Pulmonary and systemic circulatory responses to inhalation of 50% nitrous oxide were studied in 11 patients with pulmonary hypertension prior to elective mitral valve replacement. All patients were ...premedicated with intramuscular morphine and scopolamine. Compared with awake control measurements while breathing 50% oxygen in nitrogen, heart rate, cardiac index, systemic and pulmonary vascular pressures, systemic vascular resistance, and systemic and pulmonary heart rate, systolic blood pressure products remained unchanged after administration of 50% nitrous oxide for 10 minutes. The only significant change was an increase in pulmonary vascular resistance from 159 +/- 18 dynes.sec.cm-5 before nitrous oxide inhalation to 213 +/- 27 dynes.sec.cm-5 during nitrous oxide inhalation (p less than 0.05). We conclude that nitrous oxide increases pulmonary vascular resistance in patients with preexisting pulmonary hypertension; however, this increase is not associated with alterations in other measured or calculated hemodynamic variables and is probably not of sufficient magnitude to recommend avoiding nitrous oxide in these patients.
Systemic circulatory responses to atracurium (0.2 and 0.4 mg/kg) were studied in 15 healthy (ASA I or II) adult patients during enflurane (1.0 to 1.25% inspired) and nitrous oxide (70% inspired) ...anesthesia. All patients were premedicated with intramuscular morphine (10-15 mg) and glycopyrrolate (0.2 mg). Compared with control measurements during enflurane-nitrous oxide anesthesia, heart rate, cardiac and stroke index, central venous pressure, and systemic mean arterial pressure remained unchanged at 2, 5, and 10 min after administration of both doses of atracurium. Systemic vascular resistance was minimally decreased (7% compared to control) (0.01 less than P less than 0.05) at 10 min following both doses of atracurium. No patient demonstrated a decrease in systemic mean arterial pressure greater than 6 mmHg. The authors conclude that atracurium in doses which produce adequate skeletal muscle relaxation during steady-state enflurane anesthesia produces no clinically significant alteration in hemodynamic variables.
The present study evaluated the hemodynamic effects produced by the intravenous infusion of diazepam (0.5 mg/kg over 10 minutes) and the simultaneous inhalation of 50% nitrous oxide in oxygen ...administered to 19 patients with coronary artery disease who were receiving chronic propranolol therapy (106 +/- 67 mg/day). In addition, hemodynamic changes produced by direct laryngoscopy and intubation of the trachea were measured. Data during the induction of anesthesia were compared to measurements obtained in a previously reported group of similar patients anesthetized in the same manner but not receiving propranolol. In the present study, as in previously observed patients not receiving propranolol, induction of anesthesia with diazepam-nitrous oxide did not result in any significant change from awake measurements with respect to heart rate (HR), mean arterial pressure (MAP), or rate-pressure product (RPP). Cardiovascular responses were similar in patients with awake resting heart rates greater than 70 beats per minute (nine patients) and less than 70 beats pr minute (10 patients). This suggests that propranolol does not alter the benign hemodynamic effects produced by this type of induction of anesthesia. Laryngoscopy and tracheal intubation significantly (p less than 0.01) increased MAP at 1 minute and HR and RPP at 1 and 2 minutes after the start of laryngoscopy. These changes were transient, returning to control values within 3 minutes after intubation. Patients with awake resting HR less than 70 beats per minute had greater increases in HR and RPP at 1 minute than did patients with resting HR greater than 70 beats per minute (p less than 0.05). This suggests that propranolol even in doses adequate to produce significant slowing of HR in awake patients does not ensure protection against increases in HR and MAP associated with laryngoscopy and intubation of the trachea.
The characteristics of phase II neuromuscular block following repeated intravenous injections of succinylcholine (SCh) were determined in 15 adult patients during enflurane, halothane, or ...fentanyl-nitrous oxide anesthesia. The onset of phase II block (train-of-four ratio (T4) equal to 0.5) occurred following a cumulative SCh dose of 4.4 +/- 0.3 (SEM) mg/kg of enflurane, 5.1 +/- 0.5 mg/kg of halothane, or 6.4 +/- 0.5 mg/kg of fentanyl. The cumulative SCh dose producing phase II block during fentanyl-nitrous oxide anesthesia was significantly greater than during enflurane (p less than 0.01) or halothane (p less than 0.05) anesthesia. Based on these data it is predicted that the likelihood of phase II block developing is less during fentanyl administration than during enflurane or halothane anesthesia. An abrupt transition from phase I to phase II neuromuscular block, as evidenced by an accelerated decrease in the T4 ratio, was observed during enflurane or halothane anesthesia as the cumulative SCh dose approached 3 to 5 mg/kg. The transition phase was delayed during fentanyl-nitrous oxide anesthesia, occurring after a cumulative SCh dose of 4 to 7 mg/kg. Following this transition, tachyphylaxis (decreased time between SCh injections) was observed in each study group. The T4 ratio in all three study groups stabilized at 0.15 to 0.25 after 7 to 8 mg/kg.
Circulatory responses following intravenous diazepam (0.5 mg/kg) and the subsequent addition of 50% nitrous oxide were studied in 14 patients undergoing elective aortocoronary saphenous vein bypass ...operations. No patient was receiving propranolol. Preanesthetic medication was with morphine and scopolamine. Diazepam was continuously infused over a 10-minute period. At the conclusion of the infusion, systolic and mean arterial pressures were 13% lower than control awake values (p less than 0.05). Heart rate, cardiac output, right atrial pressure, pulmonary arterial pressure, pulmonary artery occluded pressure, and systemic and pulmonary vascular resistance were not changed. The subsequent addition of nitrous oxide resulted in no further statistically significant changes except for a 2.4 torr increase in right atrial pressure (p less than 0.05). In contrast, previous data collected from similar patients demonstrated significant reductions in blood pressure and cardiac output while systemic and pulmonary vascular resistance and pulmonary artery occluded pressure were increased when nitrous oxide was added following the administration of morphine (1 to 2 mg/kg). It is concluded that the observed minimal circulatory changes following diazepam administration and the subsequent addition of nitrous oxide make diazepam-nitrous oxide a valuable alternative to a morphine-nitrous oxide induction of anesthesia in patients with coronary artery disease.
The ICARUS T600 liquid argon (LAr) time projection chamber (TPC) underwent a major overhaul at CERN in 2016-2017 to prepare for the operation at FNAL in the Short Baseline Neutrino (SBN) program. ...This included a major upgrade of the photo-multiplier system and of the TPC wire read-out electronics. The full TPC wire read-out electronics together with the new wire biasing and interconnection scheme are described. The design of a new signal feed-through flange is also a fundamental piece of this overhaul whose major feature is the integration of all electronics components onto the signal flange. Initial functionality tests of the full TPC electronics chain installed in the T600 detector at FNAL are also described.
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