Effect of propranolol on circulatory responses to induction of diazepam-nitrous oxide anesthesia and to endotracheal intubation

The present study evaluated the hemodynamic effects produced by the intravenous infusion of diazepam (0.5 mg/kg over 10 minutes) and the simultaneous inhalation of 50% nitrous oxide in oxygen administered to 19 patients with coronary artery disease who were receiving chronic propranolol therapy (106 +/- 67 mg/day). In addition, hemodynamic changes produced by direct laryngoscopy and intubation of the trachea were measured. Data during the induction of anesthesia were compared to measurements obtained in a previously reported group of similar patients anesthetized in the same manner but not receiving propranolol. In the present study, as in previously observed patients not receiving propranolol, induction of anesthesia with diazepam-nitrous oxide did not result in any significant change from awake measurements with respect to heart rate (HR), mean arterial pressure (MAP), or rate-pressure product (RPP). Cardiovascular responses were similar in patients with awake resting heart rates greater than 70 beats per minute (nine patients) and less than 70 beats pr minute (10 patients). This suggests that propranolol does not alter the benign hemodynamic effects produced by this type of induction of anesthesia. Laryngoscopy and tracheal intubation significantly (p less than 0.01) increased MAP at 1 minute and HR and RPP at 1 and 2 minutes after the start of laryngoscopy. These changes were transient, returning to control values within 3 minutes after intubation. Patients with awake resting HR less than 70 beats per minute had greater increases in HR and RPP at 1 minute than did patients with resting HR greater than 70 beats per minute (p less than 0.05). This suggests that propranolol even in doses adequate to produce significant slowing of HR in awake patients does not ensure protection against increases in HR and MAP associated with laryngoscopy and intubation of the trachea.