Cardiac arrest and resuscitation of a 31-year-old healthy female in a 10km fun run.
Running events are increasingly popular, at times involving >50,000 participants with varying experience and fitness levels. Unfortunately, this twe of event is occasionally marred by the death of a participant due to sudden cardiac arrest (SCA) (1). Retrospective analysis of data from mass running events reveals that SCA occurs at a rate of 0.55 to 0.8 per 100,000 participants (2:3). Given the established risk of this potentially treatable condition, on-site medical services must be prepared to provide life saving cardiac interventions. This case report describes a successful finish line resuscitation and confirms the need for high-quality medical planning and response at mass gathering events.
The case occurred during a 10km run which attracted over 49,000 participants. A main medical tent at the finish line was staffed by pre-hospital providers, nurses, physicians, and allied health professionals. Two smaller tents and mobile response teams were located along the route, providing first-aid services. The finish line area was patrolled by medical providers who acted as spotters. Eight automatic external defibrillators (AEDs) were distributed throughout the course and advanced life support (A.LS) equipment and personnel were based in the main tent. In addition, the onsite medical team coordinated with the local ambulance service, which included mobile ALS providers.
The patient, a previously well 31-year-old female on no regular medications, collapsed 10 meters past the finish line. Although feeling well during the run, she became light-headed shortly after completing the race, and subsequently collapsed. Seizure-like activity was witnessed. A fellow runner trained in cardiopulmonary resuscitation (CPR) immediately began chest compressions. First-aiders at the scene requested AIS back-up from the finish line medical team. Within three minutes, the team arrived with an AEI). Analysis revealed a shockable rhythm (ventricular fibrillation), which was converted to sinus rhythm after a single shock (Figure 1). After one additional minute of CPR, there was return of spontaneous circulation as evidenced by a femoral pulse. Within five minutes, the patient began to awaken and was transported on a medical gator through the crowded finishing chute to a standby ambulance, and from there to a local hospital.
[FIGURE 1 OMITTED]
On arrival in the emergency department (ED), the initial electrocardiogram (ECG) showed sinus tachycardia at 106 beats/minute. The PR interval and QRS duration were normal at 138ms and 82ms. The a interval was prolonged at 488ms (Figure 2). Bloodwork re-vealed no electrolyte abnormalities. The patient was admitted to the Cardiac Care Unit for monitoring and investigation.
She remained hemodynamically stable and demonstrated no evidence of arrhythmia during her hospital stay. Daily EGGS revealed normalization of QTc interval to 421 to 434ms, and evolution of nonspecific T-wave inversion in the anterior leads. Cardiac magnetic. resonance imaging (MRI) confirmed the absence of structural cardiac abnormalities. Bruce protocol exercise test on Day 3 revealed a QT-interval that failed to shorten with exercise, leading to a relative lengthening of the QTc. The test duration was 13 minutes and 50 seconds with a maximum heart rate of 203 beats per minute and prolonged tachycardia with a heart rate of 139 beats per minute after an 11-minute recovery period.
A MedtronicTM implantable cardioverter defibrillator (ICD) was implanted on Day 5 and the patient was discharged home on Day 7. Genetic tests for the five most common long QT mutations were negative. There was no family history of cardiac disease or sudden unexplained death. All immediate family members subsequently underwent screening ECGs, which were normal. The patient has been maintained on beta-blockade and has experienced no further cardiac events or arrvthmias. She has returned to cautious aerobic activity
This case report highlights a successful resuscitation following a witnessed cardiac arrest at a mass gathering event. The most likely etiology for this patient's arrest was congenital long QT syndrome (LQTS) . LQTS refers to a group of disorders defined by delayed cardiac repolarization as manifested by a prolonged QT interval on ECG. individuals with LQTS are predisposed to a characteristic polymorphic ventricular tachycardia, torsade des pointes, which can degenerate to ventricular fibrillation and SCA. LQTS can result from congenital and/or acquired causes. See Table 1 for further detail (4). Congenital LQTS is caused by mutations in ion channels or related proteins that determine conduction of the cardiac action potential. Hundreds of mutations have been identified in at least 12 LQTS-susceptibility genes (5).
Table 1--Causes of Long QT Syndrome Congenital Acquired Inherited Metabolic chairnelopathies Roman o-Ward Hypocalcernia, Syndrome hypokalemia, hypomagnesemia Jervell and Lange-Nielsen Syndrome Idiopathic Anti-Arrytbmics Amiodarone, Diospyramide, Dofetilide, ibutilide, Quinidine, Procainamide, Sotalol Antibistarnines Asteinizole, Terfenidine Anti-Infectives Clan thromycin, Erythrornycin, Pentamidine, Sparfi oxcin Anti-Malarial Chioroquine, Halofantrinc Psychotropics Chiorprornazine, Flaloperidol, Thioridazone, SSRIs Heart Disease Left ventricular hvpertrop hy, heart failure, invocardial isehemia
Common presentations of LQTS include palpitations, presyncope, syncope, or cardiac arrest. In this population, cardiac events are commonly triggered by adrenergic stimuli such as exercise (6). The diagnostic approach to LQTS should include a detailed clinical history of the cardiac event, any history of palpitations or syncope, and a family history of SCA or unexplained deaths. Physical examination and cardiac imaging are important for ruling out structural causes. Prolongation of the QT interval on a resting ECG is the hallmark of LQTS. The upper limit of normal for the corrected QT interval among males is .450ms and .470ms among females (7). Exercise testing can be a useful adjunct as individuals with LQTS often fail to appropriately shorten their gic with exercise provocation compared with controls (8). Genetic testing for common LQTS mutations may aid in diagnostic and treatment decisions, however, in a number of patient with LQTS a mutation cannot be identified; negative genetic analysis does not rule out the diagnosis (9).
[FIGURE 2 OMITTED]
Published guidelines direct the management of patients with LQTS to reduce the risk of sudden cardiac death (10). Avoidance of QT-prolonging drugs and medications that could derange electrolytes is essential; however, the foundation of therapy is beta-blockers (BBs). BBs may exert reduced mortality for patients with LQTS by reducing adrenergic stimulation and therefore arrhythmia activity (6). ICDs are recommended for survivors of SCA and patients who continue to be symptomatic despite BB therapy (10).
The current case report describes resuscitation following SCA in the setting of LQTS. To our knowledge, this has not been previously documented at a mass running event. The timely delivery of CPR, early defibrillation, and the provision of advanced care was essential to the survival of this patient and illustrates the importance of rapid response, on-site medical services at such events.
Sheila Turns, NP, PhD, for her academic leadership and careful editing of this manuscript, as well as SportMedBC, Rockdoc Consulting, Inc., and the British Columbia Ambulance Service for their commitment to high quality care at mass gatherings in our region.
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(2.) Kim JH, Malhotra R, Chiampas G, d'Hemecourt P, Troyanos C, Cianca 5, et al. Cardiac arrest during long distance running races. N Ent,-Med 2012; 366:130-40.
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(4.) Van Noord C, Eijgelsheim M, Stricker BHC. Drug-and non-drug-associated QT interval prolongation. BrJ Clin Pbannacol. 2010; 70:16-23.
(5.) Kapa S,Tester DJ, Salisbury BA, Harris-Kerr C, Pungliya MS, Alders M, et al. Genetic testing for long-QT syndrome: Distinguishing pathogenic mutations from benign variants. Circulation. 2009;120:1752-60.
(6.) Goldenberg I, Zareha W, Moss AJ. Long QT syndrome. Curr Prob Cardiol. 2008; 33:629-94.
(7.) Moss AJ, Robinson JL. Long QT syndrome. Heart Dis Stroke. 1992; 1:309-14.
(8.) WongJA, Gula 1 j, Klein GJ,Yee R, Skanes AC, Krahn AD. Utility of treadmill testing and genotype prediction in long QT syndrome. arc Anhytinn Electrophysiol 2010; 3:120-5.
(9.) Roden DM. Long-QT syndrome.. N EngJ Med. 2008; 358:169-76.
(10.) Zipes DP, CammAJ, Borggefe M, Buxton AE, Chaitman B, Fromer NI, et aLACC/AHAJESC. 2006 guidelines for management of patients with ventricular arrhythmias and prevention of sudden cardiac death. Circulation. 2006; 8:746-837.
*Adam Lund, BSc, MI), MDE, FRCPC (a); Steven Skitch, BSc, PhD (b); Allison Chew, BEng(Comp), MPH, MD (c); Kerrie Lewis, LPN, EMR (d); Marc Alfonso, EMR (e)
a) Clinical Assistant Professor, Department of Emergency Medicine **
b) Medical Student **
c) Resident **
d) Project Manager, Mass Gathering Medicine Interest Group, Department of Emergency Medicine **
e) Outdoor Emergency Care (OEC) Technician
* Corresponding Author: email@example.com
** University of British Columbia, Vancouver, British Columbia, Canada All authors attest that they have no conflicts of interest to disclose related to the submitted case report.
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|Author:||Lund, Adam; Skitch, Steven; Chew, Allison; Lewis, Kerrie; Alfonso,Marc|
|Article Type:||Clinical report|
|Date:||Jun 22, 2012|
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