Comparison of the Ventilatory Effects of Etomidate and Methohexital

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Abstract
Using a dual-isohypercapnic technique, the effect of equipotent doses of methohexital (1.5 mg/kg) and etomidate (0.3 mg/kg) on the ventilatory response of CO2 (.ovrhdot.VERCO2) was studied in 6 healthy volunteers. Speed of induction and duration of hypnosis did not differ significantly between the 2 drugs. Within 2 min after injection, the slope of .ovrhdot.VERCO2 decreased significantly after both methohexital (from 2.52 to a minimum of 0.15 l .cntdot. min-1, mmHg-1, P < 0.05) and etomidate (from 2.56 to a minimum of 0.62 l .cntdot. min-1 .cntdot. mmHg-1, P < 0.05); the magnitude of this depression did not differ significantly between the drugs. Methohexital caused a significant decrease in minute ventilation at end-tidal PCO2 [pressure for CO2] of 46 mmHg (.ovrhdot.VE 46) from 14.6 to 4.3 1 .cntdot. min-1 within 60 s after injection (P < 0.05). After etomidate .ovrhdot.VE 46 gradually increased from 17.9 l .cntdot. min-1 to a maximum of 31.6 1 .cntdot. min-1 at 3.5 min after injection (P < 0.05); respiratory rate increased significantly, while changes in tidal volume were not significant. Effects of etomidate and methohexital on .ovrhdot.VE 46 differed significantly (P < 0.001). While etomidate and methohexital similarly depress the medullary centers that modify ventilatory drive in response to changing CO2 tensions, ventilation at any given CO2 tension is greater after etomidate than after methohexital. Etomidate may cause a CO2-independent stimulation of ventilation, suggesting its use for induction of anesthesia in cases where maintenance of spontaneous ventilation is desirable.

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