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Cardiovascular Responses to Nitrous Oxide During Light, Moderate, and Deep Halothane Anesthesia in Man
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1978
Year
Nitrous OxideCardiac AnaesthesiaPercent HalothaneCardiovascular DiseasePeripheral ResistancePhysiologyAnesthesia PracticeCardiovascular ResponsesAnesthesiaMedicineCardiologyDeep Halothane AnesthesiaAnesthetic PharmacologyCent HalothaneAnesthesiology
The cardiovascular effects of addition of 20, 40, and then BO percent N2O or nitrogen during controlled ventilation with light (0.8 percent), moderate (1.2 percent), and deep (1.6 percent) halothane-O2 anesthesia were determined in 39 volunteers and compared to results obtained in 18 additional volunteers who received similar concentrations of halothane-O2 anesthesia alone over the same time interval. Halothane resulted in significant and similar reductions in heart rate at all concentrations studied hut produced concentration-related decreases in mean arterial blood pressure, stroke volume, and cardiac output and increases in right atrial pressure. Halothane did not significantly change peripheral resistance at any concentration. Addition of N2O did not change arterial blood pressure or heart rate at any concentration of halothane but produced increases in right atrial pressure in all groups. Peripheral resistance was reduced and stroke volume and cardiac output increased when N2O was added to 0.8 percent halothane. Subjects anesthetized with 1.2 percent halothane showed no significant change in stroke volume or cardiac output with addition of any concentration of N2O, while those anesthetized with 1.6 per cent halothane sustained reductions in stroke volume and cardiac output with 60 percent N2O. Peripheral resistance remained unaltered during addition of N2O to 1.2 percent halothane but significantly increased with 1.6 percent halothane. Addition of nitrogen to halothane produced changes that were similar to those occurring during continued halothane-O2 administration. These data demonstrate that addition of N2O during halothane-O2 anesthesia produces significant changes in cardiovascular dynamics which are variable and dependent upon the concentrations of halothane and N2O employed. Our findings suggest that N2O blocks the reduction of peripheral vascular resistance and increases in cardiac output, stroke volume, and heart rate seen with continued halothane-O2 administration when added to moderate or deep levels of halothane.