Perioperative management and outcome of patients having cardiac surgery combined with abdominal aortic aneurysm resection.

Patients with abdominal aortic aneurysms (AAA) have a high incidence of associated cardiac disease. If a patient presents with both severe coronary artery disease and a large AAA, a staged procedure of cardiac surgery (CS) followed by AAA resection may present too great a risk of aneurysm rupture and death. A combined procedure may be recommended in this circumstance; however, the literature contains only individual successful case reports of such a procedure. A series of 10 patients who underwent CS and AAA repair to define the risks and outcome of this complex patient population is presented. Methods used included a retrospective analysis of hospital chart data from patients undergoing combined CS and AAA resection from 1980 to the present at this institution. The data analyzed included age, sex, chief complaint, past medical history, indications for surgery, abdominal aneurysm size, coronary anatomy, valvular pathology, preoperative left ventricular function, anesthetic agent and dose, order of surgery, prebypass complications, intraoperative complications, cardiopulmonary bypass time, aortic cross-clamp time, abdominal aortic cross-clamp time, blood product use, and postoperative complications. Seven of the 10 patients had a successful outcome (S group), whereas 3 of the 10 patients died postoperatively (D group). The staged procedure of first performing CS and then the AAA resection has a combined operative mortality of 4%. When the nature of both lesions is severe and a combined procedure is necessary, there is an associated in-hospital mortality of approximately 30% at this institution. The S group patients had an unremarkable postoperative course with a relatively short hospital stay when compared to the staged procedure.

Systemic lidocaine and human somatosensory-evoked potentials during sufentanil-isoflurane anaesthesia.

The effect of systemically administered lidocaine on somatosensory evoked potentials (SSEPs) during general anaesthesia has not been widely reported. Knowledge of the influence of anaesthetic agents on evoked potentials assists in interpreting evoked potential waveforms. Accordingly, we studied the behaviour of cortical and subcortical (recorded at the second cervical vertebra) SSEPs after administration of intravenous lidocaine (3 mg.kg-1 bolus followed by infusion at 4 mg.kg-1.hr-1) during a sufentanil-based anaesthetic regimen in 16 patients undergoing abdominal or orthopaedic surgery. When compared to awake baseline recordings, the sufentanil-nitrous oxide, low-dose isoflurane anaesthetic depressed N1 amplitude by approximately 40% and prolonged latency by 10%. Fifteen minutes after establishment of this anaesthetic, the amplitude and latency of N1 were 1.13 +/- 0.56 microV and 19.81 +/- 1.63 msec, respectively. Within five minutes of adding lidocaine, amplitude decreased further to 0.84 +/- 0.39 microV (P = 0.001), while latency was extended to 20.44 +/- 1.48 msec (P = 0.01). Lidocaine did not affect cervical amplitude and prolonged latency only minimally. Despite the observed effects on amplitude and latency, SSEP waveforms were preserved and interpretable. Plasma lidocaine levels obtained at 5, 20, and 40 minutes after lidocaine were 5.17 +/- 1.33, 3.76 +/- 1.14, and 3.66 +/- 0.9 micrograms.dl-1, respectively. Our results indicate that systemically administered lidocaine at therapeutic plasma levels acts synergistically with a sufentanil-based anaesthetic to depress the amplitude and prolong the latency of SSEPs.

The effect of intrathecal morphine on somatosensory evoked potentials in awake humans.

Although the effect of systemic opioids on somatosensory evoked potentials has been well described, little is known about the interaction between intrathecally administered opioid analgesics and somatosensory evoked potentials. Accordingly, the influence of intrathecally administered morphine on posterior tibial nerve somatosensory cortical evoked potentials (PTSCEPs) was investigated in 22 unpremedicated, awake, neurologically normal patients scheduled to undergo elective abdominal or pelvic procedures. Patients were randomly assigned to receive either preservation-free intrathecal morphine sulfate (ITMS) or placebo. After baseline PTSCEP, heart rate and, mean blood pressure were recorded, ITMS (15 micrograms.kg-1) was injected via standard dural puncture with the patient in the lateral position. PTSCEPs, heart rate, and mean blood pressure were recorded again at 5, 10, 20, 30, 60, 90, and 120 min. Control patients were treated identically (including position, sterile preparation, and subcutaneous tissue infiltration with local anesthetic), except for lumbar puncture, and were unaware of their randomization. Before administration of ITMS, PTSCEP P1, N1, P2, N2, and P3 latencies were 39.4 +/- 3.2, 47.6 +/- 3.9, 59.2 +/- 3.2, 70.4 +/- 3.7, and 84.6 +/- 5.5 ms, (mean +/- standard deviation), respectively. The corresponding P1-N1, N1-P2, and P2-N2 amplitudes were 2.4 +/- 1.1, 2.4 +/- 1.1, and 2.3 +/- 0.9 microV, respectively. There were no significant changes over time between the control and ITMS groups. PTSCEPs resulting from left-sided stimulation were not different from those elicited by right-sided stimulation. All ITMS patients had intense postoperative analgesia for at least 24 h. It is concluded that ITMS does not affect PTSCEP waveforms in the 35-90 ms latency range during the awake state.(ABSTRACT TRUNCATED AT 250 WORDS)

Intrathecal morphine does not reduce minimum alveolar concentration of halothane in humans: results of a double-blind study.

The effect of intrathecal morphine on the minimum alveolar concentration (MAC) of halothane was investigated in 22 patients undergoing elective abdominal surgery. The patients were randomly assigned to the control (CTRL) or intrathecal morphine sulfate (ITMS)-treated groups. Approximately 2.5 h before induction of anesthesia with halothane, the ITMS-treated group received 15 micrograms/kg preservative-free ITMS (Duramorph; Elkins-Sinn, Cherry Hill, NJ) while in the right lateral decubitus position. The CTRL group was treated in an identical fashion except that, after placement of the introducer needle, actual dural puncture was omitted. After inhalational induction with halothane as the sole anesthetic agent, the patients' responses to surgical incision were recorded. MAC was determined with the modified up-down method of Dixon and verified with probit analysis. MAC (+/- SE) after ITMS was 0.76 +/- 0.06, compared with a CTRL MAC of 0.78 +/- 0.15 (not significant). Under the conditions of this study, the MAC of halothane in humans was not significantly affected by ITMS.

Alpha-adrenergic agonist drugs, left ventricular function, and emergency from cardiopulmonary bypass.

The relationship between preoperative left ventricular (LV) dysfunction and the use of alpha-adrenoceptor agonists during weaning from cardiopulmonary bypass was studied in 102 patients undergoing coronary artery surgery. LV function was evaluated subjectively by examination of the 30 degree right anterior oblique left ventriculogram. Group 1 consisted of 75 patients with normal or mild impairment in LV function, whereas group 2 consisted of 27 patients with moderate-severe LV dysfunction. Cardiovascular parameters were measured at baseline, during hypothermic bypass with the aorta clamped, during normothermic bypass after unclamping, and 1 and 15 minutes after separation from bypass. Thirty-seven patients in group 1 (49%) and 11 patients in group 2 (39%) required some form of inotropic and/or vasopressor support during weaning from bypass. Group 2 required significantly higher cumulative doses of phenylephrine after bypass compared with group 1 (1.69 +/- 0.70 mg, n = 9, v 0.24 +/- 0.04 mg, n = 27, P less than 0.05). Similarly, the dose of norepinephrine infusion in group 2 was 3.3 times that in group 1 (10 +/- 6 micrograms/min, n = 2, v 3 +/- 0.6 micrograms/min, n = 2, P = NS). The higher doses of alpha-adrenoceptor agonists required in patients with moderate-severe LV dysfunction may be due to differences in alpha-adrenoceptor agonist affinity and/or receptor density.

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)

The effect of ketamine on human somatosensory evoked potentials and its modification by nitrous oxide.

The effect of ketamine alone and in combination with N2O (70% inspired) on median nerve somatosensory evoked potentials (SSEPs) was investigated in 16 neurologically normal patients undergoing elective abdominopelvic procedures. The anesthetic regimen consisted of ketamine (2 mg/kg iv bolus followed by continuous infusion at a rate of 30 micrograms.kg-1.min-1) [corrected], neuromuscular blockade (atracurium), and mechanical ventilation with 100% oxygen. SSEP recordings were obtained immediately preinduction and at 2, 5, 10, 15, 20, and 30 min postinduction. Thereafter, N2O was added with surgical incision and maintained for 15 min. At 5-min intervals, SSEP recordings were again taken during and after N2O. With minor exceptions, mean cortical and noncortical latencies as well as noncortical-evoked potential amplitude were unaffected by either ketamine or N2O. Ketamine induction increased cortical amplitude significantly with maximal increases occurring within 2-10 min. For example, at 5-min postinduction, mean N1-P1 amplitude increased from 2.58 +/- 1.05 (baseline) to 2.98 +/- 1.20 microV and P1-N2 amplitude increased from 2.12 +/- 1.50 (baseline) to 3.99 +/- 1.76 microV. Throughout the 30-min period after ketamine induction, mean P1-N2 amplitude increased generally by more (57-88%) than did mean N1-P1 amplitude (6-16%). N2O added to the background ketamine anesthetic produced a rapid and consistent reduction in both N1-P1 and P1-N2 amplitude. Thus, at 1 min after N2O, mean N1-P1 amplitude decreased from 2.74 +/- 1.11 to 1.64 +/- 0.63 microV, while P1-N2 amplitude decreased from 3.32 +/- 1.52 to 1.84 +/- 0.87 microV.(ABSTRACT TRUNCATED AT 250 WORDS)