Syncope

Syncope does not typically occur with exertion.

ERS represents only 3–20% of syncope cases (1).

In a study of 7,500 athletes, 6.2% had reported a syncopal episode in the preceding 5 yrs. Of these cases of syncope, 87.7% were unrelated to exercise, 12% were postexertional, and only 1.3% were exertional (2,3).

Only a minority of syncopal events are associated with physical activity, accounting for only 3–20% of cases.

Athletes who present with exertional syncope (during exertion) have a greater probability of cardiac causes.

Stroke volume may be an important pathophysiologic factor in ERS.

Exercise-associated collapse (EAC) is defined as occurring when an athlete essentially collapses and is unable to stand or walk unaided as a result of light-headedness, faintness, dizziness, or syncope.

Victims of EAC are often able to assist in their own recovery, as opposed to those of a true ERS event.

Postsyncopal athletes are best evaluated in a head-down, legs-up position because this may be therapeutic for EAC.

Begin with assessment of mentation and circulatory status.

If pulseless and unresponsive, basic life support (BLS) should be started, as suggested by the new cardiopulmonary resuscitation guidelines.

Once cardiorespiratory status has been established, a thorough history should be obtained, with a particular focus on any presyncopal symptoms and prior episodes.

Is it a true syncope?

Does the initial evaluation lead to certain diagnosis, suspected diagnosis, or unexplained diagnosis?

Is heart disease present?

According to the guidelines on syncope of the European Society of Cardiology and a similar statement of the American Heart Association, the initial evaluation of patients with syncope is based on a thorough history and physical examination, supine and upright BP measurement, and standard ECG.

Comprehensive neurologic assessment, especially with regard to cognitive function

Vital statistics should be obtained, with the caveat that a rectal temperature is the most reliable means of assessing core temperature after exertion if heat stroke is suspected as a cause for the syncopal episode.

BP in both arms, pulse, and hydration status will provide additional immediate clues.

Cardiac and pulmonary examinations should attempt to identify any structural cardiac abnormalities.

Careful evaluation of the carotid or radial pulse may demonstrate the bifid pulse (2 systolic peaks) of hypertrophic cardiomyopathy or the slow rising pulse (pulsus parvus et tardus) of aortic stenosis.

Chest palpation in an attempt to identify the point of maximal impulse, as well as any thrills or heaves that may identify pathologic conditions

Auscultation should be performed with the patient in the supine, seated, and standing positions.

Murmurs, gallops, and pathologic splitting all should be noted.

Listening to the patient during squatting, while standing, and during a Valsalva maneuver may help to rule out dynamic outflow obstruction.

A systolic murmur that gets louder with standing or during a Valsalva maneuver suggests the obstruction of hypertrophic cardiomyopathy.

A patient with an identified systolic murmur and a systolic pressure gradient between the upper and lower extremities of >10 mm Hg should suggest a diagnosis of aortic stenosis.

The major causes of syncope among athletes would be cardiac, neurologic, or metabolic.

Neurologic tests include EEG, brain imaging (MRI, MRA, CT scans), and neurovascular studies (Doppler, US).

Metabolic syncope is seen frequently during the event and has readily identifiable conditions.

Most patients suffer from cardiac syncope.

Drugs could precipitate a syncopal attack, and a detailed medication history including recreational drug use is essential. The drugs most likely to induce syncope include nitrates, vasodilators, and β-blockers.

The treatment should be aimed initially at increasing salt and fluid intake.

The patient should be encouraged to maintain hydration.

If the prodrome of an episode is recognized, the patient should lie flat until the episode passes.

These measures, along with patient education, frequently will be all that is required.

Generally, in athletes without structural cardiac defects, in whom syncope occurred after exercise, return to play is likely.

In fact, athletes with syncope had a low recurrence rate and no major adverse events in a follow-up period of >6 yrs (2,3).