Open-water swimming could potentially be fatal, cardiologists warn

Doctors warn against a potentially life-threatening condition endemic to swimmers.
Ayesha Gulzar
Swimmer training on the open sea.
Swimmer training on the open sea.


A recent study links swimming in open water to a lung condition called swim-induced pulmonary edema (SIPE). The case study reports that the heart and the lungs can be affected by SIPE.

SIPE causes fluid buildup in the lungs and is described by an umbrella term called Immersion Pulmonary Edema (IPE). The condition is found in open-water swimmers, scuba divers, snorkelers, military swimmers, and triathletes.

It's characterized by shortness of breath (dyspnea), low blood oxygen (hypoxemia), coughing up frothy sputum (hemoptysis), extreme fatigue, symptoms of respiratory distress, and a sensation of 'wet' lungs.

The First Published Case

IPE case studies have been reported since the 1980s. However, the first published evidence of IPE involving myocardial edema – swelling of the heart muscle – was published in 2022. According to the case study, a "fit and well female in her fifties" with no previous notable medical history started to hyperventilate while swimming.

"When I got out, I undid my wetsuit and immediately felt the sensation of my lungs filling with fluid," the patient reported, following which she began coughing a metallic-tasting pink frothy sputum.

Fortunately, the responders recognized the symptoms of IPE, which was later confirmed by a chest X-ray, revealing fluid in her lungs. Signs of heart and tissue damage were observed through blood tests and an MRI.

An Elusive Pathophysiology

As the body exerts itself during immersion, blood is redirected from the peripheral vascular system to the core, increasing thoracic volume and thereby increasing pressure in the pulmonary vasculature.

Additionally, predisposing factors include cold water, over-hydration, negative inhalation pressure, diabetes, hypertension, high physical exertion, and underlying cardiac pathology.

However, according to Stefanie D. Martina from the Divers Alert Network, all these factors need not be present for the sudden onset of IPE as this syndrome has also been reported in warm waters, low immersion activity, lower exertion levels, varying depths, and otherwise healthy individuals.

Other contributing factors may exist, but the exact pathophysiology is currently elusive. IPE is also underdiagnosed due to shared postmortem findings with drowning and prolonged resuscitation efforts. Due to a lack of data and a poor understanding of pathophysiology, there are currently no ways to portend susceptibility.

Another critical factor to note is that of recurrence; Researchers have reported an 18-33 percent recurrence rate, meaning that IPE patients should be presumed to have a predisposition, and patient counseling is imperative.

Prevention and Treatment

Researchers at Duke University have recently completed phase two of a clinical study, according to which administering a generic form of Viagra, Sildenafil, to IPE patients resulted in reduced pulmonary vascular pressures with no adverse effects on exercise hemodynamics.

According to Dr. James Oldman of the Royal United Hospitals Bath, no standard medical guidelines regarding the recognition and management of IPE currently exist.

While doctors advise slower-paced swimming, avoiding cold water, and tight-fitting wetsuits, substantial scientific evidence in favor of these guidelines is lacking in scientific literature.

In conclusion, while researchers navigate the elusive path of IPE diagnosis, treatment, and prevention, remaining abreast of developments can prove lifesaving.

The case report has been published in the journal BMJ Case Reports.


Immersion pulmonary oedema (IPE) is an under-reported and poorly understood phenomenon thought to be related to exercise-induced haemodynamic changes while submersed in water. Previous work has demonstrated reversible myocardial dysfunction during acute episodes. We present a case of IPE with concomitant, transient, left ventricular myocardial oedema characterised via MRI. This is a novel finding and may be evidence of left ventricular strain due to pressure overload or secondary to a subclinical myocarditis.

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