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.

Nalbuphine antagonism of fentanyl-induced ventilatory depression: a randomized trial.

The authors anesthetized 18 patients with good pulmonary and ventricular function for coronary artery bypass grafting with high doses of fentanyl. When the patients were arousable and their vital signs stable in the intensive care unit, the authors administered nalbuphine or placebo (randomly and double-blinded) until extubation criteria were met, and subsequently gave nalbuphine for analgesia. In one of ten placebo patients, tracheal extubation was accomplished without nalbuphine. This patient then retained CO2 and required nalbuphine; the other nine placebo patients could not be extubated after placebo trials and were given nalbuphine. In all other patients in both groups, tracheal extubation was successful following nalbuphine (median dose 60 micrograms/kg, range 30-180 micrograms/kg). One patient became renarcotized 4 h after tracheal extubation without an increase in plasma fentanyl concentration; he received an additional dose of nalbuphine and recovered without further incident. Nine patients required treatment with vasoactive agents or beta-blockers for hypertension or tachycardia associated with the administration of nalbuphine. Eight of 18 patients were not satisfied with nalbuphine analgesia, and required morphine for relief of their pain. Recurrent elevations of fentanyl concentrations in plasma were observed and appeared to be related to increasing motor activity. Nalbuphine is an effective opioid antagonist after fentanyl anesthesia, but its use is associated with side effects, and analgesia for the post-sternotomy patient may be unsatisfactory unless the dose is carefully titrated to the minimum required to antagonize respiratory depression.

High-dose fentanyl for rapid induction of anaesthesia in patients with coronary artery disease.

Nine premedicated patients, chronically maintained on beta-adrenergic blocking agents and demonstrating good ventricular function without significant valvular or left main coronary artery disease, were investigated to determine their haemodynamic responses to rapid induction of anaesthesia and tracheal intubation during elective coronary artery bypass surgery. Fentanyl 50 micrograms X kg-1 and pancuronium 0.15 mg X kg-1 were administered intravenously over 20 seconds followed by tracheal intubation 90 seconds thereafter. The rapid sequence of anaesthetic induction and tracheal intubation was well tolerated by all patients. Though statistically significant changes were detected in heart rate, pulmonary capillary wedge pressure and systemic vascular resistance, these changes were small and not considered clinically significant and no signs of ischaemia were detected on the ECG. The present study demonstrates that high-dose fentanyl is capable of inducing anaesthesia rapidly and protecting against the haemodynamic changes associated with tracheal intubation.

Absence of seizures during induction of anesthesia with high-dose fentanyl.

Anesthesia was induced in six patients scheduled for elective aortocoronary bypass (ACB) surgery with intravenous fentanyl, either 50 (n = 2) or 150 micrograms/kg (n = 4) over 20 or 60 sec, respectively. Patients had been given their usual antianginal medications before surgery and were premedicated with morphine sulfate. Arterial plasma fentanyl levels were measured repetitively at frequent intervals, and eight leads of the cortical electroencephalogram (EEG) were recorded continuously. Peak plasma fentanyl concentrations exceeded 1750 ng/ml at the end of the injection of 150 micrograms/kg and then decreased by more than 75% within 3 min. In an additional two patients, incremental doses of fentanyl (25, 25, 50, 50 micrograms/kg; total 150 micrograms/Kg) maintained fentanyl concentrations between 30 and 650 ng/ml for the entire 15 min of the study. In all cases, diffuse slow-wave EEG activity, characteristic of fentanyl anesthesia, was seen. Motor activity, including wrist flexion and ocular movements, was observed during the onset of fentanyl-induced truncal rigidity, but no seizure-like activity was found in the EEG.

High-dose hydromorphone (Dilaudid) for coronary artery bypass surgery.

The hemodynamic effects of high-dose hydromorphone hydrochloride (H), 1.25 mg/kg, were investigated in 10 patients with normal ventricular function undergoing coronary artery bypass graft (CABG) surgery. One patient with unstable angina was excluded from the study because of hypotension and facial flushing after a 6-mg test dose of H. Nine patients showed no significant change in heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), left ventricular stroke work index (LVSWI), systemic vascular resistance (SVR), pulmonary capillary wedge pressure (PCWP), or coronary perfusion pressure (CPP) after H; central venous pressure (CVP) increased significantly (P less than 0.05). Loss of consciousness did not occur reliably after H. The addition of 50% N2O to H produced significant decreases in CI and LVSWI (P less than 0.05). Hemodynamic responses to tracheal intubation, skin incision, and sternotomy included depression of CI, elevation of SVR, and increased MAP (P less than 0.05). Vasodilators were required in eight patients before aortic cannulation and after extracorporeal circulation. Mean time to awakening was 7.6 hr after the full dose of H, and extubation was performed the morning after surgery (21 hr after H) according to our usual practice. We conclude that very large doses of H (equivalent in analgesic terms to 10 mg/kg of morphine sulfate) are well tolerated by most patients undergoing CABG surgery, but unconsciousness and complete suppression of sympathetic responses require supplementation of H with additional anesthetic agents or vasodilators.