British journal of anaesthesia
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Delayed onset of obstruction in the Oxford endotracheal tube during anaesthesia is described in five patients. The effects of intra-cuff voluem and pressure on the wall of the tube were investigated and discussed with special refernce to the ffects of body heat and repeated use on the consistency of the tube. It is concluded that inward collapse of the tube wall is caused by a combination of factors, namely: frequent use, softening of the tube wall by body heat, the gradual increasing of intra-cuff volume and pressure by diffusion of nitrous oxide into the cuff, replacing a damaged cuff by a new one and heat sterilization. Deflation and re-inflation of the cuff to minimal occlusive volume at hourly intervals is suggested as a precautionary measure in the prevention of inward collapse of the tube wall.
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Serial measurements of maternal blood-gases, alveolar-to-arterial oxygen tension difference (PAO2--PaO), calculated pulmonary venous admixture (physiological shunt), deadspace/tidal volume ratio (VD/VT), and respiratory minute volume have been made in a carefully selected group of normal pregnant patients at 12, 24, 32 and 38 weeks of gestation and 5 weeks after delivery. All measurements were made in the semi-recumbent position with a left lateral pelvic tilt. Mean arterial PO2 was consistently greater than 100 mm Hg throughout pregnancy, although the value decreased from 106.4 mm Hg at 12 weeks of gestation to 101.8 mm Hg at the 38th week. Despite this decrease there was no change in (PAO2--PaO2) VD/VT, or percentage shunt with increasing gestation; nor did these values differ significantly from non-pregnant values in the same patients.
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Comparative Study Clinical Trial Controlled Clinical Trial
The effects of adding adrenaline to etidocaine and lignocaine in extradural anaesthesia I: block characteristics and cardiovascular effects.
The addition of adrenaline 5 mug/ml, 1 : 200 000 to 1% etidocaine hydrochloride administered extradurally (L2-3) shortened significantly the onset time for sensory blockade, particularly with respect to the spread of the analgesia from the injection site, and shortened the already rapid onset of motor block. Etidocaine hydrochloride 1% plain caused a slower onset of block, laster longer and produced more profound analgesia over the caudal dermatomes than did 2% lignocaine hydrochloride. ⋯ With regard to cardiovascular variables, there were no significant differences between subjects receiving the plain etidocaine and the plain lignocaine. However, subjects receiving etidocaine with adrenaline exhibited increased cardiac stimulation and a decrease in total peripheral resistance over the first 150 min.
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Measurements of complement conversion and white cell variations were made on sequential blood samples obtained from a single volunteer following repeated administration of Althesin. The results suggest a mechanism by which a clinically significant hypersensitivity reaction to the drug might be mediated. Studies of patients receiving routine anaesthesia revealed a very high incidence of subclinical "hypersensitivity" reaction, some of which appear to be immune-mediated. These reactions occurred irrespective of whether the patients were induced with Althesin, methohexitone or propanidid.
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Plasma concentrations of lignocaine were measured in three groups of anaesthetized patients following spraying of the trachea and larynx with a lignocaine 10% aerosol spray. Greater venous plasma concentrations occurred in patients who were paralysed with suxamethonium. ⋯ In individual patients a concentration 50% in excess of the mean value may occur. The use of lignocaine 100 mg as a 10% aerosol spray can be considered safe.