Acta anaesthesiologica Scandinavica
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Acta Anaesthesiol Scand · Nov 1988
Cardiac arrest during anaesthesia. A computer-aided study in 250,543 anaesthetics.
With the aid of a computer-based anaesthetic record-keeping system, all cardiac arrests during anaesthesia at the Karolinska Hospital between July 1967 and December 1984 were retrieved. There were a total of 170 cardiac arrests and 250,543 anaesthetics in the data file, which gives an incidence of 6.8 cardiac arrests per 10,000 anaesthetics. Sixty patients died, constituting a mortality of 2.4 per 10,000 anaesthetics: 42 were considered as inevitable deaths (rupture of aortic or cerebral aneurysm, multitrauma, etc.); 13 cases of cardiac arrest were considered as non-anaesthetic, i.e. complications due to surgery and other procedures. ⋯ The most common cause of cardiac arrest due to anaesthesia was hypoxia because of ventilatory problems (27 patients), postsuccinylcholine asystole (23 patients) and post-induction hypotension (14 patients). The highest mortality was seen when spinal or epidural anaesthetics were given to patients with impaired physical status including hypovolaemia. The incidence of cardiac arrest has declined considerably during the period studied, and this coincides with an increasing number of qualified anaesthetists employed in the department during the same period.
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Acta Anaesthesiol Scand · Nov 1988
Randomized Controlled Trial Comparative Study Clinical TrialQT interval of the ECG, heart rate and arterial pressure using five non-depolarizing muscle relaxants for intubation.
The QT interval, heart rate and arterial pressure were measured during anaesthetic induction in 186 patients without cardiovascular diseases or any preoperative drugs. The study was randomized and double-blind. The patients were premedicated with either pethidine 1 mg/kg + atropine 0.01 mg/kg or with only pethidine 1 mg/kg i.m. ⋯ The QT intervals were prolonged only in relation to the increased heart rate. At 6.5 min, the values in all groups were decreased to about the same level as before intubation. The mean control values of the heart rate were between 80 and 90 b.p.m. in the atropine-treated groups and between 70 and 80 b.p.m. in the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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Acta Anaesthesiol Scand · Nov 1988
Randomized Controlled Trial Clinical TrialEpidural clonidine for treatment of postoperative pain after thoracotomy. A double-blind placebo-controlled study.
Clonidine has been reported to produce analgesia in humans in different painful conditions. The aim of the present study was to investigate if epidural clonidine produced a clinically important analgesia to severe postoperative pain. Using a controlled, randomized double-blind design, one group of patients received a single dose of epidural clonidine 3 micrograms/kg (n = 10) and a control group epidural 0.9% saline (n = 10), when reporting postoperative pain after thoracotomy performed under standardized anaesthesia. ⋯ The side-effects of epidural clonidine were tolerable, and no treatment for arterial hypotension was required. No early or delayed respiratory depression occurred. In conclusion, clonidine 3 micrograms/kg epidurally seems to lack clinically important analgesic effects on severe postoperative pain, at least following thoracotomy.
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Acta Anaesthesiol Scand · Nov 1988
Continuous-flow apneic ventilation with small endobronchial catheters.
This study compares gas exchange and hemodynamic parameters during bronchial insufflation with two different internal diameter (ID) catheters (2.5 and 1.4 mm) at a constant mean gas exit velocity. Anesthetized, paralyzed dogs were instrumented to monitor arterial, central venous, and airway pressures, blood gases, temperature, ECG, and ventilated using continuous flow apneic ventilation (CFAV) via 2.5-mm or 1.4-mm ID bronchial insufflation catheters positioned 1.25 bronchial diameter units (BDU) beyond the carina. Initially, flow was adjusted to provide adequate oxygenation and ventilation through the 2.5-mm ID catheters. ⋯ After a 30-min stabilization period, physiological parameters were again recorded. No significant differences were noted in arterial, central venous, or airway pressures, temperature, heart rate, pH, PaCO2, and PaO2 between the 2.5-mm and 1.4-mm ID bronchial insufflation catheters. However, significantly less bronchial insufflation flow (69.7%) was required to maintain oxygenation and ventilation for the 1.4-mm ID bronchial insufflation catheters.
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Acta Anaesthesiol Scand · Oct 1988
Alterations in the pharmacokinetic properties of amide local anaesthetics following local anaesthetic induced convulsions.
The comparative pharmacokinetic properties of lidocaine, bupivacaine, etidocaine and mepivacaine were investigated in convulsing and non-convulsing dogs. The same dose of a given local anaesthetic was administered as either a 30-s intravenous (IV) bolus to produce convulsions or as a 15-min IV infusion producing no convulsions. Derived pharmacokinetic data were found to be different in convulsing and non-convulsing animals. ⋯ Overall, the most profound effects of convulsions on pharmacokinetic data were seen with mepivacaine. Convulsions were associated with increases in heart rate ranging from 117% (lidocaine, P less than 0.05) to 129% (mepivacaine, P less than 0.05), increases in cardiac output ranging from 78% (mepivacaine) to 232% (bupivacaine, P less than 0.05) and increases in mean arterial pressure ranging from 45% (lidocaine, P less than 0.05) to 80% (bupivacaine, P less than 0.05). The results suggest that when local anaesthetic-induced seizures occur in man, it cannot be assumed that these drugs will be distributed and eliminated as predicted by intravenous infusion of non-toxic doses.