Myocardial Oxygen Consumption and Coronary Haemodynamics during Fentanyl-Droperidol-Nitrous Oxide Anaesthesia in Patients with Ischaemic Heart Disease

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Abstract
Eight patients with stable ischemic heart disease were investigated to determine the effects of fentanyl (15 .mu.g/kg).sbd.droperidol (150 .mu.g/kg).sbd.N2O (75%) anesthesia, without concomitant fluid challenge, on myocardial O2 consumption and lactate uptake, and central and coronary hemodynamics. Anesthesia induced reductions in mean arterial pressure (-35%, P < 0.01), systemic vascular resistance (-30%, P < 0.01), left ventricular stroke work index (-50%, P < 0.01) and total body O2 consumption (-23%, P < 0.01), with no changes in heart rate, cardiac output or mean pulmonary arteriolar occlusion pressure. Mixed venous O2 content increased (P < 0.05). Systemic vasodilatation, circulatory adaptation to an overall lower metabolic rate and clinically negligible cardiodepression are the likely mechanisms behind the central hemodynamic response to this form of anesthesia. Coronary sinus blood flow (measured by the continuous thermodilution technique) decreased (P < 0.01) in parallel with the decrease in coronary perfusion pressure. Thus, coronary vascular resistance remained unchanged. As expected from the hemodynamic findings, myocardial O2 consumption decreased (-37%, P < 0.01). Coronary sinus O2 content and myocardial O2 extraction did not change, nor was myocardial lactate uptake affected. No ST-T-segment depressions or dysrhythmias were recorded. Apparently, myocardial oxygenation was adequate despite the reduction in coronary perfusion pressure. There was poor correlation between changes in myocardial O2 consumption and rate pressure product (r = 0.455) or triple product (r = 0.375).