Abstract

A lung model was used to simulate gas exchange for a 70 kg adult under anaesthesia. It was demonstrated that the modified Mapleson D circuit (Bain) with low fresh gas flows determined according to body weight is a partial rebreathing system. With controlled ventilation this can be compensated for by increasing minute ventilation above the predicted and the arterial carbon dioxide level can then be regulated by adjusting the fresh gas flow. During spontaneous ventilation this compensation is critically dependent on the patient's ability to increase minute ventilation. Therefore in any particular case the arterial carbon dioxide is unpredictable and totally dependent on carbon dioxide responsiveness, carbon dioxide production, physiological dead-space, respiratory wave form, and apparatus dead-space. Although normocarbia can be achieved by certain ideal patients despite low fresh gas flows it can be done only if minute ventilation is markedly increased. This enforced hyperpnoea will significantly encroach on the respiratory reserve of these patients and may well be unattainable in some. We conclude that any decrease in respiratory drive, increase in carbon dioxide production, increase in physiological or apparatus dead-space (i.e. a mask) will produce potentially dangerous hypercarbia using a Bain circuit with a fresh gas flow of 100 ml/kg/minute. This hazard is not easily recognized. The only way to minimize these factors during spontaneous ventilation is by the use of a non-rebreathing circuit. To do this with a T-piece or Bain circuit the fresh gas flow must be between 200 and 300 ml/kg/min for an average adult, with this requirement being highly dependent on all the variables outlined. One must decide whether the low economy and high level of operating room pollution with this wide range of flow outweigh the advantages of trying to make the Mapleson D a universal circuit.

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