CHANGES IN MYOCARDIAL-METABOLISM AND TRANSCARDIAC ELECTROLYTES DURINGSIMULATED VENTRICULAR-TACHYCARDIA - EFFECTS OF BETA-ADRENERGIC-BLOCKADE

Myocardial ischemia, electrolyte changes, and fluctuations in autonomi c tone may play an important role in the presentation of malignant ven tricular arrhythmias. beta-Adrenoceptor blocking agents have been show n to decrease the incidence of ventricular fibrillation and sudden car diac death in patients with coronary artery disease. Therefore we inve stigated the changes in myocardial metabolism and transcardiac electro lytes during simulated ventricular tachycardia before and after beta-a drenergic blockade. Six patients with normal coronary arteries (group 1) and 12 patients with documented coronary artery disease (group 2) w ere included in the study. The right ventricle was paced with electrod e catheters to a constant cycle length of 400 msec for 3 minutes. Bloo d samples were withdrawn simultaneously from the coronary sinus and fe moral artery to determine the transcardiac differences in metabolic va riables and electrolytes before the pacing, at the end of the pacing, and 2 minutes thereafter. After pacing, the patients were given intrav enous propranolol (0.15 mg/kg), and the protocol was repeated. Intraar terial blood pressure and electrocardiogram were monitored continuousl y. There was a rapid decline of the mean arterial blood pressures afte r initiation of the pacing in both study groups, whereafter the pressu res began to rise. Propranolol somewhat blunted the blood pressure rec overy, especially in group 2. Norepinephrine levels increased during t he pacing in both patient groups, and, the increase was accentuated by beta-adrenergic blockade. The femoroarterial coronary sinus differenc e in lactate turned negative, and pH, PCO2 and potassium differences i ncreased in group 2 during pacing. However, the myocardial energy stat e remained relatively good as estimated from the nonsignificant change in the transcardiac differences of the plasma adenosine catabolites. There were no changes in the metabolic variables or transcardiac elect rolytes in group 1 patients during pacing. Propranolol did not prevent the metabolic ischemia, but it did prevent the pacing-induced decreas e in coronary sinus potassium and increase in transcardiac potassium d ifference. Propranolol also decreased arterial levels of free fatty ac ids and their extraction in group 2 patients during pacing. In conclus ion, blood pressure decay during simulated ventricular tachycardia is followed by instantaneous sympathoadrenergic activation. In patients w ith coronary artery disease, this process is accompanied by metabolic ischemia and net transfer of extracellular potassium into the intracel lular space. The metabolic and electrolyte changes may result in alter ations of electrophysiologic milieau, thereby also modifying the clini cal characteristics of ventricular tachycardia. Propranolol decreases arterial levels of free fatty acids and prevents changes in transcardi ac electrolytes observed in coronary artery disease patients during si mulated ventricular tachycardia. These effects of propranolol may be o f clinical significance.