Canadian Anaesthetists' Society journal最新文献

This study was designed to test the hypothesis that administration of clinical doses of cimetidine could affect the metabolic degradation of enflurane to inorganic fluoride via inhibition of the mixed function oxidase enzyme (MFOE) system. In Part 1 of the study 38 female patients undergoing gynaecologic surgery received, double blind, either cimetidine, 300 mg PO the night prior to surgery and 300 mg IV 30 minutes prior to anaesthesia induction or a placebo. In Part 2, 24 patients received either cimetidine as in Part 1, but with continued administration for 24 hours into the postoperative period, or a placebo. Anaesthesia in all cases was with enflurane in oxygen, via a closed circuit. In both Parts 1 and 2 of the study there were no statistically significant differences between the two groups in serum fluoride levels at baseline, four hours or 24 hours postoperatively, or in the total urinary fluoride excretion during the first or second postoperative days. The authors speculate that this is due either to separate interactions of cimetidine and enflurane with the MFOE system or to the relatively low rate of enflurane metabolism.

Expired carbon dioxide measurements (PeCO2) were used (1) to assess the adequacy of initial alveolar ventilation, and (2) to document intraoperative airway events and metabolic trends. Three hundred and thirty-one children were studied. Thirty-five intraoperative events were diagnosed by continuous PeCO2 monitoring; 20 were potentially life-threatening problems (malignant hyperthermia, circuit disconnection or leak, equipment failure, accidental extubation, endobronchial intubation, or kinked tube); only two of these were also diagnosed clinically. The duration of anaesthesia may be a factor: 3.9 hours for cases with events vs. 2.5 hours for cases without events (p less than 0.002). There was a higher incidence of hypercarbia (peak expired PeCO2 greater than or equal to 50) in children who were not intubated (29 per cent) compared to those who had an endotracheal tube in place (12 per cent) (p = 0.0001). Hypocarbia (peak expired PeCO2 less than or equal to 30) was more frequent in intubated cases (11 per cent) than in unintubated cases (three per cent) (p = 0.03). There was a high incidence of hypocarbia in infants less than one year of age (p = 0.02). We conclude: (1) life-threatening airway problems are common during anaesthesia in paediatric patients; (2) quantitative measurement of PeCO2 provides an early warning of potentially catastrophic anaesthetic mishaps; (3) the incidence of events increases with duration of anaesthesia.

Oscillometry using an automatic monitor was compared with invasive blood pressure monitoring in 21 patients scheduled for surgery under general anaesthesia with deliberate hypotension. Six ranges of mean blood pressure measurements were studied, two of which were hypotensive. An excellent correlation was found between the two methods (systolic: r = 0.94; mean: r = 0.93; diastolic: r = 0.88) but there was a large variability among individual subjects. For systolic, diastolic and mean intra-arterial readings above an approximative value of 10.64 KPa (80 mmHg), the oscillometric monitor was found to underestimate blood pressure. Inversely, it was found to overestimate blood pressure for intra-arterial readings under the approximative value of 10.8 KPa (80 mmHg). We conclude that the non-invasive monitor represents a good trend estimation of the invasive radial blood pressure technique, but that wide inter-individual variability and the overestimation of blood pressure below an approximative value of 10.64 KPa (80 mmHg) precludes interchange of techniques when absolute values are considered, especially during controlled hypotension. However, oscillometry could represent a better estimate of central aortic pressure.

The potential for inducing hypotension during fentanyl anaesthesia by administering either diltiazem (n = 7) or sodium nitroprusside (n = 7) was investigated during total hip arthroplasty. Haemodynamic variables were obtained in the lateral position before, during and after administration of the hypotensive agent. Diltiazem 0.15 mg X kg-1 given as an IV bolus followed by a 12.5 +/- 3 micrograms X kg-1 X min-1 continuous infusion decreased mean arterial pressure (MAP) from 77 +/- 11 mmHg to 63 +/- 16 mmHg (p less than 0.05) while other haemodynamic parameters showed only minor and insignificant changes. Hypotension continued for at least 30 min after the cessation of diltiazem. With sodium nitroprusside MAP decreased immediately from 81 +/- 11 mmHg to 59 +/- 9 mmHg (p less than 0.01) and rapidly returned to its control value after cessation of the infusion. CI and Qs/Qt rose significantly (p less than 0.05) while the systemic vascular resistance index (SVRI) (p less than 0.01) and pulmonary vascular resistance index (PVRI) (p less than 0.05) fell significantly. The haemodynamic profile was significantly different between hypotensive agents for MAP (p less than 0.02), heart rate (HR) (p less than 0.01), SVRI (p less than 0.05), and PVRI (p less than 0.05). HR was lower with diltiazem than with nitroprusside. A bradycardia less than 50 beats/min was observed in five patients in the diltiazem group. MAP, SVRI and PVRI were lower with nitroprusside than with diltiazem. Diltiazem can induce and maintain moderate hypotension without tachycardia and decreased cardiac output in humans during fentanyl anaesthesia but the modulation of the level of arterial pressure and the depression of atrioventricular conduction are unpredictable.

Serum potassium levels were measured in 15 patients with brain tumours between 3-7 cm diameter, during thiopentone/70 per cent N2O in O2 anaesthesia, with mask ventilation controlled to maintain a constant end-tidal CO2 concentration. Potassium levels were determined one minute before and one and ten minutes after administration of succinylcholine 1.0 mg X kg-1 IV. No statistically significant increase in serum potassium occurred following succinylcholine, nor were there any ECG changes associated with succinylcholine administration. Use of succinylcholine in patients with brain tumours does not appear to cause elevation of serum potassium levels or ECG changes.