Vasovagal syncope (VVS), also known as neurocardiogenic syncope and vasodepressor syncope, is a frequent and usually benign form of syncope that results from an errant reflex arc of cardiac mechanoreceptors (4,19). It is considered a subset of neurally mediated (reflex) syncope (17). While VVS is common, it rarely occurs during exercise (5). An athlete who presents with exertional syncope should not be diagnosed with VVS until a thorough cardiac evaluation excludes arrhythmias and structural heart disease. The 36th Bethesda Conference Guidelines do not restrict athletes with VVS from returning to participation (12,20).
We describe a case of exertional syncope in a collegiate swimmer, which, after thorough workup, was attributed to VVS. The athlete was allowed to return to swimming with individual supervision. To our knowledge, this is the first reported case of VVS during swimming competition.
A 21-year-old white female collegiate swimmer, competing in a 400-yd individual medley, stopped swimming and began to sink at 110 yd, after her turn and underwater kick off the wall while holding her breath. This was between her butterfly and backstroke segments. A teammate removed her from the water. She was breathing and had a pulse but was verbally unresponsive with her arms and legs shaking. She became verbally responsive after several minutes. A team physician performed vital, lung and heart exams within 3 min of the event and they were normal. She was drowsy but oriented. Emergency Medical Services (EMS) arrived within 10 min and performed a rhythm strip showing normal sinus rhythm. Her oxygen saturation was normal. Her blood glucose was 109. She refused to go to the emergency department for further monitoring despite recommendations. She was monitored and evaluated by the team physician and athletic trainer for several hours. The swimmer denied experiencing prodromal symptoms but described feeling profound fatigue which subsequently persisted for 24 h after the event. Further physical exam showed a body mass index of 22.6 with healthy appearance. She was 6′1″ and 171 lbs. She had no abnormal facial features, ocular abnormalities, excessive joint laxity, arachnodactyly, or abnormal arm span/height ratio. She was an elite swimmer with years of experience competing on the national level. She denied any illegal drug or supplement use.
She had complained previously of chest pains and shortness of breath with dry-land exertion at her preparticipation physical examination for college but denied experiencing the symptoms with swimming. Before she was cleared for participation, a cardiology evaluation was performed with an ECG, echocardiogram, and stress echocardiogram to rule out arrhythmias, mitral valve prolapse, and other structural abnormalities, and with a cardiac CT to rule out an anomaly of coronary arteries. The results were all normal. She had no family history of arrhythmia, cardiac disease, or sudden unexplained death.
During her first 2 years of collegiate swimming, but prior to this exertional syncopal event, she had several presyncopal episodes and one reported syncopal event that occurred after dry-land training of running stadium steps. She also had one episode that occurred at an away competition after a race and after exiting the pool. At that time, she was taken to the emergency room with a reported normal evaluation result. None of these prior events were during exertion or in the water. She had experienced prodromal symptoms consisting of lightheadedness, shakiness, chest tightness, and shortness of breath with all of these previous episodes. For the previous events, cardiology reevaluation and pulmonology evaluation had been performed with ECG and a 24-h Holter monitor, and lab work had been done, including thyroid, electrolytes, blood glucose, and HgA1c tests, with all of the results being normal. Pulmonary function tests did show small airway dysfunction improved with bronchodilators. She was treated with twice-daily inhaled budesonide/formoterol and inhaled albuterol as needed with improvement in chest tightness and shortness of breath symptoms. These were her only medications. Recommendations to increase hydration and salt intake were made. She also had a history of anhidrosis. The previous nonexertional events had been diagnosed as VVS and it was felt that her exercise-induced bronchospasm may have contributed to her symptoms. After this exertional event, she was restricted from swimming or any exertion until further workup.
Cardiology reevaluation was performed on her with a new ECG (Fig. 1), a transthoracic echocardiogram, and a 48-h Holter monitor. She also underwent cardiac magnetic resonance imaging (MRI) with gadolinium to rule out arrhythmogenic right ventricular dysplasia (ARVD). All of the results of these tests were normal. A neurologist evaluated her with an electroencephalogram (EEG), and she underwent a brain MRI without contrast, in which the results were normal, and neurology deferred to cardiology for further workup as they did not feel her syncope was neurologic in origin. An electrophysiology study was performed on her, which did not induce an arrhythmia, followed by a tilt table test that replicated her previous postexertional episodes’ prodromal symptoms of lightheadedness, dizziness, shortness of breath, and limb jerking along with frank syncope, which was very consistent with VVS. Her systolic blood pressure was 50 mm Hg at the time of symptoms. However, since she had not experienced her typical prodromal symptoms with her most recent episode, the exertional event during competition in the pool, further evaluation was obtained.
An epinephrine challenge was performed to evaluate for long QT syndrome (LQTS) and showed subtle QT and T wave changes. An electrophysiologist with extensive athlete experience reviewed the results and concluded they showed an unusual response to epinephrine but were negative for LQTS. He recommended a diagnostic stress test for further characterization of the QT response. This showed an appropriate decrease in QT interval during maximal exercise, inconsistent with LQTS (Fig. 2). In addition, both her mother and father had resting ECG performed with normal QT intervals. At this point, her syncopal episodes including the recent exertional event were concluded to result from VVS, with the exertional event likely triggered by decreased venous return from the Valsalva maneuver during a vigorous flip turn with breath holding.
While her syncope was felt to be benign, there was concern that she could have another event in the water. Constant supervision by an individually assigned lifeguard during both training and competition was arranged, and she was allowed to return to swimming. She was started on metoprolol ER 12.5 mg to blunt sympathetic/parasympathetic responses that could trigger vasovagal events. This did not inhibit performance, and she was able to complete her season with no further events.
VVS is a disorder of autonomic cardiovascular regulation (19). An increase in adrenergic tone is believed to be one trigger (6). It occurs when contractions of a volume-depleted ventricle stimulate cardiac mechanoreceptors triggering a reflex arc that paradoxically leads to increased vagal tone and subsequent peripheral vasodilation, decreased HR, and syncope (4).
Fear and pain are the most common triggers. Exercise also may trigger VVS, but it is usually postexertional and seen with upright posture. VVS that occurs during exertion and in a nonupright position is unusual. Because syncope in this setting is more likely to be from a potentially lethal cardiac condition, the diagnosis of exertional VVS should be a diagnosis of exclusion (4).
Syncope in athletes is not uncommon. In one study by Colivicchi et al. (5) of 7,568 athletes undergoing preparticipation physical examination, 6.2% reported a syncopal spell in the last 5 years. Syncope was unrelated to exercise in 86.7%, postexertional in 12%, and exertional in 1.3%. All of the cases of nonexertional or postexertional syncope were diagnosed with a neurally mediated cause. Of the athletes with exertional syncope, 33% had a potentially life-threatening cardiovascular abnormality requiring disqualification. The remaining 66% were diagnosed with neurally mediated syncope (5). This demonstrates that while exercise-associated syncope is usually benign, a third of exertional syncope cases are caused by serious and potentially life-threatening cardiovascular disorders and need to be evaluated thoroughly.
Syncope is defined as a transient loss of consciousness (T-LOC) caused by global cerebral hypoperfusion (17). This definition separates syncope from other causes of T-LOC such as epileptic seizures (17). The differential diagnosis of exertional T-LOC is broad and includes neurally mediated syncope, T-LOC from abnormal cerebral metabolic activity, syncope from orthostatic hypotension, and cardiac syncope (5,13,17). Cardiac causes of syncope can be further divided into structural causes like hypertrophic cardiomyopathy or anomalies of the coronary arteries and genetic channelopathy-associated arrhythmias like LQTS. The Table presents a summary of potential causes of exertional T-LOC.
In our athlete, because syncope occurred during exertion as opposed to postexertion, a structural cardiac cause was of significant concern. However, this was ruled out by extensive imaging including echocardiography, cardiac CTA, and cardiac MRI.
Exercise-associated collapse (EAC) is a common cause of exercise-related syncope. EAC refers to athletes who cannot support themselves upright from dizziness, lightheadedness, faintness, or syncope. It is likely the most common cause of collapse of athletes at the finish line of athletic events. EAC is believed to be predominantly the result of transient postural hypotension caused by lower extremity pooling of blood once an athlete stops moving, with subsequent impairment of cardiac baroreflexes (3,13). This was ruled out in our athlete as she was in a supine position and still under exertion when the episode happened.
The athlete described in this report was witnessed to have some shaking of her limbs, attributed to a seizure. While neurologic causes are important to consider, convulsive syncope or motor activity during syncope is associated commonly with cerebral anoxia from both neurocardiogenic syncope and life-threatening arrhythmias such as LQTS. It is misdiagnosed frequently and treated as epilepsy. A cardiovascular cause of syncope must be considered and cardiovascular assessment should supersede neurologic workup (1,10,14,15,18). A seizure was ruled out in our athlete as she had no confusion immediately after her event followed by a normal neurology evaluation, EEG, and brain MRI.
Hypoxia and hypocapnia are other causes of loss of consciousness seen in shallow water and mostly have been associated not only with breath-holding divers but also with sprint swimmers, underwater sport athletes, and spear fishermen amongst others. The mechanism that could be considered in this case would be hyperventilation prior to the race causing hypocapnia in blood and tissues but slightly increasing the oxygen stores in the lungs. This delays the carbon dioxide-driven response to breathe, and loss of consciousness can happen suddenly because the athlete easily can override voluntarily the weak respiratory stimulus from hypoxia (7,11). In this case, however, the swimmer was competing in an aerobic distance event, not a sprint, and did not appear to hyperventilate prior to her event or breath hold during her race other than several seconds off each wall which is typical with flip turns.
In this case, LQTS, specifically types 1 and 2, were considered. Type 1 is most common and typically occurs during exercise, especially swimming where a vagotonic reflex is thought to result from sudden exposure of the patient’s face to cold water (9,16). Type 2 has been associated with seizures and is triggered usually by an emotional event, loud sounds, or exercise. Both types were plausible in this case but essentially ruled out by the cardiac workup. The athlete was offered genetic testing as the final confirmation against LQTS, but she declined and then left our institution after the season, limiting further follow-up.
A tilt table test (TTT) is important in diagnosing VVS. Because false-positive results may occur, especially in athletes who may have an increased susceptibility to orthostatic hypotension, it is imperative that the test reproduce clinical symptoms along with hypotension and syncope in an upright position to diagnose VVS (4,13). Unfortunately, there is no gold standard diagnostic test for VVS, and TTT can act only as an aid to the clinical history. However, the European Society of Cardiology suggests various indications for TTT where its diagnostic yield can be high, such as in negative comprehensive cardiovascular workup, to distinguish syncope from epilepsy when limb movements were observed, or if syncope could happen in high-risk settings (pilot, water, etc.) (4,8,13,17).
Once a diagnosis of VVS is established, effective treatments may include beta-blockers and trigger avoidance, increased salt intake, and careful hydration (4). Disopyramide, alpha agonists, and selective serotonin reuptake inhibitors may be used in recalcitrant cases. Our athlete was placed on a low-dose beta-blocker (metoprolol ER) treatment, remained symptom free, and did not experience decreased performance. The use of beta-blockers have had contradictory results in a variety of studies, and therefore, the European Society of Cardiology Guidelines state that beta-blockers are not indicated for treatment of VVS. However, the outcome used in the clinical trials was a negative tilt response which is not useful to assess efficacy. Beta-blockers may be helpful and can be considered in those with evidence of adrenergic hypersensitivity, younger patients, and those with a vasovagal response during tilting after isoproterenol infusion (2,17).
The 36th Bethesda Conference Guidelines serve as a gold standard reference in the evaluation, treatment, and return to play of athletes with syncope. It states that VVS is a common finding in highly trained athletes, but structural cardiovascular disease should be excluded definitively prior to making the diagnosis. The guidelines also do not restrict competitive sport activities for athletes with VVS if appropriate workup has been performed (20).
In a water athlete, safe return to play is an important consideration as drowning could occur with an episode. Our institution was able to provide an individual lifeguard for all training and competitions. It was felt that safe return was possible with this oversight. Unfortunately, our athlete was lost to follow-up when she transferred from our institution, but these precautions would have been recommended for the duration of her competitive swimming career.
In conclusion, while VVS is a common cause of syncope and has been associated with exercise, it rarely occurs during exercise (5). To our knowledge, there have been no reported cases of VVS in a swimmer while competing. A cause of syncope is diagnosed in only 50% of presentations, and of these, detailed history and physical exam can provide a diagnosis in the majority of cases (20). If the cause is not identified readily, further cardiovascular evaluation guided by early consultation with a cardiologist is necessary to exclude deadly arrhythmias or structural heart disease in an athlete who presents with exertional syncope (20).
The authors declare no conflicts of interest and do not have any financial disclosures.
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