Elsevier

Resuscitation

Volume 109, December 2016, Pages 71-75
Resuscitation

Clinical paper
Ventricular fibrillation waveform measures and the etiology of cardiac arrest

https://doi.org/10.1016/j.resuscitation.2016.10.007Get rights and content

Abstract

Background

Early determination of the acute etiology of cardiac arrest could help guide resuscitation or post-resuscitation care. In experimental studies, quantitative measures of the ventricular fibrillation waveform distinguish ischemic from non-ischemic etiology.

Methods

We investigated whether waveform measures distinguished arrest etiology among adults treated by EMS for out-of-hospital ventricular fibrillation between January 1, 2006–December 31, 2014. Etiology was classified using hospital information into three exclusive groups: acute coronary syndrome (ACS) with ST elevation myocardial infarction (STEMI), ACS without ST elevation (non-STEMI), or non-ischemic arrest. Waveform measures included amplitude spectrum area (AMSA), centroid frequency (CF), mean frequency (MF), and median slope (MS) assessed during CPR-free epochs immediately prior to the initial and second shock. Waveform measures prior to the initial shock and the changes between first and second shock were compared by etiology group. We a priori chose a significance level of 0.01 due to multiple comparisons.

Results

Of the 430 patients, 35% (n = 150) were classified as STEMI, 29% (n = 123) as non-STEMI, and 37% (n = 157) with non-ischemic arrest. We did not observe differences by etiology in any of the waveform measures prior to shock 1 (Kruskal–Wallis Test) (p = 0.28 for AMSA, p = 0.07 for CF, p = 0.63 for MF, and p = 0.39 for MS). We also did not observe differences for change in waveform between shock 1 and 2, or when the two acute ischemia groups (STEMI and non-STEMI) were combined and compared to the non-ischemic group.

Conclusion

This clinical investigation suggests that waveform measures may not be useful in distinguishing cardiac arrest etiology.

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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      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

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      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.

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