Diagram showing the portion of normal sinus rhythm during which<unk>  is a risk These factors influence the chance of<unk> : * 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 ) * 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: # 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) # Relative exercise-induced hypoxia and acceleration of the excitoconductive system of the heart make it more susceptible to stretch-induced ventricular fibrillation. The cellular mechanisms of<unk>  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. 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<unk>  risk window exists in time and in space. This helps to explain why precordial impacts tend to have benign consequences. Impact energies of at least are estimated to be required to cause cardiac arrest, when applied in the right time and spot of the precordium of an adult. Impacts up to have already been measured with hockey pucks and lacrosse balls, in karate punches, and in boxer Rocky Marciano's punch. The 50-joule threshold, however, can be considerably lowered when the victim's heart is under ischemic conditions, such as in coronary artery insufficiency. 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<unk>  (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. 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.
Commotio cordis
Grisi siknis
Torus palatinus
Caput Medusae
Dolichonychia
Caput medusae
Pleurothotonus
Epiphora 