Swimming-Induced Pulmonary Edema and Sildenafil
Does sildenafil reduce pulmonary artery pressure (PAP) and pulmonary artery wedge pressure (PAWP) in swimming-induced pulmonary edema (SIPE)–susceptible individuals during submerged exercise?
The study cohort was comprised of 10 subjects with a history of SIPE (mean age 41.6 years). Two subjects had experienced SIPE while diving, five during a triathlon or in training for a triathlon, and two during both. Another subject experienced SIPE when she fell off her windsurfer into a cold river. The control group was comprised of 20 subjects (mean age 36.2 years). These individuals were instrumented with radial artery and pulmonary artery catheters before they performed moderate cycle ergometer exercise for 6-7 minutes while submerged in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. They measured heart rate, mean arterial pressure (MAP), mean PAP (MPAP), and PAWP immediately before submersion and at 1 minute afterward. Effective arterial elastance (Ea) was calculated as (2 x Psys + Pdia)/(3 x stroke volume), where Psys and Pdia represent systolic and diastolic arterial pressures. Pulmonary artery compliance was calculated as stroke volume/PA pulse pressure.
The investigators found that work rate and MAP during exercise were similar in both groups. Average VO2 and cardiac output (CO) in SIPE-susceptibles and controls were: 2.42 L.min-1 vs. 1.95 L.min-1, p = 0.2; CO 17.9 L.min-1 vs. min-1, p = 0.01. SVR was higher in the SIPE-susceptible group (p = 0.0106). Accounting for differences in CO between groups, MPAP at CO = 13.8 L.min-1 was 22.5 mm Hg in controls vs. 34.0 mm Hg in SIPE-susceptibles (p = 0.004) and the corresponding PAWP 11.0 mm Hg vs. 18.8 mm Hg (p = 0.028). After sildenafil, there was a significant decrease in PAP, but there were no statistically significant differences in MPAP or PAWP between SIPE-susceptibles and controls. Blood gases were not significantly different between groups except after sildenafil, when pH was slightly higher compared to both control (p = 0.0087) and pre-sildenafil (p = 0.02), and PaO2 was higher in the SIPE-susceptible group compared to pre-sildenafil (p = 0.0337).
The authors concluded that the reduction in pulmonary vascular pressures after sildenafil, with no adverse effect on exercise hemodynamics, suggests that it may be useful in SIPE prevention.
Although this was not a randomized study, the findings are important because it suggests that pulmonary edema associated with swimming submerged in cold water is associated with both higher PAWP and MPAP. Also, it is interesting to note that PAP was reduced with a single dose of sildenafil, suggesting that vasoconstriction is an important mechanism, and this therapy is probably beneficial in these individuals.
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