Commotio Cordis 

Updated: Jan 04, 2016
Author: Steven M Yabek, MD, FAAP, FACC; Chief Editor: Stuart Berger, MD 



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 (CPVT). Sudden death due to ventricular fibrillation may also occur following a blunt, nonpenetrating blow to the chest, specifically the precordial area, in an individual with no underlying cardiac disease. This is termed commotio cordis.[1]

Much of our 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 New England Cardiac Arrhythmia Center at the Tufts University and School of Medicine in Boston, Massachusetts and data derived from the US Commotio Cordis Registry (Minneapolis, Minnesota).

Relatively recent data from the registry of the Minneapolis Heart Institute Foundation show that commotio cordis is one of the leading causes of sudden cardiac death in young athletes, exceeded only by hypertrophic cardiomyopathy and congenital coronary artery abnormalities.[2]

Commotio cordis typically involves young, predominantly male, athletes in whom a sudden, blunt, nonpenetrating and innocuous-appearing trauma to the anterior chest results in cardiac arrest and sudden death from ventricular fibrillation. The rate of successful resuscitation remains relatively low but is improving slowly. 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. While only 216 instances have been reported to the US Commotio Cordis Registry (as of 2012),[3, 4] this is probably a considerable underestimation of its true incidence since this entity still goes unrecognized in many instances and continues to be underreported.


Although reported more often in recent years, commotio cordis remains a relatively 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 only 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 30-millisecond window that occurred 10-40 milliseconds before the T-wave peak.[5] This window represents only about 6% 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.

Impacts delivered outside the 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 (possibly 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.[5]

A wide variation in individual vulnerability to ventricular fibrillation from appropriately timed strikes has been noted in the animal model. Animals with a higher susceptibility to ventricular fibrillation had, in general, longer QRS and QTc durations at baseline.[5] More research is clearly indicated to verify these observations and the potential relevance to human subjects.

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 occurring at a velocity of 40 mph. Also, the hardness and shape 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.



United States

Approximately 10-20 commotio cordis events are added to the US Commotio Cordis Registry every year.[6] The actual incidence is, in all likelihood, considerably greater because of lack of recognition and underreporting.


There has been a progressive decline in fatality related to commotio cordis episodes. Survival during the initial years of the US Registry (1970-1993) was only 10%. During the most recent years for which data are available (2006-2012), survival has increased to 58%.[4] This can be attributed to earlier recognition of a commotio cordis event and earlier commencement of CPR and public-access defibrillation using increasingly available AEDs.


Data collected by the US Commotio Cordis Registry show that nearly 80% of commotio cordis episodes occur in whites.[4]


According to data collected by the US Commotio Cordis Registry, 95% of cases of commotio cordis occur in males.[4]


Although reported in a wide range of ages (6 wk 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 26% are younger than 10 years and 75% are younger than 18 years.[4]




In most reported cases of commotio cordis, 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 most instances. In some instances, 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 the latest reported data from US Commotio Cordis Registry, at the time of the incident, 53% of persons struck were engaged in organized competitive athletics. The remainder were involved in normal daily activities (23%) or recreational sports (24%).

Baseball, softball, hockey, and lacrosse are the sports most commonly involved. Other associated organized activities included soccer, football, boxing, and karate. 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 has become less of an exception compared with earlier eras. Although efforts at resuscitation occur frequently, often involving trained bystanders or emergency medical technicians, the onset of 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 and timely CPR efforts and defibrillation that occur within 3 minutes of the collapse. The survival rate is only 5% or less 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.


Persons with a commotio cordis event are typically found to be unresponsive, apneic, pulseless, and without an audible heartbeat. Many are cyanotic. Grand mal seizures have been evident in some. 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. The ribs and sternum are not structurally injured.


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 ischemiclike 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 of resuscitative efforts. At present, whether these conditions have a pathophysiologic role in commotio cordis has not been confirmed, but seems unlikely.





Laboratory Studies

Findings from the workup of patients with commotio cordis have been limited mostly to postmortem studies on individuals who died as a result of the event. In general, patients who experience an episode of commotio cordis are surprisingly free of abnormal laboratory, imaging, or histologic findings, with the exception of the abnormalities revealed by ECG.

Postmortem toxicologic screening of blood and urine are universally negative. Results of serum toxicologic studies in patients who survive commotio cordis are also negative. Cardiac enzyme levels are usually within reference range and show no evidence of myocardial necrosis (ie, infarction). One survivor was reported to have a mildly elevated creatine kinase (CK) level, but the CK-MB fraction was within reference range.

Imaging Studies

Echocardiography in a survivor of commotio cordis almost always shows an anatomically and functionally normal heart. No evidence is found for any of the underlying cardiac conditions (eg, hypertrophic cardiomyopathy, anomalous origin of a coronary artery from the wrong sinus, aortic root disruption) that are sometimes associated with sudden cardiac death during athletics. The cardiac valves are normal, although an incidental finding of mitral valve prolapse has been described. Some survivors demonstrate mildly diminished global left ventricular systolic function or limited areas of hypokinesis. These abnormalities are of short duration, lasting only a few days.

A few patients have undergone cardiac catheterization and cineangiography following a commotio cordis episode. In general, cardiac and coronary artery anatomy were found to be normal. The patients did not demonstrate evidence of coronary artery spasm or thrombosis. Isolated findings of hypokinesis or akinesis have been documented within the left ventricle in a few patients, similar to that reported by echocardiography.

Other Tests

The most common initial ECG findings in both nonsurvivors and survivors are ventricular fibrillation and asystole. Timing of the ECG following impact seems to be the major determinant in which rhythm is present. Patients undergoing resuscitation efforts during transport to an emergency department also have ventricular fibrillation if they have not been electrically defibrillated. If an ECG is recorded relatively late during the resuscitative effort, asystole is the most common finding. In all likelihood, ventricular fibrillation was the initial rhythm following impact.

Patients who survive commotio cordis frequently demonstrate impressive ST-segment elevation, which is particularly evident in precordial leads V1 -V3. The significance of this finding remains unclear because myocardial ischemia, the most common cause of ST-segment elevation, has not been shown to result from commotio cordis in humans or in animal models.

Complete heart block, left bundle-branch block, and, occasionally, idioventricular escape rhythms are also noted in persons who survive commotio cordis. These latter ECG findings, which last only 2-3 days, are remarkably similar to what was noted in the commotio cordis swine model when chest wall impacts were timed to occur outside the period of greatest vulnerability.

No permanent ECG findings have been described. No ECG evidence for congenital QTc prolongation, Brugada syndrome, or arrhythmogenic right ventricular cardiomyopathy have been found in any patients who survived commotio cordis.

Histologic Findings

Data from many autopsy examinations of patients who died from commotio cordis revealed virtually normal cardiac morphology in every instance. In many cases, the patient has small oval or circular abrasions or bruises over the precordium. Most are located directly over the left ventricle. Generally, no evidence is found of rib fractures, hemothorax, hemopericardium, or external myocardial contusion. The heart is found to be completely free of congenital or acquired structural entities known to predispose young people and athletes to sudden death. No evidence for aortic rupture or traumatic injury has been found. Overall cardiac weight, wall thickness, and chamber dimensions are normal. Careful examination of the coronary arteries reveals no evidence of either damage or thrombosis.

Histologic examination results are almost always normal and reveal no evidence of acute or chronic myocardial infarction, infection, or inflammation. Evidence of active or healed myocarditis or arrhythmogenic right ventricular cardiomyopathy has not been reported. Rarely, hemorrhage has been reported in the anterior left ventricular wall and in the A-V node and specialized conduction system. The significance of these findings is uncertain.



Medical Care

The treatment of commotio cordis is not different from any other cardiopulmonary emergency associated with a nonperfusing cardiac rhythm. For victims of witnessed ventricular fibrillation arrest, as occurs in commotio cordis, early cardiopulmonary resuscitation (CPR) and rapid defibrillation can significantly increase the chances of survival.

The 2010 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommend early CPR that emphasizes chest compressions immediately after the emergency response system has been activated. The guidelines deemphasize the importance of rescue breaths and pulse checks. Although a chest compression to ventilation ratio of 30:2 and a compression rate of at least 100 per minute are still recommended for adults and children (above age 1 y), bystander "hands-only" CPR (compression only) also significantly improves survival compared with no bystander CPR. Rapid defibrillation significantly increases the chances for survival to hospital discharge. CPR, beginning with chest compressions, should resume immediately after a shock and should continue for 2 minutes before a rhythm or pulse check is conducted.

Performing CPR while the AED or defibrillator is readied for use is strongly recommended. A shorter time interval between the last chest compression and the shock is directly correlated with the success of defibrillation.

The relatively low rate of survival from commotio cordis is probably caused by the delay in instituting effective CPR measures because bystanders frequently fail to appreciate the severity of the event, lack knowledge of commotio cordis, or mistakenly believe that the trauma was insignificant. Many observers have commented that they believed that the wind was knocked out of the person. Experience suggests that survival is associated with resuscitation efforts begun within 1-3 minutes of collapse.

Electrical defibrillation

The hallmark of effective resuscitation is rapid, direct current defibrillation. Time to defibrillation is probably the single most important determinant of survival in cardiac arrest. The likelihood of successful defibrillation decreases rapidly over time, in part because ventricular fibrillation generally evolves to asystole within a few minutes. Experimental data gathered using the commotio cordis swine model suggest that defibrillation within 1 minute of ventricular fibrillation onset results in a 100% survival rate and that defibrillation after 2 minutes results in an 80% survival rate. In animals in which ventricular fibrillation was present for more than 4 minutes, the survival rate was 0% unless CPR was instituted after defibrillation (in which case, the likelihood of survival increased to 65%). In humans, every 1-minute delay in defibrillation beyond the first 3 minutes decreases the likelihood of survival by approximately 10%.

Because emergency paramedical technicians cannot be expected to arrive at the scene of a cardiac arrest in less than 5 minutes, the expanded use of public-access automated external defibrillators (AEDs) may save the lives of countless young people who experience cardiac arrest due to blunt trauma to the precordium. AEDs, even when used by persons with minimal training, can recognize and automatically terminate fatal arrhythmias. AEDs are now approved for use in children as young as 1 year. Ideally, AEDs should have a specific "low-output" setting or a special pediatric pad and cable set which attenuates the charge for use in children aged 1-8 years. Even without these, all AEDs can be used in children of any age older than 1 year.

Precordial thump

Use of the precordial thump during CPR is controversial. No prospective studies have evaluated the efficacy of precordial thump in resuscitation. Recently, limited studies in animals and humans have shown precordial thumps to be ineffective in terminating ventricular fibrillation.[7] The 2010 AHA Guidelines for adult ACLS mention that one immediate precordial thump may be considered after a witnessed cardiac arrest if an AED or defibrillator is not immediately available. Precordial thump is not mentioned at all as an option in pediatric CPR or pediatric advanced life support (PALS).



Medication Summary

Medications may be required to treat arrhythmias following basic cardiopulmonary resuscitation (CPR), electrical defibrillation, or both.




The 36th Bethesda Conference on Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities had a number of recommendations regarding commotio cordis.[8]

Children and adolescents aged 13 years and younger should use age-appropriate safety baseballs.

Although commercial chest wall protectors prevent traumatic injury in some instances, the construction of many products is not sufficient to prevent transmission of blows to the heart. Among professional athletes who suffered a commotio cordis event, 1/3 were wearing commercially availabe chest protectors.

All sports venues should have immediate access (within 5 min) to an automated external defibrillator (AED).

Survivors of commotio cordis should undergo a thorough cardiac evaluation, including a 12-lead ECG, ambulatory Holter monitoring, and complete echocardiography.

Eligibility for returning to competitive sports following a commotio cordis episode is, at present, a decision left to individual clinical judgment. No evidence suggests that survivors of commotio cordis have a greater risk of future arrhythmic events. The role of subclinical long QT syndrome as a potential cause for increased susceptibility, as suggested by animal studies, needs further investigation.

Because risk is proportional to the hardness and compactness of the object that strikes the precordium, consideration may be given to the use of specially designed, softer-than-normal safety baseballs in recreational and Little League baseball.


Survival from a commotio cordis event is improving. Based on the most recent US Commotio Cordis Registry data, 58% of individuals have survived a commotio cordis episode in recent years. Overall, survival trends following exercise- or sports-related sudden cardiac arrest from all causes in young athletes is improving.[9]

Failure of timely resuscitation efforts may relate to several factors, the most important of which is the presence of structural heart disease. In those with an anatomically normal heart suffering a commotio cordis event, the duration and intensity of exercise prior to arrest, higher than normal endogenous catecholamine levels and a decrease in systemic vascular resistance may all play a role in limiting the success of resuscitation.[10]

Standard chest compressions following electrical defibrillation may predispose to episodes of repeated refibrillation, thereby limiting the effectiveness of resuscitation. Despite the current AHA Guidelines, some studies have demonstrated that chest compressions can result in electrical capture of the ventricles, which, under certain conditions, may lead to so-called "long-short" electrical sequences that reinitiate fibrillation.[11]