Sufentanil and succinylcholine for rapid-sequence anesthetic induction and tracheal intubation: hemodynamic and hormonal responses.

Rapid-sequence induction and tracheal intubation are used in the management of patients at risk of aspiration. Patients with coronary artery disease (CAD) are at additional risk of adverse hemodynamic responses to intubation. The hemodynamic and hormonal responses to intubation with sufentanil, 7 micrograms/kg, and succinylcholine, 1.5 mg/kg, were studied in patients with CAD and good left ventricular function (ejection fraction greater than or equal to 0.4) who were undergoing elective coronary artery bypass grafting. Tracheal intubation occurred 60 seconds after administration of sufentanil and succinylcholine. Heart rate, systemic and pulmonary arterial pressures, pulmonary artery occlusion and central venous pressures, and cardiac outputs were measured at various time intervals before and after induction of anesthesia. Systemic vascular resistance and cardiac index were calculated. Arterial blood samples were drawn before and after anesthetic induction for the determination of catecholamine concentrations in serum. Rapid-sequence administration of sufentanil and succinylcholine resulted in a moderate decrease (24%) in mean arterial pressure from 95 to 72 mm Hg, and the mean arterial pressure remained less than the control value at 1, 3, and 5 minutes after intubation. Systemic vascular resistance also decreased (23%) after administration of sufentanil and returned to control values 5 minutes after intubation. There were no changes in cardiac index until 5 minutes after intubation, at which time it decreased (18%) from 2.8 to 2.3 L/min/m2.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil plasma concentration v. effect relationships in cardiac surgical patients.

Effects of alfentanil, preceded by lorazepam, on suppression of haemodynamic and somatic responses to noxious stimuli was studied in patients undergoing CABG. Plasma concentration of alfentanil, somatic and haemodynamic responses were measured at loss of consciousness, tracheal intubation, sternotomy and during multiple application of electrocoagulation. Additional alfentanil was administered i.v. to control unwanted responses. Study 1 (six patients): lorazepam 0.08 mg kg-1 by mouth 1-2 h before operation, alfentanil priming infusion (60 micrograms kg-1 min-1 for 10 min) followed by maintenance infusion (4.5 micrograms kg-1 min-1). With mean plasma alfentanil 1178 (SEM 54) ng ml-1, two patients required supplementary alfentanil to suppress somatic motor responses; one patients required nitroglycerin to control an increase in arterial pressure which was unresponsive to additional alfentanil following sternotomy. Study 2 (13 patients): lorazepam 0.04 mg kg-1 by mouth as premedication; one of three maintenance infusion rates of alfentanil: 5.4 (n = 4), 6.6 (n = 5), or 7.8 (n = 4) micrograms kg-1 min-1, each preceded by a proportional priming infusion. With plasma alfentanil 2181 (62) ng ml-1, somatic motor responses requiring additional alfentanil occurred in nine patients; haemodynamic responses in four of seven patients tested could not be controlled by alfentanil. The highest plasma concentration of alfentanil to prevent response to a stimulus other than tracheal intubation was different between the two studies (P less than 0.05). We conclude that alfentanil alone is insufficient to suppress haemodynamic and somatic motor responses to noxious stimulation during CABG and that the role of premedication is significant.