Journal of Emergencies, Trauma, and Shock
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Year : 2018  |  Volume : 11  |  Issue : 3  |  Page : 225-227
An unusual case of commotio cordis resulting in ventricular flutter

Division of Pediatrics Cardiology and Cardiac Surgery, Connecticut Children's Medical Center, University of Connecticut, Connecticut, USA

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Date of Submission20-Jul-2017
Date of Acceptance08-Jun-2018
Date of Web Publication01-Oct-2018


A 16-year-old male developed palpitations immediately following chest impact with a soccer ball. The patient was noted to have ventricular flutter in a delayed presentation that was successfully treated. While ventricular fibrillation is the predominant arrhythmia following commotio cordis, ventricular flutter may occur as well. Ventricular flutter may be better tolerated in a young athletic individual with structurally normal heart and may lead to a delayed presentation.

Keywords: Commotio cordis, palpitations, ventricular flutter

How to cite this article:
Davey BT, Quintana C, Upadhyay S. An unusual case of commotio cordis resulting in ventricular flutter. J Emerg Trauma Shock 2018;11:225-7

How to cite this URL:
Davey BT, Quintana C, Upadhyay S. An unusual case of commotio cordis resulting in ventricular flutter. J Emerg Trauma Shock [serial online] 2018 [cited 2021 Apr 20];11:225-7. Available from:

   Introduction Top

Commotio cordis refers to sudden cardiac arrest after direct chest impact.[1],[2] Most impacts occur in competitive sports, with some reports during recreational activities and violent altercations.[2],[3] Although early recognition and cardiopulmonary resuscitation improve survival, commotio cordis remains a potentially fatal condition. This report describes an interesting case of an adolescent male with commotio cordis resulting in ventricular flutter with delayed presentation to medical attention.

   Case Report Top

A previously healthy 16-year-old male was hit in the center of his chest with a soccer ball from 20 feet away while playing competitive soccer. He immediately developed palpitations and stopped play for several minutes to recover. He returned to play despite persistent palpitations and made a penalty kick, but did not return to baseline. He subsequently developed diaphoresis, shortness of breath, lethargy, nausea, and emesis and then presented to the emergency department 8 h after the event.

The patient had no prior history of syncope, palpitations, exercise intolerance, or recent illness. His family history was negative for congenital heart disease, arrhythmias, cardiomyopathy, and sudden death. He denied alcohol and cocaine exposure, but reported marijuana use 3 weeks prior. He took a friend's lisdexamfetamine pill that morning to concentrate on studying for a test.

Physical examination revealed an ill, pale-appearing patient with normal mental status and no external signs of trauma. He had “cyanotic lips” and felt cool and clammy. His heart rate (HR) was 225–240 beats per minute (bpm) and blood pressure (BP) was 160/100 mmHg with 100% oxygen saturation. An electrocardiogram (ECG) demonstrated ventricular flutter at 227 bpm, prompting administration of amiodarone 150 mg intravenous over 10 min [Figure 1]. Hemodynamic instability with a hypotension to 95/64 mmHg and altered mental status prompted rapid sedation and analgesia with midazolam and fentanyl and then external direct current cardioversion with 125 Joules. Sinus rhythm returned with a HR of 86 bpm and BP of 106/67 mmHg.
Figure 1: This image demonstrates the patient's electrocardiogram upon presentation to the emergency department. Ventricular flutter with a rate of approximately 230 bpm is noted

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An amiodarone drip of 1 mg/min was initiated with transfer to the Connecticut Children's Medical Center. Transthoracic echocardiography demonstrated normal ventricular systolic function, no pericardial effusion or regional wall motion abnormalities, and normal coronary artery origins. No further ectopy or tachyarrhythmia was appreciated by telemetry and subsequent Holter monitoring of amiodarone. A follow-up ECG demonstrated sinus arrhythmia with no ventricular preexcitation and normal QTc interval [Figure 2]. An exercise stress test demonstrated no arrhythmia at peak exercise or during recovery. The patient was permitted to return to sports with a chest protector. There were no further events or symptoms at more than 1 year of follow-up. He was strongly discouraged to use any stimulant medications.
Figure 2: This electrocardiogram after recovery demonstrates sinus arrhythmia with sinus bradycardia at 52 bpm, PR interval of 183 ms, QRS duration of 94 ms and QTc interval of 428 ms and early repolarization pattern

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   Discussion Top

Commotio cordis is the second most common cause of sudden death in young male athletes after hypertrophic cardiomyopathy.[2],[4] The most frequent arrhythmia described is ventricular fibrillation leading to sudden death on initial presentation.[5],[6] Victims typically collapse upon impact; 20% of patients remain conscious for several seconds and very few present minutes or hours after impact.[7],[8],[9]

Increased chest wall compliance and altered repolarization patterns play a role in commotio cordis pathophysiology. Determinants of injury include precordial location, repolarization phase, projectile density, and impact velocity (30–50 miles/h).[4],[6] The vulnerable phase of repolarization occurs 10–20 ms before peak of the T wave [2] [Figure 3]. Studies suggest that transmitted impact force causes myocardial ion channel upregulation and massive ion influx leading to arrhythmias such as ventricular fibrillation. Poor cerebral and myocardial perfusion cause immediate collapse. Dense-core, hard and small projectiles such as baseball, hockey and lacrosse balls have a higher incidence of ventricular fibrillation and increased morbidity compared to hollow objects.
Figure 3: The vulnerable phase of repolarization occurs 10–20 ms before peak of the T wave when a chest wall impact can lead to dangerous arrhythmias

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Ventricular fibrillation is the most common mechanism of cardiac arrest following commotio cordis, although other arrhythmias including ventricular tachycardia, complete heart block, asystole, supraventricular tachycardia, and atrial fibrillation are reported.[5],[9],[10] Delayed presentation of commotio cordis is uncommon.[8] While our patient experienced palpitations immediately after impact, he did not demonstrate hemodynamic compromise until receiving amiodarone. This may be because ventricular flutter at a relatively slower rate of 225–240 bpm is more stable compared to ventricular fibrillation.

Stimulant medications have been attributed to sudden cardiac arrest.[11] Lisdexamfetamine has not been specifically reported with cardiac arrest; however, it carries an Food and Drug Administration warning regarding such.[12] It may potentiate arrhythmia mechanisms in patients with previously undiagnosed arrhythmias. A primary role of lisdexamfetamine in this patient's arrhythmia cannot be excluded, but is unlikely with no risk factors and the temporal association of symptoms to chest impact.

The gold standard for primary prevention of commotio cordis is avoidance of chest wall impacts. Although chest protectors can lower the risk of ventricular fibrillation compared to impacts without chest protectors, the quality of the product varies and the use does not eliminate the risk of commotio cordis.[13] In addition, softer equipment such as “safety baseballs” also lower the risk of ventricular fibrillation but fail to eliminate the risk.[14] Early access to automated external defibrillators improves survival rates, but survival remains as low as 25% despite resuscitation within 3 min.[15]

   Conclusion Top

Commotio cordis is a rare, dreadful event following precordial impact with a high velocity projectile, typically resulting in ventricular fibrillation and immediate collapse. Rapid identification and resuscitation are the key to survival; nonetheless, the survival rate is low. Only 4% of projectile-related deaths are associated with air-filled balls. In this unique case, an air-filled ball induced an arrhythmia which allowed for preserved perfusion with delayed presentation to medical attention. Any palpitations following chest injury require immediate medical attention.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Link MS, Maron BJ, VanderBrink BA, Takeuchi M, Pandian NG, Wang PJ, et al. Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis. J Am Coll Cardiol 2001;37:649-54.  Back to cited text no. 1
Maron BJ, Estes NA 3rd. Commotio cordis. N Engl J Med 2010;362:917-27.  Back to cited text no. 2
Link MS. Pathophysiology, prevention, and treatment of commotio cordis. Curr Cardiol Rep 2014;16:495.  Back to cited text no. 3
Berkson D, Queller H, Holmes N, Yun DS, Sandella B, Sargent T, et al. Commotio cordis in a 17-year-old baseball catcher. Pediatr Cardiol 2010;31:689-92.  Back to cited text no. 4
Fujita S, Nakamura T, Koura U, Toga A, Ina S, Higashiyama H, et al. Commotio cordis presenting as a temporary complete atrioventricular block in a 2-year-old girl with congenitally corrected transposition of the great arteries. Pediatr Cardiol 2011;32:1043-7.  Back to cited text no. 5
Maron BJ, Gohman TE, Kyle SB, Estes NA 3rd, Link MS. Clinical profile and spectrum of commotio cordis. JAMA 2002;287:1142-6.  Back to cited text no. 6
Fox SA, Templeton C, Hancock-Friesen C, Chen R. Commotio cordis and ventricular pseudoaneurysm. Can J Cardiol 2009;25:237-8.  Back to cited text no. 7
Tome R, Somri M, Teszler CB, Yanovski B, Gaitini L. Delayed ventricular fibrillation following blunt chest trauma in a 4-year-old child. Paediatr Anaesth 2006;16:484-6.  Back to cited text no. 8
Ota K, Bratincsak A. Atrial fibrillation induced by commotio cordis secondary to a blunt chest trauma in a teenage boy. Pediatrics 2015;135:e199-201.  Back to cited text no. 9
Alp H, Baysal T, Karaarslan S. Supraventricular tachycardia due to blunt chest trauma in an adolescent. Ulus Travma Acil Cerrahi Derg 2014;20:211-3.  Back to cited text no. 10
Nissen SE. ADHD drugs and cardiovascular risk. N Engl J Med 2006;354:1445-8.  Back to cited text no. 11
Cowles BJ. Lisdexamfetamine for treatment of Attention-Deficit Hyperactivity Disorder. Ann Pharmacother 2009;43:669-73.   Back to cited text no. 12
Kumar K, Mandleywala SN, Gannon MP, Estes NA 3rd, Weinstock J, Link MS, et al. Development of a chest wall protector effective in preventing sudden cardiac death by chest wall impact (Commotio cordis). Clin J Sport Med 2017;27:26-30.  Back to cited text no. 13
Link MS, Maron BJ, Wang PJ, Pandian NG, VanderBrink BA, Estes NA 3rd, et al. Reduced risk of sudden death from chest wall blows (commotio cordis) with safety baseballs. Pediatrics 2002;109:873-7.  Back to cited text no. 14
Palacio LE, Link MS. Commotio cordis. Sports Health 2009;1:174-9.  Back to cited text no. 15

Correspondence Address:
Dr. Brooke T Davey
Connecticut Children's Medical Center, 282 Washington Street, Hartford, CT 06016
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JETS.JETS_78_17

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