The effects of nitrous oxide on myocardial metabolism and hemodynamics during fentanyl or enflurane anesthesia in patients with coronary disease.

Twenty patients about to have coronary artery bypass grafts were studied before and after 15 min of 50% nitrous oxide added to either fentanyl (75 micrograms/kg) or enflurane (0.5%) anesthesia. Arterial and central pressures and cardiac output were measured, plus coronary sinus blood flow and arterio-coronary sinus differences in oxygen, hemoglobin, and lactate contents. Fentanyl-N2O and enflurane-N2O both decreased systemic resistance, heart rate, cardiac output, and hence arterial pressure. Stroke work decreased significantly with little or no change in wedge pressure: ventricular function was impaired. Coronary flow and myocardial O2 consumption decreased with fentanyl-N2O. Oxygen extraction increased with enflurane-N2O, as did lactate contents of coronary sinus blood. Hemodynamic depression occurred from the combined effects of nitrous oxide and fentanyl or enflurane. The beta-blocked myocardia of nonstimulated coronary patients were becoming ischemic globally on 50% oxygen, after significant hypotension. From this and other evidence, we conclude that nitrous oxide may not be benign in patients with coronary arterial disease.

Myocardial metabolism and haemodynamic responses with enflurane anaesthesia for coronary artery surgery.

Ten patients were studied before, during and after enflurane anaesthesia for coronary vein grafting. All had good ventricular function and nine were receiving effective beta blockade. Cardiac output and vascular pressures were measured, plus coronary sinus blood flow (CBF), myocardial oxygen consumption (MVO2) and lactate extraction (MLE). Enflurane induction (10 minutes, mean 1.72 per cent end tidal) reduced blood pressure (MAP), due to decreased cardiac index (CI), with no change in heart rate or systemic resistance. Intubation returned MAP and CI to control level but the heart rate increased. Subsequently, enflurane kept MAP, CI and stroke work below the awake level. CBF decreased on induction, rose again on intubation and remained normal before bypass. MVO2 fell on induction from an increase in CS oxygen content, which remained elevated. Normal MLE continued in every patient. There was no evidence of myocardial ischaemia in patients on beta blockade, when haemodynamics were maintained at or below those of the sedated, awake state.

Myocardial metabolism and haemodynamic responses during high-dose fentanyl anaesthesia for coronary patients.

Fentanyl (mean dose 109 micrograms X kg-1) and oxygen were given to ten patients having coronary vein grafts. Serial studies were done before, during and after operation, of central and mean arterial pressures (MAP), cardiac index (CI) and coronary sinus flow (CBF) by thermodilution, myocardial oxygen consumption (MVO2) and lactate extraction (MLE). On induction CI and stroke work index decreased, but heart rate and MAP were unchanged as systemic resistance increased. Mean MAP and heart rate remained at the awake levels. Mean CBF remained unchanged along with stable MAP and coronary resistance. Oxygen content of CS blood increased on induction and remained elevated until the incision; it was above the awake level early postoperatively. MVO2 was low normal when the patients were awake and remained so. Normal MLE continued with a few exceptions. High-dose fentanyl did not uniformly abolish autonomic reflexes. Heavy premedication, complete beta adrenergic blockade and a high initial doses of fentanyl plus its continued infusion, aided in retaining a hypodynamic circulation and myocardial oxygenation.