Effects of vasoactive drugs on flows through left internal mammary artery and saphenous vein grafts in man.

Vasoactive agents are commonly used in the postcardiopulmonary bypass period to elevate the mean arterial pressure of myocardial revascularization patients. Concern exists that administration of vasoactive agents in this setting may affect flow through saphenous vein and internal mammary artery grafts. Twenty-eight patients were randomly assigned to receive one of the six two-drug combinations of phenylephrine, norepinephrine, and epinephrine. After termination of cardiopulmonary bypass baseline, hemodynamic measurements and electromagnetic flow probe measurements of saphenous vein and internal mammary artery graft flow were made. The first agent was then infused to elevate mean arterial pressure 20 mm Hg. After 5 minutes of stability, hemodynamic and graft flow measurements were repeated. The infusion was terminated, 5 minutes of stability were obtained, and baseline measurements were repeated. The second agent was then infused, and measurements were repeated after a 5-minute stabilization period. Phenylephrine induced a nonsignificant increase in saphenous vein graft flow (68 +/- 31 versus 81 +/- 49 ml/min) and a significant decrease in internal mammary artery graft flow (40 +/- 16 versus 32 +/- 12 ml/min). Norepinephrine induced a significant increase in saphenous vein graft flow (80 +/- 39 versus 97 +/- 39 ml/min) and no significant change in internal mammary artery graft flow (44 +/- 20 versus 45 +/- 20 ml/min). Epinephrine induced a significant increase in both saphenous vein (82 +/- 38 versus 96 +/- 40 ml/min) and internal mammary artery (38 +/- 12 versus 55 +/- 24 ml/min) graft flows. We conclude that administration of vasoactive agents in the postcardiopulmonary bypass period may significantly affect saphenous vein and internal mammary artery graft flows.

Blood loss and transfusion requirements in patients implanted with a mechanical circulatory support device undergoing cardiac transplantation.

Patients implanted with mechanical circulatory support devices (MCSD's) are at high risk for post-operative bleeding at cardiac transplantation. However, the magnitude of the risk and transfusion requirements for MCSD patients at the time of transplantation have not been previously reported. The purpose of this study was to characterize and compare the bleeding characteristics and transfusion requirements of 3 sub-groups of cardiac transplant patients: primary (n = 45), redo (n = 26), and MCSD (n = 23) patients.

Use of transesophageal echocardiography for delivery of a parturient with severe pulmonary hypertension.

The anesthetic management of a parturient with severe pulmonary hypertension during labor and subsequent cesarean delivery is presented. Transesophageal echocardiography was used intraoperatively to manage the patient's hemodynamics, while pulmonary artery pressure monitoring was of little use. The benefits of transesophageal echocardiography for management of these patients are discussed.

The effect of esmolol given during cardiopulmonary bypass.

beta-Adrenergic antagonism decreases the size of myocardial infarction and provides myocardial protection during hypothermic arrest for cardiac surgery. However, concern regarding the negative inotropic and chronotropic effects of beta-adrenergic antagonism persisting after cardiopulmonary bypass (CPB) has impeded the use of esmolol for this purpose during cardiac surgery. This is a randomized, double-blind prospective study of the effects of esmolol infused during CPB and the effects of hypothermic CPB on esmolol. Patients scheduled for CPB were randomized to receive intravenous esmolol (300.micrograms.kg-1.min-1 during CPB after a bolus of 2 mg/kg prior to CPB) or placebo. Infusion was stopped at 10 min after release of aortic cross-clamp. Hemodynamics were measured, as well as serum esmolol, catecholamines, lactate, and potassium. Postoperative variables measured included electrocardiographic changes, creatine kinase (CK)-MB fractions, post-CPB dysrhythmias and drugs, hospitalization time and cost, and mortality. Esmolol was administered to 16 patients and placebo to 14. Esmolol levels reached a high of 10.5 +/- 0.9 micrograms/mL during CPB, but decreased to 0.1 +/- 0.02 microgram/mL within 30 min after stopping infusion. Cardiac indices (cardiac index, stroke volume index, left cardiac work index, left ventricular stroke work index, right cardiac work index, and right ventricular stroke work index) were higher in the esmolol group for the first hour post-CPB (P < 0.05). Systemic arterial lactate and coronary sinus lactate were lower in the esmolol group after CPB (P < 0.05), but myocardial lactate extraction was not significantly different between groups. After CPB, hemoglobin was lower in the esmolol group (P < 0.05) due to longer CPB and aortic cross-clamp time (P < 0.05), but oxygen consumption was less than in the control group (P < 0.05). Post-CPB serum potassium was higher in the esmolol group (P < 0.05). Results are confounded by more chronically beta-adrenergically blocked patients randomized to the esmolol group (P < 0.05). Esmolol infused during CPB in this series of patients was associated with high concentrations during CPB but did not result in any adverse clinical effects after CPB.

Clinical comparison of sevoflurane and isoflurane in healthy patients.

We compared blood pressure and heart rate changes in healthy patients during anesthesia with sevoflurane (n = 50) versus isoflurane (n = 25) and the rate of recovery after such anesthesia. After premedication with intravenous administration of midazolam, induction of anesthesia with thiopental, and intubation of the trachea facilitated with succinylcholine or vecuronium, anesthesia was maintained with approximately 1 MAC (sevoflurane, 2.05%; isoflurane, 1.15%) of the volatile anesthetic in oxygen for the duration of the operation. Anesthetic concentration was varied as indicated to maintain arterial blood pressure at +/- 20% of baseline values. Sevoflurane and isoflurane produced similar systolic and diastolic arterial blood pressures, but heart rate after incision was faster in patients given isoflurane. Recovery of response to command was shorter in patients given sevoflurane than that in patients given isoflurane (7.5 +/- 0.5 min versus 18.6 +/- 2.0 min). Consistent with this finding, venous blood drawn after anesthesia showed a more rapid initial decay with sevoflurane. Nausea and vomiting were comparable in both groups. We conclude that sevoflurane anesthesia, as compared with isoflurane, is associated with possible advantageous effects on heart rate and recovery.

Cardiovascular effects of sevoflurane compared with those of isoflurane in volunteers.

BACKGROUND: Sevoflurane is a new inhalational anesthetic with desirable clinical properties. In some clinical situations, an understanding of the detailed cardiovascular properties of an anesthetic is important, so the authors evaluated the hemodynamic effects of sevoflurane in healthy volunteers not undergoing surgery. METHODS: Twenty-one subjects were randomized to receive sevoflurane, isoflurane, or sevoflurane: 60% N2O. Anesthesia was induced and maintained by inhalation of the designated anesthetic. Hemodynamic measurements were performed before anesthesia, during controlled ventilation, during spontaneous ventilation, and again during controlled ventilation after 5.5 h of anesthesia. RESULTS: A few subjects became excessively hypotensive at high anesthetic concentrations (2.0 minimum alveolar concentration [MAC] sevoflurane, 1.5 and 2.0 MAC isoflurane), preventing data collection. Sevoflurane did not alter heart rate, but decreased mean arterial pressure and mean pulmonary artery pressure. Cardiac index decreased at 1.0 and 1.5 MAC, but in subjects with mean arterial pressure > or = 50 mmHg returned to baseline values at 2.0 MAC when systemic vascular resistance decreased. Sevoflurane did not alter echocardiographic indices of ventricular function, but did decrease an index of afterload. Sevoflurane caused a greater decrease in mean pulmonary artery pressure than did isoflurane, but the cardiovascular effects were otherwise similar. Administration of sevoflurane with 60% N2O, prolonged administration or spontaneous ventilation resulted in diminished cardiovascular depression. CONCLUSIONS: At 1.0 and 1.5 MAC, sevoflurane was well tolerated by healthy volunteers. At 2.0 MAC, in subjects with mean arterial pressure > or = 50 mmHg, no adverse cardiovascular properties were noted. Similar to other contemporary anesthetics, sevoflurane caused evidence of myocardial depression. Hemodynamic instability was noted in some subjects at high anesthetic concentrations in the absence of surgical stimulation. The incidence was similar to that with isoflurane. The cardiovascular effects of sevoflurane were similar to those of isoflurane, an anesthetic commonly used in clinical practice since 1981.