David J. Benefiel

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 isoflurnne (with nitrous oxide) either nt a low concentration alone or at a higher concentration with phenylephrine added to support blood pressure. Blood pressure wns maintained within 20% of each patients average ward systolic pressure. Seven leads of electrocardiograms (ECC) and echocardiograms were analyzed for segmental wall motion. The echocardiograms were analyzed using standard formulae for end-systolic meridional wall stress (SWS) and rntecorrected 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 perioperntive 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 hemodynamicnlly similar; in particular, the heart rates were not different. Increased wall stress in anesthetized patients is associated with an increased incidence of myocardial ischemia as evidenced by new segmental wall motion and wall thickening abnormalities (SWMA).

No finding of increased myocardial ischemia during or after carotid endarterectomy under anesthesia with nitrous oxide

Nitrous oxide (N2O) has been implicated as a cause of myocardial ischemia. We investigated whether substitution of N2O for a portion of the anesthesia supplied by isoflurane increased myocardial ischemia in patients at risk for such ischemia. Seventy patients having carotid endarterectomies (63 patients) or other carotid surgery (seven patients) were prospectively, randomly assigned to an anesthetic regimen that included or excluded N2O. All other aspects of anesthetic management were similar, except for greater concentrations of oxygen and isoflurane in patients not given N2O. Perioperative monitoring for myocardial ischemia and infarction included 12− or 5-lead electrocardiography, transesophageal echocardiography, and creatine kinase isoenzyme levels. By transesophageal echocardiographic or electrocardiographic criteria, 44% of patients given oxygen but only 21% of those given N2O had myocardial ischemia intraoperatively (P = 0.065). Similarly, myocardial infarction, identified by changes in creatine kinase isoenzymes, occurred in only one patient given N2O but in three given oxygen (not significantly different). Thus we found no trend indicating a greater incidence of myocardial ischemia or infarction associated with the use of N2O.

Anaphylactoid reactions to vascular graft material presenting with vasodilation and subsequent disseminated intravascular coagulation.

This report describes five patients who had immediate adverse reactions following placement of a vascular graft. All had unusually persistent decreases in systemic vascular resistance, and four of these patients had bleeding as an early manifestation of this reaction. In two of three patients in whom the graft was replaced, uneventful recovery followed. Both patients in whom the graft was not replaced died. Blood samples from two of the patients demonstrated activation of complement and of the kinin system, whereas control patients did not demonstrate increased levels of activation products from these cascade systems. Recognition of this syndrome is important to patient survival, which appears to depend on rapid replacement of the graft.