Active Voice: Sildenafil for Prevention of Swimming-Induced Pulmonary Edema?
By Richard E. Moon, M.D.
Viewpoints presented in SMB commentaries reflect opinions of the authors and do not necessarily reflect positions or policies of ACSM.
Richard Moon, M.D., FACP, FCCP, obtained his medical degree from McGill University in Montreal, Quebec, Canada. Thereafter, he trained in internal medicine, pulmonary and critical care, and anesthesiology. He is a practicing anesthesiologist at Duke University in Durham, North Carolina, where he serves as medical director of the Center for Hyperbaric Medicine & Environmental Physiology. His research focuses on understanding the physiology of environmental extremes: altitude, diving and immersion.
This commentary presents Dr. Moon’s views on the topic of a research article he and his colleagues authored together. Their article appeared in the September 2017 issue of Medicine & Science in Sports & Exercise® (MSSE).
The first description of swimming-induced pulmonary edema (SIPE) in 1981 was followed some years later by case series studies carried out in military recruits and triathletes – the phenomenon came as a complete surprise. SIPE consists of shortness of breath, cough productive of bloody secretions, hypoxemia and pulmonary edema occurring during swimming or scuba diving, usually in cold water. It often requires emergency treatment with oxygen and hospitalization. SIPE tends to recur in susceptible individuals, and deaths have been reported.
Why young, healthy individuals with high levels of physical fitness should experience a condition commonly associated with heart failure has been a mystery. Immersion in water is known to cause blood from the extremities and splanchnic vessels to redistribute into the thorax, causing pressures in the pulmonary vessels to rise. It was hypothesized that SIPE in susceptible individuals is due to excessively high pressures in the pulmonary arteries, veins and capillaries, perhaps caused by exaggerated venoconstriction in cold water causing greater peripheral-to-central blood redistribution or left ventricular stiffness (abnormal diastolic properties).
Our investigator group examined this issue by instrumenting healthy individuals, who had experienced one or more SIPE episodes, with arterial and pulmonary artery catheters, and compared their pulmonary and systemic pressures during 10 minutes of exercise in cold (20 degrees Celsius) water with the same responses in a group of volunteers who had never experienced SIPE. In 2016, we reported our findings from this study in the journal Circulation. Indeed, we observed higher pressures in the pulmonary vessels in the SIPE-susceptible individuals. We also studied the effect of oral sildenafil on pulmonary vascular pressures under the same conditions of exercise, while subjects were submersed in cold water. We chose sildenafil because of its known effect of lowering pulmonary artery pressure and its lack of adverse effects on the heart or on athletic performance. When compared with baseline measurements, we demonstrated that sildenafil significantly lowered pressures in the pulmonary vessels. Although we had not proven that it would prevent SIPE, this study provided strong evidence to suspect that it would.
Now to our more recent study, the findings of which we reported in the September 2017 issue of MSSE. One of our volunteer subjects, a 46-year-old exceptionally fit triathlete, had experienced SIPE at least five times, one of which required that she be treated in a hospital. Following her participation in our study, she was prescribed 50 mg sildenafil by her physician – to be taken before each of her triathlons. Since then, from May 2011 to November 2015, she successfully completed 20 triathlons, of which five were ultra-distance events (10-kilometer swim, 420.6-kilometer bike, 84.4-kilometer run) - with no SIPE experienced in any of these competitions.
This observation provides preliminary evidence that sildenafil may be an effective prophylactic drug for individuals susceptible to SIPE who wish to participate in events that previously have evoked SIPE. However, it is important to acknowledge that this is only a single individual and additional evidence is required before concluding that the drug is effective in this setting.
Moreover, it is important to note that this drug may be safe only in preventing SIPE that occurs during surface swimming. The reason is that sildenafil can increase oxygen levels in the brain and therefore may increase susceptibility to CNS oxygen toxicity and seizures when individuals breathe hyperoxic gas mixtures, including air, under pressure, as in scuba diving (see: www.ncbi.nlm.nih.gov/pubmed/19179645). Sildenafil may, therefore, be dangerous for scuba divers because seizures that occur underwater are likely to cause death due to drowning.