Clinical paperVentricular fibrillation waveform measures and the etiology of cardiac arrest☆
Introduction
Resuscitation following cardiac arrest is challenging and relies on a coordinated set of rescuer actions described by the links in the chain of survival.1 Typically there is a standard resuscitation protocol. This protocolized approach specifies the selection, dose, and timing of therapies and potentially belies the heterogeneity of arrest etiology and acute time-sensitive physiology.2, 3, 4 In ventricular fibrillation, the etiology of arrest is often attributed to either acute ischemia or non-ischemic arrhythmia.5, 6, 7, 8 Among acute ischemic arrests, some are caused by complete epicardial coronary artery occlusion sometimes manifesting as ST elevation myocardial infarction (STEMI), while others result from other presentations of critical coronary ischemia manifesting as non-STEMI.6, 7, 8 Currently there are no diagnostic tools to distinguish such etiologies of arrest during active resuscitation. Moreover, even after a patient achieves return of spontaneous circulation (ROSC), the 12 lead electrocardiogram (ECG) may not reliably discriminate the underlying etiology of arrest.6, 7, 8 Thus, a real-time appreciation of the cardiac arrest etiology could have implications for resuscitation therapy. Although ventricular fibrillation appears as a chaotic and disorganized rhythm, characteristics of the ventricular fibrillation waveform such as amplitude, frequency, and organization can be systematically quantified in real-time. These measures have correlated with arrest physiology and are strongly related to clinical outcome.9, 10, 11 Evidence from animal studies indicates that ventricular fibrillation waveform measures are differentially affected by ischemia such that these waveform measures may differ at the outset or over the course of resuscitation.12, 13, 14 We undertook a study of clinical ventricular fibrillation arrest to assess whether quantitative measures of the ventricular fibrillation waveform can distinguish among STEMI, non-STEMI, and non-ischemic etiology of arrest.
Section snippets
Methods
We conducted a retrospective investigation of Emergency Medical Services (EMS)-treated ventricular fibrillation cardiac arrest occurring among persons 18 years or older between January 1st, 2006 and December 31st, 2014 in greater King County, WA. Since the investigation aimed to evaluate the relationship between quantitative waveform measures and the etiology of arrest, we used a convenience sample restricted to cases with an adequate EMS defibrillator recording, defined as a minimum 5-second
Results
During the study period, King County EMS agencies treated 1655 cardiac arrest patients who presented with ventricular fibrillation, did not have a public access defibrillator applied, and had a defibrillator that enabled CPR detection. Of these, 580 died in the pre-hospital setting or in the emergency department. Of the remaining 1075, 645 were excluded for reasons including lack of a 5-second, CPR-free ECG epoch prior to the first shock, missing defibrillator recording, technical difficulties
Discussion
In this clinical study of out-of-hospital ventricular fibrillation, we compared whether four quantitative waveform measures could distinguish the etiology of cardiac arrest. The study compared clinically-relevant etiology groups to include ACS consistent with STEMI, ACS consistent with non-STEMI, and non-ischemic causes of arrest given the potential for distinct strategies for resuscitation or post-resuscitation care. We did not observe clinically-meaningful differences according to etiology
Conflict of interest statement
The authors have no disclosures regarding this investigation.
Role of the funding source
The study was funded in part by the Laerdal Foundation, Life Sciences Discovery Foundation, and Philips Inc. These organizations had no role in the design, data acquisition, evaluation, interpretation, presentation, or decision to submit for publication.
Acknowledgements
The authors are grateful for the dedication and skills of the emergency dispatchers and EMS providers of King County, WA.
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Cited by (10)
The effect of the localisation of an underlying ST-elevation myocardial infarction on the VF-waveform: A multi-centre cardiac arrest study
2021, ResuscitationCitation Excerpt :Setting and population: We studied patients ≥ 18 years with a presumed cardiac cause of OHCA and VF as first observed rhythm, transported to the hospital. Only transported patients are included, to establish a reliable diagnosis of STEMI and its localisation using hospital diagnostics such as cardiac biomarkers or coronary angiography (CAG) findings.15,16,24 Exclusion criteria were: no (analysable) VF-tracing or insufficient clinical information to determine STEMI-status and its localisation, or a STEMI not involving the anterior or inferior myocardial wall (e.g. isolated posterior or isolated lateral STEMI), in accordance with a previous study.19
Coronary angiography findings in patients with shock-resistant ventricular fibrillation cardiac arrest
2021, ResuscitationCitation Excerpt :In a previous report from our registry, we studied all, non-selected OHCA-cases and found survival to discharge rate of 15%.32 Importantly, the present data corroborate with previous studies using similar inclusion criteria.33,34 Second, we defined shock-resistant VF according to the number of defibrillation shocks, in line with previous studies.35
European Resuscitation Council Guidelines 2021: Adult advanced life support
2021, ResuscitationCitation Excerpt :This technology is under active development and investigation, but current sensitivity and specificity are insufficient to enable introduction of VF waveform analysis into clinical practice. Although one large RCT,171 and 20 observational studies172–191 published since the 2010 guidelines review 140,141 have shown promise and some improvements in this technology, there remains insufficient evidence to support routine use of VF waveform analysis to guide the optimal timing for a shock attempt.1,104 Biphasic waveforms are now well established as a safe and effective waveform for defibrillation.
End-tidal carbon dioxide (ETCO<inf>2</inf>) and ventricular fibrillation amplitude spectral area (AMSA) for shock outcome prediction in out-of-hospital cardiac arrest. Are they two sides of the same coin?
2021, ResuscitationCitation Excerpt :For instance, in case of coronary obstructions, even with high quality CPR, coronary perfusion could be suboptimal and fail to restore myocardial energy. In this regard, AMSA has been found to be lower in patients with an acute36–38 or previous39 myocardial infarction. Another possible explanation of the discrepancy between ETCO2 and AMSA may be represented by those patients with a dilated heart at the moment of cardiac arrest, for whom low AMSA values have been reported.39
The ventricular fibrillation waveform in relation to shock success in early vs. late phases of out-of-hospital resuscitation
2019, ResuscitationCitation Excerpt :This may affect the VF-waveform and undermine the use of AMSA and its changes as a determinant of shock success. Moreover, there remains uncertainty about the impact of underlying heart disease on the VF-waveform and its implications with regard to shock outcome. 29,32–35 Underlying etiology might impact a priori chances of shock success, thereby potentially influencing the relation between AMSA-measures and shock success, especially in later phases of resuscitation.
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A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi: 10.1016/j.resuscitation.2016.10.007.