Swimming-Induced Pulmonary Edema

Case Presentation

A 60-year-old triathlete with a history of repaired coarctation of the aorta, bicuspid aortic valve and mild central mitral regurgitation with normal valve morphology presented with recurrent episodes of cough, chest tightness and wheezing when swimming in cold water. She started competitive swimming at the age of 55 and first noticed symptoms during a half Ironman triathlon in New England when the water temperature was 10°C. She had taken pre-race salt tablets and wore a wetsuit. During the swim she developed a cough, diffuse chest tightness and dyspnea but finished the race despite experiencing a "drowning" sensation. She did not develop hemoptysis and her symptoms began to subside after the race, taking 48 hours to completely resolve. She had not previously experienced similar symptoms when swimming in warmer water nor had she ever experienced symptoms while running or cycling.

Swimming-Induced Pulmonary Edema

While swimming, running and cycling, the fundamental elements of the modern triathlon, are all endurance sporting disciplines, swimming may present some unique cardiopulmonary physiologic challenges. Water immersion results in compressive forces on the body and increases pressure on the peripheral capacitance vessels. This results in central redistribution of blood volume into the thoracic cavity with increased venous return and biventricular preload.1 This redistribution, further exacerbated by the compressive forces of tightly fitting neoprene wetsuits which are common place among triathletes, can be hemodynamically significant with attendant increases in central venous pressure by 12-18mmHg and stroke volume by greater than 25% during water immersion at rest.2,3

Water also places thermal stress on the body with attendant physiologic effects. Healthy subjects immersed in 14°C water demonstrated higher blood pressures and sympathetic tone characterized by higher norepinephrine levels when compared to immersion in 32°C water.4 Furthermore, cold water immersion has been associated with increases in left ventricular end diastolic volume as a result of increased peripheral vasoconstriction.5 Exercise in cold water has also been shown to increase both mean pulmonary artery pressure (MPAP) and pulmonary artery wedge pressure (PAWP).6

Swimming-induced pulmonary edema (SIPE), also known as immersion pulmonary edema, is a form of pulmonary edema that occurs during water sport activity in young, otherwise healthy individuals. It has been reported in surface swimming, snorkeling, scuba diving and breath-hold diving. It was first reported in scuba divers in 1981 and has since been reported in military trainees, swimmers and triathletes.7 At present, SIPE is an understudied condition with an unknown true prevalence. Reported prevalence estimates range from 1.8-60% among combat swimmer trainees and 1.4% in triathletes.8,9

SIPE is a form of hemodynamic pulmonary edema caused by an exaggerated increase in pulmonary vascular pressures in response to immersion in water, intense physical activity and host factors.10,11 Prior evaluation supports a hydrostatic mechanism of pulmonary edema but the pathophysiology remains poorly understood.10 In normal subjects, acute increases in PAWP that exceed 18-25mmHg can cause hydrostatic alveolar edema.12 It has also been shown that elevated hydrostatic pressures can result in microscopic breaks in the membranes of the blood-gas barrier, known as capillary stress failure, a finding that may explain the high prevalence of hemoptysis seen in those with SIPE.13,14 Thus, hydrostatic pulmonary edema coupled with capillary stress fracture provide a plausible mechanism for the development of SIPE in susceptible individuals.


Subjects are asymptomatic prior to water immersion and develop symptoms during or after swimming. In a review of 70 young healthy males diagnosed with SIPE, the most commonly reported symptoms were dyspnea (100%), cough (96%), hemoptysis (56%), wheeze (9%) and chest tightness (9%).15

Physical Examination

During the acute illness, examination is consistent with pulmonary edema with findings of rales, crackles and/or wheezing. Low oxygenation saturations can be seen with pulse oximetry and hypoxemia on arterial blood analysis. The degree of desaturation is beyond what can be seen in elite athletes with short capillary transit times.16 Chest radiograph will show findings consistent with pulmonary edema and pleural effusions may be seen. To date, no studies have examined non-invasive estimates of pulmonary arterial pressure or pulmonary vascular resistance among patients with acute SIPE.

Risk Factors

Given the physiologic changes and blood redistribution that occurs with water immersion, training habits that are routinely used for terrestrial endurance competition, including salt tablet ingestion and pre-race hydration, may augment preload and thus increase the risk of developing SIPE. A history of systemic or pulmonary hypertension also increases this risk by further increasing pulmonary pressures and, in the case of hypertension, may expose underlying cardiac diastolic dysfunction.17 Female gender and older age have also been noted as risk factors. Water specific risk factors include cold water temperature and the use of wetsuits, both of which can independently and synergistically augment preload.18 Athletes that have experienced an episode of SIPE appear to be at relatively high risk of recurrence with reported recurrence rates ranging from 13-75%.8,11 To date, a definitive screening test to identify athletes that may be particularly susceptible to SIPE is not available.


Four diagnostic criteria for SIPE have been previously proposed:19

  1. Acute onset of dyspnea or hemoptysis during or immediately after swimming.
  2. Hypoxemia, defined by oxygen saturation <92% or an alveolar-arterial oxygen gradient of >30mmHg.
  3. Chest radiograph consistent with alveolar filling process or interstitial pulmonary edema that resolves within 48hrs.
  4. No history of water aspiration, laryngospasm or preceding infection.


At present, there have been no randomized trials of SIPE therapy and thus the evolving standard of care is based on logic and anecdotal experience. The acute treatment of SIPE begins with immediate removal from the water, placing the individual in a warm environment, and removal of a constrictive wetsuit if present. Additional supportive care, including oxygen, diuretics and β2 agonists may be considered on a case-by-case basis. While SIPE can be fatal, the majority of athletes recover and are completely symptom free within 48 hours.

Anecdotally, vasodilators including sildenafil and dihydropyridine calcium channel blockers have been used for the prevention of SIPE with success.* The effect of sildenafil in SIPE susceptible subjects has recently been reported.10 Compared to controls, MPAP and PAWP were higher after cold-water exercise in the SIPE group. After sildenafil, SIPE susceptible subjects had a significant decrease in pulmonary artery pressures, resulting in similar MPAP and PAWP when compared to controls. The authors of this study suggested that sildenafil-induced reduction in pulmonary vascular pressures during submerged exercise is likely the result of vasodilatation of both pulmonary vessels and peripheral veins. Similar to our experience, there are published case reports in which pre-workout sildenafil can prevent the development of SIPE.20

Our approach is to counsel athletes on modifiable risk factors including cold-water swimming, wetsuits, salt tablets and pre-race hydration. If the athlete is not hypertensive, we recommend 50mg of sildenafil prior to swims. If the patient is hypertensive, we adjust the blood pressure regimen to include a daily dihydropyridine calcium channel blocker. Neither of these medications are prohibited by the World Anti-Doping Agency.21 Importantly, due to concern that PDE-5 inhibitors may increase susceptibility to seizures as a result of central nervous system oxygen toxicity, we do not recommend their use in scuba divers.22 We routinely recommend that all athletes test the tolerability of pharmacotherapy in non-race conditions with active surveillance prior to race day use.

Case Follow-Up

Our athlete underwent an echocardiogram and maximal effort cardiopulmonary exercise test to confirm that progression of valvular disease and new-onset obstructive coronary artery disease were not responsible for her symptoms. She was advised to avoid salt tablets and overhydration and was started on sildenafil prior to cold-water swims and races. Since initiating targeted sildenafil prophylactic therapy, she has not had recurrence of symptoms and has routinely secured successful podium finishes in numerous races.

*These are off-label uses for both medications.


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Clinical Topics: Anticoagulation Management, Congenital Heart Disease and Pediatric Cardiology, Diabetes and Cardiometabolic Disease, Heart Failure and Cardiomyopathies, Prevention, Pulmonary Hypertension and Venous Thromboembolism, Sports and Exercise Cardiology, Valvular Heart Disease, Vascular Medicine, Atherosclerotic Disease (CAD/PAD), Congenital Heart Disease, CHD and Pediatrics and Prevention, CHD and Pediatrics and Quality Improvement, Acute Heart Failure, Pulmonary Hypertension, Exercise, Hypertension, Sports and Exercise and Congenital Heart Disease and Pediatric Cardiology, Sports and Exercise and ECG and Stress Testing, Mitral Regurgitation

Keywords: Respiratory Sounds, Pulmonary Wedge Pressure, Diving, Heart Valve Diseases, Swimming, Stroke Volume, Pulmonary Edema, Athletes, Exercise Test, Phosphodiesterase 5 Inhibitors, Neoprene, Vasodilator Agents, Calcium Channel Blockers, Risk Factors, Blood Pressure, Cold Temperature, Coronary Artery Disease, Cough, Central Venous Pressure, Vasodilation, Breath Holding, Hemoptysis, Diuretics, Oxygen, Laryngismus, Norepinephrine, Hydrostatic Pressure, Fractures, Stress, Factor X, Factor XI, Aortic Coarctation, Mitral Valve Insufficiency, Pulmonary Artery, Vasoconstriction, Heart Valve Diseases, Oximetry, Hypertension, Pulmonary, Dyspnea, Hypoxia, Brain, Hypertension, Vascular Resistance, Blood Volume, Edema, Thoracic Cavity, Pleural Effusion, Sensation, Dihydropyridines, Nervous System, Off-Label Use

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