Canadian Anaesthetists' Society journal
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To examine a possible mechanism which could cause arterial hypoxaemia following pulmonary embolism, we collapsed and did not ventilate one lung in each of eleven dogs, to produce hypoxic pulmonary vasoconstriction. In five dogs (Starch Group), PaO2 fell from 10 to 7.7 kPa (76.6 to 58.4 torr) as shunt fraction (Qs/Qt) rose from 19 to 31 per cent. Mean pulmonary artery pressure (ppa), paCO2 and VD/VT remained constant. ⋯ We conclude from these results that emboli are preferentially distributed to ventilated lung. After embolization PPA increases. At least in this pulmonary embolism model the increased PPA may overcome hypoxic pulmonary vasoconstriction, redistribute blood to non-ventilated lung and create arterial hypoxaemia.
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This paper reports the case of a 2 1/2-year-old male who appeared to have drowned in the family swimming pool. Immediate continuous cardiopulmonary resuscitation eventually restored circulation and respiration. ⋯ Prompt and continuous use of measures to support cerebral resuscitation were successful and the child subsequently was completely normal. A reevaluation of current information seems indicated in regard to the prognosis of the near-drowned child.
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Comparative Study
An evaluation of gas density dependence of anaesthetic vaporizers.
Four commonly used vaporizers were studied for the effect of carrier gas density on vaporizer output. Vapour concentrations from a halothane Cyprane (Fluotec) Mark 2 increased in relation to the density of carrier gas, whereas the concentrations delivered by an enflurane Ohio vaporizer decreased. The halothane Cyprane (Fluotec) Mark 3 and enflurane Cyprane vaporizers were largely independent of density. Of clinical importance, nitrous oxide/oxygen (75/25), compared with oxygen alone, increased the vapour concentration outputs of the halothane Mark 2 up to 30% and decreased the outputs of the enflurane Ohio unit up to 20%.