Exercise-Associated Collapse

Etiology

Exercise-associated collapse was previously called heat syncope, and the etiology is not fully understood.[2] It is thought to be caused by transient orthostatic hypotension resulting from impaired baroreflexes associated with volume depletion, peripheral vasodilation, and decreased vasomotor tone leading to decreased preload, reduced cardiac output, and presyncope or syncope.[4]

Epidemiology

Exercise-associated collapse is most common in endurance events such as marathons, ultramarathons, and triathlons but can occur in various activities of various intensities, including military training and competitive team sports.[1] The greatest risk factors for exercise-associated collapse include a history of a previous collapse, dehydration, elevated environmental temperature, elevated humidity, calorie restriction, history of chronic health issues, and alcohol consumption.[5] There does not appear to be an increase in risk associated with age, sex, or ethnicity.[3]

Pathophysiology

While the exact mechanism of exercise-associated collapse remains to be determined, it was previously believed to be caused by dehydration and/or hyperthermia. More recent evidence indicates that transient postural hypotension resulting from an interaction of athletic bradycardia, lower extremity pooling post-endurance workout, and impaired cardiac baroreflexes are the principal causes.[6] Trained endurance athletes tend to have mild left ventricular dilation and hypertrophy that allows for more efficient cardiac output and a subsequent lower resting heart rate. During endurance exercise, heart rate increases to account for subsequent increases in metabolic demand. Increased metabolic demand requires increased vasodilation for the high-demand muscle groups, usually the lower extremities. This vasodilation is offset by the lower extremity muscles functioning as a ‘second heart’ by moving the increased lower body blood volume back to the heart to support the high cardiac output needed during vigorous exercise. However, this ‘second heart’ effect is lost with the cessation of exercise. When done abruptly, such as upon crossing the finish line of a marathon, venous pooling in the lower extremities results due to impaired baroreflex control. When coupled with a quick return towards a resting heart rate as seen in trained athletes, insufficient blood supply results, creating a hypotensive setting. This exercise-associated postural hypotension may result in symptoms caused by a decline in systolic blood pressure below supine values, leading to an exertional-related collapse when standing.[7]

History and Physical

It is common for exercise-associated collapse to occur in the pre-hospital setting, such as a mass participation athletic event. Healthcare providers should suspect EAC when athletes present with collapse during exertion or just after discontinuation of intense physical exertion, such as marathon running, cycling, triathlon, hiking, backpacking, or endurance-based military field training or combat operations. The likelihood of EAC is increased if the exertional event occurred in hot, humid weather, but other etiologies should be considered if a patient presents with significantly abnormal vital signs, including significant hypertension and hyperthermia. Prompt identification and differentiation from other common exertional injuries are essential to caring for a collapsed athlete. Alternative etiologies include, but are not limited to, sudden cardiac arrest, exertional heat stroke, exercise-associated hyponatremia, exercise collapse associated with sickle cell trait, insulin-related hypoglycemia, seizures, and anaphylaxis. Presenting symptoms of EAC include lightheadedness, orthostasis, faintness, fatigue, and generalized weakness. The individual will often present with some alteration in mental status ranging from mild to significant. Severe symptoms include syncope after discontinuation of exertion.[8]

Evaluation

Initial physical assessment of a collapsed athlete will include ABCDE screening (airway, breathing, circulation, disability, and exposure). If ABCs are verified, a brief history may be conducted to evaluate for altered mental status. Vital signs, including a core rectal temperature, are essential for differentiating underlying etiologies, especially hyperthermia.[9]

Treatment / Management

Management is dictated by the presence or absence of neurologic symptoms. The goal of treatment is the return of vascular tone and the resolution of postural hypotension to resolve symptoms. If the patient is normothermic, place the patient in Trendelenburg position or supine with the legs elevated 12 to 24 inches above the heart. Often, this alone significantly improves mental status and physical symptoms.[9] 

When resting at baseline, the patient is eligible for oral fluid resuscitation and ambulation with assistance. This should be under the auspices of personnel trained to look for signs of other forms of exertional injury like EAH or heat injuries due to the high incidence of presentation overlap. Ambulation allows for the return of skeletal muscle 'second heart' effect and oral rehydration allows for increased intravascular volume status, both aimed at improving postural orthostatic hypotension.[10]

If the patient's mental status is not improving after 5 minutes of Trendelenburg positioning, other etiologies should be considered. Intrvenous access should be obtained, and fluid rehydration should be considered. However, point-of-care electrolyte and glucose evaluation should be considered to evaluate for hypoglycemia and hyponatremia before fluid administration. Any persistent mental changes, rectal temperature higher than 102, systolic blood pressure lower than 110, or heart rate above 100 should be considered for transfer to a higher level of care.[7]

Differential Diagnosis

EAC falls on the spectrum of exertional injuries but should be considered a diagnosis of exclusion to other etiologies of exertional falls. As stated above, ABCDE or a similar initial assessment method should be utilized.[11] This should help rule out sudden cardiac arrest or other cardiovascular incidents. A core rectal temperature evaluates for hyperthermic or hypothermic factors such as exertional heat stroke or other heat injuries. Point-of-care electrolytes and glucose testing look for causes such as exercise-associated hyponatremia and exertional hypoglycemia. A patient history from the individual known contact is important to evaluate for sickle cell trait status for exercise collapse associated with sickle cell trait ECAST, seizure history for potential epilepsy, or allergy history for potential anaphylaxis.[2]

Prognosis

Many athletes recover rapidly with only minimal intervention, and most are effectively treated in the pre-hospital setting and do not require treatment at a hospital. Results from a study evaluating participants in the Gothenburg half marathon demonstrated only 1.19 to 2.21 per 1000 needed more intervention than ambulation and oral hydration.[3] A requirement for advance care usually indicates another underlying etiology to the presenting symptoms and suggests the need for a broader workup. The most common cause for needing advanced care was hyperthermia, hyponatremia, and hypoglycemia.[2]

Complications

There are few complications directly associated with EAC. Most of the time, patients have a complete recovery with minimal intervention and limited sequala.[7] Individuals with a history of EAC are at an increased risk for a repeat episode in the future.[5] Individuals can have injuries incurred when they EAC associated falls, but these are secondary effects and are not due to the collapse itself.