ObjectivesTo test the hypothesis that, in newborn piglets, the presence of a tension pneumothorax modifies the cardiovascular responses to hypoxia/hypercarbia.DesignProspective laboratory study.SettingPerinatal cardiovascular research laboratory at a university school of medicine.SubjectsSeven newborn piglets.InterventionsWe sequentially exposed the piglets to a baseline (control I) measure, hypoxia/hypercarbia, tension pneumothorax with normoxia/normocarbia, and tension pneumothorax with hypoxia/hypercarbia added.Measurements and Main ResultsBrain 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.ConclusionsTension 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. (Crit Care Med 1994; 22:1453–1460)