To determine the electrophysiological effects of propofol and to explain the potential mechanism(s) whereby it causes bradyarrhythmias, 10 closed-chest pigs weighing 20-25 kg were studied. Each animal was premedicated by intramuscular administration of ketamine hydrochloride, intubated, and mechanically ventilated. Femoral arterial and venous catheters were placed, and a comprehensive electrophysiologic evaluation was performed at baseline and after two doses (1 mg/kg i.v. bolus and 0.1 mg/kg/min infusion and an extra 1-mg/kg i.v. bolus and 0.2 mg/kg/min infusion) of propofol. The electrophysiological effects obtained on low- and high-dose propofol were compared to baseline values. Propofol caused a dose-related decrease in sinus cycle length (baseline 565 ± 36 ms, low-dose propofol 541 ± 28, high-dose propofol 527 ± 26 ms; p < 0.05), a prolongation of the corrected sinus node recovery time (baseline 119 ± 35 ms, low-dose propofol 126 ± 32, high-dose propofol 130 ± 30 ms; p < 0.01), and an increase in the His-ventricular interval (baseline 33 ± 4 ms, low-dose propofol 36 ± 4, high-dose propofol 40 ± 3 ms; p < 0.005). All other electrophysiological parameters remained unchanged, and there were no cases of spontaneous atrioventricular block or sinus pauses. We conclude that propofol causes dose-related depression of sinus node and His-Purkinje system functions, but has no effect on the atrioventricular node function and on the conduction properties of atrial and ventricular tissues in normal pig hearts.

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We evaluated the benefits of bilateral deep cervical plexus block regional anesthesia in healthy and high risk patients undergoing thyroid and parathyroid surgery and assessed its effects on respiratory function. Twenty-one patients undergoing thyroid and parathyroid operations were studied. Bilateral superficial and deep plexus blocks were performed in all patients except one (who received only superficial plexus block because of a slightly prolonged prothrombin time) with 0.375-0.5% bupivacaine with 1:200,000 epinephrine. Intraoperatively, supplemental intravenous sedatives/narcotics were titrated to achieve patient comfort and cooperation. To allay anxiety, patients were allowed to listen to music via headphones intraoperatively. Forced vital capacity was measured before block, 10 minutes after the block and in the recovery room in half the patients. Eighteen patients tolerated the procedure well with supplemental sedation. Two patients required supplemental inhalation anesthesia via mask and one required tracheal intubation because of coughing prior to surgery. Three high risk patients tolerated the procedure well requiring only intraarterial line monitoring. Postoperatively, 11 patients had minimal incisional pain, 13 patients had mild pain on swallowing and 2 patients complained of nausea. There were no significant differences in the baseline forced vital capacity vs. forced vital capacity measured after the block and in the recovery room. This study indicates that regional anesthesia is an appropriate alternative to general anesthesia in selected patients undergoing thyroid and parathyroid surgery and did not compromise respiratory function.

Although both ketamine and halothane inhibit potassium currents through the Kv2.1 channel, their mechanisms of action at this potential target may be different. Deletion of the C-terminal sequence resulted in decreased sensitivity to both anesthetics. Although it is not clear whether anesthetics interact directly with the C-terminus, which is thought to reside intracellularly, this portion of the channel protein clearly influences the actions of both anesthetics.

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