קרדיולוגיה - האיגוד הישראלי לרפואה דחופה

Written by Alex Clark

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Sparky likes lidocaine

This target trial emulation utilized the Resuscitation Outcomes Consortium Cardiac Epistry to compare lidocaine (n=987) with amiodarone (n=1464) in adults with atraumatic, shockable OHCA refractory to at least three defibrillation attempts. Because the study used cases from 2011–2015, when ACLS guidelines recommended amiodarone as first-line, investigators used inverse probability weighting and doubly robust regression to reduce treatment-selection bias. Lidocaine was associated with higher rates of ROSC at ED arrival (41.0% vs. 34.6%; absolute difference 6.43%; 95%CI 2.6–10.3%) but not with significantly improved survival to hospital discharge (26.2% vs. 23.5%; absolute difference 2.78%; 95%CI–0.6 to 6.2%) or favorable neurologic outcome (17.7% vs. 16.2%; absolute difference 1.5%; 95%CI–1.5 to 4.5%). Although appropriately cautious in their interpretation, the authors suggest the upper bounds of the confidence intervals leave open the possibility for clinically meaningful benefit of lidocaine. While the target trial emulation strengthens causal inference compared to traditional observational analyses, the study still has severe limitations when it comes to drawing any conclusions of superiority, including the older registry data with potentially outdated practices, the inability to assess timing of antiarrhythmic administration, and the potential for residual confounding.

How does this change my practice?

Source

The post PODCAST: ​Which Is Better? Amiodarone vs. Lidocaine for OHCA first appeared on האיגוד הישראלי לרפואה דחופה.

Pulmonary embolism ECG findings are one of the most commonly tested Emergency Medicine board topics — and one of the easiest places to get tricked. Let's quickly cover what is the right answer on boards, and how in real life there is an even better option.

The post PODCAST: The PE ECG Finding Everyone Memorizes… But Gets Wrong first appeared on האיגוד הישראלי לרפואה דחופה.

Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.

Course Highlights:

Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function.

Hemodynamic Criteria:

Cardiac Index (CI): >4.0 L/min/m2.

Cardiac Output (CO): >8 L/min.

Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state).

The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses.

Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).

Effective Arterial Blood Volume: Paradoxically low despite high total CO.

Neurohormonal Cascade:

Activation of Renin-Angiotensin-Aldosterone System (RAAS).

Increased Sympathetic Nervous System tone.

Increased Antidiuretic Hormone (ADH) secretion.

Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion.

Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy.

Hyperthyroidism/Thyrotoxicosis:

Direct T3 effects: increased chronotropy/inotropy.

Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation.

Myeloproliferative Disorders:

High cell turnover and increased oxygen consumption drive compensatory CO increase.

Sepsis (Hyperdynamic Phase):

Cytokine-mediated global vasodilation.

Note: Often transient; may transition to sepsis-induced myocardial depression.

Arteriovenous Fistulas (AVF) / Malformations (AVM):

Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population).

Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation.

Chronic Liver Disease (Cirrhosis):

Formation of “spider angiomata” and internal AV shunts.

Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide).

Thiamine Deficiency (Wet Beriberi):

Accumulation of pyruvate/lactate → systemic vasodilation.

Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema.

Chronic Lung Disease:

Hypoxia/Hypercapnia-driven systemic vasodilation.

Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output.

Others: Paget’s disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma.

Acute Phase:

Immediate ↓ SVR.

↑ Stroke volume and Heart Rate (SNS-mediated).

Endothelial shear stress → Nitric Oxide release → further arterial dilation.

Subacute Phase (Days to 2 Weeks):

RAAS-driven volume expansion.

↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP).

Natriuretic peptide surge (BNP/ANP) peaks around Day 10.

Chronic Phase (Weeks to Months):

Adaptive hypertrophy.

Decompensation occurs when dilation exceeds contractility limits.

Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF):

Maneuver: Manually compress the AVF (or inflate cuff to >50 mmHg above SBP) for 30 seconds.

Positive Result: Reflexive bradycardia or a transient rise in systemic BP.

Significance: Confirms the shunt is a major contributor to the cardiac workload.

Peripheral Pulse Assessment:

Water Hammer Pulses: Rapid upstroke and collapse.

Quincke’s Pulse: Visible capillary pulsations in the nail beds.

Traube’s Sign: “Pistol-shot” sounds auscultated over the femoral arteries.

Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs).

Left Ventricle: Hyperdynamic function; EF typically >60%.

Left Atrium: Significant dilation (Left Atrial Volume Index >34 mL/m2; Case study noted 72 mL/m2).

IVC: Plethoric with minimal respiratory variation.

Doppler: High flow velocities across the AV access if applicable.

BNP/NT-proBNP: Often markedly elevated (e.g., >70,000 in severe cases), though mean values in literature hover around 700–800 pg/mL.

Hematology: CBC to evaluate for severe anemia (trigger for HOHF if Hgb<7–8 g/dL) or myeloproliferative markers.

Endocrine/Metabolic: TSH (Thyrotoxicosis), Serum Thiamine (Beriberi), LFTs (Cirrhosis).

Diuresis: Aggressive IV loop diuretics (Bumetanide/Furosemide).

Ultrafiltration: Preferred in ESRD patients failing to respond to dialysis or with refractory congestion.

Vasodilator Caution: Avoid aggressive Nitroglycerin or ACE-inhibitors initially.

Rationale: Baseline SVR is already pathologically low; further reduction may precipitate profound hypotension/circulatory collapse.

Anemia: Transfuse to goal Hgb>7–8 g/dL to reduce demand.

Beriberi: High-dose IV Thiamine (100–500 mg).

Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole).

Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites.

Flow Reduction (Banding): Surgical narrowing of the fistula to target flow <600 mL/min.

RUDI Procedure: Revision Using Distal Inflow (moving inflow to a smaller, more distal artery).

Ligation: Complete closure of the AVF.

Note: Requires bridge to Tunneled Dialysis Catheter or AV graft (higher resistance than fistulas).

The “Normal EF” Trap: Do not be reassured by an EF of 55–65%; in the context of pulmonary edema and high CO, this is potentially HOHF.

Pulse Pressure: Look for a wide pulse pressure (e.g., 180/60) as a marker of low SVR.

ESRD Logic: If an ESRD patient is “wet” immediately after HD, the problem is likely flow (AVF), not just fluid.

The post PODCAST: High-Output Heart Failure first appeared on האיגוד הישראלי לרפואה דחופה.

Cardiac arrest care has always been about the fundamentals—high-quality CPR, timely defibrillation, and effective ventilation. But as our guest experts Dr. Sheldon Cheskes and Dr. Rob Simard make clear in this EM Cases update as we reflect on the latest 2025 AHA guidelines, the fundamentals are evolving in ways that challenge some of our most ingrained habits and assumptions. In Part 1 of this series, we take a deep dive into the practical bedside application of CPR, defibrillation, and ventilation—moving beyond “cookbook” algorithms toward a more nuanced, performance-driven approach. From rethinking pad placement and shock strategy, to interpreting ETCO₂ in context rather than chasing arbitrary numbers, to recognizing that even subtle leaning on the chest during compressions can undermine outcomes—this episode is packed with pearls that demand we recalibrate how we run resuscitations. We explore why measuring CPR quality—and feeding that information back in real time—is no longer optional but central to care. We unpack concepts like compression-adjusted ventilation, the role of arterial lines during arrest, and feedback devices. And perhaps most provocatively, we challenge traditional dogma and the questions: Is the two-minute cycle too rigid? Should we be shocking earlier? Is head up CPR a viable technique?  and much more…

Podcast production, sound design & editing by Anton Helman; Voice editing by Erik Krosby

Written Summary and blog post by Anton Helman March, 2026

Cite this podcast as: Helman, A. Simard, R. Cheskes, S. Cardiac Arrest Update: Beyond the 2025 Guidelines Part 1: CPR, Defibrillation and Ventilation. Emergency Medicine Cases. March, 2026. https://emergencymedicinecases.com/cardiac-arrest-update-cpr-defibrillation-ventilation. Accessed March 27, 2026

The 2025 AHA ACLS Guidelines reaffirm what saves lives in cardiac arrest: rapid recognition, high-quality CPR, early defibrillation for shockable rhythms, timely vasopressor use, and coordinated post–cardiac arrest care. Those pillars are not new—and that’s the point. Survival gains in many systems have come less from novel drugs and more from better execution: faster emergency activation, higher bystander CPR rates, earlier AED deployment, and tighter choreography during resuscitation. What the guidelines cannot fully capture is the nuance required when the algorithm becomes sparse. In the ED, the most consequential decisions often occur precisely where evidence is uncertain and the flowchart stops giving direction—especially in VF after multiple shocks, epinephrine, and amiodarone with no ROSC. At that inflection point, the clinician has to think physiologically: Are we generating coronary perfusion pressure? Are we preserving it with compression fraction? Are we undermining ourselves with hyperventilation? Is VF truly shock-refractory or simply recurrent? Is our defibrillation technique actually delivering current through myocardium—or just delivering electricity into a high-impedance chest?

This episode focuses on those bedside inflection points—the places where small adjustments in timing, technique, and interpretation can plausibly change outcomes.

Chain of Survival

CPR

Monitoring, resuscitation targets and ventilation

Defibrillation

Refractory and recurrent VF, Dual Sequence Defibrillation

Epinephrine

Cardiac arrest care is defined less by what we add and more by how well we execute what already matters. The latest guideline-informed perspective reinforces that survival is driven by a series of interdependent steps, each of which must be optimized.

The chain of survival now explicitly includes:

The greatest impact comes from the earliest links—rapid activation, bystander CPR, and early defibrillation. By the time a patient reaches the ED without ROSC, prognosis is already significantly diminished, underscoring that ED care is only one part of a larger system.

High-quality CPR is one of the only interventions with a clear and consistent relationship to survival and neurological outcome. Even experienced clinicians frequently perform CPR poorly. CPR is physically demanding, and degradation in performance happens rapidly. Even within 45 seconds, compression quality begins to decline, which is why switching compressors every two minutes is not just recommended—it is essential. What is often under-appreciated is that CPR is not simply about generating movement—it is about generating forward blood flow. Every component—rate, depth, recoil—directly influences cardiac output during arrest. If any of these are suboptimal, perfusion to the heart and brain falls.

In practice, this means that the team leader must actively monitor CPR as a primary intervention, not assume it is being done correctly. High-performing teams treat CPR like a continuously titrated therapy. We often teach “rate 100–120, depth 5–6 cm, full recoil,” but those are surrogates. The real goal is uninterrupted perfusion.

Aortic diastolic pressure/arterial lines #1

If you rank physiologic targets by direct mechanistic link to ROSC and defibrillation success, aortic diastolic blood pressure is the most causally plausible bedside surrogate for CPP—when you have an arterial line. Diastolic pressure directly reflects the pressure gradient driving coronary blood flow, and both animal and human physiologic data support the association between higher diastolic pressures during CPR and higher ROSC likelihood. In practical terms, if an arterial line is present, many experienced resuscitationists aim for diastolic BP ≥25–30 mmHg (often higher if achievable) for whether CPR is generating meaningful myocardial perfusion.

The operational nuance for placing an arterial line is staffing and opportunity cost. In a lean resus (one physician and one nurse), arterial line placement can be counterproductive if it distracts from compressions, defibrillation timing, and ventilation discipline. With adequate personnel, an a-line can serve three high-yield roles:

Pitfall: Treating an arterial line like a life-saving intervention in itself. The line is a monitor—not a therapy—and it must never cost compression quality or pause time.

ETCO2 has strong physiologic plausibility because it reflects pulmonary blood flow and thus cardiac output generated by compressions. Higher ETCO₂ generally correlates with better perfusion and higher probability of ROSC, and a sudden sustained rise can signal ROSC. However, ETCO₂ is indirect and confounded by ventilation, airway problems, lung pathology, and metabolic state. It is best used as a trend and a quality monitor rather than a rigid interventional endpoint.

Compression fraction is foundational because it preserves CPP. It is not a “physiologic metric” in the same way, but it is causally upstream: if compression fraction is low, neither diastolic pressure nor ETCO₂ can be trusted to improve meaningfully.

Pearl: If you can measure only one physiologic CPR target, diastolic pressure has the strongest causal plausibility as a surrogate for CPP. ETCO₂ is extremely useful, but it is an indirect surrogate and must be interpreted in context.

End-tidal CO₂ confounders:

For example, a patient with chronically elevated CO₂ may have misleadingly high values, while a prolonged downtime may produce low values despite adequate CPR. The key clinical application is to interpret ETCO₂ in context, rather than using it as a standalone decision-making tool.

A persistently low ETCO₂ should trigger one question first: Is this a CPR quality problem, or a physiology problem?
If ETCO₂ is <10–15 mmHg:

Falsely low ETCO₂ can result from hyperventilation, excessive tidal volumes increasing intrathoracic pressure, poor compressions, severe PE, low metabolic CO₂ production in prolonged arrest, airway leaks/disconnections, or severe obstructive lung disease. Falsely elevated ETCO₂ can occur with hypoventilation, bicarbonate administration (transient CO₂ load), ROSC, or certain V/Q mismatch patterns.

Pitfall: ETCO₂ used as a discreet target is a common pitfall. Rather ETCO2 is a trend monitor. Use it to detect deterioration in perfusion, guide CPR optimization, and identify ROSC.

Key recurring problems include:

Each of these has a direct physiologic consequence. For example, leaning prevents ventricular filling during recoil, reducing preload. Incorrect rate disrupts optimal coronary perfusion pressure. Hyperventilation increases intrathoracic pressure, impairing venous return.

CPR errors are cumulative. Multiple small deviations can combine to produce profoundly ineffective circulation, even when CPR appears “acceptable” at a glance.

When CPR quality was first objectively measured in large studies, no system was consistently delivering high-quality CPR. Only after introducing measurement and feedback did performance improve.

In practical terms, this has several implications:

Interruptions in CPR are physiologically devastating. Coronary and cerebral perfusion pressures fall rapidly during pauses, and it takes multiple compressions to rebuild them. Minimizing interruptions is not about rushing—it is about anticipation.

Effective teams:

Ultrasound pulse checks can improve accuracy if performed with strict discipline. The value is not “more data”; it is faster confirmation of pulsatility at a known anatomic target. The danger is that ultrasound becomes a pause-extending distraction. The probe must be ready, positioned during compressions, and used to confirm flow during a brief pause—then compressions resume immediately. If interpretation requires longer thinking, capture/record a short clip and interpret after compressions restart.

Pearl: To minimize CPR interruption record the PoCUS pulse check for 3-5 seconds and resume CPR immediately, then interpret the recording

Feedback devices are appealing because they target something we know matters—compression quality—but the evidence is mixed and stronger for CPR process metrics than for survival. Real-time audiovisual feedback can modestly improve compression rate, depth, recoil, and sometimes compression fraction. Metronomes can help prevent drift in rate but do not ensure depth or recoil and have not convincingly improved outcomes alone. Analogue tactile “clicker” devices show promising signals in low-certainty data, likely because they enforce adequate depth with an unmistakable cue.

In practice, the most defensible role for feedback devices is within a quality improvement program. Measuring CPR quality across arrests, reviewing performance, identifying recurring failure modes, and retraining accordingly is where devices may produce system-level benefit. Even sensor-only measurement can improve performance through observation effects—teams compress better when they know compressions are being measured.

Head-up CPR has a physiologic rationale that is easy to like: elevating head and thorax may reduce intracranial pressure and improve cerebral venous drainage, potentially improving cerebral perfusion. But the concept is usually bundled with strategies to augment forward flow (active compression–decompression CPR, impedance threshold devices). Without those adjuncts, tilting could reduce venous return and compromise cardiac output.

Operationally, head-up CPR is difficult to do well with manual compressions. Maintaining consistent depth, recoil, and compression fraction while the patient is tilted is challenging. For practical reasons, head-up CPR typically needs to be paired with mechanical CPR to provide consistent compressions while allowing controlled elevation. The evidence base remains early and limited, with feasibility studies and small datasets—often bundled interventions—making it hard to isolate which component drives any observed signal. The strongest evidence for head-up CPR comes from animal studies, where combining head elevation with an impedance threshold device and mechanical CPR shows clear improvements in cerebral perfusion and intracranial pressure. However, they are explicit that translating these results into humans has been problematic, and that human studies are small and conflicting, with no convincing demonstration of improved survival. Although one center (Minnesota) has reported success with head-up CPR, other systems have not been able to replicate those results, raising concern that outcomes may depend heavily on highly specialized protocols and early implementation that are difficult to reproduce.

Mechanical CPR is not recommended for routine use, but it has clear roles in specific situations:

A key limitation is that application of the device can cause significant interruptions if not performed efficiently. There is a clear learning curve, and teams must train to apply devices rapidly (ideally within 10 seconds).

Ventilation mismanagement is one of the most common iatrogenic harms during cardiac arrest. Hyperventilation increases intrathoracic pressure, reduces venous return, decreases CPP, and increases intracranial pressure—reducing cerebral perfusion. Even experienced providers hyperventilate during the adrenaline of a code. The recommended approach remains simple but hard to execute: once an advanced airway is in place, provide one breath every 6 seconds (10/min), deliver each breath over ~1 second, and use only the tidal volume needed for visible chest rise. Over-ventilation is often not recognized in real time, which is why ventilation feedback devices and structured strategies are an important future direction.

Instead of timing breaths by counting seconds (which often fails under stress), synchronize ventilation with compressions using a 12:1 compression-to-ventilation ratio (one breath after every 12 compressions). At a compression rate near 120/min, this naturally generates ~10 breaths/min and reduces drift into hyperventilation. It anchors behavior to the rhythm of CPR rather than the wall clock.

Ventilation strategy during arrest is a major area of future research. The OPTIVO trial (Optimized Ventilation in Cardiac Arrest) is designed to evaluate whether a more physiologically optimized ventilation strategy—controlling rate and volume to minimize intrathoracic pressure and preserve venous return—improves outcomes compared with conventional practice. In parallel, ventilation feedback devices that provide real-time rate and tidal volume cues may reduce hyperventilation during chaotic resuscitation. Additionally, the evidence for the traditional 500–600 mL tidal volume target is weak; there are active investigations into whether 300–400 mL may be preferable. Early use of a ventilator in CPR mode to control asynchronous ventilation during arrest has a strong physiologic rationale but requires further study.

Pearl: If you can’t reliably deliver one breath every 6 seconds, use compression-adjusted ventilation (12:1) to “hard-wire” the correct rate into the resuscitation rhythm.

Defibrillation is deceptively simple—push a button and shock—but success depends on whether current actually traverses myocardium and whether perfusion has primed the heart to respond. Many “by the book” failures are not failures of the algorithm, but failures of technique and choreography.

Peri-shock pause is the major culprit: stopping compressions too early, charging after the pause begins, delaying compressions after the shock, and allowing rhythm checks to sprawl into extended hands-off time. Technical errors also matter: poor pad adhesion, pads placed on hair or moisture, incomplete chest exposure, or pad placement that does not maximize current through ventricular myocardium. A final strategic mistake is repeating identical shocks indefinitely without escalating defibrillation conditions—vector change, pad repositioning, energy escalation, or advanced strategies in refractory VF.

The two-minute CPR cycle is a practical teaching tool, not sacred physiology. Recurrent VF often occurs early after a shock within 30 seconds. Where rhythm filtering allows detection of refibrillation during compressions, there is physiologic plausibility to re-shock promptly when VF is clearly present rather than waiting an arbitrary full cycle. This is not stacked shocks with long pauses—it is the idea that we should avoid unnecessary time in VF while preserving compression fraction.

Emerging evidence suggests that anterior–posterior (AP) pad placement may deliver more current through the ventricles compared to anterior–lateral (AL). This is particularly relevant in ventricular fibrillation, where the goal is to deliver current through the ventricular myocardium. In contrast, atrial fibrillation cardioversion targets the atrium, explaining why AL may be ore effective for termination of atrial fibrillation.

Practically, AP placement can be achieved with minimal interruption:

A key conceptual shift is understanding that current—not energy—is what matters in defibrillation. This brings pad placement into focus. Incorrect placement, particularly placing the lateral pad too low or anterior (effectively shocking the spleen!), can result in ineffective current delivery. Many pad placements effectively “miss the heart,” delivering current through non-cardiac structures.

Pearl: Start with the fastest, cleanest, most consistent pad placement that preserves compression fraction. Escalate to vector change deliberately when shocks fail—without paying for it in pause time. Some systems start with AP positioning which appears to maximize current through the heart when compared to AL pad positioning.

In hairy patients, poor pad adhesion increases impedance and reduces effective current delivery. The key is to solve the contact problem without delaying shocks.

Pearl: Manually applying pressure to the pads in hirsute and/or sweaty patients during defibrillation is safe for the provider and increases current, the key factor in effective defibrillation

The 2025 AHA Guidelines provide no recommendations after 3 shocks, epinephrine and amiodarone are given in VF.

The traditional two-minute CPR cycle is increasingly questioned. Most patients who refibrillate do so within 30 seconds, not two minutes. This raises concern that waiting a full cycle before re-shocking may delay effective therapy.

While evidence is not definitive, the physiologic argument supports:

Dual sequential external defibrillation (DSED) uses two defibrillators and two pad sets to deliver two shocks in rapid sequence. This not simply “more joules,” but improved myocardial coverage through multiple vectors and a potential priming effect where the first shock alters the VF substrate, increasing susceptibility to the second shock delivered milliseconds later.

A major controversy is whether DSED harms CPR quality by introducing complexity and longer pauses. In the DOSE-VF trial, chest compression fraction was similar across all groups, including DSED. This suggests that, in trained systems, DSED can be implemented without compromising CPR quality, which is critical since CPR quality is strongly tied to outcomes. The practical implication is that DSED is a training problem, not an unavoidable pause problem: if your system cannot do it without prolonged hands-off time, it may not be worth it; if it can be integrated cleanly, it becomes a preferred escalation strategy.

DOSE-VF trial is a high quality sizeable randomized trial comparing:

The trial demonstrated that both vector change and DSED improved outcomes compared to standard defibrillation, including higher rates of ROSC and improved survival. While both vector change and DSED performed better than standard care, DSED is favored when feasible according to our experts.

Traditionally, DSED has been reserved for refractory VF after three failed shocks. However, there exists emerging data suggesting that earlier use of DSED may be beneficial. There are several small European studies showing a signal that early DSED—even after the first failed shock—might improve outcomes, and importantly, that early use does not appear harmful. Many institutions in North America already use DSED after the second shock, while others are waiting for more data before moving it as early as after the initial shock. This challenges the traditional “late rescue therapy” mindset and suggests that DSED may be more effective when used before prolonged ischemia and myocardial deterioration occur.

Stellate ganglion block is grounded in a simple physiologic idea: sympathetic overdrive fuels electrical instability. In prolonged refractory VF or electrical storm physiology, the myocardium is often bathed in catecholamines—from endogenous stress response and from exogenous epinephrine. This sympathetic surge lowers arrhythmia threshold and can perpetuate recurrent or refractory VF despite shocks and antiarrhythmics.

The stellate ganglion provides major sympathetic input to the heart. Blocking it produces a rapid temporary chemical sympathectomy, aiming to reduce arrhythmogenic drive and stabilize the myocardium so defibrillation and perfusion strategies can succeed. Observational evidence and systematic reviews suggest high rates of arrhythmia suppression or reduction in electrical storm, with low rates of serious complications. It is best thought of as a bridge therapy—buying time for definitive management such as PCI, ECMO, or ablation.

SG = Stellate Ganglion, CA = Carotid Artery SCM = Sternocleidomastoid

Complications are uncommon. Transient Horner’s syndrome and hoarseness may occur. Serious complications (vascular injury, pneumothorax, major bleeding) are rare with ultrasound guidance. Evidence is largely observational and protocols vary, but the physiologic rationale is coherent and the bedside feasibility is high in trained hands.

Epinephrine works because it raises aortic diastolic pressure via alpha-mediated vasoconstriction, increasing CPP and the probability of ROSC. The problem is that while epinephrine improves ROSC and survival to hospital admission, it has not consistently improved neurologically intact survival in a large, definitive way. That tradeoff matters most in shockable rhythms where defibrillation is the primary therapy and excessive catecholamine exposure may worsen electrical instability.

Guideline dosing remains 1 mg IV/IO every 3–5 minutes. High-dose epinephrine has not shown benefit and may cause harm. The nuanced bedside discussion is about rhythm-specific strategy: in VF, many clinicians stop epinephrine after 2–3 doses if VF remains refractory or recurrent, especially when catecholamine-driven instability is suspected. In PEA/asystole, early epinephrine appears more clearly associated with improved ROSC, and continued dosing is reasonable while aggressively searching for reversible causes—though prolonged futile resuscitations should still trigger a reassessment of goals and likelihood of meaningful outcome.

Pitfall: Continuing epinephrine for multiple doses without addressing reversible causes or without reconsidering whether catecholamines are perpetuating instability in refractory VF.

IM epinephrine is being explored as a way to deliver earlier epinephrine when IV access is delayed, particularly in the prehospital setting. Observational and pilot data suggest shorter time to first dose and signals for improved ROSC and early survival, especially in non-shockable rhythms, with uncertain impact on neurologically intact survival. The physiologic concern is absorption: in a low-flow arrest state, skeletal muscle perfusion is reduced, making IM uptake potentially delayed or unpredictable. The practical stance is cautious optimism: IM may be a bridge when IV/IO is delayed, but it should not replace rapid vascular access until randomized outcome data clarify its effect.

The AHA guideline direction emphasized here is a practical hierarchy: IV preferred, IO as backup. The reason is not that IO never works, but that IO reliability and pharmacokinetics may be less consistent than previously thought, and RCTs have not shown superiority despite perceived faster placement. Malposition and silent failure are key concerns.

Where PoCUS adds real value is confirmation of IO placement. Doppler ultrasound during flush can confirm medullary flow quickly without interrupting CPR, identifying nonfunctional IOs that otherwise would be assumed to work.

Pearl: If you’re using IO in arrest, especially when expected drug effects are absent, PoCUS Doppler confirmation can convert IO from a hopeful access point to a verified delivery route.

The post PODCAST: Cardiac Arrest Update: Beyond the 2025 Guidelines Part 1: CPR, Defibrillation and Ventilation first appeared on האיגוד הישראלי לרפואה דחופה.

In this episode, Sam Ashoo, MD and T.R. Eckler, MD discuss the February 2026 Emergency Medicine Practice article, Emergency Department Diagnosis and Management of Acute Coronary Occlusion

00:00 – Introduction & Welcome

01:21 – Episode Overview: Acute Coronary Occlusion

02:06 – Why This Topic Matters: Statistics & New Guidelines

03:35 – Nomenclature: ACO vs STEMI/NSTEMI

06:15 – Differential Diagnosis for STEMI

07:41 – Pre-Hospital Care & EMS Role

11:37 – Patient History & Presenting Symptoms

12:28 – Physical Examination Findings

14:54 – EKG: The Most Important Test

17:00 – STEMI Definition & Criteria

20:32 – STEMI Equivalents: Scarbosa Criteria

22:40 – Smith Modified Scarbosa Criteria

24:10 – Hyperacute T Waves

25:30 – Posterior STEMI

28:40 – De Winter Sign

29:38 – Non-STEMI EKG Findings

31:30 – AVR ST Elevation

32:47 – Wellens Syndrome

33:54 – Reciprocal ST Segment Changes

36:15 – Inferior MI Patterns

37:54 – Laboratory Testing

39:51 – Imaging: Chest X-Ray & Echocardiography

42:25 – Supplemental Oxygen: What the Evidence Shows

44:50 – Analgesia & Pain Management

46:35 – Pharmacotherapy: Aspirin & Antiplatelet Agents

49:18 – Reperfusion Therapies & Thrombolytics

53:05 – Cardiac Arrest in STEMI Patients

53:55 – Closing Remarks & CME Information

The post PODCAST: Acute Coronary Occlusion first appeared on האיגוד הישראלי לרפואה דחופה.

Date: January 3, 2026 

Reference: Shroyer et al. Accuracy of cath lab activation decisions for STEMI-equivalent and mimic ECGs: Physicians vs. AI (Queen of Hearts by PMcardio). Am J Emerg Med. 2025 Nov.

Guest Skeptic: Dr. Amal Mattu has been on the faculty at the University of Maryland since 1996. He has developed an academic niche in emergency cardiology and electrocardiography, and he also enjoys teaching and writing on other topics, including emergency geriatrics, faculty development, and risk management. Amal is currently a tenured professor and Vice Chair of Emergency Medicine at the University of Maryland School of Medicine, and a Distinguished Professor of the University of Maryland-Baltimore.

Case: A 58-year-old man with diabetes and hypertension arrives at the emergency department (ED) 30 minutes after the sudden onset of substernal chest pressure radiating to the left arm, now improved to 3/10. His vital signs are BP 146/88, HR 92, RR 18, O2 sat 98% on room air. The initial 12-lead ECG shows RBBB with left anterior fascicular block and subtle anterior ST‑depression with proportionally tall, broad T waves in V2 to V4. This is an appearance that can be seen with Hyper-Acute T Wave Occlusive Myocardial Infarction (HATW‑OMI) or an ST-Elevated Myocardial Infarction (STEMI)‑mimic in conduction disease. A debate ensues between emergency medicine and cardiology on whether to activate the cath lab now or get troponins plus serial ECGs?

Background: Emergency physicians need to be experts at interpreting ECGs. For decades, we’ve been taught STEMI criteria, only to learn repeatedly that important exceptions exist (posterior OMI, de Winter, hyperacute T waves, modified Sgarbossa in LBBB, etc.). Those exceptions have evolved into two distinct categories. There are the STEMI‑equivalents (OMI without classic ST‑elevation) and STEMI‑mimics (ST‑elevation without OMI). That expanding exception list increases diagnostic complexity and uncertainty. This is the area where artificial intelligence (AI), utilizing computer vision and machine learning, could provide a benefit.

ECG-specific AI models now aim squarely at this problem. The study we are reviewing today evaluated the Queen of Hearts (QoH) AI. It is a deep neural network trained to detect occlusive myocardial infarction (OMI) on 12-lead ECGs. The model is described as “91% accurate” in prior work and is undergoing FDA review as of March 24, 2025, but whether it outperforms practicing clinicians on the hardest cases (STEMI‑equivalents and mimics) remained unclear.

ECG diagnostic accuracy is important in emergency medicine because misclassification cuts both ways. Missed OMI delays reperfusion, while overcalls send patients and teams to the cath lab unnecessarily, putting patients at risk and using up valuable resources. A diagnostic aid that catches true positive OMIs while reducing false activations could improve outcomes and team throughput.

Reference: Shroyer et al. Accuracy of cath lab activation decisions for STEMI-equivalent and mimic ECGs: Physicians vs. AI (Queen of Hearts by PMcardio). Am J Emerg Med. 2025 Nov.

Authors’ Conclusions: “Physicians frequently misinterpret STEMI-equivalent and STEMI-mimic ECGs, potentially impacting CLA decisions. QoH AI demonstrated superior accuracy, suggesting a potential to reduce missed OMIs and unnecessary catheterization laboratory activations. Prospective studies are needed to validate these findings in clinical practice.” 

Quality Checklist for a Diagnostic Study:

Results: They recruited 95 physicians to interpret the ECGs. There were 53 EM physicians and 42 cardiologists (23 general, 15 interventional, 4 EP electrophysiology). Experience: EPs 7 years (IQR 3 to 15) vs cardiologists 15 years (IQR 9.2 to 21).

The most frequently misclassified by humans were LBBB (±OMI), transient STEMI, HATW‑OMI, and de Winter. QoH AI missed LBBB‑OMI and LV aneurysm. RBBB + fascicular block and HATW‑OMI produced the largest EP-cardiologist disagreement.

1) Spectrum Bias: The investigators intentionally selected “ambiguous” STEMI‑equivalent and STEMI‑mimic ECGs and fixed the OMI prevalence at 50% for the reader study. That design improves efficiency in comparing readers and the AI, but it does not reflect the spectrum or prevalence we see in day-to-day ED practice and therefore threatens external validity. In diagnostic accuracy research, spectrum bias occurs when the distribution of disease/non-disease, disease severity, or look-alikes in the sample differs from that in the clinical population in which the test will be used. It can change sensitivity and specificity in either direction. Selecting borderline cases may deflate both compared with routine practice, and it will certainly distort PPV/NPV because predictive values are prevalence‑dependent. The authors acknowledge this by noting the 50% OMI prevalence and the deliberate use of ambiguous ECGs “may not accurately reflect predictive values observed in real-world settings.”

2) Differential Verification & Imperfect Gold Standard: Not every patient had the same reference standard. While most OMI determinations used angiography, some mimic cases without angiography were adjudicated by serial troponins, echocardiography, and clinical follow-up. Using different reference standards in different subgroups constitutes differential verification (double gold‑standard) bias and can bias sensitivity and specificity up or down, depending on whether the disease can resolve or only become detectable over time. In addition, any composite or clinical adjudication process is an imperfect gold standard, which can either inflate or deflate the index test’s performance depending on how errors correlate across tests. The authors explicitly note these issues in their discussion.

3) Incorporation/Review Bias: The paper reports that cardiologists performing angiography were not masked to the ECG. When the result of (or information from) the index test helps determine the reference diagnosis, that is incorporation (review) bias. This typically inflates both sensitivity and specificity of the index test because the gold standard classification is partially “contaminated” by the test under study. In this context, seeing a concerning ECG may tilt the invasive assessment and adjudication toward “culprit” lesion labelling or influence borderline calls, making ECG-based classification look better than it truly is.

4) Unit‑of‑analysis & Precision Limitations: This was a reader study with 95 clinicians classifying the same small set of 18 ECGs. Even with appropriate statistics, the small number of cases means performance estimates can be fragile, and the 95% confidence intervals reflect that imprecision. To their credit, the authors modelled accuracy with multi-level robust variance to account for clustering (multiple readers rating the same cases), but the design still limits precision and generalizability across the full morphology spectrum of each category. The authors themselves state that “one representative ECG per type…cannot represent all ST‑T variants”, and that asking physicians to read far more than 18 tracings was impractical. This imprecision concerns should raise our skeptical radar, and we should factor this into our study interpretation.

5) External Validity: The study is single-center and uses an online survey without the interruptions, time pressure, serial ECGs, bedside echo, or troponin trends that influence ED decision‑making. The authors explicitly caution that the controlled survey conditions do not replicate real clinical environments and could over- or under-estimate real-world accuracy. AI performance can also be domain‑dependent (ECG device/process, patient mix). Showing “simulation” superiority does not guarantee clinical utility until confirmed in prospective practice studies. This is a limitation known in the diagnostic literature (including the AI diagnostic literature) that emphasizes the potential difference between an artificial scenario and prospective bedside clinical application. In other words, until it is released into the wild involving other hospitals and workflows, we don’t know if it will have a net positive patient-oriented outcome (POO) of benefit.

Comment on the Authors’ Conclusion Compared to the SGEM Conclusion: We generally agree with the authors’ conclusions.

Case Resolution: Given the concerning RBBB + LAFB with anterior repolarization changes and ongoing symptoms, we activate the cath lab. If available, an AI read supporting OMI would reinforce the call. If it disagreed, we would not delay for the algorithm. In the lab, the patient is found to have a proximal LAD culprit and undergoes PCI.

Dr. Amal Mattu

Clinical Application: The most significant finding that immediately makes me doubt the utility of the study is the chart that shows sensitivity and specificity. Even without all of the nerdy details, it is obvious that a 65% sensitivity for picking up OMIs (or my long-preferred term: acute coronary occlusion, ACO) is not possible. Any emerg phys or cardiologist who is missing 35% of ACOs is going to be fired, sued many times over, and driven out of medicine! Without reading any of the paper, as soon as I see that chart, I know it can’t be right unless the clinicians at his institution are incompetent.

No one has discussed the costs associated with integrating AI systems into all those ECG machines.

This QoH AI system is not ready for implementation in clinical practice outside a research study. The use of AI has the potential to augment clinical decision-making, but it is not currently done on autopilot without a human-in-the-loop.

What Do I Tell the Patient? Your ECG shows changes that could mean a blocked heart artery. We think the best course of action is to take you to the cath lab now to restore blood flow if needed. We also use a computer tool to double-check ECGs. It supports our concern, but it doesn’t replace us as doctors. The goal is to act fast and safely to get you the care you need.

Keener Kontest: Last week’s winner was Dr. Steven Stelts from Auckland, NZ. He knew the enzyme inhibited by etomidate to decrease cortisol and aldosterone is 11-beta-hydoxylase.

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The QT interval is a vital part of ECG interpretation, reflecting the heart’s electrical recovery after each beat. When prolonged, it can set the stage for torsades de pointes. Understanding how to measure and correct the QT interval, identify high-risk medications, and act quickly when TdP occurs is essential for every clinician. This guide walks you through the physiology, interpretation, common causes, and emergency management of QTc prolongation to keep your patients safe.

The post PODCAST: Understanding QTc Prolongation: Causes, Risks, and Management first appeared on האיגוד הישראלי לרפואה דחופה.

Jonathan H. Kim, MD, MSc1; Austin J. Rim, MD1; James T. Miller, MS1; et al

Question  What is the contemporary incidence of cardiac arrest and death among marathon and half-marathon runners in the US?

Findings  In this case series and cohort study from the Race Associated Cardiac Event Registry, the incidence of cardiac arrest during marathons and half-marathons has remained relatively stable since 2010, compared with 2000-2009. The risk of dying from cardiac arrest during long-distance running races has decreased by approximately 50% compared with 2000-2009.

Meaning  Effective emergency action planning during marathons and half-marathons, inclusive of immediate access to defibrillation, has likely led to significant improvements in cardiac arrest outcomes, equivalent to settings with publicly accessible automated external defibrillators.

Importance  More than 29 million participants completed marathons and half-marathons in the US between 2010-2023, approximately 3 times the number from 2000-2009. Contemporary long-distance race-related cardiac arrest incidence and outcomes are unknown.

Objective  To determine the incidence and outcomes of cardiac arrests during US marathons and half-marathons between 2010-2023 from a record of race finishers and a comprehensive review of cases from media reports, direct contact with race directors, USA Track & Field claims, and interviews with survivors or next of kin.

Design, Setting, and Participants  Observational case series from the Race Associated Cardiac Event Registry; cohort data from US marathon and half-marathon runners from January 1, 2010, to December 31, 2023. Case profiles were reviewed to determine etiology and factors associated with survival. Incidence and etiology data were compared with historical reference standards (2000-2009).

Exposure  Recreational long-distance running (marathon and half-marathon distance).

Main Outcomes  Incidence proportions of sudden cardiac arrest and death.

Results  Among 29 311 597 race finishers, 176 cardiac arrests (127 men, 19 women, 30 sex unknown) occurred during US long-distance running races. Compared with 2000-2009, cardiac arrest incidence remained unchanged (incidence rate, 0.54 per 100 000 participants [95% CI, 0.41-0.70] vs 0.60 per 100 000 [95% CI, 0.52-0.70], respectively). However, there were significant declines in cardiac death incidence (0.20 per 100 000 [95% CI, 0.15-0.26] vs 0.39 per 100 000 [95% CI, 0.28-0.52]) and case fatality rate (34% vs 71%). Cardiac arrests remained more common among men (1.12 per 100 000 [95% CI, 0.95-1.32]) than women (0.19 per 100 000 [95% CI, 0.13-0.27]) and during the marathon (1.04 per 100 000 [95% CI, 0.82-1.32]), compared with the half-marathon (0.47 per 100 000 [95% CI, 0.38-0.57]). Among runners for which a definitive cause of cardiac arrest could be determined (n = 67/128 [52%]), coronary artery disease rather than hypertrophic cardiomyopathy was the most common etiology. Decreased cardiopulmonary resuscitation time and an initial ventricular tachyarrhythmia rhythm were associated with survival.

Conclusions and Relevance  Despite increased participation in US long distance running races, cardiac arrest incidence remains stable. There has been a marked decline in cardiac arrest mortality, and coronary artery disease was the most common etiology among cases with sufficient cause-related data. Effective emergency action planning with immediate access to defibrillation may explain the improvement in survival.

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Millions of people participate in long-distance running, particularly marathons and half-marathons, annually.1 While the health benefits of regular exercise are well established,2 long-distance running can cause significant cardiovascular stress, potentially increasing the risk of cardiac arrest in individuals with underlying heart conditions.3 This concern is particularly notable as the number of middle-aged and elderly runners—a population at higher average cardiovascular risk than younger runners—continues to rise.4 Understanding the incidence, causes, and outcomes of cardiac arrest in long-distance runners is crucial for informing risk, identifying prevention strategies, and optimizing race-day medical preparedness.

In this issue of JAMA, Kim et al5 report on a comprehensive prospective observational study that investigated the incidence and outcomes of cardiac arrest during marathons and half-marathons in the US between 2010 and 2023. Their study provides valuable insights into the incidence, risk factors, etiologies, and survival trends associated with cardiac arrest in long-distance runners.

The researchers used data from the Race Associated Cardiac Event Registry (RACER), a prospective registry of marathon and half-marathon runners in the US.1 A targeted, multistep algorithm was used to identify cases of cardiac arrest through media reports, direct contact with race directors, and USA Track & Field claims data. This systematic approach minimized the risk of underreporting and ensured a more accurate representation of cardiac arrest incidence. A similar approach was used in an earlier report using RACER data, allowing for comparisons over time.1

A total of 176 cardiac arrest cases were identified among 29 311 597 race finishers between 2010 and 2023. The incidence of cardiac arrest remained relatively stable over this period compared with the previous decade (2000-2009), with an incidence proportion of 0.54 per 100 000 participants. However, the study revealed a significant decline in cardiac arrest mortality from 2010-2023 compared with 2000-2009 (34% vs 71%, P < .001).1,5 The study also highlighted key demographic factors associated with higher cardiac arrest incidence. Men were found to be at a higher risk than women, with an incidence rate of 1.12 per 100 000 compared with 0.19 per 100 000 in women. Marathons were associated with a higher incidence proportion of cardiac arrest, compared with half-marathons (1.04 per 100 000 vs 0.47 per 100 000).

Coronary artery disease was identified as the most common cause of cardiac arrest, accounting for 40% of cases. This finding contrasts with earlier studies that identified hypertrophic cardiomyopathy as the predominant cause.1 The authors suggest that the shift in etiology may be due to improved case ascertainment methods and a potential bias in previous studies toward identifying hypertrophic cardiomyopathy cases. It is also possible that diagnosis and treatment of hypertrophic cardiomyopathy has improved to the point that it now accounts for only a small minority of cardiac arrest cases in marathon runners.

The strengths of the study include its large sample size, comprehensive case identification methods, and detailed analysis of clinical profiles that may help identify individuals at the highest risk for cardiac arrest during long-distance running. The study also has limitations. Race finishing times were used as surrogates for race participants, which may have resulted in some participants being counted more than once. This would have the potential effect to underestimate cardiac arrest risk slightly. There is no reason to believe this limitation would have differed in the prior RACER analysis; thus, relative comparisons between periods are likely still valid. The study was unable to ascertain the cause of cardiac arrest in approximately 50% of cases, which may limit the accuracy of the etiologic findings.

Despite these limitations, the study has important clinical implications. The decline in cardiac arrest mortality likely underscores the importance of effective emergency action planning during races, including immediate access to defibrillation. Rapid access to prehospital automated external defibrillators has been associated with a favorable survival and neurologic outcome in distance runners who experience a cardiac arrest.6 The findings of the study also may reinforce the importance of primary cardiac prevention in older runners, particularly men, who are at higher risk of coronary artery disease. This is in line with some lines of thinking that would support use of low-dose aspirin before races to prevent cardiovascular events, including cardiac arrest, in patients with an increased estimated atherosclerotic risk.7

This study provides valuable insights into the incidence, causes, and outcomes of cardiac arrest during long-distance running races. While the overall incidence of cardiac arrest has remained stable, the significant decline in mortality highlights the positive impact of improved medical preparedness for races. The study’s findings emphasize the need for continued efforts to enhance primary and secondary prevention strategies for runners, ensuring the safety of participants in long-distance running events.

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