Inspiratory force in the intubated patient during spontaneous respiratory effort following general anaesthesia.
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Biomedical subjects
Publications and source records attributed to M Ibler.
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Fentanyl is a strong, synthetic analgesic which may cause muscular rigidity when administered intravenously. To obtain a quantitative measure of the possible increase in muscle tone after intravenous fentanyl, the muscular tension of the right rectus abdominis was measured in 20 patients before and after administration of this drug. A traction transducer apparatus was fastened between the anterior and posterior rectus sheath in a right oblique laparotomy incision. Premedication was with pentobarbitone, and the anaesthesia and muscle relaxation were effected by thiopentone or enibomal and nitrous oxide-oxygen with 75% nitrous oxide, and suxamethonium infusion (0.2%) until the measurement of tension was started. Immediately after the action of suxamethonium had ceased, fentanyl, about 0.004 mg/kg body weight, was administered. An increase in tone was found in 15 cases (75%). The mean increase was 9.2 N. The influence of the anaesthesia upon the result is discussed, and it is concluded that fentanyl must be responsible for the increase in muscle tone.
The systolic time intervals were studied in 16 surgical patients without heart disease between 29 and 75 years of age by a non-invasive technique before and after an induction dose of enibomal (Narcodorm). The pre-injection period/left ventricular ejection time-ratio (PEP/LVET-ratio) increased between 8 and 60% and (1/PEP-2) decreased between 3 and 50%, indicating a reduction of myocardial contractility under the influence of enibomal. Factors responsible for circulatory depression during barbiturate anaesthesia are discussed.
The systolic time intervals and calculated parameters of PEP/LVET (pre-injection period/left ventricular ejection time-ratio) and 1/PEP2 before and after induction of anaesthesia with the barbiturate enibomal (Narcodorm) were studied noninvasively in eight surgical patients after pre-treatment with a bolus dose of glucagon. The mean difference between the PEP/LVET-ratio before and after induction was 0.06, and the mean difference between 1/PEP2 before and after induction was -8. The corresponding values in the control group consisting of 12 patients were 0.09 and -28, respectively, suggesting a somewhat greater depression of cardiac function in this group. However, no statistically significant difference at the 5% level was found between changes in the glucagon group and controls. The influence of barbiturates and glucagon on cardiac function is discussed.
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