Isoflurane—A Powerful Coronary Vasodilator in Patients with Coronary Artery Disease

Abstract

The coronary hemodynamic effects of 1% end-tidal isoflurane [an anesthetic] administered in O-N by intermittent positive-pressure ventilation (IPPV) were investigated in 21 patients with stable coronary artery disease. Besides standard central hemodynamic measurements, coronary sinus blood flow was measured by continuous thermodilution, and arterial and coronary sinus blood were analyzed for O2 and lactate. Isoflurane decreased coronary perfusion pressure (-35%) by a combination of systemic vasodilation and decrease in cardiac performance. Coronary sinus blood flow did not change; consequently, coronary vascular resistance was reduced (-26%). Both myocardial O2 consumption (-36%) and extraction (-29%) were reduced. Ten patients developed ST-T-segment depressions or T-wave inversions in combination with markedly decreased myocardial lactate extraction (-52%) during isoflurane, suggesting regional ischemia. Patients without ECG changes had unchanged myocardial lactate extraction. Phenylephrine and nitroglycerin i.v. were used to restore coronary perfusion pressure to awake control level, and heart rate was kept at control by atrial pacing in the last 10 patients of the series. Five of these patients had ECG and metabolic evidence of regional myocardial ischemia during steady-state isoflurane anesthesia. Coronary blood flow increased to awake control level, and coronary vascular resistance was unaffected. Myocardial O2 extraction remained at the same low level as during administration of isoflurane alone, suggesting persistent myocardial overperfusion (coronary vasodilation). When perfusion pressure was raised, the ECG changes reverted towards awake pattern in 2 of the 5 patients in parallel, with increase in myocardial lactate extraction. In the 3 remaining patients, ECG remained abnormal, as did myocardial lactate extraction. End-tidal isoflurane 1% apparently induces coronary vasodilation that is not related to normal autoregulation and both decreased coronary perfusion pressure and redistribution of myocarial blood flow may contribute to development of reginal myocardial ischemia.