Effects of thiopentone on cardiac performance, coronary hemodynamics and myocardial oxygen consumption in chronic ischemic heart disease.

Abstract

Thiopentone was administered as induction agent for general anesthesia to eight patients with stable ischemic heart disease; 6 mg/kg of the drug induced decrease in arterial blood pressure (-27%), systematic vascular resistance (-20%), stroke volume index (-14%), mean pulmonary arteriolar occlusion pressure (-15%) and left ventricular stroke work index (-38%), while heart rate increased by 10% and cardiac output remained unchanged. Total body oxygen consumption decreased by 30%. Myocardial oxygen consumption decreased by 39% with unchanged or decreased myocardial oxygen extraction and myocardial lactate uptake decreased by 40%. Arterial and coronary sinus hypoxanthine levels were unchanged and no ST-T-segment changes or dysrhythmias were recorded. In the present experimental setting, the results indicate that thiopentone substantially decreased myocardial oxygen requirements. In spite of the marked reduction in coronary perfusion, myocardial oxygen demand was matched by supply, myocardial dysoxia was not induced and cardiodepression was clinically negligible. Rate pressure product was a poor indicator of changes in myocardial oxygen consumption after thiopentone administration.