Pulseless Electrical Activity, or Electromechanical Dissociation

In this issue of the Journal, Holmström et al.¹ analyzed unique prospectively collected data. The authors obtained the data on 641 observed sudden cardiac arrest (SCA) cases that occurred in the presence of Emergency Medical Services (EMS) personnel and, thus, argued that an available electrocardiogram (ECG) reflected the true SCA initial rhythm. Holmström et al.¹ utilized the data of the prospective community-based studies of the SCA, the Oregon Sudden Unexpected Death Study (OregonSUDS), and the Ventura Prediction of Sudden Death in Multi-ethnic Communities (PRESTO) study. Adjudication of SCA cases was based on EMS reports, initial ECG strip recorded at the time of SCA, medical records, death certificates, and autopsy reports. The authors aimed to compare and contrast the clinical characteristics of individuals presented with the shockable versus non-shockable initial rhythms and, therefore, included “pulseless ventricular tachycardia (VT)” cases in the ventricular fibrillation (VF) group. Previously diagnosed coronary artery disease (CAD) was noted in 53.4%, and heart failure (HF) in 30.3% of the population. The authors found that anemia, older age, chronic kidney disease (CKD), obesity, and prearrest dyspnea were the most important predictors of pulseless electrical activity (PEA). In contrast, CAD, prearrest chest pain, and young age were the most important predictors of VF. The authors should be congratulated on their important endeavors. However, several aspects of comparison between “shockable VT/VF” and “non-shockable PEA” deserve additional comments.

The development of SCA in the presence of EMS personnel is an infrequent clinical scenario. Theoretically, two different underlying stories can be unfolding. In one clinical scenario, an EMS team would attend to a patient who was initially presented with trivial clinical symptoms (e.g. chest pain, dyspnea) and, by a random chance, at the moment of ECG recording, a patient would develop SCA. In such a clinical scenario, an EMS team had a unique opportunity to capture a rare moment of SCA initiation and record the true initial SCA rhythm. The probability of such a clinical scenario is minuscule, but it is not zero. The second (more frequent) clinical scenario includes an EMS response to an SCA case with a successful return of spontaneous circulation (ROSC) when a subsequent (second, third, and so on) SCA event is developed at the time of continuous ECG monitoring on the scene or during the transportation of a patient to a hospital.² Such a second clinical scenario is more frequent because continuous ECG monitoring is routinely performed after ROSC, which increases the probability of observing initiating SCA rhythm. While one can speculate that the unobserved cardiac rhythm that initiated the first SCA event with successful ROSC was the same as an observed cardiac rhythm that initiated subsequent SCA events, such an assumption cannot be proven and remains speculative. Moreover, the probability of PEA increases with each subsequent SCA episode, even if the very first initiating rhythm was shockable.² This does not detract from the study but should be taken into account for its appropriate interpretation.

PEA, or electromechanical dissociation (EMD), is defined as organized depolarization or electrical activation of the heart without cardiac output or generation of blood pressure.^3–5 Substantial, high-quality, carefully performed experimental and clinical studies of EMD were conducted in the 1980s-1990s.^3–5 One of the experimental models of EMD is described as induced VF without cardiopulmonary resuscitation but with an application of defibrillation after a few minutes, resulting in restoration of electrical activity without generation of blood pressure.³ Diffuse myocardial ischemia is one of the major pathophysiological mechanisms of EMD, suggesting that obtaining an effective coronary perfusion pressure should be the treatment goal. Chronotropic medications, calcium chloride, and pacing are ineffective.^3–5 There were reports that selective alpha-adrenergic agonist methoxamine improves resuscitation success.^{4, 5}

Other distinct mechanisms of EMD³ include a substantial reduction in preload (e.g., due to significant hemorrhage or pericardial tamponade), an increase in afterload (e.g., due to massive pulmonary embolism), and a terminal/final stage of mechanical pump failure.⁶ Acute mechanical pump failure in end-stage systolic heart failure can manifest either as EMD or incessant VT/VF, representing agonal cardiac rhythm.⁶ Accordingly, even if VT/VF is a technically “shockable rhythm,” incessant VT/VF and electrical storms in patients with implanted cardioverter defibrillators may indicate development of terminal pump failure (sometimes, as a cascading failure) that cannot be resuscitated.⁶

A relatively recent, comprehensive review of cardiac arrest (including PEA) mechanisms, pathophysiology, and resuscitation was published in Circulation Research by Patil, Halperin, and Becker.⁷ Weisfeldt’s concept of “three-phase” time-dependent model of SCA from VF and pulseless VT is broadly applicable to a wide range of clinical scenarios and guides SCA resuscitation.⁸ The first (electrical) phase of SCA due to VF lasts for approximately 5 minutes when defibrillation delivers the greatest resuscitation success. The second (circulatory) phase lasts approximately from 5^th to 10^th minute after VF onset. The best therapy during the circulatory phase is to give vigorous chest compressions first, prior to defibrillation. The third (metabolic) phase starts after 10 minutes of SCA and requires metabolic resuscitation. The challenge is that for out-of-hospital SCA, it is difficult to know in which phase the victim is. Both the 2^nd and the 3^rd phases of SCA due to VF can clinically manifest as PEA.

Wider use of the point-of-care ultrasound/ echocardiography (POCUS) led to more frequent detection of pseudo-PEA.^{9, 10} Pseudo-PEA manifests by weak myocardial contractions that only produce detectable aortic pressure, which can be measured either invasively or on echocardiography. Patients with pseudo-PEA are more likely to achieve ROSC and good neurological outcomes than patients with true PEA, and synchronization of external chest compressions with cardiac systole improves outcomes.^11–13 Recent data suggest that pseudo-PEA constitute more than half of PEA cases (42-86%).^{9, 14} POCUS data were not available in the study by Holmström et al.,¹ and, therefore, pseudo-PEA cases were missed. Early detection of pseudo-PEA (by using POCUS) and the development of specific therapies for pseudo-PEA can potentially significantly improve outcomes of SCA due to PEA. Even if the study by Holmström et al.¹ was not designed to detect pseudo-PEA, one can speculate that more than half of their PEA cases were, in fact, pseudo-PEA cases. Clinical characteristics of the PEA population can serve as important clinical clues, prompting evaluation for pseudo-PEA. More research on pseudo-PEA is needed in order to identify and manage patients successfully.