Cardiovascular and respiratory consequences of tension pneumothorax

A. N. Hurewitz, U. Sidhu, E. H. Bergofsky, B. Leff, I. Averbuch, R. Grimson, A. D. Chanana

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17 Scopus citations


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 At the maximum value of 45 (≃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, 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.

Original languageEnglish (US)
Pages (from-to)545-549
Number of pages5
JournalClinical Respiratory Physiology
Issue number6
StatePublished - 1986
Externally publishedYes

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


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