eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology
Commotio Cordis
Updated: Jul 17, 2007
Introduction
Background
Sudden unexpected cardiac death in young people that occurs during sports participation is usually associated with previously diagnosed or undiagnosed structural or 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 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).
Recent data from the registry of the Minneapolis Heart Institute Foundation show that CC is the second leading cause of sudden death in young athletes, behind hypertrophic cardiomyopathy.1 However, CC is rarely described in the pediatric literature and is mentioned in very few current texts on critical care, emergency medicine, and pediatric cardiology.
CC 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 CC 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 projectile or bodily contact caused impact to the person's precordium. More than 180 cases of CC have been reported to the US Commotio Cordis Registry (Minneapolis, Minn).2 In all likelihood, CC remains significantly underdiagnosed and underreported.
Pathophysiology
Although reported more often in recent years, CC remains a rare event. This is based, in part, on the pathophysiology of the disorder, which requires precise synchronization of a number of relevant variables. In a series of studies using a swine model of CC, the critical timing and location of blunt chest trauma required to induce ventricular fibrillation and sudden death were demonstrated.
Ventricular fibrillation can be triggered by chest wall impact immediately over the heart and occurs most frequently with impact over the center of the left ventricle. Impact over other precordial sites causes ventricular fibrillation less often. Similarly, nonsustained polymorphic ventricular tachycardia, ST-segment elevation, transient complete heart block, left bundle-branch block, and left ventricular wall motion abnormalities occurred 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 the experimental studies, when 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. Consistently, 90% of low-energy precordial impacts, produced by striking the precordium with a wooden object similar in size and weight to a baseball, resulted in immediate ventricular fibrillation if the impact was delivered within a 15-millisecond window that occurred 15-30 milliseconds before the T-wave peak. This window represents only about 3% 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 this period of vulnerability on the T-wave upstroke or during other portions of the electrical cycle never 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 activation of the mechanosensitive K+ ATP -channel probably provide the basis for ventricular fibrillation and sudden death following blunt thoracic trauma, as well as the ischemiclike ECG changes noted in those rare individuals who survive CC.
In a slightly different swine model of CC, ventricular fibrillation was reproduced by simulated baseball strikes of 30 mph. The force of chest trauma was shown to be inversely related to fatal outcome in CC. Conversely, the hardness of the object that strikes the chest was shown to be directly related to ventricular fibrillation. Perfectly timed strikes with regulation baseballs resulted in ventricular fibrillation in 35% of instances (compared to 90% when using the wooden object).
Softer-than-normal baseballs reduced the risk of ventricular fibrillation to 8% with very soft baseballs, 22% with moderately soft baseballs, and 29% with the least soft baseballs. The predilection for CC to affect individuals younger than 16 years in particular likely relates to chest configuration (ie, narrower anterior-posterior diameter) and increased chest compliance in young children, predisposing them to cardiac electrical disturbances that occur following only modest precordial trauma.
Frequency
United States
The actual prevalence of CC among children and adolescents in the United States is largely unknown. Although more than 128 cases have been reported to the US CC Registry, many instances likely go unreported.2
Mortality/Morbidity
According to the US CC Registry, approximately 15% of persons with CC have been resuscitated.1
Race
According to data collected by the US CC Registry, 87% of cases of CC are in whites.1
Sex
According to data collected by the US CC Registry, 95% of cases of CC occur in males.1
Age
Although reported in a wide range of ages (3 mo to 50 y), CC occurs most frequently in male children aged 4-16 years, with a mean age of 14 years. Data from the US CC Registry show that 43% are younger than 12 years and that only 22% are aged 18 years or older.1
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 he performs a brief purposeful activity, movement, or behavior (eg, picking up and throwing a ball, crying) before final collapse.
- According to data collected by the US CC Registry, at the time of the incident, 47% of persons struck were engaged in organized competitive sports.1 The remainder were involved in normal daily activities or recreational sports.
- Baseball, softball, and hockey are the sports activities most commonly involved. Other associated organized activities included karate, lacrosse, and football. Rare cases have also been associated with basketball, cricket, martial arts, boxing, street fights, and motor vehicle accidents.
- In most instances (68%), 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.1 Other projectiles have included hockey pucks and lacrosse balls. In 32%, 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 CC event is unusual. 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 that are begun within 1-3 minutes of the collapse and are associated with chest thumps or electrical defibrillation. In events in which resuscitation is known to have been started in less than 3 minutes, the survival rate was 25%. The survival rate was only 3% in cases in which resuscitative efforts were delayed longer than 3 minutes. Although a number of individuals have been resuscitated with the restoration of a normal heart rhythm, many of these individuals experience irreversible ischemic encephalopathy and ultimately die as a result of the injury.
Physical
- Persons with CC 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 CC. 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 CC both result from sudden ventricular fibrillation. Precordial impacts probably result in activation of the normally inactive mechanosensitive K+ ATP channel, which 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.
- Impacts that occur only during a narrow, vulnerable period of repolarization result in ventricular fibrillation. Impacts during other portions of the cardiac cycle result in ST-segment elevation.
- Some observers believe that CC 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 CC has not been determined.
More on Commotio Cordis |
Overview: Commotio Cordis |
| Differential Diagnoses & Workup: Commotio Cordis |
| Treatment & Medication: Commotio Cordis |
| Follow-up: Commotio Cordis |
| References |
| Next Page » |
References
Maron BJ. Sudden death in young athletes. N Engl J Med. Sep 11 2003;349(11):1064-75. [Medline].
Doerer JD, Haas TS, Estes NAM, Link MS, Maron BJ. Evaluation of chest barriers for protection against sudden death due to commotio cordis. Am J Cardiol. March 15 2007;99(6):857-9. [Medline].
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].
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].
Futterman LG, Lemberg L. Commotio cordis: sudden cardiac death in athletes. Am J Crit Care. Jul 1999;8(4):270-2. [Medline].
Link MS, Estes NA 3rd. Mechanically induced ventricular fibrillation (commotio cordis). Heart Rhythm. Apr 2007;4(4):529-32. [Medline].
Link MS, Ginsburg SH, Wang PJ, et al. Commotio cordis: cardiovascular manifestations of a rare survivor. Chest. Jul 1998;114(1):326-8. [Medline].
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].
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].
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].
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].
Maron BJ, Gohman TE, Kyle SB. Clinical profile and spectrum of commotio cordis. JAMA. Mar 6 2002;287(9):1142-6. [Medline].
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].
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].
Vincent GM, McPeak H. Commotio cordis: a deadly consequence of chest trauma. Phys Sportsmed. Nov 2000;28(11):31-9. [Full Text].
Further Reading
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
Overview: Commotio Cordis