Sudden cardiac death is usually caused by chance arrhythmic events that are triggered by an interaction between structural heart abnormalities and transient, functional electrophysiologic disturbances. In the majority of cases the initiating event is a ventricular tachyarrhythmia, either pulseless ventricular tachycardia (VT) that degenerates rapidly to ventricular fibrillation (VF) or "primary" VF. 78 From a public health standpoint, strategies for preventing and treating SCD in the community can be targeted primarily at VT and VF because these rhythms are not only the most frequent, but also the most potentially treatable, currently identified initiating event.
The mechanisms responsible for triggering fatal ventricular dysrhythmias are only partially understood. Frequent ventricular ectopy alone, in the absence of significant underlying structural heart disease, does not generally result in cardiac arrest. However, ventricular extrasystoles in the presence of transient myocardial ischemia, left ventricular dysfunction, and/or cardiomegaly often trigger runs of VT that may degenerate into pulseless VT or VF.
Many types of structural heart disease can predispose to SCD. One common denominator is dispersion of ventricular depolarization and/or repolarization, allowing "islands" of ventricular tissue to depolarize and repolarize at different rates. This lack of homogeneity in electrical activation and recovery fosters the development of circus movement reentry, which can initiate and sustain ventricular tachyarrhythmias. Myocardial ischemia and/or infarction can also transiently diminish the homogeniety of left ventricular depolarization and repolarization.
Left ventricular hypertrophy (often due to hypertension and/or valvular heart disease) or conduction disturbances (left or right bundle branch block or a nonspecific intraventricular conduction disturbance) can create similar functional disturbances on a more chronic basis. An example of this SCD mechanism is the mysterious illness that causes death during sleep in young Asian (especially Thai) men who have no evidence of structural heart disease. 9 Many of these men have an abnormal cardiac conduction system that can be diagnosed by electrophysiologic testing. It is interesting to note that many of these Asian men who are at risk of SCD can be identified from a standard electrocardiogram (ECG), which shows a characteristic pattern of right bundle branch block with ST-segment elevation in V 1-3.
The long QT syndrome, in which the corrected QT interval is pathologically prolonged, is also associated with SCD. 10 Prolongation of the corrected QT interval probably represents dispersion in ventricular repolarization and can be congenital (with or without nerve deafness) or acquired (due to hypokalemia, hypomagnesemia, hypocalcemia, anorexia, ischemia, central nervous system pathology, terfenadine-ketoconazole combinations, or certain antipsychotic or antiarrhythmic drugs). The "corrected QT interval" can be calculated easily by the following formula:
where QTc is the corrected QT interval in seconds, QTm is the measured QT interval in seconds, and R-R is the interval between any two consecutive R waves on the ECG in seconds. This formula, known as Bazett's equation, while seeming to be complex, is actually quite simple and easy to remember. Since the QT interval is heart rate dependent, the formula "corrects" the measured QT interval to a heart rate of 60 beats per minute (at which the R-R interval is 1.0 s). Since the square root of 1 = 1, the QTc equals the QTm at a heart rate of 60 beats per minute (at which the normal QT interval limits are 0.35 to 0.44 s).
Most SCD victims have cardiac abnormalities on postmortem examination. The most common autopsy findings in SCD victims are evidence of coronary atherosclerosis and its complications, cardiomegaly with left ventricular hypertrophy and contraction band necrosis. The latter appears to be a marker for catecholamine stimulation and occurs with high frequency regardless of whether cardiopulmonary resuscitation (CPR) was performed. 11
Factors affecting survival of out-of-hospital VF include witnessed collapse, prompt initiation of CPR, early defibrillation, younger age, and arrest occurring away from home.12 Comorbid illnesses, such as a history of congestive heart failure, contribute to hospital mortality following successful resuscitation but only account for one-fourth of the variation in survival from SCD. Cardiac arrest during AMI is associated with a significantly improved outcome compared to cases not occuring in the setting of AMI.13 Although the reason for improved long-term survival of AMI patients is not fully known, it is probably due to the fact that such patients have transient electrical instability, unlike patients with chronic cardiomyopathy, in whom there is a persistent vulnerability to VT or VF.
The outcome of resuscitation is strongly influenced by the patient's initial cardiac rhythm. The likelihood of survival is relatively high (up to 40 to 60 percent) if the initial rhythm is VT or VF (particularly if the VF is "coarse," the arrest was witnessed, and prompt CPR and defibrillation are provided). If the initial rhythm is not VT or VF, survival is typically less than 5 percent in most reported series. Asystolic patients whose cardiac arrest was unwitnessed rarely survive neurologically intact to hospital discharge. The only common exceptions are witnessed cardiac arrest patients whose initial asystole is due to increased vagal tone or other relatively easily correctible factors, such as hypoxia of brief duration.
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