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1
Question:

A 24-year-old man is evaluated due to a syncopal episode that occurred immediately after he completed a 13-mile half-marathon.  The patient felt light-headed and then passed out.  He was immediately placed in a supine position and regained consciousness after 2-3 minutes.  The patient has no chest pain, palpitations, or shortness of breath.  He has never had a similar episode.  There is no family history of sudden death.  The patient does not use alcohol or illicit drugs.  Temperature is 37 C (98.6 F), blood pressure is 98/56 mm Hg, pulse is 80/min, and respirations are 14/min.  Complete physical examination and ECG show no abnormalities.  Which of the following is the most likely mechanism of this patient's syncope?

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Explanation:

Exercise-associated collapse

Pathophysiology

  • Cessation of exercise results in sudden decrease in venous return to the heart (preload)

Manifestations

  • Athlete collapses immediately after cessation of exercise
  • Dizziness or light-headedness, syncope
  • Normal to minimally elevated core temperature

Management

  • Trendelenburg positioning  (ie, feet inclined above the head)
  • Oral hydration

This patient with syncope after completing a half-marathon experienced exercise-associated collapse (EAC).  EAC is characterized by the inability to stand or walk associated with light-headedness or syncope immediately following vigorous physical activity.

EAC is thought to occur due to physiologic adaptations in endurance athletes, who have significantly higher cardiac output than untrained individuals due to hypertrophy of the left ventricle (ie, athlete's heart).  During strenuous exercise, the skeletal muscles, particularly in the lower extremities, exert significant pressure on the venous system, which increases venous return to the heart.  When an athlete abruptly stops exercising (eg, finishing a run), the muscles no longer exert pressure and venous return dramatically decreases.  The sudden decrease in cardiac preload fails to meet increased cardiac demands, resulting in transient postural hypotension with syncope or collapse.  This may be compounded by inhibition of the baroreflex and dehydration, which often occur with intense exercise.

The Trendelenburg position (ie, feet inclined above the head) helps redistribute blood to the heart and brain, improving symptoms.

(Choice B)  The physiologic effects of exercise include increased circulating catecholamines, decreased parasympathetic activity, and increased sympathetic activation, all of which result in increased, rather than decreased, cardiac contractility.

(Choice C)  Left ventricular outflow obstruction (eg, hypertrophic cardiomyopathy) can cause syncope and sudden cardiac death.  However, patients often have dyspnea on exertion or chest pain, and ECG abnormalities (eg, widespread repolarization changes) are typical.

(Choice D)  Resting bradycardia in well-conditioned athletes is thought to be due in part to an increased parasympathetic regulation of cardiac pacemaker cells.  However, because exercise training results in elevated stroke volume, this is not associated with hypotension or syncope.  Furthermore, this patient has a normal heart rate.

(Choice E)  Electrolyte abnormalities (eg, hyperkalemia) cause cardiac irritability and promote the development of tachyarrhythmias.  Although arrhythmias can cause collapse, they usually occur during, not immediately after, exercise.  Furthermore, electrolyte abnormalities result in characteristic ECG changes (eg, peaked T waves).

Educational objective:
Exercise-associated collapse typically occurs after intense exercise in well-conditioned athletes.  It is characterized by loss of postural tone or syncope immediately following the cessation of exercise and occurs due to impaired venous return to the heart.