Commotio Cordis

Etiology

Commotio cordis most commonly results from an impact to the left chest with a hardball (e.g., a baseball) during sports activity. The sudden focal distortion of the myocardium results in ventricular fibrillation, causing sudden cardiac arrest in an otherwise structurally normal heart. It is distinct from a traumatic injury to the heart, like cardiac contusion or rupture or penetrating chest injuries.

Epidemiology

Commotio cordis plays a distressing role as a leading cause of sudden cardiac death in young athletes. Reported cases remain relatively infrequent (less than 30 cases are reported each year), although it is increasingly recognized. The US Commotio Cordis Registry (Minneapolis, MN) has been established to facilitate the aggregation of information.

Children appear to be at the highest risk for commotio cordis. The mean age reported in the registry is 15 years, and very few cases have been reported above 20 years old. This may be a result of a combination of a thinner chest wall relative to an adult and an increased likelihood to participate in activities where they are likely to be hit in the chest. 

Ninety-five percent of reported cases occur in boys, which is likely again a reflection of selection for participation in sports which provides the risk factors necessary for commotio cordis to occur. However, the anatomical differences in the chest wall thickness may also play a role.

The reported survival rate among African Americans is lower than in whites (4% vs. 33%). This may be a result of a higher rate of delayed resuscitation (44% vs. 22%) and less frequent use of automated external defibrillators (AEDs) (4% vs. 8%).[3]

One would expect survival to be similar to other cases of ventricular fibrillation, if not even higher, because of the lack of structural heart disease. While initial cases reported very low survival, a significant increase in reported survival has been noted in recent years, likely due to improved recognition and early treatment.[3]  The most recently reported survival rates exceed 50%.

Pathophysiology

Contention exists around the exact mechanism for commotio cordis.  However, experimental studies have shown that there are several factors involved. First, contact occurs directly over the heart in the anterior chest.[4] The contact occurs during ventricular repolarization, specifically during the upstroke of the T-wave before its peak. If the impact occurs later than this, it is more likely to result in a transient complete heart block, left bundle branch block, or ST-segment elevation.[5] While this period occupies only about 1% of the cardiac cycle, the relative proportion is increased with increasing heart rate, as may occur during exercise.

The impact energy must be sufficient to cause ventricular depolarization, estimated to be about 50 joules. This is easily achieved by a thrown baseball, for example, and the risk for commotio cordis appears to peak around 40 miles per hour. At higher speeds (with more energy), there is more likely to be resultant structural damage to the heart and/or chest wall rather than isolated ventricular fibrillation.[6] Smaller balls also carry a higher risk for commotio cordis, likely due to the impact being concentrated on a smaller surface area.[7]

The mechanical force resulting from the precordial impact causes a stretch in myocardial cell membranes, which likely activates ion channels (mechanical-electrical coupling).[8]  If the right number of these channels are in a vulnerable period of repolarization, the result of the depolarization may be ventricular fibrillation.[9]

History and Physical

A history consistent with commotio cordis involves a sudden impact with the anterior chest overlying the heart, followed by immediate cardiac arrest. This is most commonly a baseball; however, any impact may be present in the appropriate circumstances. Ventricular fibrillation may be observed if monitoring or an AED is available. Patients generally have no history of structural heart disease to explain the dysrhythmia, and the injury is not attributable to physical damage to the heart, cardiac contusion, or rupture. Penetrating injury is not the cause for arrest.

Physical exam findings may reveal a contusion overlying the heart, but this often takes time to develop, so it should not be relied upon to confirm the diagnosis. A pulse is not present with ventricular fibrillation, and there is evidence of inadequate organ perfusion (i.e., unconsciousness).

Evaluation

During resuscitation, rhythm strip analysis may help guide interventions. Point-of-care ultrasound may be useful to exclude concomitant injuries like pneumothorax or pericardial effusion/tamponade. Radiography has essentially no role in the management of commotio cordis but may be important to identify concomitant serious injuries like a sternal fracture.

The American Heart Association (AHA) and the American College of Cardiology (ACC) provide a strong recommendation based on moderate-quality evidence that after resuscitation, patients with commotio cordis should undergo “a comprehensive evaluation for underlying cardiac pathology and susceptibility to arrhythmias.”[10]

An electrocardiogram (ECG) may reveal evidence of myocardial injury, but it may be difficult to distinguish whether it occurred primarily or secondary to cardiac arrest. Troponin and echocardiogram may be useful to determine the presence of myocardial contusion.  An echocardiogram may also help identify if there are other underlying structural abnormalities. Stress testing or cardiac catheterization may be considered to evaluate for coronary artery disease, as appropriate.  Pharmacological testing for Brugada syndrome and long-QT syndrome should also be considered.

Treatment / Management

Initial efforts should focus on resuscitation from cardiac arrest due to ventricular fibrillation. This includes closed chest compressions and early defibrillation. If the arrest is prolonged, it may be prudent to provide rescue ventilation and/or medications to improve coronary perfusion pressure (e.g., epinephrine). For an isolated blunt cardiac injury resulting in dysrhythmia, stabilization of the electrical activity may be the only necessary intervention. After resuscitation, appropriate post-arrest care should be implemented.[11]

It may be appropriate to consider other forms of traumatic arrest, depending on the clinical scenario. These may include tension pneumothorax, cardiac or coronary laceration or tamponade, traumatic valvular injury, pulmonary laceration or great vessel injury, hemorrhagic shock, etc., or extrathoracic injuries, depending on the mechanism of injury.

Prevention remains an important consideration. Unfortunately, the use of chest wall protectors has failed to demonstrate a decrease in the incidence of commotio cordis.[12] Thirty-seven percent of the reported cases have occurred with chest protectors in place.[3] The AHA/ACC provides the following recommendations:[10](B3)

1. "Measures should be taken to ensure successful resuscitation of commotio cordis victims, including training of coaches, staff, and others to ensure prompt recognition, notification of emergency medical services, and institution of cardiopulmonary resuscitation and defibrillation." (strong recommendation, based on moderate-quality evidence).
2. "It is reasonable to use age-appropriate safety baseballs to reduce the risk of injury and commotio cordis" (moderate recommendation, based on moderate-quality evidence).
3. "Rules governing athletics and coaching techniques to reduce chest blows can be useful to decrease the probability of commotio cordis" (moderate recommendation, based on limited evidence).

Differential Diagnosis

• Myocardial infarction
• Hypertrophic cardiomyopathy
• Ventricular fibrillation
• Prolonged QT syndrome
• Viral myocarditis