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The influence of hypervolaemia upon circulation and pulmonary ventilation was studied in six piglets (body weights 8.5-10.5 kg). A new functional principle for artificial ventilation was used. The alveolar ventilation was unchanged at normovolaemia and hypervolaemia. Arterial blood gases were sampled and end-tidal carbon dioxide concentrations were measured continuously. Central circulation was followed by pressure recordings and an electromagnetic flow meter for cardiac output measurements. Mean values +/- SEM of end-inspiratory tracheal pressures increased from 0.98 +/- 0.06 kPa at normovolaemia to 1.57 +/- 0.06 kPa at hypervolaemia (p less than 0.02). In all animals total compliance decreased (p less than 0.02). Simultaneously the insufflation time for the tidal volume decreased by 13 per cent (p less than 0.05). Arterial oxygen tensions decreased from 8.5 +/- 0.48 kPa to 7.0 +/- 0.77 kPa (p less than 0.05). During hypervolaemia aortic pressures increased from 13.1 +/- 1.3 kPa to 14.9 +/- 0.8 kPa (p less than 0.05), pulmonary artery pressures from 2.8 +/- 0.33 kPa to 5.0 +/- 0.53 kPa (p less than 0.02) and cardiac output from 1.07 +/- 0.17 1 . min-1 to 1.5 +/- 0.19 1 . min-1 (p less than 0.02). The stroke work for the right heart increased by 74 per cent (p less than 0.02) and for the left heart by 62 per cent (p less than 0.02). Pulmonary vascular resistance was unchanged, while systemic vascular resistance was significantly decreased (p less than 0.05). The positive effect upon systemic circulation gained by the use of excessive fluid therapy resulted in an overcirculation within the lungs which reduced pulmonary ventilation. This reduction could most probably be related to a closure of terminal airways secondary to lung hyperperfusion, increasing the pulmonary shunt.

Circulatory and ventilatory effects of hypervolaemia in artificially ventilated piglets