defibrillators 28
Preparing the Patient 29
Safety Issues 30
Synchronized Cardioversion 32
Ventricular Tachycardia 32
Refibrillation versus Refractory VF 33
Pacing 33
Summary 33
Chapter 6
ALS Core ECG Rhythms and Recognition 34
Chapter 7
Drugs in Resuscitation 43
Chapter 8
ALS Algorithms 50
Chapter 9
Resuscitation in Special Situation 53
Chapter 10
Post Resuscitation Care 57
Chapter 11
Ethics of resuscitation and end of life issues 60
Appendix
64Skill Station Competency Checklist
National Committee on Resuscitation Training (NCORT) 70

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Medicine is now driven with new advancing
technology as well as drugs. The practice of
resuscitation is like-wise faced with new
and changing evidence from the scientific
community. What was practiced before is
now being reviewed and updated.
With the growing availability of trained first
responders and Public Access Defibrillators,
it becomes ever more important to support
Basic Life Support skills with those taught in
the Advanced Life Support. This is to
ensure the best possible outcome for
victims of cardiac arrests, either in or out of
hospital.
With this manual, I applaud the efforts of
the National Committee on Resuscitation
Training to ensure, the continuing updated
teaching of Advanced Life Support in line
with the international community. I hope
this will prove useful to participants in
updating themselves on the current best
practices in the field of resuscitation.
Thank you.
With this manual, I
applaud the efforts
of the National
Committee on
Resuscitation
Training to ensure,
the continuing
updated teaching of
Advanced Life
Support in line with
the international
community
Datuk Dr.Noor Hisham Bin Abdullah
Ketua Pengarah Kesihatan
Kementerian Kesihatan Malaysia

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The necessity and importance of practicing
cardiac life support is undeniably important
in the current age and era where medical
advancement is so widely available and
practiced. In the efforts to further inculcate
good practice and train personnel to be
more receptive in emergencies, this course
proves to be widely important. The
development and improvement of the
guidelines in managing cardiac
resuscitation is constantly being reviewed
and updated in order to provide better
understanding and care.
The development of this Advanced Life
Support Manual was a collaborative effort
by The National Advanced Life Support
Subcommittee with incorporation of course
content from the ILCOR (International
Liaison Committee on Resuscitation
Training ). Through this joint effort, I hope
this manual serves the purpose of training
and improving the quality of care offered.
I would also like to express my gratitude to
the committee for their continued efforts
in developing this manual. With that, I wish
all of you the best in this journey of self-
improvement, in working towards
bettering healthcare and inadvertently,
quality of life and care.
Thank you.
The development
and improvement
of the guidelines in
managing cardiac
resuscitation is
constantly being
reviewed and
updated in order to
provide better
understanding and
care
DATUK DR JEYAINDRAN TAN SRI SINNADURAI
Timbalan Ketua Pengarah Kesihatan
(Perubatan)

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Congratulations to National Committee on
Resuscitation Training (NCORT) for
producing such a high quality Advanced
Life Support (ALS) training that is tailored
to local settings.
Resuscitation plays a vital role in improving
the survival of patients who are facing life
and death situations. Hence, it is
important that a guideline should provide
simple and yet efficient algorithms for the
healthcare providers to follow in various
life threatening situations. ALS guidelines
have evolved as a result of evidence-based
findings and advances in medicine. Thanks
to the effort of all members in NCORT, this
current edition has showed us the
systemic approach in the resuscitation
practice based on the up to date evidence
we have so far.
With the development of this guideline, it
is hoped that it will provide the essential
steps for our healthcare providers to
perform good quality cardiopulmonary
resuscitation and post-resuscitation care,
thus improving the prognosis of the
patients.
Thank you.
With the
development of
this guideline, it is
hoped that it will
provide the
essential steps for
our healthcare
providers to
perform good
quality
cardiopulmonary
resuscitation and
post-resuscitation
care
Dato’Dr. Hj Azman Bin Hj. Abu Bakar
Pengarah
Bahagian Perkembangan Perubatan

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Course Overview
The Advanced Life Support Course aims to train doctors and healthcare providers working in
critical care areas in the resuscitation of patients beyond the ABC of resuscitation.
The course emphasizes on enhancing your skills in the treatment of arrest patients through
active participation in a series of simulated cardiopulmonary cases. These simulations are
designed to reinforce important concepts, including
 Basic Life Support (BLS)
 Advanced Life Support (ALS)
 Effective resuscitation team dynamics
Course Objectives
Upon completion of this course, you should be able to
 Manage cardiac arrest until return of spontaneous circulation (ROSC),
termination of resuscitation, or transfer of care
 Demonstrate effective communication as a member or leader of a resuscitation team
and recognize the impact of team dynamics on overall team performance
Course Description
The course concentrates on skills both individually and as part of a team. Lectures are short and
few. Therefore you are expected to have read the ALS provider training manual before the course.
In addition, strong BLS skills are the foundation of ALS. You must have passed the 1-rescuer
BLS/Automated External Defibrillator (AED) course before enrolment into the ALS course. The
course programme is as follows:

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Day 1
0730 - 0800h Registration
0800 - 0810h Course overview
0810 - 0840h Lecture
- Airway Management
- Drugs
- Algorithm
- Post resuscitation care
1000 – 1015h Tea Break
1015 - 1215h Skill stations:
Airway, Defibrillation and
ECG recognition + drugs with each station
lasting 45 minutes
1215 - 1300h ‘Put it all together’
1300 - 1400h Lunch
1400 - 1700h Megacode practice
Day 2
- Ethics in resuscitation
0830 - 0930h Theory test
0930 - 1300h Megacode practice
1300 - 1400h Lunch
1400 - 1700h Test on Airway and Megacode

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The BLS Primary Survey
The BLS goal is to support or restore effective oxygenation, ventilation, and circulation until ROSC or
until ALS interventions can be initiated. Performance of the actions in the BLS Primary Survey
substantially improves a patient’s chance of survival and a good (or better) neurologic outcome.
Before conducting the BLS Primary Survey, you should assess Danger, check patient Responsiveness,
Shout for help (activate emergency medical system and get an AED).
The BLS Primary Survey is an ABCD approach using a series of sequential assessments. Each assessment
is followed by appropriate action(s) if needed. As you assess each step (the patient’s airway, breathing,
circulation, and determine if defibrillation is needed), you stop and perform an action, if necessary,
before proceeding to the next assessment step. Assessment is a key component in this approach. For
example:
• Check for responsiveness before shouting for help and open the airway
• Check breathing before starting chest compressions
• Attach an AED, then analyze for a shockable rhythm before delivering a shock
Remember:
Assess...then perform appropriate action.
Table 1 below shows an overview of BLS Primary Survey. DRS is included before ABCD for
completeness.
Assess Action
Danger
- Are there blood spills, sharps, electric
wires?
- Is the scene dangerous?
Wear PPE (gloves, apron, mask) if available
Make sure you, the victim and
bystanders are safe
Responsiveness
- Is the patient responsive?
Tap shoulders and Say ‘Hello!
Hello! Are you OK?’
Shout for help
‘Emergency!Emergency!
Call ambulance 999 or bring emergency
trolley & defibrillator if available

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Assess Action
Airway
- Is the airway open?
Open the airway using non-invasive techniques
(head tilt-chin lift; jaw thrust without
head extension if trauma is suspected)
Breathing
- Is the patient breathing and are
respirations adequate?
Look for normal breathing in not more
than 10s (almost simultaneously when
performing head tilt chin lift)
Circulation
- Is the patient breathing and are
respirations adequate?
Perform high-quality CPR if not breathing or
abnormal breathing (gasps) is seen until an
AED arrives. Pulse check should be done
simultaneously with breathing assessment.
Defibrillation
- Is there a shockable rhythm?
Check with a manual defibrillation
or use an AED
Provide shocks as indicated Follow each
shock immediately with CPR, beginning with
chest compressions
NB. Make every effort to minimize interruptions in chest compressions. Limit interruptions in chest
compressions to no longer than 10s
Avoid:
• Prolonged rhythm analysis • Frequent or inappropriate pulse checks
• Taking too long to give breaths • Unnecessarily moving the patient
The ALS Secondary Survey
The ALS Secondary Survey is conducted after the BLS Primary Survey when more advanced
management techniques are needed.
Advanced airway interventions may include the laryngeal mask airway (LMA), or endotracheal tube
(ETT).
Advanced circulatory interventions may include drugs to control heart rhythm and support blood
pressure.
An important component of this survey is the differential diagnosis, where identification and treatment
of the underlying causes may be critical to patient outcome.
In the ALS Secondary Survey, you continue to assess and perform an action as appropriate until transfer
to the next level of care. Many times assessments and actions in ALS will be performed simultaneously
by team members

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Table 2: The ALS Secondary Survey
Assess Action
Airway
- Is the airway patent?
- Is an advanced airway indicated?
- Maintain airway patency in unconscious patients by
use of head tilt – chin lift/jaw thrust , orophyaryngeal
airway (OPA) or nasopharyngeal airway (NPA)
- Use advanced airways if needed (e.g. LMA or ETT)
Breathing
- Are oxygenation and
ventilation adequate?
- Is an advanced airway indicated?
- Is proper placement of airway
device confirmed?
- Is tube secure and placement
reconfirmed frequently?
- Are exhaled CO₂ and
oxyhemoglobin saturation
monitored?
- Give supplementary oxygen
- Assess the adequacy of oxygenation and ventilation by
• Clinical criteria (colour, chest rise, auscultation)
• Oxygen saturation
• Capnometry or capnography
The benefit of advanced airway placement is weighed
against the adverse effects of interrupting chest
compressions. If bag-mask ventilation is adequate,
insertion of an advanced airway may be deferred until
the patient fails to respond to initial CPR and
defibrillation or until ROSC.
If advanced airway devices are used:
- Confirm proper integration of CPR and ventilation
- Confirm proper placement of advanced airway
devices by
• Clinical criteria (colour, chest rise, auscultation)
• Capnometry or capnography
- Secure the device to prevent dislodgment
- Continue exhaled CO₂ measurement
Circulation
- What is the initial cardiac rhythm?
- What is the current cardiac rhythm?
- Have you established access
for drug and fluid?
- Does the patient need
volume (fluid) for resuscitation?
- Are medications needed for
rhythm or blood pressure?
- Obtain IV / IO access, give fluids if needed.
- Attach ECG leads and monitor for arrhythmias or
cardiac arrest rhythms (e.g. VF, pulseless VT, asystole,
and PEA)
- Give appropriate drugs to manage rhythm (e.g.
amiodarone, lidocaine, atropine, magnesium) and
blood pressure (adrenaline).
- Other inotropes or vasopressors to be considered
after ROSC is achieved.(e.g. dopamine, noradrenaline,
adrenaline )
Differential Diagnosis
- Why did this patient develop
cardiac arrest?
- Why is the patient still in arrest?
- Can we identify a reversible cause
of this arrest?
● Search for, find and treat reversible causes (i.e.
definitive care). Look for 5H and 5T causes.
● 5H: Hypoxia, Hydrogen ion, Hypothermia,
Hypovolemia, Hypo/hyperkalemia.
● 5T: Tamponade (cardiac), Tension pneumothorax,
Thrombosis (pulmonary or coronary), Toxins

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Roles
Team Leader
Organizes the group, monitors individual performance of team members, backs up team members,
models excellent team behavior, trains and coaches, facilitates understanding and focuses on
comprehensive patient care.
Team Member
Must be proficient to perform skills within their scope of practice. They are clear about their role
assignment, prepared to fulfill the role responsibilities, well-practiced in resuscitation skills,
knowledgeable about the algorithms and committed to success.
Team Dynamics and Communication
Closed Loop Communication
When communicating with team members, the leader should use closed loop communication.
The leader gives an order or assignment and then confirms that the message is heard. The team
member verbally repeats the order to confirm that the order or assignment is heard and informs the
leader when the task is complete.
Clear Messages
All messages and orders should be delivered in a calm and direct manner without yelling or shouting. The team
leader should speakclearly while the team members should question an order if they areunsurewhat is said.
Clear Roles and Responsibilities
Every member of the team should know his/her role and responsibilities. To avoid inefficiencies, the team
leader should clearly delegate tasks. A team member should not accept assignments above his/her level of
expertise.
Knowing One’s Limitations
Every member of the team should know his/her imitations and capabilities and the team leader should be
aware of them. A new skill should not be attempted during the arrest, instead call for expert help at an early
stage.

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Knowledge Sharing
A critical component of effective team performance is information sharing. The team leader can ask
for suggestions when the resuscitation efforts seem to be ineffective.
ConstructiveIntervention
During a code, a team leader or member may need to intervene if an action is about to occur at an
inappropriate time. For example, the person recording the event may suggest that adrenaline be
given as the next drug because it has been 5 minutes since the last dose. In actual fact the adrenaline
should be repeated every 3 to 5 minutes. All suggestions for a different intervention or action should
be done tactfully by the team leader or member.
Reevaluation and Summarizing
An essential role of the team leader is monitoring and reevaluation of the status of the
patient, interventions that have been done and assessment findings.
Mutual Respect
The best teams are composed of members who share a mutual respect for each other and work
together in a collegial, supportive manner. All team members should leave their egos at the door.
Team debriefing
A team debriefing could be done, led by the Team leader after the resuscitation has been
completed and the patient has been admitted to a critical care ward to discuss pertinent issues that
occurred during the resuscitation and reinforce teaching points among members.

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Overview of Airway Management
The support of ventilation and oxygenation during CPR and peri-arrest period is important. The
purpose of ventilation during CPR is to maintain adequate oxygenation and sufficient elimination of
carbon dioxide. Airway management during resuscitation is dependent on patient factors, the phase of
resuscitation (during CPR or after ROSC) and the skill of the rescuers.
A variety of airway management modalities e.g. bag valve mask (BVM), supraglottic airway devices
(e.g. LMA,SUPREME,Igel) and endotracheal tube (ETT) are often used during resuscitation as a part of
stepwise approach to airway management. After ROSC, ultimately an endotracheal intubation is
needed for the post resuscitation care.
Oxygen during CPR
1. When supplementary oxygen is available, use the maximal feasible inspired oxygen
concentration during CPR. The detrimental effects of hypoxia during low cardiac output state
(CPR) supersede hyperoxia that may exist in the immediate post cardiac arrest period.
2. After ROSC, titrate the inspired oxygen concentration to achieve the SpO2 in the range of 94 –
98%.
Adjuncts for Airway Management and Ventilation.
1. There are various modalities for managing the airway during resuscitation. It depends mainly
on the rescuer skill and the familiarities of the technique to provide effective oxygenation and
ventilation. Options includes bag mask ventilation (BMV), supraglottic airway devices (SGAs)
and endotracheal intubation.
2. There is inadequate evidence to show the difference in survival or favorable neurological
outcome with the use of bag mask devices (BMV), supraglottic airway devices (SGAs) and
endotracheal tube (ETT). Either BMV or an advanced airway (SGAs,ETT) may be used for
oxygenation and ventilation during CPR. Advanced airways should be inserted if the rescuer is
familiar with the devices and technique of insertion.
3. Supraglottic airway devices e.g. LMA, Supreme, I-gel are relatively easier to insert in
comparison to endotracheal intubation. Interruption to chest compression should be
minimized during insertion of an advanced airway.
4. Once an advanced airway has successfully been inserted, cyclical CPR (30:2) should be stopped.
The ventilation rate should be 10 breaths per minutes (1 breath every 6 seconds) while chest
compression being performed at the rate of 100 – 120 per minutes.
5. Delivery of oxygen through a cannula or surgical cricothyrodotomy may be lifesaving in CICO
conditions (Cannot Intubate Cannot Oxygenate).

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Oxygen Delivering Devices
Oxygen supplement is always appropriate for patient in respiratory distress. There are various devices
that can deliver supplemental concentration from 21% - 100%.
Table . Delivery of Supplemental Oxygen: Flow Rates and Percentages of Oxygen Delivered.
Device Flow Rates Delivered Oxygen (%) -approximate
Nasal cannula
1L/minute
21 - 24
2L/minute 25 - 28
3L/minute
4L/minute
29 - 32
33 - 36
5L/minute 37 - 40
6L/minute 41 - 44
Simple face mask 6-10L/minute 35 - 60
Venturi mask
(Device specific)
4-8L/minute
10-12L/minute
24 - 40
40 - 50
Mask with O2
10-15L/minute 70 - 80
Reservoir
• Rebreathing
• Non-rebreathing 10-15L/minute 95 - 100

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Nasal Cannula
• Consists of 2 prongs
• Every 1L/minute increase in O2 flow rate increase in FiO2 by 4%
• Usually 1-6L/minute O2 given
• Do not use more than 6L/minute O2 as this does not increase oxygenation much, yet dries up nasal
passages and is uncomfortable to patient
• O2
concentration depends on: - O2
supply flow rate
- Pattern of ventilation
- Patient inspiratory flow rate
Simple Face Mask
 Made from silicone rubber or transparent plastic
 Various size, from paediatric to big adult
 Fits loosely on the face, which allows room air to be inhaled, if needed
 O₂ concentration depends on:
- O₂ supply flow rate - Patient inspiratory flow rate
- Pattern of ventilation - Tight fit of the mask
 Supplies 35% to 60% oxygen with flow rates of 6 to 10L/ minute
 Does not supply oxygen > 60%

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Venturi Mask
• Based on Bernoulli principle
- O2 is passed through a narrowed orifice and this creates a high-velocity stream of gas. This
high-velocity jet stream generates a shearing force known as viscous drag that pulls room
air into the mask through the entrainment ports on the mask.
• Gives desired concentration of oxygen to patient (24% to 60%)
• Ideally used for patient with Chronic Obstructive Pulmonary Disease (COPD)
Mask with O2
Reservoir
• The addition of a reservoir bag to a standard face mask increases the capacity of the O2
reservoir by 600 to 1000 ml. If the reservoir bag is kept inflated, the patient will inhale
only the gas contained in the bag.
• There are two types of mask-reservoir bag devices:
Rebreathing system Non-rebreathing system
• Novalveandsogasexhaledinthe initialphase
ofexpirationreturnstothereservoir bag
• Providesupto70%to80%O2 withflowratesof
10-15L/minute.
• Presenceofaone-wayvalvethatpreventsany
exhaledgasfromreturningtothereservoir bag
• Providesupto95%to100%O2 withflowrates
of10-15L/minute.

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Non-invasiveAirway Devices
Oropharyngeal Airway
• A semicircular tube to hold the tongue away from the posterior wall of the pharynx
• Used in comatose patient or patient with loss of airway reflex
• May cause laryngospasm in semi-comatose patient
• Various sizes (3,4,5)
- The appropriate size is measured from angle of mouth to angle of jaw

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Nasopharyngeal Airway
• An uncuffed tube made of soft rubber or plastic
• Used in patient where mouth opening is difficult
• More tolerable by semi-comatose patient
• Used with caution in patient with base of skull fracture or with ENT bleeding
• May cause airway bleeding
• Various sizes (size indicates internal diameter)
- The appropriate size is measured from tip of the nose to tragus of the ear
Manual Assist Ventilation
In an unconscious or semiconscious victim, the healthcare provider should open the airway by head
tilt-chin lift or jaw thrust (if suspected cervical injury). Oropharyngeal or nasopharyngeal airways may
be used to prevent the tongue from occluding the airway.

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Mouth to Mask Ventilation (Pocket Resuscitation Mask)
• Pocket resuscitation mask is a one way valve mask
• Advantages:
- Eliminates direct contact - Oxygenates well if O2 attached
- Easier to perform than bag-mask ventilation - Best for small-handed rescuers
• Two ways of carrying out mouth to mask ventilation depending on whether there are 1 or 2 rescuers
1- RescuerTechnique
• Performed from sides
• Rescuer slides over for chest
compressions
• Fingers-head tilt-chin lift
2- RescuerTechnique
• The rescuer chest compression
• The ventilator stands at
head end
Bag-maskVentilation
Non breathing Valve
Ventilation
Bag
Oxygen
Supply Inlet
Connection
Air/Oxygen
Intake Valve
Oxygen
Reservoir
Exhalation
Port
Face Mask
Oxygen Supply
Tubing

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• The bag-mask device consists of a self-inflating bag with a non-rebreathing valve
- Can be used with a face mask or an advanced airway eg Supraglottic airway devices
(SGAs) or endotracheal tube (ETT)
- Provides positive pressure ventilation
- Cannot be used to allow spontaneous breathing
• The provider should use an adult (1 to 2 L) bag and deliver just enough volume to produce
visible chest rise
• Bag-mask ventilation can produce gastric inflation with complications, including
regurgitation and aspiration
• Two ways of holding the bag-mask device on the face for adequate ventilation:
AdvancedAirways
Bag-mask ventilation is not suitable for prolonged periods of ventilation as it also inflates the
stomach. Therefore, ALS providers should be trained to use advanced airways (supraglottic airway
devices (SGAs) and ETT).
Supraglottic Airway Devices (SGAs)
Supraglottic airways are devices designed to maintain an open airway and facilitate ventilation.
Insertion of a supraglottic airway device does not require visualization of vocal cords, therefore can
be done with minimal chest compression interruptions.
Laryngeal Mask Airway
 An advanced airway device that is considered an acceptable alternative to the ETT
 Technically easier to insert and minimally interrupt chest compression during resuscitation
 Ventilating patient via LMA may still cause gastric aspiration
 Composed of a tube with a cuffed mask-like projection at the end of the tube and connected
to a pilot balloon.
1 Hand (E-C Clamp Technique) 2 Hand (E-C Clamp Technique)

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Recommended Size Guidelines for LMA
The following table shows the Recommended Size Guidelines and the Amount of Air needed to
inflate the LMA cuff:
Size of LMA Weight of patient Max Air in Cuff Not to Exceed
Size 1 < 5 kg 4 ml
Size 1.5 5 to 10 kg 7 ml
Size 2 10 to 20 kg 10 ml
Size 2.5 20 to 30 kg 14 ml
Size 3 30 to 50 kg or small adult 20 ml
Size 4 50 to 70 kg (adult) 30 ml
Size 5 > 70 kg (large adult) 40 ml
Insertion of LMA
Before any attempt to insert an LMA, the following equipment has to be prepared:
• Personal protective equipment - mask, eye shield/goggle, gloves
• Appropriate size LMA
• Syringe with appropriate volume (10, 20 or 50 ml) for LMA cuff inflation
• Water soluble lubricant
• Ventilation equipment
• Tape or other device(s) to secure LMA
• Stethoscope
The following are the steps necessary for successful insertion of LMA:
Step 1: Size selection - as per Recommended Size Guidelines

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Step 2: Examination of LMA
• Inspect surface of LMA for damage, including cuts, tears, or scratches
- Do not use the LMA if the airway tube is damaged in any way
• Inspect interior of LMA airway tube to ensure that it is free from blockage or loose
particles
-Any particles present in the airway tube should be removed as patient
may inhale them after insertion
• Inflate cuff to ensure that it does not leak
• Deflate cuff to ensure that it maintains a vacuum
Step 3: Check inflation and deflation of cuff
• Inflate cuff with the recommended volume of air
• Slowly deflate cuff to form a smooth flat wedge shape which will pass easily around
the back of the tongue and behind the epiglottis
Step 4: Lubrication of LMA Cuff/Mask
• Use a water soluble lubricant to lubricate
• Only lubricate LMA cuff/mask just prior to insertion
• Only lubricate back of LMA cuff/mask thoroughly
• Avoid excessive lubricants on interior surface or in the bowl of cuff/mask as
inhalation of the lubricant following placement may result in coughing or obstruction
Step 5: Position head for insertion
• LMA can be inserted even if the head is in the neutral position as long as the mouth
opening is adequate
• Avoid LMA fold over:
-Assistant pulls the lower jaw downwards
- Visualize the posterior oral cavity
- Ensure that LMA is not folding over in the cavity as it is inserted

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1
3
2
4
Below are a series of diagrams showing the insertion of LMA:
Method for holding the LMA for
standard insertion technique
To facilitate introduction of LMA into
the oral cavity, gently press the
middle finger down onto the jaw
With the head tilt and the neck
flexed, insert the cuff of LMA into
the oral cavity; direction of force
goes against the hard palate
The index f i n g e r p u s h e s L M A
i n a cranial direction following the
contours of the hard and soft palates

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5 6
8 9
Maintaining pressure with finger on
LMA in the cranial direction, advance
LMA until definite resistance is felt
at the base of the hypopharynx: note
flexion of the wrist
Gently maintain cranial pressure with
non-dominant hand while removing
index finger
Bite Block
Tape
To allow LMA to seat optimally, inflate
without holding LMA
Inflate cuff with just enough air to
obtain a seal - this should correspond to
intracuff pressures around 60 cm H2O;
do not over-inflate
Tape the bite-block and LMA airway
tube downwards against the chin

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Finally connect tobag-mask or ventilator and look for chest rise
Confirm equal breath sounds over both lung fields &absence of ventilatory sounds over
epigastrium
Final words on LMA
• Test cuff before use
• Don’t lubricate anterior side of LMA mask
• Insert only in comatose patient
• Keep cuff inflated until patient awake
LIMITATION OF SGAs
1. In the presence of high airway resistance or poor lung compliance (pulmonary oedema,
bronchospasm) there is a risk of significant leak around the cuff causing hypoventilation.
The leaks gas normally escapes through the patient’s mouth but some gastric inflation may
occur.
2. No data demonstrating whether or not it is possible to provide adequate ventilation via
SGAs without interruption of the chest compression. Uninterrupted chest compressions are
likely to cause some leaks around the SGAs cuff when ventilation is attempted. Attempt
continuous chest compression initially but abandon this if persistent leaks occur.
3. There is theoretical risk of aspiration of stomach contents; however this complication has
not been documented widely in clinical practice.
4. If the patient is not deeply unconscious, insertion of the SGAs may cause coughing, straining
or laryngospasm. This will not occur in cardiopulmonary arrest patients.
5. If adequate ventilation is not achieved, withdraw the SGAs and re-attempt insertion after
ensuring good alignment of the head and neck.
Endotracheal Tube (ETT)
The ETT was once considered the optimal method of managing airway during cardiac arrest. It keeps
the airway patent, permits suctioning of airway secretions, enables delivery of a high concentration of
oxygen, provides an alternative route for the administration of some drugs, facilitates delivery of a
selected tidal volume, and with the use of a cuff, may protect the airway from aspiration. However,
there is insufficient evidence to support or refute the use of any specific technique to maintain an
airway and provide positive pressure ventilation in resuscitation. Endotracheal intubation should only
be performed by trained personnel with high level of skill and competence.
Equipment for Endotracheal Intubation:
The equipment necessary for endotracheal intubation may be remembered as mnemonics MALES:
M - Mask (Bag-mask), Magill forceps
A - Airways (Oropharyngeal/Nasopharyngeal Airway)
L - Laryngoscope, LMA, Lubricant gel
E - Endotracheal tubes + Stylet + tape for securing ETT
S - Suction (Catheter/Yaunker), Syringe, Stylet

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Laryngoscope
• Consists of handle (which contains a battery power source) and blade
• 2 types of blades: Macintosh blade (curved) for adults Miller blade (straight) for newborn and infants
• Make sure that the light on the blade works and is bright when lit up
Endotracheal Tube
Choosing The Correct Size ETT
Preparation for Endotracheal Intubation
It is important to get ready before any attempt in intubation:
 Equipment ready and in good order: MALES
 Adequate oxygen source
 wall or cylinder
 if oxygen source is from oxygen cylinder, check O₂ pressure
 Enough helping hands
 Equipment to confirm correct placement of ETT i.e. Stethoscope, CO2 detector devices
 Resuscitation and intubation drugs available and ready
Age Internal Diameter (mm) Anchor for Oral ETT
Adult Male 7.5 - 8.0 20 - 22 cm
Adult Female 7.0 - 7.5 18 - 20 cm
Newborn to 3 months 3.0 weight (kg) +6
Infants 3.0 - 3.5 weight (kg) +6
Children >1year
If using cuffed ETT
(Age/4) + 4.0
(Age/4) + 3.5
3 times size of ETT used/
(Age/2)+12

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The Technique of Endotracheal Intubation
The following steps are necessary for successful endotracheal intubation during cardiac arrest:
Step 1: Position patient in the “sniffing the morning air” position
 Flexion at lower cervical spine
 Extension at atlanto-occipital joint
To align the axes of upper airway as shown in the diagram below
Extend-the-head-on-neck (“look up”): aligns axis A relative to B
Flex-the-neck-on-shoulder (“look down”): aligns axis B relatives to C
Extend-the-head-on-neck (“look up”): aligns axisArelative to B
Flex-the-neck-on-shoulders (“look down”): aligns axis B relative to C
Step 2: Preoxygenation
• 100% O2 for 3 minutes or with 4 vital capacity breaths
Step 3: Laryngoscopy and insertion of ETT
A
A
B
C
B
C

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3A: Laryngoscopy
 Use left hand to hold laryngoscope
 Enter at right side of mouth and push tongue towards left aside
 Move the laryngoscope blade towards midline and advance to the base of the tongue.
Advance the blade to the vallecula if the curved blade is used or to just beyond tip of
epiglottis if the straight blade is used
 Lift upward and forward to bring up the larynx and vocal cords into view. The direction of
force necessary to lift the mandible and tongue is 45 degrees. Do not use teeth as a fulcrum
or a lever
3B: Insertion of ETT
• Insert the ETT through the vocal cords. View the proximal end of the cuff at the
level of the vocal cords and advance it about 1 to 2.5cm further into the trachea
• Inflate the ETT with enough air to occlude the airway (usually 10 to 20ml)
Important point to note:
Interruption to chest compression during endotracheal intubation should be
less than 5 seconds.
Laryngoscopic View Laryngoscope blade position
Hand Position Laryngoscope blade position

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Step 4: Confirm correct position of ETT
• Observe colour of patient
• Visualise chest rise with delivery of first manual breath
• Detect vapour in ETT
• 5 points auscultation for breath sounds (auscultate epigastrium, anterior chest
at bilateral mid-clavicular lines and thorax at bilateral mid-axillary lines)
• Detect end-tidal CO2
with capnography or CO2
detector device
Step 5: Secure ETT with tape
Step 6: Ventilate with a tidal volume of 6-8 ml/kg (visible chest rise) at a rate of 8-10 breath
per minute
Waveform Capnography
Continuous waveform capnography is recommended as the most reliable method of confirming and
monitoring correct placement of the endotracheal tube (ETT). Studies of waveform capnography to
verify ETT position in patients in cardiac arrest have shown high sensitivity and specificity in identifying
correct ETT placement. It can also detect a patient’s deterioration associated with declining clinical
status or ETT displacement.
End-tidal CO2 during resuscitation:
 Confirms ETT placement; note that EtCO2 detection will not differentiate between tracheal
and endobronchial tube placement. Careful auscultation is essential.
 Correlates with cardiac index
 Assesses adequacy of ventilation
 Indicates quality of CPR
 Signifies ROSC
 Carries prognostic value for survival during resuscitation
Waveform Capnography.
Normal range (approximately 35 to 45 mmhg)

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Complications of Endotracheal Intubation
During intubation Hypoxia from the procedure itself, esophageal intubation and/or
laryngospasm and bronchospasm
Hypertension/hypotension, tachycardia/bradycardia and arrhythmias
from/parasympathetic/sympathetic response
Trauma to teeth, lips, tongue, mucosa, vocal cords, trachea
Vomiting and aspiration
Arytenoid dislocation hoarseness
Spinal cord trauma in cervical spine injury
When ETT in-situ Migration to bronchus/esophagus
Obstruction from kinking, secretions or over-inflation of cuff Disconnection
from breathing circuit
Accidental extubation/ETT dislodgement
Lip ulcer in prolonged oral intubation
Sinusitis or otitis or nasal ulcer in prolonged nasal intubation
During extubation: Laryngospasm
Edema of upper airway
Pulmonary aspiration
After Extubation Sore throat
Hoarseness
Long Term Subglottic stenosis
Vocal cord granuloma
Laryngeal granuloma

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TracheobronchialSuctioning
Suction Catheter
• Size (FG) = ETT internal diameter (mm) x 3/2 or outer diameter should not exceed 1/2 to 2/3
ETT internal diameter
• Minimal trauma to mucosa with molded ends and side holes
• Long enough to pass through tip of ETT
• Minimal friction resistance during insertion through ETT
• Sterile and disposable
Suction Pressure
• 100 to-120mmHg (adults) • 80 to-100mmHg (children) • 60 to-80 mmHg (infants)
Complications of Tracheobronchial Suctioning:
• Sudden severe hypoxia, secondary to decrease in functional residual capacity during
the application of negative pressure in the trachea
• Cardiac arrest if severe hypoxia
• Increase in intra-arterial pressure and tachycardia due to sympathetic response to suction
Technique of Tracheobronchial Suctioning:
Step 1
Always preoxygenate with 100% O2 for 3-5 minutes to reduce risk of
hypoxia and arrhythmias
Step 2
Using sterile technique, the suction catheter is inserted without
closing the side opening in the proximal end of the catheter
Step 3
The suction catheter is advanced to the desired location which is
approximately at the level of the carina where trachea bifurcates
Step 4
Suction is applied intermittently by closing the side opening while
the catheter is withdrawn with a rotating motion
Step 5
Limit duration of suctioningto 10-15 seconds. If arrhythmias occur,
immediately discontinue suctioning and manually bag patient with O2
Step 6
Prior to repeating the procedure, patient should be ventilated with
100% O2 for about 30 seconds.
Point to note:
Inpatientwithelevated intracranial pressure(e.g.headinjury),temporary
hyperventilation before and after suctioning may be indicated

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What is Defibrillation?
• The passage of an electrical current across the myocardium to depolarise a critical
mass of myocardium and enable restoration of coordinated electrical activity
• An electrophysiological event that occurs 30-50 ms after shock delivery-the heart is stunned
and hopefully the sino-atrial (SA) node will take over
• Aims to restore sinus rhythm
• Shocksuccesstypically defined as the termination of ventricular fibrillation (VF) within 5
seconds after the shock. Shock success using this definition does not equal to resuscitation
outcome
• Indicated only for VF or pulseless ventricular tachycardia (pVT) where a single shock is given
followed immediately by chest compression without any pulse check or rhythm reanalysis
after a shock.
The Importance of Early Defibrillation
Early defibrillation is critical to survival from sudden cardiac arrest (SCA) for the following reasons:
1) Most frequent initial rhythm in out-of-hospital, witnessed SCA is VF
2) Treatment for VF is defibrillation
3) The probability of successful defibrillation diminishes rapidly over time
4) VF tends to deteriorate to asystole over time
For every minute that passes between collapse and defibrillation, survival rates from witnessed
VF SCA decrease 7% to 10% if no CPR is provided. When bystander CPR is provided, the decrease
in survival rate is more gradual and averages 3% to 4% per minute from collapse to defibrillation.
CPR prolongs VF, delays the onset of asystole and extends the window of time during which
defibrillation can occur. Basic CPR alone, however, is unlikely to terminate VF and restore a
perfusing rhythm.
Defibrillators
Modern defibrillators are classified according to 2 types of waveforms: monophasic and
biphasic. Monophasic waveform defibrillators were introduced first, but biphasic waveforms are
used in almost allAutomated External Defibrillators (AEDs) and most manual defibrillators sold today.
Energy levels vary by type of device and manufacturer.
Although it is recognized that some areas continue to use the older monophasic waveforms,
defibrillation using biphasic waveform are preferred (2015 guidelines). Studies show greater success
in arrhythmia termination.

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There are two types of Biphasic waveforms:
Monophasic Waveform Defibrillators
• Deliver current of one polarity (i.e. direction of current flow)
• Categorized by the rate at which the current pulse decreases to zero:
- Monophasic damped sinusoidal waveform (MDS) current returns to zero gradually
- Monophasic truncated exponential waveform (MTE) current returns abruptly (truncated) to zero
Biphasic Waveform Defibrillators
• Equivalent or higher efficacy for termination ofVF when compared with monophasic
waveforms
• Different biphasic waveforms have not been compared with regard to efficacy
• Use the manufacturer’s recommended energy dose (120 to 200J). If the manufacturer’s
recommended dose is not known, defibrillate at 200J, the maximal dose
Preparing The Patient
Electrode/Paddle Size
• Minimum 150 cm2
, 8 to 12 cm in diameter for both handheld paddle electrodes and self-
adhesive pad electrodes although defibrillation success may be higher with electrodes 12
cm in diameter rather than with those 8 cm in diameter
• Small electrodes (4.3cm) harmful and may cause myocardial necrosis
Electric/Paddle force
• 8kg in adult
• 5kg in 1-8years when using adult paddles
Transthoracic Impedance
• Use gel pads or electrode paddles or self-adhesive pads to reduce transthoracic impedance.
The average adult human impedance is 70 to 80 Ω. When transthoracic impedance is too
high, a low-energy shock will not generate sufficient current to achieve defibrillation
Electrode/PaddlePlacement
• Can be at antero-lateral, antero-posterior, anterior-left infrascapular and anterior-right
infrascapular locations on the chest/back. All these 4 positions are equally effective. For ease
of placement and education, anterolateral is a reasonable default electrode placement.
• Ensure that the paddle and gel or pads are in full contact with the skin
• Special considerations:

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Breasts
- Place lateral pads/paddles under breast tissue
- Move pendulous breasts gently out of the way
Wet Chest
- Briskly wipe the chest dry before attaching electrode pads and attempting defibrillation
Hirsutism
- Shave hirsute males prior to application of pads
- Remove excess chest hair by briskly removing an electrode pad (which will remove some hair)
or by rapidly shaving the chest in that area
Automated Implanted Cardioverter Defibrillator
- Avoid placing the pads or paddles over the device as there is a potential for pacemaker or ICD
to malfunction after defibrillation when the pads are in close proximity to the device
- Use antero-posterior and antero-lateral locations
Presence of Transdermal Medication Patch (eg patch containing nitroglycerin,
nicotine, analgesics, hormone replacement, anti-hypertensives)
- Do not place electrodes over transdermal medication patch which may block delivery of energy
from the electrode pad to the heart and may cause small burns to the skin
- Removemedicationpatchandwipetheareabeforeattachingtheelectrodepadifdefibrillationis
needed
Safety Issues
Fire
• Ignitedbysparksfrompoorlyapplieddefibrillatorpaddlesinthepresenceofanoxygen-enriched
atmosphere
• Avoid defibrillation in an oxygen-enriched atmosphere
• Use self-adhesive defibrillation pads
• Ensure good pad–chest-wall contact
• If manual paddles are used, gel pads are preferable to electrode pastes and gels
because the pastes and gels can spread between the 2 paddles, creating the potential
for a spark
AccidentalElectrocution
• Charge paddles after being placed on patient’s chest rather than prior to being taken out
from thedefibrillator
• Ensure that none of the rescuer team members is in contact with
patient/victim/resuscitation trolley prior to defibrillator discharge
Safety and Clearing The Patient
“Clear, shocking”
• Always announce that a shock is about to be delivered
• Perform a visual check making sure no one is in contact with the patient
• “Clear” the patient and rescuers before each shock

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• Make sure that no oxygen is flowing across the patient’s chest or openly across the
electrode pads
• Carry out the above steps quickly to minimize the time from the last compression to
shock delivery
When pressing the shock button, the defibrillator operator should face the patient, not the machine.
This helps to ensure coordination with the chest compressor and to verify that no one resumed the
contact with the patient.
No need to use exact words, but a clear and firm warning of about a delivering a shock and everyone
must stand clear of patient. The entire sequence should take less than 5 seconds.
An Example:
These steps are summarized below:
1 Attach electrodes to patient’s chest
2 Turn defibrillator on – select leads
3 Analyse the rhythm? shockable
4 Apply coupling agent or pads to patient’s chest
5 Select energy level
6 Apply paddles to chest
7 Charge the paddles
8 The “Clear” chant
9 Check monitor again
10 Discharge shock and return the paddles to the machine
• To avoid pre-shock pause of more than 5 sec. Even a 5-10 seconds delay will reduce the chance of
survival. Use of adhesive pad is encouraged to reduce delay.
• To continue giving high quality chest compression for 2 minutes after delivery of shock to improve
coronary perfusion pressure and cerebral perfusion. Only to check the pulse and rhythm after a
complete 2 minutes of cycle of CPR.

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Synchronized Cardioversion
• A shock delivery that is timed (synchronized) with the QRS complex
• Avoidsshockdeliveryduringtherelativerefractoryportionofthecardiaccyclewhenashockcouldproduce VF
Use of Synchronized Cardioversion
• Indicatedinahemodynamicallyunstablepatient(lowbloodpressure)withaperfusingrhythm(pulsepresent)
• Recommended in supraventricular tachycardia due to re-entry, atrial fibrillation, atrial flutter,
and atrial tachycardia
• Recommended in monomorphic VT with pulses
• Not effective for treatment of junctional tachycardia or multifocal atrial tachycardia
Recommended Energy Level for Synchronized Cardioversion (ERC Guidelines)
Ventricular Tachycardia (VT)
• If pulseless VT (pVT)
- Treat as VF.
 Unstable Polymorphic (Irregular) VT With or Without a Pulse
- Treat as VF using defibrillation doses.
 Unstable Monomorphic (Regular) VT With a Pulse
- Treat with biphasic waveform cardioversion (synchronized) at 120J-150J or monophasic
waveform cardioversion at 200J. If the initial shock fails, increase the dose in a stepwise
fashion.
 Witnessed and monitored patient with VF/pVT,(in catheter lab, coronary care unit, critical
care area where manual defibrillator is rapidly available) 3 quick and successive (stacked )
shocks is recommended. Reason being, the chest compression is unlikely to improve the
already very high chance of ROSC when defibrillation occurs early in the electrical phase,
immediately after onset of VF. If this initial three-shock strategy is unsuccessful, the ALS
algorithm should be followed and these three-shocks are treated as first single shock given.
Waveform Biphasic energy Monophasic energy
Narrow regular (SVT, Atrial
flutter)
70-120J 100J
Narrow irregular
(Atrial fibrillation)
120-150J 200J
Broad complex tachycardia (VT) 120-150J 200J
Monomorphic VT 120-150J 200J

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Refibrillation versus Refractory VF
Refibrillation is recurrence of VF during a documented cardiac arrest episode, occurring after initial
termination of VF while the patient remains under the care of the same providers.
Usage of escalating energy level is beneficial for the termination of the refibrillation and patient with
failed shock.
Refractory VF is when fibrillation persist after three defibrillation shocks. Amiodarone 300mg bolus
followed with infusion 900mg to be given. (Amiodarone 150mg after 300 mg bolus, maximum daily
dose 2.2g).
Points to know:
Synchronized cardioversion is preferred for treatment of an organized ventricular rhythm.
However, for some arrhythmias, the many QRS configurations and irregular rates that
comprise polymorphic ventricular tachycardia make it difficult or impossible to reliably
synchronize toa QRS complex. If there is any doubt whether monomorphic or polymorphic VT
is present in the unstable patient, do not delay shock delivery to perform detailed
rhythm analysis-provide high energy unsynchronized shocks (i.e. defibrillation doses,
360J monophasic or 120-200J biphasic).
Pacing
• Not recommended for patients in asystolic cardiac arrest as it is not effective and may delay
or interrupt the delivery of chest compressions
It is reasonable for healthcare providers to be prepared to initiate pacing in patients who do not
respond to atropine (or second-line drugs if these do not delay definitive management).
Immediate pacing might be considered if the patient is severely symptomatic. If the patient does
not respond to drugs or transcutaneous pacing, transvenous pacing is probably indicated.
Summary
The recommendations for electrical therapies described in this section are designed to improve
survival from SCA and life threatening arrhythmias. Whenever defibrillation is attempted,
rescuers must coordinate high-quality CPR with defibrillation to minimize interruptions in chest
compressions and to ensure immediate resumption of chest compressions after shock delivery.

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ALS Core ECG Rhythms
and Recognition
2. Sinus Arrhythmia
 Variation in the P-P interval of more than 120 ms (3 small boxes).
 The P-P interval gradually lengthens and shortens in a cyclical fashion, usually
corresponding to the phases of the respiratory cycle.
 Normal sinus P waves with a constant morphology (i.e. no evidence of premature atrial
contractions).
 Constant P-R interval (i.e. no evidence of Mobitz I AV block).
 Regular rhythm.
 Normal P wave morphology and axis (upright in I and II, inverted in aVR).
 Narrow QRS complexes (< 100 ms wide).
 Each P wave is followed by a QRS complex.
 The PR interval is constant. ( P-R interval < 0.2sec )
1. Normal Sinus Rhythm

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3. Sinus Tachycardia
• Heart rate > 100 bpm.
• Regular rhythm.
• P wave for every normal QRS complex
• P waves may be hidden within each preceding T wave at higher rate.
4. Sinus Bradycardia
• Sinus rhythm.
• A resting heart rate of < 60 bpm.
• Normal QRS complex

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5. Premature atrial complexes (PAC)
 An abnormal (non-sinus) P wave is followed by a QRS complex.
 The P wave typically has a different morphology and axis to the sinus P waves.
 The abnormal P wave may be hidden in the preceding T wave, producing a
“peaked” or “camel hump” appearance.
6. Premature Ventricular Complexes (PVCs)
 Broad QRS complex (≥ 120 ms) with abnormal morphology.
 Premature — i.e. occurs earlier than would be expected for the next sinus
impulse.
 Discordant ST segment and T wave changes.
 Usually followed by a full compensatory pause.

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7. Atrial Fibrillation
 Irregularly irregular rhythm.
 No P waves.
 Absence of an isoelectric baseline.
 Variable ventricular rate.
 QRS complexes usually < 120 ms.
 Fibrillatory waves may mimic P waves leading to misdiagnosis.
8. Atrial Flutter
• Rhythm can be regular or variable.
• Rapid identical undulating waves.
• No P waves.
• Sawtooth appearance known as flutter waves.

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9. Supraventricular Tachycardia
 Narrow complex tachycardia .
 P waves not seen.
 Rate > 150 bpm.
 Regular rhythm.
10. Ventricular Tachycardia
 Very broad complexes (~ 200 ms).
 Regular ventricular rate.
 Possibly some superimposed P waves.

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11. Torsades de Pointes
 Rate 150 – 250 bpm.
 QRS showed continuous changing of axis (hence ‘turning of point ‘ ).
 Prolonged QT interval.
 Irregular ventricular rhythm.
12. Ventricular Fibrillation
 Chaotic irregular deflections of varying amplitude.
 No identifiable P waves, QRS complexes, or T waves.
 Rate 150 to 500 per minute.
 Amplitude decreases with duration (coarse VF-> fine VF).

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13. First Degree Heart Block
 PR interval > 200ms (five small squares).
 Sinus rhythm.
 Normal P wave followed by normal QRS complex.
 ‘Marked’ first degree block if PR interval > 300ms.
14. 2
nd
Degree AV Block Mobitz I (Wenkebach phenomenon)
 Progressive prolongation of the PR interval culminating in a non-conducted
P wave.
 The PR interval is longest immediately before the dropped beat.
 The PR interval is shortest immediately after the dropped beat.

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15. 2
nd
Degree AV block, Mobitz II
 Intermittent non-conducted P waves without progressive prolongation of the
PR interval (compare this to Mobitz I).
 The PR interval in the conducted beats remains constant.
 The P waves ‘march through’ at a constant rate.
 The RR interval surrounding the dropped beat(s) is an exact multiple of the
preceding RR interval (e.g. double the preceding RR interval for a single
dropped beat, treble for two dropped beats, etc).
16. Complete Heart Block
 In complete heart block, there is complete absence of AV conduction – none
of the supraventricular impulses are conducted to the ventricles.
 Atrial and ventricular rate regular but indipendently dissociated.
 The P wave is normal.

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17. Asystole
 No ventricular activity.

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Adrenaline
Introduction
• Naturally occurring cathecholamines with
alpha and beta effects
• Administration in cardiac arrest will cause
intense vasoconstriction (alpha adrenergic
action) and divert cardiac output to vital
organ such as brain and heart
• Can improve ROSC although no difference in
survival (Retrospective study)
• Facilitate defibrillation by improving
myocardial blood flow during CPR
Indications
• Cardiac arrest: The first drug to be used
in cardiac arrest of whatever cause
• Symptomatic bradycardia:
Can be considered after atropine as
an alternative infusion to dopamine
• Severe hypotension
• Anaphylaxis
Dose and Administration For Cardiac Arrest
 IV/IO: 1mg ( 1 ml 1:1000 ), administered
every 3-5minutes followed by 20ml flush
If IV/IO is difficult to establish, adrenaline can
be given through ETT at dose of 2-2.5mg
For Symptomatic Bradycardia (2nd degree
Type 2 and Type 3 Heart Block)
 Infusion at 2-10µg/minute, titrated to
response
For Anaphylactic Shock
 IM : adult or children > 12 years give 0.5 mg
as initial dose ( 0.5 ml of 1:1000 )
 IV: titrate 50-100 mcg (0.5 to 1 ml) according
to response ( use 10 ml 1:10000 )
Side-effect and Precautions
• Severe Hypertension
• Tachyarrhythmias
• Tissue necrosis if extravasation occurs
Following ROSC, even small doses of
adrenaline (50-100µg) may induce tachycardia,
myocardial ischaemia, VT and VF. If further
dose is required, it must be titrated carefully
to achieve an appropriate blood pressure
Atropine
Introduction
• An anticholinergic agent
• Antagonises the action of the
parasympathetic neurotransmitter
acetylcholine at muscarinic receptors.
Therefore, it blocks the effect of
the vagus nerve on both the sino-atrial
(SA) node and the atrio-ventricular
(AV) node, increasing sinus automaticity
and facilitatingAV node conduction
Dose and Administration
• The recommended dose for bradycardia
is 0.5mg IV every 3 to 5 minutes to a
max total dose of 3mg
• Doses of atropine sulfate of < 0.5mg
may paradoxically result in further
slowing of the heart rate
• Atropine administration should not
delay external pacing for patients with
poor perfusion
Use atropine cautiously in the presence of
acute coronary ischemia or MI; increased heart
rate may worsen ischemia or increase infarction
size. Will not be effective in infranodal (type II)
AV block and new third-degree block with wide
QRS complexes

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Indication
• First line drug for symptomaticBradycardia
• Organophosphate poisoning
Side Effects and Precautions
• Use atropine cautiously in the presence
of acute coronary ischemia or MI;
increased heart rate may worsen ischemia
or increase infarction size.
• Will not be effective in infranodal (type II)
AVblock and new third-degree block with
wide QRS complexes
Adenosine
Introduction
• Naturally occurring purine nucleotide
• Slows transmission across AV node but
has little effect on other myocardial cells
or conduction pathways
• Highly effective for terminating
paroxysmal SVT with re-entrant circuits
that include AV node (AVNRT)
• Give 6 mg adenosine as a rapid IV push
through a large (e.g. antecubital) vein
followed by a 20mL saline flush.
If unsuccessful, this can be followed with up
totwodoseseachof12mg every1-2
minutes
• In other narrow-complex tachycardias,
adenosine will reveal the underlying atrial
rhythmsbyslowingtheventricularresponse
Indications
• First drug for most form of stable
narrow- complex PSVT
• Effective in terminating stable narrow-
complex PSVT due to reentry involving
AV node or sinus node
• May be considered for narrow-
complex reentry tachycardia while
preparing for cardioversion
• Transient unpleasant side effects, in
particular nausea, flushing, and chest
discomfort
• Caution if need to be given in asthmatic
patient
• In WPW syndrome, blockage of
conduction across the AV node by
adenosinemaypromoteconductionacross
an accessory pathway
• In supraventricular arrhythmias, this may
cause a dangerously rapid ventricular
response
• It may also precipitate atrial fibrillation
associated with a dangerously rapid
ventricular response
• The initial dose should be reduced to 3 mg
in patients taking dipyridamole or
carbamazepine
Amiodarone
Introduction
• An antiarrhythmic with complex
pharmacokinetics and
pharmacodynamics properties
• Act on sodium, potassium and
calcium channels
• Poses alpha and beta-adrenergic
blocking properties.
• Refractory pulseless VT /VF ; IV/IO 300mg bolus
(dilute in 20mL Dextrose 5% solution)
Can repeat after the 5th shock :150 mg
• Unstable tachyarrhythmias; 300mg IV over 10-
20 minutes
• Stable tachyarrhythmias; 300mg IV over 20-60
minutes
• Maintenance infusion; 900 mg IV over 24h

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• A membrane-stabilising anti-arrhythmic
drug that increases the duration of
the action potential and refractory
period in atrial and ventricular
myocardium
• A mild negative inotropic action
• Causes peripheral vasodilation
through non-competitive alpha
blocking effects. Atrioventricular
conduction is slowed, and a similar
effect is seen with accessory pathways.
Indications
• Refractory pulseless VT/VF ( persistent
after at least 3 shock and adrenaline )
• Unstable tachyarrhythmias ( failed
3x cardioversion )
• Stable tachyarrhythmias
Adverse Effects and Precautions
• Can cause hypotension, bradycardia
and heart block
• Theadverse hemodynamiceffects of the IV
formulation of amiodarone are
attributed to vasoactive solvents
(polysorbate 80 and benzyl alcohol)
• Beware of accumulations with multiple
dosing (cumulative doses >2.2g are
associated with hypotension)
Calcium
Introduction
• Essential for nerve and muscle activity
• Playsavitalroleinthecellularmechanism
underlying myocardialcontraction
• No data supporting any beneficial
action for calcium after cardiac arrest
• Some studies have suggested a
possible adverse effect when given
routinely during cardiac arrest (all
rhythms)
Indications
Only in Pulseless ElectricalActivity caused by
• hyperkalaemia
• hypocalcaemia
• overdose of calcium channel blocker
• The initial dose of 10 ml 10% calcium
chloride (6.8 mmol Ca2+
) may be repeated
if necessary
• Administer calcium chloride via a central
line only
• Calcium can slow heart rate and
precipitate arrhythmias
• In cardiac arrest, calcium may be given by
rapid intravenous injection
• In the presence of a spontaneous
circulation give it slowly
• Do not give calcium solutions and sodium
bicarbonate simultaneously via the
same route

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Introduction
• A chemical precursor of noradrenaline
that stimulates both alpha and beta
adrenergicreceptors
• In addition, there are receptors specific for
dopamine (DA1, DA2 dopaminergic
receptors)
• Stimulates the heart through both alpa and
beta receptors
• Both a potent adrenergic receptor agonist
and a strong peripheral dopamine receptor
agonist. These effects are dose dependent.
Indications
• Second-linedrugforsymptomaticbradycardia
• Use for hypotension
• Usual infusion rate is 2-20µg/kg/minute
and dose titrated according to response
• Can cause tachycardia, hypertension
• Can precipitate arrhythmias
• May cause excessive systemic and
splanchnic vasoconstriction for higher dose
(10-20µg/kg/minute)
• Correct hypovolemia with volume replacement
before starting on dopamine
• Use with caution in cardiogenic shock with
accompanying CHF and LV dysfunction
Lignocaine
Introduction
• Act as a sodium channel blocker
Indications
• Alternative to amiodarone in
cardiac arrest from VT/VF
• Stable monomorphic VT with
preserved ventricularfunction
Dopamine
• Cardiac arrest from VT/VF Initial dose:
1-1.5mg/kg IV or IO
• For refractory VF: may give additional
dose 0.5-0.75mg/kg and repeat 5-
10 minutes up to 3 times or maximal
dose of 3mg/kg
• In overdose it can cause slurred speech,
altered consciousness, muscle twitching
and seizure
• It also can cause hypotension,
bradycardia, heart block and asytole

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Introduction
• A calcium channel blocking drug that
slows conduction and increases
refractoriness in the AV node
• The action may terminate re-entrant
arrhythmias and control of the
ventricular response rate in atrial
Indications
• Used for narrow-complex paroxysymal
SVT (unconverted by vagal maneuvers or
adenosine )
• Arrhythmias known with certainty to be
of supraventricular origin
• 2.5– 5 mg IV over 2 min: repeated
doses
5-10 mg every 15-30 min to a
maximum 20 mg
• If given to patient with ventricular
tachycardia may cause
cardiovascular collapse
• May decrease myocardial
contractility and critically reduce
cardiac output in patients with
severe LV dysfunction
Introduction
• An electrolye important for maintaining
membranestability
• Hypomagnesemia can cause myocardial
hyperexcitability especially in the presence
of hypokalemia or digoxin
• Insufficient evidence to recommend for or
against its routine use in cardiac arrest
Indications
• Torsadesdepointes
• Hypomagnesemia
• Lifethreateningventriculararrhythmiasdueto
digitalistoxicity
• Cardiac arrest due to Torsades
de pointes orhypomagnesemia:
1-2g diluted in 10 mL D5% to
be given over 5-20 minute
• Torsades de pointes with
pulse or AMI with
hypomagnesemia:
Loading dose of 1-2g mixed
with 50 mL D5% over 5-60
minute, followed with 0.5 to
1g/hour (titrate to control
Torsades)
• Occasional fall in blood pressure
with rapid administration
• Use with caution if renal failure is
present
Magnesium
Verapamil
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Introduction
Strong beta-1 and alpha-adrenergic effects
and moderate beta-2 effects
Is a potent vasoconstrictor with positive
inotropic effect
Indication
• Used for hypotension in post
resuscitation period
• Cardiogenic shock
0.05– 1mcg/kg/min as continuous infusion
Cause tissue necrosis if extravasation occurs
Do not administer Sodium Bicarbonate
through the same IV line containing
Noradrenaline
Increase afterload and beta-effects may
increase myocardial work and oxygen
consumption
Very high dose can lead into peripheral limb
ischaemia
Noradrenaline
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Introduction
 Used as a positive inotropic drug of
choice in the post-resuscitation
period
 It has beta-agonist activity causes
vasodilatation and increase in heart
rate especially direct stimulation of
Beta-1 receptors
Indication
• In hypotension with poor output
state
• With present of pulmonary oedema
and hypotension prevents the use of
other vasodilators
5– 20 mcg/kg/min as continuous infusion
• May worsen hypotension especially at
the initial treatment.
• Can increase risk of arrhythmia,
including fatal arrhythmias
Introduction
• A strong alkaline agent with
high sodium and bicarbonate load
• Not recommended for routine use
in cardiac arrest
Indications
• Known prexisting hyperkalemia
• Known preexisting bicarbonate
responsive acidosis e.g. : aspirin
overdose, diabetic ketoacidosis,
tricyclic antidepressant or cocaine
• Prolonged r e s u s c i t a t i o n with
effective ventilation. Upon return of
spontaneous circulation after long
arrest interval
• Not useful nor effective in
hypercarbic acidosis (e.g. cardiac
arrest or CPR)
without tracheal intubation
• 1 mEq/kg IV bolus
• May cause tissue necrosis if
extravasation occurs
• Do not administer together with
IV line used for vasopressors or
Calcium
SodiumBicarbonate
Dobutamine
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Introduction
• A chemical precursor of noradrenaline
that stimulates both alpha and beta
adrenergicreceptors
• In addition, there are receptors specific for
dopamine (DA1, DA2 dopaminergic
receptors)
• Stimulates the heart through both alpa and
beta receptors
• Both a potent adrenergic receptor agonist
and a strong peripheral dopamine receptor
agonist. These effects are dose dependent.
Indications
• Second-linedrugforsymptomaticbradycardia
• Use for hypotension
• Usual infusion rate is 2-20µg/kg/minute
and dose titrated according to response
• Can cause tachycardia, hypertension
• Can precipitate arrhythmias
• May cause excessive systemic and
splanchnic vasoconstriction for higher dose
(10-20µg/kg/minute)
• Correct hypovolemia with volume replacement
before starting on dopamine
• Use with caution in cardiogenic shock with
accompanying CHF and LV dysfunction
Lignocaine
Introduction
• Act as a sodium channel blocker
Indications
• Alternative to amiodarone in
cardiac arrest from VT/VF
• Stable monomorphic VT with
preserved ventricularfunction
Dopamine
• Cardiac arrest from VT/VF Initial dose:
1-1.5mg/kg IV or IO
• For refractory VF: may give additional
dose 0.5-0.75mg/kg and repeat 5-
10 minutes up to 3 times or maximal
dose of 3mg/kg
• In overdose it can cause slurred speech,
altered consciousness, muscle twitching
and seizure
• It also can cause hypotension,
bradycardia, heart block and asytole
48 Page

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Introduction
Strong beta-1 and alpha-adrenergic effects
and moderate beta-2 effects
Is a potent vasoconstrictor with positive
inotropic effect
Indication
• Used for hypotension in post
resuscitation period
• Cardiogenic shock
0.05– 1mcg/kg/min as continuous infusion
Cause tissue necrosis if extravasation occurs
Do not administer Sodium Bicarbonate
through the same IV line containing
Noradrenaline
Increase afterload and beta-effects may
increase myocardial work and oxygen
consumption
Very high dose can lead into peripheral limb
ischaemia
Noradrenaline

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BLSAdult Algorit
Adapter from 2015 American heart Association Guidelines for resuscitation
CPR 2 min
Adrenaline every 3-5 min
Consider advanced airway,
capnography
CPR 2 min
IV/IO, Adrenaline every 3-5 min
Consider advanced airway,
capnography
Can consider:
-3 stacks of shocks in witnessed,
monitored VF/pVT
-Escalation of energy in
refibrillation/failed shock

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Adapted from European Resuscitation Council (ERC) 2015 Guidelines for resuscitation.

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Adapted from European Resuscitation Council (ERC) Guidelines for resuscitation.

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Cardiac arrest in special circumstances
Special causes: 4 hs’ & 4 ts’ [ Hypoxia; Hypo/ Hyperkalaemia and other electrolytes disorders; Hypo/
Hyperthermia; Hypovolaemia ,Tension pneumothorax; Tamponade (cardiac); Thrombosis (coronary
and pulmonary); Toxins (poisoning) ]
 Survival after an asphyxia-induced cardiac arrest is rare and survivors often have severe
neurological impairment. Thus, during CPR early effective ventilation of supplementary oxygen is
essential. Those who are unconscious but have not progressed to a cardiac arrest are much more
likely to make a good neurological recovery.
 A high degree of clinical suspicion and aggressive treatment can prevent cardiac arrest from
electrolytes abnormalities especially from life-threatening hyperkalaemia. Early recognition and
prompt treatment must be done immediately and a new algorithm has been introduced for
management of hyperkalaemia. Other electrolytes disorders are also important to be managed
correctly to minimize complications leading to cardiac arrest namely hypercalcaemia,
hypocalcaemia, hypermagnesaemia and hypomagnesaemia.
 Hypothermic patient without signs of cardiac instability (systolic blood pressure > 90 mm Hg,
absence of ventricular arrhythmias or core temperature > 28o
C ) can be rewarmed externally
using minimally invasive techniques ( e.g. with warm forced air and warm intravenous fluid ).
Patients with signs of cardiac instability should be transferred directly to a centre capable of
extracorporeal life support (ECLS). The mainstay of therapy for hyperthermia including heat
stroke is still supportive and rapidly cooling the victim.
 Hypovolaemia is a potentially treatable cause of cardiac arrest that usually results from a reduced
intravascular volume (i.e. haemorrhage), but relative hypovolaemia may also occur in patients
with severe vasodilation (e.g. anaphylaxis, sepsis). Early recognition and immediate treatment
with intramuscular adrenaline remains the mainstay of emergency treatment for anaphylaxis.
Intravenous adrenaline should only be used by those experienced in the use and titratioin of
vasopressors in their normal clinical practice ( e.g. anaesthetists, emergency physicians, intensive
care doctors).
 The mortality from traumatic cardiac arrest (TCA) is very high. The most common cause of death
is haemorrhage. It is recognized that most survivors do not have hypovolaemia, but instead have
other reversible causes (hypoxia, tension pneumothorax, cardiac tamponade) that must be
immediately treated. The new treatment algorithm for TCA was developed to prioritize the
sequence of life-saving measures. Chest compressions should not delay the treatment of
reversible causes. Principles of damage control resuscitation in trauma including hypotensive
resuscitation, haemostatic resuscitation and damage-control surgery. Cardiac-arrest of non-

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traumatic origin leading to a secondary traumatic event should be recognized and treated with
standard algorithms.
 Diagnosis of tension pneumothorax in a patient with cardiac arrest or haemodynamic instability
must be based on clinical examination. During CPR, presentation is not always classical, but when
it is suspected in the presence of cardiac arrest or severe hypotension, chest decompression
should be carried out immediately before radiographic confirmation.
 There is limited evidence for recommending the routine transport of patients with continuing CPR
after out-of-hospital cardiac arrest (OHCA) of suspected cardiac origin. Transport may be
beneficial in selected patients where there is immediate hospital access to the catheterisation
laboratory and an infrastructure providing pre-hospital and in-hospital teams experienced in
mechanical or haemodynamic support and percutaneous coronary intervention (PCI) with ongoing
CPR.
 Recommendations for administration of fibrinolytics when pulmonary embolism is the suspected
cause of cardiac arrest remain unchanged. Routine use of surgical embolectomy or mechanical
thrombectomy is however not recommended. Consider these methods when there is a known
diagnosis of pulmonary embolism.
 Routine use of gastric lavage for gastrointestinal decontamination in poisoning is no longer
recommended. The preferred method of gastrointestinal decontamination in patients with intact
or protected airway is activated charcoal especially if given within 1 hour of the time of ingestion.
Reduced emphasis is placed on hyberbaric oxygen therapy in carbon monoxide poisoning. For up-
to-date guidance in severe or uncommon poisonings, seek advice from a poison centre.
Cardiac arrest associated with concomitant diseases
Asthma
Patients most at risk include those with:
 Previous history of intubation due to asthma;
 Beta-2 agonists dependence;
 Poor compliance with medication
 Food allergy in a patient with asthma.
The main causes of cardiac arrest in asthma patient are.
 Hypoxaemia
 Severe bronchospasm
 Mucous plugging leading to asphyxia ;
 Cardiac arrhythmias due to hypoxia, electrolyte abnormalities or asthma medication (e.g.
beta-adrenergic agonists, aminophylline).
 Tension pneumothorax
 Development of Auto-PEEP in mechanically ventilated patient due to reduction in venous
return.

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Treatment of cardiac arrest in asthmatic patient.
Follow standard BLS guidelines. Start Advanced Life Support, consider early intubation, due to
significant risk of gastric inflation and hypoventilation of the lungs when attempting to ventilate a
severe asthmatic (690). Minimizing development of air trapping during CPR with respiratory rates of 8–
10 breaths per minute and a tidal volume required for a normal chest. If dynamic hyperinflation of the
lungs is suspected during CPR, compression of the chest while disconnecting tracheal tube may relieve
air trapping.
Patients with ventricular assist devices (VADs)
Full training in the procedures for equipment failure and the cardiac arrest situation associated with
ventricular assist devices (VADs) is recommended. External chest compression may be particularly
useful to decompress a non-functional right ventricle in cardiac arrests that might be the cause of the
loss of cardiac output. Few implantable left ventricular assist devices (LVAD) in the market currently
such as a HeartMate (Thoratec, Pleasanton, CA, USA) or HeartWare (HeartWare, Framingham, MA,
USA).
Management of cardiac arrest in patient with VADs are ; Start ALS algorithm ;Check the rhythm;
perform defibrillation for shockable rhythms (VF/pVT), start pacing for asystole and turn the pacing off
in pulseless electrical activity (PEA).
ERC recommended, because it is possible for a patient to have asystole or VF, but still have adequate
cerebral blood flow due to adequate and continued pump flow. If the patient is conscious and
responding then you will have more time in which to resolve this arrhythmia and external chest
compressions will not be needed.
Obesity
The World Health Organization (WHO) uses body mass index (BMI; weight in kg divided by height in
m2) to define obesity in adults as;
• Overweight (25.0–29.9kgm−2);
• Obese (30.0–34.9kgm−2);
• Very obese (≥35.0 kg m−2 ).
No changes to sequence of actions are recommended in resuscitation of obese patients. CPR may be
challenging because of physical and physiological factors related to obesity: patient access and
transportation, patient assessment, difficult IV access, airway management, quality of chest
compressions, the efficacy of vasoactive drugs, and the efficacy of defibrillation because none of these
measures are standardised to a patient’s BMI or weight. (710). Higher inspiration pressure is needed
for positive pressure ventilation due to increased intra-abdominal pressure.
Cardiac arrest associated with pregnancy
The main causes of cardiac arrest are; Haemorrhage, embolism (thromboembolic and amniotic fluid),
hypertensive disorders of pregnancy, abortion and genital tract sepsis account for most deaths directly
associated with pregnancy, and pre-existing medical conditions for those indirectly related to

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pregnancy. During cardiac arrest, Gravid uterus compromised venous return and eventually and cardiac
output limits the effectiveness of chest compressions. During cardiac arrest, Gravid uterus (from 20th
weeks onwards) compromised venous return and eventually and cardiac output limits the effectiveness
of chest compressions.
The recommendation as follow:
 Place the patient in the left lateral position or manually and gently displace the uterus to the
left.
 Give oxygen, guided by pulse oximetry to correct any hypoxaemia.
 Give a fluid bolus if there is hypotension or evidence of hypovolaemia.
 Immediately re-evaluate the need for any drugs being given.
 Activate Code Red. Obstetric and neonatal specialists should  be involved early in the
resuscitation.
 Identify and treat the underlying cause, e.g. rapid recognition and  treatment of sepsis,
including early intravenous antibiotics.
The key steps for BLS in a pregnant patient
 Call for expert help early (including an obstetrician and a neonatologist).
 Start BLS according to standard guidelines.
 Ensure high-quality chest compressions with minimal interruptions.
 The hand position for chest compressions may need to be slightly  higher on the sternum for
patients with advanced pregnancy e.g.  third trimester.
 Manually displace the uterus to the left to reduce IVC compression.
 Add left lateral tilt if this is feasible and ensure the chest remains  supported on a firm
surface (e.g. in the operating room) – the optimal angle of tilt is unknown. Aim for between
15 and 30◦.
 Start preparing for emergency Caesarean section.
 Early tracheal intubation will however make ventilation of the lungs easier in the presence of
increased intra-abdominal pressure.
Discussion with O&G team regarding the the need for an emergency hysterotomy or Caesarean section
as soon as a pregnant woman goes into cardiac arrest (about 4 min after cardiac arrest). Based on ERC
guidelines 2015 recommendations are :
 At gestational age less than 20 weeks, urgent Caesarean delivery need not be considered,
because a gravid uterus of this size is unlikely to significantly compromise maternal cardiac
output.
 At gestational age approximately 20–23 weeks, initiate emergency hysterotomy to enable
successful resuscitation of the mother, not considering survival of the delivered infant, which
is unlikely at this gestational age.
 At gestational age approximately ≥24–25 weeks, initiate emergency hysterotomy to save the
life of both the mother and the infant.
Follow standard post resuscitation guidelines. No contraindication of Targeted temperature
management (TTM) in early pregnancy together with continuous fetal heart monitoring.

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Post Resuscitation Care
Successful return of spontaneous circulation (ROSC) is not the end point of cardiac arrest
resuscitation. In fact, it is the first step towards goal of complete neurological recovery in cardiac
arrest patient.
There is increase recognition on the existence of post cardiac arrest syndrome in cardiac arrest victim
whom has been successfully resuscitated and achieved ROSC. This involves a complete
pathophysiological process.
Post cardiac arrest syndrome ≡ post anoxic ( no flow/cardiac arrest )
- ischaemic ( minimal flow/CPR )
- reperfusion ( ROSC ) syndrome
The presentations of post cardiac arrest syndrome include myocardial dysfunction ( first 2-3 days )
and anoxic brain injury. In addition, the ischaemic-reperfusion problem activates immunological and
systemic inflammatory response and contributing to multi-organ failure and increase risk of infection.
Therefore, a comprehensive, structured, multidisciplinary system of care should be implemented in a
consistent manner for the treatment of post cardiac arrest patient. The post resuscitation phase
starts at the location where ROSC is achieved. But, once stabilized, the patient should be transferred
to the most appropriate area of high level care ( eg : intensive care unit, coronary care unit or cardiac
catheterization laboratory ).
The clinical intensity of post cardiac arrest syndrome varies, but is roughly proportional to the
duration of the cardiac arrest and CPR. The overall outcome depends on the underlying cause of
collapse, the availability of early high quality CPR and post cardiac arrest care.
To ensure the success of post cardiac arrest care, healthcare provider must:
• Optimize the patient’s hemodynamic and ventilation status
• Initiate targeted temperature management
• Provide immediate coronary reperfusion with Percutaneous Coronary Intervention ( PCI )
• Provide neurologic care and prognostication and other structured intervention
Post Resuscitation Care Protocols
1. Controlled Ventilation
• If there is any doubt about patient’s neurological function, controlled ventilation with
advanced airway ( ETT ) should be initiated.
• Sedation ± muscle relaxant should be used to reduce oxygen consumption.
• Waveform capnography should be used to monitor CO2 and oxygenation should be
monitored continuously with pulse oximeter.

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• Titrate FiO2, aims SpO2 94-98% ( avoid hyperoxaemia )
• Aims PaCO2 35-45 mmHg ( maintain normocarbia )
• Continuous EEG ( electroencephalography ) is recommended (if available) to detect
seizures if neuromuscular blocking agent is used
2. Hemodynamic optimization
• Significant myocardial dysfunction is common during post cardiac arrest period. This
accounts for the major cause of death post ROSC but typically recovers by 2-3 days.
• Post cardiac arrest myocardial dysfunction causes hemodynamic instability, which
manifests as hypotension, low cardiac index and arrhythmias. Echocardiography is
indicated during post cardiac arrest care period
• Most of the patient will require inotropic support and intravascular volume expansion.
Some may need invasive device such as IABP (intra-aortic balloon pump) to maintain
hemodynamic stability.
• In post cardiac arrest victims who are maintained a MAP ≥ 70 mmHg as part of post
resuscitation care management, have been reported to have better neurological outcome
and survival.
3. Coronary reperfusion (early PCI)
• Overall, the most common cause of cardiac arrest is cardiovascular disease and associated
coronary ischaemia. Therefore, a 12- lead ECG should be obtained as soon as possible
post cardiac arrest to detect ST elevation/ LBBB
• Coronary angiography should be performed emergently in collapsed patient with
suspected cardiac etiology of arrest and ST elevation on ECG
• Even in the absence of ST elevation, emergent coronary angiography is reasonable for
collapsed patient of suspected cardiac origin
• Factors such as patient age, duration of CPR, hemodynamic stability, presenting cardiac
rhythm, neurological status upon hospital arrival and perceived likelihood cardiac etiology
can influence the decision to undertake the timing for the coronary intervention.
4. Targeted Temperature Management
The term targeted temperature management (TTM) is now preferred over the previous term
therapeutic hypothermia
Hypothermia :
 Suppresses many pathways leading to delayed cell death
 Reduces the CmRO2 ( cerebral metabolic rate for oxygen )by about 6% for each 10○
C
reduction in core temperature reduces the release of excitatory amino acids and free
radicals
 Blocks the intracellular consequences of excitotoxin exposure
 Reduces inflammatory response associated with post cardiac arrest syndrome
Recommendations:
 The comatose adult patient with ROSC after cardiac arrest, must have TTM
 Select and maintain a constant core temperature between 32-36○
C for at least 24 hours
 Prehospital cooling with large volume of cooled intravenous drip immediately after ROSC is
not recommended

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5. Seizure Control
• Seizure is common after cardiac arrest. It occurs in approximately one third of patients who
remain comatose after ROSC. Myoclonus is the most common presentation
• Seizure may increase CmRO2 and has potential to worsen the brain insult caused by cardiac
arrest. It should be treated with anticonvulsant
• However, prophylactic use of anticonvulsant in post cardiac arrest patient is not
recommended
6. Glucose Control
• Maintain blood glucose level at ±10mmol/l
• Do not implement strict glucose control in patient with ROSC post cardiac arrest because it
increases the risk of hypoglycaemia
• Hyperglycaemia in patient post cardiac arrest is bad but hypoglycaemia is more disastrous.
Prognostication
Death is common after ROSC post cardiac arrest. Therefore, optimal timing for prognostication in
post resuscitation care patient is essential
The earliest time for prognostication in patient treated with TTM may be 72 hours after return to
normothermia.
The earliest time to prognosticate a poor neurological outcome in patient not treated with TTM is 72
hours after cardiac arrest. However, time must be given to allow the effect of sedation/ muscle
relaxant to wear off.
Care of the resuscitation team & patient’s relatives
Audit all the resuscitation attempts.
Such documentations allow us:
• To reconstruct the sequence of events with correlation of intervention and response during
resuscitation.
• To evaluate the appropriateness of care
• To evaluate the outcome and effects of resuscitation training.
However, feedback for the resuscitation team should be constructive and not based on fault/blame
culture. Whether the resuscitation attempt was successful or not, the patient’s relatives will require
considerable support. Consider the needs of all those associated with the arrest.

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Ethics of resuscitation and end of life issues
Cardiopulmonary resuscitation (CPR) is performed with the aim to preserve life and to achieve
acceptable quality of life. CPR practice, like any other medical therapies, continue to evolve, as such,
the ethical considerations inevitably should evolve as well. The process of resuscitation may carry risk
of causing suffering and prolonging the process of dying, and it is not an appropriate goal of medicine
to prolong life at all costs. The decision to not initiate and withhold CPR, are influenced by ethical,
legal, religious and cultural background of the community. In the absence of an advanced
medical planning or directives, CPR responders are expected to act in the best interest of the victim until
a clear direction of care or prognosis can be established, following discussion with his/her next of kin.
An ALS provider should be familiar with the relevant legal aspects in ethical issues in resuscitation.
Beneficience
Life sustaining therapy including CPR should be done in the best benefit of the victim.
However, a balance between risk and benefit when attempting CPR should be considered.
Withholding CPR should be considered if the risk for proceeding with CPR outweighs its benefit.
Non-maleficience
CPR should not be attempted in those whom it will not succeed, where no benefit is likely but
there is obvious risk of harm.
Autonomy
A person with decision making capacity should be allowed to make informed decisions pertaining
to their health and resuscitation options. An advanced medical plan or directives, once
established should be respected in uplifting his rights to medical autonomy.
Justice
This implies to our duty in distributing care equally within the society. If CPR is provided,
it should be available to all who shall benefit from it.
As modern medicine continues to evolve alongside technologies that can sustain and prolong
life, it is imperative that the ethical basis of resuscitation should evolve as well. New resuscitation
techniques and strategies like extracorporal CPR requires new approaches in dealing with decision
to discontinue support. Health care providers will inevitably face difficulties to decide on the
direction of resuscitation without a good understanding of such therapy, its appropriate use,
limitations, implications and likely benefits.
A shift from doctor-centered (beneficence) to patient-centered (autonomy) care in
resuscitation and end of life decisions have been emphasized in the 2015 guidelines. Greater
importance has been given to respecting patient’s wishes for CPR as part of medical therapy. As
such healthcare providers are responsible to equip themselves with sound knowledge in
resuscitation, communication and ethical issues pertaining to it, in making end of life decisions.

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Advanced medical care/planning
Advanced medical care or plan when made, should be clearly documented and visible in
patient’s case notes for other healthcare personnel to recognize on the spot. An advance
decision is an expression of patient’s preferences inclusive of either written or verbal. Most
importantly, the healthcare team and those close to him/her are aware of his/her wishes.
However, over time the situation or perspectives of patient might change and DNAR orders
could be revised accordingly. Exemption from DNAR should also be clearly specified to avoid
confusion. In absence of an advanced resuscitation plan, it is acceptable for first responders
to perform resuscitation measures until a clear plan is established.
Withdrawal and withholding therapy
Healthcare providers should consider withholding or withdrawing CPR when :
- Safety of provider can no longer be sufficiently assured
- In presence of obvious mortal injury or irreversible death
- Advanced medical directive becomes available
- There is strong evidence that further CPR would be against
patient’s values and preferences or considered ’futile’
- Asystole for more than 20 minutes despite ongoing ALS by trained
personnel, in absence of reversible cause.
Family presence during resuscitation (FPDR)
The concept of family members being present during resuscitation process has become an
accepted practice since the 1980s and was highlighted in AHA 2010 guidelines. Health care
providers often feel that the presence of family members during resuscitation may interrupt
or interfere with the resuscitative process and thus affecting the outcome. Post traumatic stress
disorder amongst family members and potential medicolegal issues are other concerns for not
allowing family members to be present during CPR. However, recent trials have proven that
FDPR did not lead to higher PTSD, anxiety or mortality.
Therefore, as we move towards a family and patient-centered care, family members should be
given the OPTION to be present during resuscitation attempt after considering the cultural,
religious and social background. Observing the resuscitation attempt may allow time for family
members and loved ones to accept the reality of death, reduce guilt or disappointment and may
help the grieving process. Whenever possible, an experienced staff should facilitate and support
the relative during this process.
A proper written document eg. policy, procedure or standard of care on FPDR in patient-care
areas should be made available to assist and ensure health care providers are aware of such
arrangement, thus providing family members the opportunity to be with their loved ones
during this trying period. In Malaysia, such practice should be allowed when proper written policy
or guidelines are in place.

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Advanced life support training manual final 2017

Advanced life support training manual final 2017

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Advanced life support training manual final 2017