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.

Figures

Fig. 1.

Minute ventilation (V̇e), alveolar ventilation (V̇a), ventilatory frequency (f), tidal volume (Vt), and fractional dead space (Vd/Vt) during exercise trials. Early, 6 min of exercise; late, 16 min of exercise. V̇e increased from early to late exercise at the surface, but not at depth. V̇e was reduced by depth and further reduced by hyperoxia. Vt did not significantly change from early to late exercise and did not differ between conditions; f increased from early to late exercise at the surface and was reduced by depth and further reduced by hyperoxia. Vd/Vt was increased by hyperoxia and was not affected by depth alone or by continued exercise. V̇a increased from early to late exercise only at the surface. V̇a was reduced by depth and hyperoxia. Mean values ± SD are shown. *Statistical significance (P < 0.05) between a pair of conditions; §significant difference (P < 0.05) between early and late exercise at the surface. PiO2, inspired Po2; ATA, atmospheres absolute.

Fig. 2.

Mean pulmonary artery pressure (MPAP), pulmonary arterial wedge pressure (PAWP), cardiac output (CO), and pulmonary vascular resistance (PVR) during exercise trials. Early, 6 min of exercise; late, 16 min of exercise. During normoxia, MPAP was increased by depth. This increase was attenuated by hyperoxia. PAWP did not differ among conditions or from early to late exercise. In normoxia, CO was increased by depth, an effect that was attenuated by hyperoxia. There was no significant change in CO from early to late exercise. PVR was decreased by hyperoxia but not by depth alone. There was no change in PVR from early to late exercise. Mean values ± SD are shown. *Statistical significance (P < 0.05) between a pair of conditions.

Fig. 3.

MPAP during exercise trials. Each circle represents a single measurement for a subject. The mean for all subjects at each time point is indicated by a horizontal bar. Measurement of MPAP at 1-min intervals during exercise showed a decrease in MPAP from early to late exercise that was significant at the surface (P = 0.003) but not at depth. Interindividual variation in MPAP was wide (range 16.0–39.6 mmHg at the surface, 14.1–42.1 mmHg in normoxia at depth, and 16.6–36.0 mmHg in hyperoxia at depth).

Fig. 4.

Alveolar-arterial Po2 (PaO2-PaO2) difference. In normoxia, there was no effect of depth on the PaO2-PaO2 difference. From early to late exercise, the PaO2-PaO2 difference increased 51.5% in normoxia but not in hyperoxia. Mean values ± SD are shown. *Statistical significance (P < 0.05) between a pair of conditions; ‡statistically significant difference (P < 0.05) between early and late exercise.