Exertional Syncope and Presyncope
Faint Signs of Underlying Problems
Kevin J. McAward, MD; James M. Moriarity, MD
Practice Essentials Series Editors:
THE PHYSICIAN AND SPORTSMEDICINE - VOL 33 - NO. 11 - NOVEMBER 2021
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In Brief: Physicians often see patients who have syncope or presyncope, but episodes associated with exercise are uncommon. Transient syncopal episodes usually require minimal evaluation and intervention. Most cases of exercise-associated syncope have neurocardiogenic origins and are benign, but fainting may signal a potentially fatal underlying problem. More serious causes of exertional syncope include structural cardiovascular abnormalities and cardiac arrhythmias. All physicians who care for active patients should be aware of the potential seriousness of this early warning sign and evaluate patients accordingly. Familiarity with the Bethesda guidelines will help clinicians decide when it is safe for an athlete to return to play following a syncopal episode.
Fainting is a universal phenomenon that is common to all cultures. Its occurrence has given inspiration to romantic and gothic authors, furniture makers (the fainting couch), psychologists (weakened temperament), metaphors (swoon with joy), sexists (the weaker sex), physicians (syncope and dropsy), and childhood pranks (eg, Valsalva's maneuver, breath holding, chest squeeze to induce fainting episode).
Syncope, as defined by the medical literature, is a sudden transient loss of consciousness and postural tone caused by cerebral hypoperfusion from which recovery is spontaneous without chemical or electroconversion resuscitation.1-3 Near syncope or presyncope is the sensation of eminent fainting.
Over a period of 26 years, the Framingham study for syncope4 evaluated 2,336 men and 2,873 women who were ages 30 to 62 years at enrollment. At least one syncopal episode was reported by 71 men (3.0%) and 101 women (3.5%) during the study. Evidence of cardiac or neurologic morbidity and mortality was also recorded. Syncope was not associated with stroke (including transient ischemic attack), myocardial infarction, or sudden death. In 40% of cases, the exact cause of syncope remained undiagnosed, and 30% of patients who experienced syncope had recurrent episodes. Despite its primarily benign outcome, up to 3% of all visits to emergency departments and up to 6% of all hospital admissions are for syncopal episodes.5
Syncope associated with exercise is far less common. Colivicchi et al6 studied a cohort of 7,568 young athletes (5,132 males, 2,436 females, age 16.2 [+2.4 years]). Syncopal episodes were reported by 474 athletes. No relationship to exercise was found in 411 athletes (86.7%), postexertional syncope occurred in 57 (12.0%), and exertional syncope in 6 (1.3%). Of the 6 athletes with exertional syncope, 1 had hypertrophic cardiomyopathy, 1 had right ventricular outflow tract tachycardia, and 4 demonstrated a positive response to tilt table testing.6
Corrado et al7 prospectively studied 33,000 Italian athletes from 1979 to 1996 and identified 49 cases of sudden death. Forty of these deaths occurred during or immediately after exercise. Seven of the 40 athletes experienced syncopal episodes prior to death.
In a study of sudden death8 in 6.3 million US military recruits from 1977 through 2021, 126 nontraumatic sudden deaths were reported, 108 were related to exercise, and 64 of these demonstrated cardiovascular disease when autopsied. Coronary artery anomalies were present in 21 individuals, myocarditis in 13, atherosclerotic coronary artery disease in 10, and hypertrophic cardiomyopathy in 8. Forty-four of the 126 deaths (35%) remained unexplained. Syncope was reported as a prodromal symptom in 6 recruits who had coronary artery pathology and in 2 who had myocardial pathology.
Causes of Exertional Syncope
In their review of exertional syncope in athletes, O'Connor et al1 cite cerebral or metabolic factors and arterial perfusion abnormalities as the principal causes of syncope. Cerebral or metabolic causes of syncope and presyncope include seizure disorder, hypoglycemia, hyponatremia, hyperthermia, and hypoxia. Most of the metabolic causes of syncope can be diagnosed by history and rapid lab testing.
Seizure disorder is more difficult to diagnose, because clinical manifestations vary and tonic/clonic muscle activity often accompanies transient cerebral hypoperfusion and metabolic abnormalities. In a study9 of 77 nonfatal cases of exercise-related hyponatremia, 28% had seizures and 43% were disoriented. Aura is typical of seizure activity, as is disorientation after the event. Slow return to consciousness, unconsciousness lasting more than 5 minutes, or disorientation immediately after the event are also associated with syncope-related seizure activity.10
Critical decreases in cerebral arterial perfusion result in brain tissue anoxia and the familiar symptoms of syncope and presyncope. The symptoms of presyncope include nausea, vomiting, lightheadedness, visual or auditory change, headache, paresthesia, yawning, fatigue, and a sense of depersonalization. Progression to loss of consciousness initiates a diagnosis of syncope. Attention to these symptoms in the patient's history—not just at the time of exertion—can prove valuable in diagnosis. For example, a runner who experiences presyncope during a race may have previously had the same symptoms during micturition. This provides a clue to a benign cause of syncope similar to micturition syncope.
The major causes of syncope can be divided into three major groups: neurocardiogenic, arrhythmic, and structural. Each has different characteristics, and the management can differ greatly.
Fainting caused by permutations in homeostatic maintenance of arterial blood pressure and systemic vascular resistance is called neurocardiogenic syncope. Systemic peripheral resistance and blood pressure control are mediated through stretch mechanoreceptors in the heart and great vessels and integrated in the vasomotor center of the medulla (table 1).11 The term "neurocardiogenic syncope" embraces a wide variety of proposed pathophysiologic conditions, including vasovagal syncope, vasodepressor syncope, cardioinhibitory syncope (Bezold-Jarisch reflex), carotid artery reflex syncope, situational syncope, and baroreceptor dysfunction. There is no agreement on the teleologic benefit of vasovagal syncope and no certain agreement on its cause.10
|All of these conditions share the final pathway of withdrawal of sympathetic tone and fall in systemic vascular resistance (SVR). They differ in the origin of the afferent stimulus that triggers the response. Exercise and the postexercise state are unique situations in the discussion of neurocardiogenic syncope, because the physiologic parameters of stroke volume, heart rate, and SVR are different during exercise and rest. Accordingly, tilt table testing, which provides information on the causes of syncope at rest, may not be as applicable to exertional syncope. The complexity of arterial blood pressure control during exercise and the many factors that influence SVR make a single cause of exercise-related syncope unlikely, and a broad-based definition of neurocardiogenic syncope is necessary.
A brief review of arterial blood pressure control and systemic vascular resistance during exercise and rest will help in understanding the possible causes of exercise-related syncope. At rest, 80% of total blood volume is in systemic circulation (extrathoracic), of which about 75% is in the veins and 25% is in the arteries. The remaining 20% of total blood volume is in central circulation (intrathoracic) in the heart, lungs, and intrathoracic veins. Central blood volume can be changed by an increase or loss of total blood volume or by redistribution of systemic blood volume to central blood volume. Shifts of extrathoracic blood to intrathoracic spaces from active venoconstriction of splenic and splanchnic beds, increases in muscle pump activity, and respiratory siphoning caused by deeper respiration can double central blood volume.
Arterial blood pressure is regulated by the autonomic nervous system and its two branches, the parasympathetic and sympathetic chains. Afferent neural signals that are sensitive to stretch emanate from high-pressure baroreceptors (ie, the carotid sinus and aortic arch) and low-pressure cardioreceptors in the atria, ventricles, and pulmonary vessels and terminate in the nucleii tractus solitarii of the medulla oblongata. The nucleii tractus solitarii connects with nearby sympathetic efferent neurons in the rostral ventrolateral nucleus and parasympathetic efferents in the nucleus ambiguus. Together, these areas constitute the vasomotor center of the medulla. Increased stretch in the baroreceptors from increases in systemic blood pressure reduces the sympathetic outflow to the arteries and increases parasympathetic outflow to cardiac conduction tracts. Increased stretch in the cardioreceptors from increases in filling volume inhibits sympathetic outflow and increases parasympathetic activity to cardiac conduction. Unloading the cardioreceptors enhances high-pressure baroreceptor activity, decreases parasympathetic activity, and increases sympathetic outflow signals to the heart and systemic vasculature.
The vasomotor center also receives afferent signaling from supramedullary centers in the amygdala, limbic cortex, and hypothalamus that may override input from baroreceptors. Conscious stimuli such as fright, noxious smells, distressing sights, emotional distress, or rage may invoke different sympathetic and parasympathetic responses in individuals. The common vasovagal faint experienced during these circumstances may be caused by supramedullary afferent stimulation of the nucleus ambiguus parasympathetic fibers and inhibition of the rostral ventrolateral nucleus sympathetic fibers.
Exercise is known to influence the activity of the vasomotor center via afferent input from supramedullary centers. For exercise to progress, vascular resistance must be reduced in exercising skeletal muscle to facilitate increased oxygen delivery. Simultaneously, vascular resistance must increase in nonexercising skeletal muscle to reduce blood flow and preserve cardiac output. In addition, exercise produces higher systemic arterial pressure, which under normal circumstances would be ameliorated by active baroreceptor and cardioreceptor responses. Supramedullary input from higher brain structures has an active role in resetting baroreceptor threshold sensitivity and activity and in selectively regulating SVR in skeletal muscle, thus permitting exercise to progress.
Other influences on circulatory control and SVR include reflex arc inhibition at the local muscle and organ level and hypothalamic-stimulated thermoregulatory input to the vasomotor center. Superficial pain stimulation often invokes a sympathetic response with increased heart rate and SVR. In contrast, deep muscle pain, joint dislocation, testicular injury, and organ distention provoke a parasympathetic response, decrease heart rate and SVR, and produce shock-like symptoms. Heat stress and rising core body temperatures activate hypothalamic thermoregulatory centers that elicit vasodilatory, sympathetic neuromediated increases in dermal blood flow that can reach 5 to 7 L/min of available cardiac output and contribute to loss of central blood volume.
Tilt table testing and the application of lower body negative pressure (LBNP) provide greater understanding of the possible mechanisms involved in syncope during exercise. Thomson et al12 investigated cardioreceptor activity in 30 patients who had recurrent syncope and tilt tests indicating abnormal vasovagal and vasodepressor responses. Using LBNP devices to retard venous return, forearm blood flow was monitored to measure vascular resistance and assess low-pressure cardioreceptor activity. Declining venous return would be expected to decrease cardioreceptor stretch and increase reflex sympathetic tone to SVR, resulting in a decrease of forearm blood flow. In the control subjects, significant decreases in forearm blood flow indicated increased SVR. In the test subjects, forearm resistance did not change or actually decreased. Central venous pressure declines were identical in both groups. The results suggest that cardioreceptor activity in test subjects fails to decline, or, in some cases, is actually stimulated, thus failing to initiate increases in vascular resistance.
In a follow-up study, Thomson et al13 studied the effects of LBNP on venous tone at rest and decreases in splenic volume during exercise. The test group consisted of 25 patients who had known vasovagal syncope, including five who had experienced syncope or near syncope during exercise. Application of LBNP reduced forearm venous volume in control subjects and in all but one test subject, indicating active venoconstriction in response to reductions in venous return. However, when both groups exercised on a stationary bicycle with increases of 25 W every 4 minutes until exhaustion or symptoms developed, test subjects demonstrated no change or increased splenic volume with concordant falls in right atrial pressure. The control subjects demonstrated decreases in splenic volume and no change or increases in right atrial pressure. Two of the five test subjects who reported presyncope or syncope during exercise developed symptoms during the test.
Combined, these two studies suggest that cardioreceptor activity is abnormal in patients with histories of syncope at rest and during exercise. The mechanism involved is failure to elicit increases in sympathetic arterial resistance and increases in splanchnic and splenic venous tone in response to postural or exercise-induced changes in venous return to central circulation. Such patients would be especially at risk for syncope postexercise and during prolonged exercise in hot, humid conditions.
In patients who experience vasovagal syncope with classic presyncopal symptoms of lightheadedness, sweating, and sudden loss of postural tone, tilt table testing has shown abnormal vagal and sympathetic baroreflex activity. With initial onset of tilt, control and tilt-positive patients show increases in blood pressure, pulse, and SVR. As tilt time progresses, arterial pressure declines in tilt-positive patients, followed by drops in SVR and diastolic pressure. Declining heart rate is a relatively later occurrence and ushers in presyncopal symptoms. Frank syncope is initiated by complete withdrawal of sympathetic tone and asystolic pauses. Horizontal positioning restores sympathetic activity, SVR, and heart rate.
Interestingly, syncope is not prevented by prophylactic pacemaker activation, indicating that sympathetic withdrawal and not an overly active para- sympathetic effect on heart rate is the culprit in vasovagal syncope.14 LBNP application has also been used to detect abnormalities in baroreflex sensitivity in patients who have documented histories of syncope.
Using microneurography in peroneal nerves with LBNP, Bechir et al15 published data showing increased sympathetic tone at rest and blunted efferent sympathetic response for induction of increases in SVR. Additional analysis of R-R intervals and pressure correlates used to measure efferent sympathetic activity to cardiac conduction tissue also demonstrated blunted sympathetic outflow in response to LBNP. The conclusion was that patients who have syncope seem to depend more on muscle sympathetic activity to maintain cardiac preload and arterial pressure at rest, and they are less able to increase sympathetic vasoconstrictor outflow in response to orthostasis. Bechir et al used the term "dysfunctional baroreflex activity" to reflect a possible lack of afferent stimuli from the mechanoreceptors and/or baroreceptors, or a dysfunction of the efferent limb to the vascular bed and heart.
Cardioinhibitory reflexes (Bezold-Jarisch) have been implicated as the cause of exercise-induced syncope. Mechanoreceptors in the ventricles (activated by stretch and increased ionotropic force) elicit reflex withdrawal of sympathetic vascular tone and initiate parasympathetic activity to cardiac conduction sites. It has been proposed that, with declining venous return and decreased end diastolic filling pressure, the heart forcibly contracts against an "empty chamber," thus eliciting the cardioinhibitory reflex.16 The latter mechanism may account for the appearance of vasovagal syncope in orthostatic stresses. It remains unclear if this relationship truly exists. Patients who have had cardiac transplants have classic vasovagal syncope even though they have denervated hearts.17,18 Additionally, studies using echocardiography also fail to demonstrate either an empty ventricle or a more vigorous contraction as measured by end-systolic length or fractional systolic shortening during syncopal episodes.19,20 Therefore, vasovagal syncope is not synonymous with the Bezold-Jarisch reflex, nor is cardioinhibitory receptor activation always present in syncopal episodes.
In summary, exercise-related syncope that is not caused by structural or arrythmogenic abnormalities is most likely to be neurocardiogenic in origin. It is likely to recur and has no long-term adverse results. The mechanism of syncope may be related to alterations in afferent cardioreceptor sensitivity and diminished efferent baroreceptor response that, combined, contribute to reduced venous return during exercise and a diminished ability to increase systemic vascular resistance. It is possible that the abrupt withdrawal of SVR elicits a cardioinhibitory reflex that accounts for the profound bradycardia and asystolic pauses that follow, but it is unlikely that cardioinhibitory activity is the sentinel occurrence in syncope. The fact that most athletes do not have exercise-induced syncope raises the question of why some do. Clearly, tilt table testing and LBNP studies are selectively abnormal in patients who have syncope with and without exercise, but they add data to clinical decision making.
When an individual begins a bout of exercise, multiple adaptive mechanisms combat the cardiovascular stress. The adrenal glands secrete epinephrine to increase the depolarization rate of the sino-atrial node, which precipitates a tachycardia that helps maintain cardiac output. Cardiac cycle times decrease as well, including the QT interval. In contrast to the cardiac performance enhancement, high sympathetic state can generate a pathologic arrhythmia by direct effect on conduction pathways, ischemia induction, and alteration in sodium-potassium movement across cell membranes. Arrhythmias may also occur in active patients who have acute rupture of atherosclerotic plaques in response to exercise.
In athletes older than 35 and in a significant number of individuals younger than 35, coronary artery disease caused by atherosclerosis is the most common cause of sudden death during exercise.21 Coronary artery disease can induce short-term or prolonged arrhythmias, such as ventricular tachycardia.
Arrhythmogenic right ventricular dysplasia is the most common cause of sudden death in athletes in some parts of the world; however, it seems to be uncommon in the United States.7,22,23 In this disease, myocardial tissue is replaced with fibrofatty tissue that disrupts the normal conducting system of the heart. The stress of exercise may lead to ventricular tachycardia.
Long QT syndrome is a congenital or acquired condition in which the QT segment lengthens after correction for heart rate (figure 1). Many different medications, both prescription and nonprescription, can lead to its development. Each of the seven subtypes of congenital long QT syndrome has characteristic mutations and histories. Of the seven, three are much more prevalent: LQT1, LQT2, and LQT3. LQT1 is most associated with morbidity triggered by exercise, although LQT3 does have an unusual predilection to occur with swimming. Long QT syndrome may lead to torsades de pointes, a life-threatening arrhythmia that may be self-limited or may progress to ventricular fibrillation. Individuals who are predisposed to this arrhythmia have a high likelihood of developing problems with significant exertion.
Polymorphic ventricular tachycardia with normal QT interval is another possible arrhythmic cause of syncope. The incidence of this disorder is unknown, but it may be the cause of 1 in 7 sudden unexplained deaths.24 The disorder tends to be familial, although sporadic cases can occur.
Brugada syndrome is a very uncommon arrhythmic cause of syncope and presyncope in the West but is more common in young Southeast Asian men. This syndrome involves a mutation on the same gene as LQT3. The transport of sodium ions into the cells is affected, but the structure of the heart is not abnormal.
Wolff-Parkinson-White syndrome is an idiopathic or hereditary condition that is characterized by ventricular pre-excitation. Rarely, it progresses to ventricular fibrillation, but it does not usually increase the risk of sudden death. Wolff-Parkinson-White syndrome has been correlated to an increased risk of syncope and presyncope.
Any of these arrhythmias may lead to a syncopal event when exercising. Unfortunately, the warning signs are few, and the result can be serious. Any history of syncope or presyncope with exercise warrants an investigation to exclude these potential causes of arrhythmia.
Abnormal cardiac structure may not affect function at rest, but with exercise, cardiac output and arterial pressure may be markedly compromised. About 2% to 50% of young individuals who experienced sudden death have abnormal cardiac structure at autopsy.21,23,25 Syncope is a common prodromal symptom of structural heart disease and should be regarded as a sentinel warning sign.
As with cardiac rhythm, exercise modulates cardiac structure. With increased sympathetic activity affecting the heart during exercise, myocardial structure becomes more dynamic with increases in cardiac wall motion and inotropic activity. Cardiomyopathies, fatty infiltration, and scarring from previous bouts of myocarditis or infarction may impair normal myocardial response to exercise.
Arterial anomalies. In the study of sudden death in military recruits by Eckart et al,8 autopsies revealed that the most common coronary artery anomaly found was the left coronary artery arising from the right sinus of Valsalva with a course between the pulmonary artery and aorta. Dynamic cardiac contraction is thought to "pinch off" coronary artery circulation, thus myocardial tissue becomes hypoxic. Anomalous coronary artery is present in 0.3% to 0.8% of the population.26-31
Hypertrophic cardiomyopathy. The most publicized of cardiac abnormalities, hypertrophic cardiomyopathy (HCM), occurs in 1 in 500 people in the general population.27 This genetic condition is the most common cause of sudden death in young athletes, and it should be considered when a first-time exercise-associated syncopal event occurs in an adolescent.26 The abnormal structure of the left ventricle in HCM can lead to lethal arrhythmias, myocardial bridging (ie, compressed tunneled coronary arteries), and ischemia that could result in infarction.27,28 The hypertrophic septum also raises ventricular diastolic pressure with prolongation of ventricular relaxation and an overall decrease in cardiac output.32 Outflow obstruction from an enlarged ventricular septum is worsened with decreased diastolic filling and contracted ventricular cavity dimension. With changes in contractility and cardiac pressures during exercise, symptoms such as presyncope and syncope may develop.
Valve abnormalities. Congenital or acquired structural defects in coronary valves, especially aortic stenosis, can precipitate syncope. In aortic stenosis, outflow obstruction from a noncompliant valve limits cardiac output in response to exercise demand. Increased ventricular pressure may stimulate ventricular stretch receptors and initiate reflex reductions in SVR, thus resulting in a vasodepressor syncopal response.30
Mitral valve prolapse (MVP) can precipitate exertional syncope through multiple mechanisms. Some patients will develop significant mitral regurgitation during exercise, thus increasing their risk of cardiovascular morbidity.31 MVP also seems to precipitate multiple types of arrhythmia leading to syncope. Studies have shown an increased risk of sudden death when MVP is combined with a history of syncope, especially if associated with mitral valve regurgitation.33-35
When an athlete collapses, the ABCs of basic life support (airway, breathing, and circulation) should be immediately assessed. The patient should be moved from any dangerous situation to an appropriate area for triage. Initial resuscitation and evaluation should be done in a head-down, legs-up position. Intravenous fluids should not be administered in most instances, because fluid has not been proven helpful and could actually be harmful if given to a fluid-overloaded patient. If the patient remains unconscious or requires cardiorespiratory support, emergency services should be notified urgently. If the patient regains full consciousness in less than 5 minutes, emergency services are not necessary. Evaluation of the cause can be completed after the patient has stabilized.
Most syncopal episodes have a benign origin. True syncope, by definition, does not require emergency life support procedures. If intervention is necessary, a structural or arrhythmic cause can be suspected and a thorough workup initiated.
Timing is extremely important. The history surrounding the event should be carefully evaluated before considering the possible causes. Syncope that occurs immediately after exertion, such as the end of a cross-country race, is most commonly neurocardiogenic syncope. When syncope occurs during exertion, serious concern should be raised for structural and arrhythmic causes.
Age is the second important factor in the diagnosis of exertional syncope. The incidence of atherosclerotic heart disease increases with age and is the most common cause of sudden death in athletes older than 35. Primary consideration of atherosclerosis in older athletes who have exertional presyncope or syncope is paramount.
History. Past syncopal episodes, especially after exertion or after a distressing stimulus, are consistent with neurocardiogenic syncope. Patients should be asked to recall any precipitating events, such as startling noises, full-bladder sensation, colonic cramping, bee sting, or a disturbing visual image such as blood or another person vomiting. If the faint was witnessed, it is important to identify any associated clues to the cause, such as seizure activity or emesis.
At a preparticipation examination, when evaluating an athlete who has a history of syncope, it is vital to get the history from the parent or guardian as well as the athlete. A recent study36 showed that the histories can vary greatly. Medical history, current prescriptions, and over-the-counter medications may provide clues to underlying chronic pathology or other cause in the development of syncope. A family history of sudden death, early cardiac disease, or long QT syndrome should be ascertained. Illicit or performance-enhancing substances, such as cocaine and ephedra, can predispose patients to cardiac disease as well as associated symptoms of chest pain, palpitations, and dyspnea that demand investigation for structural heart problems.
Physical exam. Physical findings often provide some clues to the underlying cause of the collapse. Observation of an obtunded patient may suggest a postictal state or other underlying neurologic or metabolic process. Patients with a cyanotic appearance are most likely experiencing a cardiac or respiratory event. The patient with neurocardiogenic syncope is usually alert and oriented within a few moments of the episode if placed in a head-down, legs-up position. Audible wheezing may be noted. Body habitus, such as a marfanoid stature, may suggest an underlying structural cardiac or aortic abnormality and may also provide information toward a cause. Clubbing may be a sign of pulmonary disorder. Generalized edema or poor skin turgor may be signs of electrolyte disturbance or dehydration. Also, external clues, such as ID bracelets and insulin pumps, may be excellent pointers to the underlying cause.
Vital signs, including body temperature, should be taken with attention to hypotension, bradycardia, tachycardia, and hyperthermia. Orthostatic blood pressures after at least 3 to 5 minutes of standing provide valuable information regarding central blood volume status. Pulse irregularity should be noted. Cardiac examination for changes in heart sounds, murmurs, thrills, and rubs should be performed. Dynamic cardiac auscultation (ie, supine, seated, and standing) may help identify hypertrophic cardiomyopathy. The decrease in venous return with standing or Valsalva's maneuver intensifies the murmur associated with this obstructive malformation.
Any athlete who experiences first-time presyncope or syncope related to exertion should have an electrocardiogram (ECG) before being cleared to return to sport. Conditions such as HCM, prolonged QT interval, heart block, and pre-excitation syndromes such as Wolff-Parkinson-White may have characteristic findings indicating an arrythmogenic or structural cause of the event. If the ECG is normal and the history and examination highly suggest neurocardiogenic syncope, no further testing is needed.37,38 The ECG of a well-trained athlete may have some acceptable abnormal findings, including sinus bradycardia, first- or second-degree AV block, increased voltage of R or S waves, and incomplete right bundle branch block.
If the history and physical exam provide no clues to the cause of the syncope or presyncope, or the event occurred during—as opposed to just after—exertion, further cardiac workup is warranted.1 Likewise, an athlete who has an abnormal exam, abnormal ECG, or history of likely cardiac events, should undergo further diagnostic testing, including echocardiography, maximal exercise testing (preferably in the exercise mode that accompanied the event), Holter or event monitor recordings, and possibly nuclear cardiac imaging, tilt table testing, electrophysiologic studies, and cardiac catheterization.
Echocardiography and stress echocardiography are useful for evaluating valvular abnormalities, ventricular or septal hypertrophy, pulmonary hypertension, and wall motion defects. Technical attention to visualizing the coronary artery architecture should be requested. Maximal exercise stress testing, if possible in the activity that caused the syncope, is also recommended to observe for ischemic changes, provocation of arrythmia, blood pressure response, and exercise capacity.
Controversy exists about the sensitivity and specificity of tilt table testing. While it will often reproduce syncope, tilt table testing has potential for false-positives and false-negatives in athletes, because of baseline increased vagal tone and decreased orthostatic tolerance.37 Event recorders, 24-hour ECG recorders, and implantable loop recorders are useful investigations if the cause of syncope is likely an arrhythmia. Asymptomatic arrhythmia uncovered during recording may not be the cause of syncope. Implantable loop recorders may become the investigation of choice for unexplained syncope, because they seem to yield a diagnosis more often with less cost.39,40 Cardiac catheterization is sometimes needed if ischemia caused by atherosclerosis or myocardial bridging is considered.
If the history or physical exam suggests noncardiac causes, baseline laboratory investigations, including blood sugar and complete blood count, should be considered. Brain natriuretic peptide is a hormone released from the myocardial cells after increased wall stress and increased cardiac volumes. Investigation is underway to see whether this simple lab test could distinguish cardiac versus noncardiac causes of syncope.41
Recommendations for Athletes
Athletes should be encouraged to stay well-hydrated and nourished before training and competition, including maintaining salt intake, especially during hot, humid conditions. Of course, recommending salt intake needs to be tempered against the individual's medical history (ie, salt should not to be recommended to hypertensive patients). Avoiding caffeine can also help maintain hydration and prevent transient arrhythmias.
Numerous medications have been tried to alleviate recurrent benign episodes; beta-blockers are probably the most commonly used. While very successful, their utility for athletes is limited, because they can interfere with athletic performance. Mineralocorticoids,42 alpha1-agonists,43 and selective serotonin reuptake inhibitors44-46 have been prescribed as treatments for neurocardiogenic syncope. Although some of the data are positive, more clinical studies are needed on the effectiveness of medication to treat exercise-induced syncope.
The 36th Bethesda Conference guidelines for participation (table 2) are generally accepted as valuable recommendations for return to play.47 Athletes who have a history of neurocardiogenic syncope are typically not restricted from activity. If a structural or arrhythmogenic cause is identified, the athlete must be restricted from play according to the current 36th Bethesda Conference recommendations.47 Further consultation with a cardiologist or cardiothoracic surgeon is recommended.
Heeding Ominous Signs
Exertional syncope is an uncommon occurrence that is most often caused by neurocardiogenic mechanisms. It may, however, be the only symptom of a potentially life-threatening abnormality. Presyncope or syncope occurring during active exercise has a greater likelihood of having structural or arrythmogenic causes and warrants complete cardiac evaluation.
Dr McAward is a family medicine physician and a primary care sports medicine physician at Memorial Sports Medicine Institute in South Bend, Indiana. Dr Moriarity is a family medicine physician and head team physician at the University of Notre Dame in Notre Dame, Indiana. Address correspondence to Kevin M. McAward, MD, 111 W Jefferson, South Bend, IN 46601; e-mail to [email protected].
Disclosure information: Drs McAward and Moriarity disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.