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Why do fit swimmers get short of breath and cough up blood?

Why do fit swimmers get short of breath and cough up blood?

 


A healthy, competitive long-distance swimmer in his 50s was rushed to the hospital with acute shortness of breath from a routine open-water swimming event and vomited up pink, frothy sputum. BMJ case report.

The water she swam in was about 17°C (62.6°F) and she was wearing a wetsuit.

In hospital, she denied chest discomfort, palpitations, dizziness, or any preceding viral symptoms. On her clinical examination, she was short of breath, coughing, and her heart rate was 100 beats per minute. Oxygen saturation was her 96%, blood pressure was her 138/69 mm Hg and body temperature was her 36.5°C (97.7°F), according to a cardiac ultrasound at her Royal United Hospitals Bath NHS Foundation Trust in England. her specialist, Dr. James Willis, and colleagues reported.

The group noted that the woman’s symptoms and tachycardia resolved spontaneously within 2 hours of her arrival at the hospital.

Her cardiovascular system was normal except for the presence of bibasal fine crepitation. An admission electrocardiogram revealed her sinus rhythm with T-wave inversions in leads I, AvL, and V2, the cardiac axis was normal, and the QT interval was corrected. Her CT of the chest ruled out large-vessel pulmonary embolism and showed perihilar ground-glass consolidation bilaterally, with more pronounced changes in the lower lobes.

A blood test initially revealed an elevated white blood cell count (14.7 × 109/L), neutrophils (12.6 × 109/L), Troponin T (23 and 32 ng/L), and N-terminal pro-brain natriuretic peptide (NT-Pro BNP; 974 ng/L).

Based on her history of acute shortness of breath when swimming in cold water wearing a wetsuit and pulmonary edema without evidence of aspiration or structural heart disease, and her rapid recovery, she was diagnosed with swim-induced pulmonary edema. (SIPE). , a subtype of immersion pulmonary edema.

The clinician also learned that she had received Pfizer’s COVID-19 booster vaccination six hours before the group’s night swim. However, given the timing of symptoms, COVID-19 boosters were ruled out as a contributing factor.

“Interestingly, cardiac MRI showed prolonged T2 relaxation times in the basolateral anterior, anterolateral, and inferior lateral regions indicative of myocardial edema,” say Willis and colleagues. They added that there is evidence of subbasolateral, non-ischemic late-intermedial gadolinium enhancement suggestive of possible fibrosis. Left ventricular diameter and systolic and diastolic function were all normal.

The patient told the clinician that he had experienced similar mild symptoms two weeks earlier while swimming in the ocean and had problems with training for running and swimming in the pool, but that he was feeling a little better. “It’s bad,” he said.

The patient was monitored, discharged the next day, and laboratory and ECG findings returned to normal.

“Interval cardiac MRI showed resolution of myocardial edema and subbasal lateral fibrosis,” Willis and colleagues reported. They also observed residual subbasal myocardial fibrosis and normal left ventricular size and function.

Approximately eight weeks later, the patient underwent CT coronary angiography, which showed normal coronary anatomy “with mild burden of non-flow-restricting atheromatous plaque, along with resolution of pulmonary edema.”

discussion

Although the pathophysiology of SIPE remains unclear since it was first reported in 1989, it has been hypothesized that it may be associated with takotsubo-like stress cardiomyopathy, cold-induced coronary spasm or ventricular pressure overload, or an inflammatory process. It has been. SIPE likely has not yet been reported, with an estimated incidence of 1.1% to 1.8% in swimmers.

Affected people are often healthy and well. Risk factors include older age, female sex, high blood pressure, long distance swimming, cold water temperatures, and pre-existing heart disease.

diagnose SIPE is based on acute onset of dyspnea and/or hemoptysis during or immediately after swimming in the absence of aspiration, laryngospasm, or preceding infection. hypoxia; X-ray evidence of pulmonary edema; and rapid resolution within two days, detailed the case authors.

At presentation, CT angiography helps rule out coronary artery abnormalities. Cardiac MRI may be used to more precisely define cardiac structure and function, and MRI renal angiography and 24-hour urinary catecholamines were performed to rule out less common causes of pulmonary edema. the authors explained.

Pre-existing decreases in lung volumes and expiratory flow, and increases in resting mean pulmonary artery pressure (PAP) and pulmonary artery wedge pressure (PAWP) also related at SIPE.

Affected individuals must be removed from the water, seated in an upright position, and ceased activity. Treatment is primarily supportive, but often requires oxygen therapy and sometimes diuretics, bronchodilators, and continuous positive airway pressure. According to the authors, as in this case, the patient usually recovers completely within 1-2 days after leaving the water.

Importantly, SIPE is responsible for approximately 10% of scuba-diving deaths, and left ventricular hypertrophy is confirmed in all cases. Between 13% and 22% of affected individuals have recurrent episodes and patients should be informed of this and considered predisposed to SIPE. Therefore, they are instructed to modify their swimming and diving activities as needed. Especially in cold water activities.

The case authors recommend avoiding the use of non-steroidal anti-inflammatory drugs (NSAIDs) after episodes of SIPE and optimizing for comorbidities that exacerbate diastolic function. “prevention Sildenafil has been shown to lower PAP and PAWP, which appears to be effective. preventive We will measure people with a history of recurrent SIPE,” they added.

The case authors noted their aim was to raise awareness among doctors and swimmers about the relatively unrecognized condition. guidance For divers. However, “there are no formal national medical guidelines for the recognition and management of this complex condition,” they said, raising a high level of suspicion in patients with post-immersion dyspnea.

  • author['full_name']

    Kate Nizel Freelance medical journalist based in Belleville, Ontario.

Disclosure

The authors report no conflicts of interest.

Primary information

BMJ case report

Source reference: Oldman J, et al., “Myocardial edema in the setting of immersion pulmonary edema — cause or effect?” BMJ Caseworker 2023; DOI: 10.1136/bcr-2022-251274.

Sources

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2/ https://www.medpagetoday.com/casestudies/pulmonology/102653

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