Effects of hyperoxia on ventilation and pulmonary hemodynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema.

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.

Cigarette smoking and decompression illness severity: a retrospective study in recreational divers.

BACKGROUND: Severe decompression illness (DCI) could be more likely in cigarette smokers because of airway obstruction or vascular disease. The present study evaluated the severity of DCI as a function of cigarette smoking in recreational divers. METHODS: We examined all DCI reports recorded in the Divers Alert Network (DAN) database from 1989 through 1997. Smoking history was quantified as heavy (>15 pack-years), light (0 to 15 pack-years), and never smoked. DCI symptoms were classified as severe (alteration in consciousness, balance or bladder/bowel control, motor weakness, visual symptoms, convulsions), moderate (other neurological symptoms), or mild (pain, skin, or nonspecific symptoms). The proportional odds model and generalized logits were used for the adjusted analysis when accounting for other covariates. RESULTS: There were 4,350 patients included in the analysis. After adjustment for confounding variables, heavy smokers were more likely to have severe vs. mild symptoms than nonsmokers (OR = 1.88) (95% CI 1.36, 2.60) or light smokers (OR = 1.56) (95% CI 1.09, 2.23). Heavy smokers and light smokers were more likely to have severe vs. moderate symptoms than nonsmokers (OR = 1.36) (95% CI 1.06, 1.74) and (1.22) (1.02, 1.46), respectively. Although these data do not reveal whether smoking predisposes to DCI, the results are consistent with a tendency, when DCI occurs, for cigarette smoking to trigger more severe symptoms. CONCLUSIONS: The data suggest that when DCI occurs in recreational divers, smoking is a risk factor for increased severity of symptoms.