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How to recognise sudden cardiac arrest on the pitch
  1. Jelle SY de Jong1,
  2. Harald T Jorstad1,
  3. Roland D Thijs2,
  4. Ruud W Koster1,
  5. Wouter Wieling3
  1. 1Clinical and Experimental Cardiology, Amsterdam UMC - Locatie AMC, Amsterdam, The Netherlands
  2. 2Neurology, Leiden University Medical Center, Leiden, The Netherlands
  3. 3Internal Medicine, Amsterdam UMC - Locatie AMC, Amsterdam, The Netherlands
  1. Correspondence to Mr Jelle SY de Jong, Clinical and Experimental Cardiology, Amsterdam UMC - Locatie AMC, Amsterdam 1105 AZ, The Netherlands; j.s.dejong{at}amsterdamumc.nl

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Sudden cardiac arrest (SCA), which occurs at a rate of about 1 in ~50 000 athlete years, is the most common cause of death in exercising young athletes.1 SCA is most frequently caused by lethal cardiac arrhythmias—that is, ventricular fibrillation (VF). If clinicians recognise key features of SCA early and accurately, they can immediately begin cardiopulmonary resuscitation (CPR) and use an automated external defibrillator (AED) as needed.2 This review aims to (1) assist health professionals recognise the signs (and avoid common pitfalls) of SCA and (2) emphasise best practice responder strategies for SCA on the pitch.

Case example of SCA

Miklos Feher, a striker for Benfica, suffered a SCA on 25 January 2004. The event can be viewed at: https://youtu.be/T7-kKy_XDQU. The underlying cause of death was later reported to be VF in a patient with hypertrophic cardiomyopathy.

Clinical question

How can clinicians and sports professionals rapidly recognise SCA on the field of play? Recognising SCA on the pitch can be challenging due to the sports setting, other mimicking causes and the rapid onset of signs following cerebral hypoperfusion. To prevent death or serious sequelae, it is key that clinicians recognise SCA immediately and start adequate management (ie, CPR and defibrillation).

Clinical features of SCA

Figure 1 is a schematic of SCA from time T=0–60 s with corresponding signs, ECG, blood pressure tracing and breathing pattern. Prolonged, sudden cerebral hypoperfusion causes a typical …

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Footnotes

  • Correction notice This article has been corrected since it published Online First. The first author's name has been amended.

  • Contributors All authors made substantial contributions to the conception or design of the work, drafted the work or revised it critically for important intellectual content, gave final approval of the version published, agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests HTJ reports grants from Amsterdam Movement Science, NOC*NSF, outside the submitted work. RDT reports grants from Dutch National Epilepsy Fund, grants from The Netherlands Organisation for Health Research and Development (ZonMW), grants from NUTS Ohra Fund, grants from Medtronic, grants from Christelijke Vereniging voor de Verpleging van Lijders aan Epilepsie, The Netherlands, grants from AC Thompson Foundation, personal fees from Medtronic, personal fees from UCB, personal fees from GSK, outside the submitted work.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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