EMERGENCY CARDIAC LIFE SUPPORT

MADE EASY

EMERGENCY DEPARTMENT
HOSPITAL KUALA LUMPUR
FOREWORD

Cardiac Life support is the core business of Emergency

Medicine. Cardiac emergencies comprise 20% of cases seen
in the emergency department. It involves day-to-day exposure
and emphasis on timely based best approach in management
of life threatening cardiac emergencies. Emergency officers
must be well trained and be up to date with latest knowledge,
skill and practices based on accredited international guidelines.
The cardiac life support mode of training in the Emergency department can be incorporated
into:

 Clinical Based Medical Practice (CBMP)

 Clinical Based Medical Education (CBME)

Emergency Officers must undergo time-based assessment in both theory and practical with a
logbook observation. Competency Certification will be awarded and will be renewed on yearly
basis.

AHA and ESC emphasize the rapid initiation of high quality & continues CPR in pulseless
arrest. Since 2015, AHA guidelines supersedes airway with chest compression. Good quality
CPR reduces the mortality rate with good beneficial outcome.

The matrix of high quality CPR is to:

 Push hard, push fast

 Compression depth at 5-6 cm
 Allow complete chest recoil

Time saved is Myocardium saved…

Prof. Dato Sri Dr. Abu Hassan Asahari

Senior Consultant Traumatologist
Head of Emergency Department
Hospital Kuala Lumpur
PREFACE

Dr Sri Rao Dr Rathini Dr Haryanti

Welcome to our very own ‘Cardiac Life Support’ course. It is solely organized by the
Emergency Department of Hospital Kuala Lumpur. Previously this training programme
focussed on trainee house officers only, however due to the growing need to train more
emergency department staff in view of the capacity, the rising events of cardiac cases from
Pre Hospital to the emergency department; we established our very own training programme
called “Emergency Cardiac Life Support”.

It is a 2-day course comprising of theory, lectures, discussions, as well as practical

session. a pre and post-test assessment will be conducted for participants to self-evaluate
after the course. Our participants will be the emergency department house officers, medical
officers, medical students, nurses, and medical assistants. We aim to deliver knowledge and
skills and provide accreditation to be a competent cardiac life saver.

Our team comprise of a Senior Emergency Physician, Dr Sri Rao, who is currently in
the sub-specialty programme of Critical Care Medicine, Dr Rathini, Emergency Physician of 3
year’s experience and Dr Haryanti, Emergency Physician of 1.5 year’s experience. Our
supporting team consists of senior medical officers with experience of more than 1 year in
Emergency Department, Dr Vyjayanthi, Dr Yeo, Dr Khalil, Dr Zafirah, Dr Hazney and Dr
Faizal.

We are also proud to share with you our very own ‘ Emergency Cardiac Life Support’
handbook which gives the participants an overview about the programme equipped with basic
knowledge on ECG, algorithms in cardiac emergency as well as real-life case sharing
scenarios. We hope you take this great opportunity of learning and equipping yourself with
the updated knowledge and it will be our pride to know you have saved lives together with us.

Dr.Sri Rao/ Dr.Rathini/ Dr.Haryanti

CCM COMMITTEE

Consultant : Prof Dato Seri Dr Abu Hassan Asaari Bin Abdullah

Specialists i) Dr Sri Rao A/L Siva
Supervisor: ii) Dr Rathini A/P Inthiran
iii) Dr Haryanti Bt Ramli
Secretary i) Dr Vjayanthi A/P Sonamuthu
ii) Dr Hazney Bt Ibrahim
Treasury i) Dr Mohamad Faizal Bin Ismail
ii) Dr Nurul Zafirah Bt Abd Aziz
Logistic Dr Ahmad Khalil Bin Ibrahim
Liaison Officer Dr Yeo Siew Kim
Staff Nurse i) Sister Zulia Bt Ramli
ii) Sn Jesyrr Vani A/P Kaniasan
Medical Assistant i) Ma Kwan Yong Kit
ii) MA Syamsulhazmi Bin Mohd Norddin
iii) Ma Fizerul Bin Amar Shariffddin
CONTENTS

Page
FOREWARD 2
PREFACE 3
CCM COMMITTEE 4
OBJECTIVES 6
PREHOSPITAL CARDIAC EMERGENCY 7
CHEST PAIN IN EMERGENCY DEPARTMENT 8
TEAM DYNAMICS IN CARDIAC RESUSCITATION 9
INTRODUCTIONS TO CARDIAC EMERGENCY
11
1. 12 LEAD BASICS
17
2. TACHY ARRYTHMIA ALGORITHM
19
3. PULSELESS ELECTRICAL ACTIVITY AND ASYSTOLE ALGORITHM
4. BRADY ARRYTHMIAS & CONDUCTION BLOCKS ALGORITHM
21
5. STEMI RECOGNITION ALGORITHM
23
6. STEMI MIMICKERS :
25
i. LVH
ii. PACED RHYTHM
iii. EARLY REPOLARIZATION
iv. PERICARDITIS
v. LEFT VENTRICULAR ANEURYSM
vi. OSBORN WAVES (HYPOTHERMIA)
vii. TAKASUBO CARDIOMYOPOPATHY
7. STEMI EQUILAVENTS :
29
i. LBBB
ii. SGARBOSSA
iii. ISOLATED POST STEMI
iv. LEFT MAIN CORONARY OCCLUSION
v. DE WINTER ST/T WAVES
vi. HYPERACUTE T WAVES
8. OTHERS:
33
i. HYERKALAEMIA
ii. BRUGADA
iii. WPW
iv. WELLENS
v. AORTIC DISSECTION

DRUGS 37
PRETEST 40
PROGRAMME ITENARY 42
NOTES 43
OBJECTIVE

Aims and Objectives

Aim:

To achieve literacy in cardiac life support among medical personnel

Objectives:

1. To enhance team dynamics, skills and communication among team members during a cardiac
arrest to improve the survival outcome of patients
2. To recognize and manage cardiac emergencies
3. To learn the matrix of High Quality Cardio-pulmonary Resuscitation
4. Know the management of post cardiac care and the disposition of patients
5. To be able to play a major role in real life cardiac resuscitation
PREHOSPITAL CARDIAC EMERGENCIES

Pre hospital services play a big role in the management of cardiac emergencies. Recognition and
initiation of right treatment to cardiac emergencies is directly linked to mortality outcome of the patients.

All emergency personnel responding to pre hospital cases must be certified in Advanced Cardiac Life
Support (ACLS). The ambulance must be well equipped with cardiac resuscitative equipment (E.q. AED,
Vitals monitors, Airway kits etc.) and life saving drugs to resuscitate at site and en route to hospital.
Anticipate any form of dangerous arrhythmias (SVT, AF, VT) to pulseless arrest.

High quality CPR must be ensured continuously in pulseless arrest, vitals monitored and right drugs
delivered and entire resuscitation must be well documented. It is good practice for the treating
emergency personnel to inform and prepare the receiving emergency department for undeterred
continuum of optimum resuscitation care. Good early communication ensures better preparation and
outcome.

 Pre Hospital Preparation

o Equipment:
i. Airway Kits (Oxygen, Definite airway adjuncts, Suction device)
ii. Automated External Defibrillator
iii. Portable defibrillator & Vital Monitors with ECG.
iv. Fluids (Crystalloid & Colloid)
v. Venous branula and infusion pumps
vi. Mechanical automated CPR machines
o Drugs: Naloxone, Flumazenil, Adrenaline, Vasopressin, Lidocaine, Morphine,
Dextrose 50%
o Communication by walkie-talkie between responder to medical base.

 Pre Hospital Cardiac Assessment

o Approach to patient based on advanced Life Support
i. If conscious, monitor Airway-Breathing–Circulation (A-B-C)
ii. If Unconscious with pulse, monitor Airway-Breathing –Circulation (A-B-C)
iii. If Unconscious without pulse, initiate cardiac compression-airway –breathing (C-
A-B)
CHEST PAIN TRIAGING IN EMERGENCY DEPARTMENT

Typical or atypical chest pain comprise of 20% of the cases seen in the emergency departments.
Typical presentations have typical symptom so they can be send to the right triage zone with
appropriate intervention. However atypical presentation with subtle symptoms can be under triaged and
sent to less priority zone where intervention can be much delayed.

At Primary triage, risk stratification is the key work to manage all cases suspected of cardiac in origin.
TIMI score or Grace score is often the choice of risk stratification score used to delineate the severity of
the problem and to triage accordingly.

A modified TIMI score (minus the troponin marker) will be studied or used at the primary or secondary
triage to reduce miss triage of high risk CV cases that appear or present as low risk category. TIMI
score of 3 or more will be regarded as high risk category and will be triaged to either Red or Amber
Zone. Those who score 1 to 2 will be triaged to either Amber-Yellow zone as moderate risk and those
who score zero will be triaged as low risk to yellow zone for first initial assessment. Serial ECG and
troponins play a big role in aiding the atypical presentation or low risk cases suspected of cardiac in
origin.

The Components of modified TIMI score are:

 Age less or equivalent to 65

 More or equivalent to 3 CAD risk factors (DM/ HPT/ Cholesterol/ Smoking/ Family history,
Renal failure)
 Known CAD (>50% stenosis)
 ASA use in past 7 days
 Severe angina (more than 2 episodes in 24 hrs)
 ECG changes

The way forward or future plan is to establish a Chest Pain Unit (CPU) within the emergency
department to handle all cases related or suspected to be cardiac in origin. This will reduce high risk
cases to be under triaged or unwarranted early discharge of cases with high mortality in 30 days
(MACE).

A simple algorithm on page X displays the suggested mode of triaging in ED using modified TIMI score.
TEAM DYNAMICS IN CARDIAC RESUSCITATION

Resuscitation is a team effort that includes various roles going on at the same time and more than one
individual. Hence it is important for each person in the team to recognize their role and know what is
expected of them during the process. It is equally important that the team leader knows their role during
the process and what is expected to be done until termination of efforts or patient is to be transferred for
post cardiac care management.

For every role that is played in the resuscitation effort, the general rule that must be remembered is:

1. Know your role and responsibility in the resuscitation effort

a) Team work is essential and since each team member has a unique role to play, if one fails
to understand their role the entire team efforts will be affected. Hence, take a role that one
is familiar with than unfamiliar with. Signs on inefficiency of a role includes:
i. Repetition of the same task more than once
ii. Essential task missed
iii. Multitasking of some team members despite adequate man power
b) Prioritize on key roles when insufficient man power until help arrives. Certain duties can be
doubled by some team members.
c) Familiar with one’s limits. This applies to team members and the team leader so that help
can be called for when needed. It is not advisable at the time of resuscitation to be trying
out new methods.
d) Openness towards constructive intervention suggestions during resuscitation when
necessary and to be done tactfully without causing a confrontation.
2. Communication is key
a) Sharing of knowledge when faced with a problem or doubt during resuscitation. This
includes providing feedback opinions to team leader.
b) Frequent summarizing and evaluation of team efforts and patient status during and after
resuscitation efforts to keep team members in the loop on their efforts.
c) Close loop communications between team leader and members. How this works is when
the team leader gives a task to a fellow member, a conformation must be given back to the
team leader that the task is received and understood by the receiving team member. Once
the task is done, the team member must report back to the team leader for the next task to
be given with the team leader acknowledging the completion of task.
d) Clear precise message between members. If message was not clear, the receiver should
ask to repeat or explain briefly what is to be expected.
e) One way communication at a time to avoid confusion from multiple voices.
f) Have a mutual respect for each team members. Any conflict of interest or confrontations
encountered can affect resuscitation works.
A high performance resuscitation team consist of 6 people ideally.

Team leader should:

1. Assign and organize the team

2. Monitors and provide assistance to each team members, occasionally taking on roles that are
not assigned
3. Mentor team members
4. Facilitate team work and understanding of each members’ role
5. Focus on overall patient care throughout the resuscitation duration including treatment
decisions and when to call of resuscitation efforts
6. Maintain close loop communications and feedback constantly to the team

Team members consists of many roles but in general:

1. Proficient in their individual skills that has been assigned

2. Be clear about their assigned roles and responsibility. If in doubt or not confident with their
assigned roles, to notify team leader immediately for reassignment
3. Well skilled in most resuscitation skills required
4. Know the algorithms
5. Committed to the team and patients

Specific roles of the team members

Compressor:

1. Patient assessment
2. Performs the 5 cycle chest compression
3. Operates the AED/monitor/defibrillator in alternating sequence after every 5 cycles or 2
minutes or if fatigue sets in

AED/Monitor/Defibrillator:

1. Sets up and monitors the AED/monitor/defibrillator

2. Takes over the compressors role after each cycle or if fatigued during rhythm analysis

Airway:

1. Maintains patency of airway

2. Ventilates with bag-valve mask
3. Applies air way adjuncts when needed
Medications:

1. Obtains IV/IO access

2. Administers medications as needed

Time Keeper/Recorder:

1. Monitors and records events throughout process including timing of interventions,

administration of medication and announce timing for next course of action
2. Monitors and records the length of time and duration of interruptions during the compression
process
3. Maintains close loop communication with the team leader and the team members always

An ideal position of team member during a resuscitation effort is as below:

INTRODUCTIONS

Lead placement

ECG axis (top) and morphology of ECG rhythm with progression of chest leads (bottom)

Placement of ECG leads in normal (top) and right sided (bottom) ECG investigation

Posterior leads placement for posterior ECG investigation

 Normal 12 lead ECG

12- LEAD ECG

P wave
First positive deflection of a cardiac cycle corresponding to atrial contraction

 <120ms ( <3 boxes)

 <2.5mm in limb leads (<3 small boxes)
 <1.5mm in precordial leads ( <2 small boxes)

P mitrale - broad, double notched P wave in lead II

indicating LEFT ATRIAL ENLARGEMENT,
commonly in mitral stenosis

P pulmonale - tall peaked P waves in lead II

indicating RIGHT ATRIAL ENLARGEMENT,
commonly in pulmonary hypertension

Inverted P wave - indicates origin of conduction

not from SA.

Q wave
Negative deflection preceding R wave
Q waves
> 40ms ( >1 box) wide
>2mm deep
>25% of QRS complex height
Commonly in V1-V3
R wave
First positive deflection after P wave, representing ventricular depolarization
Dominant R waves in V1
Normal in paediatrics age group and young adults
ECG :
RVH
RBBB
Post MI
WPW Type A
Incorrect lead placement
Dextrocardia
Hypertrophic cardiomyopathy
Muscular Dystrophy

Dominant R wave in aVR

Sodium channel blocking agents poisoning
Dextrocardia
Incorrect limb lead placement
VT
Poor R wave progression
Commonly in V3 of <3mm
Previous anterior septal MI
LVH
Inaccurate lead placement
Normal variant
T wave
Positive deflection after QRS complex indicating ventricular depolarization in all leads except aVR and
V1
<5mm in limb leads, <15mm in chest leads
Inverted T waves
Normal in paediatrics age group or ventricular
strain pattern
PE - in V1-V3 and inferior leads

Biphasic T wave
Hypokalaemia- down then up

Ischaemia - up then down

Camel hump indicates hypokalaemia

PR interval
From start of P wave to start of QRS complex
120-200ms (3-5 small boxes)

QT interval
From start of Q wave to end of T wave
Normal CORRECTED QTC interval is <440ms in men and <460ms in women

ST Segment
Flat line from end of S wave to start of T wave
May appear elevated or depressed

J point
Junction between end of QRS complex and
start of ST segment

QRS complex
From start of Q wave to end of S wave
Normal duration is 70-100ms
Abnormal presents as narrow or broad

Putting it together

Interpreting anatomy of lesions base on ECG abnormality

ALGORITHMS

Tachyarrhythmia with pulse

Narrow QRS complex
Atrial fibrillation Irregularly irregular pattern with narrow QRS and
NO P waves preceding QRS ( maybe fibrillatory
pattern)
RR intervals are variable

Atrial flutter
No P wave or T wave, replaced by saw tooth
pattern
QRS narrow
Rhythm maybe regular or irregular

SVT
Absent P wave
Narrow QRS with regular rhythm, reaching a rate
of >150/minute

Broad complex
Ventricular tachycardia As per pulseless arrest rhythm
Consider pharmacological reversal agents if
patient is stable.
If unstable, SYNCHRONIZED cardioversion if
rhythm is regular
Pulseless arrest
Ventricular Fibrillation
Wide QRS with no P or T wave
Irregular pattern and rhythm

Use 200J defibrillation mode (Biphasic)

Ventricular tachycardia
Regular QRS rhythm with no P or T wave

Use 200J defibrillation mode

PEA ( Pulseless Electrical Activity)

Can be any rhythm, even a sinus rhythm BUT NO
PALPABLE PULSE

DO NOT SHOCK IN THIS CASE, continue CPR

Asystole
Flat line with no P, QRS or T wave

DO NOT SHOCK IN THIS CASE

Check that leads are attached, equipment is not

faulty and that the height of the complex is not too
small to be read ( put to the maximum height)
before committing to the asystole pattern
Bradyarrhythmia
Sinus bradycardia
Heart rate of less than 60/minute
PR interval is not more than 5 boxes

st
1 degree
Prolong regular PR interval of more than 5 boxes

2nd degree Mobitz 1/Wenckebach

Gradual prolongation of PR interval followed by a
loss/drop of QRS complex and a repeat of the
cycle

Mobitz 2
Constant PR interval but with sudden loss of QRS
complex after a P wave. Rate is constant as well

Fixed block
Fixed ration of P to QRS complex ie, 2 P waves to
1 QRS complex

rd
3 degree heart block
Total dissociation of P and QRS complexes
STEMI / NSTEMI / ACS
Occlusion of the arteries of the coronary vessels

Plague can be stable ( stable angina) or unstable

ie ruptures followed by thrombus formation leading
to further narrowing of the lumen

Normal ECG pattern

ST segment elevation above the PR level

ST segment depression below the PR level

T wave inversion
STEMI MIMICKERS
Early Repolarization

Features:
Widespread minor ST segment elevation prominently in leads V2-V5 and J point notching
ST to T wave in V6 height ratio less than 25%
Concordant T Waves with QRS complex
No reciprocal ST segment changes like in MI

Left ventricular aneurysm

Features:
Minimal ST elevation in V1-V3 associated with deep Q waves and T wave inversion
Osborn wave

Features:
Positive deflection of J point, prominent in precordial leads
Seen in hypothermia
Paced rhythms

Ventricular spikes followed by wide QRS complex with discordant ST segments and T waves ( QRS
wave the opposite of ST segments and T waves from baseline)

Pericarditis

Features:
Widespread ST segment concave elevation
PR depression throughout over most limb leads (I, II, III, aVL, aVF) and precordial leads (V2-V6)
Reciprocal changes of ST depression and PR elevation in lead aVR ( may involved V1)
Sinus tachycardia
Left ventricular hypertrophy

Features:
Sokolov-Lyon Criteria
S wave in V1 + tallest R wave in V5/V6 = >35mm (>7 boxes)

Voltage criteria (must also fulfill non voltage criteria)

Limb leads
R wave in lead I + S wave in lead III >25 mm (>5 boxes)
R wave in aVL >11mm (>2 boxes)
R wave in aVF > 20mm (>4 boxes)
S wave in aVR >14mm (>3 boxes)

Precordial leads
R wave in V4, V5 or V6 >26mm (>5 boxes)
R wave in V5 or V6 + S wave in V1 > 35 mm (> 7 boxes)
Largest R wave + largest S wave in precordial leads > 45 mm (>9 boxes)

Non-voltage criteria (must be fulfilled if using voltage criteria)

Increase R wave peak time > 50 ms in leads V5 or V6
St segment depression and T wave inversion in left sided leads (left ventricular strain pattern)
Takotsubo Cardiomyopathy

Features:
Base on Mayo clinic criteria
New ECG changes (ST elevation or T wave inversion) or moderate troponin rise
Transient akinesis/dyskinesis of left ventricular (apical or mid segment) with regional wall abnormalities
extending beyond single vessel territory
Absence of coronary artery stenosis >50% per culprit lesion
STEMI Equivalent’s
De Winters

Features:
Tall prominent symmetrical T waves in precordial leads
Upsloping ST segment depression >1mm at J points of precordial leads
Absent ST elevation in precordial leads
ST segment in aVR elevated (0.5mm - 1mm)

* Variant of anterior STEMI presentations on ECG without typical ST segment elevations hinting towards
Left anterior descending artery occlusion

Hyperacute T waves

Features:
Early changes in STEMI
Broad and symmetrical T wave
Isolated Posterior STEMI

Features:
Over anterior leads in V1 - V3
Horizontal ST depressions
Tall and broad R waves (>30ms)
Upright T wave
Dominant R wave with R/S ratio >1 in V2

Over posterior leads (V7-V9)

ST segment elevation >0.5mm
Left Bundle Branch Block

Features:
Broad QRS more than 120ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads ( I, aVL,V5-V6) with absent Q wave ( but can have a small Q
wave in aVL)
Prolong R wave peak time >60 ms in left precordial leads (V-V6)
Appropriate discordance of ST segments and T wave to QRS complex
Poor R wave progression in chest leads
Left axis deviation
W pattern in V1,M pattern in V6 ( WiLLiaM) of R wave
Incomplete LBBB features:
QRS complex <120ms

Left Main Coronary Artery Occlusion

Features:
Widespread horizontal ST depression that is prominent in I, II and V4-V6
ST elevation in aVR >1mm
ST elevation in aVR>V1

Sgarbossa

Sgarbossa criteria:
> 1 lead with >1 mm of concordant ST elevation
>1 lead from V1-V3 with >1 mm concordant ST depression
>1 lead anywhere with >1mm ST elevation and proportionally excessive ST elevation (defined as >25%
of depth of preceding S wave.
Discordant: QRS complex is the opposite of the ST segment (one goes up, the other goes down and
vise versa)
Others

Aortic dissection

Mimics inferior STEMI or can be normal ECG

History is important as well as physical examination - some may present with ECG changes but no
chest pain

Brugada

Brugada Type 1 features:

Coved ST segment of >2mm in >1 leads (V1-V3) followed by a negative T wave

Must be associated with one of the clinical findings:

Documented ventricular fibrillation or polymorphic ventricular tachycardia
Family history of sudden cardiac death <45 years
Coved-type ECG’s in family memebrs
Inducible VT with programmed electrical stimulation
Syncope
Nocturnal agonal respiration

Brugada Type 2 features:

>2mm saddle back ST segment elevation
Warrants further investigation

Brugada Type 3 features:

Mimics morphology of type 1 or 2 but <2mm ST segment elevation

Warrants further investigation

Associated with high risk of sudden cardiac death in a structurally normal heart in patients of 40’s
Hyperkalaemia

Feature:
Peaked tall symmetrical T waves

Serum Expected changes

Potassium
5.5 - 6.5 mmol/L Tall tented T wave
6.5- 7.5 mmol/L Loss of P wave
7.5 - 8.5 mmol/L Widening QRS complex
>8.5mmol/L Sine wave

Wellens

Implies critical stenosis of left anterior descending artery with high risk of evolving into a full blown
anterior MI

Features:
Deeply inverted or biphasic T waves in V2-V3 but may extend from V1-V6
Isoelectric or minimally elevated ST segment <1mm
No precordial Q waves
Preserved precordial R wave progression
Recent history of angina
Pain free during ECG captured
Normal or slightly elevated cardiac markers
Wellen’s Type A features:
Biphasic pattern, positive initially then negative
Accounts 25% of cases

Wellen’s Type B features:

Deeply symmetrically inverted T waves
Accounts 75% of cases
Wolf-Parkinson White Syndrome

Features:
Delta wave in QRS complex
Shortened PR interval
Drugs

DRUGS INDICATIONS PRECAUTIONS/CONTRAIN DOSE

DICATIONS
Adenosine First line drug in stable Contraindicated in poisoning IV rapid push:
SVT (only if pathology or drug induced tachycardia, Pt in mild reverse
is reentry involving AV second or third degree heart Trendelenburg position
or SA node) block before administration,
record the rhythm before
May be considered for May be ineffective if patients administering
unstable narrow are on theophylline or
complex reentry caffeine. Consider larger Push bolus 6mg rapidly via
tachycardia while dosing for effects to take large peripheral veins (
preparing for place preferably cubital fossa
cardioversion veins) over 1 to 3 seconds
If patients on dipyridamole or followed by bolus of 20 mls
Regular and carbamazapine, heart NS, immediately elevate
monomorphic wide transplant patients or the extremity while
complex tachycardia administration via central monitoring the cardiac
venous access, reduce initial monitor, record the rhythm
dose to 3mg during this process

Warn patients before Second dose of 12mg can

administering of possible side be given in 1 to 2 minutes
effects: if failed to revert
Flushing, chest pain or
tightness, brief episodes of
asystole or bradycardia,
ventricular ectopy

Caution if used in irregular,

polymorphic wide complex
tachycardia or VT as may
cause deterioration including
hypotension

Transient periods of sinus

bradycardia and ventricular
ectopy are common on
termination of SVT

Safe and effective in

pregnancy
Amiodarone VF/pulseless VT not May cause hypotension if VF/pVT Cardiac arrest
responding to shock infused rapidly not responding to CPR,
treatment, CPR and shock and vasopressor
vasopressor Cumulative dosing of >2.2gm First dose: 300mg IV/IO
over 24 hours have been push
Recurrent associated with significant
hemodynamically hypotension Second dose ( if needed):
unstable VT 150mg IV/IO
Caution when administering
Be wary of toxicity when with other drugs that prolongs Life threatening
using this drug. Only QT interval ( like arrhythmias ( including
use in patients with life procainamide) VT)
threatening
arrhythmias. Proper Long half-life ( up to 40 days) Maximum cumulative dose
monitoring is :
mandatory. 2.2gm IV over 24 hours
administered as follows:

Slow infusion: 360mg IV

over 6 hours (1mg per
minute)

Maintenance infusion:
540mg IV over 18 hours
(0.5mg per minute)
Atropine Symptomatic sinus Increases myocardial oxygen Bradycardia with or
bradycardia demand, hence use with without ACS
Can be given caution in the presence of 0.5mg IV every 3 to 5
ETT route Maybe beneficial for AV myocardial ischaemia and minutes as needed, to a
nodal block but not hypoxia maximum of 0.04mg/kg (
likely for type 2 second 3mg)
rd
degree or 3 degree AV Do not use in hypothermia
blocks or a block in bradycardia Consider shorter dosing
nonnodal tissue intervals and higher doses
May not be effective in Type in severe conditions
rd
Organophosphate 2 AV blocks and new 3
poisoning antidote degree block with wide QRS Organophosphate
complexes. May show poisoning
No longer used in PEA paradoxical slowing on 2-4 mg or higher
or asystole algorithm monitor hence, be prepared
to pace or give ionotropic
support

Doses <0.5mg may result in

 paradoxical slowing of the
heart rate
Dopamine Second line drug for Prior to initiating, correct any IV infusion
symptomatic hypovolemia with adequate Infuse at a rate or 2 to 20
IV infusion bradycardia fluid replacements mcg/kg/min, titrate to
response slowly
Use for hypotension as Cautionary use in cardiogenic
a inotrope agent shock with CHF

May cause tachyarrhythmias

and excessive
vasoconstriction

Do not mix with sodium

bicarbonate
Epinephrine Cardiac arrest Raised blood pressure and Cardiac arrest
VF, pulseless VT, heart rate may induce IV/IO 1mg ( 10ml of
asystole, PEA myocardial ischaemia, 1:10000 solution) every 3
angina, and increased to 5 mins during
Symptomatic myocardial oxygen demand resuscitation followed with
bradycardia 20mls of NS flush and
Can be considered as Higher doses maybe required elevation of the extremity
an alternative infusion to treat poison, drug induced for 10 to 20 seconds after
to dopamine after shock but practice caution as administration
atropine it can contribute to post
resuscitative myocardial Higher dose Up to
Severe hypotension dysfunction 0.2mcg/kg may be used
Can be considered for specific indications eg
when pacing and Beta blockers or CCB
atropine fails, when overdose
hypotension
accompanies Continuous infusion
bradycardia, or with Start with 0.1 to 0.5
phosphodiesterase mcg/kg/min and titrate to
enzyme inhibitor effect

Anaphylaxis, severe Endotracheal route 2 to

allergic reactions 2.5mg diluted in 10mls NS
Combine with large
volumes of fluids, Profound bradycardia or
corticosteroids, hypotension
antihistamines 2 to 10mcg per min
infusion and titrate to
response
Lidocaine As an alternative to Do not use as prophylaxis in Cardiac arrest from
amiodarone in VF/pVT AMI VF/pVT
Can be given cardiac arrest Initial dose: 1 - 1,5 mg/kg
via ETT route Reduce the maintenance IV/IO
Stable monomorphic VT dose in impaired liver function
with preserved or LV dysfunction For refractory VF, may
ventricular function give additional 0.5 to
Discontinue if signs of toxicity 0.75mg/kg IV push, repeat
Stable polymorphic VY develops every 5 to 10 mins to a
with normal QT interval maximum of 3 doses or
and preserved LV total of 3mg/kg
function when
ischaemia and Perfusing Arrhythmia
electrolytes are being In stable VT,wide complex
treated tachycardia of uncertain
type, significant ectopy:
Can be used for stable 0.5 to 0.75 mg/kg and up
polymorphic VT with to 1 to 1.5mg/kg may be
baseline used

QT-interval prolongation Repeat 0.5mg to

if torsades suspected 0.75mg/kg every 5 to 10
mins to a maximum of
3mg/kg

Maintenance infusion
1 to 4 mg per minute (30 to
50 mcg/kg/min)
Magnesium Torsades de pointes or Watch out for drop in blood Cardiac arrest due to
Sulphate suspected pressure after rapid hypomagnesemia or
hypomagnesemia is administration Torsades de Pointes
present ONLY 1 to 2 g ( 2 to 4 ml of 50%
Practice caution in renal solution diluted in 10mls
Life threatening failure patients given IV/IO)
ventricular arrhythmias
from digitalis toxicity Torsades de Pointes
with a pulse or AMI with
hypomagnesemia
Load with 1 to 2 gm mixed
in 50 to 100mls diluent
over 5 to 60 mins IV
Followed with 0.5 to 1 g
per hour IV (titrate to
control the torsades)