Related Experiment Videos
Cardiopulmonary consequences of decompression stress
Respiration Physiology
|August 1, 1980
Summary
Clinically silent venous gas emboli (VGE) from hyperbaric decompression alter cardiac output and pulmonary vascular resistance in sheep, despite no gas exchange issues. This indicates decompression stress impacts cardiopulmonary function.
Area of Science:
- Cardiopulmonary physiology
- Hyperbaric medicine
- Diving physiology
Background:
- Clinically undetectable venous gas emboli (VGE) are common after hyperbaric decompression.
- The cardiopulmonary effects of these VGE during uneventful decompression are not well understood.
Purpose of the Study:
- To investigate the cardiopulmonary effects of clinically uneventful decompression in unanesthetized sheep.
- To assess the impact of venous gas emboli on gas exchange and hemodynamics.
Main Methods:
- Unanesthetized sheep were instrumented for hemodynamic and blood gas monitoring.
- Animals underwent hyperbaric exposure (6.03 ATA) or a control period (1 ATA).
- Measurements included pulmonary artery pressure, cardiac output, blood gases, and Doppler bubble detection.
Main Results:
- Venous gas emboli (VGE) were detected in all hyperbaric-exposed animals.
- Cardiac output (CO) decreased by 20% and pulmonary vascular resistance (PVR) increased by 60% post-decompression.
- These hemodynamic changes exceeded predictions, but gas exchange and ventilation/perfusion (V/Q) scans remained normal.
Conclusions:
- Clinically uneventful decompression stress significantly alters cardiac output and pulmonary vascular resistance in sheep.
- Hemodynamic changes occur without detectable impairment in gas exchange.
- These findings highlight subclinical cardiopulmonary effects of decompression.