Sudden arrhythmic death as a result of a blunt chest wall blow has been termed 
Commotio Cordis (CC). CC is being reported with increasing frequency with more 
than 180 cases now described in the United States Commotio Cordis Registry. The 
clinical spectrum is diverse; however young athletes tend to be most at risk, 
with victims commonly being struck by projectiles regarded as standard 
implements of the sport. Sudden death is instantaneous and victims are most 
often found in ventricular fibrillation (VF). Chest blows are not of sufficient 
magnitude to cause any significant damage to overlying thoracic structures and 
autopsy is notable for the absence of any structural cardiac injury. Development 
of an experimental model has allowed for substantial insights into the 
underlying mechanisms of sudden death. In anesthetized juvenile swine, induction 
of VF is instantaneous following chest impacts that occur during a vulnerable 
window before the T wave peak. Other critical variables, including the impact 
velocity and location, and the hardness of the impact object have also been 
identified. Rapid left ventricular pressure rise following chest impact likely 
results in activation of ion channels via mechano-electric coupling. The 
generation of inward current through mechano-sensitive ion channels results in 
augmentation of repolarization and non-uniform myocardial activation, and is the 
cause of premature ventricular depolarizations that are triggers of VF in CC. 
Currently available chest protectors commonly used in sport are not adequately 
designed to prevent CC. The development of more effective chest protectors and 
the widespread availability of automated external defibrillators at youth 
sporting events could improve the safety of young athletes.