Isoflurane-nitrous Oxide Research Articles

SINGLE BREATH INDUCTION OF ANAESTHESIA WITH ISOFLURANE

This study has compared a single breath induction technique and a conventional inhalation induction technique using isoflurane in nitrous oxide and oxygen. Each group consisted of 36 unpremedicated patients. Single breath induction was associated with fewer problems on induction, but required more patient co-operation. Ninety-four percent of patients were willing to repeat the single breath induction technique, compared with 74% of patients receiving a conventional inhalation induction.

Effect of Spontaneous Sighs on Arterial Oxygenation during Isoflurane Anesthesia in Humans

The presence, frequency, and volume of spontaneous sighs was evaluated in 21 (ASA 1-2) supine patients aged 44 +/- 15.2 (SD) yr, during isoflurane-nitrous oxide anesthesia. Before induction the inspiratory capacity of each patient was determined. After induction of anesthesia and tracheal intubation patients breathed spontaneously except for three manual inflations to each patient's predetermined inspiratory capacity at the beginning and end of surgery. Arterial blood gas tensions were measured before and 5 min after each set of mechanical deep breaths and each hour during surgery, the mean duration of which was 2 +/- 0.09 hr. Spontaneous sighs occurred in 13 of 21 patients. The average frequency was 6 +/- 4 sighs/hr. At FIO2 = 0.5, nonsighing patients had an initial PaO2 of 229 +/- 59 mm Hg and sighers had an initial PaO2 of 162 +/- 57 mm Hg (P less than 0.05). Arterial oxygen did not change in sighing patients during the course of surgery, while in nonsighing patients the PaO2 decreased from the initial value of 229 +/- 60 mm Hg to 170 +/- 63 mm Hg (P less than 0.05). Mechanical deep breaths administered at the end of surgery produced no improvement in oxygenation in either sighers or nonsighers. The presence or absence of sighs did not correlate with PaO2 or PACO2. Though the results suggest that spontaneous sighs in some patients may function to help maintain arterial oxygenation, all patients maintained their PaO2 while breathing spontaneously under general anesthesia in the supine position.

Nitrous Oxide Does Not Increase the Incidence of Nausea and Vomiting after Isoflurane Anesthesia

A total of 110 patients undergoing elective abdominal hysterectomy were anesthetized in random order with either isoflurane in nitrous oxide and oxygen or isoflurane in air and oxygen. Fentanyl was used as an adjunct to isoflurane in all patients, 0.05 mg every 45 min. No difference was found between the two anesthetic techniques in the incidence of nausea, vomiting, or both during the first 24 hr after operation. The overall incidence was 62 and 67% for air-O2 and N2O-O2 groups, respectively. Patients who had had nausea or vomiting after previous anesthetics had nausea or vomiting significantly more frequently than patients who did not. It is concluded that nitrous oxide does not contribute to the occurrence of nausea or vomiting after isoflurane anesthesia for gynecologic laparotomies.

The Effects of Isoflurane and Isoflurane-Nitrous Oxide Anesthesia on Brainstem Auditory Evoked Potentials in Humans

Monitoring of brainstem auditory evoked potentials (BAEP) during neurological surgery can provide useful information. However, in order to interpret intraoperative BAEP changes, it is necessary to delineate the influence of anesthesia, including inhalation agents. In this study, we examined the influence of isoflurane and isoflurane-nitrous oxide anesthesia on BAEP in ten healthy volunteers during normothermic, normocapnic, and normotensive conditions. Isoflurane significantly increased the latencies of peaks III, IV, and V at all end-tidal concentrations studied (1.0%, 1.5%, and 2.0%). Addition of 50% nitrous oxide did not influence these findings. The increase in latencies with isoflurane anesthesia, however, was nonlinear and appeared to plateau after 1.5%. We suggest that during isoflurane anesthesia, an intraoperative increase in peak V latency beyond 1.0 msec is best explained by factors other than direct effects of isoflurane.

Respiratory Sinus Arrhythmia during Recovery from Isoflurane???Nitrous Oxide Anesthesia

Heart rate and respiratory patterns were monitored in ten ambulatory female patients undergoing elective laparoscopy. The patients were anesthetized with isoflurane-nitrous oxide. An index of cardiac vagal tone determined from the heart rate pattern by quantifying the amplitude of respiratory sinus arrhythmia was elevated over four 10-min periods: before induction of anesthesia; during maintenance of anesthesia; upon arrival in the recovery room; and 20-30 min later when the patient was fully conscious. All ten patients' vagal tones were lowest during maintenance of anesthesia. During the recovery periods vagal tone increased and approached the conscious level. On-line analysis of respiratory sinus arrhythmia may provide a physiological index of the level of anesthesia and the rate of recovery.

Untersuchungen der Kreislaufwirkungen von Vecuronium sowie von Pancuronium unter verschiedenen Anästhesie-Bedingungen

The cardiovascular effects of equipotent doses (1,25 X ED95) of vecuronium (70 micrograms/kg iv) and pancuronium (80 micrograms/kg iv) were studied in 16 patients scheduled for elective coronary artery bypass surgery during steady-state conditions of isoflurane (0,4-0,5 vol% end-tidal)-nitrous oxide anaesthesia. All patients were chronically treated with oral beta receptor-blocking agents. Vecuronium did not cause any significant cardiovascular changes whereas pancuronium produced increases in heart rate (13%), cardiac index (15%) and mean arterial pressure (4%) while systemic vascular resistance decreased (8%). In a second part of this study we analysed whether the magnitude of the vagolytic effects of pancuronium is influenced by the anaesthetic procedure and/or by preoperative beta-blocker therapy. A group of 8 patients who were pretreated with beta-receptor blockers and received fentanyl (7 micrograms/kg) during the anaesthetic procedure showed low control values of heart rate (HR), cardiac index (CI), mean arterial pressure (MAP) and the rate-pressure product (RPP) which were due to both, the antisympathetic effects of beta-blocker therapy and the central vagomimetic properties of fentanyl. The administration of pancuronium (80 micrograms/kg) caused the greatest percentage increases in HR (20%), CI (22%), MAP (8%) and RPP (31%) in this group of patients. In contrast, patients (n = 8) anaesthetized with isoflurane-nitrous oxide who were not on preoperative beta-receptor blocker medication, demonstrated higher haemodynamic control values and less increases in HR (10%), CI (10%) and RPP (15%), MAP did not change. The clinical significance of these findings is discussed.

The Effects of Isoflurane and Isoflurane-Nitrous Oxide Anesthesia on Brainstem Auditory Evoked Potentials in Humans

Monitoring of brainstem auditory evoked potentials (BAEP) during neurological surgery can provide useful information. However, in order to interpret intraoperative BAEP changes, it is necessary to delineate the influence of anesthesia, including inhalation agents. In this study, we examined the influence of isoflurane and isoflurane-nitrous oxide anesthesia on BAEP in ten healthy volunteers during normothermic, normocapnic, and normotensive conditions. isoflurane significantly increased the latencies of peaks III, IV, and V at all end-tidal concentrations studied (1.0%, 1.5%, and 2.0%). Addition of 50% nitrous oxide did not influence these findings. The increase in latencies with isoflurane anesthesia, however, was nonlinear and appeared to plateau after 1.5%. We suggest that during isoflurane anesthesia, an intraoperative increase in peak V latency beyond 1.0 msec is best explained by factors other than direct effect of isoflurane.

Time-dependent changes in cerebral and cardiovascular parameters in isoflurane-nitrous oxide-anesthetized dogs.

The purpose of this study was to examine the time-dependent effects of isoflurane-nitrous oxide anesthesia on cerebral blood flow and metabolism and on cardiovascular parameters. Eleven 15-kg mongrel dogs were anesthetized with 0.8% isoflurane (approximately 1.3 MAC (minimal anesthetic concentration], 70% nitrous oxide, and 30% O2 and were paralyzed with pancuronium. Blood flow (using the radioactive microsphere technique) and cerebrovascular and cardiovascular parameters were measured 6 times at 30-minute intervals beginning 2 hours after the induction of anesthesia. In this experiment, cerebral blood flow was markedly elevated at 2 hours after the induction of anesthesia, but then declined progressively by 40 to 50% over the 2 1/2-hour time period investigated, approaching values for normal awake dogs. The decline was accompanied by a progressive decrease in the cerebral metabolic rate of oxygen and a constant rise in cerebrovascular resistance. Blood flow to organs outside the central nervous system declined progressively, but with more variability between tissues. The mean arterial pressure increased slightly, and the peripheral vascular resistance almost doubled, but cardiac index, cardiac work, and stroke volume all decreased gradually. We conclude that isoflurane-nitrous oxide anesthesia produces significant cerebral vasodilatation in dogs, but that this effect diminishes over time. These time-dependent circulatory changes merit further investigation in humans.

Plasma Cholinesterase Activity and Tachyphylaxis during Prolonged Succinylcholine Infusion

Fifteen patients were studied during general anesthesia (nitrous oxide-fentanyl, N = 7 or nitrous oxide-isoflurane, N = 8) to determine the relationship between plasma cholinesterase activity and succinylcholine requirements during prolonged infusion. Using train-of-four stimulation, neuromuscular block was maintained at 90% for at least 1 hour, and plasma cholinesterase was measured at 30-minute intervals. During the infusion, succinylcholine requirements increased in every patient (tachyphylaxis), but there was no significant change in plasma cholinesterase activity. Succinylcholine requirements during the 1st hour of infusion in patients given fentanyl were correlated with preinfusion cholinesterase activity. It is concluded that tachyphylaxis to succinylcholine is not the result of increased metabolism from enzyme induction and that succinylcholine requirement is related to plasma cholinesterase activity.

Cardiovascular effects of isoflurane in surgical patients.

Cardiovascular responses to isoflurane–nitrous oxide–oxygen anesthesia were studied in 32 older patients undergoing surgical operations. In half of the patients, anesthesia was induced with isoflurane alone, in the remainder, with isoflurane and thiopental All were intubated and mechanically ventilated to maintain normal Paco Stroke volume, heart rate, cardiac output, systemic resistance, systolic, diastolic and mean pressures, and central venous pressure changes were generally similar to those found by other investigators in patients not undergoing surgical operations, except that we observed an increased systemic resistance. A decrease in stroke volume was counterbalanced by increases in pulse rate and systemic resistance, so that the total effect on cardiac output and arterial pressures was negligible. The cardiovascular responses that we found suggest that isoflurane may counteract primary myocardial depression by autonomic mechanisms similar to those seen with diethyl ether anesthesia.