Canadian journal of anaesthesia = Journal canadien d'anesthésie
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Randomized Controlled Trial Clinical Trial
The management of temperature during hypothermic cardiopulmonary bypass: II--Effect of prolonged hypothermia.
In animals mild hypothermia (32-35 degrees C) reduces ischaemic brain injury, but this has not been investigated in humans. During hypothermic cardiopulmonary bypass (CPB) patients are made hypothermic (usually to 30-32 degrees C) but are then rewarmed at a time when they are still at risk of ischaemic brain injury. We investigated the feasibility and safety of maintaining mild hypothermia throughout the CPB period. ⋯ There were no differences between groups in intra- or postoperative blood loss or blood use, inotrope use, dysrhythmias, or myocardial infarction. The hypothermic group received more muscle relaxant for the treatment of shivering postoperatively. Our results suggest that mild hypothermia following CPB did not increase morbidity although larger studies are needed for confirmation.
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Comparative Study
High-dose vecuronium neuromuscular block: a comparison of arrhythmias and onset of block during sufentanil anaesthesia.
This study compared the heamodynamic effects of sufentanil with those observed following concomitant sufentanil and high-dose vecuronium administration to determine whether vecuronium induces bradyarrhythmias. Sixty coronary artery bypass patients were stratified into beta blocker (n = 30) or non-beta blocker (n = 30) groups and following induction with sufentanil (9 +/- 3 micrograms.kg-1) and midazolam (0.07 +/- 0.04 mg.kg-1), received either succinylcholine 1 mg.kg-1 (SxCh), vecuronium 0.3 mg.kg-1 (Vec 0.3), or vecuronium 0.5 mg.kg-1 (Vec 0.5). Using a Holter ECG monitor, bradyarrhythmias were classified as mild (HR 46-50), moderate (HR 40-45) or severe (HR < 40). ⋯ Following induction, there were similar reductions in mean heart rate and mean arterial pressure in all three muscle relaxant groups in both the beta and the non-beta blocker groups; however, there was no difference in the incidence of mild, moderate or severe bradyarrhythmias among the SxCh, Vec 0.3 or Vec 0.5 groups. The Vec 0.5 beta blocker group had a higher incidence of mild bradyarrhythmias (32 +/- 36%) than the Vec 0.5 non-beta blocker group (2 +/- 3%, P = 0.017). Using EMG recording, the onset time of maximal neuromuscular block for the Vec 0.3 group (108 +/- 17 sec) was longer (P < 0.05) than the SxCh (76 +/- 21 sec) and Vec 0.5 (82 +/- 13 sec) groups, which were similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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During hypothermic cardiopulmonary bypass (CPB) patients are cooled, usually to between 30-32 degrees C, and, after myocardial blood flow is restored, they are rewarmed with blood heated in the pump-oxygenator. We audited our local practice by recording tympanic and nasopharyngeal temperatures in 11 patients undergoing hypothermic CPB. ⋯ This may be of some importance because it has become widely appreciated by neuroscientists that mild degrees of brain cooling (2-5 degrees C) are capable of conferring dramatic protection from ischaemic brain injury and, conversely, mild temperature elevation may be markedly deleterious. If control of brain temperature is considered desirable then we would suggest that nasopharyngeal temperature be monitored during rewarming on CPB.
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Randomized Controlled Trial Comparative Study Clinical Trial
Sedative and ventilatory effects of midazolam infusion: effect of flumazenil reversal.
The purpose of this study was to evaluate the effects of flumazenil (1 mg i.v.) on the ventilatory response of premedicated patients receiving a continuous infusion of midazolam for sedation. After assessing baseline ventilatory function using a modified Read rebreathing method for determining hypercapnic ventilatory drive, 16 healthy outpatients were administered fentanyl, 50 micrograms i.v., and midazolam 2 mg i.v., followed by a variable-rate midazolam infusion, 0.3-0.5 mg.min-1. Upon termination of the midazolam infusion, serum midazolam concentrations were measured and ventilatory function was reassessed. ⋯ In some patients, the ventilatory response to hypercarbia actually decreased after flumazenil administration compared with the immediate prereversal (sedated) values. It is concluded that midazolam infusion, 0.43 mg.min-1, did not impair CO2-responsiveness. Flumazenil's effect on central ventilatory drive was more variable than its reversal of midazolam-induced sedation.