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

Commotio Cordis

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

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.

Relationship of the anatomy of the human thorax to the internal viscera (heart and lungs) and bones (sternum and ribs).

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.

Differential Diagnoses

Anomalous Left Coronary Artery From the Pulmonary Artery
Cardiomyopathy, Hypertrophic
Long QT Syndrome
Myocardial Infarction in Childhood
Myocarditis, Viral
Ventricular Fibrillation

Workup

Laboratory Studies

• In the past, findings from the workup of patients with commotio cordis (CC) have been limited mostly to postmortem studies and tests on individuals who died as a result of the event. Additionally, the relatively few patients who survived the acute episode and who received the attention of trained medical personnel have provided little insight into the likely findings from laboratory and other studies in patients who survive commotio cordis. 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.
• Blood studies/toxicology: Results of 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: Echocardiography in a patient who survives 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 was described in one survivor. 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.
• Angiography: A few patients have undergone cardiac catheterization and cineangiography upon arriving at a hospital 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 incidences of areas of hypokinesis or akinesis have been documented within the left ventricle, similar to that reported based on findings of 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 dysplasia has been found in any patient who survived commotio cordis.

Histologic Findings

• Data from many autopsy examinations of patients who died as a result of 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 exists. 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 arteriovenous (AV) node and specialized conduction system. The significance of these uncommon histologic findings is uncertain.

Treatment

Medical Care

The treatment of commotio cordis (CC) is not different from any other cardiopulmonary emergency associated with asystole. Attention to airway maintenance, chest compressions, and ventilation are key. Current guidelines recommend immediate defibrillation (if available) following a sudden, witnessed collapse. Chest compressions and ventilation (30:2 ratio) should be used for 5 cycles (about 2 min) prior to defibrillation when the collapse is unwitnessed. One shock should be administered and then followed immediately by cardiopulmonary resuscitation (CPR), starting with chest compressions, for 5 cycles before checking the rhythm. 

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 automated external defibrillators (AEDs) may save the lives of countless young people who go into 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.⁶ The guidelines mention that one immediate precordial thump may be considered after a witnessed cardiac arrest if a defibrillator is not immediately available.
  • Precordial thump is not mentioned at all as an option in pediatric CPR or pediatric advanced life support (PALS). Because a single thump can be delivered quickly, its use as emergency therapy for pediatric commotio cordis, in which the child is pulseless and no defibrillator or cardiac monitor is immediately available, should be reinvestigated. If used in this setting, it should never be allowed to delay electrical defibrillation and should always be followed by standard CPR modalities.

Medication

• Medications may be required to treat arrhythmia following basic cardiopulmonary resuscitation (CPR), electrical defibrillation, or both.
• Follow current American Heart Association (AHA) guidelines.

Follow-up

Deterrence/Prevention

• The recently published 36th Bethesda Conference on Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities had a number of recommendations regarding commotio cordis (CC).⁷
  • 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 in all instances. In a recent review, 18% of commotio cordis events occurred in individuals wearing a chest protector.³
  • 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.
• 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.

Prognosis

• Survival from a commotio cordis event is the exception. Based on the most recent US Commotio Cordis Registry data, only 24% of individuals have survived a commotio cordis episode. Overall, survival trends following exercise-related sudden cardiac arrest from all causes in young athletes continues to be dissapointing.⁸
• Despite greater awareness of sudden cardiac death in athletes and the increasing availability of AEDs at athletic venues, overall successful resuscitation and survival from 2000-2006 was only 11%. Most resuscitation failures have been attributed to delayed onset of cardiopulmonary resuscitation (CPR) and defibrillation. Survival has usually been associated with effective CPR efforts that are begun within 1 minute of the collapse. However, in a report of 9 witnessed and sudden cardiac arrests among intercollegiate athletes, only 1 survived, despite initiation of CPR within 1 minute in 8 of the 9 cases and defibrillation at an average of 3 minutes in 7 of 9 cases.⁹ Two of the individuals had a commotio cordis event. In 6 cases, a cardiac abnormality was identified.   
• 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.⁹
• Standard chest compressions following electrical defibrillation may predispose to episodes of repeated refibrillation, thereby limiting the effectiveness of resuscitation. Studies have demonstrated that chest compressions result in electrical capture of the ventricles which, under certain conditions, can lead to so-called "long-short" electrical sequences that initiate fibrillation.¹⁰

Miscellaneous

Medicolegal Pitfalls

• Although mortality from commotio cordis (CC) is seemingly a chance event and clearly accidental in almost every instance, criminal charges have been pursued in some cases. Several cases reported to the US Commotio Cordis Registry (occurring on and off the athletic field) have resulted in murder or manslaughter convictions. This may be primarily related to the lack of understanding of how blunt chest impact can result in an unintended electrophysiologic cardiovascular catastrophe.
• In 1998, a man from Washington, DC, was sentenced to a prison term of up to 18 years following the sudden death of his 11-year-old son immediately following 2 seemingly innocuous, but punitive, chest blows. The Cook County Chicago Office of the Medical Examiner recently reported deaths involving 2 boys, aged 3 years and 14 months. In both instances, deliberate fatal blows were delivered to the anterior chest with a closed fist. Both children collapsed immediately, were found to be in ventricular fibrillation by paramedics, and could not be resuscitated.

Multimedia

Media file 1: Relationship of the anatomy of the human thorax to the internal viscera (heart and lungs) and bones (sternum and ribs).

References

1. Maron BJ. Sudden death in young athletes. N Engl J Med. Sep 11 2003;349(11):1064-75. [Medline].

2. Link MS, Wang PJ, Pandian NG, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med. Jun 18 1998;338(25):1805-11. [Medline].

3. Maron, BJ: Clinical Features of Commotio Cordis. Presentation of Registry Data at Heart Rhythm Society Scientific Sessions [database online]. Boston, Massachusetts: May 15, 2009.

4. Animal Model of Commotio Cordis: Presentation at Heart Rhythm Society Annual Scientific Sessions [database online]. Boston, Masachusetts: Link MS; May 15, 2009.

5. Link MS, Maron BJ, Wang PJ, et al. Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis). J Am Coll Cardiol. Jan 1 2003;41(1):99-104. [Medline].

6. Amir O, Schliamser JE, Nemer S, Arie M. Ineffectiveness of precordial thump for cardioversion of malignant ventricular tachyarrhythmias. Pacing Clin Electrophysiol. Feb 2007;30(2):153-6. [Medline].

7. Maron BJ, Estes NAM, Link MS. 36th Bethesda Conference: Eligibility recommendations for competitive athletes with cardiovascular abnormalities. Task Force 11: Commotio Cordis. J Am Coll Cardiol. Apr 19 2005;45(8):1371-3. [Medline].

8. Drezner JA, Chun JS, Harmon KG, Derminer L. Survival trends in the United States following exercise-related sudden cardiac arrest in the youth: 2000-2006. Heart Rhythm. Jun 2008;5(6):794-9. [Medline].

9. [Guideline] Drezner JA, Rogers KJ. Sudden cardiac arrest in intercollegiate athletes: detailed analysis and outcomes of resuscitation in nine cases. Heart Rhythm. Jul 2006;3(7):755-9. [Medline].

10. Osoria J, Dosdall DJ, Robichaux Jr RP, Tabereaux PB, Ideker RE. In a Swine Model, Chest Compressions Cause Ventricular Capture and, By Means of a Long-Short Sequence, Ventricualar Fibrillation. Circ Arrhythmia Electrophysiol. 2008/10;1:282 - 9.

11. Abrunzo TJ. Commotio cordis. The single, most common cause of traumatic death in youth baseball. Am J Dis Child. Nov 1991;145(11):1279-82. [Medline].

12. Futterman LG, Lemberg L. Commotio cordis: sudden cardiac death in athletes. Am J Crit Care. Jul 1999;8(4):270-2. [Medline].

13. Link MS, Bir C, Dau N, Madias C, Estes NA 3rd, Maron BJ. Protecting our children from the consequences of chest blows on the playing field: a time for science over marketing. Pediatrics. Aug 2008;122(2):437-9. [Medline].

14. Link MS, Estes NA 3rd. Mechanically induced ventricular fibrillation (commotio cordis). Heart Rhythm. Apr 2007;4(4):529-32. [Medline].

15. Link MS, Ginsburg SH, Wang PJ, et al. Commotio cordis: cardiovascular manifestations of a rare survivor. Chest. Jul 1998;114(1):326-8. [Medline].

16. Link MS, Maron BJ, VanderBrink BA, et al. Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis. J Am Coll Cardiol. Feb 2001;37(2):649-54. [Medline].

17. Link MS, Wang PJ, VanderBrink BA, et al. Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio cordis). Circulation. Jul 27 1999;100(4):413-8. [Medline].

18. Maron BJ, Gohman TE, Kyle SB. Clinical profile and spectrum of commotio cordis. JAMA. Mar 6 2002;287(9):1142-6. [Medline].

19. Maron BJ, Link MS, Wang PJ, Estes NA 3rd. Clinical profile of commotio cordis: an under appreciated cause of sudden death in the young during sports and other activities. J Cardiovasc Electrophysiol. Jan 1999;10(1):114-20. [Medline].

20. Maron BJ, Strasburger JF, Kugler JD, et al. Survival following blunt chest impact-induced cardiac arrest during sports activities in young athletes. Am J Cardiol. Mar 15 1997;79(6):840-1. [Medline].

21. Vincent GM, McPeak H. Commotio cordis: a deadly consequence of chest trauma. Phys Sportsmed. Nov 2000;28(11):31-9. [Full Text].

Keywords

commotio cordis, CC, low-impact chest trauma, cardiac concussion, ventricular fibrillation, cardiac arrest, sudden cardiac death, myocardial infarction, heart attack, anomalous origin of a coronary artery, hypertrophic cardiomyopathy, congenital prolongation of the QTc interval, asystole, automated external defibrillators, AED, blunt chest impact, precordium, arrhythmogenic right ventricular cardiomyopathy, primary electrical disorders, catecholaminergic ventricular tachycardia, primary electrical phenomenon, coronary artery vasospasm, myocardial contusion, precordial trauma, trauma to the precordium, precordial thump, precordial blunt trauma, treatment, diagnosis

Contributor Information and Disclosures

Author

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, American College of Cardiology, American Heart Association, Heart Rhythm Society, New Mexico Pediatric Society, Society for Pediatric Research, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Ira H Gessner, MD, Professor Emeritus, Pediatric Cardiology
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, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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 College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital 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, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

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