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Commotio Cordis

  • Author: Steven M Yabek, MD, FAAP, FACC; Chief Editor: Stuart Berger, MD  more...
Updated: Jan 05, 2016


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 cause of sudden cardiac death in young athletes, exceeded only by hypertrophic cardiomyopathy and congenital cornoary 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]

Contributor Information and Disclosures

Steven M Yabek, MD, FAAP, FACC Pediatrix Cardiology Associates of New Mexico (a Division of Mednax Medical Group), Presbyterian Hospital Medical Center

Steven M Yabek, MD, FAAP, FACC is a member of the following medical societies: American Academy of Pediatrics, Heart Rhythm Society, Western Society for Pediatric Research, New Mexico Pediatric Society, American College of Cardiology, American Heart Association, Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Hugh D Allen, MD Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, Western Society for Pediatric Research, American College of Cardiology, American Heart Association, American Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD Medical Director of The Heart Center, Children's Hospital of Wisconsin; Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, Medical College of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

Ira H Gessner, MD Professor Emeritus, Pediatric Cardiology, University of Florida College of Medicine

Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

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