Manually assisted and controlled respiration: its use during inhalation anesthesia for the maintenance of a near-normal physiologic state: a review.
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Anesthesia for craniotomies should guarantee hemodynamic stability, preservation of cerebral autoregulation, and rapid postoperative recovery of consciousness. Increases in intracranial pressure (ICP) and postoperative respiratory depression should be avoided. Combined anesthesia (KA) with N2O and volatile anesthetics may increase cerebral blood flow (CBF), ICP, and cerebral oxygen consumption. According to recent studies, total intravenous anesthesia (TIVA) with propofol and alfentanil seems to best fulfill the requirements. Using transcranial Doppler sonography (TCD) (TC2-64, EME), we studied the influence of TIVA and KA under normo- and hyperventilation on the blood flow velocity (BFV) and pulsatility of the middle cerebral artery (MCA). METHODS. Two groups of 10 patients each undergoing craniotomy were investigated. Systolic and mean BFV, pulsatility index, mean arterial blood pressure, heart rate, and arterial CO2 tension were measured at four time intervals: (1) preoperatively; (2) 15 min after anesthesia induction under normoventilation, preoperatively; (3) 25 min after anesthesia induction under hyperventilation, preoperatively; and (4) 6 h postoperatively. The patients were premedicated with flunitrazepam 1 mg PO. TIVA was induced with 60 mg propofol, 1 mg alfentanil, and 6 mg vecuronium; simultaneously infusions of propofol (15 mg/min) and alfentanil (0.3 mg/min) were started and were maintained until the dura was completely opened. The infusion rates were then reduced to 6 mg/min propofol until skin suturing and 0.1 mg/min alfentanil until dural suturing was completed. Patients were ventilated with O2/air (fiO2 = 0.5). In the KA group anesthesia was induced with 4-6 mg/kg thiopental, 0.15 mg fentanyl, and 6 mg vecuronium and maintained with boluses of fentanyl, N2O (fiO2 = 0.5), and isoflurane (1.3 MAC). The time course is illustrated in Figs. 1 and 2 and the results are shown in Tables 1 and 2. They were tested using a one-factor analysis of variance and the Kruskal-Wallis range test. RESULTS. There was a significant decrease in systolic and mean BFV combined with an increase in pulsatility index after induction of TIVA, while KA induction effected no significant change in cerebral hemodynamics. The subsequent hyperventilation caused a similar decrease in mean BFV and increase in pulsatility index in both groups. CONCLUSION. Using the assumption that the diameter of the MCA is nearly constant, the reduction in BFV associated with an increase in pulsatility during TIVA is explainable as a decrease in CBF. By having a comparable influence on hemodynamics, the reduction in CBF with increase in cerebral vascular resistance seems to make TIVA the more advantageous anesthesia technique for patients with reduced intracranial compliance.
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To assess administration of inhaled anesthesia during high-frequency oscillation, we evaluated the performance of a high-frequency oscillator that permitted incorporation of a precision vaporizer. The ventilator design used a single gas source for both vaporizer circuit and ventilatory support. The performance was evaluated in conjunction with a test lung device. The vaporizer performance was accurate when high-frequency, low-volume gas flow was used to provide source gas for the vaporizer. The ventilator provided accurate halothane delivery to the test lung device. Based on the results of this study, inhaled anesthesia can be accurately administered in conjunction with high-frequency oscillation. A single gas source that transverses the vaporizer before breathing circuit entrainment is critical for accurate results.
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Transient hyperammonemia was observed in rats after inhalation anesthesia with ether. The elevation of blood ammonia concentration induced by ether anesthesia was greatest in carbon tetrachloride injured and indomethacin-treated rats, but not observed in phenobarbital-treated rats. The results suggest interaction between ether metabolism and ammonia metabolism in the liver.
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