title: Effects of hyperoxia on ventilation and pulmonary hemodynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema.
abstract: Immersion pulmonary edema (IPE) can occur in otherwise healthy swimmers and divers, likely because of stress failure of pulmonary capillaries secondary to increased pulmonary vascular pressures. Prior studies have revealed progressive increase in ventilation [minute ventilation (Ve)] during prolonged immersed exercise. We hypothesized that this increase occurs because of development of metabolic acidosis with concomitant rise in mean pulmonary artery pressure (MPAP) and that hyperoxia attenuates this increase. Ten subjects were studied at rest and during 16 min of exercise submersed at 1 atm absolute (ATA) breathing air and at 4.7 ATA in normoxia and hyperoxia [inspired P(O(2)) (Pi(O(2))) 1.75 ATA]. Ve increased from early (E, 6th minute) to late (L, 16th minute) exercise at 1 ATA (64.1 +/- 8.6 to 71.7 +/- 10.9 l/min BTPS; P < 0.001), with no change in arterial pH or Pco(2). MPAP decreased from E to L at 1 ATA (26.7 +/- 5.8 to 22.7 +/- 5.2 mmHg; P = 0.003). Ve and MPAP did not change from E to L at 4.7 ATA. Hyperoxia reduced Ve (62.6 +/- 10.5 to 53.1 +/- 6.1 l/min BTPS; P < 0.0001) and MPAP (29.7 +/- 7.4 to 25.1 +/- 5.7 mmHg, P = 0.002). Variability in MPAP among subjects was wide (range 14.1-42.1 mmHg during surface and depth exercise). Alveolar-arterial Po(2) difference increased from E to L in normoxia, consistent with increased lung water. We conclude that increased Ve at 1 ATA is not due to acidosis and is more consistent with respiratory muscle fatigue and that progressive pulmonary vascular hypertension does not occur during prolonged immersed exercise. Wide variation in MPAP among healthy subjects is consistent with variable individual susceptibility to IPE.
authors.affiliation: Center for Hyperbaric Medicine and Environmental Physiology, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
authors.forename: Dionne F
authors.initials: DF
authors.lastname: Peacher
authors.forename: Shelly R H
authors.initials: SR
authors.lastname: Pecorella
authors.forename: John J
authors.initials: JJ
authors.lastname: Freiberger
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Natoli
authors.forename: Eric A
authors.initials: EA
authors.lastname: Schinazi
authors.forename: P Owen
authors.initials: PO
authors.lastname: Doar
authors.forename: Albert E
authors.initials: AE
authors.lastname: Boso
authors.forename: Aaron J
authors.initials: AJ
authors.lastname: Walker
authors.forename: Matthew
authors.initials: M
authors.lastname: Gill
authors.forename: Dawn
authors.initials: D
authors.lastname: Kernagis
authors.forename: Donna
authors.initials: D
authors.lastname: Uguccioni
authors.forename: Richard E
authors.initials: RE
authors.lastname: Moon
mesh_terms: D000328:Adult; D002245:Carbon Dioxide / Q000097:blood; D004242:Diving / Q000502:physiology; D015444:Exercise / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D018496:Hyperoxia / Q000503:physiopathology*; D007101:Immersion / Q000503:physiopathology*; D008297:Male; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology; D010313:Partial Pressure; D016684:Prone Position / Q000502:physiology; D011651:Pulmonary Artery / Q000502:physiology; D011654:Pulmonary Edema / Q000503:physiopathology*; D012123:Pulmonary Ventilation / Q000502:physiology*; D013550:Swimming / Q000502:physiology*; D014797:Vital Capacity / Q000502:physiology; D055815:Young Adult
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen