- Unexpected death occurring within an hour of onset of symptoms.
- Primary electrical mechanisms include ventricular fibrillation, ventricular tachycardia, asystole, and pulseless electrical activity.
Each year in the United States, more than 250,000 individuals die suddenly of some form of cardiovascular disease. Because of
the many advances made during the past 30 years in clinicians’ ability
to identify and modify the risk factors associated with sudden death,
to resuscitate victims of cardiac arrest, and to prescribe specific
antiarrhythmic therapy to prevent recurrences, age-adjusted sudden
death mortality rates have declined dramatically. However, the number
of elderly individuals in the population has increased, and sudden
cardiac arrest remains an important problem.
In a simplistic sense, any death can be considered sudden. For general clinical purposes, however, the term “sudden cardiac
death” is usually reserved for those deaths in which the
patient had stable cardiac function until the terminal event, with
death occurring within a short time (often defined as less than
1 hour) of the onset of symptoms. Some experts prefer the term “instantaneous
death,” namely, death with immediate collapse without preceding
symptoms. Instantaneous death is usually assumed to be due to primary
arrhythmia, but other catastrophic events, such as a massive pulmonary
embolism, the rupture of an aortic aneurysm, or a stroke, can also cause
instantaneous death. It is also important to note that not all arrhythmic deaths
are sudden. For example, a patient who is resuscitated from a cardiac
arrest may die days or weeks later from complications of the arrest.
This death would be due to an arrhythmia but would not meet the
standard definition for instantaneous or sudden death.
Effective evaluation and treatment of patients at risk for cardiac arrest and sudden death require an understanding of the responsible pathophysiologic mechanisms, the strategies proposed for primary prevention, the techniques and results of resuscitation, and the treatment modalities for secondary prevention in survivors of an
Rosamond W et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and
stroke statistics—2008 update: a report from the American
Heart Association Statistics Committee and Stroke Statistics Subcommittee.
Circulation. 2008 Jan 29;117(4):e25–146.
A number of different electrophysiologic mechanisms may be responsible for sudden cardiac death. When ambulatory electrocardiographic (ECG) recordings from the time of an out-of-hospital cardiac arrest are
examined, ventricular fibrillation and rapid ventricular tachycardia
are the most commonly documented initial arrhythmias. Bradyarrhythmias, including
atrioventricular block, asystole, or electromechanical dissociation,
are also observed. The prevalence of these latter arrhythmias is
higher in the setting of progressive and advanced underlying heart
disease; in the elderly; and in patients whose sudden death is precipitated
by an acute catastrophe, such as a pulmonary embolism, an acute
myocardial infarction, rupture of a major vessel, or a major neurologic
insult. The focus of this chapter will be principally those sudden
deaths for which an arrhythmia was the primary cause.
Although sudden death occurs in all forms of heart disease, in the United States and Europe, coronary artery disease is the most
common cardiac diagnosis seen in sudden death victims (Table 25–1). Several mechanisms can produce potentially
fatal arrhythmias among patients with coronary artery disease, and
it is often difficult to define the precise factors that underlie
a given episode. At one extreme is the patient with a previously
normal ventricle who has an acute occlusion of a major epicardial
coronary artery in whom ventricular fibrillation then develops during
the first minutes of an acute infarction. This patient represents
an example of pure ischemic injury without associated prior scar.
At the other end of the spectrum is the patient with a history of
a single-vessel occlusion and an old myocardial infarction, in whom
postinfarction scarring has provided the anatomic substrate for a
rapid reentrant ventricular tachycardia that results in hemodynamic
collapse and sudden death. Acute ischemia need not be involved.
In coronary artery disease, the individuals at highest risk for sudden
death have both multivessel disease and myocardial scarring from
one or more prior infarctions. Even in such individuals, sudden
cardiac arrest may be the first clinical manifestation of the disease.
As treatment of acute myocardial infarction has become more aggressive
during the past 20 years, the nature of the typical scar that results
from a myocardial infarction has also changed. Dense scar tissue
with aneurysm formation, the classic substrate associated with uniform
morphology ventricular tachycardia, is now seen less often. After pharmacologic
or mechanical reperfusion, the current standards of therapy, the
infarct zone shows mostly patchy fibrosis, and in such areas disorganized arrhythmias
predominate. In patients with this complex substrate, sudden death
is thought to result from a complex interaction between some triggering event,
such as ischemia, autonomic nervous system dysfunction, electrolyte imbalance,
or drug toxicity, and the unstable electrophysiologic milieu created
by prior infarction.
Table 25–1. Cardiac Conditions Associated with Sudden Death.
| Save Table
Table 25–1. Cardiac Conditions Associated with Sudden Death.
|Diseases of the coronary arteries|
|Acute ischemia or infarction|
|Prior myocardial infarction|
|Congenital coronary anomalies|
|Diseases of the aorta|
|Diseases of the myocardium|
|Valvular heart disease|
|Arrhythmogenic right ventricular cardiomyopathy|
|Congenital heart disease|
|Primary pulmonary hypertension|
|Neuromuscular disorders with cardiac involvement|
|Primary electrophysiologic disorders|
|Long-QT syndrome: acquired and congenital|
|Catecholaminergic polymorphic ventricular tachycardia|
|Congenital atrioventricular block|
Autopsy and clinical studies have highlighted this complexity.
Coronary artery thrombi or plaque rupture may be detected in up
to 50% of sudden death victims, but new Q wave myocardial
infarctions will develop in only about 25% of patients
resuscitated from an out-of-hospital cardiac arrest. Angiographic
studies in cardiac arrest survivors have shown that a high ...