Effects of He-O2 breathing during experimental decompression sickness following air dives.
The effects of ventilation with He-O2 during decompression sickness (DCS) and venous air embolism were studied. Fifteen anesthetized dogs were mechanically ventilated and subjected to repeated air dives until pulmonary artery pressure at least doubled within 10 min postdive. At 30 min postdive, ventilation was either continued with air (controls, n = 7) or changed to He-O2 (n = 8) for an additional 90 min. All animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, hypoxemia, hypercarbia, and pulmonary edema. Breathing air or He-O2 postdive did not alter these responses, but He-O2 breathing produced an 11% increase in pulmonary vascular resistance (PVR). In 3 other anesthetized dogs that were not subjected to dives, ventilation was changed to He-O2 at various times during an intravenous infusion of air; He-O2 breathing caused a 22% increase in PVR. We conclude that breathing He-O2 during DCS resulting from air dive can intensify pulmonary vascular obstruction.
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D003665:Decompression Sickness / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D004285:Dogs; D006371:Helium / Q000008:administration & dosage*; D008297:Male; D010100:Oxygen / Q000008:administration & dosage* / Q000097:blood; D011651:Pulmonary Artery / Q000503:physiopathology; D011652:Pulmonary Circulation; D014655:Vascular Resistance
D006371:Helium; D010100:Oxygen