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Sudden cardiac death

Sudden cardiac death (SCD) accounts for up to

50% of cardiovascular-related deaths in the

United States and other developed countries.

By definition, SCD refers to the acute and

natural death from cardiac causes within a

short period (often within an hour of onset of

symptoms).

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Sudden cardiac death

The time and mode of death are unexpected,

and often death occurs in patients without

any prior potentially fatal conditions.

Most cases of SCD are associated with

underlying cardiac arrhythmias; however,

other causes have been identified.

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PATHOPHYSIOLOGY AND MECHANISM OF

SUDDEN CARDIAC DEATH

The mechanism of SCD is complex and is often

associated with an interplay between

anatomical substrates, functional substrates,

and transient events that lead to the initiation

of ventricular arrhythmias (VT or VF)

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Causes of sudden cardiac death

Electrophysiologic abnormalities--

Coronary artery disease--

Primary cardiomyopathies--

Myocarditis--

Valvular heart disease-- Arrhythmogenic right ventricular dysplasia--

Pulmonary hypertension--

Hypertensive heart disease--

Congenital heart disease--

Inflammatory and infiltrative disease of myocardium--

Neuromuscular disease--

Intracardiac obstruction--

Acute aortic dissection--

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Interactions of various factors that

cause sudden cardiac death

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Sudden Cardiac Death

Incidence

400,000 - 500,000/year in U.S.

Only 2% - 15% reach the hospital Half of these die before discharge

High recurrence rate

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Underlying Arrhythmia of Sudden

Death

VT

62%Bradycardia

17%

Torsades

de Pointes

13%

Primary

VF

8%

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ARRHYTHMIC MECHANISM OF SUDDEN

CARDIAC DEATH

In approximately 80 percent of cases, a sustainedventricular arrhythmia is preceded by an increase inventricular ectopy

These spontaneous arrhythmias are present for avariable period of time prior to the development of asustained ventricular tachyarrhythmia

In about one-third of cases, the tachyarrhythmia is

initiated by an early R on T ventricular prematurebeat; in the remaining two-thirds, the arrhythmia is

initiated by a late cycle VPB

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ARRHYTHMIC MECHANISM OF SUDDEN

CARDIAC DEATH

A bradyarrhythmia or asystole is an important

but less common cause of SCD, being

observed in only about 10 percent of cases

A bradyarrhythmia is more often associated

with a nonischemic cardiomyopathy

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ETIOLOGY OF SUDDEN CARDIAC DEATH

There are many cardiac and noncardiac causes for a

sustained ventricular tachyarrhythmia that can result

in SCD

In one study of 809 patients with a cardiac arrest, 34percent had a noncardiac origin, most commonly due

to trauma, nontraumatic bleeding, intoxication, near

drowning, or pulmonary embolism

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Clinical Substrates Associated with VF

Arrest

Myocardial ischemia and infarction

Acute myocardial infarction is associated with an

approximate 15% risk of VF within the first 24 to

48 hours, with the incidence falling to only 3percent over the next several days

When VF is provoked by an AMI, symptoms of the

infarction are present for minutes to hours before

sudden death occurs; over 80 percent of VF

episodes occur within the first 6 hours

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Clinical Substrates Associated with

VF Arrest

Congestive heart failure

The presence of CHF increases overall mortality

and the incidence of SCD in both men and women

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CHF Predict Increased Sudden Death and Overall

Mortality

During a 38 years follow-up of subjects in the Framingham

Heart Study, the presence of CHF significantly increased

sudden death and overall mortality in both men andwomen. *P

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Risk of Sudden Death: Data from GISSI-2 Trial

Patients withoutLV Dysfunction

Patients with

LV DysfunctionNo PVBs

1-10 PVBs/h

> 10 PVBs/h

0.86

A

0.88

0.90

0.92

0.94

0.96

0.98

1.00

0 30 60 90 120 150 180

Days

Sur

vival

p log-rank 0.002

0.88

0.90

0.92

0.94

0.96

0.98

1.00

0 30 60 90 120 150 180

Days

Sur

vival

B

p log-rank

0.0001

0.86

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Clinical Substrates Associated with

VF Arrest

Left ventricular hypertrophy

Hypertension with LVH appears to increase the risk of

SCD

In one study, patients with hypertension and LVH whodied suddenly had less extensive coronary disease

than normotensives who had SCD

These findings suggest that the hypertrophied

myocardium is more susceptible than normalmyocardium to the the effects of ischemia

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Clinical Substrates Associated with VF Arrest

Absence of structural heart disease (primary electrical

disease) Rarely, SCD occurs in patients younger than 40 years of

age who have no evidence of structural heart disease

However, in approximately 90 percent of these casesautopsy reveals evidence of underlying heart diseasethat was unrecognized, including myocarditis,hypertrophic cardiomyopathy, arrhythmogenic RVdysplasia, sarcoidosis, or asymptomatic coronary heart

disease The remaining 10 percent of patients have idiopathic

ventricular fibrillation ("primary electrical disease)

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Clinical Substrates Associated with VF

Arrest

Myocardial ischemia and infarction

Acute myocardial infarction is associated with an

approximate 15% risk of VF within the first 24 to

48 hours, with the incidence falling to only 3percent over the next several days

When VF is provoked by an AMI, symptoms of the

infarction are present for minutes to hours before

sudden death occurs; over 80 percent of VF

episodes occur within the first 6 hours

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Brugada's syndrome One interesting subgroup are patients with

Brugada's syndrome who have a peculiar ECGpattern consisting of a RBBB and ST segment

elevation in V1 to V3 One study reported data on 63 such patients, 41 of

whom were diagnosed after an episode of SCD

During a 34 month follow-up, a recurrent

arrhythmic event occurred in 34 percent ofsymptomatic patients and in 27 percent ofasymptomatic patients

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Commotio cordis

Sudden death has been described in young athletes

who have been struck in the precordium with a

projectile object such as a baseball, hockey puck, orfist

One study described an animal model in which low-

energy blows to the chest wall delivered during

repolarization, just before the peak of the T wave,produced ventricular fibrillation

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OUTCOME OF RESUSCITATION

When the initial rhythm is asystole, the likelihood of

successful resuscitation is low and, when performed out

of hospital, less than 10 percent survive to hospitalization

The outcome is much better when the initial rhythm is a

sustained VT (65 to 70% survival)

Approximately 25 percent of patients with VF survive to

be discharged; in the majority of these patients an acute

myocardial infarction is the underlying mechanism

Patients who have SCD due to PEA also have a pooroutcome

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FACTORS RELATED TO THE OUTCOME OF

RESUSCITATION

The only effective way to reestablish organized

electrical activity and myocardial contraction is

prompt electrical defibrillation

It has been estimated that organ damage becomesirreversible after approximately 4 minutes of VF

As a result, the longer the duration of the cardiac

arrest, the lower the likelihood of resuscitation or

survival even if initial resuscitation is successful

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RESUSCITATION

The Seattle Heart Watch program has reported onthe outcome of patients resuscitated at the scene bya bystander trained in CPR compared with CPRinitiated by emergency medical personnel

There was no difference in the percentage ofpatients resuscitated at the scene and admitted aliveto the hospital (67 versus 61 percent)

However, the percentage discharged alive wassignificantly higher among those with bystander-initiated CPR (43 versus 22 percent, p< 0.001)

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Bystander-initiated CPR ImprovesOutcome

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RESUSCITATION

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

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PROVOKING FACTORS

Electrolyte disturbances

Any reversible metabolic abnormalities should be

identified and corrected, particularly hypokalemia

and hypomagnesemia which may predispose toventricular tachyarrhythmias

Antiarrhythmic drugs

Whenever possible, antiarrhythmic drugs should

be discontinued prior to any diagnostic studies

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PROVOKING FACTORS

Use of anillicit drugsuch as cocaine can

directly cause arrhythmia or produce coronary

artery vasospasm and ischemia

Aprolonged QTinterval which may be

acquired (due, for example, to a drug or

electrolyte disturbance) or inherited

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CARDIAC EVALUATION

It is essential that the patient undergo a completecardiac examination to establish the nature and

extent of underlying heart disease

The LV function and coronary anatomy should be

assessed utilizing physical examination, echo, cardiac

catheterization, and, if warranted, myocardial biopsy

Since global LV dysfunction due to myocardial

stunning may be present as a result of the cardiac

arrest, baseline evaluation of left ventricular function

should be performed at least 48 hours after

resuscitation

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ARRHYTHMIA EVALUATION

There are different approaches (termed

conservative and aggressive) to the evaluation

and treatment of SCD

Ongoing controlled trials may in the future

provide information as to which of these

approaches is associated with the best

outcome

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Conservative approach

The conservative approach involves a complete

arrhythmia evaluation to establish at baseline the

type, frequency, and reproducibility of spontaneous

ventricular ectopy, and the inducibility of aventricular tachyarrhythmia

This involves the use of noninvasive ambulatory

monitoring for 48 hours, an exercise test, and an

invasive electrophysiologic study

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Conservative approach

For patients with SCD, in whom sustained

monomorphic VT is induced at baseline, the use of

antiarrhythmic agents to prevent the induction of

sustained VT may be an adequate and effective firstapproach

For those patients who have recurrent arrhythmia,

the ICD could be considered as an additional or

alternative therapy

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Aggressive approach

The aggressive approach uses the ICD in all

victims of SCD whose chance of recurrence with

therapy cannot be accurately predicted

High, medium and low risk are all objective, sincerecurrence of ventricular fibrillation is often

lethal

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Aggressive approach

When using an aggressive approach, the value of

diagnostic testing is to find conditions that do not

require ICD insertion, like episodic prolonged sinus

arrest, severe AV nodal or infranodal disease causingintermittent third degree AV block, and preexcitation

with AF leading to VF

These and some other arrhythmias should be treated

with pacemaker, radiofrequency ablation ortherapies other than ICD

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