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Curriculum/Cardiovascular/Arrhythmias

ARR-01 · Part 1 of 2

Arrhythmias:
acute decisions.

Assess pulse and perfusion, classify the rhythm, and choose the next intervention. Cases below connect the ECG to treatment, contraindications, and monitoring.

Start the opening case
Scope & review details
Release0.13.6
Acute / narrative review2026-10-08
Pass review due2027-01-08
ScopeAdults · first 10 minutes
Contents
Opening case00:00

Tachycardia with new confusion

A 68-year-old with ischemic cardiomyopathy becomes confused and diaphoretic. Pulse 184/min, blood pressure 74/42 mm Hg. The rhythm is regular and wide. You have IV access, pads are going on, and the patient still has a pulse.

What is the decision?

Compare your next step
Immediate synchronized cardioversion.

The organized tachycardia is plausibly driving shock. Sedate only if feasible without delaying treatment. Sustained polymorphic VT needs an unsynchronized shock; pulse loss moves to CPR and the arrest pathway.

AHA 2025 · wide-complex tachycardia

First, decide what the rate is doing.

A fast monitor number can be the problem, or a response to the problem. Sinus tachycardia in hemorrhage is not asking for a circuit breaker. A sudden organized tachycardia with new shock may be. Work on rhythm and perfusion together; do not make the patient wait for a perfect rhythm name.

Keep pads and a rescue plan ready during a drug attempt. “Stable” describes this moment, not the next ten minutes. AHA 2025 guidance

The master decision tree

Pulse → instability → width → regularity.

Identify the rhythm and whether it is causing poor perfusion before choosing a drug. A regular wide-complex rhythm with a pulse and shock requires a different action from stable SVT.

01Pulse?No pulse → cardiac-arrest pathway. Pulse present → continue.
02Is the rhythm causing instability?Hypotension, shock, altered mental status, ischemic chest discomfort, or acute heart failure—linked causally to the rhythm.
Yes · causal instabilityFor a causative tachyarrhythmia, electrical therapy usually outruns medication. Synchronize tachycardias with an organized QRS; polymorphic VT cannot reliably synchronize and requires an unsynchronized shock.
No · presently stableObtain a 12-lead when feasible, treat reversible causes, and classify before choosing a rhythm-specific drug.
03QRS width?Narrow <120 ms usually means ventricular activation through the His–Purkinje system. Wide ≥120 ms expands the differential and raises the price of a wrong assumption.
NarrowRegular

Think AVNRT/AVRT, atrial tachycardia, flutter with fixed conduction, or sinus tachycardia.

For suspected stable re-entrant SVT: modified Valsalva, then adenosine when appropriate. Sinus tachycardia calls for treatment of its cause, not conversion. Ask whether the rhythm is AV-node-dependent or whether adenosine will only reveal atrial activity.

NarrowIrregular

Think AF, flutter with variable conduction, MAT, or frequent ectopy.

Choose rate/rhythm therapy from ventricular function, pressure, congestion, sympathetic state, duration, anticoagulation context, and the precipitating illness.

WideRegular

Treat uncertain wide-complex tachycardia as VT until a safer explanation is established.

Stable regular monomorphic WCT may receive an antiarrhythmic infusion and expert consultation. Adenosine is confined to stable, regular, monomorphic WCT when an AV-node-dependent mechanism is plausible.

WideIrregular

Pause: polymorphic VT, pre-excited AF, AF with aberrancy, toxicity, and artifact live here.

Do not reflexively give an AV-nodal blocker. In pre-excited AF it can favor accessory-pathway conduction; sustained polymorphic VT requires immediate unsynchronized shock.

Mechanism anchor

A wide QRS is a warning label, not a diagnosis.

Think of width as the ventricular delivery route. Narrow usually means activation used the native conduction highway. Wide means it took a detour—or started in the ventricle. The detour does not name the rhythm, but it raises the cost of the wrong drug.

Regularity tells you how many clocks are arguing.

A regular rhythm suggests one repeating circuit or focus. Irregularity can reveal competing atrial wavefronts, variable AV conduction, changing ventricular activation, or polymorphism. That is why a drug that fits AVNRT can be useless—or dangerous—one branch over.

Explore this decision

Podcast · EMplify · EB Medicine Wide Complex Tachycardia An ED discussion to connect a wide QRS to the patient, the differential and the next intervention.

Sam Ashoo, MD, and T. R. Eckler, MD · 27 Apr 2026 · page updated 27 May 2026 · About 50 minutes · choose a chapter

Look or listen for
Start with bedside steps at 7:54. For a focused return, use the accessory-pathway discussion at 14:09 or stability assessment at 27:58. Times below are the publisher’s chapter labels; seek in its player.
Before opening
Without naming a drug, list the findings that would make you abandon a diagnostic or infusion-first plan.
Bring it back
Return to the unstable-WCT case and explain what changed the treatment priority.
Access
Public podcast page/player and chapter list. No transcript was found on that page. The companion article/CME is subscriber material.
Review scope
Publisher description and chapter list checked; audio and subscriber article not reviewed.
Boundary
Expert discussion, not a protocol. Keep the current AHA pathway and local resuscitation policy beside it; the recording has not been auditioned here.

Publisher chapters

  • 7:54 · Bedside steps
  • 14:09 · AF with an accessory pathway
  • 27:58 · Stable versus unstable
  • 38:00 · Treatment
  • 44:49 · Risk-management pitfalls
Open Wide Complex Tachycardia at EMplify · EB Medicine Return to the unstable-WCT case

Source and access checked 2026-10-16.

One case · four lenses

After unstable wide-complex tachycardia.

Review medication execution, evolving physiology, discharge planning, and the diagnostic/procedural plan after the opening case.

AccountabilityExecution under time pressure

Make the next intervention executable and intercept medication-system failure before administration.

  1. Name the syndrome, not a fragile diagnosis.“Unstable regular wide-complex tachycardia with a pulse” is enough to act safely.
  2. Build and verify the electrical plan.Confirm sync markers, pads, energy strategy, sedation feasibility, airway support, and the post-conversion branch.
  3. Prepare the rescue branch.Sustained polymorphic VT → immediate unsynchronized shock. Pulse loss → start CPR and follow arrest rhythm analysis; defibrillate VF/pVT.
  4. Own the last safe medication mile.Prioritize high-risk orders; verify selection, dose, concentration, route, pump strategy, compatibility, monitoring, and stop rules before the drug enters the line.
AccountabilityMedication coherence over days

Turn a successful conversion into a coherent daily plan, then a safe transition the next team and patient can actually follow.

  1. Reconstruct the trigger and substrate.Ischemia, scar, HF decompensation, infection, thyroid disease, sleep apnea, electrolyte loss, alcohol, stimulant exposure, and medication changes.
  2. Reconcile every indication.Separate acute rescue from chronic prevention, resolve duplications and interactions, and avoid therapeutic inertia after the reason for a drug changes.
  3. Reassess the whole regimen daily.Specify rhythm endpoints, QT/QRS thresholds, electrolyte targets, renal/hepatic reassessment, adherence barriers, and what finding triggers escalation or de-escalation.
  4. Close the transition.Document the cardiology/EP plan, anticoagulation logic, monitoring ownership, patient teach-back, access, and the exact follow-up question.
AccountabilityDynamic physiology + ICU safety

Ask whether the arrhythmia is the driver of shock, a consequence of shock, or both—and re-answer as the physiology changes.

  1. Interrogate hemodynamics.Preload, contractility, vascular tone, RV/LV function, mechanical support, ventilator effects, catecholamine exposure, and perfusion markers.
  2. Model changing PK/PD.Low hepatic flow, AKI/CRRT, acidemia, altered protein binding, cumulative infusions, and active metabolites can change effect within hours.
  3. Reduce the arrhythmogenic environment.Treat ischemia, hypoxia, acidosis, fever, agitation, pain, electrolyte loss, and unnecessary sympathomimetics or QT/QRS-active drugs.
  4. Plan, document, and debrief recurrence.Defibrillation readiness, pacing, sedation/sympathetic control, EP escalation, mechanical support, handoff, and medication-safety learning after the event.
Counter-lensDiagnosis + procedure + prognosis

Explain what circuit or focus exists, why this patient developed it, and which diagnostic or procedural decision changes the trajectory.

  1. Build the differential from anatomy.Ventricular scar re-entry, SVT with aberrancy, pre-excitation, focal automaticity, triggered activity, drug/toxin effect, and metabolic conduction delay.
  2. Use ECG findings as likelihood modifiers.AV dissociation, capture/fusion, concordance, axis, morphology, prior BBB, and comparison with baseline—without pretending any one algorithm is absolute.
  3. Choose definitive diagnostics.Post-conversion ECG, echo, ischemic workup, medication/toxin history, family history, CMR, ambulatory monitoring, genetics, or EP study as the case warrants.
  4. Define the endpoint.Acute termination, recurrence suppression, ablation, device therapy, substrate treatment, prognosis, and shared decisions.
What the practice standards changed in these lenses

The shared floor is comprehensive medication management: assess the patient and medication problem, build and implement a collaborative plan, follow outcomes, communicate, and keep developing competence. Specialty changes what must happen first and what failure is most costly.

ED

ASHP emphasizes resuscitation presence, prospective interception of high-risk medication errors, medication preparation/administration support, toxicology, order triage, discharge work, quality improvement, education, and research.

Medicine

The BCPS/general clinical-pharmacy frame emphasizes patient-centered plans, evidence appraisal, repeated monitoring/modification, communication, education, medication-use systems, and transitions across a broad adult population.

Critical care

The ASHP–ACCP–SCCM position and BCCCP outline add daily interdisciplinary rounds, dynamic PK/PD, devices and organ support, resuscitation, stewardship, ICU medication safety, quality analytics, and ICU-to-ward transitions.

Physician · generalist

This remains a deliberate counter-lens: diagnostic synthesis, procedural eligibility, prognosis, and shared decisions. It is not presented as a pharmacy board-certification domain.

Credential boundary: BCPS is the current broad pharmacotherapy baseline. BCCCP supplies the critical-care specialization. BPS has published a validated BCEMP outline effective December 1, 2026; until then, it is a forthcoming specialty blueprint, not a credential the learner is expected already to hold.

Acute case ladder

Pick one of twelve cases—not a queue to finish. Choose an action and explain your reason before comparing. Then change the patient and rehearse the recommendation.

Original synthetic patients · difficulty is an authoring guide, not a validated score. Case choices and spoken rehearsal are not saved or graded as clinical competence.

Straightforward

Recognize the branch and make the first move.

EDPalpitations at 190/min

A 35-year-old has abrupt palpitations, a regular narrow rhythm at 190/min, BP 126/78, and no ischemic symptoms. They can cooperate. A brief seated strain has not helped.

What would you do next, and what result would make you reconsider the rhythm diagnosis?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Use a standardized modified Valsalva maneuver if appropriate: strain followed promptly by supine repositioning and passive leg elevation. If unsuccessful, prepare the adenosine pathway with ECG recording and rescue capability.

Why

REVERT studied stable SVT and found more conversion with the postural modification than standard Valsalva. A loosely performed seated strain is not the same intervention. AV-nodal interruption treats circuits that depend on the node.

Hazard to avoid

Repeated vagal or drug attempts must not delay electrical treatment if perfusion deteriorates. If transient AV block reveals ongoing flutter, the atrial rhythm is not terminated by blocking the node.

Every option, and when it would fit

  1. Give adenosine now; the first seated strain already failed.

    Adenosine can interrupt an AV-node-dependent circuit, but a casual seated strain is not a standardized modified maneuver. This stable, cooperative patient has an opportunity for an effective non-drug attempt first.

    Different patient or conditions: If a properly performed maneuver fails and the rhythm remains eligible regular SVT, use adenosine with ECG recording, rapid delivery/flush, and rescue readiness. Contraindications still matter.

  2. Try a standardized modified Valsalva, with an adenosine/rescue plan ready. Best fit here

    Best fit here. The patient can cooperate and has preserved perfusion. The postural modification changes venous return and the vagal response; the circuit must depend on AV-nodal conduction for interruption to terminate it.

    Different patient or conditions: Only while the patient remains stable and can safely perform the maneuver. Deteriorating perfusion or an irregular wide rhythm changes the branch.

  3. Use immediate synchronized cardioversion because the rate is 190/min.

    A rate alone does not establish causal instability. Electrical treatment is effective, but this stem supports trying the appropriate stable-SVT pathway rather than treating a number as shock.

    Different patient or conditions: If the tachycardia causes hypotension, shock, altered mentation, ischemic discomfort, or acute HF, prioritize synchronized cardioversion. It also remains an option when eligible stable treatment fails or is contraindicated.

  4. Use IV amiodarone as the broadest first-line SVT drug.

    Broad antiarrhythmic activity is not a reason to bypass a well-defined AV-node-dependent SVT pathway. It introduces a slower and more complex medication attempt without addressing the immediate diagnostic question.

    Different patient or conditions: Amiodarone has selected VT and AF roles; those require a different rhythm/substrate assessment. It is not a substitute first step for this cooperative stable-SVT patient, and IV amiodarone is not an exception in pre-excited AF.

Make it executable

Record the rhythm during the maneuver and any adenosine attempt. Verify the selected product/local rapid-push and flush method before administration; watch for transient AV block, ongoing atrial activity, conversion and recurrent symptoms. Recheck perfusion rather than repeating attempts automatically.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

The rhythm is now irregular and wide, with variable QRS shapes. The patient is still perfusing.

Does the adenosine plan still fit? What dangerous mechanism must you consider?

Review the changed case

No: possible pre-excited AF changes the branch. Avoid AV-nodal blockers, reassess stability, and prepare the appropriate rhythm-specific drug or electrical pathway. If perfusion deteriorates, do not delay electrical treatment for more diagnostic certainty.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

I'd try a properly performed modified Valsalva while this patient is stable and cooperative. If that fails and the rhythm remains regular and narrow, prepare adenosine with continuous ECG recording and rescue capability. If AV block reveals flutter, reassess rather than assuming conversion. If perfusion deteriorates, move to electrical treatment.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Adenosine

Sources: REVERT-2015 ACC-SVT-2015 · Original patient; guideline/label-based teaching and expert synthesis.

EDBradycardia with confusion

A patient is hypotensive and confused with complete AV block and a wide escape rhythm at 28/min. Atropine has not improved ventricular rate or perfusion.

What should lead the treatment plan now?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Prepare and establish effective pacing with resuscitative support, while evaluating reversible causes. Confirm mechanical as well as electrical capture; ECG spikes alone do not prove perfusion.

Why

Vagolysis may not improve distal conduction disease. Atropine response is not a definitive localization test, and a critically slow escape rhythm needs stabilization rather than prolonged diagnostic speculation.

Hazard to avoid

Do not mistake pacing artifact for effective capture or allow sedation preparation to delay life-saving stabilization. Assign monitoring, analgesia/sedation, and escalation responsibilities.

Every option, and when it would fit

  1. Wait for more atropine trials before preparing pacing.

    Atropine has already failed to improve this unstable complete block. More diagnostic speculation or repeat dosing must not delay effective perfusion support.

    Different patient or conditions: Atropine is reasonable in acute bradycardia with hemodynamic compromise, particularly when a nodal/vagal mechanism may respond. It is not a prerequisite to delaying pacing in deteriorating high-grade block.

  2. Accept pacing spikes on the monitor as successful resuscitation.

    Electrical artifact is not mechanical capture. Even apparent electrical capture needs a perfusion check: pulse/pressure, mentation and other bedside evidence must improve.

    Different patient or conditions: Spikes help evaluate pacing delivery but are never sufficient proof of perfusion. Check capture and escalate ineffective pacing.

  3. Use synchronized cardioversion to reset the slow rhythm.

    Cardioversion treats selected tachyarrhythmias; it does not supply missing ventricular impulses in complete AV block. This is a pacing/perfusion problem, not a rapid-circuit termination problem.

    Different patient or conditions: Synchronized cardioversion fits a causative unstable organized tachycardia with a pulse. That different rhythm is not present here.

  4. Establish effective pacing/resuscitative support, confirm mechanical capture and evaluate reversible causes in parallel. Best fit here

    Best fit. Transcutaneous pacing can bridge to transvenous pacing; adrenergic support may also be needed according to response and resources. Stabilization and cause-finding occur together.

    Different patient or conditions: This patient has persistent compromised perfusion after atropine. Toxin-related or metabolic causes add targeted treatment; neither pacing nor a chronotropic drug replaces that work.

Make it executable

Assign pacing/capture checks, pressure monitoring and analgesia/sedation without delaying stabilization. Verify any epinephrine/dopamine infusion using the current local protocol and correct concentration/pump. Escalate failed capture or persistent hypoperfusion; investigate ischemia, hypoxia, electrolytes and medicines/toxins.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

New information suggests beta-blocker poisoning rather than isolated conduction disease.

What does this add to your stabilization plan?

Review the changed case

Continue resuscitative stabilization while adding toxin-specific evaluation and management with toxicology support. The standard bradycardia algorithm alone is not a complete poisoning plan, and apparent electrical capture is not proof of adequate perfusion. This foundation case does not supply a full toxicologic treatment protocol.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

Atropine hasn't restored perfusion; I'd prioritize effective pacing and resuscitative support now rather than delay for repeated drug trials. Confirm mechanical capture, not just spikes, and assign monitoring and analgesia/sedation responsibilities without delaying stabilization. Evaluate reversible causes and escalate promptly. If poisoning is suspected, add toxicology support and toxin-specific management.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Atropine

Sources: AHA-ALS-2025 ACC-BRADY-2018 · Original patient; guideline/label-based teaching and expert synthesis.

EDNew confusion during rhythm evaluation

A 61-year-old with a regular monomorphic WCT at 176/min was initially talking with BP 112/70. Before medication starts, they become confused; BP is 72/40 and a pulse remains. Pads are attached.

What is the next action now—not the plan from three minutes ago?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Immediate synchronized cardioversion for the organized tachycardia with a pulse and causal instability.

Why

The perfusion change overrides the earlier drug plan. Synchronization avoids delivering a shock during the vulnerable repolarization period of an organized rhythm.

Hazard to avoid

Do not keep calling this 'stable VT' because that was true at the first set of vitals. Sedation and ECG confirmation must not become causes of delay.

Every option, and when it would fit

  1. Start the planned procainamide infusion first.

    The patient no longer meets the premise of a tolerated drug attempt. Infusion-related hypotension and treatment delay matter when perfusion is already failing.

    Different patient or conditions: A selected stable monomorphic WCT patient may be eligible for a monitored drug attempt with rescue ready. Restored stability would require reassessment; it does not excuse delaying shock now.

  2. Perform immediate synchronized cardioversion, with sedation only if it will not delay treatment. Best fit here

    Best fit. The organized tachycardia now plausibly causes shock and altered mentation. Confirm synchronization markers and reassess pulse; do not wait for a perfect VT-versus-SVT label.

    Different patient or conditions: Synchronized treatment fits organized unstable tachycardia with a pulse. Sustained polymorphic VT needs an unsynchronized shock; loss of pulse changes to the arrest pathway.

  3. Try diagnostic adenosine because the QRS morphology is uniform.

    Regular monomorphic morphology is necessary for the selected WCT adenosine exception but not sufficient: stability is also required. This patient is unstable.

    Different patient or conditions: Only selected stable, regular, monomorphic WCT when the mechanism is uncertain, with continuous monitoring and rescue capability.

  4. Wait for the 12-lead to prove VT.

    A diagnostic test that delays stabilization has the wrong priority. The syndrome—organized tachycardia with causal instability—is enough to treat.

    Different patient or conditions: A 12-lead is valuable when obtainable without delaying urgent care, and after conversion to clarify mechanism and substrate. It is not a gate before treatment here.

Make it executable

Confirm pulse, pads and sync markers; assign shock and airway/rescue responsibilities. Sedate only if feasible without delay. After treatment, reassess ECG, pressure and consciousness, and investigate ischemia, electrolytes and medication triggers.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

Before the shock, the rhythm becomes sustained polymorphic VT with no consistently identifiable QRS for synchronization.

Would you keep trying to synchronize?

Review the changed case

No. Deliver an immediate unsynchronized shock for sustained polymorphic VT. If the pulse is lost, begin CPR and follow the VF/pulseless-VT arrest pathway. Do not delay shock to obtain a QT measurement.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

The patient's perfusion has deteriorated, so I'd stop the drug-first plan and cardiovert this organized tachycardia now. Confirm sync markers; sedation only if it will not delay treatment. If it becomes sustained polymorphic VT, use an unsynchronized shock; if pulseless, start CPR and the arrest pathway.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Procainamide Adenosine

Sources: AHA-ALS-2025 · Original patient; guideline/label-based teaching and expert synthesis.

Explore the reasoning

Review · EHRA consensus · endorsed by HRS, APHRS and LAHRS Management of electrical storm or clustered ventricular arrhythmias For the next question after stabilization: what if VT keeps returning despite apparently successful treatment?

Radosław Lenarczyk and colleagues · Europace · 8 Apr 2024 · evidence search through Nov 2023 · Advanced optional reading · §8 acute management

Look or listen for
Read §8.1 on triggers and assessment, then §§8.2.3–8.2.8 on ICD management, sedation, drug therapy and escalation. Keep structural heart disease and primary electrical disease separate.
Before opening
A patient has recurrent ICD shocks. What might perpetuate the cycle besides failure of the antiarrhythmic drug?
Bring it back
Outline the ED pharmacist’s immediate work and the questions that require electrophysiology/ICU input. State where shock, sedation, hemodynamics and definitive treatment fit.
Access
Open-access full text. Repository access may occasionally show a browser check; the PubMed record also links the publisher.
Review scope
Methods and selected acute-management sections inspected, including device, sedation, pharmacotherapy and escalation. No complete dose-table audit or independent clinician approval.
Boundary
A consensus review, explicitly not a guideline; evidence strength varies. This adds optional context, not a new electrical-storm module. Use current AHA/local resuscitation guidance, not older regional shock/drug sequences as a US order set.
Open Management of electrical storm or clustered ventricular arrhythmias at EHRA consensus · endorsed by HRS, APHRS and LAHRS PubMed record and publisher access — Management of electrical storm or clustered ventricular arrhythmiasReturn to acute case practice

Source and access checked 2026-10-16.

More to weigh

Select therapy, check eligibility, and define the stop rule.

EDWide-complex tachycardia with a pulse

A 67-year-old with prior MI has regular monomorphic WCT at 168/min. They are alert with BP 118/72. There is no acute HF, major renal impairment, or baseline QT prolongation. Cardioversion is available.

If the team selects procainamide, what would you monitor and what ends the attempt?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Prepare continuous ECG/pressure monitoring and an immediate electrical rescue plan. During the selected infusion, stop for rhythm suppression, hypotension, QRS widening >50%, or the protocol maximum.

Why

PROCAMIO favored procainamide over its studied amiodarone regimen in tolerated WCT, but the comparison was small and open-label. The result informs this selected pharmacologic attempt, not a mandate to infuse every VT patient.

Hazard to avoid

A normal-looking pressure at one moment is not sustained stability. Do not stack successive QT/conduction-active agents without reassessing cumulative effects.

Every option, and when it would fit

  1. Finish the planned infusion even if pressure falls; conversion takes time.

    This treats the drug plan as more important than evolving perfusion. Procainamide can lower pressure and widen conduction; deterioration ends the tolerated-VT attempt.

    Different patient or conditions: There is no appropriate role for continuing an infusion through the stated stop criteria. Continued treatment is conditional on ongoing eligibility and the protocol's limits.

  2. Add amiodarone immediately if procainamide has not converted the first few minutes.

    Stacking conduction/QT-active drugs can compound hypotension and proarrhythmia. Failure is a reason to reassess and use electrical treatment when indicated, not to reflexively layer agents.

    Different patient or conditions: Amiodarone may be an alternative selected WCT pathway before this exposure. After another antiarrhythmic, further drug selection requires explicit specialist reassessment of cumulative exposure and risk; no automatic combination is endorsed.

  3. Monitor ECG and pressure continuously; stop at termination, hypotension, excess QRS widening or the protocol maximum. Best fit here

    Best fit for the selected attempt. Read QRS and pressure as treatment endpoints, not just safety paperwork. Pads and synchronized cardioversion must be immediately available if the patient deteriorates.

    Different patient or conditions: This stem intentionally excludes major renal impairment, baseline QT prolongation and acute HF. Their presence would change eligibility, agent selection or preference for electricity.

  4. Give diltiazem because AF with aberrancy has not been excluded.

    An uncertain wide rhythm is not permission to assume supraventricular origin. Nodal blockade and negative inotropy may cause collapse without treating VT.

    Different patient or conditions: Diltiazem belongs in eligible rate-control contexts with an established diagnosis, suitable LV function and no pre-excitation—not undifferentiated WCT.

Make it executable

Use the current approved infusion protocol to verify dose, concentration, pump rate and line/access requirements. Obtain a baseline QRS, QT and pressure; specify who monitors, who stops the infusion, and who performs cardioversion. Do not improvise a second agent when the first fails.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

During the attempted drug treatment, VT persists and the patient becomes confused and hypotensive.

Do you continue the comparison of antiarrhythmics, or change the treatment sequence?

Review the changed case

Stop the infusion attempt and prepare synchronized cardioversion for VT with a pulse and hemodynamic instability. The patient's deterioration, not the trial's preferred drug, controls the next step. Reassess the pulse; pulse loss changes to the arrest pathway.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

If we choose a drug attempt for this currently tolerated monomorphic WCT, procainamide is reasonable in the stated substrate. I'd monitor ECG and pressure continuously with cardioversion ready. Stop for termination, hypotension, QRS widening over 50%, or the protocol maximum. Any deterioration changes the plan to electricity; don't stack agents without reassessment.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Procainamide Amiodarone

Sources: PROCAMIO-2017 AHA-ALS-2025 · Original patient; guideline/label-based teaching and expert synthesis.

EDRecent-onset palpitations

A perfusing patient with symptomatic recent-onset AF wants rhythm restoration. The team is discussing a drug–shock approach versus electrical cardioversion alone.

What must you establish before borrowing the RAFF2 result?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Check onset certainty, thromboembolic risk and anticoagulation requirements, stability, contraindications, and whether this is primary AF or secondary to an acute illness. Clarify sedation feasibility and the patient's preference.

Why

RAFF2 studied selected stable acute AF patients. High conversion rates do not erase the trial's eligibility or the separate stroke-prevention decision. Drug–shock was not statistically superior in the primary conversion comparison.

Hazard to avoid

Do not interpret a nonsignificant superiority test as proof of equivalence, or interpret successful conversion as completion of the anticoagulation plan.

Every option, and when it would fit

  1. Establish onset, stroke/anticoagulation context, primary versus secondary AF, contraindications and patient preference first. Best fit here

    Best fit. A conversion trial answers how a strategy performed in its selected population; it does not establish this patient's eligibility. A shared treatment plan needs both symptom/rhythm goals and thromboembolic protection.

    Different patient or conditions: For stable acute AF, this assessment precedes elective strategy selection. If AF itself causes instability, emergency cardioversion takes priority while anticoagulation is addressed as soon as feasible.

  2. Choose drug–shock because RAFF2 proved it superior.

    The primary comparison did not demonstrate statistical superiority. Drug-first can avoid sedation in some eligible patients, but exposure, adverse effects and patient preference remain part of the choice.

    Different patient or conditions: A drug–shock strategy may fit a trial-like eligible acute primary-AF patient with no drug contraindication and electrical rescue available. It is a strategy option, not an obligation created by the trial.

  3. Choose shock alone because conversion removes the need for anticoagulation.

    Successful conversion does not erase atrial stunning, pre-existing thrombus or long-term stroke risk. The procedure and anticoagulation decisions are linked but are not interchangeable.

    Different patient or conditions: Electrical cardioversion may fit an eligible stable patient who prefers rapid restoration and can undergo sedation, or an unstable patient requiring urgent treatment. Anticoagulation still requires its own plan.

  4. Treat every acute AF episode as primary AF, even during sepsis.

    This ignores the possibility that AF is a manifestation of another illness. A high conversion rate in selected primary AF does not tell you to prioritize conversion over treatment of the precipitant.

    Different patient or conditions: No universal primary-AF assumption is appropriate. A rhythm strategy may still be necessary if AF is contributing materially to instability; that is a patient-specific causal assessment.

Make it executable

Before an elective conversion attempt, verify anticoagulant history/adherence, onset reliability, contraindications and sedation/airway arrangements. Document the chosen rhythm endpoint, post-conversion monitoring, recurrence plan and the clinician responsible for anticoagulation follow-up.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

Further history makes onset uncertain. The patient also has sepsis, and AF developed during that illness.

What changes before you select a conversion strategy?

Review the changed case

Reassess the precipitating illness, perfusion, rate/rhythm goals, and cardioversion safety, including thromboembolic risk and anticoagulation. The selected recent-onset primary-AF trial does not supply a ready-made plan for uncertain-onset AF during sepsis. Identify whether the arrhythmia itself is causing instability.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

Before picking drug–shock versus shock alone, I'd verify onset, anticoagulation and thromboembolic risk, stability, and whether this is primary AF. RAFF2 supports high conversion in selected patients, not automatic eligibility or proof of equivalent strategies. Let's also clarify sedation feasibility and the patient's preference, then leave an explicit anticoagulation plan.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Procainamide

Sources: RAFF2-2020 ACC-AF-2023 · Original patient; guideline/label-based teaching and expert synthesis.

EDPalpitations and pulmonary edema

A 73-year-old has known EF 25%, acute pulmonary edema, AF at 145/min and BP 98/64. They are alert and warm, receiving respiratory support. AF onset is uncertain and they have missed anticoagulant doses. The team is evaluating whether AF is the cause or a contributor. They ask about rate-control eligibility while reassessing perfusion.

Which medication recommendation best accounts for this substrate?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Intercept IV diltiazem and unqualified beta-blockade. Continue stabilization/precipitant treatment; choose any eligible rate-control attempt with explicit monitoring and cardioversion/stroke-risk awareness.

Why

The same nodal effect can be helpful in stable AF and harmful when contractile reserve is failing. Digoxin and amiodarone have different onset, clearance and conversion consequences; they are not interchangeable rescue labels.

Hazard to avoid

Do not normalize the rate at the expense of perfusion, or assume every pulmonary-edema patient needs the same drug. Determine whether AF is actually driving instability.

Every option, and when it would fit

  1. Use IV diltiazem because it usually lowers the rate quickly.

    Rapid rate reduction is not the only endpoint. Negative inotropy can worsen this patient with substantial LV systolic dysfunction and acute decompensation.

    Different patient or conditions: IV diltiazem may fit hemodynamically stable AF with EF >40%, suitable pressure and no pre-excitation. That is a different patient.

  2. Use an esmolol bolus without concern because it washes out quickly.

    A short half-life permits titration; it does not prevent immediate hemodynamic harm from beta-blockade in decompensated HF. The current physiology, not reversibility alone, sets eligibility.

    Different patient or conditions: Carefully selected beta-blockade can fit stable eligible rate-control patients. This stem does not justify an unqualified bolus in active decompensation.

  3. Treat the HF/precipitants and reassess causal instability; consider digoxin or selected IV amiodarone only after their separate safety checks. Best fit here

    Best fit. Digoxin can be considered when usual nodal agents are contraindicated, but onset and renal exposure matter. IV amiodarone may fit selected decompensated/critically ill patients; it can also cardiovert, so uncertain onset and missed anticoagulation matter.

    Different patient or conditions: If AF itself causes hemodynamic instability, prioritize synchronized cardioversion. In a still-perfusing patient, choice depends on urgency, pressure, renal function, interactions and rhythm/stroke goals—not a universal 'HF drug'.

  4. Give IV amiodarone solely for rate control and ignore cardioversion risk.

    The name of the intended goal does not prevent rhythm conversion. A medication can cross the rate/rhythm boundary while the patient's anticoagulation remains incomplete.

    Different patient or conditions: Amiodarone may still be selected after assessing alternatives and accounting for possible conversion and thromboembolic protection. In emergency instability, necessary cardioversion must not wait for elective anticoagulation requirements.

Make it executable

Check renal trajectory, electrolytes, baseline QT/conduction, cumulative drugs and anticoagulant adherence. Use a current regimen/preparation reference for the selected intervention; monitor pressure, respiratory status and rhythm. Stop/reassess deterioration and have electrical rescue ready.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

Despite support, pressure falls to 74/42 with new confusion. The team judges the tachyarrhythmia a major cause of worsening perfusion.

Should missed anticoagulant doses delay the emergency intervention?

Review the changed case

No. Prioritize synchronized cardioversion for AF causing instability. Address anticoagulation as soon as feasible with the treating team, but do not import elective waiting or imaging requirements into a life-threatening emergency. Continue treating the HF and precipitant.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

I'd avoid IV diltiazem with EF 25% and active decompensation; esmolol's short half-life doesn't make an unqualified bolus safe. Let's treat the HF, reassess whether AF is driving instability, and choose between eligible alternatives using urgency, renal function and pressure. If amiodarone is chosen, account for possible conversion and the missed anticoagulation. Deterioration caused by AF changes the plan to emergency cardioversion.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Diltiazem Esmolol Digoxin Amiodarone

Sources: ACC-AF-2023 AHA-ALS-2025 Esmolol label Digoxin label · Original patient; guideline/label-based teaching and expert synthesis.

Explore the reasoning

Podcast · CardioNerds Acute Management of Atrial Fibrillation · episode 431 Hear how comorbid illness and ventricular function reshape the rate-versus-rhythm conversation.

Jonathan Chrispin, MD, with Naima Maqsood, Kelly Arps and Jake Roberts · 24 Oct 2025 · Case discussion · duration not confirmed

Look or listen for
Use the first patient in the written notes, then the decompensated-HF discussion. Compare the reason for a fast rate with the harm caused by it.
Before opening
In AF plus pulmonary edema, what would tell you whether the rhythm is driving instability or accompanying another illness?
Bring it back
Revisit the AF/decompensated-HF case. Give a recommendation, its hemodynamic boundary and a rescue plan before revealing the existing feedback.
Access
Public publisher player and detailed written show notes; show notes are not a verbatim transcript. No chapter times verified.
Review scope
Show notes checked against the lesson’s acute safety boundary; recording not auditioned.
Boundary
The notes’ general advice to anticoagulate before rhythm control is not a reason to delay emergency cardioversion for instability caused by AF. Use current AF/AHA guidance for cardioversion eligibility and anticoagulation.
Open Acute Management of Atrial Fibrillation · episode 431 at CardioNerds Return to the AF/decompensated-HF case

Source and access checked 2026-10-16.

Complex

Clearance, interactions, and a changing patient alter the plan.

WardAn elevated level after a loading dose

A patient received an IV digoxin load. A concentration was drawn 1 hour later and flagged high. The patient is perfusing without new ectopy, AV block, GI symptoms, or visual complaints.

What can this level tell you—and what can it not tell you?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Confirm dose and sample times, renal function, electrolytes, and ECG. Arrange a properly timed sample when needed; a concentration obtained before distribution is complete should not be interpreted as a trough.

Why

Digoxin distributes into tissue over hours. A high early circulating concentration is not by itself a diagnosis of toxicity, and a loading decision is not interchangeable with maintenance dosing.

Hazard to avoid

Timing is not an excuse to ignore symptoms or dangerous arrhythmias. If findings suggest toxicity, act on the clinical syndrome and seek toxicology support rather than waiting for a convenient number.

Every option, and when it would fit

  1. Give digoxin immune Fab immediately based on the flagged one-hour concentration alone.

    An early post-load concentration is affected by distribution and cannot independently diagnose toxicity. Treating a flagged number without the clinical syndrome confuses exposure measurement with the decision to give an antidote.

    Different patient or conditions: Fab may be needed for severe suspected digoxin toxicity, including dangerous arrhythmias or other life-threatening findings. Seek toxicology support; do not wait for a perfectly timed sample when the patient is clinically toxic.

  2. Verify dose/sample timing, ECG, symptoms, renal function and electrolytes; obtain a correctly timed level if needed. Best fit here

    Best fit. The patient currently lacks the toxicity features described in the stem. Tissue distribution explains why a one-hour level differs from a post-distribution concentration.

    Different patient or conditions: Use this interpretation while monitoring the actual patient. New symptoms, conduction change or ventricular arrhythmia override reassurance from timing or a later lower number.

  3. Dismiss toxicity permanently because the sample was drawn early.

    Timing limits interpretation of this sample, not the possibility of toxicity. Renal decline, interacting exposure and electrolyte changes can alter risk while the laboratory number becomes less striking.

    Different patient or conditions: There is no appropriate permanent dismissal. A clinically well patient may not need antidote, but still needs contextual reassessment.

  4. Repeat a loading dose now because a one-hour level is unusable.

    A poorly timed sample does not mean the previous dose vanished. Loading and maintenance decisions require the dose history and evolving response, not replacement of a 'bad lab' with another drug exposure.

    Different patient or conditions: Additional loading is only a deliberate, reference-verified clinical decision after cumulative dose, renal status, response and safety assessment—not an automatic reaction to sample timing.

Make it executable

Reconstruct cumulative dose and collection times from the administration record, not recollection. The label advises a pre-dose or at-least-six-hour post-dose sample. Reassess ECG, renal trajectory, potassium and magnesium; keep clinical-toxicity escalation separate from the sampling plan.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

Creatinine has now risen, potassium is abnormal, and the patient has nausea plus new ventricular ectopy. The reported digoxin concentration is less dramatic than before.

Does the lower concentration reassure you? What deserves priority now?

Review the changed case

No. Renal deterioration, electrolyte changes, symptoms, and ventricular ectopy raise concern for toxicity. Assess and treat the clinical syndrome with ECG/electrolyte monitoring and toxicology support as indicated; do not dismiss it because the number is lower or postpone necessary care until another sample arrives.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

I wouldn't diagnose toxicity from a level drawn one hour after the IV load. Let's verify dose and sample times, ECG, symptoms, renal function, and electrolytes, then obtain a properly timed level if needed. That timing caveat doesn't override dangerous clinical findings: new arrhythmias or symptoms require immediate reassessment and toxicology support when indicated.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Digoxin

Sources: Digoxin label · Original patient; guideline/label-based teaching and expert synthesis.

Internal medicineA new prescription at admission

A patient has taken dofetilide uneventfully for months. A new TMP–SMX prescription is entered, and the latest renal function is worse than baseline.

Is separating administration times enough?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

No. Intercept the contraindicated trimethoprim combination and choose an appropriate antimicrobial alternative with the team. Review renal function, current QT, other interactions, and whether the rhythm prescription remains within its protocol.

Why

Trimethoprim interferes with renal cation secretion, increasing dofetilide exposure. Timing separation does not remove this clearance interaction; renal deterioration adds another exposure problem.

Hazard to avoid

A previously tolerated regimen is not protected from a new interacting medication. Do not convert a contraindication into a 'monitor more closely' plan without changing the prescription.

Every option, and when it would fit

  1. Separate TMP–SMX and dofetilide by several hours.

    This is a clearance interaction, not two drugs meeting in the gut. Trimethoprim inhibits renal cation secretion; spacing administrations does not remove increased dofetilide exposure.

    Different patient or conditions: Timing separation may solve selected absorption interactions, but has no appropriate role as the sole fix for this contraindicated combination.

  2. Give both but obtain one extra ECG.

    Monitoring can detect harm; it does not make a contraindicated combination acceptable. Worsening renal clearance adds risk beyond the interaction itself.

    Different patient or conditions: ECG surveillance remains essential after changing the prescription. It is not an alternative to intercepting the combination.

  3. Intercept TMP–SMX and reassess QT, renal function, other drugs and the dofetilide protocol with the team. Best fit here

    Best fit. Remove the contraindicated exposure, then reassess the remaining rhythm regimen. The substitute antimicrobial must fit the infection, organism, allergy and organ function rather than simply have a different name.

    Different patient or conditions: The patient already takes dofetilide; review is especially important with illness, renal change or an interruption. Any restart needs its own monitored reinitiation assessment.

  4. Hold dofetilide today, then let the patient resume the old dose at home tomorrow.

    This bundles a plausible hold for review with an unsafe automatic restart. The interruption, QT, current clearance and remaining interactions control the reinitiation plan.

    Different patient or conditions: Holding therapy may be part of the treating team's safety plan. Reinitiation is not a routine home refill; use the monitored protocol and do not assume that yesterday's dose remains eligible.

Make it executable

Check the active order and last administrations immediately. Escalate abnormal QT or ventricular arrhythmia; do not initiate a new dose while eligibility is unresolved. For reinitiation, the label requires at least three days of continuous ECG monitoring with CrCl calculation and resuscitation capability.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

The antibiotic interaction has been addressed. You learn that the patient stopped dofetilide during the illness and now wants to restart it at home.

Is resolving the interaction enough to approve an outpatient restart?

Review the changed case

No. Verify the interruption and obtain a protocol-based reinitiation plan with the treating team. Dofetilide reinitiation requires monitored care; renal function, QT, and current interactions still matter. Do not treat this as a routine refill or assume the old tolerated dose remains appropriate.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

I'd stop the TMP–SMX order and find an appropriate antimicrobial alternative with the team. Trimethoprim raises dofetilide exposure through a clearance interaction, so separating times doesn't solve it. With renal function worsening, also review the current dose protocol, QT, and other interactions. If dofetilide was interrupted, clarify the monitored reinitiation plan rather than simply restarting it.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Dofetilide

Sources: Dofetilide label · Original patient; guideline/label-based teaching and expert synthesis.

EDRecurrent arrhythmia after vomiting

An 80-year-old taking sotalol has gastroenteritis and new AKI. Between episodes, sinus rate is 46/min, QTc is approximately 580 ms and potassium is 3.1 mmol/L. Several brief polymorphic VT episodes caused presyncope and self-terminated. The patient is currently perfusing in sinus rhythm; pads are attached.

What is the prevention plan now, and what makes you stop talking and shock?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Prevent recurrence by removing acquired triggers and correcting electrolytes with IV magnesium as appropriate. Be ready for immediate unsynchronized shock if polymorphic VT becomes sustained.

Why

The patient is currently between episodes, which gives a brief chance to change the substrate. It does not mean the next run is safely tolerated. QT-active exposure and slow-rate pauses can continue after a medication is withheld.

Hazard to avoid

Never collapse 'torsades treatment' into magnesium alone. Do not add a QT-prolonging drug or label selected isoproterenol as routine treatment for every long-QT phenotype.

Every option, and when it would fit

  1. Withhold the culprit, give IV magnesium/correct electrolytes, monitor continuously and obtain expert help for persistent pause-triggered recurrence; shock immediately if sustained. Best fit here

    Best fit for recurrent acquired long-QT torsades between self-terminating runs. Renal loss of clearance, repolarization delay, hypokalemia and pauses converge. Recurrence prevention is a separate job from terminating sustained polymorphic VT.

    Different patient or conditions: Magnesium fits the long-QT recurrence problem even if the serum magnesium is not low. Persistent bradycardia/pause-triggered episodes may need expert-guided pacing or selected isoproterenol—not a universal chronotropic strategy.

  2. Give amiodarone because all polymorphic VT gets the same antiarrhythmic.

    This ignores the substrate. Additional QT-active treatment can promote acquired torsades instead of solving its trigger.

    Different patient or conditions: Selected normal-QT polymorphic VT recurrence, particularly with ischemia, has a different drug discussion. Do not transfer that plan to a known prolonged-QT case.

  3. Give more beta-blockade to suppress every ventricular arrhythmia.

    In this acquired, bradycardic/pause-triggered setting, further slowing can worsen the trigger. Arrhythmia suppression is not one mechanism across all long-QT syndromes.

    Different patient or conditions: Beta-blockers have distinct roles in selected congenital long-QT or adrenergic arrhythmia contexts. Those require a different diagnosis and specialist plan, not extrapolation into this acquired pause-dependent episode.

  4. Wait for another magnesium level, then try synchronized cardioversion if the next episode persists.

    Neither a serum result nor synchronization should delay treatment of sustained polymorphic VT. Its changing complexes cannot be synchronized reliably.

    Different patient or conditions: Electrolyte sampling informs correction without delaying rescue. Synchronized cardioversion fits organized tachycardia; sustained polymorphic VT requires an unsynchronized shock.

Make it executable

Check the last sotalol doses, renal trajectory and all QT-active agents. Verify the current IV magnesium preparation/rate and electrolyte protocol, accounting for organ function. Monitor ECG, pressure and recurrent pauses; obtain urgent specialist support for persistent recurrence while maintaining defibrillation readiness.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

The next polymorphic VT episode persists. The patient becomes unresponsive while the monitor continues to show changing QRS complexes.

Does magnesium or pacing come before the electrical rescue?

Review the changed case

No. Deliver an immediate unsynchronized shock for sustained polymorphic VT. Assess pulse promptly; if pulseless, start CPR and the VF/pulseless-VT arrest pathway. Magnesium, trigger correction and expert-guided rate support address recurrence and must not delay shock.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

This looks like acquired long-QT torsades with sotalol accumulation, low potassium and pauses. I'd withhold the culprit, correct electrolytes and give IV magnesium using the current protocol, with continuous monitoring and pads on. Persistent pause-triggered recurrence needs urgent expert-guided rate support. If a run becomes sustained, shock unsynchronized immediately; don't wait for magnesium or a pacing wire.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Sotalol Magnesium Isoproterenol

Sources: AHA-ALS-2025 Sotalol label · Original patient; guideline/label-based teaching and expert synthesis.

Explore the reasoning

Video · CardioNerds · Cardiovascular Fundamentals The QT Interval with Dr. Nino Isakadze A visual refresher on QT measurement and its pitfalls before interpreting a proarrhythmia risk.

Nino Isakadze, MD · Publication date not confirmed · Focused lecture · duration not confirmed

Look or listen for
Follow the measurement explanation. Keep separate what is measured, how rate correction is chosen and what the number can tell you in this patient.
Before opening
Which assumptions would you check before accepting the monitor’s QTc as the final answer?
Bring it back
Return to the sotalol/AKI/pauses case. Explain the risk using the patient’s rhythm, exposure and electrolytes—not the QTc alone.
Access
Official YouTube video linked by the creator’s fundamentals page. Captions and chapter times not checked.
Review scope
Creator description and official video title/channel checked; recording not auditioned. Date and duration remain unverified.
Boundary
Measurement foundations only; do not use this older fundamentals series as the current torsades or cardioversion treatment pathway.
Open The QT Interval with Dr. Nino Isakadze at CardioNerds · Cardiovascular Fundamentals Return to the sotalol/AKI/pauses case

Source and access checked 2026-10-16.

Very difficult

Separate competing mechanisms and coordinate rescue, medication review, and handoff.

EDA rapid rhythm with varying QRS complexes

A patient has a very rapid irregular wide rhythm with changing QRS morphology. They are currently alert, but pressure is drifting down. Diltiazem has been suggested because the rhythm looks like AF.

Which drugs must you intercept, and what is the deterioration branch?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Avoid AV-nodal blockers in pre-excited AF, including adenosine, beta-blockers, diltiazem/verapamil, digoxin, and IV amiodarone. If stable, specialist-supported procainamide or ibutilide may be options; hemodynamic instability prioritizes electrical cardioversion.

Why

Preferentially blocking the AV node can favor rapid accessory-pathway conduction and precipitate VF. The broad utility of amiodarone elsewhere does not make IV amiodarone an exception here.

Hazard to avoid

Treat the high-risk pattern before demanding a perfect historical WPW diagnosis. Monitor for pulse loss; VF/pulseless VT follows the arrest/defibrillation branch.

Every option, and when it would fit

  1. Give diltiazem to slow the AV node before deciding about cardioversion.

    This is the dangerous shortcut. In pre-excited AF, suppressing AV-nodal conduction can favor very rapid accessory-pathway ventricular activation and degeneration to VF.

    Different patient or conditions: Diltiazem may fit confirmed AF without pre-excitation, with suitable ventricular function and pressure. Changing only the drug dose does not make it safe in pre-excited AF.

  2. Use IV amiodarone because it is safer than other nodal blockers in WPW.

    IV amiodarone is not a safe exception to the pre-excited-AF prohibition. Its familiar use in other arrhythmias can make this wrong choice particularly tempting.

    Different patient or conditions: IV amiodarone has selected VT or non-pre-excited AF roles. It must not be borrowed for this high-risk pre-excited-AF pattern.

  3. Try adenosine to see whether the irregular wide rhythm is SVT.

    The diagnostic adenosine exception is confined to a stable, regular, monomorphic WCT—not an irregular, variably wide rhythm. A brief nodal block can be harmful here.

    Different patient or conditions: A different stable regular narrow orthodromic AVRT, or selected stable regular monomorphic WCT, may be eligible with monitoring and immediate rescue. That does not transfer to this rhythm.

  4. Intercept nodal blockers, reassess perfusion immediately, and prepare electrical cardioversion; consider procainamide/ibutilide only if truly stable and eligible. Best fit here

    Best fit. Act on the hazardous pattern while establishing the mechanism. A drifting pressure demands repeated causal-instability assessment; a medication discussion must not delay needed electricity.

    Different patient or conditions: Stable pre-excited AF may permit a specialist-supported drug strategy after QT, HF, renal and other eligibility checks. Instability prioritizes electrical cardioversion; sustained polymorphic VT requires unsynchronized shock.

Make it executable

State 'possible pre-excited AF—no nodal blockers' during the order check. Keep pads on, monitor ECG/perfusion continuously, and assign electrical rescue. Before an eligible drug attempt, verify formulation, protocol, QT, electrolytes, LV function and prior antiarrhythmic exposure.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

A different patient with a known accessory pathway has a stable, regular narrow-complex tachycardia consistent with orthodromic AVRT.

Does the pre-excited-AF prohibition mean adenosine is never appropriate in a patient with an accessory pathway?

Review the changed case

No. Orthodromic AVRT depends on AV-nodal conduction and is a different circuit from pre-excited AF. Adenosine can be appropriate for selected regular narrow SVT with ECG monitoring and immediate rescue capability. It can precipitate AF, so do not discard that safety preparation or transfer the plan to an irregular wide rhythm.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

I'd intercept diltiazem: this irregular, variably wide rhythm could be pre-excited AF, where nodal blockade can accelerate accessory-pathway conduction. IV amiodarone is not a safe exception. Reassess perfusion now and have electrical cardioversion ready as pressure declines. If truly stable, discuss procainamide or ibutilide with specialist support; don't wait for a historical WPW label.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Procainamide Ibutilide Adenosine

Sources: ACC-AF-2023 ACC-SVT-2015 · Original patient; guideline/label-based teaching and expert synthesis.

ED revisitMedication review after discharge

A patient returns to the ED with dizziness after a hospital course of amiodarone. It was stopped at discharge. They also take warfarin and digoxin; renal function is worse than baseline. The discharge note says to resume the old outpatient doses without further INR checks. They are currently alert and perfusing; ECG and laboratory reassessment are underway.

What belongs in the handoff?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Document the amiodarone exposure, last dose, INR trend, current warfarin plan, and a defined follow-up INR/adjustment responsibility. Review other interacting medications and whether any rhythm agent is still needed.

Why

Amiodarone and its active metabolite have prolonged disposition. Interaction onset and offset may lag visible rhythm control; 'discontinued' is not synonymous with 'cleared.'

Hazard to avoid

Do not automatically restore a pre-exposure warfarin dose based solely on the medication list. Conversely, an adjustment made during exposure may need reassessment as the interaction wanes.

Every option, and when it would fit

  1. Reconstruct exposure and current physiology, then give warfarin and digoxin separate monitoring/adjustment plans. Best fit here

    Best fit. The rhythm medication list does not show residual exposure. INR surveillance addresses anticoagulation, not digoxin exposure, conduction toxicity or renal clearance.

    Different patient or conditions: Needed after meaningful amiodarone exposure when interacting drugs remain. The magnitude and duration depend on the actual course and patient; do not impose one permanent dose reduction.

  2. Restore all pre-admission doses because amiodarone was stopped.

    Discontinuation is not clearance. Automatic dose restoration can ignore persistent metabolic/transport interactions and new renal dysfunction.

    Different patient or conditions: A previous regimen may become appropriate only after current INR, ECG, symptoms, renal status and waning exposure support it. The old medication list alone is insufficient.

  3. Use the INR to decide whether digoxin also needs adjustment.

    INR reflects vitamin-K-antagonist effect, not digoxin concentration or toxicity. One convenient laboratory test cannot stand in for two different exposure-response systems.

    Different patient or conditions: INR is useful for warfarin decisions. Digoxin needs its own clinical/ECG, electrolyte, renal and appropriately timed concentration assessment when indicated.

  4. Give more digoxin whenever AF recurs because amiodarone is no longer on the list.

    A recurrent rhythm does not establish inadequate digoxin exposure. Bradycardia, renal impairment or toxicity can coexist with atrial arrhythmia; additional loading could worsen the patient.

    Different patient or conditions: Digoxin can fit selected rate-control problems after independent eligibility and cumulative-dose review. It is not a reflex response to recurrence or a substitute for urgent stabilization.

Make it executable

At the ED revisit, review rate, rhythm, perfusion, bleeding and toxicity symptoms before attributing everything to AF. Verify last amiodarone dose, total course, INR trend, warfarin doses, digoxin timing and renal change. Name the next clinician and the tests they must act on.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

Medication reconciliation also finds digoxin. Renal function has worsened since admission.

Does the INR follow-up plan cover the additional risk?

Review the changed case

No. Add a separate digoxin review: dose, concentration and sample timing when indicated, symptoms, ECG, electrolytes, and renal function. Amiodarone exposure and impaired renal clearance may both affect risk. INR monitoring addresses warfarin, not digoxin exposure or toxicity.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

I wouldn't automatically restore the old warfarin regimen just because amiodarone is off the list. Let's document exposure and the INR trend, agree on the current warfarin plan, and name who will check and act on follow-up INRs. The interaction can persist and then wane, so this needs reassessment rather than a permanent dose assumption.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Amiodarone Digoxin

Sources: Amiodarone label Digoxin label · Original patient; guideline/label-based teaching and expert synthesis.

EDChest pain with recurrent wide-complex runs

A 59-year-old with ongoing ischemic chest pain has sustained polymorphic VT, terminated by immediate defibrillation. In the brief sinus rhythm afterward, QTc is 430 ms and there are new ischemic ST changes. Potassium and magnesium are normal. Recurrent runs occur as the team activates urgent coronary evaluation.

Which recurrence plan fits the current substrate without delaying another shock?

Choose your action. Then explain the mechanism and the finding that would change your plan.

Commit & compare

Next step

Prioritize electrical rescue for sustained episodes and urgent ischemia treatment. Consider an eligible recurrence-suppression strategy rather than routine magnesium or rate acceleration.

Why

The key discriminator is the substrate between episodes, not the dramatic tracing alone. Termination, recurrence prevention and definitive cause treatment are related but separate tasks.

Hazard to avoid

Do not let a medication discussion delay defibrillation or urgent coronary care. Normal QT does not identify every cause of polymorphic VT; alternative mechanisms need specialist review if the ischemic explanation becomes uncertain.

Every option, and when it would fit

  1. Treat this as acquired torsades solely because the QRS axis twists.

    Morphology alone does not establish torsades. The available between-episode QT and ischemic context point to a different recurrence mechanism.

    Different patient or conditions: A prolonged between-episode QT with culprit drugs, electrolyte losses or pause-triggered runs would support the acquired long-QT branch. Reassess if those facts change.

  2. Use magnesium as the routine main antiarrhythmic despite normal QT and electrolytes.

    Magnesium is not routinely recommended for normal-QT polymorphic VT. Treating every twisting rhythm alike distracts from the ongoing ischemic trigger.

    Different patient or conditions: Magnesium fits recurrent polymorphic VT associated with long QT or correction of a demonstrated deficiency. That does not replace shock or ischemia treatment in this patient.

  3. Start isoproterenol to accelerate the rate regardless of the ischemia.

    Selected pause-dependent acquired torsades is not a general license to increase adrenergic drive. This stem has ischemic symptoms and normal QT, not a bradycardic long-QT recurrence problem.

    Different patient or conditions: Expert-guided isoproterenol may fit selected acquired pause-dependent torsades; it is not routine here and can aggravate ischemic demand. Other causes require specialist-specific treatment.

  4. Continue immediate defibrillation for sustained episodes, urgently treat the ischemia, and discuss eligible lidocaine/amiodarone for recurrence with the team. Best fit here

    Best fit. Shock terminates the sustained episode, but it does not remove ischemia. Normal-QT recurrence has different pharmacologic options from acquired long-QT torsades; the optimal drug evidence is limited.

    Different patient or conditions: This plan assumes the current normal-QT/ischemic findings. Agent selection still needs pressure, conduction, organ function and prior-exposure review. A newly prolonged QT changes the branch.

Make it executable

Keep pads attached and assign immediate shock/pulse reassessment. Confirm the between-episode ECG, evolving ischemic findings and prior drugs; verify the selected recurrence regimen using the correct formulation/protocol. Monitor pressure and conduction while coordinating definitive ischemia care.

For medication, use the current product/local protocol to verify dose, preparation, route, rate and organ adjustment. This case is not a complete medication order.

Change the patient

A different patient has QTc 590 ms, new QT-active medications and repeated pause-triggered runs after vomiting; there is no ischemic presentation.

Which parts of your original drug plan fail to transfer?

Review the changed case

The immediate unsynchronized-shock branch still applies if polymorphic VT is sustained. Recurrence prevention changes to acquired long-QT trigger removal, magnesium/electrolyte correction and selected expert-guided rate support. Do not reflexively add a QT-active agent from the ischemic/normal-QT plan.

Practice the provider recommendation

For the original patient, say what you recommend and why. Include the patient-specific hazard, monitoring or rescue plan, and anything you still need to clarify.

Check your reasoning: intervention and sequence → mechanism → alternative and boundary → execution/monitoring → stop/rescue → unresolved information and handoff. A matching phrase is not the goal.

Compare with an example recommendation

The sustained episode needs immediate defibrillation; afterward the normal QT and ischemic presentation make routine torsades treatment a poor fit. I'd keep electrical rescue ready, coordinate urgent ischemia treatment and discuss an eligible lidocaine or amiodarone recurrence plan after exposure and hemodynamic review. If the between-episode QT becomes prolonged, reassess the substrate rather than repeating the same drug plan.

Bring this decision back later

On a later session—tomorrow or another interval that fits—close the explanations and start with the changed patient. Generate the recommendation before checking it. Then name one different finding that would make another option appropriate. Keep the emergency stop/rescue branch explicit; an unsafe option does not need a redeeming scenario.

Drug detail: Lidocaine Amiodarone Magnesium Isoproterenol

Sources: AHA-ALS-2025 · Original patient; guideline/label-based teaching and expert synthesis.

Cases from the literature

Published case reportQRS widening during renal impairment

A patient receiving flecainide develops renal impairment and marked QRS widening.

What would you review before calling a new wide rhythm simply 'recurrent AF with aberrancy'?

Compare with the published report

What the authors reported

The authors describe flecainide toxicity in renal impairment, with marked QRS widening, treated successfully with IV sodium bicarbonate.

Clinical interpretation

Review baseline QRS, renal trajectory, flecainide dose history, and interacting drugs. Accumulating sodium-channel blockade can change the ECG and the treatment problem. In suspected toxicity, involve toxicology/cardiology; this report does not supply a general dosing protocol.

Limit: One uncontrolled report supports a mechanism and a safety signal, not an incidence estimate or comparative treatment effect.

Drug detail: Flecainide

Subedi R, Dean RK, Chaudhary A, Szombathy T. Proc (Bayl Univ Med Cent). 2018;31:328–330. DOI: 10.1080/08998280.2018.1463042. Indexed primary full-text excerpts and bibliographic record; no figure reproduced. Accessed 2026-10-08.

Published case reportLoss of consciousness after gastroenteritis

An older patient taking sotalol is hospitalized with gastroenteritis, develops acute kidney injury and has an episode of loss of consciousness.

Which admission changes could make the home medication unsafe before the first hospital dose?

Compare with the published report

What the authors reported

An octogenarian hospitalized with gastroenteritis developed prerenal AKI, sotalol accumulation, severe QT prolongation, and torsades with loss of consciousness. Reported treatment included temporary pacing, IV magnesium, and withdrawal of sotalol.

Clinical interpretation

Review renal function, volume loss, QT, heart rate/pauses, electrolytes, and additional QT-active agents. A chronic prescription needs fresh eligibility when clearance and physiology change.

Limit: This is a single case reported in an abstract. No unreported QT, creatinine, or dose values are inferred; it does not compare pacing with alternative treatments.

Drug detail: Sotalol Magnesium

Michiels V, Miljoen H, Vrints C. Acta Cardiol. 2009;64:839–842. DOI: 10.2143/AC.64.6.2044756. Primary abstract reviewed; full text not reviewed. Accessed 2026-10-08.

Interactive · rhythm-to-action

Choose the next safe move.

Four cases. One rule: choose from the patient plus the tracing—never the tracing alone. These strips are schematic, not diagnostic.

Case1 / 4Score0
Your browser cannot render the schematic rhythm strip. The rate, width, regularity, and case description remain available as text.
Rate — QRS — Regularity — Schematic · not diagnostic

Emergency department

Loading case…

What is the best next action?

Baseline assessment · six decisions

Explain the answer you choose.

The clue that changes the plan matters more than the score. Every distractor gets a bedside autopsy: why it fails here, and when it might fit.

01
A patient with a pulse has a regular wide-complex tachycardia at 190/min, BP 68/38 mm Hg, acute confusion, and cool extremities. What should lead?

Correct: B. The rhythm is plausibly causing shock and altered mentation. An organized tachycardia with a pulse is synchronized so energy avoids the vulnerable repolarization period. Medication or a perfect tracing must not delay electrical therapy.

  • A: reasonable in selected stable WCT, not as the lead intervention in causal instability.
  • C: adenosine is limited to stable regular monomorphic WCT when an AV-node-dependent mechanism is plausible.
  • D: unsynchronized energy is for VF/pulseless VT or polymorphic VT that cannot be synchronized reliably—not every organized WCT with a pulse.
02
A stable patient has an irregular wide-complex tachycardia with very rapid varying ventricular rates and known WPW pattern on a prior ECG. Which next step is the dangerous reflex?

Correct: D. In pre-excited AF, AV-nodal blockade can shift conduction toward the accessory pathway and permit dangerously rapid ventricular activation. Stable pre-excited AF is generally treated with a pathway-active rhythm strategy such as procainamide or ibutilide; instability calls for cardioversion.

  • A/B: guideline-supported pharmacologic options in an appropriate stable patient, with drug-specific contraindications and monitoring.
  • C: anticipatory preparation is appropriate because the rhythm can deteriorate.
03
A stable regular narrow-complex tachycardia persists after a correctly performed modified Valsalva maneuver. Why is adenosine a mechanistically coherent next step?

Correct: A. Adenosine’s very short A1-mediated AV-nodal effect can terminate AVNRT/orthodromic AVRT or briefly reveal continued atrial activity when the AV node is not part of the circuit.

  • B: it does not make pre-excited AF safe; AV-nodal blockade is contraindicated there.
  • C: the effect lasts seconds, not long enough for durable AF rate control.
  • D: adenosine is not a class I sodium-channel blocker and does not treat scar-mediated VT.
04
What is the most accurate interpretation of PROCAMIO when selecting therapy for a tolerated regular wide-QRS tachycardia?

Correct: C. PROCAMIO was a small randomized open-label trial in tolerated wide-QRS tachycardia. Procainamide produced fewer prespecified major cardiac adverse events and more termination, but the study does not erase contraindications or establish superiority across shock, severe HF, prolonged QT, polymorphic rhythms, or every WCT mechanism.

  • A: overgeneralizes population and mechanism.
  • B: hierarchy alone does not replace directness, quality, and clinical applicability.
  • D: the comparison was procainamide versus amiodarone.
05
A patient has recurrent polymorphic VT with a clearly prolonged QT after several QT-active medications. Which statement best reflects both guidance and evidence?

Correct: B. The 2025 AHA guideline states that magnesium may be considered for recurrent polymorphic VT associated with long QT (Class 2b, C-LD), alongside trigger and electrolyte correction. Direct randomized torsades evidence is absent—an ideal example of bedside guidance and evidence certainty being separate questions.

  • A: treatment is mechanistic and does not require a low measured serum value.
  • C: routine magnesium is not recommended for polymorphic VT with a normal QT.
  • D: beat-to-beat morphology changes make reliable synchronization difficult; sustained polymorphic VT requires immediate unsynchronized shock.
06
After successful conversion of the opening-case VT, which action best represents the internal-medicine lens rather than simply repeating ED stabilization?

Correct: D. The internal-medicine lens owns the trajectory after stabilization: cause, recurrence risk, medication reconciliation, monitoring, definitive evaluation, and a transition plan.

  • A/B/C: all are high-value ED-pharmacist actions in the first minutes; they remain relevant during handoff but do not replace longitudinal planning.
Your resultNot submittedProficiency target: ≥85% and no safety-critical miss. This six-item baseline is diagnostic, not a mastery credential.

Next: why this drug, for this patient?

Part 2 connects channel behavior, changing drug exposure, and the studies that shaped treatment.

Open Part 2: mechanism & treatment strategy

Clinical studies

EHRA compendium close read

Open the shared arrhythmia evidence register.