Commotio Cordis -- Sudden Cardiac Death With Chest Wall Impact

Christopher Madias, M.D.; Barry J. Maron, M.D.; Jonathan Weinstock, M.D.; N. A. Mark Estes III, M.D.; Mark S. Link, M.D.

Disclosures

J Cardiovasc Electrophysiol. 2007;18(1):115-122. 

In This Article

Pathophysiology

The likely cause of death in CC is VF initiated by a chest wall blow.[1,4,19,26] The mechanism of impact-induced VF is under investigation; however, development of an experimental swine model has shed substantial light on the pathophysiology of this phenomenon. Available evidence suggests that the underlying mechanism is multifactorial and requires the precise confluence of several determinants. The swine model attempts to mimic the clinical profile of CC and entails propelling impact objects (baseballs and lacrosse balls) at the chest wall of anesthetized juvenile swine. Release and subsequent impact of the object is gated to the cardiac cycle by a cardiac stimulator with triggering from the surface electrocardiogram.[19] The most significant finding that emerged from the initial experiments was that development of VF required the precise timing of chest wall impact. When chest wall impact occurred in a narrow window of the cardiac cycle-10-30 msec before the peak of the T wave—VF was consistently produced (Fig. 1).[4,19] VF was instantaneous and was not preceded by premature ventricular contractions, ST-segment changes, or heart block. Impacts during depolarization (on the QRS) frequently resulted in transient complete heart block.[3] Chest impacts occurring in other portions of the cardiac cycle did produce various electrophysiologic effects—including ST-segment elevation, premature ventricular contractions (PVC), and left bundle branch block—but never resulted in VF.[3,19] Angiography performed immediately after impact did not reveal any evidence of stenosis or spasm in epicardial coronary arteries. Myocardial perfusion imaging with technetium 99 m sestamibi performed after impact revealed only small, mild apical defects in a minority (25%) of the animals tested. Left ventriculograms and echocardiograms also performed immediately after impact revealed mild apical or distal septal hypokinesis in regions distant from the area of precordial impact. On pathologic examination, structural cardiac damage has not been observed with impact velocities of less than 50 mph.[19]

Six-lead electrocardiogram from an 11-kg swine undergoing a 30-mph chest wall impact with an object the shape and weight of a standard baseball. Ventricular fibrillation is produced immediately on impact within the vulnerable zone of repolarization (10-30 ms prior to the peak of the T wave).[22] Reprinted with permission from The American College of Cardiology Foundation.

In this model, several other factors have been identified as crucial to the development of VF. Using echocardiographic guidance, the importance of impact location directly over the anatomic position of the heart was revealed.[22] With an impact velocity of 30 mph, VF occurred most commonly with blows directly over the center of the cardiac silhouette (30% of impacts) versus those over the left ventricular base (13% of impacts) or apex (4% of impacts). Impacts at sites that did not overlay the heart did not result in VF or other electrophysiologic effects.

Our model also identified a relationship between the hardness of the impact object and the likelihood of inducing VF.[3,19,23] In an experiment designed to assess the effectiveness of safety baseballs in preventing VF, impact with softer baseballs was associated with a lower incidence of VF (Fig. 2). Finally, the importance of the velocity of chest wall impacts was also systematically evaluated.[21] Baseballs were propelled with velocities ranging from 20 to 70 mph and timed to impact on the vulnerable 20 ms window on the upstroke of the T wave. The incidence of impact velocity relative to incidence of VF exhibited a Gaussian relationship. The threshold velocity to cause VF was 25-30 mph, and as impact velocity increased, the incidence of VF rose to a peak of nearly 70% of impacts at 40 mph. At velocities ≥50 mph, however, the likelihood of VF decreased.[21] This observation is consistent with the clinical scenario of CC that occurs in youth baseball, where baseball velocities are estimated to range between 30 and 50 mph.[4]

The incidence of ventricular fibrillation in 8-12 kg swine undergoing 30 and 40 mph chest wall impacts. Safety baseballs of different hardness (Reduced Injury Factor [RIF]) are compared to impacts with a regulation Little League baseball. RIF 1 baseballs are the softest balls, marketed for use in T-Ball and by kids aged 4-7 years. RIF 5 and RIF 10 are intermediate in hardness and marketed for 8- to 10-year-olds and 11- to 13-year-olds, respectively. The * denotes P < 0.03 for the differences in incidence of ventricular fibrillation between the regulation baseball and the softest safety baseball at 30 mph impacts. The denotes P < 0.01 for the differences between the incidence of ventricular fibrillation, the regulation baseball, and the safety baseballs at 40 mph impacts. No differences were evident among the safety baseballs of different hardness.[23] Reprinted with permission from The American Academy of Pediatrics.

The importance of the hardness, location, and velocity of chest wall impacts in CC likely relates to the effects of these variables on induction of a critical left ventricular (LV) pressure that is necessary to induce VF. In the experiments of impact velocity, higher velocities correlated with the generation of greater peak instantaneous LV pressures. As with impact velocities, the risk of VF correlated with the LV pressure rise created by the chest wall blow in a Gaussian distribution (Fig. 3).[4,20,21] The highest incidence was evident with peak LV pressures of 250-450 mmHg and decreased with pressures above and below this range. Thus, these data suggest that there is a lower and upper limit of vulnerability of LV pressures resulting in VF, and that the instantaneous LV pressure rise produced by the chest blow mediates the electrophysiologic consequences of CC.

The probability of ventricular fibrillation relative to the peak left ventricular (LV) pressure and LV pressure over time (dP/dt) in 8-12 kg swine undergoing 30 mph chest wall impacts with a baseball. The data exhibit a Gaussian distribution (P < 0.0001 by logistic regression). The highest incidence of ventricular fibrillation was evident with peak LV pressures between 250 and 450 mmHg.[21] Reprinted with permission from The American College of Cardiology Foundation.

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