학술논문
Cardiovascular effects of hypoxia/hypercarbia and tension pneumothorax in newborn piglets.
Document Type
Academic Journal
Author
Brann BS 4th; Department of Pediatrics, Brown University School of Medicine, Women and Infant's Hospital of Rhode Island, Providence 02905.; Mayfield SR; Goldstein M; Oh W; Stonestreet BS
Source
Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 0355501 Publication Model: Print Cited Medium: Print ISSN: 0090-3493 (Print) Linking ISSN: 00903493 NLM ISO Abbreviation: Crit Care Med Subsets: MEDLINE
Subject
Language
English
ISSN
0090-3493
Abstract
Objectives: To test the hypothesis that, in newborn piglets, the presence of a tension pneumothorax modifies the cardiovascular responses to hypoxia/hypercarbia.
Design: Prospective laboratory study.
Setting: Perinatal cardiovascular research laboratory at a university school of medicine.
Subjects: Seven newborn piglets.
Interventions: 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.
Measurements and Main 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.
Design: Prospective laboratory study.
Setting: Perinatal cardiovascular research laboratory at a university school of medicine.
Subjects: Seven newborn piglets.
Interventions: 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.
Measurements and Main 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.