Pseudo-pulseless electrical activity: A distinct hemodynamic state in cardiac arrest and its implications for resuscitation

Abstract

Pulseless electrical activity (PEA) is conventionally defined as organized electrical cardiac activity in the absence of a palpable pulse. It is managed as a single non-shockable arrest rhythm within advanced life support algorithms. Increasing use of point-of-care ultrasound and objective perfusion monitoring has revealed substantial physiological heterogeneity within this category. A clinically important subset demonstrates persistent cardiac mechanical activity despite absent palpable pulses, commonly referred to as PEA with cardiac mechanical activity (pseudo-PEA). In this review, pseudo-PEA is defined as the absence of a palpable pulse in the presence of cardiac mechanical activity visualized on point-of-care ultrasound. Across observational cohorts and systematic reviews, the presence of cardiac activity during PEA is consistently associated with higher rates of return of spontaneous circulation and short-term survival compared with cardiac standstill, suggesting that pseudo-PEA often represents a profound but potentially reversible low-flow state rather than complete electromechanical dissociation. Current resuscitation algorithms do not explicitly distinguish pseudo-PEA from true PEA, which may contribute to non-targeted therapy, delayed correction of reversible causes, and premature termination decisions. This narrative review synthesizes the physiological basis of pseudo-PEA, evaluates available diagnostic and prognostic evidence, and examines the operational risks of intra-arrest ultrasound, particularly interruption of chest compressions. We propose a physiology-guided resuscitation approach that integrates time-limited ultrasound with objective perfusion assessment. While this framework offers a more nuanced understanding of cardiac arrest physiology, the available evidence remains largely observational. Pseudo-PEA should therefore inform clinical reasoning rather than dictate management in isolation. Further prospective studies are required to determine whether physiology-guided strategies improve meaningful survival outcomes.

Key Words: Pulseless electrical activity with cardiac mechanical activity; Pulseless electrical activity; Cardiac arrest; Point-of-care ultrasound; End-tidal carbon dioxide; Coronary perfusion pressure; Physiology-guided cardiopulmonary resuscitation

Core Tip: Pulseless electrical activity (PEA) is traditionally treated as a uniform non-shockable cardiac arrest rhythm. Yet, bedside ultrasound and perfusion monitoring increasingly reveal a subgroup with residual cardiac mechanical activity called PEA with cardiac mechanical activity. This review reframes PEA with cardiac mechanical activity as a low-flow arrest state rather than true electromechanical dissociation, summarizes prognostic and physiological evidence supporting this distinction, and highlights the limitations of rhythm-based resuscitation algorithms. We propose a structured, physiology-guided resuscitation strategy that integrates time-limited ultrasound with perfusion targets to guide treatment escalation while preserving the quality of cardiopulmonary resuscitation.

INTRODUCTION

Pulseless electrical activity (PEA) is one of the most frequently encountered presenting rhythms in both in-hospital and out-of-hospital cardiac arrest. Despite improvements in cardiopulmonary resuscitation (CPR), systems of care, and post-cardiac arrest management, the outcomes continue to be poor especially in terms of neurologically -intact survival[1,2]. Contemporary life support algorithms emphasize both simplicity and reproducibility; accordingly, PEA is managed as a single non-shockable pathway centered on high-quality CPR, periodic epinephrine administration, rhythm reassessment, and systematic evaluation for reversible causes, the so-called “Hs and Ts”[1,2].

However, PEA is not a mechanistic diagnosis. At the bedside, it serves as an operational label applied when organized electrical activity is observed on the monitor but a palpable pulse cannot be reliably identified during the brief resuscitation pause. Although this approach is necessary in a time-critical setting, it inevitably groups physiologically distinct states under a single category.

The widespread availability of point-of-care ultrasound (POCUS) has highlighted this limitation. Multiple observational studies suggest that a substantial proportion of patients, who fulfil clinical criteria of PEA, exhibit persistent cardiac mechanical activity on echocardiography[3-5]. These patients, commonly described as having PEA with cardiac mechanical activity (pseudo-PEA), have higher rates of return of spontaneous circulation (ROSC) and short-term survival compared to patients with cardiac standstill, suggesting preserved myocardial viability and the presence of a potentially reversible low-flow circulatory state rather than complete electromechanical dissociation[3,4,6]. For this review, pseudo-PEA is defined pragmatically as the absence of a palpable pulse, in the presence of cardiac mechanical activity on POCUS. This activity exists alongside a spectrum that ranges from coordinated ventricular contraction to minimal- or agonal-myocardial motion. Despite this variability, the difference between motion-present and motion-absent states is reproduced across the emergency department and in-hospital cohorts, as well as in systematic reviews that support its clinical relevance[6,7].

Manual pulse palpation has well-established limitations in low-output states. During cardiac arrest, pulse checks are prone to false-negative diagnosis, especially in the presence of severe vasodilation, low stroke volume, obesity, or peripheral edema[8]. Ultrasound- or Doppler-assisted techniques may improve the detection of residual circulation, when performed in a structured manner[8,9]. However, these potential benefits must be weighed against the risk of interrupting chest compressions. Observational studies have consistently shown that unstructured or prolonged ultrasound use during CPR increases hands-off time, which is associated with reduced coronary and cerebral perfusion, eventually leading to worse outcomes[10,11]. As a result, modern resuscitation practice encounters a central operational tension, i.e. ultrasound can refine the physiological assessment in PEA, but only if applied in a manner that preserves the quality of CPR.

Against this background, a need exists to move beyond rhythm-based classification towards a physiology-informed understanding of PEA. Pseudo-PEA can be conceptualized as a state in which the electrical activity persists and myocardial contraction is present, yet insufficient to generate effective perfusion. This condition is dynamic, potentially reversible, and highly sensitive to preload, afterload, and the quality of resuscitation. Furthermore, it is also important to acknowledge that the current evidence base remains largely observational, and optimal management strategies are not yet well defined. This review develops a conceptual framework for pseudo-PEA as a low-flow arrest phenotype, synthesizes the available physiological and diagnostic evidence, and proposes a pause-minimizing resuscitation approach that integrates time-limited ultrasound with objective perfusion assessment.

CONCEPTUAL FRAMEWORK: ELECTRICAL ACTIVITY, MECHANICAL FUNCTION, AND CIRCULATORY FLOW

The clinical label of PEA is shaped by the practical constraints of bedside resuscitation rather than by a single underlying pathophysiological mechanism. Current advanced life support algorithms require clinicians to determine the presence or absence of a pulse during brief interruptions in chest compressions, typically limited to 10 seconds, to minimize the loss of coronary and cerebral perfusion[2]. However, pulse palpation is inherently insensitive in low-flow states. Its accuracy depends on multiple factors including vascular tone, pulse pressure, examiner’s experience, and the patient’s characteristics such as obesity or peripheral edema[9,12]. As a result, the clinical diagnosis of PEA encompasses a heterogeneous range of physiological conditions rather than a single pathophysiological entity.

This spectrum ranges from true electromechanical dissociation, in which the organized electrical activity persists in spite of minimal or complete absence of myocardial contraction, to low-flow states in which the cardiac mechanical activity is preserved yet it fails to generate a palpable pulse, consistent with pseudo-PEA. In some cases, though clinically inapparent, the physiologically meaningful pulsatile flow may be present but it remains undetectable by palpation.

Physiology cascade: From electrical depolarization to organ perfusion

Cardiac arrest physiology is accurately conceptualized as a cascade of events rather than a binary state. Electrical depolarization is relatively energy-efficient and it may persist despite the impairment of myocardial metabolism, even late into circulatory collapse. On the other hand, the mechanical contraction requires intact excitation-contraction coupling, adequate oxygen delivery, and sufficient availability of adenosine triphosphate. In states of ischemia or metabolic failure, the contractile function may be compromised earlier than the generation of electrical impulse, thus resulting in organized electrical activity with inadequate mechanical output.

However, contraction alone does not guarantee effective circulation. The generation of a palpable pulse and meaningful organ perfusion rely upon stroke volume, arterial elastance, systemic vascular resistance, and unobstructed forward flow. The progressive impairment of myocardial energetics further reduces the contractile effectiveness, ultimately resulting in circulatory collapse and cardiac standstill. Within this framework, the pseudo-PEA represents a low-flow state along a continuum from preserved electrical activity to complete circulatory failure.

Coronary perfusion pressure (CPP), approximated by the gradient between aortic diastolic pressure and right atrial pressure, is a critical factor that determines the success of resuscitation during CPR[13,14]. Both experimental and clinical studies demonstrate that the restoration of diastolic pressure, rather than systolic pressure alone, is strongly associated with ROSC[14]. Consequently, 2 patients with identical electrocardiographic rhythms and similar degrees of myocardial contraction may experience profoundly different myocardial and cerebral perfusion depending on the vascular tone, intrathoracic pressure, right ventricular loading conditions, and the quality of chest compressions[15,16]. This relationship among electrical activity, mechanical contraction, and effective forward flow is illustrated schematically in Figure 1.

Figure 1 Electrical-mechanical-circulatory continuum in cardiac arrest. Schematic illustrating the relationship among electrical activity, myocardial contraction, and effective circulatory flow. Circulatory flow declines earliest, followed by mechanical function, while electrical activity persists longest. Pseudo-pulseless electrical activity is represented as a low-flow state with preserved electrical activity and variable mechanical function but inadequate perfusion. Cardiac standstill reflects absence of mechanical activity despite organized electrical activity, while asystole represents absence of both electrical and mechanical activity. PEA: Pulseless electrical activity.

Why pulse palpation is an inadequate surrogate for circulatory flow

Manual pulse palpation has long served as a clinical discriminator between circulation and cardiac arrest even though its limitations have been well documented. Comparative studies using invasive arterial waveforms, Doppler ultrasound, and point-of-care echocardiography demonstrate frequent false-negative pulse assessments in low-output states[9,12,17]. In the presence of severe vasodilation or reduced stroke volume, the pulsatile flow sufficient to sustain myocardial and cerebral perfusion may fail to generate a palpable peripheral pulse.

The absence of a palpable pulse should not be automatically equated with the absence of circulation. When objective markers such as end-tidal carbon dioxide (EtCO₂) or arterial diastolic pressure suggest ongoing perfusion, the underlying physiology differs substantially from the true cardiac standstill. In this context, pseudo-PEA reflects a limitation of pulse-based assessment rather than a distinct rhythm.

Definitions and terminologies used in this review

For clarity and consistency, in this review, pseudo-PEA is defined as the absence of a palpable pulse in the presence of cardiac mechanical activity, visualized on POCUS[3,5,8]. This definition reflects its practical application during resuscitation and aligns with the majority of observational studies.

Cardiac mechanical activity exists along a spectrum. In some patients, coordinated myocardial contraction is observed with visible change in chamber size, whereas in others, only minimal or agonal myocardial motion is seen. These patterns reflect varying degrees of myocardial viability and circulatory effectiveness rather than distinct diagnostic entities. For conceptual clarity, this review descriptively refers to these patterns as organized and disorganized cardiac activity without implying rigid classification.

True PEA, or the cardiac standstill phenotype, refers to the organized electrical activity in the absence of a visible myocardial contraction on ultrasound. This distinction is clinically relevant, as multiple observational studies have demonstrated varying prognostic implications between motion-present and motion-absent states, although such findings remain associative[4-7].

A few alternative terminologies, including PEA with motion (PREM) and PEA with standstill, have been proposed to distinguish between PEA with and without visible cardiac activity on ultrasound. PREM broadly corresponds to motion-present states (pseudo-PEA), whereas PEA with standstill reflects cardiac standstill. These terms are inconsistently applied across the studies, which may introduce ambiguity. Accordingly, this review favors an explicit description of the ultrasound findings over the use of alternative acronyms. The ultrasound findings should be interpreted in clinical context and not used in isolation to guide termination decisions.

EPIDEMIOLOGY AND PROGNOSIS: WHAT CHANGES WHEN PSEUDO-PEA IS IDENTIFIED

Reclassification of “PEA” using ultrasound reveals prognostically distinct phenotypes

The integration of POCUS into cardiac arrest management has fundamentally altered the epidemiologic understanding of PEA. While it was historically considered a single non-shockable rhythm, it is now being recognized as a heterogeneous group of physiological states with markedly different outcomes. Across the emergency department and other in-hospital cohorts, ultrasound reclassification consistently demonstrates that a substantial proportion of the patients, who meet the bedside definition of PEA, exhibit persistent cardiac mechanical activity[3-7].

This distinction is clinically meaningful. The observational studies show that the presence of cardiac activity during PEA arrest is associated with the maximum rate of ROSC, survival to hospital admission, and less consistently, survival to discharge. In a prospective multicenter cohort, evaluating ultrasound use during advanced life support in non-shockable arrest, cardiac activity emerged as a strong predictor of short-term survival. However, survival to discharge among the patients with persistent cardiac standstill was found to be rare[4]. These findings were supported by quantitative data from the observational cohorts, in which the ROSC was achieved in approximately 40%-70% of patients with pseudo-PEA compared to markedly lower or no ROSC in cardiac standstill. Further, their survival to hospital discharge was observed almost exclusively among patients with preserved cardiac activity. These associations persisted after adjustment for arrest location, witnessed status, and initial rhythm, thus supporting a biologically relevant separation between motion-present and motion-absent phenotypes. However, potential selection bias, variability in ultrasound use and resuscitation practices should also be considered. Some of the key clinical studies that evaluate the ultrasound-defined cardiac activity during PEA and their associated resuscitation outcomes are summarized in Table 1[3-8,18-21].

Table 1 Key studies evaluating ultrasound-defined cardiac activity in pulseless electrical activity and pseudo-pulseless electrical activity.

Ref.	Design/setting	Population	Ultrasound phenotype	Key outcomes	Interpretation, limitations, and strength of evidence
Gaspari et al[3], 2016	Prospective, multicentre observational; ED and OHCA	n = 793; non-shockable arrests (PEA + asystole)	Cardiac activity present vs absent on POCUS during ACLS	Cardiac activity independently associated with survival to admission and discharge; survival to discharge exceedingly rare without activity	Large multicentre cohort; includes asystole; observational design limits causal inference
Gaspari et al[4], 2017	Retrospective secondary analysis of prospective registry	n = 225; PEA patients with cardiac activity	Organized vs disorganized cardiac activity	Organized activity associated with higher ROSC and survival to admission; differential association with vasoactive escalation (hypothesis-generating)	Non-randomized; subject to indication and selection bias; not designed to evaluate treatment efficacy
Devia Jaramillo et al[18], 2020	Single-center observational cohort; ED (Colombia)	n = 108; cardiac arrests	Pseudo-PEA vs true PEA vs other rhythms	Pseudo-PEA associated with higher ROSC and survival to discharge than true PEA	Single-center ED cohort; favorable case mix may limit generalizability
Kedan et al[5], 2020	Systematic review	10 studies; ED and IHCA	Cardiac activity on POCUS (binary)	Consistent association between cardiac activity and ROSC and short-term survival	Heterogeneous definitions and study designs; limited neurologic outcome data
Blyth et al[6], 2012	Systematic review	12 observational studies	Cardiac activity during arrest	Cardiac activity predicts ROSC and survival to admission	Older studies; variability in ultrasound timing and protocols
Tsou et al[7], 2017	Systematic review and meta-analysis	15 studies; > 1200 patients	Cardiac activity on focused echocardiography	Moderate prognostic accuracy for ROSC and discharge; higher accuracy for survival to admission	Heterogeneity across studies; not sufficient as a sole criterion for termination decisions
Rabjohns et al[20], 2020	Narrative review; ED-focused	Review of 9 pseudo-PEA articles	Pseudo-PEA vs true PEA; diagnostic, therapeutic, and prognostic literature	Summarized evidence supporting ultrasound-based diagnosis, mechanism-directed treatment, and better prognosis of pseudo-PEA than true PEA	Useful ED-oriented synthesis, but narrative design and small underlying studies limit certainty
Jian et al[19], 2025	Systematic review and meta-analysis (PEA-specific)	PEA patients only	Cardiac activity on POCUS	Highest prognostic accuracy for survival to admission; moderate for ROSC and discharge; inadequate alone for termination decisions	PEA-specific synthesis strengthens relevance, but definitions of “cardiac activity” remain heterogeneous
Elhalwagy et al[21], 2025	Systematic review and meta-analysis	12 studies; 494355 patients	Pseudo-PEA contextualized within broader PEA vs asystole literature	PEA showed better survival and neurologic outcomes than asystole; authors suggest pseudo-PEA may partly explain this difference	Important updated synthesis, but indirect for pseudo-PEA because much of the pooled comparison is PEA vs asystole rather than directly pseudo-PEA vs true PEA
Latsios et al[8], 2025	Narrative review	ED and ICU arrests	Pseudo-PEA vs standstill	Reinforces prognostic separation and integration with perfusion markers	Narrative synthesis; does not provide pooled outcome estimates

The table summarizes study design, patient population, ultrasound definitions, and associations with return of spontaneous circulation and survival outcomes. All included studies are observational; findings represent associations rather than causal effects. ACLS: Advanced cardiac life support; ED: Emergency department; OHCA: Out-of-hospital cardiac arrest; IHCA: In-hospital cardiac arrest; PEA: Pulseless electrical activity; POCUS: Point-of-care ultrasound; Pseudo-PEA: Pulseless electrical activity with cardiac mechanical activity; ROSC: Return of spontaneous circulation; ICU: Intensive care unit.

Pseudo-PEA identifies opportunity, not certainty

Although pseudo-PEA is associated with improved outcomes compared to cardiac standstill, it should not be interpreted as a pre-ROSC state. Rather, it reflects a critically reduced and unstable circulatory state in which perfusion remains highly vulnerable to changes in preload, afterload, intrathoracic pressure, and CPR quality in spite of its presence.

This distinction has important clinical implications. Interpreting pseudo-PEA as “near ROSC” may lead to false reassurances and delayed targeted intervention. In parallel, when it is recognized as a severe low-flow physiology, it might underscore the need to promptly correct the reversible contributors. Despite higher ROSC rates, pseudo-PEA remains associated with substantial mortality and neurological injury, thus emphasizing that its prognostic advantage is relative rather than absolute[3-7]. Thus, its clinical value lies in the identification of potentially salvageable physiology rather than the prediction of inevitable recovery.

Quality of cardiac motion and its prognostic implications

Beyond the binary presence or absence of cardiac activity, the quality of myocardial motion may provide additional prognostic information. Secondary analyses suggest that organized cardiac activity, characterized by coordinated chamber contraction and visible changes in cavity size, is associated with higher rates of ROSC and survival to hospital admission than the disorganized or agonal motion[4]. This characteristic represents a gradation within motion-positive states rather than a discrete classification.

Such observations are biologically plausible. Coordinated contraction reflects preserved excitation-contraction coupling and myocardial energy reserves, whereas agonal motion likely represents advanced metabolic failure. However, these observations arise from non-randomized analyses and should be cautiously interpreted.

The inferences from systematic reviews and meta-analyses further support the prognostic value of ultrasound-detected cardiac activity during PEA arrest, demonstrating its moderate accuracy for predicting ROSC and survival outcomes[5-7,19-21]. However, heterogeneity in definitions, variability in ultrasound application, and potential self-fulfilling bias limit the certainty of these findings. Accordingly, ultrasound findings should be considered a tool for risk stratification rather than taking it as a deterministic prognostic marker.

Implications for termination of resuscitation decisions

Recognition of pseudo-PEA is particularly relevant for the termination of resuscitation (TOR), a domain in which the rhythm-based frameworks have historically dominated. Current guidelines do not explicitly incorporate ultrasound-defined cardiac activity into TOR criteria. However, observational data consistently demonstrates that motion-present states carry a higher probability of ROSC and short-term survival compared to cardiac standstill[1,2,4].

Pseudo-PEA does not mandate prolonged resuscitation, but it should prompt caution against premature termination. It supports reassessment of CPR quality, perfusion markers, and reversible causes. On the contrary, persistent cardiac standstill, combined with refractory low perfusion and prolonged low-flow time, may support TOR decisions. This represents a shift from rhythm-based finality to physiology-informed judgment.

PATHOPHYSIOLOGY OF PSEUDO–PEA

Pseudo-PEA can be best understood as a low-flow hemodynamic state rather than a complete electromechanical dissociation. Here, the defining feature is persistence of myocardial mechanical activity that fails to generate a palpable pulse because either the forward flow is critically reduced or the pressure generation is inadequate, or at times, both. Clinically, pseudo-PEA represents a circulatory collapse that occurs at the threshold between profound shock and true cardiac arrest.

A palpable pulse requires not only myocardial contraction, but also sufficient stroke volume, adequate arterial elastance, and effective transmission of pressure to peripheral circulation. Therefore, ventricular contraction alone is insufficient to guarantee pulse palpability or organ perfusion. In pseudo-PEA, cardiac motion may be preserved. However, the stroke volume remains inadequate, systemic vascular resistance is too low to convert flow into pressure, or mechanical obstruction prevents forward flow.

These mechanisms can be understood through ventricular-arterial coupling. When arterial elastance is markedly reduced, as in case of severe vasoplegia, the increase in cardiac output may fail to generate meaningful arterial pressure despite the presence of preserved contractility[22]. Conversely, in states of excessive afterload or impaired contractility, pressure generation may remain limited in spite of adequate filling.

Across the arrest phenotypes, myocardial blood flow is a principal determinant of successful resuscitation during CPR. CPP, approximated by the difference between aortic-diastolic pressure and right atrial pressure, remains a key determinant of successful resuscitation[13]. The restoration of diastolic pressure, rather than systolic pressure alone, is consistently associated with ROSC[13,14]. When diastolic pressure cannot be maintained due to multiple reasons like vasodilation, impaired compression mechanics, elevated right-sided pressures, or dynamic hyperinflation, the myocardial perfusion falls and contractility deteriorates followed by the rapid progression of pseudo-PEA to cardiac standstill.

Dominant mechanistic pathways leading to pseudo-PEA

Pseudo-PEA arises through several dominant mechanistic pathways that frequently overlap in individual patients. So it is crucial to identify primary physiological failure to understand the persistence of myocardial activity despite inadequate perfusion.

Preload failure and impaired venous return

Severe hypovolemia due to hemorrhage, dehydration, third-spacing, or late distributive shock may permit preserved myocardial contractility, but negligible stroke volume, because ventricular filling remains inadequate. In this setting, the circulatory failure occurs at the level of venous return rather than myocardial function. When chest compressions are effective, preload restoration can rapidly improve the EtCO₂ and perfusion, thus underscoring the recruitable nature of this pseudo-PEA phenotype.

Mechanical obstruction to forward flow

Cardiac tamponade, massive pulmonary embolism, and acute right ventricular pressure overload represent classic obstructive pathways to pseudo-PEA. In these states, myocardial contraction may persist; however, effective circulation is impeded, resulting in marked reductions in left ventricular preload and systemic output despite the ongoing electrical and mechanical activities. Acute right ventricular failure is particularly relevant, as severe dilation and septal shift can abruptly compromise the left ventricular filling and precipitate the low-flow arrest in spite of the preserved contractility[23].

Vasodilatory collapse and failure of pressure generation

Profound vasoplegia, as seen in sepsis, anaphylaxis, or post-cardiac arrest inflammatory states, may prevent the conversion of flow into diastolic pressure in spite of the preserved cardiac output. CPP falls primarily because aortic diastolic pressure cannot be sustained, even when myocardial contraction appears to be adequate. In this phenotype, the limiting factor is vascular tone rather than preload or intrinsic contractility.

Severe pump failure and myocardial stunning

Pseudo-PEA may also result from extensive ischemia, myocarditis, advanced cardiomyopathy, or post-resuscitation myocardial stunning. Ultrasound typically demonstrates globally-reduced ventricular contraction or dilated chambers with minimal change in cavity size. Myocardial stunning, following cardiac arrest, is well documented and it may persist despite the restoration of coronary perfusion, thus limiting effective stroke volume generation and delaying the recovery of forward flow[23,24].

Despite the differing mechanisms, these pathways converge on a final state of critically inadequate perfusion in spite of the presence of preserved electrical activity and variable mechanical contraction (Figure 2). Pseudo-PEA, therefore, represents a time-sensitive physiology in which myocardial viability persists yet it depends on uninterrupted CPR and rapid correction of dominant hemodynamic abnormality.

Figure 2 Mechanistic framework of pseudo-pulseless electrical activity as a low-flow state. Schematic linking ultrasound phenotypes to dominant physiological mechanisms, including preload limitation, vasodilatory collapse, mechanical obstruction, and pump failure, and their impact on coronary perfusion pressure and forward flow. CPP: Coronary perfusion pressure; MI: Myocardial infarction; PE: Pulmonary embolism; PEA: Pulseless electrical activity.

Standard PEA algorithms emphasize high-quality CPR, epinephrine administration, and the systematic evaluation of reversible causes[1,2]. Though appropriate, this approach might be incomplete in pseudo-PEA since the primary problem is impaired perfusion rather than the absence of mechanical activity. The escalation of adrenergic therapy, without addressing the underlying physiology, may increase the myocardial oxygen demand or worsen the afterload mismatch. Observational data supports the hypothesis that pseudo-PEA may represent a subgroup in which physiology-guided resuscitation strategies warrant further investigation, thus underscoring the need for prospective validation[4-7,18-21].

DIAGNOSIS OF PSEUDO-PEA

Recognition of pseudo-PEA requires the identification of cardiac mechanical activity in patients who meet the operational definition of PEA. The diagnostic goal is limited to determining whether myocardial contraction is present or not, despite the absence of a palpable pulse.

POCUS remains the most reliable metric to make this distinction during resuscitation. Across multiple observational cohorts and systematic reviews, the presence of any cardiac motion on ultrasound has consistently differentiated pseudo-PEA from true PEA or cardiac standstill[3-7,18,19]. For recognition purposes, a binary assessment, i.e. presence or absence of cardiac mechanical activity, is sufficient. A single cardiac window obtained during the scheduled rhythm or pulse check is sufficient for this assessment without requiring any detailed functional or etiologic assessment.

Because cardiac motion does not necessarily equate to effective perfusion, objective perfusion signals should be used to support recognition when available. Persistently measurable EtCO₂ during CPR, low-amplitude pulsatile arterial waveforms, or Doppler-detected central arterial flow indicate residual circulation that may not be detectable by manual palpation[13,14,17-21]. Although these findings support the recognition of pseudo-PEA, they do not redefine the concept.

Ultrasound use must be a time-bound and structured phenomenon. Probe positioning should occur during the ongoing compressions, with image acquisition confined to scheduled pauses. In this setting, ultrasound should answer a single question, i.e. whether cardiac mechanical activity is present or not without expanding the diagnostic scope or interrupting the CPR (Figure 3).

Figure 3 Diagnostic framework for pseudo-pulseless electrical activity during cardiopulmonary resuscitation. The figure outlines rhythm identification, pulse assessment, time-limited ultrasound evaluation of cardiac mechanical activity, and adjunctive use of perfusion markers without prolonging interruptions in chest compressions. ACLS: Advanced cardiac life support; CPR: Cardiopulmonary resuscitation; DBP: Diastolic blood pressure; EtCO₂: End-tidal carbon dioxide; PEA: Pulseless electrical activity; POCUS: Point-of-care ultrasound; Pseudo-PEA: Pulseless electrical activity with cardiac mechanical activity.

PROPOSED PHYSIOLOGY-GUIDED RESUSCITATION ALGORITHM FOR PSEUDO-PEA

Once the cardiac mechanical activity is identified, in the absence of a palpable pulse using time-limited POCUS during scheduled rhythm or pulse checks, ultrasound assessment should be integrated with standard pauses in chest compressions. The total interruption should be limited to ≤ 10 seconds and image acquisition should ideally be completed within a few seconds (typically ≤ 5 seconds). At this stage, the focus shifts from rhythm classification to understanding whether the ongoing resuscitative efforts are producing adequate myocardial and cerebral perfusion or not. This approach complements, rather than replaces, established resuscitation principles. High-quality chest compressions, appropriate ventilation and oxygenation, and guideline-directed epinephrine administration continue throughout the procedure in line with the American Heart Association and European Resuscitation Council recommendations[1,2].

Within this framework, the presence of cardiac mechanical activity should not be equated with effective circulation. Pseudo-PEA represents a low-flow state in which the myocardial contraction is insufficient to generate a meaningful forward perfusion. On the contrary, true PEA reflects cardiac standstill with no mechanical activity. This distinction underscores the importance of integrating ultrasound findings with perfusion markers and clinical context rather than merely interpreting cardiac motion in isolation.

After diagnosing pseudo-PEA, objective perfusion assessment becomes central to decision-making. Continuous or trending markers, particularly EtCO₂ and, when available, arterial diastolic pressure, are used to identify whether CPR and adjunctive therapies are generating effective forward flow and coronary perfusion[13-15,24]. Although no single threshold is definitive, persistently low EtCO₂ values (< 10 mmHg) or low diastolic pressures (< 20-25 mmHg) suggest inadequate perfusion despite visible cardiac activity. Conversely, rising EtCO₂ or improving diastolic pressure may indicate effective resuscitation and evolving circulatory recovery. These values should be interpreted in context rather than as absolute decision cutoffs.

The dominant physiological limitation, then, guides therapeutic priorities inferred from the ultrasound phenotype and perfusion response. In preload-limited states, the restoration of effective venous return is emphasized. In suspected obstructive physiology, expedited confirmation and institution-specific pathways for obstruction relief are considered, when feasible. In vasodilatory collapse, restoration of vascular tone and diastolic pressure is prioritized to preserve coronary perfusion. In pump-failure phenotypes, excessive afterload escalation is avoided, and a balance is ensured between perfusion pressure and residual contractile reserve. These mechanisms frequently overlap and reassessment is iterative rather than linear.

Epinephrine administration continues as per the current resuscitation guidelines. In selected settings, persistently inadequate perfusion, despite ongoing cardiac mechanical activity, may prompt one to consider escalation beyond bolus-only vasopressor therapy; however, this approach is supported by observational data and should be regarded as a hypothesis-generative rather than a directive[4-7,18,19].

Physiological response is reassessed at scheduled rhythm and pulse checks, typically after one to two CPR cycles, using objective perfusion markers and brief, time-limited ultrasound confirmation, when indicated. Improvement in perfusion supports the continuation of targeted therapy. By contrast, deterioration towards cardiac standstill or persistently refractory low perfusion, despite optimized CPR and correction of reversible contributors, prompts reassessment of overall resuscitation goals in accordance with institutional, ethical, and guideline-based standards[1,2]. Ultrasound findings should not be used in isolation to justify the TOR.

The emerging ultrasound-integrated resuscitation models further support a shift towards real-time physiological assessment and mechanism-based interpretation, rather than relying solely upon rhythm-based decision-making[8,25]. However, most of the available evidence remains conceptual or derived from non-adult populations and its applicability to adult pseudo-PEA should further be validated. The proposed algorithm (Figure 4) should therefore be viewed as an evidence-backed, hypothesis-generating framework, designed to guide physiology-based resuscitation, while preserving CPR quality and adherence to established life-support principles.

Figure 4 Physiology-guided resuscitation pathway for pseudo-pulseless electrical activity. The algorithm illustrates targeted optimization of coronary and cerebral perfusion using objective hemodynamic and metabolic markers, integrated within guideline-directed advanced cardiac life support, with iterative reassessment of rhythm and perfusion. ACLS: Advanced cardiac life support; AHA: American Heart Association; CPR: Cardiopulmonary resuscitation; ERC: European Resuscitation Council; POCUS: Point-of-care ultrasound; PEA: Pulseless electrical activity; Pseudo-PEA: Pulseless electrical activity with cardiac mechanical activity; EtCO₂: End-tidal carbon dioxide; ROSC: Return of spontaneous circulation; TOR: Termination of resuscitation; LV: Left ventricle; PE: Pulmonary embolism.

LIMITATIONS AND FUTURE DIRECTIONS

The concept of pseudo-PEA is supported predominantly by observational cohorts, secondary analyses, and systematic reviews of heterogeneous studies. Although the presence of cardiac mechanical activity on ultrasound is consistently associated with improved short-term outcomes, causality cannot be inferred. Patients with pseudo-PEA likely differ from those with cardiac standstill in ways not fully captured by available data, including arrest etiology, pre-arrest physiology, and intensity of resuscitation. The proposed physiology-guided approach should therefore be viewed as a conceptual framework rather than a validated protocol.

Definitions of pseudo-PEA and what constitutes “meaningful” cardiac activity vary widely across studies, ranging from any visible myocardial motion to coordinated chamber contraction. This variability limits comparability and precludes the establishment of universally applicable decision-making thresholds. Similarly, perfusion markers such as EtCO₂ and arterial diastolic pressure - central to the proposed framework are derived from heterogeneous data. They should be interpreted as dynamic trends within a clinical context rather than fixed targets.

Studies evaluating vasoactive escalation or physiology-guided strategies in pseudo-PEA are subject to indication bias and should be regarded as hypothesis-generating. In addition, the potential for a self-fulfilling effect must be considered, as awareness of cardiac activity on ultrasound may influence clinician behavior, including the duration and intensity of resuscitation efforts. While ultrasound provides valuable physiological insight, unstructured or prolonged use during CPR may increase hands-off time, underscoring the need for strict adherence to time-limited imaging protocols[10-12,15,26].

Future research should focus on prospective, protocolized evaluation of physiology-guided resuscitation strategies in pseudo-PEA. An important question is whether integrating time-limited ultrasound with objective perfusion markers improves neurologically intact survival without compromising CPR quality[27,28]. Randomized or cluster-based comparisons with standard advanced cardiac life support approaches will be necessary. Standardization of definitions, ultrasound reporting, and outcome measures will also be essential to improve reproducibility. Ultrasound findings should be interpreted alongside other clinical data rather than used in isolation to guide termination decisions.

At a systems level, further work is needed to determine how emerging resuscitation infrastructure can be incorporated into physiology-guided care without increasing no-flow time. For example, video-assisted dispatcher CPR has been associated with improved CPR quality and survival despite potential delays in initiation[29]. Although not validated for pseudo-PEA recognition, these findings highlight the broader systems context in which physiology-guided resuscitation must operate.

Pseudo-PEA also highlights the limitations of purely rhythm-based cardiac arrest classification. Recognizing it as a low-flow phenotype may better align clinical frameworks with bedside physiology. Until prospective evidence becomes available, pseudo-PEA should inform clinical reasoning and risk stratification rather than mandate specific therapeutic pathways.

CONCLUSION

Pseudo-PEA represents a low-flow hemodynamic state within the spectrum of non-shockable cardiac arrest, in which myocardial activity persists yet it fails to generate effective perfusion. Recognizing this phenotype challenges the traditional pulse-based definitions of arrest and highlights physiological heterogeneity underlying the clinical label of PEA. Use of time-limited POCUS, alongside objective perfusion markers, allows identification of residual circulation that may not be clinically apparent while maintaining the central priority of uninterrupted, high-quality CPR. This approach shifts the focus from rhythm alone to the adequacy of perfusion and the underlying hemodynamic limitation. The available evidence remains largely observational, and important uncertainties persist. At present, pseudo-PEA is best viewed as a framework that supports more informed clinical reasoning rather than a basis for prescriptive management. Prospective studies are needed to determine whether physiology-guided resuscitation strategies improve meaningful survival outcomes. Even so, acknowledging pseudo-PEA as a low-flow arrest phenotype represents a step toward a physiology-driven understanding of cardiac arrest, aligning bedside assessment more closely with underlying circulatory function.