A 17-year-old male track athlete presents to your emergency department with a complaint of syncope. He had been running a moderate-paced two mile warm-up when he collapsed suddenly. He had no prodromal symptoms, and witnesses state he was unconscious for approximately 30 seconds. No seizure activity or post-ictal behavior was noted. He denies any previous history of syncope or chest pain, and family history is unremarkable. He has normal vital signs and physical exam. His rapid glucose and chest radiograph are normal; 12 lead ECG shows prominent QRS complexes which the computer interprets as “probably age-related; otherwise normal ECG.” He is currently asymptomatic, and both he and his parents would like to leave, so he can rest up for that weekend’s state meet. The track coach is present and states that this young man could be on his way to a Division I track scholarship. Can he run this weekend?
There is an expectation that athletes are among the healthiest members of society. But every now and then an athlete succumbs to sudden cardiac death. Needless to say, it is a highly emotional event. Sports Illustrated recently ran a full-spread article on hypertrophic cardiomyopathy reflecting public anxiety over these uncommon but devastating events. An athlete who collapses on the field will, more often than not, be transported to the ED. We will often be the first physician to treat, and will be the first called to answer for our decisions.
Is this athlete at risk for sudden cardiac death? Maybe. Sudden cardiac death strikes athletes of all ages; for convenience we categorize the young athlete (age35), being aware that overlap is present. Sudden death in younger athletes occurs in approximately 1 per 150,000 athletes per year. In this group, death is most often due to a complication of a congenital structural or conduction abnormality exacerbated by exertion. The most common structural abnormality in the United States is hypertrophic cardiomyopathy (HCM), a disease characterized by asymmetric enlargement of the left ventricle. Exertion results in functional obstruction of the ventricle which, theoretically, generates unstable rhythms. In the majority of cases, the inciting rhythm is ventricular fibrillation.
Athletes with HCM may complain of exertional chest pain, dyspnea, or syncope, but the majority remains asymptomatic up until the time of death. The textbook systolic ejection murmur of HCM increases with standing or valsalva (via decreased venous return and increased turbulence) and decreases with squatting (as venous return increases), but is often absent on examination. Most athletes with HCM will have an abnormal resting ECG, with increased voltage, prominent Q waves, inverted T-waves, and repolarization abnormalities being common. The diagnosis is confirmed by an echocardiogram demonstrating abnormal enlargement of the ventricular septum.
Other diagnoses that must be excluded include congenital coronary artery anomalies (which may become functionally obstructed during exertion), myocarditis, QT prolongation, and connective tissue disease. QT interval prolongation (QTc >0.46 seconds) may be due to a congenital conduction defect, antibiotics or other QT-prolonging medications. Athletes with Marfan’s syndrome (often undiagnosed) are susceptible to thoracic aortic dissection, secondary to connective tissue elasticity of the aortic root and development of aneurysm.
“Commotio cordis” has become increasingly recognized as a cause of death in young athletes without evidence of heart disease. A blunt (and often mild) blow to the chest results in ventricular fibrillation, most likely due to impact during repolarization. Participants in projectile sports (baseball, hockey, lacrosse) appear to be at greatest risk.
In the case of young athletes experiencing sudden cardiac arrest, survival with good neurological outcome depends on three well known factors:
1. Immediate CPR
2. A presenting rhythm of ventricular fibrillation
3. Rapid defibrillation.
Initiation of resuscitative measures (CPR alone or in combination with an AED) in less than 3 minutes results in an approximately 28% survival rate, whereas measures commenced after 3 minutes result in a 2% survival rate. Sideline physicians should insist on access to an AED or manual defibrillator, and should quickly assess rhythm and shock when indicated.
Consider cardiovascular causes when a young athlete presents to the ED with a complaint of exertional chest pain or syncope. Key aspects of the evaluation include:
1. Play close attention to the patient’s rhythm and hemodynamic stability.
2. Physical exam is most often normal, but this does not rule out disease. Be vigilant for pathologic murmurs, asymmetric pulses, or stigmata of Marfan’s Syndrome.
3. Consider the diagnosis of thoracic aortic dissection in tall (>72 inch male, >70 inch female) athletes who present with chest pain or stroke-like syndromes.
4. Obtain a 12-lead ECG. Be aware that non-pathologic adaptation to intensive training may result in ECG changes similar to those found in HCM. In the symptomatic athlete, any change should be presumed to be pathologic, and the athlete should be referred for further evaluation. HCM cannot be ruled out with a good echocardiogram.
5. The EP should never clear the athlete for return-to-play without the concurrence of a treating cardiologist. Withstand the temptation and pressure by parents, coaches, and the athletes themselves to return them to play without a full evaluation. Consider admission for anyone with any evidence of hemodynamic instability, ECG or rhythm abnormalities, or poor follow-up.
After a great deal of wrangling with the echo lab, the track star received an urgent echocardiogram which revealed a thickened ventricular septum. The shocked coach was convinced to purchase an AED for the team. The athlete was sidelined making him and his family very disappointed, but grateful that a catastrophe had been averted.
Brian Springer is the sports medicine director for the Wright State University Department of Emergency Medicine.