Commotio cordis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2]Cafer Zorkun, M.D., Ph.D. [3]


Typically, arrhythmic deaths are caused by a low/mild force striking the chest wall, a condition known as Commotio Cordis. Many of those suffering from this condition are athletes between the ages of 8 and 18 and play sports that involve projectiles, such as baseball, hockey pucks, and lacrosse balls. When a hand strikes in martial arts, its force can alter its rhythm, causing it to become arrhythmic. If a projectile strikes the athlete's heart in the middle of their chest with a low impact but is sufficient to cause their heart to become arrhythmic, it can also cause the athlete's heart to become arrhythmic. In the case of commotio cordis, a poor prognosis is associated with failure to provide immediate CPR and defibrillation. This is a hazardous condition that has a very low survival rate.


  • Commotio cordis occurs due to sudden blunt force trauma to the chest, causing sudden death without damage to the heart. It does not occur simply by striking the chest. The blow must occur just at the right time during the heartbeat and must hit close to the left ventricle.
  • In the event of an impulsive blow to the chest, you may suffer from hypertension, in which the lower chambers of your heart beat abnormally fast. This may be dangerous if you are struck again, in the same manner, a few minutes later.
  • Commotio cordis should be distinguished from a condition called a cardiac contusion, which occurs when a blunt strike to the chest damages the structural heart structures. Motor vehicle accidents are an example of such a case. [1]

There are many possible causes of commotio cordis, including the impact of being hit by an object:[2]

  • baseball
  • hockey puck
  • lacrosse ball
  • softball

The following factors increase the chance of commotio cordis[3][4]:

  • Direction of impact over the precordium (precise area, angle of impact)
  • Total applied energy (area of impact versus energy, i.e., speed of the projectile multiplied by its mass)
  • Impact occurring within a specific 10-30 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 1000 milliseconds (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% only. That explains also why the heart becomes more vulnerable when it is physically strained by sports activities:

  • The increase in heart frequency (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 windows of vulnerability size)
  • Relative exercise-induced hypoxia and acceleration of the excito- conductive system of the heart make it more susceptible to stretch-induced ventricular fibrillation.

The cellular mechanisms of commotio cordis are still poorly understood, but probably related to the activation of mechano- sensitive proteins, ion channels.

It is estimated that impact energies of at least 50 joules are required to cause cardiac arrest, when applied in the right time and spot of the precordium of an adult. Impacts of up to 130 joules have already been measured with hockey pucks and lacrosse balls, 450 joules in karate punches and an incredible 1028 joules in boxer Rocky Marciano's punch. The 50 joules threshold, however, can be considerably lowered when the victim's heart is under ischemic conditions, such as in coronary artery insufficiency[5].

There is also an upper limit of impact energy 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 was needed to induce release of creatine kinase, a marker for muscle cell damage.[6] Obviously one should take into account that 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.


  1. Quinn TA, Jin H, Lee P, Kohl P (August 2017). "Mechanically Induced Ectopy via Stretch-Activated Cation-Nonselective Channels Is Caused by Local Tissue Deformation and Results in Ventricular Fibrillation if Triggered on the Repolarization Wave Edge (Commotio Cordis)". Circ Arrhythm Electrophysiol. 10 (8): e004777. doi:10.1161/CIRCEP.116.004777. PMC 5555388. PMID 28794084.
  2. Abrunzo TJ (November 1991). "Commotio cordis. The single, most common cause of traumatic death in youth baseball". Am J Dis Child. 145 (11): 1279–82. doi:10.1001/archpedi.1991.02160110071023. PMID 1951221.
  3. Geddes LA, Roeder RA. Evolution of our knowledge of sudden death due to commotio cordis. Am J Emerg Med. 2005 Jan;23(1):67-75. Review. PMID 15672341
  4. Kohl P, Nesbitt AD, Cooper PJ, Lei M. Sudden cardiac death by Commotio cordis: role of mechano-electric feedback. Cardiovasc Res. 2001 May;50(2):280-9. Review. PMID 11334832
  5. Kohl P, Sachs F & Franz M (eds): Cardiac Mechano-Electric Feedback and Arrhythmias: from Pipette to Patient. Elsevier (Saunders), Philadelphia 2005 ISBN 9781416000341
  6. Cooper PJ, Epstein A, Macleod IA, Schaaf ST, Sheldon J, Boulin C, Kohl P. Soft tissue impact characterisation kit (STICK) for ex situ investigation of heart rhythm responses to acute mechanical stimulation. Prog Biophys Mol Biol. 2006 Jan-Apr;90(1-3):444-68. Review. PMID 16125216

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