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Hemodynamic effects of nicardipine-induced hypotension during enflurane/nitrous oxide were evaluated in 10 surgical patients. An infusion of nicardipine was titrated to maintain mean arterial pressure at 60 to 70 mmHg under enflurane 1.5 to 2.0 vol% and nitrous oxide 60 vol%. Mean arterial pressure was well controlled with the nicardipine infusion, whereas cardiac index increased with decreased systemic vascular resistance. Heart rate increased concomitantly with decreased blood pressure, which indicated that enflurane 1.5 to 2.0 vol% did not suppress baroreceptor reflex during nicardipine administration. However, rate-pressure-product was not increased by the nicardipine. Right and left ventricular systolic work indices were not increased by the nicardipine. Right ventricular ejection fraction was not also changed by the nicardipine. Although serum norepinephrine level increased during the nicardipine infusion, the values remained within physiological ranges. Our results suggest that nicardipine-induced hypotension may be safely performed during enflurane/nitrous oxide anesthesia because neither ventricular work nor myocardial oxygen demand was increased by nicardipine.

The effects of anesthetic induction by diazepam, flunitrazepam and midazolam on cardiac performance were evaluated in 33 ASA class I surgical patients (average age was 36 years). The patients were divided according to the 3 drug groups, and the effects of each drug assessed utilizing measurements of systolic time intervals. An increase in heart rate and decrease in blood pressure was observed following flunitrazepam and midazolam induction. There was no changes in PEPI (pre-ejection period index) and LVETI (left ventricular ejection time index) by benzodiazepines induction. The PEP/LVET ratio was increased by diazepam while the DPTI (diastolic pressure time index)/TTI (tension time index) was reduced by flunitrazepam and midazolam. However, these changes in PEP/LVET and DPTI/TTI were within normal limits. These data indicate that in healthy humans the induction dose of either diazepam, flunitrazepam or midazolam does not extremely influence either PEP/LVET for cardiac performance or DPTI/TTI for cardiac oxygen balance. The results also suggest that the simultaneous use of PEP/LVET and DPTI/TTI is more informative than any single variable for the evaluation of cardiac effects of anesthetics.

The combined negative inotropic effects ofisoflurane and calcium entry blockers (verapamil, diltiazem, nifedipine, nicardipine) were studied utilizing isolated heart preparations of ventricular muscles from dogs. All of these calcium entry blockers exerted dose-dependent decreases in maximal velocity of shortening (Vmax), maximal developed isometric force (Fm), and the maximal first derivative of Fm (maximal dF/dt). Dose-dependent decreases of these variables of muscle mechanics were augmented in isoflurane-depressed myocardium. At equimolar concentrations, direct myocardial depression was demonstrated in the following order of severity: nifedipine > diltiazem = verapamil > nicardipine. Percent depressions of Vmax, Fm and maximal dF/dt were significantly greater in muscles when calcium entry blockers were combined with 1MAC isoflurane than in muscles of calcium entry blockers alone. These data suggest that the negative inotropic effects of verapamil, diltiazem, nifedipine, and nicardipine were potentiated by isoflurane

Clinical evaluation of continuous\(S\bar v_{O_2 } \) monitoring during general anesthesia was made in 21 surgical patients utilizing a fiberoptic reflectometry system combined with a pulmonary artery flow-directed balloon catheter. On-line in vivo values for\(S\bar v_{O_2 } \) by the system were closely related to those obtained in vitro from a Radiometer ABL-300. There was a good correlation between changes of in vivo\(S\bar v_{O_2 } \) and corresponding changes in cardiac index. We also observed that there were significant correlations between\(S\bar v_{O_2 } \) and oxygen extraction ratio, and\(S\bar v_{O_2 } \) and oxygen delivery. These data indicate that continuous monitoring of\(S\bar v_{O_2 } \) during general anesthesia can provide on-line information not only about hemodynamic state but also on oxygen transport, which will be especially helpful in managing hemodynamicaly unstable patients during anesthesia.

We evaluate the accuracy of cardiac output measurement with esophageal Doppler ultrasonography (ECO). A total of 71 simultaneous measurement of esophageal Doppler and thermodilution cardiac output were compared in 16 patients undergoing general anesthesia in the supine position. ECO was determined easily with minimal experience, and significantly correlated with thermodilution cardiac output (TDCO) measurement ( P0.001). The regression equation obtained was Y = 0.983X + 0.019, and the correlation coefficient was 0.935. Furthermore, ECO was more reproducible than TDCO. However, ECO is not able to assess CO accurately in either lateral or prone position and after cardiopulmonary bypass in open heart surgery. Our results suggest that the esophageal Doppler technique allows a noninvasive and continuous cardiac output monitoring in patients during general anesthesia, and that it is more useful in patients for whom invasive monitoring is considered inappropriate. However, further improvement in this technique will be necessary for its routine use in clinical anesthesia.

The direct inotropic action of seven local anesthetics: procaine, mapivacaine, lidocaine, tetracaine, chloroprocaine, bupivacaine and etidocaine were compared in isolated cat papillary muscles. All of the local anesthetics produced a doserelated depression of maximal velocity of shortening (Vmax), maximal developed force (Fm) and maximal dF /dt. The more potent local anesthetics such as bupivacaine and etidocaine depressed myocardial contractility at significantly lower concentrations than the less potent local anesthetics such as lidocaine and mepivacaine. Depression of Vmax by bupivacaine or etidocaine was three times greater than that by lidocaine and ten times greater than that by procaine. At the same concentration (10−4M), direct myocardial depression was demonstrated in the following order of severity: etidocaine ≥ bupivacaine > tetracaine > chloroprocaine ≥ lidocaine > mepivacaine > procaine.