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OBJECTIVE To test the hypothesis that, in newborn piglets, the presence of a tension pneumothorax modifies the cardiovascular responses to hypoxia/hypercarbia. METHODS Prospective laboratory study. METHODS Perinatal cardiovascular research laboratory at a university school of medicine. METHODS Seven newborn piglets. METHODS We sequentially exposed the piglets to a baseline (control I) measure, hypoxia/hypercarbia, tension pneumothorax with normoxia/normocarbia, and tension pneumothorax with hypoxia/hypercarbia added. RESULTS Brain and systemic blood pressures and blood flow (radionuclide-microspheres) were measured. Hypoxia/hypercarbia resulted in increased brain perfusion (207 +/- 61% of control, mean +/- SEM, p < .05) and heart perfusion (176 +/- 58% of control, p < .05) and decreased gastrointestinal perfusion (-37 +/- 9% of control, p < .05). Tension pneumothorax with normoxia/normocarbia reduced the cardiac output (-70 +/- 8% of control, p < .05), which was redistributed toward the brain (p < .05) at the expense of the gastrointestinal tract (p < .05). Although this redistribution in cardiac output persisted during tension pneumothorax with hypoxia/hypercarbia added, sustained reductions in cardiac output (-57 +/- 11%, of control, p < .01) were associated with smaller increases in perfusion to brain (55 +/- 54 vs. 207 +/- 61% of control, tension pneumothorax with hypoxia/hypercarbia added, and hypoxia/hypercarbia time periods, respectively, p < .05) and heart (65 +/- 49 vs. 176 +/- 58% of control, tension pneumothorax with hypoxia/hypercarbia added, and hypoxia/hypercarbia time periods, respectively, p < .05) and larger decreases in blood flow to gastrointestinal tract, pancreas, and kidneys (p < .05) than with hypoxia/hypercarbia alone. CONCLUSIONS Tension pneumothorax-induced reductions in cardiac output limit the hypoxia/hypercarbia-mediated increases in perfusion to brain and heart and accentuate the hypoxia/hypercarbia-related decreases in perfusion to kidneys and splanchnic organs.
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