Resus: Commotio Cordis
On January 2, 2023, the world was dismayed when a routine football game ended with a player in critical condition after entering cardiac arrest on the field due to a hit to the chest. The culprit broadcasted on various news stations was Commotio Cordis, its Latin translation meaning “agitation of the heart”. Most cases that are reported today are seen in young male athletes. The aim of this post is to bring awareness to the pathophysiology, epidemiology, and current recommendations for management and preventative measures that can be taken to prevent this potentially fatal event.
Commotio cordis (CC) is defined as a sudden blow to the precordial chest during ventricular repolarization resulting in ventricular fibrillation (VF) and cardiac arrest in a patient with no predisposed structural cardiac condition and/or no cardiovascular history [1]. The blow is considered “low-energy” as described in a study done in 1998 [2]. In this study, young pigs were used as experimental models while impact to the chest wall was created using a wooden object identical in size and weight of a baseball thrust at 30 mph at specific timings of the cardiac cycle. Ten of the impacts recorded occurred during the ECG upstroke before the peak of the T wave in the cycle and each of these impacts produced VF. Impacts at other instances of the cardiac cycle did not produce VF. Furthermore, the study shows that hits later in the cardiac cycle could result in complete heart block, ST segment elevation, or left bundle branch block, which would all notably be seen on ECG. Figure 1 shows electrocardiogram leads of these impacts causing VF. This study was the first to demonstrate the mechanism of CC and since has been unceasingly referred to as a baseline model of its pathophysiology.
When it comes to those who are at risk for CC and how often this occurs, the national US Commotio Cordis Registry can be consulted, which has been aggregating information since 1997. Less than 30 cases are reported per year with 95% of the cases occurring in boys with a mean age of 15 years [1]. The increased incidence in younger age is due to their thinner chest, allowing more force and energy to be transferred to the myocardium of the heart. CC is second in frequency, behind hypertrophic cardiomyopathy, as a cause of sudden cardiac death in athletes [3,4]. An article published in 2013 by BJ Maron, which is the principle investigator of CC, discusses the risk factors of CC. It mentions that while there seems to be the commonality of young male athletes, there also seems to be a racial component [5]. Survival rate in African Americans is lower due to delayed resuscitation being more common in this population. This same article discussed environment as another risk factor. Specifically, athletes who partake in unorganized, recreational sports had less survivors, presumably due to the lack of a specialized medical team with an AED on standby.
Interestingly enough, we can also take the size and shape of the object itself into consideration when it comes to risk factors causing CC. A study performed by Kalin et al in 2011 evaluated the incidence of VF when projecting flat and smaller diameter spherical objects at a similar swine model as used in the previous study that determined CC pathophysiology [6]. The objects projected were all the same weight, but consisted of a flat object, and 2 round spheres at 42 and 72 mm in diameter to represent a golf ball and base ball, respectively. Velocity and timing of the cardiac cycle were kept constant during projection. The flat object did not produce a single episode of VF. The smaller sphere created more instances of VF than the larger, but the authors state this difference was not statistically significant. It was concluded that smaller diameter objects create a greater rise in left ventricular pressure, providing a favorable setup for VF. Figure 2 shows a graphical representation of this information.
With the vast knowledge and research that has developed over time, with much to owe to BJ Maron and his team of investigators, we have become better equipped at understanding the pathophysiology and epidemiology of CC. Using this, we can be more prepared with plans and resources in place for resuscitation when needed in susceptible populations. The survival rate of CC is based strictly on the immediate recognition of cardiac arrest, followed by quick defibrillation [7]. The primary reason for mortality is a delay in defibrillation and resuscitation. Studies in the 1990’s showed survival rates as low as 10-15%, giving the impression that CC was expected to be fatal. However, due to education on prompt resuscitation and increasing availability and use of AED’s, a study in 2013 has shown a 5 fold increase in survival [8]. Figure 3 below shows a representation of the increasing survival rate over recent years.
Figure 3.
CC victims should undergo a complete cardiac work up to rule out any other cause of their ventricular fibrillation and subsequent cardiac arrest, such as a congenital heart condition [9]. This testing could include ECG, echocardiogram, stress testing, ambulatory ECG, or others depending on what the physician deems necessary. Testing for long QT syndromes or Brugada syndrome is also applicable. If the patient has experienced true CC, no other cause will be found, and if the patient has a benign ECG and PE, they will likely have a benign clinical course [9]. Given how many variables it takes for CC to occur, it is unlikely that all of those variables could occur randomly a second time, making repeat instances unlikely. However, patients should be monitored for future dysrhythmias [7].
Prevention of CC has proven difficult with failure of chest protection in preventing fatal dysrhythmias according to studies and data from the national registry [10]. Despite lack of prevention, survival rates are on the rise, now over 50% [1], due to increasingly effective education and availability of medical personnel and AED’s at sporting events. BJ Maron states that these events can be a source of tragedy for the public [5], and with an event recently broadcasted on television, it can be expected that there will be a surge in education and training of recognition and management of cardiac arrest due to Commotio cordis.
POST BY: SARAH POWELL (MS4)
FACULTY EDITING BY: COLIN MCCLOSKEY, MD
References
Tainter CR, Hughes PG. Commotio Cordis. (2022). In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; PMID: 30252270.
Link, MS., et al. An Experimental Model of Sudden Death due to Low-Energy Chest-Wall Impact (Commotio Cordis). New Engl J Med. 1998;338: 1805-1811.
Westreich R, Haim M, Bereza S, Konstantino Y. Commotio Cordis: Indeed? (2019). JACC Case Rep,1(4):597-601. DOI: 10.1016/j.jaccas.2019.09.010.
Semsarian C, Sweeting J, Ackerman MJ. Sudden cardiac death in athletes. BMJ. 2015; 350.
Maron BJ. Sudden death in young athletes. New Engl J Med. 2003; 34: 1064-75.
Kalin J, Madias C, Alsheikh-Ali AA, Link MS. Reduced diameter spheres increases the risk of chest blow–induced ventricular fibrillation (commotio). Heart Rhythm 2011;8:1578–1581.
Bock JS., Benitez, RM. Blunt Cardiac Injury. Cardiology Clinics. 2012; 30: 545-555
Maron BJ, et al. Increasing Survival Rate from Commotio Cordis. Heart Rhythm. 2013; 10: 219-223.
Link MS, Estes III M, Maron BJ. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 13: Commotio Cordis. J Am Coll Cardiol. 2015; 66: 2439-43.
Doerer JJ, Haas TS, Estes III M, Link MS, Maron BJ. Evaluation of Chest Barriers for Protection Against Sudden Death Due to Commotio Cordis. Am J Cardiol. 2007; 99: 857-859.