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Pulmonary edema develops after recurrent obstructive apneas.

E C Fletcher1, M Proctor, J Yu

  • 1Division of Respiratory Medicine, Department of Medicine, Louisville Veterans Affairs Medical Center, University of Louisville School of Medicine, Louisville, Kentucky, USA. ecflet01@qwise.louisville.edu

American Journal of Respiratory and Critical Care Medicine
|November 11, 1999
PubMed
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Recurrent obstructive apneas (OAs) in dogs led to lung edema and worsened gas exchange, suggesting a link between OAs and pulmonary edema. This study provides crucial data on physiological changes during OAs.

Area of Science:

  • Cardiovascular System
  • Respiratory System
  • Pulmonary Medicine

Background:

  • Anecdotal reports suggest pulmonary edema may follow recurrent obstructive apneas (OAs).
  • However, objective data on lung water, gas exchange, or cardiac hemodynamics in such cases are lacking.
  • This study investigates the physiological consequences of induced OAs in an animal model.

Purpose of the Study:

  • To investigate the effects of recurrent obstructive apneas on lung water, gas exchange, and cardiac function.
  • To determine if induced OAs can cause pulmonary edema and alter physiological parameters.

Main Methods:

  • Repetitive obstructive apneas were induced in intubated, anesthetized dogs for 8 hours.
  • Control dogs underwent identical instrumentation without induced apneas.

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  • Measurements included arterial oxygen saturation, pulmonary capillary wedge pressure, cardiac output, and venous admixture.

    • Main Results:

    • Apneic dogs showed a significant increase in venous admixture (pulmonary shunt), indicating worsened gas exchange.
    • Histological examination revealed alveolar and interstitial fluid in apneic dogs, consistent with pulmonary edema.
    • Cardiac output and filling pressures did not significantly change, but one dog expired from heart failure.

    Conclusions:

    • Recurrent obstructive apneas can lead to pulmonary edema and impaired gas exchange.
    • The findings support a causal link between OAs and the development of lung edema.
    • Further research is warranted to explore the clinical implications in humans.