Exercised-Induced Vasovagal Syncope: Limiting the Risks
David Wang, MD, MS; Scott Sakaguchi, MD; Marcella Babcock, MA, AT,C/RTHE PHYSICIAN AND SPORTSMEDICINE - VOL 25 - NO. 5 - MAY 97
In Brief: Syncopal episodes in an athlete require a thorough evaluation because some of the possible causes are life-threatening. Two case studies demonstrate the diagnostic work-up, which typically involves electrocardiography, echocardiography, and exercise testing. Tilt-table testing can be used to confirm a diagnosis of vasovagal syncope, but only after structural heart disease has been ruled out. Treatment of vasovagal syncope includes avoiding dehydration and using one or a combination of medications shown to be useful for this condition. Care must be exercised in choosing medications; some are prohibited in organized athletics, and some can hurt performance.
An athlete fainting during play or on the sidelines creates a dramatic scene. Though vasovagal syncope is a common cause, it's important to rule out life-threatening conditions and to control fainting symptoms for the safety of the patient and other athletes. Two cases demonstrate the presentation and evaluation of vasovagal syncope and provide a springboard for discussing the special issues physicians will encounter as they manage active patients who have syncope.
A 20-year-old female collegiate volleyball player presented after experiencing syncopal episodes. On the first and second days of practice, the athlete had dizziness after 1 hour of exercise; it resolved with rest. During warm-up on the fourth day of practice, the athlete fainted without experiencing a prodrome; after the 15-second episode, her blood pressure was 116/74 mm Hg and her pulse was 60 per minute.
The patient had a history of a restrictive eating disorder and depression. She had had three syncopal episodes that were attributed by her physicians to poor nutrition and excessive workouts. Her eating disorder had been successfully treated with counseling, and her depression was controlled with fluoxetine hydrochloride and counseling. Her preparticipation exam had been normal.
Her evaluation revealed normal electrolytes, blood glucose, echocardiogram, and resting electrocardiogram (ECG). An exercise treadmill test using the Bruce protocol was limited because of symptoms of light-headedness at 92% of her predicted maximum heart rate. A head-up tilt-table test was performed. After 8 minutes at an 80° tilt the athlete developed nausea, diaphoresis, and diminished consciousness accompanied by hypotension and bradycardia. The test was repeated after metoprolol tartrate was given intravenously; the patient's symptoms were delayed to 12 minutes and diminished in severity.
Findings on the initial tilt-table test suggested a vasovagal cause for her syncope. Since an intravenous beta-blocker delayed the symptoms, treatment was initiated with oral pindolol, and she continued on fluoxetine. After 2 weeks, the patient was asymptomatic during a follow-up 45-minute tilt-table test. During the test her blood pressure transiently fell to 76/48 mm Hg at 42 minutes but returned to 101/47 mm Hg before the table was brought down.
Though the beta-blocker seemed to decrease and delay her symptoms, she continued to have prodromal symptoms with hard workouts. Despite the addition of disopyramide phosphate, she suffered another event without a prodrome when she returned to practice. Because of the fear of more events, especially without prodromes, the patient retired from competitive volleyball.
At her 6-month follow-up visit, the patient had stopped all medications but was having presyncopal episodes during her activities of daily living. She began therapy with midodrine hydrochloride and was asymptomatic while returning to volleyball at the club level.
A 22-year-old collegiate female rower presented after experiencing syncopal episodes for 8 months. These episodes of fainting or light-headedness occurred about two to three times per month, usually after workouts, but sometimes while at rest.
The patient's ECG and echocardiogram were normal except for mild left ventricular enlargement. On a treadmill test using the Bruce protocol she achieved 101% of her predicted maximum heart rate. Fifteen minutes into the test her systolic blood pressure reached 180 mm Hg. She suddenly became presyncopal, and her systolic blood pressure was found to be 80 mm Hg while at peak exercise. There was no change in her cardiac rhythm. During tilt-table testing at 80°, the patient developed frank syncope with a blood pressure of 52/19 mm Hg and relative bradycardia (60 beats per minute) at 6 minutes. A repeat test after administration of metoprolol was also positive after 10 minutes.
The athlete was initially treated with disopyramide. After experiencing numbness of the mouth, fatigue, and light-headedness, she was switched to pindolol. Though she denied presyncopal symptoms while on this medication, she had motion sickness, balance problems, and tunnel vision when she stood up. Her medication was changed to metoprolol, and she improved clinically but had difficulty with fatigue and concentration. For these reasons the patient was switched to sertraline hydrochloride. On sertraline the patient continued to have syncopal episodes, though they were less frequent. She never returned to competitive rowing.
At 18-month follow-up, she was taking sertraline and midodrine. She had had no further syncope, but continued to have symptoms of presyncope.
The Syncope Spectrum
Syncope is defined as the sudden loss of postural tone and consciousness with subsequent spontaneous recovery. It frequently occurs because of a transient decrease in blood flow to the brain, usually for more than 8 to 10 seconds (1).
Fainting is fairly common inside and outside the athletic arena, occurring in 3% of the general population and accounting for 3% of emergency department visits (2,3). The causes of syncope are numerous, but can be categorized as cardiac or noncardiac (table 1: not shown). Cardiac syncope includes mechanical (eg, valvular obstruction), electrical (eg, arrhythmias), neurally mediated (vasovagal), and orthostatic causes. Noncardiac syncope is much less common and includes metabolic (eg, hypoglycemia), neurologic (eg, seizure), and psychiatric causes (4).
Serious causes of syncope that can result in death include atherosclerotic coronary artery disease, hypertrophic cardiomyopathy, coronary artery anomalies, aortic aneurysms, aortic stenosis, dilated cardiomyopathy, myocarditis, and arrhythmias, among other less common causes. The less serious causes of syncope in athletics are more common and include medications, drug use, hypovolemia, and vasovagal mechanisms. Symptoms of the above can all be amplified in athletes who have eating disorders or are "cutting weight."
Vasovagal or neurocardiogenic syncope may be the most common type of syncope in athletes (5). Vasovagal reactions are reasonably well accepted as a cause of postexercise syncope. These reactions may occur with or without a prodrome. It is more controversial whether vasovagal syncope can occur during exercise. Our second patient clearly demonstrated a hypotensive response during her exercise test without associated arrhythmia. Another similar case was recently reported (6).
Vasovagal reactions consist of varying degrees of bradycardia (a cardioinhibitory response) and vasodilation (a vasodepressor response). These reactions can range from pro-dromal vagal symptoms such as nausea, pallor, diaphoresis, and/or blurred vision, to presyncope or outright syncope.
Many trigger types may initiate neurally mediated syncope, including venipuncture, coughing, urination, and defecation. Vigorous contractions of the ventricle in response to prolonged standing and dehydration are believed to initiate a vasovagal reaction by activating cardiovascular mechanoreceptors that form the afferent limb of the vasovagal reflex. Exercise-induced increases in the strength of ventricular contractions may directly stimulate these afferent cardiovascular mechanoreceptors (4). Increased epinephrine levels have been seen prior to syncopal episodes and contribute to these vigorous cardiac contractions (7,8). In addition, the decreased venous return caused by relative dehydration during prolonged exercise may also stimulate the ventricle.
These afferent inputs are thought to initiate a reflex in the medulla that produces the efferent response. Bradycardia seen in neurally mediated syncope is controlled by parasympathetic output from the vagus nerve (4). The enhanced vagal tone seen in endurance athletes may further sensitize the efferent limb to this neurocardiac reflex (9). One must note that noncardiac triggers exist, as is demonstrated by the "emotional" faint (10).
The vasodilatation that produces hypotension in neurally mediated syncope is less well understood than the previously described bradycardia. While bradycardia contributes to hypotension, vasodilatation has been documented to precede bradycardia in many, if not most, cases of vasovagal syncope (5). The mechanism for the vasodilatation may be withdrawal of the alpha-agonist activity in the postexercise period or peripheral beta2-agonist activity secondary to catecholamines (11). The lower heart rate and blood pressure ultimately lead to a worsening cerebral hypoperfusion and subsequent hypoxia. It is interesting that transient Doppler imaging shows paradoxical cerebrovascular arterial vasoconstriction with vasovagal reactions that could also contribute to brain ischemia (12).
Diagnostic Test Selection
Syncopal episodes related to physical exertion should be evaluated thoroughly because syncope may be the presenting symptom of a serious cardiac disease that may lead to sudden death. Syncope preceded the deaths of basketball stars Hank Gathers and Reggie Lewis. The syncope evaluation involves a thorough history and physical exam. Because the majority of cases have cardiac causes, a 12-lead ECG and echocardiogram are usually suggested. If these tests show evidence of structural heart disease, more invasive studies such as cardiac catheterization, coronary angiography, myocardial biopsy, and/or electrophysiologic studies should be considered, depending on the initial evaluation. Exercise testing may reveal cardiac arrhythmias or ischemia, both of which require aggressive evaluation. In the absence of structural heart disease, tilt-table testing may identify neurally mediated hypotension and bradycardia as the etiology for exercise-associated syncope.
As was demonstrated in the cases here, tilt-table testing can be useful in diagnosing vasovagal syncope. Head-up tilt-table testing has been found to be effective in reproducing syncope in those who are predisposed to vasovagal reactions. The sensitivity of the test may be increased by contaminant provocation with isoproterenol hydrochloride infusion (13,14). In one study (13), 24 young athletes with unexplained syncope were evaluated using tilt-table testing. Ten (41%) had a positive test at baseline, and nine (37%) had a positive test with isoproterenol, while none of 10 syncope-free controls had syncope with testing.
The results of tilt-table testing in athletes must be interpreted with caution because false-positive tests may be relatively common in this population. Endurance athletes appear to have less orthostatic tolerance, perhaps because increased total blood volume may attenuate mechanoreceptor responsiveness (15-17). Currently we (DW, SS) are looking at the incidence of false-positive tilt-table tests in asymptomatic elite athletes. This test should be used only when the patient history suggests a neurally mediated syncope and structural heart disease has been ruled out. It should not be used as a screening test.
Tilt-table protocols vary but usually follow a similar pattern. The patient lies supine on a comfortable flat table with secure straps across the chest and legs. The patient is then given sufficient intravenous fluids to avoid immediate orthostatic changes in heart rate and blood pressure. After an equilibrium period the subject is tilted head up to an angle of 60° to 80° over 10 to 20 seconds. The patient remains tilted until syncope, extreme presyncope, or a preset length of time has elapsed. The heart rate is measured continuously by ECG. Blood pressure may be monitored with an arterial catheter, a blood pressure cuff, or other noninvasive blood pressure monitor. A standard protocol has recently been published (18).
Though vasovagal reactions themselves are not fatal, treatment involving medication and adequate hydration is imperative because resulting falls can be harmful. Syncopal episodes in swimming and downhill skiing that resulted in serious harm have been seen in our institution.
Beta-blockers are commonly used to treat vasovagal syncope. Though it seems paradoxical to select a negatively chronotropic medication to treat bradycardia, the negative inotropic effects may decrease the afferent signals from the mechanoreceptors to the brain stem, thereby suppressing the efferent arm of the reflex (19).
Disopyramide has been used successfully in the treatment of neurally mediated syncope (9,20). This type 1 antiarrhythmic has profound negative inotropic effects and anticholinergic properties. The negative inotropic effects may decrease afferent mechanoreceptor activity, while the anticholinergic effects may decrease vagal (efferent) output.
The selective serotonin reuptake inhibitors (SSRIs) have also been used with success in patients who have vasovagal syncope, though the mechanism of action is speculative. A study(21) has shown that intracerebroventricular serotonin induces hypotension, inhibits renal sympathetics, and excites adrenal sympathetics. SSRIs may blunt the response to shifts in serotonin levels (22).
Fludrocortisone acetete, which has volume-expanding properties, has been used with some success. Midodrine, which received US Food and Drug Administration approval in September 1996 for the treatment of orthostatic hypotension, has peripheral alpha-adrenergic effects and has shown promise in treating vasovagal reactions (23).
Compared to nonathletes, athletes require greater care in choosing medications. Depending on the individual and the activity involved, medication may either blunt performance and be deemed intolerable, or enhance performance and be banned by sports governing bodies, as described here and outlined in table 2:
The cases presented here demonstrate typical examples of vasovagal syncope, possibly the most common cause of syncope in athletes. Vasovagal reactions do not appear to be life-threatening but certainly are a cause of great concern to athletes and their families and friends. In many cases, the condition can occur suddenly and without warning. The falls incurred from such vasovagal events can be very dangerous, making avoidance of causative exercise prudent, but not necessarily imperative.
As was demonstrated by both of the case studies, syncope can be very difficult to treat, and patients are not always able to return to their sports. However, the advent of new medications such as midodrine seems to improve the chance that affected athletes can return to their sport (27).
Dr Wang is director of general medicine and sports medicine clinics at Boynton Health Service and team physician at the University of Minnesota in Minneapolis. He is on the clinical faculty in the Department of Family Practice at the University of Minnesota Medical School and an editorial board member of The Physician and Sportsmedicine. Dr Sakaguchi is assistant professor in the Department of Internal Medicine, division of cardiology, at the University of Minnesota. Ms Babcock is the athletic medicine manager and marketing director with Two Rivers Center, Inc, Coon Rapids, Minnesota. Address correspondence to David Wang, MD, MS, Boynton Health Service, University of Minnesota, 410 Church St SE, Minneapolis, MN 55455; send e-mail to [email protected].
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