Sudden cardiac death a systematic approach

Sudden cardiac death: A systematic
approach
Speaker:
DR . Ashutosh Tiwari

Is the topic “ sudden cardiac death”
appropriate?

 In 2009 a 12 year old class VII student in Delhi collapsed on her school's football field
and died within minutes due to cardiac arrest.
 Smitu Kothari, 59, one of India’s leading social and environmental activists, died of a
cardiac arrest at Delhi in March 2009.
 Shiv Charan Mathur, Governor of Assam died of cardiac arrest in Delhi at the age of 83
in June, 2009.
 Kishore Sarja, a noted film director from South India died of cardiac arrest in June,
2009 at Bangalore at the age of 50.
 A 27-year-old pilgrim from Punjab died of cardiac arrest at the 3,880 metre high cave
shrine of Amarnath.
 And millions of music lovers across the world were left grieving the loss of pop icon
Michael Jackson, who is said to have died due to cardiac arrest induced by painkillers.
 As per WHO census statistics mortality due to cardiac causes has overtaken mortality
due to all cancers put together. Approximately 4280 out of every one lakh people die
every year from SCA in India alone.
Death in news

Mr. K is 55 yr old senior corporate manager who had bypass
surgery done in 2000 after he was found to have blockages in
all the 3 arteries and a weak heart. (Triple vessel disease with
LV dysfunction). Following a successful surgery he took his
medications regularly and maintained a healthy lifestyle. He
had two recent episodes of dizziness one of which resulted in
a transient loss of consciousness. He dismissed these
symptoms as insignificant.
 His family was devastated when he was found dead in his
bed one morning.
 Ms R is a young lady who is very concerned after her 28 yr
old brother died suddenly with no obvious disease.

 Mr K family who constantly ask themself if there was
something that could have been done to prevent this
tragedy?
 Ms R wants to know if her family members are at a similar
risk?
 Considerable research in this area has been done in the last
decade addressing these issues, which has enhanced our
knowledge to recognize and help such patients.

 DEFINITION
 Magnitude of the Problem
 WHO ARE AT RISK ?
 PATHOPHYSIOLOGY
 Clinical Characteristics of Cardiac Arrest
 SURVIVAL WITH INTERVENTION
 INTERVENTIONS
OUTLINE

Term Cardiovascular collapse Cardiac arrest Sudden
cardiac
death
Definition Sudden loss of effective
blood flow due to cardiac
and/or peripheral vascular
factors that may reverse
spontaneously (e.g.syncope)
or require interventions (e.g.,
cardiac arrest)
Abrupt cessation of cardiac
mechanical function, which
may be reversible by a prompt
intervention but will lead to
death in its absence
Sudden,
irreversible
cessation
of all
biological
functions
Qualifiers Nonspecific term: includes
cardiac arrest and its
consequences and
transient events that
characteristically revert
spontaneously
Rare spontaneous reversions;
likelihood of successful
intervention relates to
mechanism of arrest, clinical
setting, and prompt return of
circulation
none
Mechanisms Same as "Cardiac Arrest,"
plus vasodepressor syncope
or other causes of transient
loss of blood flow
VT, VF, Asystole , Bradycardia,
pulseless electrical activity

 Frequency
 United States
 approximately 325,000 deaths per year ; more than that due to lung
cancer, breast cancer, or AIDS.
 SCD is often the first expression of CAD and is responsible for
approximately 50% of deaths from CAD.
 International
 In Western industrialized nations- similar to the U. S.
 In other countries - varies as a reflection of the prevalence of CAD or
other high-frequency cardiomyopathies in those populations.
MAGNITUDE OF THE PROBLEM

Increasing SCD events in developing nations is thought to
reflect a change in dietary and lifestyle habits in these nations.
 As per WHO census statistics mortality due to cardiac causes
has overtaken mortality due to all cancers put together.
Approximately 4280 out of every one lakh people die every year
from SCA in India alone.
 It has been estimated that SCD claims more than 7,000,000
lives per year worldwide.

Mortality/Morbidity
only 20% of patients with out-of-hospital cardiac arrest survive
to hospital discharge ( in ideal conditions).
 anoxic encephalopathy(30-80%) – major adverse outcome from
a SCD event

 Race
 inconclusive data
 Some studies suggest - greater proportion of coronary deaths were "sudden" in blacks
 Gillum et al ( 1980-1985) - percentage of CAD deaths occurring out of the hospital and in
EDs was found to be higher in blacks
 Sex
 Men :women = 3:1. reflecting the higher incidence of obstructive coronary artery disease
in men.
 Observational data point to the fact - men = plaque rupture,
 women= plaque erosion.
 Whether this biologic difference accounts for the male predominance of SCD is unclear.
Who are at risk

 Age
 Bimodal- between birth and 6 months (SIDS) then again
between 45 and 75 years (coronary artery disease)
 In the Framingham study, the proportion of coronary artery disease
deaths that were sudden was
62% in men aged 45-54 years, but this percentage fell to
58% in men aged 55-64 years and to
42% in men aged 65-74 years.
 the proportion of deaths that are sudden from coronary artery disease
decreases with age.

9/9913
Incidence of Sudden Death Increases with
Age
During a 38 years follow-up of subjects in the Framingham
Heart Study, the annual incidence of sudden death increased
with age in both men and women.However, at each age, the
incidence of sudden death is higher in men than women. (Am
Heart J 1998; 136:205)

Mortality rates in deaths per 100 000 for patients with ischemic heart disease occurring out of
hospital or in emergency room (estimate for sudden cardiac death rate) (A) and occurring in
hospital, according to age, sex, and race in 48 states during 1985 (B).
Zipes D, Wellens H. Circulation 1998;98:2334-2351
Copyright © American Heart Association

Anatomy
 autopsy -acute changes in coronary plaque morphology,
such as thrombus,
plaque disruption, or both,
in 50% of cases of sudden coronary death,
in hearts with myocardial scars and no acute infarction-
active coronary lesions 46% ofcases.
 because mechanisms responsible for sudden cardiac death depend in part on
anatomic substrate, which naturally varies from one individual to another,
 the usefulness of risk assessment modalities varies from one patient and
particular type of anatomic substrate to another.

Activity
 somewhat controversial.
 Vigorous exercise -trigger sudden cardiac death and acute myocardial infarction
(possibly by increasing platelet adhesiveness and aggregability)
 Moderate exercise-may be beneficial
Evidences
 Annual incidence of SCD during exercise - 1 per 200 000 to 250 000 healthy young
 Very rare in athletes - only 20 to 25 annually in the U.S.(despite the publicity)
 Cardiac rehabilitation programs- cardiac arrests occur at a rate of 1 in 12 000
 During stress testing - cardiac arrest occurs at a rate of 1 per 2000
 Experimentally- regular exercise in dogs prevents ischemia induced VF and death by
increasing vagal activity
 Thus, regular exercise decreases cardiovascular morbidity and mortality, whereas
vigorous exercise, particularly in untrained individuals, may have an adverse effect.
 In the Maastricht Sudden Death study, 67% of the sudden death victims were
physically inactive at the time of the event.

Other risk factors
 Smoking is an important risk factor.
In the Framingham study, the annual incidence increased from 13 per 1000 in
nonsmokers to almost 2.5 times of that for people who smoked 20 cigarettes
per day.
Stopping smoking promptly reduced this risk.
 Elevated serum cholesterol appears to predispose patients to rupture of vulnerable
plaques( whereas cigarette smoking predisposes patients to acute thrombosis)
 Emotional stress can be an important trigger for sudden cardiac death, as shown by
the Northridge earthquake that struck the Los Angeles area at 4:31 AM January 17,
1994.
 Depression in a patient in the hospital after myocardial infarction is a significant
predictor of the 18-month post–myocardial infarction cardiac mortality, and the risk
associated with depression was greatest among patients with frequent premature
ventricular complexes.
 Socioeconomic factors are also important; sudden cardiac death after myocardial
infarction increases 3-fold in men with low levels of education and complex
ventricular ectopy compared with better educated men who have the same
arrhythmias.

Risk of sudden cardiac death by decile of multivariate risk: 26-year follow-up, Framingham
Study.

Impaired left ventricular function
 Left ventricular dysfunction is a major independent predictor of total and sudden cardiac
mortality in patients with ischemic and non-ischemic cardiomyopathy.
 For example, in survivors of cardiac arrest who have a LVEF <30%,
the risk of sudden cardiac death exceeds 30% over 1 to 3 years( if the patients
do not have inducible ventricular tachycardia)
 whereas it ranges between 15% and 50% in those who have inducible ventricular
tachyarrhythmias despite therapy with drugs that suppress the inducible arrhythmias or
with empirical amiodarone.

Relationship between left ventricular ejection fraction (EF) and ventricular premature
depolarizations (VPD) and survival during 3 years of follow-up after myocardial infarction.

 Certain ECG abnormalities can help identify patients at increased risk for sudden
cardiac death.
 These include the presence of AV block or
intraventricular conduction defects and
QT prolongation,
 an increase in resting heart rate to 90 bpm, and increased QT dispersion in survivors
of out-of hospital cardiac arrest.
 A recent study failed to support the usefulness of QT dispersion in predicting risk in
patients after myocardial infarction.
 The presence of complex ventricular arrhythmias, such as nonsustained ventricular
tachycardia, is also a marker.

 History can provide clues to the high-risk patient.
 For example, in patients with ventricular tachycardia after myocardial infarction,
on the basis of clinical history, the following 4 variables identify patients at
increased risk of sudden cardiac death:
 (1) syncope at the time of the first documented episode of arrhythmia,
 (2) NYHA class III or IV,
 (3) ventricular tachycardia/fibrillation occurring early after myocardial infarction (3
days to 2 months), and
 (4) history of previous myocardial infarctions.
 In some patients, family history can be important.

PATHOPHYSIOLOGY

Transient Risk Factors
 Unfortunately, most of these more stable risk factors lack sufficient sensitivity,
specificity, and predictive accuracy to pinpoint the patient at risk with a degree of
accuracy that would permit using a specific therapeutic intervention before an
actual event.
 This probably relates, at least in part, to the transient nature of many risk factors,
such as myocardial ischemia and reperfusion;
hemodynamic dysfunction;
electrolytes( hypokalemia and hypomagnesemia )
changes in pH or PO2;
influence of central and peripheral neurophysiological actions;
transient effects of toxins (drugs or alcohol)
 Structural cardiac abnormalities of the myocardium, coronary arteries, or cardiac
nerves provide the substrate on which a transient risk factor operates.
 Myocardial hypertrophy, congestive heart failure, and cardiac dilation as well as
regional autonomic dysfunction all may be important.

 Thus, if structural factors for the most part only create a substrate on which the
transient factors operate to initiate a ventricular tachyarrhythmia, risk
identification requires finding those subjects whose inherent physiological
characteristics make the initiation of electrophysiological instability more likely
when these conditions are met.
 This requires clinically identifiable,
genetically based or acquired,
individual differences in the responses of membrane channels,
receptors,
exchangers, and
pumps in the susceptible
individual,
 a formidable challenge at present.
 Patients with the congenital long-QT syndrome serve as the prototypic example
of the interaction between a molecular myocardial abnormality, an “ionopathy,”
and an inciting event, eg, exercise in LQT1 and sleep/rest in LQT3.

DRUGS
 Antiarrhythmic drugs have long been known to be capable of provoking ventricular
tachyarrhythmias and sudden cardiac death.
 Non-antiarrhythmic drugs that prolong repolarization along with class IA
antiarrhythmic agents, can cause torsade de pointes.
 Class IC drugs in the CAST study
• An antiarrhythmic drug can create the abnormality on which a transient risk
event, such as ischemia, interacts to provoke a lethal arrhythmia.
• For example, in the CAST experience, despite the increased risk of sudden cardiac
death established by the presence of complex forms of ventricular ectopy,
particularly in older age groups and in patients post myocardial infarction,
• suppression of those ventricular arrhythmias with encainide and flecainide
conferred an increased risk of death and/or no improvement in survival with
moricizine.

 The results of CAST taught us at least 3 important lessons:
(1)that mechanisms responsible for premature ventricular complexes, which were
suppressed, were different from mechanisms that caused sudden cardiac death,
presumably from a ventricular tachyarrhythmia, which was increased;
(2) that proarrhythmia from an antiarrhythmic agent could occur months after drug
initiation and was not always an early event; and
(3) that antiarrhythmic drugs could become a risk factor when the myocardial
substrate changed, presumably when ischemia developed.
 Drug-drug interactions during poly-pharmacy can be dangerous, even with
apparently innocuous medications.
 Phosphodiesterase inhibitors and other positive inotropic agents that increase
intracellular calcium loading have also been demonstrated to exert proarrhythmic
actions and increase the risk of sudden cardiac death.

ELECTROLYTES
 Hypokalemia (in some instances provoked by potassium-wasting diuretics),
hypomagnesemia, and increased intracellular calcium concentration may be
important as primary or triggering events.
 It is sometimes difficult to determine whether a patient resuscitated from
ventricular fibrillation had the arrhythmia provoked by hypokalemia,
 because in the postresuscitation period, serum concentrations of potassium may be
reduced because of the effects of catecholamine release after the cardiac arrest.
 Thus, unless there is a history of electrolyte imbalance, drugs known to deplete
potassium, special diets such as the liquid protein diet, or documented electrolyte
abnormalities when the patient is in a steady state, the diagnosis of hypokalemia
may be in doubt.
 And search for other cause or precipitator should also be made

Autonomic Nervous System
 Abnormalities of the autonomic nervous system appear to be involved in the
genesis of sudden cardiac death.
 Myocardial infarction, for example, produces regional cardiac sympathetic and
parasympathetic dysfunction not only in the infarcted area but also in regions
apical to the infarct, presumably because of interruption of afferent and efferent
nerve fibers traversing the infarct .
 Denervated regions show supersensitivity to catecholamine infusion, with
disproporti-onate shortening of refractoriness that creates autonomic
heterogeneity, resulting in dispersion of refractoriness and/or conduction, which
can be conducive to development of ventricular arrhythmias.
 Any process that creates electrical heterogeneity favors the development of
ventricular fibrillation.
 Recent data indicate that sympathetically denervated ventricular myocardium
demonstrates abnormal oxygen utilization, which could also affect
arrhythmogenesis (G.D. Hutchins, PhD, unpublished observations, 1998).

 Most data suggest that vagal stimulation, profibrillatory for the atria, mitigates the
development of ventricular arrhythmias in a variety of experimental situations.
 Whether parasympathetic stimulation is protective because of a direct
electrophysiological effect on ventricular myocardium, by opposing sympathetic
actions, or by albeit minimally prolonging refractoriness is not known.
 Reductions in heart rate variability, as well as baroreflex sensitivity, identify
patients at risk for a subsequent cardiac event.
 Vagal stimulation can terminate a specific type of ventricular tachycardia originating
in the right ventricular outflow tract, but neural innervation at that site may be
unique.

CHD
I. Coronary heart disease
A. Coronary artery abnormalities
1. Chronic atherosclerotic lesions
2. Acute (active) lesions (plaque
fissuring, platelet aggregation, acute
thrombosis)
3. Anomalous coronary artery
anatomy
B. Myocardial Infarction
1. Healed
2. Acute
CARDIOMYOPATHIES
II. Myocardial hypertrophy
A. Secondary
B. Hypertrophic cardiomyopathy
1. Obstructive
2. Non-obstructive
III. Dilated cardiomyopathy—primary
muscle disease
IV. Inflammatory and infiltrative
disorders.
A. Myocarditis
B. Noninfectious inflammatory diseases
C. Infiltrative diseases
Disease states

V.Valvular heart diseases
1. Aortic stenosis
2.others- MS
MVP
VI. Electrophysiologic abnormalities
(structural)
A.Wolff-Parkinson-White syndrome
B. Conducting system disease
VII. electrophysiological
abnormalities(inherited)
1.congenital long QT syndromes,
2.right ventricular dysplasia,
3.Brugada syndrome,
4.CPVT

Causes of sudden cardiac death in competitive athletes.

CORONARY ARTERY DISEASE
Atherosclerotic changes –
 At least 80% of patients have as the underlying anatomic substrate
 Autopsy - recent occlusive coronary thrombus in 15% to 64% of victims
with many hearts showing plaque fissuring, hemorrhage, and thrombosis.
no specific pattern of distribution of coronary artery lesions
 Interestingly, chronic ischemia may exert a protective effect by causing the
development of coronary collaterals
 So,an acute occlusion of a minimally stenosed coronary artery can result in a more
disastrous outcome
Nonatherosclerotic abnormalities
 Important in only a very small number of SCD
 Include coronary arteritis, embolism, dissection, and
anomalous origin of a left coronary artery from the pulmonary artery or of
a left coronary artery from the right or noncoronary aortic sinus of Valsalva, passing
between the aortic and pulmonary artery roots.

CARDIOMYOPATHY
 Represent the second largest group of patients who experience sudden cardiac
death.
Hypertrophic cardiomyopathy
 prevalence -2 in 1000 young adults
 incidence of SCD- 2% to 4% per year in adults
 risk factors -a history of SCA
sustained VT,
family history of SCD,
a diverse genotype,
recurrent syncope,
multiple episodes of non-sustained VT, and
massive LVH
 mechanisms -arrhythmias, abrupt hemodynamic deterioration, and/or ischemia.
Idiopathic dilated cardiomyopathy
 substrate for 10% of SCD in the adult population.
 high risk of sudden death - nonsustained ventricular tachycardia
Syncope in heart failure patients
 mechanisms –arrhythmias (ventricular tachycardia , asystole or electromechanical
dissociation)

 Arrhythmogenic right ventricular dysplasia
 gene defect recently localized to chromosomes 1 and 14
 autosomal dominant inheritance.
 familial disorder in '30% of cases
 responsible for sudden death in young individuals and adults,
 Exercise can precipitate ventricular tachycardia in these patients,
 with an annual incidence of sudden death estimated to be '2%.
 pathological patterns- fatty and
fibrofatty myocardial infiltration
ECG during sinus rhythm often exhibits T-wave inversion in V1 to V3 or complete or
incomplete right bundle-branch block, and the ventricular tachycardia has a left bundle-
branch block contour

During sinus rhythm, intraventricular conduction may be
sufficiently slow as to produce a terminal notch on the QRS
complex that Fontaine called an epsilon wave (Figure ).

Primary electrophysiological abnormalities
Represent a group in whom mechanical function of the myocardium is normal and an
electrophysiological derangement represents the primary cardiac problem.
This includes patients with the
1. congenital long-QT syndrome,
2.Wolff-Parkinson-White syndrome,
3.several types of distinctive ventricular tachycardias,
4.idiopathic ventricular fibrillation
5.Brugada’ssyndrome),
6.congenital complete AV block, and
7.a variety of acquired abnormalities,
acquired long-QT syndrome
acquired diseases of the sinus node,
AV node, and
His-Purkinje system, (such as
Lenegre’s disease or Lev’sdisease)

 It is important to remember that the absence of structural abnormalities is
established by relatively gross tests, such as cardiac catheterization and
echocardiography.
 Other imaging techniques, for example, those that evaluate sympathetic
neuralfunction, are often abnormal in these patients.
 With the development and validation of new diagnostic tools, including
autonomic imaging by positron emission tomography,
genetic testing, and
magnetic resonance imaging,
 many forms of “idiopathic” sudden cardiac death in patients with apparently
structurally normal hearts may have to be reclassified,
 because these patients may become identified as having a specific structural and/or
genetic abnormality.
 A fascinating recent discovery is that the gene responsible for the Brugada
syndrome, the cardiac sodium channel gene SCN5A on chromosome 3, is the same
gene, with different defects, that causes LQT3 syndrome.

WPW syndrome is a recognized but rare cause of sudden death.
 In a study by Klein et al of 31 patients with VF and WPW syndrome, a history of atrial
fibrillation or reciprocating tachycardia was an important predisposing factor.
 The presence of multiple accessory pathways,
posteroseptal accessory pathways, and
a pre-excited R-R interval of less than 220 ms
during atrial fibrillation are associated with higher risk for SCD.
 Symptomatic patients should be treated by
antiarrhythmic medications (eg, procainamide),
catheter ablation of the accessory pathway, or
electrical cardioversion
depending on the severity and frequency of symptoms.
 Asymptomatic patients may be observed without treatment.
 Medications such as digoxin, adenosine, and verapamil that block the AV node are
contraindicated in patients with WPW and atrial fibrillation because they may
accelerate conduction through the accessory pathway, potentially causing VF and
SCD.
Wolff-Parkinson-White syndrome

The existence of an atrio-ventricular accessory pathway in this
syndrome results in ventricular pre-excitation, which appears
with short PR interval, wide QRS complex, and delta wave on
ECG.

Prodrome, Onset, Arrest, Death
prodromal symptoms : SCD may be presaged by increasing angina, dyspnea,
palpitations, easy fatigability, and other nonspecific complaints.
 generally predictive of any major cardiac event
 not specific for predicting SCD.
The onset of the clinical transition: leading to cardiac arrest, is defined as an acute
change in cardiovascular status preceding cardiac arrest by up to 1 h.
Continuous electrocardiographic (ECG) recordings :
demonstrate changes in cardiac electrical activity (over minutes or hours)
 tendency for the heart rate to increase and
 advanced grades of PVCs
 begin with a run of nonsustained or sustained VT,
 which then degenerates into VF.
Clinical Characteristics of Cardiac Arrest

Progression to biologic death is a function of the mechanism of cardiac arrest and
the length of the delay before interventions.
VF or asystole without CPR within the first 4–6 min has a poor outcome even if
defibrillation is successful because of superimposed brain damage; there are few
survivors among patients who had no life support activities for the first 8 min after
onset.

 Outcome statistics are improved by lay bystander intervention (basic life
support ) before definitive interventions (advanced life support) especially when
followed by early successful defibrillation.
 Death during the hospitalization after a successfully resuscitated cardiac arrest
relates closely to the severity of central nervous system injury.
 Anoxic encephalopathy and infections subsequent to prolonged respirator
dependence account for 60% of the deaths.
 Another 30% occur as a consequence of low cardiac output states that fail to
respond to interventions.
 Recurrent arrhythmias are the least common cause of death, accounting for
only 10% of in-hospital deaths.
SURVIVAL WITH INTERVENTIONS

FACTORS RELATED TO THE OUTCOME OF
RESUSCITATION
The Seattle Heart Watch program has reported on the outcome of
patients resuscitated at the scene by a bystander trained in CPR
compared with CPR initiated by emergency medical personnel
There was no difference in the percentage of patients resuscitated
at the scene and admitted alive to the hospital (67 versus 61
percent)
However, the percentage discharged alive was significantly higher
among those with bystander-initiated CPR (43 versus 22 percent,
p< 0.001)

 In the setting of acute MI , it is important to distinguish
between primary and secondary cardiac arrests.
 Primary cardiac arrests are those which occur in the absence of
hemodynamic instability
 secondary cardiac arrests are those which occur in patients in
whom abnormal hemodynamics dominate the clinical picture
before cardiac arrest.
 The success rate for immediate resuscitation in primary cardiac
arrest during acute MI in a monitored setting should exceed
90%.
 In contrast, as many as 70% of patients with secondary cardiac
arrest succumb immediately or during the same hospitalization.

 survival depends on
the presence of individuals who are competent in performing basic life
support,
the rapid arrival of personnel and apparatus for defibrillation and
advanced life support, and transfer to a hospital.
 Upon emergency department (ED) presentation, the most important
determinants of survival include
(1) an unsupported systolic blood pressure (SBP) greater than 90
mmHg,
(2) a time from loss of consciousness to return of spontaneous
circulation (ROSC) of less than 25 minutes, and
(3) some degree of neurological responsiveness.

FACTORS RELATED TO THE OUTCOME OF
RESUSCITATION
9/9950
 In addition to later onset of CPR, there are a number of
other factors that are associated with a poor outcome
with CPR
 Cancer or Alzheimer's
disease
 History of >2 chronic
diseases
 A history of cardiac
disease
– Absence of any vital signs
– Sepsis
– An initial rhythm of asystole or
PEA
– CPR lasting >5 minutes
– CVA with severe neurologic
deficit

INTERVENTIONS
POPULATION
SCD WITHOUT KNOWN RISK FACTORS
SCD IN HIGH RISK GROUP
CARDIAC ARREST
CARDIAC ARREST SURVIVORS
CPR(BLS,AED,ACLS)
ICD,DRUGS
POSTRESUSCITATION CARE ,ICD
NOT AVAILABLE

NEW OLD RATIONALE
Chest compressions, Airway,Breathing
(C‐A‐B):New science indicates the
following order:
1. Check the patient forresponsiveness
2. Check for no breathing or no
normal breathing.
3. Call for help.
4. Check the pulse (not >10 seconds)
5. Give 30 compressions.
6. Open the airway and give 2breaths
7. Resume compressions.
Airway, Breathing, Chest
Compressions (A‐B‐C)
after responsiveness
was assessed, a call for
help was made,
the airway opened,
checked forbreathing,
and 2 breaths were
given,
followed by a pulse
check and compressions
ventilations are an
important part of
resuscitation,but
evidence shows
thatcompressions
are the critical
element in adult
resuscitation. In
the ABC sequence,
compressionsare
often delayed.
Compressions should be initiated
within 10 seconds of recognition
of the arrest.
Compressions were to
be givenafter airway and
breathing wereassessed
Compressions are
often delayed
while A and B
CPR

Compressions should be given at
a rate of at least 100/min. Each
set of 30 compressions should
take approximately 18 seconds or
less.
Compessions were to be
given at a rate of about
100/min. Each
cycle of 30 compressions
was tobe completed in 23
seconds or less.
rates arecommonly
quite slow and
compressions
>100/min result in
better perfusion
and better
outcomes.
Compression depths are as
follows:
• Adults: at least 2 inches (5 cm)
• Children: at least one third the
depth of the chest, approximately
2 inches (5 cm)
• Infants: at least one third the
depth of the
chest, approximately 1½ inches
(4 cm)
Compression depths were as
follows:
• Adults: 1½ to 2 inches
• Children: one third to one
half the diameter of the
chest
• Infants: one third to one
half the diameter of the
chest
Deeper
compressions
generate
better perfusion of
the coronary
and cerebral
arteries.
NEW OLD RATIONALE

Cricoid pressure is no longer
routinely recommended for use
with ventilations during cardiac
arrest.
If an adequate
number of
rescuers were
available, one
could apply
cricoid
pressure.
Randomized studies have
demonstrated that cricoid
pressure still allows foraspiration.
It is also difficult to properly train
providers to perform the
maneuver correctly
“Look, listen, and feel for
breathing” has been removed
Healthcare providers briefly
check for no breathing or no
normal breathing when checking
responsiveness to detect signs
of cardiac arrest.After delivery
of 30 compressions, lone
rescuersopen the victim’s airway
and deliver 2 breaths.
“Look, listen,
and feel for
breathing”
was used to
assess
breathing
after the
airway was
opened.
With the new chest compression–
first sequence, CPR is performed
if the adult victim is unresponsive
and not breathing or notbreathing
normally (ie, only gasping) .
Therefore, breathing is briefly
checked as part of a check for
cardiac arrest. After the first set of
chest compressions, the airway is
opened and the rescuer delivers 2
breaths.
NEW OLD RATIONALE
Airway and Breathing

Bystander-initiated CPR Improves
Outcome

AED
 user-friendly devices
 Move him or her to a dry area
 Turn on the AED's power.
 Hear voice prompts and see prompts on a
screen.
 Expose the person's chest.
 Place one sticy pad on the right center of the
person's chest above the nipple.
 Place the other pad slightly below the other
nipple and to the left of the ribcage.
 Check the person for wetness,chest
hairs,medication patch,metal
neckles,pacemaker ,ICD.
 Press the AED's "analyze" button. Stay clear
while the machine checks the person's heart
rhythm.
 If a shock is needed, the AED will let you know
when to deliver it.

Survival before (open bars) and after (shaded bars) beginning early defibrillation programs by
emergency medical technicians.

ACLS
Adult Advanced Cardiovascular Life Support 2010
American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

ICDAVID trial The
Antiarrhyt
hmic Drug
Versus
Defibrillat
or trial
Enrolled patients
with a history of
VT,VF, or syncope
Survival benefit
was noted in 507
patients receiving
the ICD compared
509 receiving
sotalol or
amiodarone
The unadjusted
survivals for ICD
vs drug groups
were
89 vs 82 % at 1
year, 82 vs 75 %at 2
years and 75 vs 65
% at 3 years
CIDS The
Canadian
ICD Study
659 patients with
VT, VF, or syncope
deemed to be 20
toarrhythmia
wererandomized
toamiodarone or
an ICD
After a 5-year
follow up, the total
mortality with the
ICD was reduced
compared to
amiodarone (25 vs
30%,p=0.072)
CASH trial The
Cardiac
Arrest
Survival in
Hamburg
In this study,
patients were
randomized to
receive an ICD,
metoprolol,
propafenone, or
amiodarone
In two year analysis,
the SCD rate was
lower with the
defibrillator than
with amiodarone or
metoprolol (0
versus 8 percent)
no difference in
total mortality
with the
defibrillator,
metoprolol, or
amiodarone (12
percent)

MADIT
I study
assessed patients with
CAD, poor LV function,
and asymptomatic
nonsustained VT, with
inducible VT or VF at EP
study, not suppressible
by antiarrhythmic drug
therapy.
the first to document a
potential benefit from
prophylactic ICDs, showed a
54% reduction in mortality in
patients implanted with a
defibrillator as opposed to
those
receiving“conventional
medical therapy”.
The results led to FDA
approval of implanted
defibrillators
The weaknesses of
this trial included
small size,
inadequate therapy
with beta blockers
and ACE inhibitors,
and the clinically
impractical
sequence of EP
study that was
required for risk
stratification.
CABG
PATCH
study
randomized patients
immediatelyfollowingsu
ccessfulaortocoronaryb
ypasssurgery, if they
met the inclusion
criteria ofalowEF(<35%),
and a positive SA- ECG,
to either an implanted-
defibrillator or control
therapy without theICD.
This study failed to show any
benefit whatsoever from the
implanted defibrillator,
but both defibrillator and no
defibrillator patients had a
low cardiac mortality (5.9%
per year),
suggesting that
surgical
revascularization
has a very
important
protective effect
against sudden
death

MADIT
II study
Criteria of
risk from
sudden
death
were the
presence
of CAD, a
prior MI,
and an EF
of <30%.
randomized a
total of 1232
patients to
either the ICD
(742 patients),
orconvention
al medical
therapy (490
patients, a 3:2
ratio).
defibrillator therapy
resulted in an
increasing mortality
benefit over
conventional therapy
over time, with an
aggregate 31%
reduction in the risk of
death at any time
interval, relative
decrease of mortality
of 12%, 28%, and 28% at 1,
2, and 3 years
respectively.
In absolute
terms, this
meant a 1%, 6%,
and 9%
reduction in
mortality at 1, 2,
and 3 years; in
other words,
the number
needed to treat
(NNT) to
prevent 1 death
by 3 years was
approximately
11.

SCD-
HeFT
Sudden Cardiac
Death in Heart
Failure Trial
2,521
patients
moderate
CHF
(NYHACla
ss II or III)
and LVEF
≤35%Rand
omized on
a 1:1:1 basis
in the 3
arms
•No difference in all-cause
mortality between
amiodarone and placebo arm
• Mortality was lower in ICD
arm vs placebo
Follow-up in SCD-HeFT patients
after a median
of 11.0 years provides critical
insights into the long-
termoutcome of patients with
moderate CHF

 patients with very poor ventricular function unquestionably benefit
from the implantation of a defibrillator, even if they are receiving
optimal medical therapy.
 The main barrier to more widespread use of prophylactic implanted
defibrillators, at least in the Indian context; though it applies as well
to the west particularly in countries with government funded health
care system, seems to be resource limitations
 both with respect to device and implantation costs, and the
availability of medical personnel to perform the procedures and
follow the patients.
Present Status of Prophylactic ICDs

 Test Used for Risk Stratification for
Sudden Death
Coronary perfusion
 Coronary angiography
 Exercise testing (including imaging)
 ST-segment changes using
ambulatory recordings
Pump function
 NYHA functional class
 Left ventricular ejection fraction
 Exercise duration
Psychosocial
 Depressionnow nothing about the
antecedents
The reason people die from this cardiovascular disorder is because we
know least about its antecedents
Arrhythmias
Long-term ambulatory recordings
Signal-averaged ECG
QT-interval duration, dispersion, and
dynamic change
T-wave alternans
Exercise testing
Programmed electrical stimulation
Neurohumoral
Heart rate variability
Baroreflex sensitivity

PHARMACOLOGICAL TREATMENT
 Of the different drugs that have been evaluated, only beta-blockers and amiodarone
have reduced sudden death in the myocardial infarction survivor.
 Class I drugs (mexiletine,encainide, flecainide, moricizine), calcium antagonists, and
class III drugs (d-sotalol, dofetilide) all failed to reduce or even increased the
incidence of sudden cardiac death after a myocardial infarction.
 Amiodarone
 In a study from South America that included patients with different causes of cardiac
disease and diminished left ventricular function (ejection fraction<35%), empirical
amiodarone was shown to beneficially affect mortality.
 But this was not confirmed in a multicenter trial, CHF-STAT.
 Two recent studies using amiodarone in patients with reduced left ventricular
function after a myocardial infarction showed a reduction in sudden (presumably
arrhythmic) deaths but not in total number of deaths.
 Importantly, these studies showed no increase in mortality compared with placebo
for patients treated with amiodarone.
 a meta-analysis from 13 trials of 6500 patients treated with amiodarone after
myocardial infarction or with heart failure showed a reduction in all-cause
mortality,death from arrhythmia, or sudden death.

 Some data suggest that amiodarone may be more effective when used for patients
with high (>90 bpm) resting heart rates.
 Preliminary data also suggest increased effectiveness when amiodarone is
combined with a beta-blocker.
 these observations need further testing before adoption.
 Beta blockers
 The BHAT study showed that beta-blockade with propranolol reduced all-cause
mortality by 25% and that the drug was especially useful in patients with
diminished left ventricular function and/or ventricular arrhythmias.
 No evidence indicates that selective beta-blockers are better than nonselective ones.
 Although beta-blocker therapy has been shown to be advantageous and should be
prescribed for most patients after a myocardial infarction unless contraindicated,
 in most countries a fraction of all patients who should receive a beta-blocker after a
myocardial infarction actually do so.
 This is especially true for women, diabetics, and the elderly.

In view of the complexity of the mechanisms involved in sudden cardiac death
there has been growing interest in the use of measures that may halt or delay progress
of cardiac disease
such as the administration of anti-ischemic drugs,
drugs to prevent plaque rupture or
thrombus formation, and
drugs that stabilize the autonomic balance or
improve pump function (Table ).
With this number and diversity of drugs, it has become increasingly difficult, if not
impossible, to evaluate the individual contribution of each drug to the reduction in
sudden cardiac death.
Aggressive therapy using thrombolysis in acute ischemic syndromes or intracoronary
interventions resulting in reduction of myocardial damage and scar formation and
prevention of ventricular remodeling will diminish the occurrence of some of the
mechanisms that play a role in a fatal arrhythmia.

TABLE . Measures to Reduce Sudden Death in Patients
Known to Have Cardiac Disease
Correcting ischemia
Revascularization
beta-Blocking agent
Preventing plaque rupture
Statin
ACE inhibitor
Aspirin
Stabilizing autonomic balance
beta-Blocking agents
ACE inhibitor
Improving pump function
ACE inhibitor
beta-Blocking agent
Prevention of arrhythmias
beta-Blocking agent
Amiodarone

Treatment algorithm for patient resuscitated from cardiac arrest.

Section 3 Sudden Cardiac Arrest Prevention
(c) Removal from Play
THANK YOU

 The MADIT I study assessed patients with coronary artery disease, poor left
ventricular function, and asymptomatic nonsustained ventricular tachycardia,
with inducible VT or VF at electrophysiologic study, not suppressible by
antiarrhythmic drug therapy.13

 This study, the first to document a potential benefit from prophylactic ICDs,
showed a 54% reduction in mortality in patients implanted with a defibrillator as
opposed to those receiving “conventional medical therapy”.

 The weaknesses of this trial included its relatively small size, inadequate therapy
with beta blockers and ACE inhibitors, and the clinically impractical sequence of
EP study and need for VT induction, followed by attempted VT/VF suppression
with procainamide, that was required for risk stratification.
 Nevertheless, the results from this study led to FDA approval of implanted
defibrillators for the particular subset of patients meeting the inclusion criteria
for this study.
Additional material

 The CABG PATCH study randomized patients immediately
following successful aortocoronary bypass surgery, if they met the
inclusion criteria of a low ejection fraction (<35%), and a positive
signal-averaged ECG, to either an implanted defibrillator or control
therapy without the ICD.14
 All devices were attached to the heart by means of epicardial
defibrillator patches (which are no longer used during the CABG
procedure.
 This study failed to show any benefit whatsoever from the
implanted defibrillator,
 but both defibrillator and no defibrillator patients had a low cardiac
mortality (5.9% per year),
 suggesting that surgical revascularization has a very important
protective effect against sudden death.

 The MADIT II study, published in March 2002,17 took a simplified approach
 to the testing of the hypothesis that implanted defibrillators would reduce
all cause mortality in at risk populations.
 The only criteria to identify patients at risk from sudden death were the
presence of coronary artery disease, a prior myocardial infarct, and an
ejection fraction of <30%.
 This study randomized a total of 1232 patients to either the ICD (742
patients), or conventional medical therapy (490 patients, a 3:2 ratio).
 Neither nonsustained VT nor an electrophysiologic study was required for
entry into this study.
 The patient population in this study was reasonably representative of
a potentially very large group of patients with chronic coronary artery
disease and prior MI.
 The mean age was 65 years, and 70% of patients were either NYHA class II or
I. A majority had a remote history of coronary bypass surgery (57%), or
coronary angioplasty (44%).

 In the vast majority, more than 6 months had elapsed since their most recent MI. Interestingly enough
the associated drug therapy that most patients in the trial had was sufficiently appropriate as to allow
generalizability in this trial.
 Seventy percent were receiving ACE inhibitors, 70% beta-blockers, and 57% digitalis. Sixty-six percent
received statins. About 12% were receiving amiodarone at last contact (presumably most often for atrial
fibrillation), and only 9% received calcium channel blockers and 3% received class I antiarrhythmic drugs.
 Patients were followed to a common primary endpoint of death from any cause. The pre-specified
mortality efficacy boundary was achieved just over 4 years after the study began, after an average
follow-up of 20 months.
 The defibrillator therapy resulted in an increasing mortality benefit over conventional therapy over
time, with an aggregate 31% reduction in the risk of death at any time interval, including a relative
decrease of mortality of 12%, 28%, and 28% at 1, 2, and 3 years respectively.
 In absolute terms, this meant a 1%, 6%, and 9% reduction in mortality at 1, 2, and 3 years; in other words,
the number needed to treat (NNT) to prevent 1 death by 3 years was approximately 11.
 This NNT compares very favorably to other cardiovascular therapies in common use, for example beta-
blockers (CIBIS 2, NNT = 23), statins (4S, NNT = 28), or ACE inhibitors (SAVE, NNT = 20).
 There was a slightly higher probability of hospitalization for heart failure in the ICD group (11 per 1000
months), versus the control group (9 per 1000 months, p=0.09).
 Subsequent further subgroup analysis showed that patients with QRS prolongation of >120 msec at
baseline received a particularly and dramatically large benefit from the implantation of an ICD, the
mortality reduction being from 53% to 21% (a 63% reduction) at 3 years in these patients.
 This latter observation is consistent with prior demonstration of QRS prolongation on the surface ECG
as being particularly potent, simple marker for the probability of all cause mortality and sudden death.

 TABLE 2. Secondary Causes of
Acquired QT Prolongation
 Antiarrhythmic agents
 Class IA: quinidine, procainamide, N-
acetylprocainamide, disopyramide
 Class III: amiodarone, low risk of
torsade de pointes
 Class IV: bepridil, mibefradil
 Antihistamines
 Terfenadine
 Astemizole
 Antimicrobials
 Erythromycin
 Trimethoprim-sulfamethoxazole
 Claritromycin
 Cotzimoxazole
 Azithromycin
 Ketoconazole
 Pentamidine
 Chloroquine
Gastrointestinal
Cisapride
Liquid protein diets
Anorexia nervosa
Lipid lowering
Probucol
Psychotropic agents
Tricyclic and tetracycline
antidepressants
Haloperidol
Phenothiazines
Risperidone
Selective serotonin reuptake inhibitors
Other agents
Organophosphates
Diuretics (reduced K1, Mg21)
Vasopressin (severe bradycardia)
Chloral hydrate amantadine
Electrolyte abnormalities
Hypokalemia
Hypomagnesemia
Hypocalcemia

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