eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Commotio Cordis

Author: Steven M Yabek, MD, FAAP, FACC, Pediatrix Cardiology Associates of New Mexico (a Division of Mednax Medical Group), Presbyterian Hospital Medical Center
Contributor Information and Disclosures

Updated: Sep 4, 2009

Introduction

Background

Sudden unexpected cardiac death that occurs in young people during sports participation is usually associated with previously diagnosed or undiagnosed structural or primary electrical cardiac abnormalities. Examples of such abnormalities include hypertrophic cardiomyopathy, anomalous origin of a coronary artery, arrhythmogenic right ventricular cardiomyopathy, and primary electrical disorders, such as congenital prolongation of the QTc interval and catecholaminergic, polymorphic ventricular tachycardia. Sudden death due to ventricular fibrillation may also occur when a baseball or other projectile strikes the precordium of an individual with no underlying cardiac disease. This is termed commotio cordis (CC).

Much of the understanding of the clinical and pathophysiologic aspects of commotio cordis is the result of work by N.A. Mark Estes III, MD, and Mark S. Link, MD, from the Cardiac Arrhythmia Center at the Tufts Medical Center in Boston, Massachusetts and the result of data derived from the Commotio Cordis Registry (Minneapolis, Minnesota).

Recent data from the registry of the Minneapolis Heart Institute Foundation show that commotio cordis is probably the second leading cause of sudden cardiac death in young athletes, exceeded only by hypertrophic cardiomyopathy.¹

Commotio cordis typically involves young, predominantly male athletes in whom a sudden, blunt, nonpenetrating and innocuous-appearing trauma to the anterior chest results in immediate cardiac arrest and sudden death from ventricular fibrillation. Resuscitation is rare. Although commotio cordis usually involves impact from a baseball, it has also been reported during hockey, softball, lacrosse, karate, and other sports activities in which a relatively hard and compact projectile or bodily contact caused impact to the person's precordium. More than 210 cases have now been reported to the US Commotio Cordis Registry.^2,3 The recent increase in reporting of cases is probably the result of increased commotio cordis awareness rather than an actual change in incidence.

Pathophysiology

Although reported more often in recent years, commotio cordis remains a rare event. This is based, in part, on the pathophysiology of the disorder, which requires precise synchronization of numerous relevant variables. In a series of studies using a swine model of commotio cordis, investigators identified the critical timing and location of blunt chest trauma required to induce ventricular fibrillation and sudden death.

Ventricular fibrillation can be triggered by chest wall impact immediately over the heart and predominantly occurs with impact over the center of the left ventricle. Impact over other precordial sites causes ventricular fibrillation less often. Nonsustained polymorphic ventricular tachycardia, ST-segment elevation, transient complete heart block, left bundle-branch block, and left ventricular wall motion abnormalities occurred in the absence of ventricular fibrillation only following impact over the cardiac silhouette in the swine model. Chest wall impact that did not overlie the heart failed to produce ventricular fibrillation or any other ECG abnormalities.

During experimental studies in which the precordial impacts were timed to occur during various points in the cardiac cycle, the electrophysiologic consequences were determined to be critically dependent on impact timing. The highest incidence of ventricular fibrillation produced by striking the precordium with a wooden object similar in size and weight to a baseball occurred when the impact was delivered within a 20-millisecond window that occurred 10-30 milliseconds before the T-wave peak. This window represents only about 4% of the cardiac cycle in an individual engaged in activities who has a heart rate of 120 beats per minute. Ventricular fibrillation was not preceded by ventricular tachycardia, conduction abnormalities, or ischemic ST changes; this suggests that the mechanism was related to a primary electrical phenomenon, not to myocardial ischemia. 

A wide variation in individual animal vulnerability to ventricular fibrillation from appropriately timed strikes was noted. Animals with an increased preimpact QTc interval seemed to have a greater likelihood of induced ventricular fibrillation, suggesting a possible genetic predisposition to commotio cordis.⁴ More research is clearly indicated to verify this observation.

Impacts delivered outside this period of vulnerability on the T-wave upstroke or during other portions of the electrical cycle rarely resulted in ventricular fibrillation; however, such impacts occasionally caused polymorphic ventricular tachycardia, complete heart block, left bundle-branch block, or ST-segment elevation, all of which were transient. In vivo studies have suggested that impact-related premature ventricular depolarizations together with elevated ventricular pressure-related activation of mechanosensitive ion channels (particularly the ATP-dependent K⁺ channel) probably provide the basis for ventricular fibrillation and sudden death following blunt thoracic trauma, as well as the ischemic-like ECG changes noted in those rare individuals who survive commotio cordis.

Other studies using the commotio cordis swine model showed a "bell-shaped" curve relating simulated baseball strike velocity and the induction of ventricular fibrillation, with the highest incidence of fibrillation (approximately 70% of strikes) occurring at a velocity of 40 mph. Also, the hardness of the object that strikes the chest was shown to be directly related to ventricular fibrillation. Softer-than-normal baseballs reduced the risk of ventricular fibrillation with very soft baseballs having the lowest incidence.

Frequency

United States

The actual prevalence of commotio cordis among children and adolescents in the United States is largely unknown. Although more than 200 cases have been reported to the US Commotio Cordis Registry, most instances still likely go unreported.

Mortality/Morbidity

According to the US Commotio Cordis Registry, approximately 24% of persons with commotio cordis have been resuscitated.³

Race

According to data collected by the US Commotio Cordis Registry, 80% of cases of commotio cordis are in whites.³

Sex

According to data collected by the US Commotio Cordis Registry, 95% of cases of commotio cordis occur in males.³

Age

Although reported in a wide range of ages (7 weeks to 50 y), commotio cordis occurs most frequently in male children aged 10-18 years, with a mean age of 15 ± 9 years. Data from the US Commotio Cordis Registry show that 27% are younger than 10 years and that only 10% are older than 25 years.³

Clinical

History

• In most reported cases of commotio cordis (CC), sudden death follows a seemingly inconsequential, nonpenetrating blow to the chest. Individuals who have witnessed the events universally believed that the chest trauma was of insufficient force to cause major injury and was out of proportion to the outcome. The person who is struck collapses immediately in approximately 50% of instances. In the remaining cases, the individual has a transient period of consciousness, during which a brief purposeful activity, movement, or behavior (eg, picking up and throwing a ball, crying) is performed before final collapse.
• According to data collected by the US Commotio Cordis Registry, at the time of the incident, 56% of persons struck were engaged in organized competitive sports.³ The remainder were involved in normal daily activities (22%) or recreational sports (22%).
  • Baseball, softball, and hockey are the sports activities that have been most commonly involved. Other associated organized activities included lacrosse, karate and football. Cases involved with daily activities have included playful boxing, a "remedy" for hiccups, parental discipline, being struck by a snowball, and an accidental kick during cheerleading, among others. 
  • In most instances (58%), the person was struck by a projectile, which was most commonly a pitched, thrown, or batted baseball or softball estimated to be traveling 30-50 mph at most. Other projectiles have included hockey pucks and lacrosse balls. In 42%, chest trauma resulted from bodily contact with another person or a stationary object. Examples of this have included a player's helmet during a football tackle, the heel of a hockey stick, a karate kick, and a body collision.
• Survival after a commotio cordis event is still the exception. Although efforts at resuscitation occur frequently, often involving trained bystanders or emergency medical technicians, the onset of cardiopulmonary resuscitation (CPR) is often delayed because observers underestimate the severity of the trauma or believe that the wind has been knocked out of the person. Survival has usually been associated with effective CPR efforts and defibrillation that occur within 1-3 minutes of the collapse. The survival rate was only 3% in cases in which resuscitative efforts were delayed longer than 3 minutes. Although numerous individuals have been resuscitated with the restoration of a perfusing heart rhythm, many of these individuals have experienced irreversible ischemic encephalopathy and ultimately died as a result of the injury.

Physical

• Persons with commotio cordis are typically found to be unresponsive, apneic, pulseless, and without an audible heartbeat; many are cyanotic.
• Grand mal seizures have been evident in some persons with commotio cordis.
• Chest wall contusions and localized bruising that correspond to the site of chest impact are noted over the precordium in approximately one third of patients.
• Typically, the ribs or sternum is not structurally injured.

Causes

• Clinical and experimental commotio cordis both result from sudden ventricular fibrillation. Precordial impacts result in left ventricular pressure elevation that causes activation of the normally inactive mechanosensitive K⁺ _ATP channel which, in turn, leads to inhomogeneity of repolarization and ST segment elevation. Critically timed impacts also produce premature ventricular depolarizations, which sets the stage for ventricular fibrillation in the presence of ischemic-like conditions.⁵
• Impacts that predominantly occur during a narrow, vulnerable period of repolarization result in ventricular fibrillation. Impacts during other portions of the cardiac cycle are less likely to produce ventricular fibrillation but may result in isolated ST-segment elevation.
• Some observers believe that commotio cordis may include a component of coronary artery vasospasm, myocardial contusion, or both. They believe that this may help explain both the difficulty and the relatively rare success of resuscitative efforts. At present, whether these conditions have a pathophysiologic role in commotio cordis has not been confirmed.

• Search for CME/CE on This Topic »

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