Commotio Cordis

Commotio cordis is sudden cardiac arrest, typically from ventricular fibrillation, caused by a blunt, non-penetrating blow to the chest, in the absence of structural cardiac injury.

Epidemiology. It is rare and mostly affects boys and young men aged 10 to 18 years, in baseball, softball, lacrosse, hockey, martial arts, cricket and other contact or projectile sports. Survival has improved to about 25 to 35% with early resuscitation and defibrillation.

Mechanism. A blow of about 30 to 50 mph delivered directly over the heart during a vulnerable window of repolarisation, 15 to 30 milliseconds before the peak of the T wave, produces ventricular fibrillation. Hard projectiles striking a pliable chest wall are the risk. Sites over the left ventricle are most dangerous.

Pathophysiology. The impact causes sudden left ventricular pressure rise, activating mechanosensitive ion channels (including ATP-sensitive potassium channels) and generating premature ventricular depolarisation that falls in the vulnerable period.

Presentation is sudden collapse within seconds of the blow, often without prior symptoms, with absent pulse and breathing, and pallor or cyanosis. Some patients have a brief period of apparent consciousness. Chest wall injury, rib fracture and cardiac contusion are generally absent.

Red flags.

• Collapse after a chest blow in sport, even when the blow appeared minor.
• Delay to defibrillation over 3 minutes.

Diagnosis is clinical by history. Rhythm monitoring shows ventricular fibrillation (sometimes asystole after prolonged arrest, or heart block). After return of circulation, do ECG, echocardiography, troponin, chest imaging and cardiac MRI to exclude structural disease, contusion, coronary injury or an underlying cardiomyopathy or channelopathy.

Differential diagnosis. Hypertrophic cardiomyopathy, long QT and Brugada syndromes, arrhythmogenic cardiomyopathy, myocarditis, coronary anomalies, blunt cardiac injury with contusion and heat illness.

Immediate. Recognise cardiac arrest, call for help, start chest compressions at 100 to 120/min and ventilations (30 to 2), and apply an automated defibrillator at once. Defibrillate for ventricular fibrillation (biphasic 150 to 200 J). Every minute of delay reduces survival by about 10%, and survival is highest if shock is delivered within 3 minutes.

Advanced life support. Continue compressions, adrenaline 1 mg IV every 3 to 5 minutes, amiodarone 300 mg IV after the third shock, and treat reversible causes. Children: shock 4 J/kg, adrenaline 10 microgram/kg.

After return of circulation. Post-cardiac arrest care: oxygen saturation 94 to 98%, normal carbon dioxide, mean arterial pressure over 65 mmHg, temperature control, 12-lead ECG, echocardiography and admission to intensive care.

Follow up. Full cardiac evaluation. Return to contact sport decided by cardiology after a normal assessment.

Prevention. Automated defibrillators and trained staff at sports venues, softer core balls for youth sport, appropriate protective chest equipment (modest effect), and training of coaches in resuscitation.

Monitoring. Rhythm for at least 24 to 48 hours, neurological observations, troponin and echocardiography.

Referral and escalation. Cardiology, sports medicine and intensive care. Genetic testing and family screening if a primary electrical disease is suspected.

Special groups. In children and adolescents, use paediatric dosing and pads sized for age.