Myocardial metabolism and hemodynamic responses with isoflurane anesthesia for coronary arterial surgery.

Isoflurane-oxygen was given for induction and maintenance of anesthesia to ten patients having coronary artery bypass grafts. All had preserved ventricular function without hypertension or other cardiac lesions; treatment with beta-blocking drugs was maintained until the operation in all patients. Cardiac output, arterial and central pressures, coronary sinus (CS) blood flow, arterial and CS oxygen, Hb, and lactate contents were measured before, six times during, and twice after anesthesia. On induction, systolic arterial pressure was purposely reduced 33% along with systemic resistance by increasing the concentration of isoflurane; cardiac index, heart rate, and coronary flow did not change. Coronary resistance decreased 23% and CS oxygen content increased 56%; but in three of ten patients myocardial lactate production took place, evidence of global ischemia. Induction of anesthesia was not smooth in three patients. Controlled hemodynamic depression could be maintained with isoflurane-oxygen, but the frequency of myocardial lactate production before and after perfusion was greater than with other general anesthetics. Isoflurane dilated portions of the coronary bed but, because anaerobic metabolism occurred concomitantly, the theory that redistribution of flow can take place resulting in ischemic areas of ventricle is supported.

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.