Swimming-Induced Pulmonary Edema With Concomitant Myocardial Injury

Abstract

Background

Swimming-induced pulmonary edema (SIPE) is an underrecognized cause of acute dyspnea in healthy athletes. Risk factors include older age, female sex, asthma, and underlying cardiopulmonary disease.

Case Summary

A 49-year-old man developed acute dyspnea during the swimming portion of a triathlon. On presentation, he exhibited hypoxemia, crackles, and radiographic pulmonary edema. Troponin elevation prompted further cardiac imaging, revealing preserved left ventricular function and focal acute myocardial edema. He was diagnosed with SIPE with concomitant myocardial injury; his condition improved with supportive care.

Review Summary

SIPE is a hydrostatic imbalance triggered by cold-water immersion, exertion, and external thoracic compression. Symptoms resolve rapidly with supportive care, and outcomes are generally positive, but recurrence can occur in up to 28% of patients. The presence of myocardial injury is an uncommon finding in SIPE, and it is unclear if this finding preceded or was secondary to it.

Take-Home Message

SIPE may present with atypical findings including myocardial injury, and cardiologists must be vigilant to prevent misdiagnosis.

Visual Summary

Visual Summary.

Timeline of Prepresentation Exercise History and Posthospitalization Course

MRI = magnetic resonance imaging; SIPE = swimming-induced pulmonary edema.

History of Presentation

In this case report, we describe a 49-year-old male triathlete who presented to the emergency department directly from the swimming portion of a summertime Olympic-distance triathlon race in Chicago, Illinois, with dyspnea. He initially attributed his shortness of breath to anxiety. The water temperature was 67 °F (19.4 °C), and he was wearing a full wetsuit. Examination revealed significant left-sided and mild right-sided crackles. His oxygen saturation was 88% to 93% on room air, requiring 2 L nasal cannula, with otherwise stable vital signs. He initially displayed rising high-sensitivity troponin I levels (61 ng/L, 251 ng/L, reference: <53 ng/L) and a B-type natriuretic peptide of 111 pg/mL (reference: <100 pg/mL); laboratory data were otherwise unremarkable. Venous blood gas excluded acidosis and hypercarbia. He received intramuscular lorazepam for possible anxiety-related dyspnea and an albuterol-ipratropium nebulizer treatment, with subjective improvement.

Take-Home Messages

• •SIPE should be considered in athletes presenting with acute hypoxemic respiratory distress during or immediately after open-water swimming events.
• •Although SIPE is primarily hemodynamic in nature and often resolves with supportive care, concomitant myocardial injury may complicate the presentation. Accordingly, patients warrant careful diagnostic evaluation, counseling on risk-reduction strategies, and longitudinal follow-up given both the risk of recurrence and potential cardiac sequelae.

Past Medical History

The patient had a history of dextrocardia, congenital absence of the right upper and middle lung lobes, asthma, and allergic rhinitis. He began endurance athletics 20 years prior, completing multiple marathons in the first 4 years before a 12-year period of sporadic activity. Four years before presentation, he resumed structured training, running 3 times weekly and swimming or bicycling 1 to 2 times per week, gradually building up training volumes. He had previously completed sprint-distance triathlons, both with and without a wetsuit, without symptoms; this was his first Olympic-distance race.

One week before the triathlon, his personal fitness tracker reported atrial fibrillation; subsequent 48-hour Holter monitoring showed no recurrence. Family history was noncontributory. Social history included alcohol intake of about 5 drinks per week, and no tobacco or drug use.

Differential Diagnosis

Asthma exacerbation was considered but was not supported by history or examination. Acute coronary syndrome and acute heart failure exacerbation were considered but were ultimately ruled out with subsequent testing. Severe mitral regurgitation from a flail leaflet was not supported by examination or echocardiography. Multifocal pneumonia was considered in the setting of asymmetric infiltrates, but the lack of fever, systemic illness, or positive infectious testing argued against this. Acute respiratory distress syndrome was excluded by the absence of systemic illness and imaging inconsistent with diffuse alveolar injury. The presentation and temporal association with immersion exercise strongly favored swimming-induced pulmonary edema (SIPE).

Investigations

Serial high-sensitivity troponin I levels peaked at 640 ng/L (reference: <53 ng/L). Electrocardiography demonstrated normal sinus rhythm without ischemic changes. Chest radiography showed asymmetric ground-glass opacities with vascular engorgement of the left lung, raising concern for unilateral pulmonary edema (Figure 1). Computed tomography pulmonary angiography excluded pulmonary embolism and revealed parenchymal changes, initially interpreted as atypical multifocal pneumonia concerning for a viral etiology (Figure 2); however, SARS-CoV-2, influenza, and a broad respiratory pathogen panel were negative, and the patient exhibited no systemic symptoms. Transthoracic echocardiography demonstrated features consistent with physiologic athletic remodeling without structural or valvular abnormalities; borderline concentric left ventricular hypertrophy (LVH) was present, and diastolic function was normal (Videos 1A and 1B). Coronary computed tomography angiography identified minimal nonobstructive coronary artery disease (CAD). Cardiac magnetic resonance imaging demonstrated focal edema in the basal inferolateral wall with hazy delayed enhancement, consistent with acute myocardial injury of uncertain etiology (Figures 3A to 3C).

Figure 1.

Chest X-Ray Demonstrating Asymmetric Left-Sided Opacities and Engorgement of the Left-Sided Pulmonary Vessels (Arrow), Likely Representing Asymmetric Pulmonary Edema in the Setting of Dextrocardia and Known Congenital Right-Sided Lobar Abnormalities (Arrow)

Figure 2.

Serial Axial Computed Tomography Scans With Pulmonary Embolism Protocol Showing Scattered Ground-Glass Opacities in Bilateral Lungs But Predominantly in the Left Upper and Lower Lobe With Relative Sparing of the Middle Lobe, Suggestive of Multifocal Pneumonia

Figure 3.

Findings on Cardiac Magnetic Imaging

(A) Short-axis plane image notable for midmyocardial delayed enhancement of the basal inferolateral wall (arrows), suggesting acute myocardial injury of unknown etiology. (B) Long-axis plane image demonstrating midmyocardial delayed enhancement (arrows), similar to (A). (C) Elevated native T2 time >60 (green outline), suggestive of regional myocardial edema of the basal inferolateral midmyocardium on T2 enhanced imaging and segmental polar mapping.

Management

Focal myocardial injury with associated troponin elevation introduced diagnostic uncertainty. The patient's clinical history lacked antecedent viral prodrome or systemic inflammatory features, making primary myocarditis less likely. Troponin elevation from demand ischemia was also considered, though the degree of biomarker release appeared disproportionate to the exertional context and degree of CAD. The troponin curve including time to peak was most consistent with an acute process temporally associated with SIPE. It is conceivable that subclinical myocarditis may have predisposed the patient to SIPE, or conversely, that SIPE itself precipitated the myocardial injury. The limited focal nature of the edema, and lack of chest pain, left ventricular (LV) dysfunction, or focal wall motion abnormalities ruled out stress cardiomyopathy, although it is possible that the mechanism was similar and potentially related to catecholamine surge. Alternative causes, including viral infection, medications, or substance use, were not supported by history, testing, or clinical course. The patient's congenital lung abnormality may have also been a predisposing factor.

The patient was managed conservatively with supportive care and demonstrated rapid clinical improvement, permitting discharge after 48 hours without diuresis. Aspirin and atorvastatin were initiated for non-obstructive CAD. Given evidence of myocardial injury, he was advised to abstain from vigorous-intensity exercise, including swimming; a recommendation extrapolated from current guidelines for myocarditis. Multidisciplinary follow-up was arranged for further diagnostic evaluation and longitudinal care.

Outcome and Follow-Up

Serial cardiac magnetic resonance imaging demonstrated resolution of myocardial edema, replaced by residual patchy midmyocardial fibrosis. LV systolic function remained preserved. Ambulatory rhythm monitoring revealed an atrial fibrillation burden of 4%, largely triggered by alcohol intake, without any ventricular arrythmias. Despite abstaining from alcohol, the patient subsequently developed increased atrial fibrillation burden and underwent ablation. There is a known association between long-term endurance sport participation and atrial fibrillation, however it is also possible that this SIPE event may have contributed. At the 2-year follow-up, he remained free of recurrent SIPE. He was not referred to sports cardiology until well after his return to running. At that time, he was not pursuing further triathlons, mainly to focus on running, but strategies for preventing recurrent SIPE were discussed.

Discussion and Mini-Review

SIPE is an underrecognized cause of acute respiratory distress in otherwise healthy athletes (Table 1). The most common presenting symptoms are cough (90.4%), dyspnea, frothy sputum production (35.6%), and hemoptysis (23.7%) immediately after strenuous swimming.^23,24 Over 80% of patients may have an oxygen saturation of >90%, however, this finding was from a study of Navy SEAL (sea, air, and land) candidates and may not represent a broader population.²⁴ The clinical algorithm for diagnosis of SIPE with acute respiratory symptoms during swimming in cold open water consists of examination for crackles, measurement of peripheral oxygen saturation, and lung ultrasonography for visualization of edema.²⁵ In practice, ultrasonography is most often replaced by chest radiography given the broad differential of patients on arrival. While there have been case reports of Takotsubo cardiomyopathy precipitated by SIPE,²² no other studies included our review were noted to demonstrate concomitant myocarditis (Table 1).

Table 1.

Review of Swimming-Induced Pulmonary Edema Cases

First Author (Year)	Age/Sex	Cardiovascular and Pulmonary Comorbidities	Reported Water Temperature (°C)	Presenting Symptoms	Time to Resolution	Treatments	Recurrence Through Follow-Up
Beinart et al (2007)1	54 y/F	HTN	22	SOB	5 d	Supplemental oxygen with continuous positive airway pressure, furosemide	No symptom recurrence
Biswas et al (2004)2	36 y/M	Type 1 DM	NR	SOB, hemoptysis	8 h	None	No symptom recurrence
Lund et al (2003)3	•21 y/M •25 y/M •27 y/M	None (all cases)	19.2 (all cases)	•SOB, cough, confusion •SOB, cough, blurred vision, confusion, weakness •SOB, hemoptysis	•24 h •48 h •5 h	Nebulized albuterol, 2 L/min supplemental oxygen (all cases)	No symptom recurrence
Melau et al (2019)4	•30 y/M •40 y/F •34 y/M	None (all cases)	14.2-14.4 (all cases)	SOB, chest tightness, productive cough with pink sputum (all cases)	•Complete regression of symptoms by transfer to large regional hospital, same day of symptom onset •Recovery within hours of transfer to nearby hospital •24 h, regress of symptoms the next day	•Rehydration, supplemental oxygen •Supplemental oxygen •Diuretics (medication and dosage not reported)	No symptom recurrence
Smith et al (2017)5	55 y/F	None	17	SOB, cough	Overnight	Furosemide 40 mg IV	Recurrence of symptoms 2 mo later with open water swimming
Yamanashi et al (2015)6	38 y/M	None	21.4	SOB	4.5 h	Methylprednisolone IV, furosemide IV	No symptom recurrence
Casey et al (2014)7	•60 y/M •55 y/F	None (both cases)	•13 •NR	•SOB •SOB, chest tightness, productive cough with pink sputum	•A few hours •Same day, before transfer to medical center	•Furosemide 50 mg IV then 40 mg IV, glyceryl trinitrate, salbutamol nebulizer •Salbutamol nebulizer	Long-term follow-up NR
Carter & Koehle (2011)8	•58 y/F •45 y/F •43 y/F	•Asthma •Asthma •None	•15 •18 •19	•SOB, hemoptysis •SOB •SOB, chest tightness, cough	•1 d •2 h •NR	•Salbutamol nebulizer •Budesonide/formoterol •Supplemental oxygen	•Recurrence 4 times in cold water •No recurrence reported •Recurrence 3 times in cold water
Paz et al (2020)9	56 y/F	None	NR	SOB, productive cough with pink sputum	24 h	Bilevel positive airway pressure ventilation, furosemide 40 mg	Long-term follow-up NR
Beinart et al (2007)1	54 y/F	HTN	22	SOB	NR	Supplemental oxygen, furosemide	Long-term follow-up NR
Tyagi et al (2021)10	18 y/M	None	NR	Presyncope, chest tightness	48 h	Furosemide 40 mg IV, continuous positive airway pressure	Long-term follow-up NR
Borza et al (2021)11	24 y/M	None	14.4	SOB, productive cough	After completing 2 courses of nebulized albuterol treatment	Nebulized albuterol, supplemental oxygen	No symptom recurrence
Barouch (2022)12	50 y/F	None	NR	SOB	48 h	None	No symptom recurrence
Pokhrel et al (2024)13	57 y/F	HTN, obesity	27.8	SOB, syncope	Improved in diffuse alveolar infiltrates at 48 h, extubated 7 d after admission	1 cycle of CPR and 2 rescue breaths with ROSC, furosemide 120 mg IV, intubated, epinephrine and vasopressin, prophylactic antibiotics for pneumonia coverage	No symptom recurrence
O'Keefe et al (2024)14	28 y/M	None	NR	SOB	NR	Supplemental oxygen	Long-term follow-up NR
Haran et al (2020)15	31 y/F	Anorexia	21.1	SOB, chest pressure, cough	5 h	Supplemental oxygen, furosemide 20 mg IV	No symptom recurrence
Marytina et al (2017)16	46 y/F	HTN	19.3	SOB, hemoptysis, lung congestion	NR	Sildenafil 50 mg	Multiple recurrence of symptoms, no recurrence once initiated on sildenafil 50 mg 1 h before swimming
Kwek et al (2017)17	21 y/M	None	30	SOB, chest discomfort, hemoptysis	2 d	Supportive treatment	No symptom recurrence, continued with diver training
Alonso et al (2017)18	28 y/F	None	15	SOB	3 d	Supplemental oxygen, furosemide 40 mg IV	No symptom recurrence and return to competition
Matthew et al (2025)19	•21 y/M •21 y/M	Monozygotic twins	NR	Acute respiratory distress (both cases)	24 h (both cases)	High-flow oxygen (both cases)	Long-term follow-up NR
Sobieszek et al (2021)20	48 y/F	None	21	SOB	3 d	Salbutamol, furosemide IV	No symptom recurrence
Deady et al (2006)21	38 y/M	None	15	SOB, chest tightness, hemoptysis	24 h	Supplemental oxygen, furosemide 20 mg IV	Long-term follow-up NR
Rigler et al (2022)22	•53 y/M •57 y/F •60 y/F	None (all cases)	NR	•SOB, chest pain, hemoptysis •SOB, chest pain •Severe SOB, hemoptysis	•8 wk •24 h •NR	•Aspirin 300 mg, ticagrelor load, sublingual nitroglycerin, started on atorvastatin and ramipril, diagnosed with concurrent TCM •Clopidogrel load, started on ramipril, bisoprolol, and aspirin, diagnosed with concurrent TCM •Supplemental oxygen, furosemide 30 mg IV then 40 mg oral, aspirin and clopidogrel load, started on ramipril and bisoprolol, diagnosed with concurrent TCM	Long-term follow-up NR

CPR = cardiopulmonary resuscitation; DM = diabetes mellitus; F = female; HTN = hypertension; IV = intravenous; M = male; NR = not reported; ROSC = return of spontaneous circulation; SOB = shortness of breath; TCM = Takotsubo cardiomyopathy.

The incidence of SIPE varies in the literature. A large-scale Swedish study described an overall incidence of 0.44%, with 90% of diagnosed patients being women (incidence rate: 0.75% in women, 0.09% in men).²⁶ The study also described an increasing incidence with age.²⁶ A systematic review described an incidence rate estimated around 1.1% to 1.8% and similarly reported older age and female sex to be notable risk factors.²⁷ A study investigating incidence in Navy SEAL candidates described an incidence of up to 5.0%.²⁴ In a study focusing on American triathletes, SIPE was identified in 1.4% of the population.²⁸ Other risk factors that have been described include overhydration prior to exercise, tight wetsuits, cold water exposure, asthma, and underlying cardiopulmonary disease, particularly hypertension and LVH.²⁷ LVH and hypertension are risk factors as they can both lead to decreased LV compliance, particularly when subjected to increased volume load; however, mild LVH is common in athletes, SIPE remains relatively rare, and SIPE may still occur in the absence of these factors. One study showed exaggerated mean pulmonary artery pressures and wedge pressures in SIPE-susceptible individuals during cold-water immersion exercise,²⁹ although another study showed no difference in pulmonary function tests, exercise capacity, or pulmonary arterial pressure response to hypoxemia in dry conditions,³⁰ making it difficult to predict with standard testing who may be at risk. Other possible predisposing mechanisms include higher venous tone (ie, decreased venous capacitance) and increased systemic vascular resistance/hypertensive response during exercise.²⁹ A systematic review of risk factors also specifically identified CAD, atrial fibrillation, diabetes, and fish oil use,²³ however not all of these factors have been consistently associated. Occurrence of SIPE does not depend on training status or experience.

The pathophysiology of SIPE is hemodynamic in nature. Cold-water immersion and exertion increase systemic vascular resistance and central blood volume, which overloads the LV, subsequently elevating pulmonary artery and capillary wedge pressures and pulmonary vascular resistance.²³ This rise in pulmonary capillary hydrostatic pressure promotes transudation of fluid into the alveolar spaces, which is further exacerbated by external thoracic compression from water immersion and wetsuits.²⁷ In susceptible individuals, the result is acute dyspnea, hypoxemia, and radiographic pulmonary edema that resolve rapidly once removed from the inciting environment.²³ Another proposed mechanism is left ventricular/right ventricular stroke volume mismatch, theorizing that with the increased systemic vascular resistance and afterload, the LV is less able to augment stroke volume with exercise, resulting in pulmonary edema.⁷

Management is supportive, typically limited to oxygen therapy and rest, with radiographic and symptomatic resolution occurring within 24 to 48 hours.^23,27 Long-term outcomes are generally favorable, although recurrence is common.²³ Preventive strategies such as avoiding overhydration, limiting cold-water exposure, and modifying wetsuit fit have been proposed, with a possible role for pharmacologic prophylaxis. A study of 10 patients with a history of SIPE investigated the prophylactic role of sildenafil, suggesting a potential role in reducing pulmonary vascular pressures without adverse effects on exercise hemodynamics.²⁹

Outcomes after hospitalization for SIPE are largely positive. While most deaths in triathlon occur during the swim portion, most were attributed to underlying cardiac disease or events.³¹ However, the true prevalence of SIPE-related events and deaths is unknown, as the presence of pulmonary edema on autopsy may make it difficult to ascertain the underlying mechanism (ie, cause vs sequelae).³¹

While symptoms tend to resolve within 48 hours, up to 38% of patients may describe symptoms at 10-day follow-up and recurrence in up to 28% of patients at 30-month follow-up.³² Overall, SIPE represents a unique diagnostic challenge in endurance athletes but is generally well tolerated, with limited long-term adverse events.

Future Directions

The current understanding of SIPE is derived predominantly from observational studies and case reports, and substantial gaps remain in identifying predisposing factors and effective preventive strategies. The episodic and unpredictable nature of SIPE makes systematic investigation difficult, and although small physiologic studies in SIPE-susceptible individuals have offered insights, they likely do not capture the full pathophysiologic spectrum. Notably, most available data originate from Western cohorts with largely Caucasian participants, thus the influence of race, ethnicity, and geographic factors remains insufficiently studied.²³ For race directors and on-site medical teams, early recognition and appropriate preparedness are essential. Equally important is athlete education, as endurance athletes may underreport or push through symptoms, increasing the risk of delayed diagnosis and adverse outcomes.

Conclusions

This case highlights SIPE as an important but underrecognized cause of acute dyspnea in endurance athletes. Recognition of its characteristic clinical features and natural history facilitates appropriate diagnosis, management, and counseling on risk mitigation. The concomitant finding of focal myocardial injury underscores the potential for SIPE to present with overlapping or confounding pathology, including myocardial injury, which may influence prognosis and follow-up. Greater awareness among clinicians and athletes is essential to avoid misdiagnosis, prevent unnecessary interventions, and reduce recurrence risk in susceptible individuals.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Video 1

Findings on Transthoracic Echocardiography

(A) Parasternal long-axis and (B) 4-chamber echocardiographic recordings demonstrate left ventricular dilation, hyperdynamic function with ejection fraction 76% by 2D biplane, and normal diastolic function. No valvular abnormalities were observed.