Journal of clinical anesthesia
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Randomized Controlled Trial Clinical Trial
Attenuation of the hemodynamic responses to endotracheal intubation with preinduction intravenous labetalol.
Endotracheal intubation following anesthesia induction frequently produces hypertension and tachycardia. This study evaluated the efficacy of preinduction IV labetalol for attenuating the hemodynamic responses to intubation following thiopental and succinylcholine induction of anesthesia. Two hours after diazepam (10 mg by mouth), 60 patients were randomized in a double-blind manner and received IV saline or labetalol at doses of 0.25, 0.5, 0.75, or 1 mg/kg in a parallel design study. ⋯ All doses of labetalol significantly attenuated the rate-pressure product increase immediately postintubation versus placebo. There was a dose-dependent attenuation of the increases in heart rate and the systolic, diastolic, and mean blood pressures versus placebo following intubation. IV labetalol at doses up to 0.75 mg/kg offers an effective pharmacologic means of attenuating preoperative hemodynamic responses to endotracheal intubation.
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The influence of increasing doses of propofol (from 6 to 12 mg/kg/h by continuous infusion) on hypoxic pulmonary vasoconstriction was studied in 10 patients prior to thoracic surgery. All patients were intubated with a left-sided double-lumen endobronchial tube. Initial anesthesia and muscle relaxation were accomplished by administering fentanyl, droperidol, and pancuronium. ⋯ There was no change in any respiratory or circulatory variables except systemic vascular resistance, which decreased significantly immediately after the propofol infusion commenced but returned to control values 15 min later for the rest of the observation period. After reestablishing two-lung ventilation, all variables did not differ from control values. In all patients, the hypoxic pulmonary vasoconstriction reflex was present after institution of one-lung ventilation and was not abolished after administration of propofol in doses from 6 to 12 mg/kg/h.
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Apneic, anesthetized patients frequently develop airway obstruction or may be disconnected from ventilatory support. The rate of PaCO2 rise is usually assumed to be equal to that of anesthetized humans who are receiving apneic oxygenation. Apneic oxygenation may eliminate CO2 because it requires a continuous O2 flow. ⋯ Piecewise linear approximation yielded a PaCO2 increase of 12 mmHg during the first minute of apnea, and 3.4 mmHg/minute thereafter. These values should be employed when estimating the duration of apnea from PaCO2 change for anesthetized patients who lack ventilatory support. In addition, it appears that the flows of O2 that most earlier investigators used when delivering apneic oxygenation probably did not eliminate significant CO2 quantities.