cardiac concussion

 

Baseball

Source: Wikipedia

 

Cardiac concussion (or commotio cordis) was first described in the 1930s, and now accounts for 5-10 cases each year in the USA. A registry of deaths and ‘near misses’ operates, with 140 cases being reported in 5 years. No such registry operates in the UK.

Cases recorded in the US indicate a mean age of 14 years, with boys being over-represented. This probably reflects the circumstances in which deaths from cardiac concussion occur;

  • sudden death in young athletes
  • with trivial non-penetrating impacts to anterior chest
  • leaving no visible trauma
  • in which resuscitation attempts unsuccessful despite early cardioversion (survival now approx 15% due to rapid defibrillation)
  • no pathological changes are seen
  • no cardiac enzyme rise is noted (although studies have not looked at cardiac Troponins)

Chest protector for 'Little League baseball'

Source: Baseball Bargains

mechanism

 

Animal research using ECG/ cardiac cycle gated impact studies (Link 1998; Link 2003) show that an impact directly over precordium at >30mph gives rise to increasing risk of VF (30% at 30 mph, 70% at 40 mph), where the impact occurs at a particularly vulnerable part of the cycle (30ms prior to T wave peak).

 

ECG trace indicating the vulnerable window in commotio cordis

Source: Wikipedia

 

Cardiac concussion involves absorption of mechanical energy from a blunt impact as harmonic oscillations which are dampened out and converted to heat. A small part of the imparted kinetic energy may be converted to electrical impulses (Hirsch and Adams 1993)

A thump in the cardiac cycle at other times gives rise to ST elevation and transient heart block.

Researchers believe the mechanism is multifactorial, with premature ventricular depolarisation acting as the trigger, but there being a change in the myocardial substrate allowing this trigger to bring about the devasating effect. Experiments indicate that the substrate change is not vagal inhibition, but it could be a rise in left ventricular pressure or the activation of stretch activated channels (potassium and others) (Koehler et al; Maron et al).

In addition, the effect of K/ATP channels (which are responsible for ST elevation and contribute to risk of VF in ischaemia) have received much interest, as their blocker (glibenclamide) reduces ST elevation and the incidence of VF following induced chest blows.

The clinical corollary of this is the ‘R on T phenomenon’ (VF caused by premature ventricular contractions falling on vulnerable portion of T wave, in ischaemic conditions (acute MI/ coronary ischaemia) but not non-ischaemic conditions such as continuous ventricular pacing).

Interestingly, cardiac arrest protocols still include the ‘precordial thump’ in some situations, such as witnessed arrest. Guidance on its use confirms that the action can convert pulseless VT to a perfusing rhythm, with the termination of VF being less common. However, it can also convert bradycardic rhythms or VT with pulse to pulseless VT or VF, accelerated VT or complete heart block – therefore it is only recommended for the pulseless person whose rhythm is being monitored (Australian Resuscitation Council).

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