Commotio cordis

Diagram showing the portion of normal sinus rhythm during which commotio cordis is a risk

These factors influence the chance of commotio cordis:[7]

• Direction of impact over the precordium (precise area, angle of impact)
• Total applied energy (area of impact versus energy, i.e., the kinetic energy of the projectile ${\displaystyle E_{\text{k}}={\tfrac {1}{2}}mv^{2}}$)
• Impact occurring within a specific 10– to 30-millisecond portion of the cardiac cycle. This period occurs in the ascending phase of the T wave, when the ventricular myocardium is repolarizing, moving from systole to diastole (relaxation).

The small window of vulnerability explains why it is a rare event. Considering that the total cardiac cycle has a duration of 1 second (for a base cardiac frequency of 60 beats per minute), the probability of a mechanical trauma within the window of vulnerability is 1 to 3 percent only. That also explains why the heart becomes more vulnerable when it is physically strained by sports activities:

1. The increase in heart rate (exercise tachycardia) may double the probability above (e.g., with 120 beats per minute the cardiac cycle shortens to 500 milliseconds without fundamentally altering the window-of-vulnerability's size)
2. Relative exercise-induced hypoxia and acceleration of the excitoconductive system of the heart make it more susceptible to stretch-induced ventricular fibrillation.[8]

The cellular mechanisms of commotio cordis are still poorly understood, but probably related to the activation of mechanosensitive proteins, ion channels. These trigger extra electrical excitation waves which, if occurring right at the trailing edge of a previous electrical cycle, can give rise to ventricular fibrillation.[9] Since the trailing edge of the preceding electrical cycle travels over the ventricular surface, the critical window for mechanical induction of ventricular fibrillation varies locally - i.e. the commotio cordis risk window exists in time and in space.[9] This helps to explain why precordial impacts tend to have benign consequences.

Impact energies of at least 50 joules (37 ft⋅lbf) are estimated to be required to cause cardiac arrest, when applied in the right time and spot of the precordium of an adult.[6] Impacts up to 130 joules (96 ft⋅lbf) have already been measured with hockey pucks and lacrosse balls, 450 joules (330 ft⋅lbf) in karate punches, and 1,028 joules (758 ft⋅lbf) in boxer Rocky Marciano's punch.[10] The 50-joule threshold, however, can be considerably lowered when the victim's heart is under ischemic conditions, such as in coronary artery insufficiency.[6]

Also an upper limit of impact energy is applied to the heart; too much energy will create structural damage to the heart muscle, as well as causing electrical upset. This condition is referred to as contusio cordis (from Latin for bruising of the heart). On isolated guinea pig hearts, as little as 5 mJ were needed to induce release of creatine kinase, a marker for muscle cell damage.[11] Obviously, this figure does not include the dissipation of energy through the chest wall, and is not scaled up for humans, but it is indicative that relatively small amounts of energy are required to reach the heart before physical damage is done.[12]

The risk would probably be reduced by improved coaching techniques, such as teaching young batters to turn away from the ball to avoid errant pitches, according to doctors. Defensive players in lacrosse and hockey are now taught to avoid using their chest to block the ball or puck. Starting in 2017, high school lacrosse players are penalized, and play stopped immediately, if they enter their own goal crease with the apparent intent of blocking shots or acting as goalkeeper.[13]

Chest protectors and vests are designed to reduce trauma from blunt bodily injury, but this does not offer protection from commotio cordis and may offer a false sense of security. Almost 20 percent of the victims in competitive football, baseball, lacrosse and hockey were wearing protectors. This ineffectiveness has been confirmed by animal studies. Development of adequate chest protectors may prove difficult.[3]

Defibrillator training kit

Automated external defibrillators and prompt CPR have helped increase the survival rate in recent years to 58%. CPR and Defibrillation must be started as soon as possible (within 3 minutes) for maximal benefit.[1] Commotio cordis is the leading cause of fatalities in youth baseball in the US, with two to three deaths per year.[14] It has been recommended that "communities and school districts reexamine the need for accessible automatic defibrillators and cardiopulmonary resuscitation-trained coaches at organized sporting events for children."[15]

Several people have been charged and convicted for deaths of victims of commotio cordis, even when the blows rendered were never given with an intent to kill.[16] In 1992, Italian hockey player Miran Schrott died after a blow to his chest from the stick of Italian-Canadian player Jimmy Boni. Boni was charged with culpable homicide, and eventually pleaded guilty to manslaughter, paying a $1,300 fine and $175,000 restitution to Schrott's family.[17]

• Pulmonary contusion
• Touch of Death
• Commotio thoracis
• R-on-T phenomenon

• Yabek, S.M. Commotio cordis. eMedicine, September 2005.