Continuing Education Activity
Exercise-associated collapse (EAC), also known as exercise-associated postural hypotension (EAPH), is defined as the inability to stand or walk unaided during or after the completion of strenuous exercise. EAC is often used as an umbrella term for any exertional fall. However, the focus of this topic pertains to causes related to postural hypotension. Other means of exertional fall, including sudden cardiac arrest, exertional heat stroke, exercise-associated hyponatremia, and exercise collapse associated with sickle cell trait (ECAST), are outside of the scope of this topic and should be studied separately. Nevertheless, astute recognition of this differential diagnosis is critical for prompt treatment.
- Describe the pathophysiology of exercise-associated collapse.
- Outline the significant risk factors and presenting signs/symptoms of exercise-associated collapse in athletes.
- Review the complications of exercise-associated collapse in athletes.
- Summarize the proper evaluation and prehospital management of exercise-associated collapse.
Exercise-associated collapse (EAC) is defined as the inability to stand or walk unaided during or after the completion of strenuous exercise. EAC was previously called heat syncope. While the etiology is not fully understood, it is thought to be caused by transient orthostatic hypotension resulting from volume depletion, peripheral vasodilation, and decreased vasomotor tone related to impaired baroreflexes leading to decreased preload, decreased cardiac output, and syncope.
Prompt differentiation of EAC from other exertional illnesses is critical, as it is a generally benign condition that can present similarly to other means of exertional falls. These presentations include sudden cardiac arrest, exertional heat stroke, exercise-associated hyponatremia, and exercise collapse associated with sickle cell trait (ECAST). A simple treatment of oral fluids and assisted walking, where medical personnel walk collapsing runners in designated safe areas, reduces the incidents of medical interventions related to EAC.
Exercise-associated collapse was previously called heat syncope, and while the etiology is not fully understood. 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.
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. 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. There does not appear to be an increase in risk associated with age, sex, or ethnicity.
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.
Trained endurance athletes tend to have mild left ventricular dilation and hypertrophy that allows for a 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 (EAPH) may result in symptoms caused by a decline in systolic blood pressure below supine values leading to an exertional-related collapse when standing.
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 (EAH), exercise collapse associated with sickle cell trait (ECAST), insulin-related hypoglycemia, seizures, and anaphylaxis.
Presenting symptoms of EAC include lightheadedness, orthostasis, faintness, fatigue, 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.
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.
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.
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.
If the patient's mental status is not improving after 5 minutes of Trendelenburg positioning, other etiologies should be considered. IV 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 > 102, systolic blood pressure < 110, or heart rate > 100 should be considered for transfer to a higher level of care.
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. 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 ECAST, seizure history for potential epilepsy, or allergy history for potential anaphylaxis.
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. A study evaluating participants in the Gothenburg half marathon demonstrated only 1.19 to 2.21 per one thousand needed more intervention than ambulation and oral hydration. 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.
There are few complications directly associated with EAC. Most of the time, patients have a complete recovery with minimal intervention and limited sequala. Individuals with a history of EAC are at an increased risk for a repeat episode in the future. Individuals can have injuries incurred when they EAC associated falls, but these are secondary effects and are not due to the collapse itself.
Deterrence and Patient Education
Individuals should be educated about having a greater risk for EAC if they have a history of chronic health issues, are dehydrated, restrict calories, and if the environmental temperature or humidity is elevated. They can reduce their risk by avoiding alcohol consumption before engaging in endurance events.
Pearls and Other Issues
Exercise-associated collapse is a benign condition that is on the exertional injury spectrum and includes conscious athletes who are unable to stand or walk on their own after the completion of an exertional event. It is associated with the sudden termination of prolonged endurance exercises and is believed to be caused by transcendent postural hypotension. The most significant risk factors contributing to EAC are dehydration, unfavorably hot and humid environments, alcohol consumption, and a history of chronic health issues or a previous collapse.
There does not appear to be an increase in risk associated with age, sex, or ethnicity. It is a diagnosis of exclusion, and other etiologies should be considered in individuals with vital sign abnormalities, persistent altered mental status, or electrolyte derangements. EAC is common in the prehospital setting of mass participation endurance events. Management is centered on excluding or identifying more severe etiologies like acute coronary syndrome, exercise-related injuries, and heat-related injuries that will need more advanced medical care.
Treatment is focused on maneuvers to reduce postural orthotic hypotension, such as elevating the feet above the heart and fluid rehydration. Most individuals diagnosed with EAC proceed to a full recovery with no sequelae. Individual athletes should be educated in reducing EAC risk by trying to avoid calorie restriction, dehydration, and limiting alcohol consumption before participating in an endurance event. They should also take time to a climate to the event location and weather.
Enhancing Healthcare Team Outcomes
Prehospital teams should be trained to quickly differentiate EAC from other more severe life-threatening conditions that can cause collapse can present similar to EAC. The proper education of physical trainers, EMTs, and other ancillary personnel at sporting events and military training in the identification and initial treatment of EAC will help expedite the treatment of more severe conditions in need of more advanced interventions and providers.