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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limitations when it comes to drawing any conclusions of superiority, including the older registry data with potentially outdated practices, the inability to assess timing of antiarrhythmic administration, and the potential for residual confounding.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.

Dr. Jonathan Thompson dives into the fascinating world of high-altitude medicine, explaining how hypoxia affects the body and lead to conditions like acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). He highlights how hypoxia is a universal concept relevant to emergency and critical care medicine, and that understanding altitude illness can improve care for patients, whether you practice on a mountain or not!

Bio: Dr. Jonathan Thompson is a former Green Beret in the U.S. Army Special Forces and former U.S. Army Special Operations Mountaineering Instructor that taught in Colorado, Alaska, and Wyoming. He completed a Masters in Physiology at the University of Michigan with a thesis on nitrate supplementation in the prevention and treatment of acute high-altitude illnesses. He is an annual, returning guest lecturer (2020-present) at the University of Michigan’s Department of Physiology instructing undergraduate and graduate students on high-altitude physiology, pathophysiology of acute altitude illnesses, and relevant treatments.

Guest: Jonathan Thompson, MD, MS; Host: Kim Bambach, MD; Audio editor: Nick Roesel

Key Learning Points:

The Bottom Line:

The best treatment is descent, and everything else is a bridge. When you’re out adventuring, don’t forget to go slow to acclimatize!

The post PODCAST: Thin Air, High Stakes: Altitude Medicine first appeared on האיגוד הישראלי לרפואה דחופה.

Dr. Jonathan Thompson dives into the fascinating world of high-altitude medicine, explaining how hypoxia affects the body and lead to conditions like acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). He highlights how hypoxia is a universal concept relevant to emergency and critical care medicine, and that understanding altitude illness can improve care for patients, whether you practice on a mountain or not!

Bio: Dr. Jonathan Thompson is a former Green Beret in the U.S. Army Special Forces and former U.S. Army Special Operations Mountaineering Instructor that taught in Colorado, Alaska, and Wyoming. He completed a Masters in Physiology at the University of Michigan with a thesis on nitrate supplementation in the prevention and treatment of acute high-altitude illnesses. He is an annual, returning guest lecturer (2020-present) at the University of Michigan’s Department of Physiology instructing undergraduate and graduate students on high-altitude physiology, pathophysiology of acute altitude illnesses, and relevant treatments.

Guest: Jonathan Thompson, MD, MS; Host: Kim Bambach, MD; Audio editor: Nick Roesel

Key Learning Points:

The Bottom Line:

The best treatment is descent, and everything else is a bridge. When you’re out adventuring, don’t forget to go slow to acclimatize!

The post PODCAST: Thin Air, High Stakes: Altitude Medicine 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.

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Chris and Wade talk about sepsis.

For EMT and AEMT classes, check out IdahoMedicalAcademy.com and use code "Summit" at checkout for 10% off.

Welcome to the Basically EMT podcast! We are very excited to be able to bring this new content to all of you and hope that you find it as fun and as informative as we do. With so many outlets for media, it can be hard to find accurate, up-to-date, and digestible material. With basically EMS we hope to be your go to station to listen for basic EMS information. Listen as our highly knowledgeable guests talk about their experiences in the field and share their expertise.

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Japanese Airway Study: Kubo A, Kunitatsu K, Nakashima T, Horitani R, Kajimoto Y, Inoue S, Hironishi M. Association between endotracheal intubation and outcomes of nonshockable out-of-hospital cardiac arrest in Japan. BMC Emerg Med. 2025 Sep 24;25(1):185. doi: 10.1186/s12873-025-01341-6. PMID: 40993541; PMCID: PMC12462024.

The post PODCAST: Association between endotracheal intubation and outcomes of nonshockable out-of-hospital cardiac arrest in Japan 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

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"Should we be giving blood transfusions to patients with traumatic cardiac arrest?" EMJ editor Prof. Richard Body and associate editor Dr. Sarah Edwards talk through some original research on the value of blood transfusions in this difficult situation. Next is the new UNCORKED study from the Trainee Emergency Research Network (TERN), with some sobering statistics on the prevalence of emergency care carried out in non-standard treatment places across the UK. Then we move to a world of high-pressure injuries, often caused by industrial spraying equipment, where things on the surface aren't quite as they seem. The last paper returns to the theme of cardiac arrests, examining the predictive value of end-tidal CO2 usage.

Read the highlights: Primary survey:

The EMJ podcast is hosted by:

Prof. Richard Body, EMJ Editor-in-Chief, University of Manchester, UK (@richardbody)

You can subscribe to the EMJ podcast on all podcast platforms to get the latest podcast every month. If you enjoy our podcast, please consider leaving us a review or a comment on the EMJ Podcast Apple (https://apple.co/4bfcMU0) or Spotify (https://spoti.fi/3ufutSL) page.

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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.

The post PODCAST: Playing with the Queen of Hearts – AI, Is It Very Smart (for ECG Interpretation)? first appeared on האיגוד הישראלי לרפואה דחופה.

Administration of blood products in the field prior to hospital arrival

Aimed at patients in hemorrhagic shock

Traditional US prehospital resuscitation relied on crystalloid

ED and trauma care now prioritize early blood

Hemorrhage occurs before hospital arrival

Delays to definitive hemorrhage control are common

Earlier blood may improve survival

ATLS and trauma paradigms emphasize blood over fluid

National organizations support prehospital blood when feasible

EMS already manages high risk, time sensitive interventions

Data are mixed and evolving

COMBAT: no benefit

PAMPer: mortality benefit

RePHILL: no clear benefit

Signal toward benefit when transport time exceeds ~20 minutes

Urban systems still experience long delays due to traffic and geography

LA County median time to in hospital transfusion ~35 minutes

~2 years of planning before launch

Pilot began April 1

Partnerships:

LA County Fire

Compton Fire

Local trauma centers

San Diego Blood Bank

14 units of blood circulating in the field

Blood rotated back 14 days before expiration

Ultimately used at Harbor UCLA

Continuous temperature and safety monitoring

Focused rollout

Trauma related hemorrhagic shock

Postpartum hemorrhage

Physiologic criteria:

SBP < 70

Or HR > 110 with SBP < 90

Shock index ≥ 1.2

Witnessed traumatic cardiac arrest

Products:

One unit whole blood preferred

Two units PRBCs if whole blood unavailable

~28 patients transfused at time of discussion

Evaluating:

Indications

Protocol adherence

Time to transfusion

Early outcomes

Too early for outcome conclusions

Multiple active programs:

Riverside (Corona Fire)

LA County

Ventura County

Additional programs planned:

Sacramento

San Bernardino

Programs meet monthly as CalDROP

Focus on shared learning and operational optimization

Trauma surgeon concerns about blood supply

Need for system wide buy in

Community engagement

Patients who may decline transfusion

Women of childbearing age and alloimmunization risk

Risk of HDFN is extremely low

Clear communication with receiving hospitals is essential

Rapid national expansion expected

Greatest benefit likely where transport delays exist

Prehospital Blood Transfusion Coalition active nationally

Major unresolved issue: reimbursement

Currently funded largely by fire departments

Sustainability depends on policy and payment reform

Hemorrhagic shock is best treated with blood, not crystalloid

Prehospital transfusion may benefit patients with prolonged transport times

Implementation requires strong partnerships with blood banks and trauma centers

Early data are promising, but patient selection remains critical

National collaboration is key to sustainability and future growth

The post PODCAST: Prehospital Blood Transfusion first appeared on האיגוד הישראלי לרפואה דחופה.