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Commotio Cordis

Editor: Patrick G. Hughes Updated: 2/5/2023 11:45:52 AM


Commotio cordis is ventricular fibrillation precipitated by blunt trauma to the heart, not attributable to structural damage to the heart or surrounding structures.[1]  Its Latin etymology, “agitation of the heart,” describes the suspected mechanism whereby significant distortion of the myocardium creates enough mechanical energy to cause inappropriate depolarization, resulting in an unstable dysrhythmia.

Cases likely attributable to commotio cordis have been described for hundreds of years.[2]  Some of the earliest reports may relate to legends like Dim Mak, an ancient Chinese martial art technique to cause death by a carefully directed blow, christened “the touch of death.”  Most cases currently reported involve young athletes playing sports.


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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.


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%.


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).


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

Deterrence and Patient Education

Current recommendations are that children should use appropriate size baseball and use chest wall protectors. All sporting arenas should have an automated external defibrillator within access.

All survivors should undergo thorough cardiac monitoring to determine the cause and prevent the event from occurring again.

The decision to return to sports should only be made after a thorough evaluation has been performed. The patient and parent or legal guardian should be asked to sign a consent that they do understand the risk of a recurrent episode.

Enhancing Healthcare Team Outcomes

Knowledge, education, and care should be coordinated between medical teams of physicians, nurses, and other health professionals, as well as with coaches, athletes, and families to identify commotio cordis and improve access to immediate treatment options. Today many sporting organizations have a healthcare professional (either a nurse or a physician) at the venue to assist and advise on safety. More important, nurses and physicians play a major role in education and teaching the public about effective resuscitation measures. Finally, these healthcare professionals also attend to any medical emergency during a sporting event.[13] (Level III)


There is evidence from a data registry that survival has improved concomitantly with increased awareness and access to medical care and public defibrillators. (Level IV) Data show that at least 59% of individuals have survived Commotio cordis in recent years, and each year the survival rates are improving. The key reasons for the mortality are the failure of timely resuscitation and the presence of congenital heart disease. However, the standardization of resuscitation out of the hospital has seen a steady increase in survivors from all types of cardiac arrest, including commotio cordis.[14][15] (Level V)



Maron BJ,Poliac LC,Kaplan JA,Mueller FO, Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. The New England journal of medicine. 1995 Aug 10     [PubMed PMID: 7609749]


Maron BJ,Doerer JJ,Haas TS,Estes NA 3rd,Link MS, Historical observation on commotio cordis. Heart rhythm. 2006 May     [PubMed PMID: 16648070]

Level 3 (low-level) evidence


Maron BJ,Haas TS,Ahluwalia A,Garberich RF,Estes NA 3rd,Link MS, Increasing survival rate from commotio cordis. Heart rhythm. 2013 Feb     [PubMed PMID: 23107651]


Link MS,Maron BJ,VanderBrink BA,Takeuchi M,Pandian NG,Wang PJ,Estes NA 3rd, Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis. Journal of the American College of Cardiology. 2001 Feb     [PubMed PMID: 11216992]

Level 3 (low-level) evidence


Link MS,Wang PJ,Pandian NG,Bharati S,Udelson JE,Lee MY,Vecchiotti MA,VanderBrink BA,Mirra G,Maron BJ,Estes NA 3rd, An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis) The New England journal of medicine. 1998 Jun 18     [PubMed PMID: 9632447]

Level 3 (low-level) evidence


Link MS,Maron BJ,Wang PJ,VanderBrink BA,Zhu W,Estes NA 3rd, Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis). Journal of the American College of Cardiology. 2003 Jan 1     [PubMed PMID: 12570951]

Level 3 (low-level) evidence


Kalin J,Madias C,Alsheikh-Ali AA,Link MS, Reduced diameter spheres increases the risk of chest blow-induced ventricular fibrillation (commotio cordis). Heart rhythm. 2011 Oct     [PubMed PMID: 21699851]

Level 3 (low-level) evidence


Bode F,Franz MR,Wilke I,Bonnemeier H,Schunkert H,Wiegand UK, Ventricular fibrillation induced by stretch pulse: implications for sudden death due to commotio cordis. Journal of cardiovascular electrophysiology. 2006 Sep     [PubMed PMID: 16948746]

Level 3 (low-level) evidence


Maron BJ,Estes NA 3rd, Commotio cordis. The New England journal of medicine. 2010 Mar 11     [PubMed PMID: 20220186]


Link MS,Estes NA 3rd,Maron BJ, Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 13: Commotio Cordis: A Scientific Statement From the American Heart Association and American College of Cardiology. Circulation. 2015 Dec 1     [PubMed PMID: 26621653]


Callaway CW,Donnino MW,Fink EL,Geocadin RG,Golan E,Kern KB,Leary M,Meurer WJ,Peberdy MA,Thompson TM,Zimmerman JL, Part 8: Post-Cardiac Arrest Care: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015 Nov 3     [PubMed PMID: 26472996]


Weinstock J,Maron BJ,Song C,Mane PP,Estes NA 3rd,Link MS, Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. Pediatrics. 2006 Apr     [PubMed PMID: 16510614]

Level 3 (low-level) evidence


Harmon KG,Drezner JA,Maleszewski JJ,Lopez-Anderson M,Owens D,Prutkin JM,Asif IM,Klossner D,Ackerman MJ, Pathogeneses of sudden cardiac death in national collegiate athletic association athletes. Circulation. Arrhythmia and electrophysiology. 2014 Apr     [PubMed PMID: 24585715]

Level 2 (mid-level) evidence


De Gregorio C,Magaudda L, Blunt thoracic trauma and cardiac injury in the athlete: contemporary management. The Journal of sports medicine and physical fitness. 2018 May     [PubMed PMID: 28967243]


Palacio LE,Link MS, Commotio cordis. Sports health. 2009 Mar     [PubMed PMID: 23015869]