What is the mechanism of sudden death?

Sudden death following cardiocircula-tory arrest is a common outcome in heart failure, with an impact on family and health care staff, which is all the greater in that it occurs more often in patients in a low New York Heart Association (NYHA) class with relatively stable disease. The mechanism may be electrical or mechanical.

Arrhythmic causes

Bradyarrhythmia may progress to asystole, causing death within minutes. More often, however, ventricular tachyarrhythmias result either in coordinated contraction, but much reduced output due to the high rate, or in uncoordinated contraction. Such tachyarrhythmias include:

Ventricular tachycardia (VT) >200 bpm, often degenerating into ventricular fibrillation (VF).

Ventricular flutter at around 300 bpm, which may also degenerate into VF.

The polymorphic VT with a sinusoidal QRS complex known as torsade de pointes, often associated with long QT syndrome, which may also degenerate into VF.

VF itself, which can occur after just a few beats of ventricular tachycardia.

All the above are more common in decompensated heart disease with left ventricular dysfunction. Ischemic cardiomyopathy, whether chronic, anginal, acute (infarction), or postinfarction, is the setting for 80% of arrhythmic sudden deaths. The combination of fibrosis, scars, aneurysm, and depressed left ventricular function provides an organic substrate for the reentry phenomena that trigger ventricular arrhythmia. Hypertrophic cardiomyopathy and dilated cardiomyopathy are also strongly associated with ventricular arrhythmia and sudden death.


Prognostic evaluation is advised in all heart failure patients to determine the most appropriate antiar-rhythmic approach. Items of fundamental importance in the history include:

The underlying heart disease. Whether the heart failure is postischemic or the result of dilated cardiomyopathy will determine the specificity and significance of further investigations, such as electrophysiological studies (EPS)

Evidence of temporary hemodynamic compromise.

Symptoms such as syncope, or even asthenia, suggest a malignant arrhythmic event

Current therapy. Is the patient taking diuretics and/or antiarrhythmic therapy?

Specific investigations, such as 24-hour Holter (ambulatory) electrocardiography, or late potentials, can then be performed, supplemented if necessary by EPS.


pathophysiology; sudden death; arrhythmia; prevention

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What is the mechanism of sudden death?

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