Module 2

Course director
Dr Michael D. Klein, MD
Medical Director of the Heart Station at
Boston Medical Center,
Clinical Professor of Medicine
Boston University School of Medicine,
Boston MA

Course Code: E.PPDiplomaCE13P2

 POST GRADUATE EXCELLENCE PROGRAM IN

CARDIAC EMERGENCIES
IN GENERAL PRACTICE

Course Information
Need for the program
The wide prevalence of cardiovascular diseases in population, more so in uninvestigated forms, put individuals at high risk of an
emergency episode. This risk will in fact be exceedingly high seeing lifestyle aberrations in population in epidemic proportions.
Cardiovascular emergencies are lifethreatening disorders, which require prompt diagnosis to avoid delay in treatment so that the
associated morbidity and mortality can be minimized. Patients may come to an emergency with varied presentations such as severe
hypertension, chest pain, dysrhythmia, or cardiopulmonary arrest. Such an occurrence of these episodes makes it imperative that
clinicians have updated knowledge about concepts related to these cardiovascular emergencies and their manifestations, and diagnosis
and management strategies related to them. This will help in considerably increasing the survival rates given that most sudden deaths
in such emergencies occur during initial hours of the onset of symptoms.

This program in “Cardiac emergencies in general practice” is designed to improve clinical skills of clinicians related to cardiology
while encountering common cardiovascular emergencies. The program is available in print format and starts with explaining in detail
finer points about the conditions, their pathogenesis and identification based on clinical presentations, and pertinent management
approaches. It is expected that the training program will inculcate the art of identifying, diagnosing, and managing confidently
common cardiovascular emergencies.

Program objectives
1. Identify different types of ventricular arrhythmias seen in clinical practice and become familiar with their management approach
2. Know the mechanisms and causes of sudden cardiac death, and be updated on its risk stratification paradigms and prevention
strategies
3. Understand the concept of post-cardiac arrest syndrome and diagnostic and management strategies in post-cardiac arrest
survivors who have received resuscitation
4. Become familiar with doses and indications of common drugs used in emergency cardiovascular care

Course director
Dr Michael D. Klein, MD
Medical Director of the Heart Station at
Boston Medical Center,
Clinical Professor of Medicine
Boston University School of Medicine,
Boston, MA

Editor
Dr Pankaj Tikku
Medical Director
Passi HealthCom

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 POST GRADUATE EXCELLENCE PROGRAM IN
CARDIAC EMERGENCIES
IN GENERAL PRACTICE

Method of participation in the program

•• Register for the program when prompted
•• Study all parts of the educational activity available in online format
•• The complete program, including two course modules, will be followed by an evaluation. Successful candidates (those who
score more than 70% in the evaluation) will be issued a certificate of participation

DISCLAIMER
THIS CONTINUING MEDICAL EDUCATION PROGRAM IS INTENDED SOLELY FOR EDUCATIONAL PURPOSES FOR QUALIFIED
HEALTHCARE PROFESSIONALS. THIS PROGRAM DOES NOT REPLACE YOUR HOME COUNTRY’S LAWS, REGULATIONS, AND GUIDELINES
CONCERNING MEDICAL CARE AND DRUG PRESCRIPTION ACTIVITIES. IN NO EVENT SHALL BOSTON UNIVERSITY BE LIABLE FOR ANY
DECISION MADE OR ACTION TAKEN IN RELIANCE ON THE INFORMATION CONTAINED IN THE PROGRAM. IN NO EVENT SHOULD
THE INFORMATION CONTAINED IN THE PROGRAM BE USED AS A SUBSTITUTE FOR PROFESSIONAL CARE. NO PHYSICIAN-PATIENT
RELATIONSHIP IS BEING ESTABLISHED.

PASSI HEALTHCOM PRIVACY POLICY

THE CONTENTS OF THIS PROGRAM ARE DEVELOPED BY PASSI HEALTHCOM PVT. LTD., IN COORDINATION WITH BOSTON UNIVERSITY
SCHOOL OF MEDICINE, USA. ALTHOUGH GREAT CARE HAS BEEN TAKEN IN COMPILING AND CHECKING THE INFORMATION, THE
AUTHORS, PASSI HEALTHCOM PVT. LTD., AND ITS AGENTS AND SPONSORS SHALL NOT BE RESPONSIBLE, OR IN ANYWAY LIABLE
FOR ANY ERRORS, OMISSIONS OR INACCURACIES, BOTH IN CONTENTS OF THIS ACTIVITY OR IN PRESCRIBING INFORMATION OF
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CURRENT APPROVED PRODUCT INFORMATION.

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POST GRADUATE EXCELLENCE PROGRAM IN

CARDIAC EMERGENCIES
IN GENERAL PRACTICE

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GENERAL PRACTICE
GRADUATE EXCELLENCE PROGRAM IN
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IN GENERAL PRACTICE

Contents
Section 1
Ventricular tachyarrhythmias 6

Section 2
sudden cardiac death 19

Section 3
Post-cardiac arrest syndrome 30

Section 4
Pharmacology in emergency cardioVascular care 39

Case studies
a case of sudden cardiac syncoPe secondary
to Prior myocardial infarction 45

sudden cardiac arrest in a 59-year old male

without heart disease 46

a 74-year old man with chest Pain 48

50
Updates

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Section
Ventricular tachyarrhythmias
1
Course Director
Dr Michael D. Klein, MD
Medical Director of the Heart Station at
Boston Medical Center,
Clinical Professor of Medicine
Boston University School of Medicine,
Boston, MA

objectiVes
• to know the different types of ventricular tachyarrhythmias and treatment approach in patients
presenting with these arrhythmias
• to discuss in brief the different treatment options for ventricular tachyarrhythmias, including
pharmacological agents, ICD and radiofrequency ablation

6

cardiac arrhythmias: focus on Vt
Cardiac arrhythmias are disorders caused by perturbation
in normal electrical activity of the heart resulting in its
disorganized rhythm. They may occur in healthy individuals
with an anatomically normal heart or may be associated with
an underlying cardiac disorder. Cardiac arrhythmias are widely
prevalent and may manifest with an array of clinical symptoms,
although a subset of affected patients remain asymptomatic.1
Commonly encountered arrhythmias include, although are
not limited to, atrial flutter and fibrillation, supraventricular
tachycardias (Svt) and ventricular tachyarrhythmias (vt).
Many arrhythmias among these have a sudden unexpected
onset and often foster risk of sudden cardiac death (SCD).
treatment of these arrhythmias can often be challenging and
should be based on the mechanism of their development.
Early diagnosis and aggressive management of potentially fatal
arrhythmias should be attempted in the intensive care unit
(ICU) with the aim to terminate the arrhythmic episode and
obviate risk of SCD.2
ventricular tachyarrhythmias (vt) are among the
commonly seen arrhythmias. The spectrum of ventricular
arrhythmias include premature ventricular complex (PvC),
sustained monomorphic vt, polymorphic vt, and ventricular
fibrillation (vf). As with other arrhythmias, they can be
detected in healthy individuals and in those with a heart
disorder. While occasionally occurring ventricular ectopics
in healthy individuals do not engender much concern,
sustained rapid vt can compromise the hemodynamic status
and even degenerate into vf. ventricular tachycardias are
commonly seen in the settings of a coronary artery disease
(CAD) and contribute to considerable morbidity and
mortality, particularly during the acute ischemic episode.
Development of implantable cardioverter-defibrillators (ICD)
and radiofrequency ablation techniques have significantly
improved survival rates in life-threatening vt. Effectiveness of
antiarrhythmic drugs, however, remains questionable.3,4
classification of Vt
various methods of classifying vt have been proposed. on
the basis of their duration, vt are divided into non-sustained
and sustained vt. While non-sustained vt are usually of
short duration and terminate spontaneously in < 30 seconds,
sustained vt are clinically more significant and last for > 30
seconds. on the basis of ECg morphology, vt (non-sustained
and sustained) are further subdivided into monomorphic
and polymorphic vts. In monomorphic vt, each QrS
complex resembles the next. In contrast, polymorphic vt
have changing QrS morphology (figure 1). Torsades de
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Figure 1 Monomorphic VT (A) and polymorphic VT (B) on
ECG
A
B
based on information from: Koplan BA, Stevenson Wg. ventricular tachycardia
and sudden cardiac death. Mayo Clin Proc. 2009 Mar;84(3):289-97.
pointes is a type of polymorphic vt that is associated with a
prolonged Qt interval and twisting of the peaks of the QrS
complexes around the isoelectric line.5 Bidirectional vt is
rarely seen in cardiology clinics and involves alternating QrS
axis morphology with rotation of 180°on a beat-to-beat basis;
originally described in association with digitalis toxicity,
bidirectional vt is now known to be a manifestation of many
other disorders.6
non-sustained Vt (nsVt): their
releVance in Practice
ventricular ectopics are not uncommon in cardiology practice.
Premature ventricular complexes (PvC) and non-sustained
ventricular tachyarrhythmias (nSvt) are two forms of
ventricular ectopics which are seen in healthy individuals
and in those with heart disorders. Although their occasional
occurrence in healthy individuals, particularly when detected
at rest, may not be considered alarming, their association
with a silent ischemic heart disease (IHD), an underlying
cardiomyopathy and risk of SCD cannot be discounted. The
PvC usually arises from an ectopic pacemaker located in the
ventricles and is a reflection of automatically or localized
reentry of this part of the ventricle. Many pathological factors
can trigger increase in automaticity of the ectopic ventricular
pacemaker; important causes among them include ischemia,
dyselectrolytemia and changes in the autonomic response (as
in athletes). Besides being an isolated phenomenon, PvC can
also occur in repetitive bursts. occurrence of three or more
PvCs at a rate greater than 100 beats per minute characterizes
a nSvt. Wide heterogeneity in clinical presentation of PvC
and/or nSvt has been noted. Most individuals with isolated
PvC and/or nSvt are asymptomatic and these ectopics are
incidentally detected on their ECg; occasionally they may be
 DIPLOMA
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associated with symptoms, especially when they complicate a
cardiac disorder. Commonly reported symptoms of PvC and
nSvt include very localized discrete chest pain, palpitations,
pre-syncopal attacks (such as dizziness, light headedness) and
rarely, syncopal episodes.7
The prognostic significance of PvC and nSvt remains
obscure, although their frequency and the clinical situation
in which they occur may be significant contributors to their
outcome. In apparently healthy individuals with an otherwise
normal heart, ventricular ectopics can occur at rest or during
exercises.8 While most investigators emphasize that occasional
ectopics in healthy individuals should be viewed as an innocuous
occurence,9 some have shown that in adults more than 30 years
of age these ectopics should be viewed with greater concern as
they may portend risk of ischemic heart disease (IHD) or SCD
in these subset of individuals.10 In contrast, PvC and nSvt
induced during exercises is often associated with increase in
risk of mortality and attempt should be made to look for an
underlying cardiac etiology in these cases.11 The risk of SCD in
exercise-induced nSvt is relatively lower in patients without
an underlying structural heart disease compared to those with
a cardiac disorder. Usually most ventricular ectopics identified
during exercises are either a result of ischemia, heart failure or
are idiopathic vt (see section on sustained vt).12
other than in healthy individuals, nSvt is also detected
in patients with heart diseases, both ischemic as well as non-
ischemic. In these patients nSvt is more likely to pursue a
fulminant course. Investigators have confirmed that frequent
runs of nSvt in patients with an underlying cardiac disorder
increases mortality risk,9 the magnitude of which varies with
the nature and extent of the cardiac disorder. In patients with
CAD, the prognostic implication of nSvt may be dependent
on the timing of its occurrence. Among patients with
myocardial infarction (MI), episodes of nSvt in the first 24
hours of the ischemic episode may not be a predictor of long-
term mortality, although these ventricular ectopics may have
a detrimental effect in increasing SCD risk when they occur
after 24 hours of infarction. Still other studies have highlighted
the prognostic significance of left ventricular ejection fraction
(lvEf) in CAD patients. Their results show that reduced
lvEf in CAD may worsen the outcome of nSvt. Usually,
patients with lvEf < 40% have a high risk of arrhythmia-
related deaths and SCD, although the risk in patients with
lvEf > 40% remains equivocal.8
In contrast to IHD, long-term outcome of nSvt in
patients with non-ischemic heart diseases appears to have
been understudied. Substantial increase in risk of SCD has
been shown with occurrence of nSvt in hypertrophic
cardiomyopathy at a young age.13 In contrast, frequent runs
8
of nSvt (≥10 beat runs) are more robust predictor of poor
prognosis in dilated cardiomyopathy.14 limited data is available
on prognostic significance of PvC and nSvt in other non-
ischemic cardiac diseases and idiopathic arrhythmogenic
conditions (described in section of sustained vt).
approach in patients with PVc and nsVt
Usually PvC and nSvt are considered low-risk arrhythmias,
especially in healthy individuals, and there is little information
about how they should be treated. Majority of patients with
these ectopics are either asymptomatic or report minimal
symptoms, such as “occasionally missing a beat”. Sometimes,
pre-syncopal attacks and syncopal episodes may also occur. A
12-lead resting ECg is often sufficient to detect a premature
ectopic. In these patients, a comprehensive history should
be taken enquiring about symptoms, their frequency and
duration. family history of SCD and presence of risk factors
for CAD should be noted.1
Management of PvC and nSvt should be attempted
keeping into consideration the clinical situation in which these
arrhythmias occur. In patients with PvC/nSvt, the primary
aim should be to identify an underlying cardiac disorder,
if present, and mitigate risk of SCD. Most asymptomatic
patients with occasional occurrence of PvC can be reassured
and followed-up at regular intervals for signs of deterioration.
Patients with exercise-induced nSvt should be subjected
to further investigations to rule out an underlying heart
disorder. young individuals < 40 years of age with nSvt
should be evaluated for non-ischemic heart diseases while
those > 40 years of age should be screened for an underlying
IHD. An underlying cardiac disorder, if identified, should be
managed accordingly. Symptomatic individuals with nSvt
need treatment with beta-blockers with/without immediate
cardioversion. Antiarrhythmic drugs may be chosen after
weighing their benefits/risks in these patients (figure 2).7,8,15
sustained Vt: the Potentially fatal
arrhythmias
In contrast to PvC and nSvt, sustained vt, monomorphic
and polymorphic, are potentially fatal cardiac arrhythmias
which can present either with or without hemodynamic
compromise. In most patients, sustained vt is associated with
an underlying structural heart disease, although its detection
in apparently healthy individuals is also known.5
A number of cardiac disorders, both ischemic and non-
ischemic, are complicated by sustained vt. Among them,
CAD appears to be most commonly linked to these fatal
ventricular arrhythmias. Sustained vt can occur either during
 DIPLOMA PROGRAM
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Figure 2 Management approach in patients with PVC or NSVT

PVC/NSVT (detected on ECG)

Asymptomatic Symptomatic

• ECHO
• Stress testing
PVC/NSVT at rest Exercise-induced PVC/NSVT • *EP testing (?)

• ECHO
• Stress testing
Reassure and follow-up
• *EP testing (?)
Underlying heart disease not detected

Underlying heart disease not detected Underlying heart disease detected Cardioversion ±
Beta-blocker

Follow-up Treat underlying disorder

*EP = electrophysiological testing (required in some patients)

based on information from:

1. Sheldon SH, gard JJ, Asirvatham SJ. Premature ventricular Contractions and non-sustained ventricular tachycardia: Association with Sudden Cardiac Death, risk
Stratification, and Management Strategies. Indian Pacing Electrophysiol J. 2010 Aug 15;10(8):357-71.
2. Katritsis Dg, Camm AJ. review nonsustained ventricular tachycardia: where do we stand? Eur Heart J. 2004 Jul; 25(13):1093-9.
3. Katritsis Dg, Zareba W, Camm AJ. nonsustained ventricular tachycardia. J Am Coll Cardiol. 2012 nov 13;60(20):1993-2004.

the acute MI episode or may develop many years after the
primary heart attack.5 Both monomorphic and polymorphic
vts can develop in the settings of acute ischemia; they are
usually preceded by ventricular ectopics in MI patients. Hence,
presence of ventricular ectopics in patients with acute MI can
be alarming as they may augur subsequent occurrence of major
arrhythmias.16 Polymorphic vt are more likely to develop
during acute MI due to ensuing abnormalities in the ventricular
repolarization during the ischemic episode. Some of these
polymorphic vt degenerate to vf, which may result in SCD
during the postinfarction period.5,16 It is worth remembering
that in most patients with acute ischemia, polymorphic vt
is associated with a normal Qt interval. This is in contrast
to another form of polymorphic vt which has a “long Qt
interval”, indicating prolonged repolarization. Polymorphic
vt with long Qt interval are characterized by a gradual
change in the amplitude and twisting of the QrS complexes
around the isoelectric line and are commonly referred to as
torsades de pointes. Although uncommonly occurring, these
polymorphic vt can frequently progress to vf and SCD.
Torsades de pointes can be congenital or acquired, the latter
form occurring either secondary to an electrolyte abnormality
(such as hypokalemia) or after administration of some class I
and class III antiarrhythmic drugs, and other drugs that can
prolong the Qt interval.17 of note, sustained vt/vf are
encountered more commonly in patients with St-elevation MI
(StEMI) compared to non-St elevation MI (nStEMI) and
increase short- and long-term mortality rates in them.18,19 The
incidence of sustained vt/vf in the settings of StEMI has
been reported to be 5-10% while their cumulative incidence in
nStEMI patients in a recently concluded study18 was shown
to be 0.9-1.5%. Monomorphic vt, although known to occur
during acute ischemia, is more commonly seen in patients
with a previous MI episode wherein the old myocardial scar
provides an ideal anatomic substrate for reentrant excitation,
hence precipitating a monomorphic vt.5

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Although CAD is by far the most common heart disease
associated with sustained vt, it is not uncommon to
encounter these arrhythmias in patients with non-ischemic
cardiac disorders, including hypertrophic cardiomyopathy,
dilated cardiomyopathy and arrhythmogenic right ventricular
dysplasia.5 Additionally, sustained vt can be detected after
cardiac surgeries and increases risk of death in the immediate
postoperative period (within 30 days). reduced lvEf (<
35%) is a strong risk factor favoring occurrence of vt in
postoperative patients.20 An often understudied cause of vt
is inherited channelopathies. Catecholaminergic polymorphic
ventricular tachycardia (CPvt) is an inherited cardiac ion
channel disorder associated with sudden onset of recurrent
syncopal episodes due to polymorphic vt, usually following
exercises or periods of acute emotion, in individuals without
a known structural heart disease. Some CPvt episodes may
terminate in SCD.21 The usual age of occurrence of CPvt
is between 7-9 years, although it has been seen in the adults
as well. Diagnosis can often be challenging due to a normal
resting ECg pattern in the absence of symptoms; evidence of
bidirectional vt may be seen in some patients. In suspected
patients, exercise treadmill testing may induce arrhythmia and
validate diagnosis of CPvt.21,22 The underlying cause of CPvt
is being investigated. Mutation in the ryanodine receptor 2
(ryr2) genes has been found to be an underlying cause in
almost half of dominantly-inherited forms of CPvt. Aberration
in calsequestrin 2 (CASQ2) genes has been reported as an
underlying cause in its autosomal recessive form. recently
investigators have identified two mutations in the CAlM1
genes, which encode for calmodulin, and may also underlie –
at least partly – the pathogenesis of this disorder.23 The long
Qt syndrome is another form of inherited channelopathy
associated with vt which engenders considerable concern
because of its association with torsades de pointes (described
previously); it can result in syncope and sudden death. The
diagnosis is primarily based on presence of Qt prolongation
on the ECg.24 Brugada syndrome, a disorder arising from
mutational defect in the cardiac sodium channels, is another
inherited cardiac disorder characterized by syncopal episodes
and/or sudden death due to vt in patients with a structurally
normal heart. The ECg in these patients is characteristic and
demonstrates rapid polymorphic vt, a pattern of right bundle
branch block with an St-segment elevation in leads v1 to v3.
While sustained vt/vf occurrence in these patients may
predispose to a sudden cardiac arrest, spontaneous termination
may culminate in a syncopal attack.25
Patients with sustained vt can have variable clinical
presentation. Most patients are symptomatic although a small
subset of patients with sustained vt may be asymptomatic
10
and can have self-termination of their vt episodes.17
Symptoms of recurrent vt, when present, include palpitation,
chest pain, dyspnea, syncopal episodes and near-syncopal
attacks. Although most patients with sustained vt have severe
symptoms, in some cases mild symptoms may be present. These
patients often present a diagnostic challenge and are frequently
misdiagnosed and treated as Svt. Since management options
for Svt are different from vt, it is prudent to differentiate the
two arrhythmias strictly on the basis of findings on a 12-lead
ECg without getting influenced by the patients’ symptom
severity.26
Some patients with an apparent good health and
anatomically normal heart can develop vt, the cause of which
remains unidentified. These patients are usually young and have
no evidence of any structural heart disease, inherited causes
of vt or dyselectrolytemia. This form of vt is referred to as
idiopathic vt. Most idiopathic vt are monomorphic. owing
to preserved cardiac functions, these patients tolerate the
tachycardia well and their overall prognosis is good, although
risk of sudden death in some individuals cannot be discounted.
two broad subgroups of idiopathic vt have been recognized;
outflow tract vt and idiopathic fascicular vt. outflow tract
vt can originate from the right or left ventricular outflow
tracts, the majority usually arising from the right ventricular
outflow tract. These vt usually occur as repetitive runs of
ventricular ectopics and nSvt (repetitive monomorphic
vt).5,27 A small subgroup of patients have idiopathic fascicular
vt wherein reentry seems to be the chief operative mechanism
for arrhythmia. These patients demonstrate evidence of right
bundle branch block QrS configuration with a left or right
axis deviation.28
approach in patients with sustained Vt
In patients with suspected vt, a baseline resting 12-lead
ECg should be advised. findings of a wide QrS complex
tachycardia (QrS 120 msec or greater) at a rate of 100 beats
per minute or greater is usually indicative of vt. It is worth
noting that although vt is the most common etiological cause
of a “wide QrS complex tachycardia”, accounting for almost
80% of these cases, some patients with broad QrS complex
can have an underlying Svt with aberrancy or a preexcited
tachycardia. Differentiating these arrhythmias may be crucial
for guiding therapy. History of a structural heart disease, CAD
or previous MI episode, a positive family history of SCD
and evidence of Av dissociation on examination (variable
intensity of first heart sound and intermittently seen cannon A
wave due to simultaneous contraction of atria and ventricles)
should strongly suggest a diagnosis of vt. furthermore, an
echocardiogram should be included in the diagnostic approach
 DIPLOMA PROGRAM
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Figure 3 Management approach in patients with sustained VT

Sustained VT*

Monomorphic VT Polymorphic VT

Stable Unstable Stable Unstable

(without hemodynamic (with hemodynamic (without hemodynamic (with hemodynamic
compromise) compromise) compromise) compromise)

Antiarrhythmic drugs Direct cardioversion Usually terminate Direct cardioversion

IV Procainamide spontaneously; if
or does not, treat as
IV Ajmaline monomorphic VT
Recurrent VT Recurrent VT
Recurrent VT

IV Amiodarone Normal EF Low EF Baseline QT Baseline QT interval

or interval normal** prolonged
IV Beta-blocker

IV Procainamide IV Amiodarone

Normal EF Low EF

Correct ischemia Correct ischemia Correct electrolyte

Correct electrolyte Correct abnormality
abnormality electrolyte +
+ abnormality IV Magnesium
IV Beta-blocker + sulphate
IV Amiodarone or
Overdrive pacing

*If an underlying heart disease is present, treat accordingly; in patients with acute MI, sustained vt may be managed with Iv lidocaine or Iv ajmaline
** Iv Isoproterenol can also be used

based on information from:

1. trappe HJ. treating critical supraventricular and ventricular arrhythmias. J Emerg Trauma Shock. 2010 Apr;3(2):143-52.
2. Collopy Kt. Stable or unstable? Assessment and management of ventricular tachycardia with pulses. EMS Mag. 2009 Jun;38(6):42-8; quiz 49.
3. Zipes DP, Camm AJ, Borggrefe M, et al.; American College of Cardiology/American Heart Association task force; European Society of Cardiology Committee for
Practice guidelines; European Heart rhythm Association and the Heart rhythm Society. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular
arrhythmias and the prevention of sudden cardiac death--executive summary: A report of the American College of Cardiology/American Heart Association task force
and the European Society of Cardiology Committee for Practice guidelines (Writing Committee to Develop guidelines for Management of Patients with ventricular
Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart rhythm Association and the Heart rhythm Society.
Circulation. 2006;114:e385-e484.

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of patients with vt to rule out a structural heart disease and
evaluate ventricular functions, including the ejection fraction
(Ef). Stress testing is also important for identifying an
underlying silent CAD. Evidence of electrolyte abnormality
should also be looked for. Invasive electrophysiologic testing
should be recommended to substantiate a diagnosis of vt,
especially in a subset of patients in whom differentiation
between vt and Svt remains difficult.29,30
In patients diagnosed with sustained vt, the initial
management approach depends primarily on the patients’
hemodynamic status. Patients who are hemodynamically
stable can be managed with antiarrhythmic drugs. However,
hemodynamically unstable patients are ideal candidates for
prompt cardioversion and defibrillation; antiarrhythmic drugs
can be used in case of no response.31 Some investigators have
recently opined that since many hemodynamically stable patients
with vt have high recurrence rates which increases their risk
of SCD, they should also be offered implantable cardioversion
along with pharmacological antiarrhythmic therapy to reduce
their arrhythmia recurrence risk.32 The guidelines of the
American College of Cardiology (ACC)/American Heart
Association (AHA) task force and the European Society of
Cardiology (ESC)33 outlines the choice of antiarrhythmic
drugs for patients with vt. These guidelines recommend Iv
procainamide (or ajmaline) for initial management of stable
sustained monomorphic vt with a normal Ef.33 While
procainamide is recommended to be given at a dose of 10 mg/
kg Iv, ajmaline, if required, should be administered at a dose
of 50-100 mg Iv over 5 minutes. Alternatively, these patients
can also be managed with amiodarone, given Iv 150-300 mg in
5 minutes, followed by infusion of 1050 mg/day.2 In unstable
patients with monomorphic vt, ACC/AHA/ESC guidelines33
recommend immediate direct current cardioversion with
appropriate sedation as the initial management approach;
for patients demonstrating recurrence despite cardioversion,
Iv procainamide (if Ef is normal) or Iv amiodarone (if Ef
is reduced) may be considered.33 for patients with sustained
monomorphic vt with an associated CAD, Iv lidocaine
(100-150 mg Iv) was the preferred antiarrhythmic drug in the
past, although more recently Iv ajmaline is recommended as a
first-line drug in these settings (see section on antiarrhythmic
drugs).2
Most patients with sustained polymorphic vt present
with a hemodynamic compromise (unstable polymorphic
vt). These patients should be offered immediate direct
current cardioversion with appropriate sedation initially. Those
with recurrent polymorphic vt with normal Qt interval
often have a coassociated ischemia; these patients should be
managed preferentially with a beta-blocker or amiodarone.33
12
Isoproterenol can also be used. It should be administered Iv
at a dose of 1-4 mcg/minute, given as infusion. Atropine can
be given at a dose of 0.5-1.0 mg Iv, maximum 0.04 mg/kg. If
amiodarone is chosen, it is recommended to be used at a dose
of 150-300 mg Iv, followed by infusion of 1020 mg/day.2 In
patients with suspected ischemia, prompt coronary angiography
can also be considered. Management of polymorphic vt with
a prolonged Qt interval should be primarily attempted with
Iv magnesium sulphate. In patients with torsades de pointes,
correction of electrolyte abnormality and withdrawal of the
offending drug is important. Magnesium sulphate should be
administered at a dose of 2 g Iv; another dose of 2 g Iv can be
repeated after 15 minutes in case of no response. This should
be followed by Iv infusion of 500 mg/hr. overdrive pacing
or general anesthesia may be considered for patients with
frequently recurring or incessant vt (figure 3).33
Ventricular fibrillations: the
medical emergency
ventricular fibrillations (vf) are characterized by a very rapid
heart rate (usually more than 300 beats per minute) and chaotic
disorganized electrical activity of the heart. Marked variability
in QrS cycle length, morphology, and amplitude characterizes
the ECg findings of patients with vf.33 Its unpredictable
onset makes vf a significant contributor to SCD in clinical
practice.34 It is rarely self-limiting and rapidly progresses to
unconsciousness and pulselessness. These attributes confer vf
the status of a medical emergency which warrants immediate
attention and aggressive resuscitative management. Despite
extensive work done, the exact mechanism underlying the
development of vf remains unknown. However, it appears
probable that vf may be triggered secondary to rapid impulse
formation and development of multiple, unstable reentry
circuits.35
In cardiology practice, vf occurs most commonly in
the settings of a CAD, usually during an acute MI episode.
In hospitalized patients with MI, vf has been demonstrated
in 5-10% of cases.36 Although long-term outcome of these
patients still needs to be established, significantly poor
prognosis of patients with vf in the immediate postinfarction
period has been unambiguously proven. In patients with
acute MI, occurrence of vf considerably increases risk of in-
hospital mortality and accounts for most deaths in the first 2
hours of postinfarction period.35,37 other than acute MI, many
other causes of vf have been identified, including hypoxia,
acidosis, severe left ventricular hypertrophy (lvH) and
advanced structural heart diseases with poor lv or rv systolic
function.35
 DIPLOMA PROGRAM
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Figure 4 Emergency management approach in patients with pulseless VT/VF

Pulseless VT/VF

Oxygenation + CPR Biphasic shock 120-200 J

I shock Monophasic shock 360 J

Continue CPR 5 cycles/2 minutes

Reassess

Shockable rhythm, no response Asystole

Repeat I shock Treat accordingly

Epinephrine 1 mg IV (can be repeated in 3-5 minutes)
OR
Vasopressin 40 IU IV (can replace 1st or 2nd dose of epinephrine)

Continue CPR 5 cycles/2 minutes

Reassess

Shockable rhythm, no response Asystole

Repeat 1 shock Treat accordingly

Antiarrhythmic drugs
• Amiodarone 300 mg IV, followed by 150 mg
IV in case of no response
• Lidocaine (in case of acute MI) 1-1.5 mg/kg
IV followed by 0.75-3 mg/kg

Continue CPR and reassess

Continue till sinus rhythm restored

based on information from:

Zipes DP, Camm AJ, Borggrefe M, et al.; American College of Cardiology/American Heart Association task force; European Society of Cardiology Committee for Practice
guidelines; European Heart rhythm Association and the Heart rhythm Society. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias
and the prevention of sudden cardiac death--executive summary: A report of the American College of Cardiology/American Heart Association task force and the European
Society of Cardiology Committee for Practice guidelines (Writing Committee to Develop guidelines for Management of Patients with ventricular Arrhythmias and the
Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart rhythm Association and the Heart rhythm Society. Circulation. 2006;114:e385-
e484.

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approach in patients with pulseless Vf be delivered. In non-responding patients, epinephrine (1 mg)

Most patients with vf present in the emergency with cardiac
arrest and are pulseless. Immediate defibrillation and initiation
of cardiopulmonary resuscitation (CPr) is required in them
to restore sinus rhythm and reduce risk of death. Defibrillators
have traditionally used monophasic waveforms to deliver
shocks in patients with cardiac arrest. Most ICDs and many
external defibrillators now deliver shock as biphasic waveforms.
Biphasic shocks appear beneficial as they require lower currents
than monophasic shocks to terminate vf episode.38
All patients with vf who present without a pulse should be
oxygenated and CPr should be promptly initiated after checking
the airways. Simultaneously direct current defibrillation should
be attempted. At the outset, one shock (ideally biphasic) should
be given; recommended energy dose for biphasic shock is 120-
200 J and for monophasic shock is 360 J. Immediately after
delivering one shock, CPr should be resumed and continued
for 5 cycles or 2 minutes. If the patient remains without a
pulse and sinus rhythm is not restored, a second shock may
should be rapidly pushed Iv/Io, which can be repeated after
3-5 minutes. Alternatively, Iv/Io vasopressin (40 IU) can be
given. Subsequent to administering vasopressors, CPr should
again be continued for 5 cycles or 2 minutes and patient then
reevaluated. If no response, another shock may be given. It is
important to rule out asystolic arrest in patients who show no
response. Administration of an antiarrhythmic drug should
also be considered in non-responding patients. These patients
can be given amiodarone (5 mg/kg or 300 mg) by rapid Iv/
Io push, followed by 150 mg Iv/Io in patients who still do
not revert to sinus rhythm. In patients with vf in the settings
of acute MI, Iv lidocaine 1-1.5 mg/kg can be given; dose of
0.75 mg up to 3 mg/kg can be repeated in them. Patients who
remain refractory to amiodarone/lidocaine may also be given
Iv magnesium (1-2 g). In these patients CPr for 5 cycles or
2 minutes followed by revaluation and deliverance of shocks/
vasopressors should be continued till normalcy in the sinus
rhythm is restored (figure 4).33

eValuate yourself
Q1. In a patient with stable sustained monomorphic vt secondary to a non-ischemic cardiomyopathy with a normal lvEf,
which of the following treatment options should be opted first?
F Cardioversion
F Wait and watch
F Procainamide
F lidocaine

Q2. In patients with vf who have a sudden cardiac arrest, the recommended energy dose for providing biphasic shock is
F 80-120 J
F 120-200 J
F 200-300 J
F 300-420 J

Q3. In patients with torsades de pointes, the following treatment option can be successful in normalizing rhythm
F lidocaine
F Procainamide
F Magnesium sulphate
F Atropine

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insight into different treatment Table 1 Antiarrhythmic drug classes

oPtions for Vt
Class Drugs
antiarrhythmic drugs 1A Procainamide
Quinidine
In the past, antiarrhythmic drugs were among the most Disopyramide
popular treatment options for terminating vt episode 1B Lidocaine
and preventing its recurrence. They were, and remain, the
1C Flecainide
mainstay of treatment for stable vt. However for unstable Propafenone
vt, immediate cardioversion/defibrillation should be opted
II Beta-blockers
first, followed by antiarrhythmic drugs in non-responding
patients.31 A wide range of antiarrhythmic drugs are now III Amiodarone
Sotalol
available and they have been variously classified; one such Ibutilide
system of classification of these drugs is shown in table 1. Dofetilide
over the last few years some shortcomings of antiarrhythmic IV Verapamil
drugs have emerged which now deters many physicians from Diltiazem
choosing these agents as a front-line treatment option for vt.
IV-like Adenosine
Antiarrhythmic drugs have a relatively narrow therapeutic
index which calls for strict adherence to their recommended
based on information from:
doses and continuous monitoring when administering these DiMarco JP, gersh BJ, opie lH. Antiarrhythmic Drugs and Strategies. Chapter 8. In:
agents. Another cause of concern with their use has been the opie lH, gersh BJ. Drugs for the Heart. 6th Edition. Elsevier Saunders;2005.218-
potential of many of these drugs to induce fatal arrhythmias, 274.
such as torsades de pointes due to class IA and III agents and
wide-QrS vt due to class IC agents.39,40 Moreover, advent
of improvised non-pharmacological treatment options, such hypotension however necessitates restricting its use to patients
as ICD, have further stacked the odds against these agents by with a normal Ef. lidocaine is a class IB antiarrhythmic
providing the clinicians with more effective and safer options to drug. It was notable for its effectiveness in terminating
manage vt. Studies performed in the past have shown greater monomorphic and polymorphic vts associated with acute MI.
effectiveness of ICDs compared to antiarrhythmic drugs in
However, more recently investigators have started restricting
reducing mortality rates in patients with vt. follow-up of
its use in these settings in light of evidence that it may favor
patients with vt and low Ef (<40%) in the Antiarrhythmics
degeneration of monomorphic vt into vf. Ajmaline, another
versus Implantable Defibrillators (AvID) study41 revealed
class I antiarrhythmic drug, is preferred in these patients.2
longer survival time of patients treated with a cardioverter-
Propafenone and flecainide are class IC antiarrhythmic drugs
defibrillator (89% at 1 year, 82% at 2 years, 75% at 3 years)
which have been found beneficial in managing vt. Their
compared to those treated with class III antiarrhythmic drugs
(82% at 1 year, 75% at 2 years, 64% at 3 years). This, and many efficacy is however reduced in patients with organic heart
other similar studies, provides robust evidence favoring the disease.43 Among class III antiarrhythmic drugs, amiodarone,
use of ICD over antiarrhythmic drugs in patients with vt and is one of the most commonly used pharmacological agent
hemodynamic compromise. revised treatment strategies for for managing vt. Its effectiveness has been documented in
vt now recommend antiarrhythmic drugs in stable patients most sustained vt; it may be preferred to procainamide in
with vt and as an adjunctive treatment option with ICD in vt associated with low Ef. Additionally, amiodarone can be
unstable patients. When used along with ICD, antiarrhythmic considered in vf patients when defibrillation fails. Sotalol,
drugs are expected to reduce the number of vt/vf episodes another class III antiarrhythmic drug, also effectively manages
and also reduce the requirement of ICD shocks, some of which vt. Its benefits in emergencies may be questionable owing to
can inadvertently increase mortality risk in the patients.42 the need to infuse it slowly.2
Procainamide, a class IA antiarrhythmic drug, has been Beta-blockers are another class of drugs which have been
widely used in patients with vt. It is one of the recommended extensively used worldwide for managing vt. They also
drugs for management of sustained monomorphic vt and reduce risk of recurrent vt and improve long-term outcome.
recurrent monomorphic vt. Its potential to cause precipitous Administration of high dose of beta-blockers to patients

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with ischemic cardiomyopathy in the Multicenter Automatic
Defibrillator Implantation trial-II (MADIt-II)44 resulted in
a significant reduction in the risk for vt/vf requiring ICD
therapy. It is noteworthy that among different antiarrhythmic
drugs, these agents have the best supporting evidence for
improving survival rates in patients with symptomatic vt
and vf.45 Along with nondihydropyridine calcium channel
blockers, beta-blockers have also been found effective for
managing idiopathic vt.5
implantable cardioverter-defibrillator (icd)
and transthoracic defibrillation
till a few years back, antiarrhythmic drugs were the only
viable treatment options available to the cardiologists for
managing fulminant vt. They are still used, though not as
commonly as in the past. Class I antiarrhythmic drugs have
been shown to be associated with many adverse effects. Class
III antiarrhythmic drugs (amiodarone and sotalol included)
demonstrate greater effectiveness than class I antiarrhythmic
drugs, although recurrent vt and risk of SCD remains a major
concern even with their use. Cardioversion and defibrillation
are two additional techniques which are being routinely used
in cardiology practice to terminate, though not prevent, life-
threatening arrhythmias. While in cardioversion energy is
usually synchronized with the QrS complex, defibrillation
involves nonsynchronized delivery of energy during any phase
of the cardiac cycle. The introduction of ICD has revolutionized
treatment approach for fatal vt. These portable devices are
implanted similar to cardiac pacemakers. They monitor rate
and rhythm of the heart and can deliver electrical shocks when
arrhythmia is detected. Many studies have confirmed their
superior efficacy to antiarrhythmic drugs in terminating fatal
vt/vf events.46
In the AvID trial,41 patients with near fatal vt/vf treated
with a cardioverter-defibrillator had longer survival compared
to those managed with amiodarone. These results were in
line with those of the Canadian Implantable Defibrillator
Study (CIDS)47 which included patients with resuscitated
vt/vf and those with unmonitored syncope. Patients who
received ICD showed a 20% relative risk reduction in all-cause
mortality and a 33% reduction in arrhythmia-related mortality
compared to those who received amiodarone. results of the
Cardiac Arrest Study Hamburg (CASH) trial,48 published
around the same time as CIDS, showed that survivors of vt-
induced cardiac arrest managed with ICD had a 23% reduction
in all-cause mortality rates compared to those treated with
amiodarone/metoprolol. These studies have encouraged
investigators to choose ICD preferentially as a front-line
treatment option for fatal/near fatal vt where imminent risk
16
of SCD is high. today, ICD is being indicated for primary
prevention of SCD in selected patients with CAD and non-
ischemic cardiomyopathy. It is also being recommended for
secondary prevention of SCD among cardiac arrest survivors
who suffered vt/vf.49
Another method of delivering defibrillating shocks in
cardiology practice is transthoracic electrical defibrillation.
In this technique, electrical pulse is applied to the surface of
the thorax through a pair of electrodes. While most external
defibrillators in the past were built to deliver monophasic
damped sine waveform shocks, it became increasingly
evident over time that a comparable or even higher rate of
cardioversion can be achieved with biphasic shocks. Most
implantable defibrillators (ICD) are designed to deliver
biphasic waveforms.50 These waveforms are now increasingly
being used in external defibrillators as well. Studies have shown
that biphasic waveforms require lower energies for inducing
comparable defibrillation to monophasic waveforms. They are
therefore likely to incur lesser post-shock myocardial injury.51
radiofrequency ablation
Despite extensive benefits, ICD is nevertheless associated
with certain limitations. It does not prevent vt recurrence
and repetitive shocks can adversely affect quality of life of
individuals.52 radiofrequency ablation (rfA) has gradually
emerged as an effective non-pharmacological treatment
option for vt in the absence of a structural heart disease.
The procedure can be performed in an outpatient setting and
involves establishing a vascular access, inducing arrhythmia and
performing mapping to identify the source of arrhythmia. This
is followed by ablation of the arrhythmic source. Satisfactory
cardiac perfusion is a prerequisite for rfA. Mapping for
locating an arrhythmogenic source can be performed only in
hemodynamically stable patients. Unmappable vt present a
challenge as rfA is difficult in these patients.53 The procedure
is specialized and hence is being performed in selected centers,
with expertise in performing this procedure. Currently rfA is
being recommended in patients with recurrent vt episodes,
symptomatic idiopathic vt, incessant vt and bundle branch
reentry vt.53,54
conclusion
ventricular tachyarrhythmias are one of the most lethal
among all arrhythmias and can impose a significant risk of
SCD. While occasional ventricular ectopics detected at rest
in healthy individuals may not be viewed with much concern,
PvC and nSvt during exercises and those in patients with
an underlying heart disease may portend risk of subsequent

major arrhythmias. Sustained vt and vf are required to be
managed more aggressively. rather unfortunately, the use of
antiarrhythmic drugs has been riddled with controversies
over the last few years and their front-line use is restricted to
symptomatic nSvt, stable vt and as an adjunct to ICD. over
the years ICD and rfA have emerged as promising treatment
options for fatal vt and offer hope of improving survival rates
in patients with vt/vf who are at a high risk of SCD.
references
1. goel r, Srivathsan K, Mookadam M. Supraventricular and ventricular
arrhythmias. Prim Care. 2013 Mar;40(1):43-71.
2. trappe HJ. treating critical supraventricular and ventricular arrhythmias. J
Emerg Trauma Shock. 2010 Apr;3(2):143-52.
3. Benito B, Josephson ME. ventricular tachycardia in coronary artery disease.
Rev Esp Cardiol (Engl Ed). 2012 oct;65(10):939-55.
4. roberts-Thomson KC, lau DH, Sanders P. The diagnosis and management of
ventricular arrhythmias. Nat Rev Cardiol. 2011 Jun;8(6):311-21.
5. Koplan BA, Stevenson Wg. ventricular tachycardia and sudden cardiac death.
Mayo Clin Proc. 2009 Mar;84(3):289-97.
6. Baher AA, Uy M, Xie f, garfinkel A, Qu Z, Weiss Jn. Bidirectional ventricular
tachycardia: ping pong in the His-Purkinje system. Heart Rhythm. 2011
Apr;8(4):599-605.
7. Sheldon SH, gard JJ, Asirvatham SJ. Premature ventricular Contractions
and non-sustained ventricular tachycardia: Association with Sudden
Cardiac Death, risk Stratification, and Management Strategies. Indian Pacing
Electrophysiol J. 2010 Aug 15;10(8):357-71.
8. Katritsis Dg, Camm AJ. review nonsustained ventricular tachycardia: where
do we stand? Eur Heart J. 2004 Jul; 25(13):1093-9.
9. Engström g, Hedblad B, Janzon l, Juul-Möller S. ventricular arrhythmias
during 24-h ambulatory ECg recording: incidence, risk factors and prognosis
in men with and without a history of cardiovascular disease. J Intern Med. 1999
oct;246(4):363-72.
10. Chiang Bn, Perlman lv, ostrander lD Jr, Epstein fH. relationship of
premature systoles to coronary heart disease and sudden death in the
tecumseh epidemiologic study. Ann Intern Med. 1969 Jun;70(6):1159-66.
11. Morshedi-Meibodi A, Evans JC, levy D, larson Mg, vasan rS. Clinical
correlates and prognostic significance of exercise-induced ventricular
premature beats in the community: the framingham Heart Study. Circulation.
2004 May 25;109(20):2417-22.
12. Dadkhah S, Dowlatshahi S, Sharain K, Sharain r. Exercise Induced non-
Sustained ventricular tachycardia and Indication for Invasive Management.
Clin Med Insights Cardiol. 2011; 5: 121–126.
13. Monserrat l, Elliott PM, gimeno Jr, Sharma S, Penas-lado M, McKenna WJ.
non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an
independent marker of sudden death risk in young patients. J Am Coll Cardiol.
2003 Sep 3;42(5):873-9.
14. grimm W, Christ M, Maisch B. long runs of non-sustained ventricular
tachycardia on 24-hour ambulatory electrocardiogram predict major
arrhythmic events in patients with idiopathic dilated cardiomyopathy. Pacing
Clin Electrophysiol. 2005 Jan;28 Suppl 1:S207-10.
15. Katritsis Dg, Zareba W, Camm AJ. nonsustained ventricular tachycardia. J
Am Coll Cardiol. 2012 nov 13;60(20):1993-2004.
16. gorenek B, Cengiz o, Kudaiberdieva g, Durak I, Dogan v, yasar B, Birdane A,
Cavusoglu y, Ata n. Mode of onset of polymorphic ventricular tachycardia in
acute myocardial infarction. Can J Cardiol. 2010 Aug-Sep;26(7):e254-7.
17
DIPLOMA PROGRAM
POST GRADUATE IN PROGRAM IN
EXCELLENCE
CARDIAC
CARDIACEMERGENCIES
EMERGENCIES
IN IN
GENERAL PRACTICE
GENERAL PRACTICE
17. Passman r, Kadish A. Polymorphic ventricular tachycardia, long Q-t
syndrome, and torsades de pointes. Med Clin North Am. 2001 Mar;85(2):321-
41.
18. Piccini JP, White JA, Mehta rH, lokhnygina y, Al-Khatib SM, tricoci P,
Pollack Cv Jr, Montalescot g, van de Werf f, gibson CM, giugliano rP,
Califf rM, Harrington RA, newby lK. Sustained ventricular tachycardia and
ventricular fibrillation complicating non-St-segment-elevation acute coronary
syndromes. Circulation. 2012 Jul 3;126(1):41-9.
19. Al-Khatib SM. Sustained ventricular arrhythmias among patients with acute
coronary syndromes with no St-segment elevation: incidence, predictors, and
outcomes. Circulation. 2002; 106: 309– 312.
20. yeung-lai-Wah JA, Qi A, Mcneill E, Abel Jg, tung S, Humphries KH, Kerr
Cr. new-onset sustained ventricular tachycardia and fibrillation early after
cardiac operations. Ann Thorac Surg. 2004 Jun;77(6):2083-8.
21. napolitano C, Priori Sg, Bloise r. Catecholaminergic Polymorphic ventricular
tachycardia. 2004 oct 14 [Updated 2013 feb 7]. In: Pagon RA, Adam MP,
Bird tD, et al., editors. genereviews™ [Internet]. Seattle (WA): University of
Washington, Seattle; 1993-2013. Available from: http://www.ncbi.nlm.nih.
gov/books/nBK1289/.
22. lee Sy, Kim JB, Im E, yang WI, Joung B, lee MH, Kim SS. A case of
catecholaminergic polymorphic ventricular tachycardia. Yonsei Med J. 2009
Jun 30;50(3):448-51.
23. nyegaard M, overgaard Mt, Søndergaard Mt, vranas M, Behr Er, Hildebrandt
ll, lund J, Hedley Pl, Camm AJ, Wettrell g, fosdal I, Christiansen M,
Børglum AD. Mutations in calmodulin cause ventricular tachycardia and
sudden cardiac death. Am J Hum Genet. 2012 oct 5;91(4):703-12.
24. Kaufman ES. Mechanisms and clinical management of inherited
channelopathies: long Qt syndrome, Brugada syndrome, catecholaminergic
polymorphic ventricular tachycardia, and short Qt syndrome. Heart Rhythm.
2009 Aug;6(8 Suppl):S51-5.
25. Brugada J, Brugada P, Brugada r. Brugada Syndrome: The Syndrome of right
Bundle Branch Block, St segment Elevation in v1 to v3 and Sudden Death.
Indian Pacing Electrophysiol J. 2001 oct-Dec; 1(1): 6–11.
26. Morady f, Shen En, Bhandari A, Schwartz AB, Scheinman MM. Clinical
symptoms in patients with sustained ventricular tachycardia. West J Med. 1985
Mar;142(3):341-4.
27. Badhwar n, Scheinman MM. Idiopathic ventricular tachycardia: Diagnosis
and management. Curr Probl Cardiol. 2007 Jan;32(1):7-43.
28. Chiarandà g, Di guardo g, gulizia M, lazzaro A, regolo t. fascicular
ventricular tachycardia. Ital Heart J Suppl. 2001 nov;2(11):1181-6.
29. lam P, Saba S. Approach to the Evaluation and Management of Wide Complex
tachycardias. Indian Pacing Electrophysiol J. 2002 oct-Dec; 2(4): 120–126.
30. de Meester A, Chaudron JM, de roy l. Usefulness of isoproterenol
in the induction of clinical sustained ventricular tachycardia during
electrophysiological study. Acta Cardiol. 1997;52(1):67-74.
31. Collopy Kt. Stable or unstable? Assessment and management of ventricular
tachycardia with pulses. EMS Mag. 2009 Jun;38(6):42-8; quiz 49.
32. Kolettis tM, Krikos vD, Apostolidis D, naka KK, Katsouras CS, Sourla E,
Michalis lK. outcome of patients with haemodynamically stable ventricular
tachycardia treated with an implantable cardioverter-defibrillator. Hellenic J
Cardiol. 2008 Jul-Aug;49(4):248-59.
33. Zipes DP, Camm AJ, Borggrefe M, et al.; American College of Cardiology/
American Heart Association task force; European Society of Cardiology
Committee for Practice guidelines; European Heart rhythm Association and
the Heart rhythm Society. ACC/AHA/ESC 2006 guidelines for management
of patients with ventricular arrhythmias and the prevention of sudden cardiac
death--executive summary: A report of the American College of Cardiology/
American Heart Association task force and the European Society of
Cardiology Committee for Practice guidelines (Writing Committee to
Develop guidelines for Management of Patients with ventricular Arrhythmias
 DIPLOMA
POST PROGRAM
GRADUATE INPROGRAM IN
EXCELLENCE
CARDIAC EMERGENCIES
IN GENERAL PRACTICE
and the Prevention of Sudden Cardiac Death) Developed in collaboration
with the European Heart rhythm Association and the Heart rhythm Society.
Circulation. 2006;114:e385-e484.
34. Jalife J. ventricular fibrillation: mechanisms of initiation and maintenance.
Annu Rev Physiol. 2000;62:25-50.
35. Cobbe SM, rankin AC. Cardiac Arrhythmias. In: Warrell DA, Cox tM, firth
JD, Benz EJ ( Jr). oxford textbook of Medicine. volume 2. 4th ed. oxford
University Press, oxford. 2005.
36. Kostić t, Perišić Z, Martinović SS, Apostolović S, Živković M, Božinović n,
Krstić n, Pavlović M. ventricular fibrillation in Acute Myocardial Infarction –
Case report. Acta Medica Medianae 2009;48(3):43-46.
37. Bougouin W, Marijon E, Puymirat E, Defaye P, Celermajer DS, le Heuzey Jy,
Boveda S, Kacet S, Mabo P, Barnay C, Da Costa A, Deharo JC, Daubert JC,
ferrières J, Simon t, Danchin n; on behalf of fASt-MI registry Investigators.
Incidence of sudden cardiac death after ventricular fibrillation complicating
acute myocardial infarction: a 5-year cause-of-death analysis of the fASt-MI
2005 registry. Eur Heart J. 2013 nov 19.
38. tang W, Weil MH, Sun S, yamaguchi H, Povoas HP, Pernat AM, Bisera
J. The effects of biphasic and conventional monophasic defibrillation on
postresuscitation myocardial function. J Am Coll Cardiol. 1999 Sep;34(3):815-
22.
39. Kobayashi y. Clinical characteristics and management of proarrhythmias
during antiarrhythmic therapy. Nihon Rinsho. 2013 Jan;71(1):79-85.
40. Kowey Pr. Pharmacological effects of antiarrhythmic drugs. review and
update. Arch Intern Med. 1998 feb 23;158(4):325-32.
41. The AvID Investigators. A comparison of antiarrhythmic-drug therapy with
implantable defibrillators in patients resuscitated from near-fatal ventricular
arrhythmias. N Engl J Med. 1997 nov 27;337(22):1576-83.
42. tanner H, Hindricks g, Kottkamp H. frequent ventricular tachycardias:
antiarrhythmic drug treatment or catheter ablation? Herz. 2005
nov;30(7):613-8.
43. Paperini l, Davini A, lattanzi f, topi A, reisenhofer B, Squarcini g, Paci A,
topi Pl. Propafenone and flecainide in the therapy of ventricular arrhythmias.
Minerva Cardioangiol. 1995 oct;43(10):449-57.
44. Brodine Wn, tung rt, lee JK, Hockstad ES, Moss AJ, Zareba W, Hall WJ,
18
Andrews M, Mcnitt S, Daubert JP; MADIt-II research group. Effects of
beta-blockers on implantable cardioverter defibrillator therapy and survival in
the patients with ischemic cardiomyopathy (from the Multicenter Automatic
Defibrillator Implantation trial-II). Am J Cardiol. 2005 Sep 1;96(5):691-5.
45. Exner Dv, reiffel JA, Epstein AE, ledingham r, reiter MJ, yao Q, Duff HJ,
follmann D, Schron E, greene Hl, Carlson MD, Brodsky MA, Akiyama
t, Baessler C, Anderson Jl. Beta-blocker use and survival in patients
with ventricular fibrillation or symptomatic ventricular tachycardia: the
Antiarrhythmics versus Implantable Defibrillators (AvID) trial. J Am Coll
Cardiol. 1999 Aug;34(2):325-33.
46. Connelly Dt. Implantable cardioverter-defibrillators. Heart. 2001
Aug;86(2):221-6.
47. Connolly SJ, gent M, roberts rS, Dorian P, roy D, Sheldon rS, Mitchell
lB, green MS, Klein gJ, o’Brien B. Canadian implantable defibrillator study
(CIDS) : a randomized trial of the implantable cardioverter defibrillator
against amiodarone. Circulation. 2000 Mar 21;101(11):1297-302.
48. Kuck KH, Cappato r, Siebels J, rüppel r. randomized comparison of
antiarrhythmic drug therapy with implantable defibrillators in patients
resuscitated from cardiac arrest : the Cardiac Arrest Study Hamburg (CASH).
Circulation. 2000 Aug 15;102(7):748-54.
49. Kedia r, Saeed M. Implantable cardioverter-defibrillators: indications and
unresolved issues. Tex Heart Inst J. 2012;39(3):335-41.
50. Kroll MW, Brewer JE. Automated external defibrillators: design considerations.
New Horiz. 1997 May;5(2):128-36.
51. faddy SC, Powell J, Craig JC. Biphasic and monophasic shocks for transthoracic
defibrillation: a meta analysis of randomised controlled trials. Resuscitation.
2003 Jul;58(1):9-16.
52. Ponti rD. role of catheter ablation of ventricular tachycardia associated with
structural heart disease. World J Cardiol. 2011 november 26; 3(11): 339–
350.
53. Stevenson Wg, Delacretaz E. radiofrequency catheter ablation of ventricular
tachycardia. Heart 2000; 84: 553–9.
54. Stevenson Wg, friedman Pl, ganz lI. radiofrequency catheter ablation
of ventricular tachycardia late after myocardial infarction. J Cardiovasc
Electrophysiol. 1997 nov;8(11):1309-19.
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Section 2
Sudden cardiac death

Course Director
Dr Michael D. Klein, MD
Medical Director of the Heart Station at
Boston Medical Center,
Clinical Professor of Medicine
Boston University School of Medicine,
Boston, MA

objectiVes
• to understand sudden cardiac death and know the factors and cardiac disorders which
increase its risk
• to get familiar with the mechanism of sudden cardiac death and know the markers which can
be used for its risk stratification
• to understand the diagnostic and management approach in survivors of sudden cardiac
arrest

19
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introduction
The concept of sudden cardiac death (SCD) is not new to
mankind. Awareness of its occurrence dates back to time
immemorial. Evidence to this effect can be found in the texts
of the ancient Egyptian medical papyrus (Ebers papyrus)
in which it was stated: ‘‘If a patient has pain in the arm and
left side of the chest, there is a threat of death.’’ today, SCD
has become one of the greatest challenges to physicians and
cardiologists owing to its common occurrence (more than
300,000 cases per year occurred in the US alone), unexpected
nature, and huge economic and social impact.1
By definition, SCD is an unexpected natural death occurring
from a cardiac cause, usually within 1 hour of symptom onset.
It can occur in patients with and without an underlying heart
disease.1-3 Coronary artery diseases (CAD) are overwhelmingly
the commonest cause, although SCD is also known to occur
in patients with non-ischemic cardiomyopathies and in
those with some rare inherited cardiac disorders.1 According
to available statistics, 80% of SCD occur in patients with
CAD. other important etiological causes of SCD include
dilated cardiomyopathy and hypertrophic cardiomyopathy,
followed by rare cardiac disorders, including congenital heart
defects and genetically-determined ion channel anomalies.2
In patients with CAD, sudden deaths can be the first, and
oftentimes, only clinical presentation.3 In most cardiac
disorders the commonest electrophysiological mechanism
which immediately precedes SCD is ventricular arrhythmia.
However, severe bradyarrhythmias may also precipitate SCD
in a small number of patients.1 Despite significant advancement
in our understanding of its pathophysiologic mechanisms and
designing novel strategies for preventing its occurrence, SCD
remains an enigma in contemporary cardiology.
factors Promoting risk of scd
There are multiple risk factors which predispose to SCD
(table 1). Since majority of SCD occur in patients with CAD,
traditional risk factors for CAD may expectably increase
risk of SCD as well. Indeed, for more than two decades,
risk factors for CAD, such as systolic blood pressure, serum
cholesterol, cigarette smoking and relative weight, have been
known to variably influence risk of SCD in asymptomatic
individuals. However, in patients with manifest CAD, extent
of atherosclerosis and ischemic damage to the myocardium,
rather than these traditional risk factors, appear to play a
more dominant role in modulating SCD risk.4 Additionally,
it has now become evident that complications of acute MI,
such as reduced ejection fraction (Ef) and heart failure, may
also contribute to SCD risk. Unfortunately, despite growing
20
Table 1 Factors which increase risk of SCD
Age, race, gender
Physical activity (exercises)
CAD risk factors (hypertension, glucose intolerance, high
cholesterol, smoking)
Hereditary factors
Chronic kidney disease
Others
based on information from:
1. Zipes DP, Wellens HJ. Sudden cardiac death. Circulation. 1998 nov
24;98(21):2334-51.
2. Kannel WB, gagnon Dr, Cupples lA. Epidemiology of sudden coronary
death: population at risk. Can J Cardiol. 1990 Dec; 6(10):439-44.
3. Poulikakos D, Banerjee D, Malik M. risk of Sudden Cardiac Death in Chronic
Kidney Disease. J Cardiovasc Electrophysiol. 2013 nov 20.
4. Arking DE, Sotoodehnia n. The genetics of sudden cardiac death. Annu Rev
Genomics Hum Genet. 2012;13:223-39.
awareness of CAD and institution of screening strategies for its
early detection, the prevalence of SCD in patients with CAD
appears to have reduced little over the last few years. This may be
attributable to suboptimal management of risk factors such as
hypertension, diabetes and dyslipidemia in the community and
frequently silent occurrence of CAD. In a recently performed
retrospective evaluation5 of clinic records and autopsy findings
of patients who had suffered SCD, suboptimally treated
hypertension and hyperlipidemia were found to be present in
27% and 25% of cases, respectively. Postmortem reports also
showed high-grade coronary stenoses in 80% of cases and
evidence of a previous silent MI in 34% cases. These findings
highlight the need for time-to-time screening of risk factors
for CAD in the community. Efforts should also be made to
intensify screening strategies for silent coronary heart disease
(CHD), which often presages unexpected occurrence of a
malignant vt/vf, and precipitation of SCD.
In addition to CAD risk factors, age, gender and ethnicity
also influences risk of SCD. Although SCD is known to occur
in all ages, its risk progressively increases with advancing age.
During the lifespan, two peaks in the incidence of SCD have
been recorded, one in infants and the other in the elderly (>
60 years of age). However, the predominant underlying cause
of SCD varies with age. The commonest cause of SCD in
individuals > 40 years of age is usually a CHD, while in younger
individuals (< 40 years), non-ischemic cardiac disorders such
as hypertrophic cardiomyopathy, and rare cardiac disorders
such as congenital heart diseases, valvular heart diseases and
arrhythmogenic right ventricular dysplasia are more likely the
precipitating causes. There is also evidence of gender difference

in risk of CAD. Men are 3-4 times more predisposed to SCD
compared to women.6 Despite this, the risk of SCD in women,
howsoever small, cannot be discounted, particularly during
the peripartum and postmenopausal periods. As women grow
older, their risk of SCD increases. In fact, the incidence of SCD
in elderly postmenopausal women (> 80 years of age) has
been found to be comparable to men due to their increased
susceptibility to atherosclerotic disease.7 Ethnic disparities
also influence SCD risk, with blacks appearing to be more
susceptible to sudden deaths compared to whites.8 other
than age, gender and ethnicity, exercises may also variably
modulate SCD risk. While moderate exercises are deemed to
be cardioprotective and may reduce risk of SCD, strenuous
exercises, particularly in untrained individuals, often increase
the risk.3 More recently, investigators have suggested a possible
role of renal impairment in increasing risk of arrhythmias
and SCD. fatal arrhythmias and SCD are known to occur in
patients with chronic kidney disease (CKD). Intriguingly,
the magnitude of risk has been found to be independent to
the stage of CKD, with studies reporting sudden deaths even
in early stages of CKD. However, the risk of SCD increases
thereafter as renal function deteriorates. Though the underlying
mechanisms of SCD in patients with CKD remains obscure,
it is plausible that electrolyte abnormality and autonomic
imbalance may be important pathological factors promoting
this risk.9 Many other factors which may increase SCD risk
Figure 1 Basic mechanism underlying occurrence of SCD
Left ventricular dysfunction
Transient risk factors
• Dyselectrolytemia
• Metabolic disturbances
• Drugs
• Increased sympathetic activity
based on information from:
Bayés de luna A, Elosua r. Sudden death. Rev Esp Cardiol (Engl Ed). 2012 nov;65(11):1039-52.
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have been identified, some still undergoing assessment in
clinical trials for their accuracy in predicting risk of sudden
death.
Many studies performed recently have attempted to
uncover a genetic link to SCD. reports citing occurrence
of SCD in inherited cardiac disorders, including Brugada
syndrome, long Qt syndrome and CPvt, validate the
veracity of this association. furthermore, many familial studies
have suggested an increase in risk for SCD if one first-degree
relative has suffered SCD.10 Uncovering molecular aberrations
which increase genetic susceptibility to SCD may be crucial
for improving risk stratification and identifying candidates for
primary prevention with implantable cardioverter-defibrillator
(ICD) treatment.
mechanism of scd
Despite extensive research, the precise mechanism underlying
occurrence of SCD continues to elude the wisdom of most
investigators. It is however known that the immediate precipitant
of SCD in most patients is a ventricular tachyarrhythmia (vt)
which rapidly degenerates into vf, and subsequently culminates
in SCD. Based on conclusion drawn from various studies, it is
conceivable that a prerequisite for fatal vt/vf in most cases is
a vulnerable myocardium. factors which make a myocardium
vulnerable to fatal arrhythmias include ischemia/infarction,
Genetic predisposition
Myocardial ischemia or infarction
Myocardium
Increased susceptibility to
arrhythmia
Sudden cardiac death
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left ventricular (lv) dysfunction, and genetic predisposition
(figure 1).1 Therefore, SCD occurs in the settings of a wide range
of cardiac disorders which impart arrhythmogenic susceptibility
to the myocardium, including CAD, cardiomyopathies,
valvular heart diseases, congenital heart diseases and cardiac
diseases with primary electrophysiological abnormalities
(table 2).3 It is noteworthy that a susceptible myocardium
provides an ideal anatomical or functional substrate on which
various transient modulators/triggers (dyselectrolytemia,
increased sympathetic activity, metabolic disturbances, drugs)
act and precipitate a lethal vt/vf episode; figure 1.1
Ischemia is one of the most important pathological factors
which enhances myocardial susceptibility to arrhythmia. During
acute phase of MI, vf accounts for a considerable percentage
of deaths. Ischemia is known to affect electrophysiological
properties of the myocardium, including its refractory and
conduction properties. Invariably during acute ischemia
membrane depolarization occurs in the myocardium which
leads to slow conduction and increased refractoriness. This
promotes development of reentrant circuits, a predominant
cause of vt in acute MI. In addition, there is also evidence
of automatic and/or triggered firing in the myocardium
secondary to ischemia, which further facilitates occurrence
of fatal vt/vf episodes.11 other than ischemia, heart failure
due to ventricular dysfunction also promotes occurrence
of arrhythmia and SCD. More SCD events occur in patients
with systolic heart failure than in those with diastolic heart
failure. While vt/vf are the most common precipitants of
SCD in mild to moderate heart failure (nyHA class II and III
heart failure), bradyarrhythmia is the immediate preceding
electrophysiological abnormality in severe heart failure
(nyHA class Iv heart failure).1 The mechanism of arrhythmia
development in heart failure is variable and may depend on its
etiological cause.
finally, how hereditary factors render myocardium
susceptible to arrhythmia is intriguing and has been a subject
of debate for long. However, based on current evidence it
appears plausible that multipronged mechanisms may account
for development of arrhythmia in these cases. In disorders
involving molecular aberrations in genes encoding cardiac
proteins, such as hypertrophic cardiomyopathy, ventricular
arrhythmias are a result of multiple interlinked mechanisms,
including intraventricular dispersion and inhomogeneity
of ventricular conduction due to variable cardiomyocyte
size, providing ideal substrate for reentry circuits.12 In ionic
channelopathies, abnormalities in formation of action potential
and regional heterogeneities in ventricular excitation promotes
development of reentry circuits and leads to the development
of fatal vf.1
22
Table 2 Cardiac disease states which increase myocardial
susceptibility to arrhythmia
Coronary artery disease
Cardiomyopathies
Valvular heart diseases
Congenital heart diseases
Primary electrophysiological abnormalities
Other cardiovascular causes
based on information from:
Zipes DP, Wellens HJ. Sudden cardiac death. Circulation. 1998 nov 24;98(21):
2334-51.
risk stratification for scd
growing awareness of SCD and its unexpected nature of
onset makes it one of the most perplexing issue in cardiology
today. risk stratification for SCD is widely recommended
to detect fatal arrhythmias early and reduce risk of SCD.
rather unfortunately, despite identification of many risk
markers, none appears to have a significantly high potential
for accurately predicting SCD risk. As a result, most risk
stratification paradigms based on these markers appear to be
inept in accurately predicting SCD risk.13 nevertheless risk
stratification for SCD is currently a widely accepted strategy,
especially in patients with CAD, for timely recognition of
lethal vt/vf episodes and early implementation of preventive
strategies. Most investigators currently prefer risk stratification
for SCD using three sets of markers; markers of abnormal
myocardial substrate or structural heart disease; markers of
abnormalities in the cardiac autonomic response; markers of
abnormal repolarization or electrical instability of the heart.14
markers of abnormal myocardial substrate or
structural heart disease
traditionally left ventricular ejection fraction (lvEf) has
been considered one of the most useful prognostic indicators
of mortality, particularly in patients with acute MI. Several
clinical trials have shown that patients with lvEf < 35-40%
have high mortality risk due to major arrhythmias and they are
considered appropriate candidates for receiving ICD therapy.
Although prognostic significance of lvEf continues to remain
undeniable, it has recently become evident that when used
alone, it may not be a sufficiently robust predictor of SCD,
as believed earlier, especially in light of evidence showing
occurrence of SCD even in patients without reduced lvEf.14,15
Another risk stratification tool which has rapidly gained

popularity for predicting SCD risk is non-sustained ventricular
tachyarrhythmia (nSvt). Several studies have shown that
repetitive runs of these ventricular ectopics may increase risk
of major arrhythmias, and therefore increase the likelihood
of SCD, particularly in individuals with an underlying heart
disease.16
Based on these observations, combined Ef and nSvt
evaluation would appear a useful strategy to improve
predictability of SCD risk. However it has been shown by some
investigators that both Ef and nSvt, although acceptable
risk markers for increased mortality, may not be accurate
predictors for SCD risk. These investigators conducted a
study17 in which they evaluated patients with acute MI for
finding risk predictors of arrhythmias and death in them. They
demonstrated that positive predictive accuracy of low Ef and
nSvt for SCD (8% and 12%, respectively) was lower than
that for predicting non-SCD (15% and 15%, respectively).
Despite these inconsistencies, both these markers are being
widely used for predicting risk of SCD, although robustness of
their predictive potential in these settings remains equivocal.
markers of abnormal cardiac autonomic
response
The autonomic nervous system has an intricate relationship
with cardiac function. Abnormalities in autonomic response
portend risk of arrhythmia and subsequent occurrence of
SCD. Multiple autonomic remodeling mechanisms have been
identified which may contribute to an arrhythmogenic substrate
and therefore increase risk of fatal arrhythmias. During recent
years, non-invasive methods for evaluating cardiac autonomic
response and predicting SCD risk have been developed. two
tests which are being widely used are analysis of heart rate
variability (Hrv) and determination of baroreflex-sensitivity
(BrS).14
Anecdotal reports in the past suggested that many ischemic
and non-ischemic cardiac disorders induced alterations in
autonomic response. There were reports of reduced cardiac
parasympathetic activity in patients with acute MI, which
owing to its inability to counter excess sympathetic activity,
promoted risk of fatal arrhythmic episodes. These assumptions
aroused interest among investigators to assess Hrv in high-
risk individuals for predicting risk of SCD. over the years
assessment of Hrv through Holter monitoring has become
an established risk stratification procedure in many cardiac
disorders, particularly in acute MI. reduced Hrv in the post-
MI period has been linked to poor prognosis.14,18 Based on
its risk prediction potential, particularly in patients with MI
and heart failure, Hrv was extensively used in the past for
23
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prognostication, although recent studies have challenged its
prognostic significance and have shown that it may have only
a low potential for predicting SCD risk.19 Another marker of
autonomic response which has been extensively used is BrS.
Similar to reduced Hrv, decreased BrS also portends poor
prognosis and may be used to identify patients at high risk of
SCD.20 Some investigators have indicated that BrS may be a
better predictor of arrhythmic events while Hrv may be more
accurate for predicting risk of deaths. Expectably, combined
assessment of Hrv and BrS may enhance potential for
predicting post-arrhythmic mortality, particularly when used
along with Ef assessment.21
markers of abnormal repolarization and
electrical instability
Electrophysiological abnormalities, such as abnormal
ventricular repolarization, and electrical instability are also
considered important contributors to arrhythmogenesis. It is
conceivable that these repolarization abnormalities combine
with changes in autonomic activity in predisposed individuals
to facilitate vt/vf development.22 various indicators of
abnormal ventricular repolarization on ECg, such as St-wave
depression and Qt prolongation, have become established
markers of mortality. Another evidence of repolarization
abnormality which has been extensively evaluated for
assessing SCD risk predictability is t-wave alternans.
This ECg phenomenon is considered a direct measure of
ventricular repolarization instability and involves periodic
beat-to-beat variation in the amplitude or shape of the t wave
on surface ECg. It has become a sensitive risk stratifier for
lethal arrhythmias and SCD.23 Although its role in predicting
arrhythmias and SCD in selected high-risk individuals has
been attested, it may be worthwhile to design more clinical
trials which can establish its role for routine risk stratification
in healthy individuals.
significance of late potentials
More recently the prognostic significance of ventricular
late potentials has been widely appreciated. These small-
amplitude, short-duration waves occur immediately after the
QrS complex and are believed to be a marker of an ischemic
myocardial substrate, which provides an ideal trigger for vf.
Because late potentials are of very low amplitude, they are
frequently obscured by noises on a regular surface ECg. The
signal-averaged electrocardiography (SAECg) has emerged
as a highly amplified and signal-processed ECg tool that can
detect these late potentials, and predict risk of arrhythmia and
SCD.14
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eValuate yourself
Q1. The most common cause of sudden cardiac deaths has been found to be
F Cardiomyopathies
F Coronary artery disease
F valvular heart diseases
F Congenital heart diseases

Q2. Which of the following statements about SCD is true?

F Men are at a lower risk of SCD than women
F Infants (children less than 1 year of age) have the lowest risk of SCD
F risk of SCD in chronic kidney disease is usually evident only in advanced stages
F risk of SCD is high if one first-degree relative has suffered a SCD event

Q3. Which of the following patients is at a significantly high risk of SCD?

F A post-MI patient with lvEf of 45%
F A healthy looking individual with incidental detection of occasional ventricular ectopics on surface ECg
F A patient with reduced Hrv in the post-MI period
F All the above are at significantly high risk of SCD

diagnostic inVestigations in that of the left ventricles. Presence of valvular abnormalities

surViVors of sudden cardiac
arrest
Sudden cardiac deaths account for considerable mortality
around the world and therefore are rapidly becoming a
significant health problem worldwide. Survivors of SCD
often pose a diagnostic and treatment challenge to clinicians.
A diligent work-up of these patients is warranted to arrive at
the underlying etiological cause of cardiac arrest. The objective
of diagnostic work-up should be to identify the underlying
arrhythmogenic substrate and trigger factors that precipitated
sudden cardiac arrest. An in-depth history should be taken in
all patients. They should be further subjected to a meticulous
physical and systemic examination, including that of the
cardiovascular system.24 family history is essential to rule out a
hereditary cause. A detailed drug history should also be sought
as many fatal arrhythmias are precipitated by medications.
Investigations required in these patients include a 12-lead
resting surface ECg and a 24-hour Holter ECg recording.
Signal-averaged ECg (SAECg) can be performed to detect
late potentials at the end of QrS complexes. Echocardiography
is advisable to identify the cardiac size and function, including
can also be identified on an echocardiogram. The reference
imaging modality for cardiac anatomy and function, cardiac
MrI, is being widely recommended now-a-days in most
survivors of cardiac arrest after an MI episode for quantifying
myocardial scar and fibrosis.25 treadmill-exercise testing and
cardiac catheterization with coronary angiography may also
be indicated in some patients.24 Invasive electrophysiological
testing may be recommended in some patients at high risk of
SCD, including those with acute MI, lv dysfunction and those
with repetitive runs of nSvt.26
PreVention of scd and
management in surViVors
In patients who suffer sudden cardiac arrest, initiating prompt
resuscitation is the key to survival, especially because there
is evidence that success rate of resuscitation reduces by
8-10% every minute following cardiac arrest. Cardiac arrests
occurring after vf are most responsive to defibrillation.
When vf deteriorates into asystole, which is oftentimes the
case, defibrillation becomes ineffective. Automated external
defibrillators (AED) are often useful for providing early

24

defibrillation in patients who suffer an out-of-hospital cardiac
arrest and may enhance chances of survival in them. once
resuscitated, patients are stabilized and transferred to an
intensive care unit (ICU) where further management starts.27
implantable cardioverter-defibrillator (icd)
The implantable cardioverter-defibrillator (ICD) has gradually
emerged as a well-accepted therapy for primary and secondary
prevention of SCD, although its use is recommended in selected
patient population. It is currently being used for primary
prevention of SCD in patients who have suffered a prior MI
and have lvEf ≤ 30-35%; however, its implantation in these
patients should be deferred till 40 days postinfarction. It is also
being recommended in patients with non-ischemic dilated
cardiomyopathy with a lvEf ≤ 35% and in those with mild to
moderate heart failure (nyHA classes II or III). A consideration
for primary prevention strategy with ICD may be expanded to
include patients with other non-ischemic cardiomyopathies
with reduced Ef, provided they remain in nyHA functional
classes II or III heart failure despite receiving optimal medical
therapy.28,29 Additionally, ICD is also being recommended in
cardiac arrest survivors as a secondary prevention strategy,
particularly in light of evidence that fatal vt/vf often recurs
and therefore patients who have had a cardiac arrest in the past
are at a risk of another such event in the future. Currently ICD
is being recommended for secondary prevention of SCD in
survivors of a prior cardiac arrest or sustained vt, regardless
of the type of underlying structural heart disease.28 It may
also be recommended for secondary prevention in other less
common cardiac disorders, such as congenital heart disorders
and inherited cardiac disorders.29
cardiac resynchronization therapy
ventricular dyssynchrony is lack of synchronous activation
and contraction of ventricles making them out of sync with
each other. It frequently leads to reduction in cardiac efficiency
and promotes development of heart failure. Alongside it often
worsens valvular regurgitation. ventricular dyssynchrony
is frequently associated with left ventricular dysfunction.
Statistics show that about 33% of patients with systolic
heart failure in nyHA classes III and Iv have an underlying
dyssynchronous ventricular contraction. oftentimes QrS
duration of > 120 ms on a 12-lead ECg is regarded as a sensitive
marker of ventricular dyssynchrony. Cardiac resynchronization
therapy (Crt) is a newly introduced technique that attempts
biventricular pacing of the ventricles, resynchronizing their
contraction and improving overall cardiac efficiency. With
time, Crt has established itself as a therapy of choice in
25
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patients with advanced heart failure. It is indicated in heart
failure patients (nyHA class III or ambulatory class Iv)
with lvEf of < 35% and QrS duration > 120 ms (i.e. with
ventricular dyssynchrony), in whom symptoms persist despite
optimal medical therapy.30 The role of Crt, however, in
managing heart failure with a narrow QrS complex remains
questionable, with a recent study showing that when used in
patients with systolic heart failure and a QrS duration < 130
msec, Crt did not reduce rate of hospitalization and death.
In fact, its use in the study participants was associated with
increase in mortality.31 Hence, currently it appears prudent to
restrict use of Crt to heart failure patients with reduced Ef
(< 35%) and ventricular dyssynchrony, i.e. those with a wide
QrS complex (> 120msec) only.
Pharmacological therapy
Despite rapid advances in cardiovascular medicine over the last
few decades, not much success has been achieved in prevention
of SCD through drug therapy. numerous clinical trials have
evaluated survival benefits of different antiarrhythmic drugs
in patients with ischemic and non-ischemic cardiac disorders.
Unfortunately, other than beta-blockers, and to an extent, renin-
angiotensin system (RAS) blockers and statins, no other class
of drugs has been found to be effective in reducing incidence of
sudden deaths. While some class III antiarrhythmic agents have
demonstrated potential to reduce vt recurrence, most have
been found wanting in reducing mortality rates. furthermore,
class I antiarrhythmic agents may increase mortality in patients
with vt and prior MI.32
Beta-blockers probably have the best evidence for
risk reduction of SCD. These drugs have invariably
demonstrated greater reduction in mortality compared to
other pharmacological agents. When deciding to choose beta-
blockers, choice of agent is important. There is incontrovertible
evidence favoring preferential use of lipophilic beta-blockers
as these agents have been found to be more beneficial than
hydrophilic beta-blockers in these settings. These agents are
being recommended in various indications, including MI and
heart failure.33 A recently published study34 in heart failure
patients, including those with post-MI heart failure, showed
that beta-blockers reduced risk of SCD by 31% and all-cause
mortality by 33%, underpinning their survival benefits in these
patients.
Another class of drugs which has shown some benefits
in reducing risk of SCD is RAS blockers. reports in the
past linked vt, occurring in patients with reduced lvEf,
to RAS activation. Although the precise mechanism of
arrhythmogenesis due to RAS activation remains obscure,
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Figure 2 Diagnostic and management approach in high-risk patients for reducing risk of SCD

Patients with ischemic or non-ischemic cardiomyopathy having a low ejection fraction (EF ≤ 35%)

• First step is to see if ICD is indicated for secondary prevention of SCD; ideal candidates would be:
» Patients who had an unexplained syncope
» Cardiac arrest survivors from VT/VF
» Patients who had unstable sustained VT
» Patients who survive cardiac arrest due to rare arrhythmogenic cardiac disorders, such as long QT syndrome,
hypertrophic cardiomyopathy and Brugada syndrome
• Also see if ICD is contraindicated; these candidates include:
» Patients with NYHA class IV heart failure
» Patients suffering from diseases associated with < 1 year of survival
» Patients with cardiogenic shock or hypotension
• In patients who are not ideal candidates for secondary prevention with ICD and in whom ICD is NOT contraindicated,
go to the next box

In these patients evaluate for class of heart failure (NYHA I-IV) and also note for presence or
absence of previous MI episode or if PCI/CABG has been recently performed; now identify
candidates who require ICD for primary prevention

Patients who should receive ICD for primary prevention

• Patients who had MI episode ≥ 40 days back and are having EF ≤ 30% with NYHA class I heart failure
• Patients in whom PCI/CABG was performed > 3 months back and are having EF ≤ 30% with NYHA class I heart failure
• Patients who had MI episode within 40 days or in whom PCI/CABG was performed within previous 3 months, and
these patients continue to have low EF and are in NYHA class I heart failure → medical management followed by
reevaluation → EF remains ≤ 30% (or ≤ 35% with NYHA class II or III heart failure)
• Patients with ischemic and non-ischemic cardiomyopathy with low EF and who are having EF ≤ 35% despite receiving
optimal medical therapy for minimum 3 months
• Patients in advanced heart failure (NYHA class III and IV) with low EF and having QRS ≥ 120 msec, cardiac
resynchronization with defibrillation should be done (with or without ICD)

based on information from:

1. Herzog E, Aziz Ef, Kukin M, Steinberg JS, Mittal S. novel pathway for sudden cardiac death prevention. Crit Pathw Cardiol. 2009; 8:1–6.
2. Aziz Ef, Javed f, Pratap B, Herzog E. Strategies for the prevention and treatment of sudden cardiac death. Open Access Emerg Med. 2010 December ; 2010(2): 99–114.

26

cardiac hypertrophy, fibrosis, and heterogeneity of the cardiac
tissue are considered prime players in arrhythmia development.
over the years, many additional electrophysiological effects of
RAS activation have been unraveled which may also contribute
to an arrhythmogenic effect. notwithstanding the underlying
mechanism, reports of a link between RAS activation and
arrhythmia development propelled investigators to evaluate
effects of RAS inhibition in preventing vt/vf development.35
Studies have confirmed that ACE inhibitors may be promising
in reducing SCD events, especially when used in patients after
an MI episode.36 More recently, the Eplerenone Post-Acute
Myocardial Infarction Heart failure Efficacy and Survival Study
(EPHESUS)37 evaluated aldosterone receptor antagonist,
eplerenone, at a dose of 25 mg/day in post MI patients with
reduced lvEf (≤ 40%), when started 3 to 14 days after acute
MI; the results of EPHESUS showed that eplerenone reduced
risk of Cv mortality by 32% and SCD by 37%, making it
another promising agent with expected benefits in reducing
SCD risk.
finally, statins have also been found to be of some benefit
in reducing SCD risk and can be incorporated as a part of the
treatment armamentarium for SCD prevention in high-risk
cases. A recently performed meta-analysis showed that statin
treatment was associated with a 19% risk reduction for SCD.38
Importantly, statins incur comparable survival benefits in
patients with non-ischemic and ischemic cardiomyopathy.39
a simplified management approach for
preventing scd
The issue of SCD risk prevention and management is complex.
Multiple pathways have been designed to address the issue.
Herzog and colleagues40 developed a novel diagnostic and
management pathway called ESCAPE, an evidence-based
eValuate yourself
Q1. Which of the following patients are not candidates for ICD therapy?
F Post-MI patients with reduced Ef (< 35%) on 15th day of postischemic episode
F Patients with hypertrophic cardiomyopathy in nyHA class III heart failure with Ef < 30% despite 3 months
of medical therapy
F Post-MI patients with reduced Ef (< 30%) and nyHA class II heart failure despite PCI performed 4 months
back
F Cardiac arrest survivors due to sustained vt
27
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novel pathway for low Ejection fraction and Sudden Cardiac
death Awareness and Prevention Eligibility, which outlined
systematic diagnostic and management approach of high-risk
patients based on lvEf, heart failure functional class, and
evidence of a prior MI or CAD. Excerpts from recommendations
provided in this pathway are shown in figure 2.40,41
therapeutic hypothermia as a novel
treatment option for cardiac arrest survivors
Death in a large majority of patients who suffer cardiac arrest
is due to neurological damage, possibly as a result of ischemic-
reperfusion injury. one of the ways of ameliorating it is
therapeutic hypothermia. The mechanism by which therapeutic
hypothermia counteracts and improves deleterious effects of
ischemia-reperfusion injury after cardiac arrest are less well-
understood, although it now appears conceivable that they may
be partly related to inhibition of cellular catabolic processes
occurring during the reperfusion period, hence resulting in
reduced cellular oxygen and glucose consumption.42 Studies
have demonstrated improved outcomes with therapeutic
hypothermia in survivors of cardiac arrest who received
resuscitation, attesting their possible role in mitigating
derangements during the postresuscitation period. It is now
known that application of mild hypothermia may improve
short-term neurological outcome of resuscitated patients after
sudden cardiac arrest. What effect this novel interventional
strategy is likely to have on long-term neurological outcome
of these patients remains to be established.43,44 Despite these
limitations, therapeutic hypothermia is rapidly becoming a
popular treatment strategy in postcardiac arrest period and
should be further evaluated for its perceived benefits in this
indication.
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Q2. Which of the following drugs has documented benefits in reducing risk of SCD?
F Amiodarone
F Procainamide
F Metoprolol
F Mexiletine
Q3. The following is an indication for cardiac resynchronization therapy
F Systolic heart failure patients with Ef = 45% and QrS complex < 120 msec
F Systolic heart failure patients with reduced Ef (≤ 35%) in nyHA grade II heart failure with QrS complex <
120 msec
F Systolic heart failure patients with reduced Ef (≤ 35%) in grade Iv heart failure with QrS complex > 120
msec
F none of these
conclusion
Sudden cardiac death (SCD) is a catastrophic event with huge
social and economic impact. It is defined as an unexpected
natural death occurring from a cardiac cause, usually within
1 hour of symptom onset. Individuals in whom SCD occurs
usually have myocardial susceptibility to arrhythmia, with
certain transient factors acting as immediate triggers to the
fatal arrhythmic episode. Most SCD events occur in patients
with CHD and tachyarrhythmia is the immediate preceding
electrophysiological abnormality in these patients. When
performing a work-up of these patients, attempt should
be made to identify the underlying anatomical/functional
substrate which renders the myocardium susceptible to fatal
arrhythmia and find the immediate triggering factors for the
event. over time, ICD has become an established therapy
for primary and secondary prevention of SCD, although its
use is still restricted to a selected subset of patients. Some
patients with severe heart failure (nyHA class Iv), low Ef (≤
35%) and QrS > 120 msec can be offered Crt, along with
optimized medical therapy, with or without ICD. Among
the pharmacological agents, beta-blockers, RAS blockers and
statins appear promising for reducing risk of SCD. Therapeutic
hypothermia is an evolving treatment option and would
require further evaluation in clinical trials before it is routinely
recommended for SCD risk reduction.
references
1. Bayés de luna A, Elosua r. Sudden death. Rev Esp Cardiol (Engl Ed). 2012
nov;65(11):1039-52.
2. rubart M, Zipes DP. Mechanisms of sudden cardiac death. J Clin Invest. 2005
Sep;115(9):2305-15.
28
3. Zipes DP, Wellens HJ. Sudden cardiac death. Circulation. 1998 nov
24;98(21):2334-51.
4. Kannel WB, gagnon Dr, Cupples lA. Epidemiology of sudden coronary
death: population at risk. Can J Cardiol. 1990 Dec; 6(10):439-44.
5. Adabag AS, Peterson g, Apple fS, titus J, King r, luepker rv. Etiology of
sudden death in the community: results of anatomical, metabolic, and genetic
evaluation. Am Heart J. 2010 Jan;159(1):33-9.
6. nofal HK, Abdulmohsen Mf. Influence of age, gender, and prodromal
symptoms on sudden death in a tertiary care hospital, eastern Saudi Arabia. J
Family Community Med. 2010 May-Aug; 17(2): 83–86.
7. rizzo S, Corrado D, Thiene g, Basso C. Sudden cardiac death in women. G Ital
Cardiol (Rome). 2012 Jun;13(6):432-9.
8. okin PM, Kjeldsen SE, Julius S, Dahlöf B, Devereux rB. racial differences
in sudden cardiac death among hypertensive patients during antihypertensive
therapy: the lIfE study. Heart Rhythm. 2012 Apr;9(4):531-7.
9. Poulikakos D, Banerjee D, Malik M. risk of Sudden Cardiac Death in Chronic
Kidney Disease. J Cardiovasc Electrophysiol. 2013 nov 20.
10. Arking DE, Sotoodehnia n. The genetics of sudden cardiac death. Annu Rev
Genomics Hum Genet. 2012;13:223-39.
11. Spector PS. Diagnosis and management of sudden cardiac death. Heart. 2005
March; 91(3): 408–413.
12. o’Mahony C, Elliott P, McKenna W. Sudden cardiac death in hypertrophic
cardiomyopathy. Circ Arrhythm Electrophysiol. 2013 Apr;6(2):443-51.
13. lopshire JC, Zipes DP. Sudden cardiac death: better understanding of risks,
mechanisms, and treatment. Circulation. 2006 Sep 12;114(11):1134-6.
14. lopera g, Curtis AB. risk Stratification for Sudden Cardiac Death: Current
Approaches and Predictive value. Curr Cardiol Rev. 2009 January; 5(1): 56–
64.
15. goldberger JJ, Buxton AE, Cain M, Costantini o, Exner Dv, Knight BP,
lloyd-Jones D, Kadish AH, lee B, Moss A, Myerburg r, olgin J, Passman
r, rosenbaum D, Stevenson W, Zareba W, Zipes DP. risk stratification for
arrhythmic sudden cardiac death: identifying the roadblocks. Circulation.
2011 May 31;123(21):2423-30.
16. Sheldon SH, gard JJ, Asirvatham SJ. Premature ventricular Contractions
and non-sustained ventricular tachycardia: Association with Sudden
Cardiac Death, risk Stratification, and Management Strategies. Indian Pacing
Electrophysiol J. 2010; 10(8): 357–371.
17. Huikuri Hv, tapanainen JM, lindgren K, raatikainen P, Mäkikallio tH,

Juhani Airaksinen KE, Myerburg rJ. Prediction of sudden cardiac death after
myocardial infarction in the beta-blocking era. J Am Coll Cardiol. 2003 Aug 20;
42(4):652-8.
18. Singer DH, Martin gJ, Magid n, Weiss JS, Schaad JW, Kehoe r, Zheutlin t,
fintel DJ, Hsieh AM, lesch M. low heart rate variability and sudden cardiac
death. J Electrocardiol. 1988;21 Suppl:S46-55.
19. Kudaiberdieva g, görenek B, timuralp B. Heart rate variability as a predictor
of sudden cardiac death. Anadolu Kardiyol Derg. 2007 Jul;7 Suppl 1:68-70.
20. Svacinová J, Moudr J, Honzíková n. Baroreflex sensitivity: diagnostic
importance, methods of determination and a model of baroreflex blood-
pressure regulation. Cesk Fysiol. 2013;62(1):10-8.
21. Hohnloser SH, Klingenheben t. Stratification of patients at risk for sudden
cardiac death with special reference to the autonomic nervous system. Z
Kardiol. 1996;85 Suppl 6:35-43.
22. Sridhar A, nishijima y, terentyev D, terentyeva r, Uelmen r, Kukielka M,
Bonilla IM, robertson gA, györke S, Billman gE, Carnes CA. repolarization
abnormalities and afterdepolarizations in a canine model of sudden cardiac
death. Am J Physiol Regul Integr Comp Physiol. 2008 nov;295(5):r1463-72.
23. Pham Q, Quan KJ, rosenbaum DS. t-wave alternans: marker, mechanism, and
methodology for predicting sudden cardiac death. J Electrocardiol. 2003;36
Suppl:75-81.
24. Sung rJ, lauer Mr. Sudden cardiac death syndrome: diagnosis and
management. J Formos Med Assoc. 2000 nov;99(11):809-22.
25. lim HS, Subbiah rn, leong-Sit P, gula lJ, Skanes AC, yee r, Klein gJ,
Krahn AD. How to diagnose the cause of sudden cardiac arrest. Cardiol J.
2011;18(2):210-6.
26. ruskin Jn. role of invasive electrophysiological testing in the evaluation and
treatment of patients at high risk for sudden cardiac death. Circulation. 1992
Jan;85(1 Suppl):I152-9.
27. Kwok KM, lee Kl, lau CP, tse Hf. Sudden cardiac death: prevention and
treatment. Hong Kong Med J. 2003 oct;9(5):357-62.
28. Zitron E, Thomas D, Katus HA, Becker r. Cardioverter defibrillator therapy
in the primary and secondary prevention of sudden cardiac death. Applied
Cardiopulmonary Pathophysiology. 2012;16:174-191.
29. Myerburg rJ, reddy v, Castellanos C. Indications for Implantable
Cardioverter-Defibrillators Based on Evidence and Judgment. J Am Coll
Cardiol. 2009;54(9):747-763.
30. owen JS, Khatib S, Morin DP. Cardiac resynchronization Therapy. Ochsner J.
2009 Winter; 9(4): 248–256.
31. ruschitzka f, Abraham Wt, Singh JP, Bax JJ, Borer JS, Brugada J, Dickstein K,
ford I, gorcsan J 3rd, gras D, Krum H, Sogaard P, Holzmeister J; EchoCrt
Study group. Cardiac-resynchronization therapy in heart failure with a narrow
QrS complex. N Engl J Med. 2013 oct 10;369(15):1395-405.
29
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32. Koplan BA, Stevenson Wg. ventricular tachycardia and Sudden Cardiac
Death. Mayo Clin Proc. 2009 March; 84(3): 289–297.
33. Hjalmarson A. Prevention of sudden cardiac death with beta blockers. Clin
Cardiol. 1999 oct;22 Suppl 5:v11-5.
34. Al-gobari M, El Khatib C, Pillon f, gueyffier f. Beta-blockers for the
prevention of sudden cardiac death in heart failure patients: a meta-analysis of
randomized controlled trials. BMC Cardiovasc Disord. 2013 Jul 13;13:52.
35. Iravanian S, Sovari AA, lardin HA, liu H, Xiao HD, Dolmatova E, Jiao Z,
Harris BS, Witham EA, gourdie rg, Duffy HS, Bernstein KE, Dudley SC Jr.
Inhibition of renin-angiotensin system (RAS) reduces ventricular tachycardia
risk by altering connexin43. J Mol Med (Berl). 2011 Jul;89(7):677-87.
36. Domanski MJ, Exner Dv, Borkowf CB, geller nl, rosenberg y, Pfeffer MA.
Effect of angiotensin converting enzyme inhibition on sudden cardiac death in
patients following acute myocardial infarction. A meta-analysis of randomized
clinical trials. J Am Coll Cardiol. 1999 Mar;33(3):598-604.
37. Pitt B, White H, nicolau J, Martinez f, gheorghiade M, Aschermann M,
van veldhuisen DJ, Zannad f, Krum H, Mukherjee r, vincent J; EPHESUS
Investigators. Eplerenone reduces mortality 30 days after randomization
following acute myocardial infarction in patients with left ventricular systolic
dysfunction and heart failure. J Am Coll Cardiol. 2005 Aug 2;46(3):425-31.
38. levantesi g, Scarano M, Marfisi r, Borrelli g, rutjes AW, Silletta Mg,
tognoni g, Marchioli r. Meta-analysis of effect of statin treatment on risk of
sudden death. Am J Cardiol. 2007 Dec 1;100(11):1644-50.
39. Dickinson Mg, Ip JH, olshansky B, Hellkamp AS, Anderson J, Poole JE, Mark
DB, lee Kl, Bardy gH; SCD-Heft Investigators. Statin use was associated
with reduced mortality in both ischemic and nonischemic cardiomyopathy
and in patients with implantable defibrillators: mortality data and mechanistic
insights from the Sudden Cardiac Death in Heart failure trial (SCD-Heft).
Am Heart J. 2007 Apr;153(4):573-8.
40. Herzog E, Aziz Ef, Kukin M, Steinberg JS, Mittal S. novel pathway for sudden
cardiac death prevention. Crit Pathw Cardiol. 2009; 8:1–6.
41. Aziz Ef, Javed f, Pratap B, Herzog E. Strategies for the prevention and treatment
of sudden cardiac death. Open Access Emerg Med. 2010 December;2010(2):
99–114.
42. Derwall M, fries M, rossaint r. Sudden cardiac death: role of therapeutic
hypothermia. Applied Cardiopulmonary Pathophysiology. 2102;16:202-211.
43. Sterz f, Holzer M, roine r, Zeiner A, losert H, Eisenburger P, Uray t, Behringer
W. Hypothermia after cardiac arrest: a treatment that works. Curr Opin Crit Care.
2003 Jun;9(3):205-10.
44. Holzer M, Bernard SA, Hachimi-Idrissi S, roine ro, Sterz f, Müllner M;
Collaborative group on Induced Hypothermia for neuroprotection After
Cardiac Arrest. Hypothermia for neuroprotection after cardiac arrest:
systematic review and individual patient data meta-analysis. Crit Care Med.
2005 feb;33(2):414-8.
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Section 3
Post-cardiac arrest syndrome

Course Director
Dr Michael D. Klein, MD
Medical Director of the Heart Station at
Boston Medical Center,
Clinical Professor of Medicine
Boston University School of Medicine,
Boston, MA

objectiVes
• to understand the concept of post-cardiac arrest syndrome and get familiar with mechanisms
of brain injury and myocardial dysfunction in resuscitated patients post-cardiac arrest
• to know the management approach during the post-cardiac arrest phase

30

what is Post-cardiac arrest
syndrome?
Sudden cardiac arrests are unfortunate terminal events of a
number of cardiac and non-cardiac disorders. Survival rates of
individuals who suffer cardiac arrests, particularly those who
suffer out-of-hospital cardiac arrests, are dismally low, although
rapid advances in resuscitation care over the last few decades
has contributed to improvement in survival of these patients.1
notwithstanding these nuanced survival benefits, overall
outcome of patients resuscitated after cardiac arrest subsequent
to resumption of spontaneous circulation (roSC) continues
to remain poor.2 Dr vladimir negovsky is credited as one of the
first investigators who recognized this paradox and attempted
to delineate the basic pathology underlying it. He named this
state as “post-resuscitation disease,” a pathophysiological state
which develops subsequent to successful cardiopulmonary
resuscitation (CPr).3 recently, this post-resuscitation phase
was renamed in a scientific statement by the International
liaison Committee on resuscitation as post-cardiac arrest
syndrome.4 Post-cardiac arrest syndrome is a constellation
of different pathological states, including hypoxic/anoxic
brain injury, myocardial dysfunction, widespread systemic
inflammation along with rapidly developing multiple organ
failure. Its occurrence post-resuscitation increases risk of death
and portends poor outcome among survivors.5
for improving standardization and prognostication, the
post-cardiac arrest period has been divided into four phases
(figure 1) based on the time elapsed after roSC. The first
phase is the immediate post-arrest phase, defined as first 20
minutes after roSC. It is followed by an early post-arrest
phase extending from 20 minutes to 6-12 hours after roSC.
Early interventions applied during this phase largely influence
the final outcome of the resuscitated patients. The third phase
is an intermediate post-arrest phase, starting from 6-12 hours
and continuing till 72 hours post-roSC. During this phase
injury pathways are still active and can be influenced by further
interventions. The final phase is the recovery phase which
occurs after 3 days of roSC. Prognostication of patients can
be most reliably done during this phase.4
PathoPhysiology of Post-cardiac
arrest syndrome
The mechanism of development of post-cardiac arrest
syndrome is complex and still incompletely understood.
However, it is widely agreed that prolonged ischemia
after cardiac arrest followed by reperfusion at the time
of resuscitation triggers a cascade of events, interplay of
31
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Figure 1 Different phases of the post-cardiac arrest period
ROSC
Immediate post-arrest phase
20 minutes
Early post-arrest phase
6-12 hours
Intermediate post-arrest phase
72 hours
Recovery phase
based on information from:
neumar rW, nolan JP, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway C, Clark
rS, geocadin rg, Jauch EC, Kern KB, laurent I, longstreth Wt Jr, Merchant rM,
Morley P, Morrison lJ, nadkarni v, Peberdy MA, rivers EP, rodriguez-nunez A,
Sellke fW, Spaulding C, Sunde K, vanden Hoek t. Post-cardiac arrest syndrome:
epidemiology, pathophysiology, treatment, and prognostication. A consensus
statement from the International liaison Committee on resuscitation (American
Heart Association, Australian and new Zealand Council on resuscitation, European
resuscitation Council, Heart and Stroke foundation of Canada, InterAmerican
Heart foundation, resuscitation Council of Asia, and the resuscitation Council of
Southern Africa); the American Heart Association Emergency Cardiovascular Care
Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council
on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical
Cardiology; and the Stroke Council. Circulation. 2008 Dec 2;118(23):2452-83.
which precipitates the systemic manifestations of this
pathophysiological state. These manifestations of post-cardiac
arrest syndrome include hypoxic/anoxic brain injury, post-
arrest myocardial dysfunction, systemic ischemia/reperfusion
injury and persistent precipitating pathology (table 1).4
onset of widespread cellular injury is triggered in
cardiac arrest survivors when ischemia due to interruption
of circulation occurs long enough to deplete cellular oxygen
stores. various factors can account for poor tissue perfusion
and ischemic cellular injury during the post-resuscitation
period. Some of these factors include compensatory increase in
systemic oxygen extraction during CPr, post-arrest myocardial
dysfunction and hemodynamic instability, which frequently
occurs during this period.4 Although the predominant cause of
ischemia in these patients remains debatable, it is plausible that
multiple critical pathways of cellular destruction, including
depletion of cellular AtP synthesis, alteration in membrane
depolarization and increase in intracytoplasmic calcium
concentration, are activated secondary to ischemia, resulting
in extensive cellular and tissue injury. With reperfusion
and roSC, paradoxically, tissue injury gets aggravated
further due to widespread formation of free radicals which
creates a systemic prooxidant state. Many free radicals are
by themselves cytotoxic, and further augment structural and
functional cellular perturbations, accelerating cell death. A
 DIPLOMA
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Table 1 Different pathological components of the post-
cardiac arrest syndrome
Hypoxic/anoxic brain injury
Post-arrest myocardial dysfunction
Systemic ischemia/reperfusion injury
Persistent precipitating pathology
based on information from:
neumar rW, nolan JP, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway C, Clark
rS, geocadin rg, Jauch EC, Kern KB, laurent I, longstreth Wt Jr, Merchant rM,
Morley P, Morrison lJ, nadkarni v, Peberdy MA, rivers EP, rodriguez-nunez A,
Sellke fW, Spaulding C, Sunde K, vanden Hoek t. Post-cardiac arrest syndrome:
epidemiology, pathophysiology, treatment, and prognostication. A consensus
statement from the International liaison Committee on resuscitation (American
Heart Association, Australian and new Zealand Council on resuscitation, European
resuscitation Council, Heart and Stroke foundation of Canada, InterAmerican
Heart foundation, resuscitation Council of Asia, and the resuscitation Council of
Southern Africa); the American Heart Association Emergency Cardiovascular Care
Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council
on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical
Cardiology; and the Stroke Council. Circulation. 2008 Dec 2;118(23):2452-83.
systemic inflammatory state ensues, with increased production
of proinflammatory cytokines, complement activation,
expression of chemoattractants and adhesion molecules on the
endothelial cell surface and local recruitment of inflammatory
cells.6 furthermore, while widespread systemic inflammation
facilitates development of a procoagulant state without
concomitant activation of endogenous fibrinolysis, thrombin
generated during intravascular coagulation reciprocally
aggravates inflammation due to its proinflammatory effects.
This vicious cycle constitutes a sepsis-like syndrome and often
culminates in multiple organ failure, infection and death.6,7
mechanism of hypoxemic/anoxic brain injury
neurons require uninterrupted circulation for maintaining
their structural and functional integrity, an attribute which
makes them highly susceptible to hypoxemia.8 Hypoxemic
injury to the brain is one of the most common causes of
mortality in patients who are resuscitated from prolonged
cardiac arrest. A retrospective review9 of medical records of
patients who suffered and survived an initial episode of cardiac
arrest showed brain injury to be the cause of subsequent death
in 23% of patients who suffered an in-hospital cardiac arrest
and 68% patients who suffered out-of-hospital cardiac arrest
(figure 2). Thus, in view of the adverse impact of brain injury,
including its contribution to overall mortality and unfavorable
neurologic outcomes among cardiac arrest survivors, it
becomes imperative to incorporate various neuroprotective
strategies in post-resuscitation care. A range of neurological
deficits may indicate to ischemic brain injury in these patients,
32
Figure 2 Contribution of neurological injury to deaths
after in-hospital cardiac arrest and out-of
-hospital cardiac arrest
80
68
70
neurological injury (%)
Patients death due to
60
50
40
30 23
20
10
0
In-hospital Out-of hospital
cardiac arrest cardiac arrest
based on information from:
laver S, farrow C, turner D, nolan J. Mode of death after admission to an intensive
care unit following cardiac arrest. Intensive Care Med. 2004 nov;30(11):2126-8.
including neurocognitive dysfunction, seizures, myoclonus
and coma. Brain death eventually ensues.4
The mechanism of brain injury in resuscitated patients
is complex and multifactorial (figure 3). Immediately
after cardiac arrest, a series of pathological events unfold
which incur ischemic injury to the brain. resuscitation and
subsequent roSC, although expected to mitigate these
effects, ironically aggravate them further, inducing a spectrum
of changes which characterize hypoxic/anoxic brain injury in
resuscitated patients. In patients who suffer a cardiac arrest,
early evidence of ischemic neuronal damage is witnessed in
large parts of the brain. These cellular changes in the neurons,
as has been described earlier, include cellular AtP depletion,
intracellular calcium accumulation and widespread neuronal
membrane breakdown. furthermore, release of glutamate
and some other neurotransmitters induces excitotoxic injury
to the neurons. Hypoxemia occurring during the ischemic
phase can also adversely affect cerebral autoregulation, which
in turn reduces cerebral perfusion.10 During the early periods
of reperfusion after roSC, cerebral circulation becomes
markedly hyperemic, probably as a result of impaired cerebral
autoregulation, facilitating extensive free radical formation,
induction of neuronal apoptotic pathways and mitochondrial
dysfunction.8 These cellular processes have neurotoxic
effects. Additionally, hyperemic circulation also results in
cerebral edema which can impair cerebral perfusion pressure.
Intracranial pressure increases, although the extent to which it
contributes to brain injury during the post-resuscitation period
remains arguable. rapidly developing myocardial dysfunction,
systemic hemodynamic compromise, hypotension and
obstruction of cerebral microcirculation by thrombi in the later
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Figure 3 Mechanism of brain injury in post-cardiac arrest syndrome

Prolonged cardiac arrest

Interruption of circulation Resuscitation and ROSC

Altered cerebral
Ischemia hypoxia Hyperemic reperfusion
autoregulation

Cerebral edema

Intracellular Impaired Apoptotic Free

Membrane Excitotoxic Other Other
calcium cerebral pathways radical
depolarization injury mechanisms mechanisms
accumulation perfusion stimulated trauma

Brain injury

based on information from:

1. neumar rW, nolan JP, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway C, Clark rS, geocadin rg, Jauch EC, Kern KB, laurent I, longstreth Wt Jr, Merchant rM,
Morley P, Morrison lJ, nadkarni v, Peberdy MA, rivers EP, rodriguez-nunez A, Sellke fW, Spaulding C, Sunde K, vanden Hoek t. Post-cardiac arrest syndrome:
epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International liaison Committee on resuscitation (American Heart
Association, Australian and new Zealand Council on resuscitation, European resuscitation Council, Heart and Stroke foundation of Canada, InterAmerican Heart
foundation, resuscitation Council of Asia, and the resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care
Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical
Cardiology; and the Stroke Council. Circulation. 2008 Dec 2;118(23):2452-83.
2. reynolds JC, lawner BJ. Management of the post-cardiac arrest syndrome. J Emerg Med. 2012 Apr;42(4):440-9.
3. geocadin rg, Koenig MA, Jia X, Stevens rD, Peberdy MA. Management of brain injury after resuscitation from cardiac arrest. Neurol Clin. 2008 May;26(2):487-506.

stages of reperfusion may also exacerbate brain hypoxemia and
result in secondary ischemic damage. Concurrence of pyrexia,
hyperglycemia and seizures in the post-resuscitation period
can contribute to deterioration in CnS functions. These
pathologies, when detected, should be promptly managed.4
mechanism of myocardial dysfunction
Myocardial dysfunction, which is reversible in nature and
amenable to treatment with inotropes and vasodilators, is also
known to frequently occur in the post-resuscitation period.
Along with neuronal dysfunction, it is also an important cause
of mortality during the post-resuscitation phase. occurrence
of myocardial dysfunction is often an early event after roSC
and is characterized by hemodynamic lability, with fluctuating
heart rate and blood pressure of the patients.4 low cardiac
index is seen within 24 hours post-resuscitation and signifies
underlying myocardial dysfunction.11 It has both systolic and
diastolic components and is completely reversible in the first
48-72 hours.11,12 It is noteworthy that severe vasodilatation
as a result of widespread systemic inflammation also occurs
after prolonged cardiac arrest and resuscitation, which along
with myocardial dysfunction, contributes to hypotension
and a shock-like state during this period. This necessitates
institution of vasopressor support along with inotropes in the
post-resuscitation period to optimize patients’ hemodynamic
functions.6
various putative mechanisms have been proposed which
may contribute to myocardial dysfunction in the post-
resuscitation phase. Though most mechanisms need to be
confirmed in well-designed clinical trials, it appears plausible
that initial catecholamine surge, myocardial stunning and
global hypokinesis after prolonged cardiac arrest may be

33
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chief contributors to this pathology.8 The cause of myocardial
stunning in the post-resuscitation period remains obscure,
although it may be a result of contractile dysfunction due to
free radical damage and increase in intracellular calcium.13
Underlying coronary artery disease (CAD), which is
commonly present in many patients who suffer cardiac arrest,
can also adversely impact myocardial functioning.8
systemic ischemia-reperfusion response
In cardiac arrest, tissue perfusion and oxygenation gets
disrupted, which does not improve much in the subsequent
period of reperfusion due to impaired vasoregulation. Coupled
with increase in peripheral oxygen extraction in the immediate
post-resuscitation phase, a gradually evolving oxygen debt
develops in most tissues which triggers widespread systemic
inflammation.4 These suggestions have been validated by
observations of increase in levels of cytokines and endotoxins in
survivors of cardiac arrest who were successfully resuscitated.14
Parallel to widespread systemic inflammation, activation of
coagulation pathways also occurs, both increasing the risk of
multiple organ failure.7 furthermore, emergency procedures
that many of these patients undergo in the ICU, including
interventions for obtaining airway and vascular access and
therapeutic modalities such as mechanical ventilation and
induced hypothermia, predispose them to increased risk of
infections. Development of infectious complications further
impact their prognosis adversely.4,6
Persistent precipitating pathology
The pathophysiology of post-cardiac arrest syndrome is
often complicated by disorders which precipitate cardiac
arrest. Some of the commonly known causes include sepsis,
pulmonary embolism and CAD. Coronary artery disease,
symptomatic or asymptomatic, is a particularly common cause
of cardiac arrest.4 In an evaluation15 of patients who suffered
cardiac arrest due to no obvious non-cardiac pathology,
angiography revealed evidence of coronary artery occlusion
in 48% patients. Similar were findings of another study,16
which evaluated patients who suffered out-of-hospital cardiac
arrest and were resuscitated, and showed ECg and enzymatic
evidence of acute MI in almost 50% patients. In view of the
above, it appears prudent to perform a 12-lead ECg in all
patients who are resuscitated from cardiac arrest to look for
evidence of MI. Emergent management through angiography
and percutaneous coronary intervention (PCI) is warranted if
an underlying acute coronary syndrome (ACS) is detected.4

eValuate yourself

Q1. Which of the following appears to be the most common cause of death during the post-resuscitation period?
F Brain injury
F Myocardial dysfunction
F Systemic ischemia/reperfusion response
F none of these

Q2. Which of these statements about post-cardiac arrest syndrome is false?

F It is associated with widespread inflammation and coagulopathy
F Myocardial dysfunction after 24 hours of roSC is irreversible
F Injury pathways remain effective in the intermediate post-arrest phase
F Evidence of MI should be looked for in all conscious patients who are successfully resuscitated after cardiac
arrest

Q3. The following has not been conclusively proven to be a cause of brain injury in the post-resuscitation period
F Ischemic neuronal injury due to interruption of circulation in cardiac arrest
F Excitotoxic neuronal injury due to release of glutamate
F neuronal injury due to free radical formation during reperfusion
F neuronal injury due to increase in intracranial pressure as a result of cerebral edema

34

management and Post-
resuscitation care
Patients who are successfully resuscitated after prolonged
ischemia due to cardiac arrest are prone to develop post-cardiac
arrest syndrome. Management of these patients should aim
to provide hemodynamic stability, improve tissue perfusion,
resurrect systemic derangements and attempt recovery of
neurological functions. A multipronged diagnostic and
management approach is instituted to achieve these objectives
(figure 4).
oxygenation and hemodynamic stabilization
In patients who are successfully resuscitated from cardiac
arrest, immediate priority should be to provide oxygenation
and hemodynamic stabilization. These patients should be
ventilated with 100% oxygen initially, and subsequent titration
can be done in the ICU to achieve and maintain peripheral
oxygen saturation of > 94%. Both hypoxia and hyperoxia can
have detrimental health consequences and therefore should be
prevented in these patients.5 Additionally, PaCo2 should also
be maintained within the reference range. Patients who suffer
out-of-hospital cardiac arrests should be optimally ventilated,
particularly in light of the fact that overzealous hyperventilation
in them, which is often the case, can further compromise
systemic hemodynamic stability and reduce cerebral blood
flow. It is advisable to start ventilation in them by providing
10-12 breaths per minute initially, and subsequently titrating
in the ICU to achieve PaCo2 of 40-45 mm Hg.17
Many patients who suffer cardiac arrest and are resuscitated
successfully are hypotensive after roSC. It is imperative to
provide cardiovascular support to improve circulation and
optimize their tissue perfusion. Establishing an emergent
intravascular (Iv) access is crucial to provide rapid Iv fluid
boluses. Hemodynamic stabilization can be best achieved using
inotropes and vasopressor agents.5,6,17 These classes of drugs
have rapidly evolved in contemporary medicine to become
cornerstone of management of several cardiac emergencies,
including shock. In patients resuscitated for cardiac arrest,
doses of inotropes and vasopressors in the post-resuscitation
period should be titrated to achieve a minimum systolic
blood pressure of ≥90 mm Hg or a mean arterial pressure
of ≥65 mm Hg.17 Epinephrine rapidly increases diastolic
blood pressure and facilitates coronary perfusion. It also
restores myocardial contractility through its inotrope effects.
Epinephrine is however associated with increase in oxygen
consumption, which may be a hindrance to its use in some
situations. Many patients in shock respond to 1 mg Iv dose
of epinephrine, which can be repeated. It has been shown that
35
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repeated 1 mg Iv doses of epinephrine can restore circulation
as efficiently as 5 mg Iv doses. vasopressin 40 IU single dose
may be administered as an alternative to epinephrine in shock
states.18 Dobutamine may also be used, particularly in patients
with post-MI cardiac arrest.1 Its starting dose is 3-5 mcg/kg/
minute, with subsequent titration required according to the
desired effect.17 In patients in whom fluid resuscitation and
vasoactive drugs prove insufficient for restoring circulation,
use of mechanical devices, such as intra-aortic balloon pump,
may be considered.4,19
revascularization
In patients who suffer cardiac arrest, MI is frequently found
to be an underlying cause. It therefore appears prudent to
obtain a 12-lead ECg in all patients resuscitated for cardiac
arrest after roSC. Evidence for St-elevation MI (StEMI)
should be specifically looked for. In patients with StEMI, an
emergent angiography followed by PCI should be performed.
In fact, considering the huge burden of asymptomatic coronary
artery disease (CAD) in the community which often remains
undetected, it may be advisable to consider emergent coronary
angiography in all patients who survive a cardiac arrest and are
resuscitated, even in the absence of evidence for StEMI. 17
therapeutic hypothermia: a neuroprotective
strategy
over the past decade, therapeutic hypothermia has gradually
emerged as one of the most successful treatment strategy for
patients who survive a cardiac arrest but remain comatose.
This treatment modality benefits by increasing the likelihood
of survival after cardiac arrest and improving neurological
outcome in these patients. In an evaluation20 of patients who
remained unconscious after resuscitation from out-of-hospital
cardiac arrest, application of moderate hypothermia was
shown to be associated with survival in 49% patients compared
to 26% patients who were provided normothermia. In another
study21 done by the Hypothermia After Cardiac Arrest Study
group, which evaluated patients resuscitated after cardiac
arrest due to vf, mortality rates at 6 months were found to
be 41% in the group assigned to hypothermia compared to
55% in the patient group which was provided normothermia.
Additionally, this study also showed improved neurological
outcome after roSC in greater number of patients who
received therapeutic hypothermia compared to those who
received normothermia (55% vs 39%, respectively). It is worth
mentioning that while robust evidence supports beneficial role
of induced hypothermia in patients who suffer out-of-hospital
cardiac arrest due to a shockable rhythm (vt/vf), its role in
patients with asystole cardiac arrest remains equivocal.4
 DIPLOMA
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Figure 4 Practical diagnostic and management approach to post-cardiac arrest syndrome

Cardiac arrest and resuscitation

ROSC

Attempt to achieve hemodynamic stability + oxygenation

Is patient conscious?

Yes No

ECG Therapeutic hypothermia

STEMI

Yes No

PCI Supportive management

based on information from:

1. Stub D, Bernard S, Duffy SJ, Kaye DM. Post Cardiac Arrest Syndrome: A review of Therapeutic Strategies. Circulation. 2011;123:1428-1435.
2. Mongardon n, Dumas f, ricome S, grimaldi D, Hissem t, Pène f, Cariou A. Postcardiac arrest syndrome: from immediate resuscitation to long-term outcome. Ann
Intensive Care. 2011 nov 3;1(1):45
3. Peberdy MA, Callaway CW, neumar rW, geocadin rg, Zimmerman Jl, Donnino M, gabrielli A, Silvers SM, Zaritsky Al, Merchant r, vanden Hoek tl, Kronick
Sl; American Heart Association. Part 9: post-cardiac arrest care: 2010 American Heart Association guidelines for Cardiopulmonary resuscitation and Emergency
Cardiovascular Care. Circulation. 2010 nov 2;122(18 Suppl 3):S768-86.

The mechanism by which hypothermia affords benefits in
the post-cardiac arrest state is multifactorial. It decreases the
cerebral metabolic rate and hence improves cerebral perfusion.
Additionally, hypothermia suppresses neuronal excitotoxic state
and decreases mitochondrial dysfunction, both factors known
to contribute to neuronal injury. Many other mechanisms of
benefits have also been proposed, although their veracity still
remains questionable.22 Currently, application of therapeutic
hypothermia (32-340 C) for 12-24 hours is recommended for
all patients who suffer out-of-hospital cardiac arrest with vf.
This treatment strategy can also be considered for patients
who suffer out-of-hospital cardiac arrest with initial pulseless
electrical activity or asystole and in those who suffer in-hospital
cardiac arrest of any rhythm. Methods which can be used to
provide therapeutic hypothermia includes surface cooling,
endovascular cooling catheters, cold packs, among others.
Monitoring the patients’ core temperature simultaneously
is recommended. Despite its benefits, hypothermia may be
associated with some concurrent adverse effects, including
arrhythmias, coagulopathy and increased risk of infections.
These should be kept into consideration when adopting this
technique.17

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other treatment options
Since maximizing neuronal recovery is an important objective
of post-resuscitation care, factors which aggravate neuronal
injury in the post-resuscitation period should be managed
effectively. neuronal injury after roSC increases with seizures,
hyperglycemia and pyrexia.4 Hyperglycemia is known to
develop in the post-resuscitation period due to highly stressful
state and adversely impacts cerebral outcomes. It is advisable
to institute prompt treatment of hyperglycemia, if detected,
and optimize blood glucose to below 180 mg/dl; a lower
blood glucose target may increase the risk of hypoglycemia,
which can also have adverse neurological consequences.19
Seizures can also accentuate neurological injury after cardiac
arrest. They can be managed using phenytoin. A few clinical
trials have also evaluated the neuroprotective role of thiopental
and magnesium in these clinical settings but have not been
able to conclude unequivocally on their effectiveness. finally,
pyrexia, which can also develop in the post-resuscitation
phase secondary to systemic inflammation, is known to impair
neurological functions; the extent to which antipyretics and
“controlled normothermia” improves pyrexia in these patients
remains to be evaluated. other than these factors, underlying
pathology of cardiac arrest should also be identified and organ-
specific investigations and management instituted.4

eValuate yourself
Q1. In post-cardiac arrest syndrome presenting as hypotensive shock on day 1 after roSC, the dose of inotropes and
vasodilators should be titrated to achieve a minimum systolic pressure of
F > 75 mm Hg
F > 80 mm Hg
F > 85 mm Hg
F > 90 mm Hg

Q2. A patient had an out-of-hospital cardiac arrest, was resuscitated and transported to a nearby hospital. He was unconscious
at the time he was wheeled into the emergency. His peripheral oxygen saturation (on oxygen) was 90%, pulse rate was rapid
and thready and blood pressure was 80/56 mm Hg. He was not following commands. to improve his neurological outcomes
after initial hemodynamic stabilization which of the following treatment option appears to be most effective?
F Thiopental
F Magnesium
F Induced hypothermia
F ECMo

Q3. In survivors of cardiac arrest after resuscitation, random blood sugar in the immediate post-resuscitation period was
found to be 256 mg/dl. The target concentration below which blood glucose should be kept to improve neurological
outcomes is
F Below 100 mg/dl
F Below 130 mg/dl
F Below 150 mg/dl
F Below 180 mg/dl

37
 DIPLOMA
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conclusion
Post-cardiac arrest syndrome is a pathological state that
develops in many patients who are successfully resuscitated
from cardiac arrest after roSC. It comprises a constellation
of abnormalities, including hypoxemic/anoxic brain injury,
myocardial dysfunction, systemic ischemia/reperfusion
injury and persisting precipitating pathology. The mechanism
of its development remains obscure, although widespread
ischemic injury from cardiac arrest appears to be the trigger
to a cascade of pathological events which get aggravated with
reperfusion and culminate in the pathological manifestations.
Management of post-cardiac arrest syndrome should attempt
to maximize neurological recovery, maintain hemodynamic
stability and treat the underlying cause. Since many patients
have MI as an underlying cause of cardiac arrest, a 12-lead
ECg should be performed to look for evidence of StEMI.
If detected, an emergent angiography and subsequent PCI
should be performed. More clinical studies are evaluating
novel therapeutic options which may soon be brought into
clinical use and improve overall outcome of these patients.
references
1. Soo l, gray D, young t, Huff n, Skene A, Hampton Jr. resuscitation from
out-of-hospital cardiac arrest: is survival dependent on who is available at the
scene? Heart 1999;81:47–52.
2. Martín-Hernández H, lópez-Messa JB, Pérez-vela Jl, Molina-latorre r,
Cárdenas-Cruz A, lesmes-Serrano A, Alvarez-fernández JA, fonseca-
San Miguel f, tamayo-lomas lM, Herrero-Ansola yP; miembros del
Comité Directivo del Plan nacional de rCP de la SEMICyUC. Managing
the post-cardiac arrest syndrome. Directing Committee of the national
Cardiopulmonary resuscitation Plan (PnrCP) of the Spanish Society for
Intensive Medicine, Critical Care and Coronary Units (SEMICyUC). Med
Intensiva. 2010 Mar;34(2):107-26.
3. negovsky vA. Postresuscitation disease. Crit Care Med. 1988
oct;16(10):942-6.
4. neumar rW, nolan JP, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway
C, Clark rS, geocadin rg, Jauch EC, Kern KB, laurent I, longstreth Wt
Jr, Merchant rM, Morley P, Morrison lJ, nadkarni v, Peberdy MA, rivers
EP, rodriguez-nunez A, Sellke fW, Spaulding C, Sunde K, vanden Hoek
t. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment,
and prognostication. A consensus statement from the International liaison
Committee on resuscitation (American Heart Association, Australian and
new Zealand Council on resuscitation, European resuscitation Council,
Heart and Stroke foundation of Canada, InterAmerican Heart foundation,
resuscitation Council of Asia, and the resuscitation Council of Southern
Africa); the American Heart Association Emergency Cardiovascular Care
Committee; the Council on Cardiovascular Surgery and Anesthesia; the
Council on Cardiopulmonary, Perioperative, and Critical Care; the Council
on Clinical Cardiology; and the Stroke Council. Circulation. 2008 Dec
2;118(23):2452-83.
38
5. Stub D, Bernard S, Duffy SJ, Kaye DM. Post Cardiac Arrest Syndrome: A
review of Therapeutic Strategies. Circulation. 2011;123:1428-1435.
6. Mongardon n, Dumas f, ricome S, grimaldi D, Hissem t, Pène f, Cariou
A. Postcardiac arrest syndrome: from immediate resuscitation to long-term
outcome. Ann Intensive Care. 2011 nov 3;1(1):45
7. Adrie C, Monchi M, laurent I, Um S, yan SB, Thuong M, Cariou A, Charpentier
J, Dhainaut Jf. Coagulopathy after successful cardiopulmonary resuscitation
following cardiac arrest: implication of the protein C anticoagulant pathway. J
Am Coll Cardiol. 2005 Jul 5;46(1):21-8.
8. reynolds JC, lawner BJ. Management of the post-cardiac arrest syndrome. J
Emerg Med. 2012 Apr;42(4):440-9.
9. laver S, farrow C, turner D, nolan J. Mode of death after admission to
an intensive care unit following cardiac arrest. Intensive Care Med. 2004
nov;30(11):2126-8.
10. geocadin rg, Koenig MA, Jia X, Stevens rD, Peberdy MA. Management
of brain injury after resuscitation from cardiac arrest. Neurol Clin. 2008
May;26(2):487-506.
11. laurent I, Monchi M, Chiche JD, Joly lM, Spaulding C, Bourgeois B, Cariou
A, rozenberg A, Carli P, Weber S, Dhainaut Jf. reversible myocardial
dysfunction in survivors of out-of-hospital cardiac arrest. J Am Coll Cardiol.
2002; 40: 2110–2116.
12. Kern KB, Hilwig rW, rhee KH, Berg RA. Myocardial dysfunction after
resuscitation from cardiac arrest: an example of global myocardial stunning. J
Am Coll Cardiol. 1996 Jul;28(1):232-40.
13. Eberli fr. Stunned myocardium--an unfinished puzzle. Cardiovasc Res. 2004
Aug 1;63(2):189-91.
14. Adrie C, Adib-Conquy M, laurent I, Monchi M, vinsonneau C, fitting C,
fraisse f, Dinh-Xuan At, Carli P, Spaulding C, Dhainaut Jf, Cavaillon JM.
Successful cardiopulmonary resuscitation after cardiac arrest as a “sepsis-like”
syndrome. Circulation. 2002 Jul 30;106(5):562-8.
15. Spaulding CM, Joly lM, rosenberg A, Monchi M, Weber Sn, Dhainaut Jf,
Carli P. Immediate coronary angiography in survivors of out-of-hospital
cardiac arrest. N Engl J Med. 1997 Jun 5;336(23):1629-33.
16. Bulut S, Aengevaeren Wr, luijten HJ, verheugt fW. Successful out-of-
hospital cardiopulmonary resuscitation: what is the optimal in-hospital
treatment strategy? Resuscitation. 2000 oct;47(2):155-61.
17. Peberdy MA, Callaway CW, neumar rW, geocadin rg, Zimmerman Jl,
Donnino M, gabrielli A, Silvers SM, Zaritsky Al, Merchant r, vanden Hoek
tl, Kronick Sl; American Heart Association. Part 9: post-cardiac arrest
care: 2010 American Heart Association guidelines for Cardiopulmonary
resuscitation and Emergency Cardiovascular Care. Circulation. 2010 nov
2;122(18 Suppl 3):S768-86.
18. overgaard CB, Dzavík v. Inotropes and vasopressors: review of physiology and
clinical use in cardiovascular disease. Circulation. 2008 Sep 2;118(10):1047-
56.
19. Binks A, nolan JP. Post-cardiac arrest syndrome. Minerva Anestesiol. 2010
May;76(5):362-8.
20. Bernard SA, gray tW, Buist MD, et al. treatment of comatose survivors
of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med.
2002;346:557-563.
21. Hypothermia After Cardiac Arrest Study group. Mild therapeutic
hypothermia to improve the neurological outcome after cardiac arrest. N Engl
J Med. 2002;346:549-556.
22. Alkadri ME, McMullan P. Induced Hypothermia as a neuroprotectant in Post-
Cardiac Arrest neurological failure. Ochsner J. 2009 Winter; 9(4): 278–281.
 DIPLOMA PROGRAM
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GENERAL PRACTICE

Section 4
Pharmacology in emergency
cardiovascular care

Course Director
Dr Michael D. Klein, MD
Medical Director of the Heart Station at
Boston Medical Center,
Clinical Professor of Medicine
Boston University School of Medicine,
Boston, MA

objectiVes
• to get familiar with the doses of different pharmacological agents used in emergency
cardiovascular care
• to know the indications in which these drugs are commonly used

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Drug Drug class Indications Dosing schedule1-31

Norepinephrine1,2,3 Sympathomimetic • Vasodilatory/cardiogenic shock
(potent a1 adrenergic with low vascular resistance
vascular agonist and (systolic BP < 70 mm Hg)
modest b agonist • As an adjunct in the treatment of
myocardial activity) cardiac arrest
Dopamine1,2,3 Sympathomimetic • Cardiogenic shock
(potent a1, b1, b2 and • Hypotension complicating acute
dopamine receptor myocardial infarction (MI) in the
agonist) presence of shock
• Post-cardiac arrest
• Symptomatic bradycardia
unresponsive to atropine or pacing
Dobutamine1,2 Synthetic • Decompensated cardiac failure
sympathomimetic • Hypotension complicating acute
(strong affinity for both MI in the absence of signs and
b1 and b2 receptors symptoms of shock
and a1 adrenergic • Shock with high systemic
receptors; no dopamine resistance
receptor activity)
• Sepsis-induced myocardial
dysfunction
• Symptomatic bradycardia
unresponsive to atropine or pacing
• Post-cardiac arrest
Vasopressin1,4,5 Vasopressor (agonist • Norepinephrine-resistant
activity on V1 receptors vasodilatory shock
of vascular smooth • Resuscitation of cardiac arrest
muscles and V2 patients
receptors of renal
collecting duct system)
Nitroglycerin6,7,8,9 Antianginal and • Stable/unstable angina and acute
antihypertensive MI
• Hypertensive emergency
associated with acute pulmonary
edema and acute coronary
syndrome (ACS)
• Perioperative hypertension
• Acute cardiac failure, continuous IV
infusion 0.01-0.03 mcg/kg/minute,
maximum 0.1 mcg/kg/minute
• Post-cardiac arrest, starting dose 0.1–0.5
mcg/kg/minute IV to attain systolic BP
≥ 90 mm Hg or mean arterial pressure
≥ 65 mm Hg, titrated to effect
• Refractory cardiac failure, starting dose
0.5-1 mcg/kg/minute IV infusion, which
may be increased to 2-20 mcg/kg/minute
to achieve desired effects
• Post-cardiac arrest, starting dose 5-10
mcg/kg/minute IV infusion to achieve
systolic BP ≥ 90 mm Hg or mean arterial
pressure ≥ 65 mm Hg, titrated to effect
2-20 mcg/kg/minute continuous IV infusion
(maximum 40 mcg/kg/minute).
• 40 IU IV bolus in patients refractory to
countershock cardiac arrest. Hypotension,
0.2 - 2.0 milliunits/kg/minute; IV infusion
of 0.01 - 0.1 IU/minute
• Antianginal, 0.3-0.6 mg sublingual
(S/L) tablet every 5 minutes until pain
relief, with maximum of 3 doses. Sprays
containing 0.4 mg/metered dose may be
used, with dosing schedule similar to S/L
tablets
• If despite S/L tablets or sprays, anginal
pain persists, initiate IV nitroglycerin 5-10
mcg/minute, increasing the dose at the
rate of 10 mcg/minute every 3-5 minutes
until pain resolves or systolic BP falls <100
mm Hg. Of note, in patients with ACS,
S/L tablets or sprays should invariably be
followed by IV nitroglycerin infusion
• Hypertensive emergencies, IV infusion
of 5 mcg/minute initially, with 5-20 mcg/
minute increments every 3-5 minutes
until desired response is achieved
(maximum infusion 100-200 mcg/minute)
• Acute pulmonary edema, S/L tablets 0.8-
2.4 mg every 5-10 minutes or IV infusion
>200 mcg/minute

40

Nitroprusside3,7,9 Arterial and venous • Severe acute low output left-sided
vasodilator cardiac failure due to mitral or
aortic regurgitation
• Hypertensive emergency
• Dissecting aneurysm
• Perioperative hypertension
• Acute pulmonary edema
• Shock or low cardiac output with
high vascular resistance
Hydralazine3,7,9 Direct-acting arteriolar • Hypertension without cardiac
vasodilator complications (as during
pregnancy)
• Perioperative hypertension
• Alternative to RAAS inhibitor in
chronic systolic heart failure with
reduced ejection fraction
• Eclampsia and preeclampsia
Labetalol7,10 Beta-blocker with • Hypertensive emergency
additional a blocking (hypertension in ischemic heart
activity disease with tachycardia, aortic
dissection, acute ischemic stroke)
• Hypertension in
pheochromocytoma
• Perioperative hypertension during
cardiac surgery
• Eclampsia/preeclampsia
Amiodarone11,12,13 Class III antiarrhythmic • Restoration of sinus rhythm in
atrial fibrillation (AF)
• Rate control in AF with rapid
ventricular response
• Sustained hemodynamically
stable monomorphic ventricular
tachyarrhythmia (VT)
• Polymorphic VT
• Of note, it is the drug of choice for • Prevention of post-infarct arrhythmia, oral
unstable VT/VF having low ejection
fraction in the settings of failed
defibrillation
• Prevention of post-infarct
arrhythmias
Lidocaine12,14 Class IB antiarrhythmic • Stable sustained monomorphic VT,
specifically associated with acute
MI
• Polymorphic VT, specifically
associated with acute MI
• Cardiac arrest due to VF
• May be considered for patients
presenting with long QT syndrome
type 3 and torsades de pointes
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• Initial IV infusion of 0.25-0.5 mcg/kg/
minute, with dose titration every 1-2
minutes until desired effects are achieved;
maximum dose 8 mcg/kg/minute. Since it
is light sensitive, cover the drug reservoir
with opaque material
• Change solution every 24 hours
Oral 50-75 mg every 6-8 hours or 3-20 mg
slow IV push every 20-60 minutes
• Initial loading dose (LD) of 20 mg IV
over 2 minutes followed by incremental
doses of 20-80 mg every 10 minutes until
desired BP is achieved, or
• LD of 20 mg IV over 2 minutes, followed
by IV infusion initiated at 1-2 mg/minute,
with upward titration until desired BP is
achieved. Of note, maximum cumulative
dose is 300 mg over 24 hours
• AF, 150 mg IV
• Rate control in AF, 300 mg IV bolus
followed by 45 mg/hour x 24 hours
• Stable monomorphic VT, 150-300 mg
IV bolus over 5 minutes followed by IV
infusion of 1050 mg/day
• Polymorphic VT, 150-300 mg IV bolus over
5 minutes followed by 1020 mg/day
400-1200 mg/day for 7 days, then taper to
100-300 mg/day
• Oral LD for arrhythmias, 1200-1600 mg
followed by maintenance dose (MD) of
200-400 mg daily
• VT/pulseless VT, 1-1.5 mg/kg IV/IO loading
dose followed by 20-50 mcg\kg\minute
infusion
• Repeat bolus if infusion started > 15
minutes after initial bolus
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Verapamil11,13,15,16 • Nondihydropyridine • Ischemic heart disease (IHD) • For supraventricular arrhythmia, 5-10 mg
calcium channel • Control of ventricular rate in AF by slow IV push over 2-3 minutes that can
blocker (CCB) with rapid ventricular response be repeated at 10-15 minute interval with
• Class IV 10 mg dose. Oral, 120-480 mg/day in 3-4
• Hemodynamically stable patients
antiarrhythmic divided doses
with supraventricular arrhythmia
• For IHD, slow release oral preparations
• Hypertrophic cardiomyopathy
180-240 mg/day
Procainamide11-13,17 Class IA antiarrhythmic • Initial treatment of stable • In VT, 10 mg/kg IV (100 mg IV bolus) over
sustained monomorphic VT 2 minutes with rate of administration 40-
• Repetitive monomorphic VT in 50 mg/minute, or
coronary artery disease (CAD) or • Oral LD of 1 g followed by up to 500 mg
idiopathic VT 3-hourly
• Recurrent or incessant • Atrial tachyarrhythmia, 500-1200 mg IV
polymorphic VT due to acute MI over 30-60 minutes
• Supraventricular tachycardia • Chronic oral therapy, 500-1000 mg every
• Control of ventricular rate in 6 hour
patients with preexcitation and
atrial fibrillation and atrial flutter
Ajmaline11,12,18,19 Class IA antiarrhythmic • Sustained hemodynamically stable • As antiarrhythmic, 50-100 mg IV over 5
monomorphic VT minutes
• Repetitive monomorphic VT in the • Ajmaline test, 10 mg over 2 minutes up to
settings of MI a target dose of 1 mg/kg
• To unmask Brugada syndrome
(atypical right bundle branch block
and right precordial ST elevation)
Diazepam20,21 Benzodiazepine • Sedative for elective cardioversion • Sedation, 5-10 mg oral tablet, or
of arrhythmias, cardiac • 5–10 mg IV bolus followed by 5–10 mg/
catheterization and coronary minute to a maximum of 70 mg
angiography
Midazolam20,21,22 Benzodiazepine • IV sedation for elective IV bolus of 5 mg followed by 1–2 mg/minute
cardioversion of arrhythmias, up to a maximum of 30 mg
cardiac catheterization and
coronary angiography
• In combination with ketamine for
sedation and pain relief in patients
with shock and cardiovascular
instability
Ketamine22,23 Anesthetic (related • Sedation, induction and • For induction of anesthesia: 0.5–1.5 mg/
to phencyclidine maintenance of general anesthesia kg IV or 4–10 mg/kg IM
hallucinogen) for cardiac catheterization. • Maintenance of anesthesia: 10–30 mcg/
However, caution needs to be kg/minute as IV infusion
practiced in the situations of
• Sedation and analgesia: 0.2–0.75 mg/kg IV
limited right ventricular functional
or 2–4 mg/kg IM, followed by continuous
reserve and increased pulmonary
infusion of 5–20 mcg/kg/minute
vascular resistance
• Induction and maintenance of
anesthesia in patients with cardiac
tamponade
• For sedation and pain relief
in patients with shock and
cardiovascular instability

42

CARDIAC
IN IN
Fenoldopam7,24 DA1 selective agonist • Hypertensive emergencies
(systemic and renal • Perioperative hypertension during
vasodilator) cardiac surgery
• Hypertensive encephalopathy
• Sympathetic crisis
Clevidipine25,26,27,28 Third-generation IV • Hypertensive emergencies and
dihydropyridine CCB urgencies when oral therapy is not
feasible or desirable
• Perioperative hypertension during
cardiac surgery
• Acute postoperative hypertension
in cardiac surgery patients
Nicardipine 7,9,29,30
Dihydropyridine CCB • Hypertensive emergency and
(short-acting) urgency
• Perioperative hypertension during
cardiac surgery
• Stroke with hypertension
• Patients with ACS and congestive
cardiac failure
• Eclampsia/preeclampsia
• Sympathetic crisis
Enalaprilat 7
ACE inhibitor • Hypertension with congestive
cardiac failure
• Patients with severe hypertension
who are at risk of cerebral
hypotension
• Prevention of worsening of renal
function in patients with diabetic
and non-diabetic nephropathy
• Perioperative hypertension
Esmolol 7,9
Cardioselective beta- • Acute MI
blocker • Perioperative hypertension
• Severe postoperative hypertension
when cardiac output, heart rate
and BP are increased
43
DIPLOMA PROGRAM
POST GRADUATE IN PROGRAM IN
EXCELLENCE
CARDIACEMERGENCIES
EMERGENCIES
GENERAL PRACTICE
GENERAL PRACTICE
An initial dose of 0.1 mcg/kg/minute,
increased by 0.05-0.1 mcg/kg/minute to a
maximum of 1.6 mcg/kg/minute
• Initial dose: 1-2 mg/hour IV infusion
• Dose titration: The initial dose may be
doubled at short intervals (90-second)
initially. As target BP is approached, the
dose increase should be lowered to less
than double and the interval between
these escalations should be increased to
every 5-10 minutes. Of note, an increase
of 1-2 mg/hour will generally produce an
additional 2-4 mm Hg decrease in systolic
BP
• Maintenance dose: The target BP is
generally achieved at the dose of 4-6 mg/
hour. Nevertheless, higher doses may be
required for severe hypertension
• Maximum dose: 16-21 mg/hour
Initial dose at 5 mg/hour IV, increased every
5 minutes by 2.5 mg/hour until target
range BP is achieved. Maximum dose is 15
mg/hour. If target BP is reached within 30
minutes, the infusion rate may be lowered to
3 mg/hour with subsequent adjustments to
maintain target range BP
1.25 mg IV over 5 minutes every 6 hours,
with increase of 1.25 mg at 12-24 hour
interval up to a maximum of 5 mg every 6
hourly
LD of 500–1000 mcg/kg IV over 1 minute,
followed by an infusion starting at 25-50
mcg/kg/minute that can be increased up
to 300 mcg/kg/minute to achieve desirable
effects
 DIPLOMA
POST PROGRAM
GRADUATE INPROGRAM IN
EXCELLENCE
CARDIAC EMERGENCIES
IN GENERAL PRACTICE
references
1. overgaard CB, Dzavík v. Inotropes and vasopressors: review of Physiology
and Clinical Use in Cardiovascular Disease. Circulation. 2008;118:1047-1056.
2. Peberdy MA, Callaway CW, neumar rW, et al. Part 9: Post–Cardiac Arrest
Care. 2010 American Heart Association guidelines for Cardiopulmonary
resuscitation and Emergency Cardiovascular Care. Circulation.
2010;122:S768-S786.
3. Poole-Wilson PA, opie lH. Digitalis, Acute Inotropes, and Inotropic Dilators.
Acute and chronic heart failure. Chapter 6. In: opie lH, gersh BJ. Drugs for
the Heart. 6th Edition. Elsevier Saunders;2005.149-183.
4. Canadian Agency for Drugs and technologies in Health (CADtH).
vasopressin as first-line therapy for cardiac arrest: A review of the guidelines
and clinical-effectiveness. CADTH Technol Overv. 2010;1(2):e0112.
5. Krismer AC, Dünser MW, lindner KH, et al. vasopressin during
cardiopulmonary resuscitation and different shock states: A review of the
literature. Am J Cardiovasc Drugs. 2006;6(1):51-68.
6. Kumar A, Cannon CP. Acute Coronary Syndromes: Diagnosis and
Management, Part I. Mayo Clin Proc. 2009;84(10):917-938.
7. varon J, Marik PE. Perioperative hypertension management. Vascular Health
and Risk Management. 2008;4(3):615–627.
8. opie lH, White HD. nitrates. Chapter 2. In: opie lH, gersh BJ. Drugs for
the Heart. 6th Edition. Elsevier Saunders;2005.33-49.
9. Angelats Eg, Baur EB. Hypertension, hypertensive crisis, and hypertensive
emergency: approaches to emergency department care. Emergencias.
2010;22:209-219.
10. Kaplan nM, opie lH. Antihypertensive Drugs. Chapter 7. In: opie lH,
gersh BJ. Drugs for the Heart. 6th Edition. Elsevier Saunders;2005.184-217.
11. trappe HJ. treating critical supraventricular and ventricular arrhythmias. J
Emerg Trauma Shock. 2010 Apr;3(2):143-52.
12. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines
for Management of Patients With ventricular Arrhythmias and the Prevention
of Sudden Cardiac Death—Executive Summary. Circulation. 2006;114:1088-
1132.
13. DiMarco JP, gersh BJ, opie lH. Antiarrhythmic Drugs and Strategies.
Chapter 8. In: opie lH, gersh BJ. Drugs for the Heart. 6th Edition. Elsevier
Saunders;2005.218-274.
14. MacIntyre P, Hillis WS. Pharmacological treatment of significant cardiac
arrhythmias. Br J Sports Med. 2000;34:401–402.
15. opie lH. Calcium Channel Blockers (Calcium Antagonists). Chapter
3. In: opie lH, gersh BJ. Drugs for the Heart. 6th Edition. Elsevier
Saunders;2005.50-79.
16. Selwyn AP, Braunwald E. Ischemic Heart Disease. Chapter 226. In: Kasper
Dl, Braunwald E, fauci AS, et al. 16th Edition (vol II). USA:Mcgraw Hill;
2005.1434-1444.
44
17. Josephson ME, Zimetbaum P. The tachyarrhythmias. Chapter 214. In: Kasper
Dl, Braunwald E, fauci AS, et al. 16th Edition (vol II). USA:Mcgraw Hill;
2005.1342-1358.
18. Schmidt C, Wiedmann f, Schweizer PA, et al. Class I antiarrhythmic drugs
inhibit human cardiac two-pore-domain K(+) (K2P) channels. Eur J
Pharmacol. 2013 Dec 5;721(1-3):237-48.
19. rolf S, Bruns HJ, Wichter t, et al. The ajmaline challenge in Brugada
syndrome: Diagnostic impact, safety, and recommended protocol. European
Heart Journal. 2003;24:1104–1112.
20. Baim DS, grossman W. Diagnostic cardiac catheterization and angiography.
Chapter 212. In: Kasper Dl, Braunwald E, fauci AS, et al. 16th Edition (vol
II). USA:Mcgraw Hill; 2005.1327-1333.
21. Mitchell ArJ, Chalil S, Boodhoo l, et al. Diazepam or midazolam for external
DC cardioversion (The DorM Study). Europace. 2003;5:391–395.
22. Sinner B, graf BM. Ketamine. Handb Exp Pharmacol. 2008;(182):313-33.
23. Pai A, Heining M. Ketamine. Continuing Education in Anaesthesia, Critical Care
& Pain. 2007;7(2):59-63.
24. oparil S, Aronson S, Deeb gM, et al. fenoldopam: a new parenteral
antihypertensive: consensus roundtable on the management of perioperative
hypertension and hypertensive crises. Am J Hypertens. 1999 Jul;12(7):653-
64.
25. Sarafidis PA, georgianos PI, Malindretos P, et al. Pharmacological management
of hypertensive emergencies and urgencies: focus on newer agents. Expert
Opin Investig Drugs. 2012 Aug;21(8):1089-106.
26. goldenberg MM. Pharmaceutical Approval Update. P&T. 2008;33(9):550-
553.
27. Aronson S. Clevidipine in the treatment of perioperative hypertension:
assessing safety events in the EClIPSE trials. Expert Rev Cardiovasc Ther. 2009
May;7(5):465-72.
28. Singla n, Warltier DC, gandhi SD, et al. treatment of acute postoperative
hypertension in cardiac surgery patients: an efficacy study of clevidipine
assessing its postoperative antihypertensive effect in cardiac surgery-2
(ESCAPE-2), a randomized, double-blind, placebo-controlled trial. Anesth
Analg. 2008 Jul;107(1):59-67.
29. Cannon CM, levy P, Baumann BM, et al. Intravenous nicardipine and labetalol
use in hypertensive patients with signs or symptoms suggestive of end-organ
damage in the emergency department: A a subgroup analysis of the ClUE
trial. BMJ open. 2013;3:e002338.
30. Peacock Wf 4th, Hilleman DE, levy PD, et al. A systematic review of
nicardipine vs labetalol for the management of hypertensive crises. Am J Emerg
Med. 2012 Jul;30(6):981-93.
31. Handbook of Emergency Cardiovascular Care for Healthcare Providers.
American Heart Association, Eds. Hazinski, Mf, Samson r, Schexnayder S.
2010.
 DIPLOMA PROGRAM
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EMERGENCIES
IN IN
GENERAL PRACTICE
GENERAL PRACTICE

case studies
Case study 1
A case of sudden cardiac syncope
secondary to prior myocardial infarction

A 67-year old male was seen following a syncopal episode lasting 10-15 seconds. It occurred on a warm day while he was
standing talking to a friend. There was no accompanying chest discomfort, shortness of breath, or palpitations. fourteen
years earlier he has sustained a large anterior myocardial infarction (MI) with right ventricular apical involvement. His
medications included: losartan, metoprolol succinate, furosemide, spironolactone, low dose digoxin, low dose aspirin, atorvastatin,
warfarin, and lantus insulin. He had stable AHA class II heart failure symptoms. He has been compliant with medications. Post
infarction transthoracic echocardiogram (TTE) showed an lvEf of 35%. Seven years later repeat TTE revealed lvEf of 30%, grade
1 lv diastolic dysfunction, normal rv size and systolic function, and normal biatrial size.
on physical examination, the weight was 64.7 kg and stable, the BP was 100/66 mm Hg RA sitting and 94/64 mm Hg RA
standing without postural dizziness, Hr was 73/minute, o2 was 99% and S3 was audible, with wide split S2. There was no jugular
venous distension ( JvD), hepatojugular reflux (HJr), ankle edema or abdominal distention. An ECg showed sinus rhythm,
left atrial enlargement, right bundle branch delay with QrS width of 174 msec, left anteriorhemiblock and frequent premature
ventricular beats; Q waves in v1-4 were indicative of the old anterior infarction (see ECg). An ICD without resynchronization
was installed.

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 DIPLOMA
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CARDIAC EMERGENCIES
IN GENERAL PRACTICE

Q1. The patient did not receive an ICD after his previous MI because:
A) He did not have sustained vt
B) He did not have vf with his acute MI
C) His lvEf of 35%, 40 days after his MI did not qualify him
D) He did not have a long Qt syndrome

Q2. When the ICD was implanted 14 years after his MI, resynchronization was not done (3rd electrode) because:
A) His Qt interval was not wide enough
B) He did not have documented vt or vf
C) His heart failure symptoms were not severe enough
D) His ECg showed a very wide QrS but with right as opposed to left bundle branch block

Answers: Q1 C; Q2 D

Case study 2

Sudden cardiac arrest in a 59-year

old male without heart disease

A 59-year old male in previously normal health collapsed while shopping in a pharmacy. Bystander CPr was initiated and
emergency medical services (EMS) summoned. They arrived within 10 minutes. A quick look ECg revealed ventricular
fibrillation (vf) and a 200 J DC countershock delivered with restoration of sinus rhythm. The patient was awake but
agitated and appeared to be moving all 4 extremities. He was conveyed rapidly to the hospital emergency department where his BP
was 140/90 mm Hg and Hr 110/minute, rr was 18/minute and the temp 99° f.
Exam showed no evidence of CHf or focal neurologic abnormalities. Blood tests were normal, except for a troponin I level of
2.6 (normal < 0.025). An ECg showed sinus tachycardia at 110/minute with normal Pr, QrS, Qtc intervals. St-t waves were
normal, except for 0.5 mm St elevation in v4-6. no premature beats were evident. The patient was initially confused but became
normally oriented over 48 hours. A transthoracic echocardiogram showed normal cardiac chamber sizes and cardiac valves. lvEf
was 65% with normal diastolic function; lv mass was normal. repeat ECg showed sinus rhythm at 79/minute with a pattern of
early repolarization anteriorly. J-waves were evident in the outer distal leads (see ECg). further history revealed sudden death in a
paternal uncle and cousin. At cardiac catheterization, left and right sided cardiac pressures were normal and there was no coronary
atherosclerosis. An implantable cardiac defibrillator was installed.

46
 DIPLOMA PROGRAM
POST GRADUATE IN PROGRAM IN
EXCELLENCE
CARDIAC
CARDIACEMERGENCIES
EMERGENCIES
IN IN
GENERAL PRACTICE
GENERAL PRACTICE

Q1. This case represents an example of:

A) Brugada Syndrome
B) Arrhythmogenic right ventricular dysplasia
C) long Qt syndrome
D) Primary coronary disease
E) J-wave, related early repolarization with primary ventricular fibrillation

Q2. J-waves are attributable to:

A) An increase in net repolarization current due to a decrease of inward currents or an increase of outward currents during early
repolarization (phase 2 of the action potential)
B) Prominent Ito epicardial mediated notch in the action potential
C) Bradycardia, offsetting slow recovery from an activation of Ito
D) Can be unmasked by sodium or calcium channel blocker drugs
Answers: Q1 E; Q2 A-D

47
 DIPLOMA
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CARDIAC EMERGENCIES
IN GENERAL PRACTICE

Case study 3

A 74-year old man with chest pain

A 74-year old man called for emergency medical services (EMS) because of chest pain which had been present for 1-2 hours
intermittently. Initial BP was 150/70 mm Hg, Pr was 81/minute and rr was 20/minute. ECg revealed sinus rhythm
with anteroseptal St elevation and inferolateral St depression (see ECg 1). to this patient, ASA, beta-blocker, heparin
and lidocaine were administered and he was rapidly transported to the emergency department. The cardiac catheterization team,
which had been alerted, performed emergency coronary angiography and a drug eluting stent (DES) was positioned in his left
anterior descending coronary (lAD) artery after which he was transported to the cardiac care unit (CCU). In the CCU, wide
complex tachycardia with QrS of 160 msec, lBBB configuration, r to S nadir of > 60 msec and small Q-wave in v6 was noted
(see ECg 2).
lidocaine infusion was stopped and amiodarone 150 mg Iv bolus followed by 1mg/minute over 6 hours and then 0.5 mg/
minute over 18 hours was given. ventricular ectopy gradually subsided over this time interval. ACE inhibitor, beta-blocker, ASA,
statin and heparin for 48 hours were continued or initiated. A predischarge transthoracic echocardiogram showed lvEf of 45%
with septal hypokinesia.

ecg 1

48
 DIPLOMA PROGRAM
POST GRADUATE IN PROGRAM IN
EXCELLENCE
CARDIAC
CARDIACEMERGENCIES
EMERGENCIES
IN IN
GENERAL PRACTICE
GENERAL PRACTICE

ecg 2

Q1. If a wide QRS ventricular tachycardia develops in the setting of an acute MI with or without a cardiac arrest, the
preferred antiarrhythmic drug would be
A) Iv bolus and infusion of lidocaine
B) Iv bolus and infusion of procainamide
C) Iv bolus and infusion of sotalol
D) Iv bolus and infusion of amiodarone

Q2. An implantable defibrillator is indicated for this patient:

A) Before hospital discharge
B) 40 days after hospital discharge
C) Is not indicated
D) 40 days after hospital discharge, if monitoring by Holter recorder or ECg shows 3 beat ventricular tachycardia

Answers: Q1 D; Q2 C

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 POST GRADUATE EXCELLENCE PROGRAM IN
CARDIAC EMERGENCIES
IN GENERAL PRACTICE
Updates
Ventricular tachyarrhythmias
Ventricular arrhythmias include a wide spectrum of arrhythmias
ranging from single ectopics to sustained ventricular tachycardias
(VT) and ventricular fibrillations (VF). With time mechanisms
of VT, particularly those associated with structural heart diseases
have been better understood and therefore a wide array of
investigation modalities (both non-invasive and invasive), many
of them recently developed, are being used in their diagnostic
and management approach. Echocardiography, cardiac CT,
cardiac magnetic resonance imaging (CMR), and nuclear
studies are being actively used in work-up for ventricular
arrhythmias; with cardiac CT and CMR-derived scar data
correlating well with electroanatomic mapping reconstructions.
Regarding pharmacotherapy, amiodarone, procainamide and
lidocaine continue to be preferred in the emergency settings
for terminating ventricular arrhythmias; recently IV sotalol
was shown to be more promising than lidocaine in terminating
sustained VT acutely.1
Sudden cardiac death
Regarding sudden cardiac death (SCD), left ventricular ejection
fraction (LVEF) has been recognized as a useful prognostic
marker for SCD over the years, although more recently it has
been shown to have limited sensitivity and specificity as a risk
stratification marker for SCD. Many novel SCD risk predictors
(including race/ethnicity, genomics, vulnerable myocardium,
and environmental triggers) have been identified, best when
used in combination, and may identify “high-risk” patients for
SCD.2 An implantable cardioverter defibrillator (ICD) remains
the standard treatment of patients who survive an out-of-hospital
cardiac arrest; however if ICD implantation is not possible due
50
Echocardiography, cardiac CT,
cardiac magnetic resonance
imaging (CMR), and nuclear
studies are being actively used
in work-up for ventricular
arrhythmias
to clinical contraindications or when patients remain undecided
about having an ICD, the ZOLL® LifeVest may be considered
as a bridge to ICD implantation or until the arrhythmic risk
subsides.3 Additionally, ICD also remains the mainstay of
prevention of SCD in ventricular arrhythmias. However, it
is noteworthy that while ICD should be strongly considered
for primary prevention of SCD in patients at highest risk,
pharmacological treatment may be considered for prevention
of SCD in select channelopathies; flecainide may be considered
in Catecholaminergic Polymorphic Ventricular Tachycardia
(CPVT) [surgical left cardiac sympathetic denervation in
refractory cases], beta-blockers in long QT syndrome (LQTS),
and quinidine for treatment of recurrent ventricular arrhythmias
in ICD-supported patients with Brugada syndrome.2 The
2017 American College of Cardiology/American Heart
Association/Heart Rhythm Society (ACC/AHA/HRS)
guidelines4 on management of ventricular arrhythmias and the
prevention of SCD have been recently provided. Some of the
prominent features are enumerated below:

Regarding management of
patients with hemodynamically
stable VT, IV procainamide can be
useful to attempt to terminate the
episode; in these subset of patients,
administration of IV amiodarone
or sotalol may also be considered
to attempt to terminate VT
•• In patients with known or suspected ventricular arrhythmias
that may be associated with structural heart disease or risk
of sudden cardiac arrest, echocardiography can be useful
for outlining structural and functional characteristics of
the heart (COR I; LOE B-NR); if structural heart disease is
suspected, CMR or cardiac CT can detect and characterize
underlying heart disorder (COR IIa; LOE C-EO). Also, in
patients with known structural heart disease, measurement
of natriuretic peptides (BNP or N-terminal pro-BNP) may
provide added prognostic information for predicting SCD
(COR IIa; LOE B-NR)
•• Regarding management of patients with hemodynamically
stable VT, IV procainamide can be useful to attempt to
terminate the episode (COR IIa; LOE A); in these subset
of patients, administration of IV amiodarone or sotalol may
also be considered to attempt to terminate VT (COR IIb;
LOE B-R)
•• On the other hand patients presenting with ventricular
arrhythmia and hemodynamic instability should undergo
direct current cardioversion (COR I; LOE A); if in
patients of ventricular arrhythmia and hemodynamic
instability, disturbance in ventricular rhythm persists or
recur after a maximal energy shock, IV amiodarone should
be administered to achieve stable rhythm after further
defibrillation (COR I; LOE A)
•• In polymorphic VT due to myocardial ischemia, treatment
with IV beta-blockers can be useful (COR IIa; LOE B-R)
Recommendations for prevention of SCD in patients with ischemic
heart disease
•• In patients of ischemic heart disease with resultant LVEF of
< 35% who are at least 40 days’ post-MI and at least 90 days’
post-revascularization, and with NYHA class II or III heart
51
POST GRADUATE EXCELLENCE PROGRAM IN
CARDIAC EMERGENCIES
IN GENERAL PRACTICE
failure despite guideline-directed management and therapy,
an ICD is recommended if meaningful survival of > 1 year
is expected (primary prevention of SCD) (COR I; LOE A)
•• In patients of ischemic heart disease with resultant LVEF
of < 30% who are at least 40 days’ post-MI and at least 90
days’ post-revascularization, and with NYHA class I heart
failure despite guideline-directed management and therapy,
an ICD is recommended if meaningful survival of > 1 year
is expected (primary prevention of SCD) (COR I; LOE A)
•• In patients with NSVT due to prior myocardial infarction,
LVEF of < 40% and inducible sustained VT/VF at
electrophysiological study, an ICD is recommended if
meaningful survival of > 1 year is expected (primary
prevention of SCD) (COR I; LOE B-R).4
(Abbreviations: COR - Class of recommendation; LOE – Level of evidence. For a complete
review of the guidelines, COR, and LOE, please visit: Al-Khatib SM, Stevenson WG,
Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow
GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD,
Myerburg RJ, Page RL. 2017 AHA/ACC/HRS guideline for management of patients with
ventricular arrhythmias and the prevention of sudden cardiac death: Executive summary:
A Report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2018
Oct;15(10):e190-e252. doi: 10.1016/j.hrthm.2017.10.035. Epub 2017 Oct 30.)
Post-cardiac arrest syndrome
Cardiac arrest can have multiple causes. Following return
of spontaneous circulation (ROSC) after a cardiac arrest,
all efforts should be made to identify the cause of arrest and
manage it immediately.5 Since acute myocardial infarction (MI)
is an important cause, early invasive coronary angiography
should be considered to identify and treat coronary artery
obstructive disease.6 Most patients in the post-ROSC phase
are hemodynamically unstable; efforts should be made to
Most patients in the post-ROSC
phase are hemodynamically
unstable; efforts should be made
to avoid hypotension and achieve
a systolic blood pressure of at
least 90 mmHg or a mean arterial
pressure of 65 mmHg following
resuscitation
 POST GRADUATE EXCELLENCE PROGRAM IN
CARDIAC EMERGENCIES
IN GENERAL PRACTICE
avoid hypotension and achieve a systolic blood pressure of
at least 90 mmHg or a mean arterial pressure of 65 mmHg
following resuscitation. Supplemental oxygen is recommended
to maintain SpO2 of 94%–98%. Judicious use of IV fluids and
inotropic drugs to optimise blood pressure, cardiac output and
urine output is necessary. Cardiac output, tissue perfusion and
oxygen delivery should be optimized to achieve an ScvO2 ≥ 70%.
Targeted temperature management (temperature of 33°C–36°C
and maintained for at least 24 hours) after ROSC may confer
neuroprotection and improved neurological outcomes. 5
However, maximum target temperature should not exceed
36°C.6 It is also advisable to maintain blood glucose between
6–10 mmol/L through regular blood glucose monitoring
and insulin therapy.5 Although prophylactic anticonvulsant is
not beneficial, seizures, if they occur, should be treated with
benzodiazepines and anticonvulsant drugs.6
52
References
1. Batul SA, Olshansky B, Fisher JD, Gopinathannair R. Recent advances in the
management of ventricular tachyarrhythmias. Version 1. F1000Res. 2017; 6: 1027.
2. Chugh SS. Sudden Cardiac Death in 2017: Spotlight on Prediction and Prevention.
Int J Cardiol. 2017 Jun 15; 237: 2–5.
3. Srinivasan NT, Schilling RJ. Sudden Cardiac Death and Arrhythmias. Arrhythm
Electrophysiol Rev. 2018 Jun; 7(2): 111–117.
4. Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal
BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky
MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL. 2017 AHA/ACC/HRS
guideline for management of patients with ventricular arrhythmias and the prevention
of sudden cardiac death: Executive summary: A Report of the American College of
Cardiology/American Heart Association Task Force on Clinical Practice Guidelines
and the Heart Rhythm Society. Heart Rhythm. 2018 Oct;15(10):e190-e252. doi:
10.1016/j.hrthm.2017.10.035. Epub 2017 Oct 30.
5. Pothiawala S, Post-resuscitation care. Singapore Med J. 2017 Jul; 58(7): 404–407.
6. Kang Y. Management of post-cardiac arrest syndrome. Acute Crit Care. 2019 Aug;
34(3): 173–178.
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IN GENERAL PRACTICE

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