Does anesthetic technique make a difference? Augmentation of systolic blood pressure during carotid endarterectomy: effects of phenylephrine versus light anesthesia and of isoflurane versus halothane on the incidence of myocardial ischemia.

Whether anesthetic technique affected the incidence of myocardial ischemia in 60 patients undergoing carotid endarterectomy was investigated. The patients were randomly assigned to receive halothane or isoflurane (with nitrous oxide) either at a low concentration alone or at a higher concentration with phenylephrine added to support blood pressure. Blood pressure was maintained within 20% of each patient's average ward systolic pressure. Seven leads of electrocardiograms (ECG) and echocardiograms were analyzed for segmental wall motion. The echocardiograms were analyzed using standard formulae for end-systolic meridional wall stress (SWS) and rate-corrected velocity of fiber shortening (Vcfc). Because of the nature of these calculations, only echocardiograms with normal regional wall motion could be accurately analyzed. The patients had postoperative ECG and creatinine phosphokinase (CPK) isoenzyme determinations and regularly scheduled clinical examinations to detect perioperative myocardial infarction and neurologic deficits. Although blood pressures were similar, the patients who received a higher concentration of anesthetic plus phenylephrine had a higher wall stress, regardless of the choice of anesthetic agent. All four techniques allowed provision of the same stump pressures (the marker surgeons used for adequacy of collateral carotid flow). No difference could be found in wall stress or incidence of myocardial ischemia between isoflurane and halothane. The patients who received phenylephrine had a threefold greater incidence of myocardial ischemia than did the patients who had light anesthesia to maintain similar systolic blood pressures and stump pressures. The groups were demographically and hemodynamically similar; in particular, the heart rates were not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Narcotics decrease heart rate during inhalational anesthesia.

We determined the heart rate (HR) response to enflurane, halothane, and isoflurane and the effects of narcotics on this response in 81 healthy patients scheduled for elective surgery. Patients were randomly assigned to one of six treatment groups: one of the three anesthetics (approximately 0.9 MAC) in 60% nitrous oxide, and either 0.15 mg/kg of intramuscular morphine 30-60 min before induction or 1 microgram/kg of IV fentanyl 10 min after skin incision. All patients received diazepam, 10 mg orally, 60-90 min before anesthesia, a rapid sequence intravenous induction, and mechanically controlled ventilation. During inhalational anesthesia and the first 10 min of surgery, no significant change in HR occurred in any group (compared to the preinduction HR), although patients given morphine premedication tended to have a decreased HR and those not given morphine premedication tended to have an increased HR. These trends partially account for significant differences that emerged between groups after induction of anesthesia. Patients given morphine premedication and halothane had lower HR (64 +/- 3 SEM) than patients given isoflurane (80 +/- 3) or enflurane (84 +/- 3) and no morphine premedication. Patients anesthetized with enflurane and morphine premedication had lower HR (71 +/- 3) than patients given enflurane without morphine premedication. Administration of fentanyl 10 min after incision (these patients had received no morphine) significantly decreased HR in the presence of any of the vapors. We conclude that inhalational anesthetics used in the clinical setting we employed do not significantly increase heart rate, and that prior administration of morphine or concurrent administration of fentanyl may significantly decrease HR.

Monitoring with two-dimensional transesophageal echocardiography. Comparison of myocardial function in patients undergoing supraceliac, suprarenal-infraceliac, or infrarenal aortic occlusion.

When the aorta must be temporarily occluded at the suprarenal or supraceliac levels during surgery, the resulting large increase in afterload may make the myocardium ischemic, even though systemic and pulmonary artery pressures and cardiac output are maintained at normal levels. These traditional indices of myocardial well-being do not appear to be sufficiently sensitive, since cardiac complications are still the most frequent cause of perioperative death and morbidity after aortic reconstruction. To evaluate two-dimensional transesophageal echocardiography as a monitor of myocardial well-being, we studied 24 American Society of Anesthesiologists physical status class III or IV adult patients who were undergoing aortic reconstruction and occlusion at the supraceliac (n = 12), suprarenal-infraceliac (n = 6), or infrarenal (n = 6) level. In addition to traditional monitors, we used a gastroscope tipped with a special 3.5 MHz two-dimensional echocardiographic transducer (Diasonics) that was placed in the esophagus to give a cross-sectional view of the left ventricle through the base of the papillary muscles. The hemodynamic effects of clamping the aorta were managed by administration of vasodilating drugs, anesthetics, and fluids to keep systemic and pulmonary arterial pressures normal. Occlusion at the supraceliac level caused major increases in left ventricular end-systolic and end-diastolic areas, decreases in ejection fraction, and frequent wall motion abnormalities; these changes were not detected by conventional monitoring devices. Occlusion at the suprarenal-infraceliac level caused similar but smaller changes, and occlusion at the infrarenal level caused only minimal cardiovascular effects. We conclude that the two-dimensional transesophageal echocardiogram offers promise as an intraoperative monitoring device.

The effect of alpha-adrenergic blockade on cardiac performance and tissue oxygen delivery during excision of pheochromocytoma.

To establish criteria for administration of the optimal dose of alpha-adrenergic receptor blocking drugs, we studied cardiac performance and tissue oxygen tension in three patients who underwent excision of pheochromocytoma. Subcutaneous oxygen tension was measured by the method of Niinikoski and Hunt. Cardiac function was assessed by thermodilution cardiac output, systemic and pulmonary arterial blood pressures, and continuous two-dimensional transesophageal echocardiography of a cross section of the left ventricle at the level of the papillary muscles. Despite large changes in cardiac output and systemic, pulmonary, and wedge pressures, intraoperative tissue oxygen tensions and ejection fractions remained normal (even at times of peak catecholamine excretion and very abnormal wedge pressures). Studies of healthy animals that received no alpha-adrenergic receptor blocking drugs showed major decrements of tissue oxygen in response to modest doses of epinephrine. We conclude that progressive administration of alpha-adrenergic receptor blocking drugs does not absolutely protect the patient from major changes in blood pressure during operation for pheochromocytoma, but that cardiac performance and oxygen supply to the tissues are unimpaired.