Cardiovascular and respiratory consequences of tension pneumothorax

The physiologic responses to acute pneumothorax were investigated in awake, standing sheep. Pleural pressure (Ppl) was raised in graded increments by injecting air from a 500 ml syringe into the pleural cavity of eight sheep to produce pneumothorax volumes of 0, 17, 35 and 45 ml.kg^-1. At the maximum value of 45 ml.kg^-1 (≃1,4000 ml), Ppl at end-expiration was raised to 10 ± 2 mmHg (mean ± SD) whereas end-inspiratory Ppl remained negative in half the sheep as the result of increased thoracic pressure swings. The most striking haemodynamic impairment was a 22% fall in stroke volume. Cardiac output, however, remained fixed at baseline values as a result of a 28% rise in heart rate. Although hypotension has been commonly held as a consequence of severe pneumothorax, mean systemic arterial pressure increased, rising by 19% in the entire group at the maximal pneumothorax tolerated. Pulmonary gas exchange was significantly disrupted by pneumothorax, as indicated by both a 40% fall in PaO₂ and a 19% reduction in arterial oxygen content. Despite a reduction in tidal volume, the sheep initially remained eucapnic by generating an increased respiratory rate and slightly increasing minute-ventilation. However, at pneumothorax volumes of 45 ml.kg^-1, the sheep were no longer able to sustain minute-ventilation and a small rise in PaCO₂ followed. The reduced arterial oxygen content and the fixed cardiac output led to a progressive reduction in systemic oxygen transport. The loss of convectional transport of oxygen as well as an impaired peripheral gradient for diffusion permitted a 21% fall of mixed venous PO₂, suggesting a significant reduction in tissue oxygenation. We conclude that an important element in the cardiovascular collapse during acute pneumothorax can be ascribed to insufficient tissue oxygen delivery as a result of the combination of arterial hypoxaemia and an inability to mount a compensatory rise in cardiac output.