Cardiovascular Collapse, Sudden Cardiac Death

Expert Lecture

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).

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.

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)

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--

Interactions of various factors that cause sudden cardiac death

 Sudden cardiac death (SCD) is a syndrome defined by its clinical presentation rather than by a discrete pathophysiology The World Health Organization definition has been widely accepted: sudden collapse occurring within one hour of symptoms However, as the name implies, SCD is instantaneous and most individuals become unconscious within seconds to minutes as a result of insufficient cerebral blood Underlying heart disease is present the vast majority of patients with SCD
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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

Primary VF 8% Torsades de Pointes 13%
VT 62% Bradycardia 17%

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ARRHYTHMIC MECHANISM OF SUDDEN CARDIAC DEATH

In approximately 80 percent of cases, a sustained ventricular arrhythmia is preceded by an increase in ventricular ectopy These spontaneous arrhythmias are present for a variable period of time prior to the development of a sustained ventricular tachyarrhythmia In about one-third of cases, the tachyarrhythmia is initiated by an early R on T ventricular premature beat; 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, 34 percent had a noncardiac origin, most commonly due to trauma, nontraumatic bleeding, intoxication, near drowning, or pulmonary embolism

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Causes of Sudden Cardiac Death

Ischemic Heart Disease CAD with MI or angina coronary artery embolism nonathogenic coronary artery disease coronary artery spasm Nonischemic heart disease CAD without MI or angina cardiomyopathy - obstructive, nonobstructive, nonischemic valvular heart disease congenital heart disease prolonged QT syndrome preexcitation syndrome complete heart block arrhythmogenic RV dysplasia
Nonischemic Heart Disease (cont) myocarditis acute pericardial tamponade acute myocardial rupture Noncardiac Disease sudden infant death syndrome drowning Pickwickian syndrome pulmonary embolism drug-induced airway obstruction no structural heart disease - primary electrical disease, chest wall trauma (commotio cordis), Brugadas syndrome (right bundle branch block and ST segment elevation V1 to V3)

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ETIOLOGY OF SUDDEN CARDIAC DEATH

Most patients who experience SCD have an underlying cardiac abnormality, particularly coronary heart disease The incidence of SCD increases with age in both men and women However, at any level of multivariate risk, women are less vulnerable to sudden death than men and a higher fraction of SCDs in women occur in the absence of prior overt coronary heart disease
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Incidence of Sudden Death Increases with Age

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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)

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ETIOLOGY OF SUDDEN CARDIAC DEATH

Symptoms of an acute ischemic episode are generally absent, and the collapse is typically instantaneous, without any warning Approximately 75 to 80 percent of patients have no ECG changes or enzyme abnormalities after resuscitation that are suggestive of an acute myocardial infarction as a precipitating factor

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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 3 percent 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 and women. *P <0.001.
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Risk of Sudden Death: Data from GISSI-2 Trial

1.00 1.00 0.98

p log-rank 0.002

0.98

0.96

0.96

Survival

0.94

Survival

0.94

0.92

0.92

0.90

0.90

p log-rank 0.0001

0.88

0.88

A
0.86 0 30 60 90 120 150 180 0.86 0

B
30 60 90 120 150 180

Days

Days

Patients without LV Dysfunction

No PVBs 1-10 PVBs/h > 10 PVBs/h

Patients with LV Dysfunction

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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 who died suddenly had less extensive coronary disease than normotensives who had SCD These findings suggest that the hypertrophied myocardium is more susceptible than normal myocardium 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 cases autopsy reveals evidence of underlying heart disease that was unrecognized, including myocarditis, hypertrophic cardiomyopathy, arrhythmogenic RV dysplasia, 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 3 percent 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 Brugada's syndrome

One interesting subgroup are patients with Brugada's syndrome who have a peculiar ECG pattern 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 of symptomatic patients and in 27 percent of asymptomatic patients
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Clinical Substrates Associated with VF Arrest

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, or fist One study described an animal model in which lowenergy blows to the chest wall delivered during repolarization, just before the peak of the T wave, produced ventricular fibrillation

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Clinical Substrates Associated with VF Arrest

Family history
A family history of myocardial infarction or SCD is associated with an increased risk for SCD

Genetic abnormality
A defect located on chromosome 1p1-1q1, has been associated with sudden death Affected individuals have progressive cardiac conduction abnormalities and symptomatic sinus bradycardia, requiring pacemaker therapy Sudden death generally occurs beyond the age of 30 and is not prevented by pacemaker therapy
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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 poor outcome

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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 becomes irreversible 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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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 bystanderinitiated CPR (43 versus 22 percent, p< 0.001)
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Bystander-initiated CPR Improves Outcome

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Causes of in-hospital mortality

The cause of death in hospital is most often noncardiac, usually being due to anoxic encephalopathy or to respiratory complications from long-term respirator dependence Only about 10 percent of patients die from recurrent arrhythmia, while approximately 30 percent die from a low cardiac output or cardiogenic shock

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FACTORS RELATED TO THE OUTCOME OF RESUSCITATION

In addition to later onset of CPR, there are a number of other factors that are associated with a poor outcome with CPR
Absence of any vital signs Sepsis An initial rhythm of asystole or PEA CPR lasting >5 minutes CVA with severe neurologic deficit

Cancer or Alzheimer's disease History of >2 chronic diseases A history of cardiac disease
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PROVOKING FACTORS
Electrolyte disturbances Any reversible metabolic abnormalities should be identified and corrected, particularly hypokalemia and hypomagnesemia which may predispose to ventricular tachyarrhythmias Antiarrhythmic drugs Whenever possible, antiarrhythmic drugs should be discontinued prior to any diagnostic studies

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PROVOKING FACTORS
Use of an illicit drug such as cocaine can directly cause arrhythmia or produce coronary artery vasospasm and ischemia A prolonged QT interval 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 complete cardiac 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 a ventricular 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 first approach 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, since recurrence 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 causing intermittent third degree AV block, and preexcitation with AF leading to VF These and some other arrhythmias should be treated with pacemaker, radiofrequency ablation or therapies other than ICD
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