Personal History: Have You Ever Nearly Lost or Actualy Lost Consciousness?
To determine the importance of a positive answer to this question, the following questions should be asked:
- Did the syncopal event occur during or immediately after exercise; if the latter, was the patient standing still or moving around?
- Prior to the syncopal event, were there any prodromal symptoms such as the following: chest pain, palpitations, visual changes, wheezing/shortness of breath, nausea, or itching?
- After the syncopal event, what was the patient’s postevent clinical status? Did they wake quickly, or was there a prolonged period of unresponsiveness? Was there any observed seizure activity or loss of urine, stool, or tongue bite marks? Were there vital signs recorded on site, particularly the immediate postsyncope measurements?
- What medications and supplements were being utilized prior to the event?
- Is there a prior personal or family history of syncope or of sudden cardiac arrest/death?
The evaluating physician’s first priority is to use the clinical history to distinguish between true syncope involving a loss of consciousness with presumed hemodynamic compromise and exercise-associated collapse associated with exhaustive effort or postexercise hypotension. In true syncope from hemodynamic causes, the athlete typically recovers quickly with restoration of arterial pressure, unless resuscitation is required. After collapse associated with an exhaustive effort, however, athletes usually will have prolonged periods of “being out of it,” even in the supine position with normal heart rate and BP. This picture is in contrast to patients with syncope due to heat stress who are universally hypotensive and tachycardic. Athletes who are impaired, seeming “unconscious,” but able to assist in their own evacuation are unlikely to be in the throes of a life-threatening arrhythmia, although other metabolic or catastrophic abnormalities are possible (e.g., hyponatremia, exertional heat stroke).
The postevent state provides important clues such as seizure activity, incontinence, and immediate vital signs (including body temperature). It must be emphasized however, that a seizure-like activity can be the result of reduced cerebral perfusion and therefore does not always imply epilepsy or neurologic problems. Reports from witnesses can be invaluable. Too often, syncope is assumed to be neurologic and the cardiac evaluation is not done, resulting in fatal outcomes.
The second critical distinction is whether the event occurred during or immediately after exercise. Orthostatic hypotension occurring after exercise, usually associated with sudden cessation of activity, is much less ominous than the sudden loss of consciousness that occurs during exercise, which suggests cardiac arrhythmia with loss of blood flow to the brain. Syncope prompted by an abrupt loud noise such as a starting gun or immersion in cold water may provide a clinical clue to prolonged QT syndrome (LQTS).
The third component of the history that provides clinical clues is a detailed assessment of events prior to the collapse. Prodromal symptoms such as palpitations (suggesting arrhythmia), chest pain (ischemia, aortic dissection), nausea (ischemia, high levels of vagal activity, or hyponatremia), wheezing, and pruritus (anaphylaxis) are significant, along with precipitating events like “only during exercise.” It is important to identify whether syncope occurs in the upright position (orthostatic hypotension) alone or also when sitting or supine (arrhythmia or nonhemodynamic cause).
The fourth component of the evaluation requires assessment of the medication and supplement history. A comprehensive medication list, including over-the-counter medications and ergogenic aids is necessary; the practice of high-risk behaviors, such as recreational drug use should be carefully investigated.
Finally, a personal and family history of sudden death is critical and, if present, may identify very high-risk subgroups with hypertrophic cardiomyopathy (HCM), LQTS, or right ventricular cardiomyopathy. Delineating a family tree will give a complete snapshot of the family history.
The Physical Examination
Vital signs (including orthostatic measurements) should be included. Blood pressure (BP) should be measured in both arms and legs as well as after 5 min of moving to a standing position.
The three tests that are core to the diagnostic evaluation of the athlete with syncope include the electrocardiogram (ECG), the echocardiogram, and the exercise stress test. Echocardiography should precede the exercise test, allowing the assessment of ventricular size and function, pulmonary pressures, and valve function/integrity. Rather than a standard Bruce protocol, a maximal symptom-limited exercise test should be used to reproduce the conditions that provoked the syncopal event. For example, a stuttering start-stop test for a basketball or soccer player or a prolonged high-intensity race pace test for a runner. The exercise ECG also should be examined for appropriate shortening of the QT interval.
Further testing should be ordered only as indicated and in consultation with the appropriate specialist. A complete review of all the advanced diagnostic tests is beyond the focus of this article. Tilt table testing should not be used in the syncope evaluation because of the high rate of false positive tests due to the steep Starling curve in athletes.
The clinician is additionally reminded that not all syncope is cardiogenic. Athletes whose history suggests seizure activity may require an electroencephalogram and magnetic resonance imaging (MRI) of the brain to exclude a structural lesion, and seizures can be related to hyponatremia or heat stroke. Hematologic and metabolic abnormalities require testing as indicated, e.g., hypoglycemia in those with diabetes, athletes with eating disorders, or patients on beta-blockers.
Case 1: Cross-Country Runner with Collapse at the Finish Line
A 17-year-old female track star was competing in the district championships in the 5,000 m. She was having an excellent race and was part of the final pack that was in contention for a medal. Just after crossing the finish line (in 17 min 55 s), she collapsed to the ground and, according to bystanders, remained “unconscious” for about an hour. ECG, echocardiogram, and Holter monitor testing results were normal, although she did not faint during the period of recording. An athlete-specific exercise test was performed on a large treadmill at 10 mph; after 10 min, the patient started to cry and then slumped in the safety harness. At the moment of fainting, her rhythm was normal, pulse was 185 bpm, and BP was 140/70. The final impression was exercise-associated collapse, and the recommendation was better training and pacing to match demands of her sport.
Key Point: History pointed away from life-threatening arrhythmia; athlete-specific exercise testing reproduced the problem during direct electrical and hemodynamic monitoring, allowing an accurate diagnosis.
Case 2: Basketball Player with Collapse on the Free Throw Line
A 21-year-old male college basketball star led a 12-point run, mostly by a series of impressive fast breaks, in the middle of the first half of an early round of the National Collegiate Athletic Association tournament. After the last jam, he was fouled and walked to the foul line. While standing waiting to shoot, he slumped to the ground. Witnesses observed generalized seizure activity. ECG showed LVH and unusual T waves in the right precordial leads, but his echocardiogram result was normal and short-term Holter monitoring did not identify any arrhythmias, although no symptoms occurred during the monitoring period. A stuttering exercise test was performed at high speed (15 mph) followed by sudden stops. After the fifth repeat, while standing quietly, there was a sudden drop in pulse to 45 bpm, BP was 60/40, and the patient fainted on the treadmill. The final diagnosis was postexercise hypotension (neurally mediated syncope). The recommendation was behavioral modification (avoid standing still if possible, learn leg crossing/butt clenching and toe bouncing maneuvers, stay well hydrated, and wear compression socks).
Key Point: Standing still after intense exercise can lead to hypotension due to loss of the muscle pump and lead to neurally mediated syncope with bradycardia and hypotension. Athlete-specific exercise testing elicited the problem and led to simple, effective, nonpharmacologic therapy.
Case 3: Football Player with Collapse while Running out for a Pass
A 19-year-old male wide receiver for a junior college football team was running a crossing pattern during practice when witnesses observed him to weave, stumble, and fall to the ground. The trainer arrived at the scene to find him alert and oriented. His BP was 135/80; pulse was 110 bpm and regular.
Physical examination result was normal; however, ECG results showed septal Q waves, LVH, and deep T wave inversions. Echocardiogram results showed a septal thickness of 1.8 cm, although without systolic anterior motion of the mitral valve. Holter monitoring revealed multiple runs of NSVT, and cardiac MRI showed multiple areas of delayed enhancement. The diagnosis was HCM; he was held from competition, and family members were screened for HCM.
Key Point: Syncope during exercise is very concerning for an arrhythmia and underlying structural heart disease.
Case 4: Lacrosse Player with Syncope during Exercise
A lacrosse player had syncope while running wind sprints. Careful history examination documented that the syncope occurred during a sprint and not between sprints. ECG results showed nonspecific ECG changes, but the echocardiogram result was normal. The exercise test result was normal; cardiac MRI was performed and showed patchy areas of delayed enhancement indicating potential myocarditis. An electrophysiology (EP) study induced atrioventricular nodal reentrant tachycardia (AVNRT) but no ventricular arrhythmias. A 24-h Holter monitor showed no arrhythmias. The athlete had a major game coming up, and there was pressure to allow him to play. The patient had ablation of the AVNRT and was allowed to return to sports. He died in practice the following week.
Key Point: The worrisome history plus noncoronary distribution of delayed enhancement on MRI are concerning for myocarditis. The conservative approach would have been to treat with a beta-blocker and angiotensin-converting enzyme inhibitor, hold out of sports for at least 3 to 6 months, perhaps implant an implantable loop recorder so that a specific diagnosis could be made if another episode of syncope occurred, and then repeat the MRI looking for resolution of delayed enhancement. Pressure to play (athlete, coach, and parent) can influence medical decision making and steer the decision away from the athlete’s best interest.
A 23-year-old male second-year medical student completed a maximal-effort Wingate test as part of a research project; prior V˙O2max testing demonstrated a maximum of 55 mL·kg−1·min−1. Immediately after the 30-s test, the student was extremely nauseous and rapidly exited the bike to move to a trash can to vomit; after two short wobbly steps, he collapsed to the ground. He was attended to immediately by the exercise staff in attendance; he had an estimated loss of consciousness for less than 30 s and had a first set of vital signs of heart rate of 140 bpm and BP of 110/60. There was no observed seizure activity and no prior complaint of chest pain. A subsequent evaluation in the sports medicine clinic demonstrated normal clinical examination results with no history of syncope; ECG results demonstrated early repolarization variation in the precordial leads. As the syncopal event occurred immediately after exercise, a treadmill stress test and echocardiogram were performed; the student completed 17 min of Bruce protocol and had a normal echocardiogram results. The diagnosis was postexertional syncope secondary to orthostatic hypotension.
Key Point: Syncope during or immediately after exercise is always concerning and warrants conscientious examination to rule out structural cardiovascular disease. Intense anaerobic exercise, which can be seen in maximal efforts like the Wingate test or weightlifting, can precipitate syncope through orthostatic hypotension and a central effect of hypocapnia leading to, or aggravating, cerebral hypoperfusion. The history of the event provides not only insight into the diagnosis but also important opportunities for prudent recommendations for prevention.