Myocardial infarction.

Abstract

Recent advances in the intensive care of patients suffering from acute myocardial infarction have shown that the immediate mortality may be lowered by the prompt recognition and treatment of cardiac arrhythmias (Hellerstein and Turell, 1958; Lancet, 1960; Brown et al., 1963; Day, 1963; Lindsay and Speikerman, 1964; Kurland and Pressman, 1965). While ventricular fibrillation is the usual cause of sudden death, a frequent precursor appears to be a slow rate due to slow nodal rhythm or complete atrio-ventricular block (Brown et al., 1963), with a tendency to episodes of asystole or ventricular tachyarrhythmia. Despite the effectiveness of some drugs such as atropine, steroids, and isoprenaline, the over-all mortality in patients with a slow rate following myocardial infarction is high (Solarz, Berkson, and Pick, 1958; Gale and Enfroy, 1959; Dali and Buchanan, 1962; Hall, 1962; Vogel, 1961; Brit. med. J., 1965; Smith and Anthonisen, 1965). This may be explained in part by the failure to keep a constant increase in heart rate and the increase in myocardial oxygen consumption caused by many of these drugs, particularly isoprenaline (Winterscheid et al., 1963). A better chance of survival seems likely if the slow rate is treated by artificial pacing, since the heart rate can then be accurately controlled without drugs which may irritate the myocardium. Unlike most patients with chronic atrio-ventricular block where the underlying cause is frequently unrelated to coronary disease, acute atrio-ventricular block following myocardial infarction is usually temporary, as is sinus bradycardia or slow nodal rhythm. It seems that the combination of a low cardiac output secondary to the slow rate together with a damaged irritable myocardium often results in ventricular fibrillation. If the cardiac output can be raised by increasing the heart rate, the risk of ventricular