Curriculum/Cardiovascular/Arrhythmias
Field manual · ARR-01

Arrhythmias:
zero-to-safe.

The first release is not a catalog of squiggles. It is a reusable way to see a rhythm, decide whether it is harming the patient, connect the tracing to electrophysiology, and choose an action that remains safe while uncertainty is still real.

Opening case00:00

The monitor says “VT.” The patient says nothing.

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?

Do not begin with the drug name. Begin with whether this rhythm is causing instability. For causal hypotension and altered mental status with a pulse, prepare immediate synchronized cardioversion; sedate only if feasible without delaying therapy.

The master decision tree

Four branches before a drug.

The sequence is deliberately clinical. It protects against two common errors: treating a monitor instead of a patient, and using an AV-nodal drug before recognizing a dangerous wide or pre-excited rhythm.

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 instabilityElectrical 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 a stable regular narrow tachycardia: modified Valsalva first, then adenosine when appropriate. 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

Why width changes risk

A narrow QRS implies rapid, coordinated ventricular depolarization through the native conduction system. A wide QRS can reflect ventricular origin, aberrant supraventricular conduction, pre-excitation, pacing, metabolic conduction delay, or sodium-channel blockade. Surface algorithms modify probability; they do not make uncertainty harmless.

Why regularity changes the drug list

Regularity suggests a repeating circuit or focus. Irregularity can expose competing atrial wavefronts, variable AV conduction, changing ventricular activation, or polymorphism—mechanisms in which a medication that is safe for AVNRT may be ineffective or dangerous.

One case · four lenses

The decision is shared. The responsibilities are not.

Switch lenses on the opening case. Each view adds setting-specific work without changing the core physiology.

Clock0–10 min

Make the next intervention executable and prevent a high-consequence medication error.

  1. Name the syndrome, not a fragile diagnosis.“Unstable regular wide-complex tachycardia with a pulse” is enough to act safely.
  2. Build the electrical plan.Confirm sync markers, pads, energy strategy, sedation feasibility, airway support, and a post-conversion 12-lead.
  3. Prepare the rescue branch.Sustained polymorphic VT → immediate unsynchronized shock. Pulse loss → start CPR and follow arrest rhythm analysis; defibrillate VF/pVT.
  4. Audit medication before it enters the line.Check QRS/QT, blood pressure, structural disease, renal function, electrolytes, interacting agents, concentration, infusion rate, and stop rules.
ArcCause → discharge

Turn a successful conversion into a coherent diagnostic, medication, and follow-up plan.

  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 the post-conversion regimen.Separate the acute infusion from chronic recurrence prevention; avoid therapeutic inertia after the indication changes.
  3. Design telemetry and laboratory monitoring.Specify rhythm endpoints, QT/QRS thresholds, electrolyte targets, renal/hepatic reassessment, and what finding triggers escalation.
  4. Close the loop.Cardiology/EP plan, ischemic evaluation, anticoagulation when relevant, patient teaching, interaction review, and access to prescribed therapy.
StateDynamic physiology

Ask whether the arrhythmia is the driver of shock, a consequence of shock, or both.

  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 for recurrence.Defibrillation readiness, pacing strategy, sedation/sympathetic control, EP escalation, mechanical support, and electrical-storm pathways.
ModelMechanism + substrate

Explain what circuit or focus exists, why this patient developed it, and what proves or changes the diagnosis.

  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.

Interactive · rhythm-to-action

Choose the next safe move.

These are schematic rhythm strips, not diagnostic tracings. The challenge is to combine the strip with the patient state rather than answer from morphology alone.

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?

Drug atlas preview

Mechanism is a safety tool.

Full monographs arrive in ARR-08. These first cards show the minimum mechanism-to-bedside chain the later atlas will expand.

A1 receptor

Adenosine

Transient AV-nodal block. Excellent for AV-node-dependent regular SVT; diagnostic for some atrial rhythms. Never a reflex for irregular/polymorphic WCT or pre-excited AF.

Half-life measured in seconds · caffeine/theophylline oppose · dipyridamole potentiates
Fast Na+ + NAPA IKr

Procainamide

Slows conduction and prolongs refractoriness. A rational option for selected stable monomorphic VT or pre-excited AF, constrained by pressure, HF, QRS/QT, kidney function, and cumulative dose.

Parent + active metabolite · renal accumulation · explicit stop rules
Multi-channel + β effects

Amiodarone

Broad electrophysiologic effects do not make it universally safest. IV hypotension, conversion when anticoagulation matters, long tissue persistence, and major chronic organ toxicity all change the plan.

IV and chronic pharmacology differ · CYP/P-gp interactions · enormous Vd
Mg2+ · afterdepolarizations

Magnesium

2025 AHA: magnesium may be considered for recurrent polymorphic VT associated with long QT (Class 2b, C-LD); direct randomized torsades evidence is absent.

Treat mechanism, not a serum number · pair with trigger removal and correction of hypokalemia

Source-to-practice lab

Read it. See it. Use it. Defend it.

Each object starts with a clinical scaffold, exposes the source’s own words and numbers, and ends with a transfer boundary and teach-back. Quotations are intentionally short; the links take you to full context.

  1. 01OrientRead the tertiary scaffold.
  2. 02InterrogateInspect methods and the exact excerpt.
  3. 03QuantifyRead absolute effects and uncertainty.
  4. 04TransferName who the result does—and does not—fit.
  5. 05Teach backDefend the bedside decision without looking.
8 minutes

Clinical pass

Read the excerpt, result, and practice boundary on the tertiary, AHA, REVERT, and PROCAMIO cards.

20 minutes

Evidence pass

Add methods, confidence intervals, and each teach-back before opening the full abstract or manuscript.

45 minutes

Four-lens pass

Read every card, then explain how the same evidence changes ED action, ICU rescue, medicine follow-up, and physician diagnosis.

Figure lab 01 · original visualization

Three trials, three different questions.

Bars use the published percentages, but the endpoint and population determine what each picture means. A larger bar is not automatically a stronger or more transferable conclusion.

REVERT · sinus rhythm at 1 minute

Technique changes the effect.

Standard Valsalva37 / 214
17%17%
Modified Valsalva93 / 214
43%43%
Absolute benefit
26 percentage points
Approximate NNT
4
Adjusted OR
3.7 (95% CI 2.3–5.8)
PROCAMIO · tolerated WCT

Read benefit and harm together.

Major cardiac adverse events

Procainamide3 / 33
9%9%
Amiodarone12 / 29
41%41%

Tachycardia terminated by 40 minutes

Procainamide22 / 33
67%67%
Amiodarone11 / 29
38%38%
RAFF2 · selected stable acute AF

Near-equal totals can conceal different workflows.

Drug → shock196 / 204
96%96%
Shock only176 / 192
92%92%
Absolute difference
4 points (95% CI 0–9)
Drug alone converted
52%
Strategy p value
0.07
Accessible data table for the three original trial visualizations.
TrialPopulationEndpointComparisonResult
REVERTStable adult SVTSinus rhythm at 1 minuteModified vs standard Valsalva43% vs 17%
PROCAMIOTolerated regular WCTMajor cardiac adverse eventsProcainamide vs amiodarone9% vs 41%
PROCAMIOTolerated regular WCTTermination by 40 minutesProcainamide vs amiodarone67% vs 38%
RAFF2Selected stable acute AFConversion to sinus rhythmDrug–shock vs shock-only96% vs 92%
Commit an interpretation before revealing the debrief

REVERT: the clinically useful measure is the 26-point absolute benefit and NNT near 4—not a claim that every SVT is 3.7 times more likely to convert.

PROCAMIO: both the adverse-event and termination signals favor procainamide, but the sample is small and the transfer boundary excludes unstable, polymorphic, and pulseless rhythms.

RAFF2: both bundled strategies converted most eligible patients. A nonsignificant 4-point difference is not proof of equivalence; workflow, sedation, preference, and eligibility still matter.

9

verified excerpts · each 20 words or fewer

Key reading cards

Reading progress is stored only on this device.

01 Wide QRS Complex TachycardiaTertiary scaffold · Foundation

“Wide complex tachycardia is a dysrhythmia with a long list of potential causes”

Continuing Education Activity · 13 quoted words
Study / source frame

A broad, open-access clinical review that organizes the differential before the learner enters individual trials and guidelines.

Result signal

No comparative effect estimate; its job is orientation, vocabulary, and differential diagnosis.

What this supports

Start with patient stability, then treat width and regularity as probability-changing features rather than a final diagnosis.

What this does not prove

Tertiary reviews compress nuance and can age. Verify management-changing claims against the current guideline and direct evidence below.

Teach-back prompt

Before opening the answer: Name four causes of wide-complex tachycardia that would change the medication plan.

Expert response: Examples include ventricular tachycardia, pre-excited AF, sodium-channel blockade, hyperkalemia, SVT with aberrancy, pacing, and artifact. The point is to connect each cause to a different hazard or rescue pathway.

Obando MA, Marra EM. StatPearls [Internet]. Updated June 26, 2023.Short quotation for commentary; credit the source and do not reproduce its figures.
Open tertiary review
02 Sustained polymorphic ventricular tachycardiaCurrent guideline · ED + ICU

“Polymorphic ventricular tachycardia is always unstable and should be treated immediately with defibrillation”

Adult ALS: polymorphic VT discussion · 13 quoted words
Study / source frame

Current emergency guidance derived from systematic, scoping, and focused evidence reviews.

Result signal

Immediate unsynchronized shock for sustained polymorphic VT is Class 1, B-NR. Magnesium for recurrence with long QT is Class 2b, C-LD.

What this supports

Shock sustained polymorphic VT without waiting for synchronization, even when a pulse is present; address the substrate after energy.

What this does not prove

A recommendation is not a randomized comparison. The guideline notes that randomized evidence for drug management of polymorphic VT is absent.

Teach-back prompt

Before opening the answer: Why is this an unsynchronized-shock pathway, and what additional action begins if the patient loses a pulse?

Expert response: Beat-to-beat QRS variation makes reliable synchronization impractical. If pulse loss occurs, begin CPR and follow arrest rhythm analysis; defibrillate VF or pulseless VT.

Wigginton JG, et al. Circulation. 2025;152(suppl 2):S538–S577.Short quotation for commentary; link to the official guideline for full context.
Open guideline
03 When atrial fibrillation is causing instabilityCurrent guideline · ED + physician

“In patients with hemodynamic instability attributable to AF, immediate electrical cardioversion should be performed to restore sinus rhythm”

Electrical cardioversion recommendations · 18 quoted words
Study / source frame

Multidisciplinary evidence synthesis for adults across the atrial-fibrillation continuum.

Result signal

Immediate synchronized cardioversion when instability is attributable to AF is Class 1, C-LD.

What this supports

The causal word matters: treat AF immediately when it is driving the instability.

What this does not prove

AF can also be a marker of sepsis, hemorrhage, PE, ACS, or another shock state. Cardioversion does not replace simultaneous causal evaluation.

Teach-back prompt

Before opening the answer: A septic patient has AF at 160/min and hypotension. What observations would make AF more likely to be the driver rather than a compensatory response?

Expert response: Look for temporal coupling, disproportionate rate, loss of atrial contribution in a preload-dependent patient, worsening with rhythm onset, and hemodynamic improvement with rate/rhythm intervention—while treating sepsis in parallel.

Joglar JA, et al. Circulation. 2024;149:e1–e156; corrected 2024.Short quotation for commentary; consult the corrected guideline for complete recommendation tables.
Open full guideline
04 Flecainide and use dependenceExpert pharmacology synthesis · Pharmacology

“This use-dependent property enables flecainide to effectively block the activation front, contributing to the termination of atrial fibrillation”

Flecainide: use-dependent sodium-channel block · 18 quoted words
Study / source frame

Expert consensus integrating ion-channel mechanisms, PK/PD, selection, monitoring, interactions, and proarrhythmia.

Result signal

This is a mechanistic statement, not a comparative clinical effect estimate.

What this supports

At faster activation rates, less time is available for flecainide to dissociate from sodium channels, strengthening blockade.

What this does not prove

The same mechanism can cause rate-related QRS widening and proarrhythmia. Mechanistic plausibility does not erase patient-selection restrictions.

Teach-back prompt

Before opening the answer: What would exercise-related QRS widening reveal about flecainide’s channel-binding behavior?

Expert response: It demonstrates use dependence: faster rates increase the fraction of blocked channels because there is less diastolic time for drug dissociation.

Merino JL, et al. Europace. 2025;27:euaf076; corrected March 2026.Short quotation for commentary; do not reproduce the source schematic. Review the March 2026 correction with the original.
Open record and figures
05 REVERT: do the maneuver correctlyPrimary randomized trial · ED pharmacist

“We have shown that a simple, cost-free, well-tolerated postural modification to the standard Valsalva manoeuvre is highly effective”

Discussion · 18 quoted words
Study / source frame

Multicenter randomized, assessor-blinded trial in 10 UK EDs; 428 primary-analysis encounters with stable SVT.

Result signal

Sinus rhythm at one minute: 43% modified versus 17% standard; absolute difference 26 percentage points; approximate NNT 4; adjusted OR 3.7 (95% CI 2.3–5.8).

What this supports

A correctly performed modified Valsalva belongs before adenosine in an appropriate stable regular narrow-complex SVT pathway.

What this does not prove

The intervention was not blinded to clinicians or patients and does not apply to instability, AF/flutter, irregular rhythms, or undifferentiated WCT.

Teach-back prompt

Before opening the answer: Calculate the absolute benefit and NNT, then name the rhythm and stability checks required before using the result.

Expert response: The absolute benefit is about 26 percentage points and NNT is about 4. Confirm a stable patient with a compatible regular SVT; exclude rhythms and states in which a vagal-first pathway is inappropriate.

Appelboam A, et al. Lancet. 2015;386:1747–1753.Short quotation for commentary; use the linked manuscript and publisher supplements rather than reproducing journal figures.
Open author manuscript
06 A newer, smaller Valsalva trialNew primary trial · Evidence critique

“Sinus rhythm was restored in 10 of 38 patients (26.3%) in the modified Valsalva group”

Abstract: Results · 15 quoted words
Study / source frame

Single-center, open-label, pragmatic randomized trial in 75 adults with stable PSVT in an Indian tertiary ED.

Result signal

Modified 26.3% versus standard 16.2%; 95% CI for the absolute difference −8.2% to 28.4%; not statistically significant.

What this supports

The direction of effect remained favorable, but the estimate was imprecise and smaller than REVERT’s.

What this does not prove

A small single-center trial with a confidence interval spanning harm and substantial benefit cannot establish equivalence or erase the larger trial.

Teach-back prompt

Before opening the answer: Why does ‘not statistically significant’ fail to prove that the two maneuvers are equivalent?

Expert response: Failure to reject no difference is not proof of equality. The wide confidence interval shows that the study cannot distinguish modest harm, no effect, or clinically important benefit.

Arora S, et al. Indian Heart J. 2026. Online ahead of print.Short quotation for commentary; the open article is CC BY-NC-ND, so link to its original figures without modification.
Open full text
07 PROCAMIO: comparative drug evidencePrimary randomized trial · ED + critical care

“Procainamide therapy was associated with less major cardiac adverse events and a higher proportion of tachycardia termination within 40 min”

Abstract: Conclusions · 20 quoted words
Study / source frame

Multicenter, randomized, open-label comparison; 74 enrolled and 62 analyzed with tolerated regular wide-QRS tachycardia, probably monomorphic VT.

Result signal

Major cardiac adverse events: 9% procainamide versus 41% amiodarone. Termination by 40 minutes: 67% versus 38%.

What this supports

For carefully selected tolerated monomorphic WCT, procainamide has stronger direct comparative evidence than amiodarone.

What this does not prove

Small, open-label, 12 exclusions from the principal analysis, and not powered for mortality. Do not extrapolate to unstable, polymorphic, or pulseless VT.

Teach-back prompt

Before opening the answer: Would you transfer this result to LVEF 15%, SBP 92 mm Hg, CKD, and QTc 510 ms? Defend the plan.

Expert response: No automatic transfer. Hypotension, severe HF, renal accumulation, and prolonged QT narrow or remove the procainamide option; reassess stability and prepare electrical therapy with expert input.

Ortiz M, et al. Eur Heart J. 2017;38:1329–1335.Short quotation for commentary; the full article is open access.
Open full text
08 RAFF2: two workable acute-AF strategiesPrimary randomized trial · ED pharmacist

“Both the drug-shock and shock-only strategies were highly effective, rapid, and safe in restoring sinus rhythm”

Abstract: Interpretation · 16 quoted words
Study / source frame

Partial-factorial randomized trial at 11 Canadian academic EDs; 396 selected adults with stable acute AF.

Result signal

Conversion: 96% drug–shock versus 92% shock-only; absolute difference 4% (95% CI 0–9; p=0.07). Procainamide alone converted 52%.

What this supports

Either pathway can work for selected stable recent-onset AF; procainamide may avoid sedation and shock in about half.

What this does not prove

This compared bundled strategies, did not establish statistical equivalence, and excluded unstable or secondary-AF presentations.

Teach-back prompt

Before opening the answer: How should prior response, sedation risk, ED resources, patient preference, and time-to-disposition alter the choice?

Expert response: Use shared, context-specific selection. High sedation risk or limited procedural resources may favor a drug-first attempt; prior drug failure, patient preference, or a need for rapid predictable conversion may favor shock-first when eligible.

Stiell IG, et al. Lancet. 2020;395:339–349.Short quotation for commentary; use the linked abstract or licensed full text for complete methods.
Open abstract
09 EAST-AFNET 4: rhythm control as prognosisPrimary randomized trial · Internal medicine

“Early rhythm-control therapy was associated with a lower risk of adverse cardiovascular outcomes than usual care”

Abstract: Conclusions · 16 quoted words
Study / source frame

International, randomized, open-label trial with blinded outcome assessment; 2,789 patients with AF diagnosed within one year plus cardiovascular conditions.

Result signal

Composite event rates: 3.9 versus 5.0 per 100 person-years; HR 0.79 (96% CI 0.66–0.94). Rhythm-therapy-related serious adverse events: 4.9% versus 1.4%.

What this supports

For selected early-AF patients, rhythm control can be a prognostic strategy rather than symptom rescue alone.

What this does not prove

Not an acute ED cardioversion trial. Therapy was heterogeneous, the trial was open-label and stopped early, and the composite cannot be assigned to one drug or ablation.

Teach-back prompt

Before opening the answer: Which new AF patients leaving the ED merit an explicit early-rhythm-control referral instead of a rate-control-only plan?

Expert response: Patients within a year of diagnosis who resemble the trial population and have cardiovascular risk or disease merit an intentional rhythm-control discussion, alongside anticoagulation and comorbidity management—not an automatic prescription for one intervention.

Kirchhof P, et al. N Engl J Med. 2020;383:1305–1316.Short quotation for commentary; consult the publisher record for full methods and supplements.
Open abstract

Watch · simulate · inspect

A curated media shelf, with a job for every click.

These are outbound resources, not endorsements of every statement they contain. Predict before opening; teach back afterward. Current guidance outranks an older demonstration when they differ.

Video · technique1:34

Modified Valsalva Maneuver

JAMA Network / JN Learning

Before opening
Predict the exact strain, repositioning, and leg-raise sequence before pressing play.
Afterward
Teach the maneuver back as an executable order, including patient selection and monitoring.

Access: Public player; an auto-generated transcript is available but may contain errors.

Boundary: Copyrighted AMA content. Link out only; do not copy, download, or embed.

Link checked 2026-07-16
Video · procedureShort skills demonstration

Synchronised cardioversion

Resuscitation Council UK

Before opening
Name the four setup checks you expect before shock delivery.
Afterward
Identify the sync-marker, safety, sedation, and re-synchronization steps shown.

Access: Full transcript and contrast controls are available.

Boundary: The older 120-J example is a device/scenario demonstration, not a universal current energy recommendation; pair it with the 2025 AHA algorithm.

Link checked 2026-07-16
Interactive simulatorSelf-paced

Manual External Defibrillation, Cardioversion, and Pacing

University of Florida Center for Safety, Simulation & Advanced Learning Technologies

Before opening
Write the device sequence for synchronized cardioversion from memory.
Afterward
Repeat locally using the text pathway: pads → rhythm → sync → energy → clear → shock → reassess → re-sync if needed.

Access: Free non-CME WebGL simulator; desktop-oriented and drag-heavy. The local text pathway is the keyboard alternative.

Boundary: Use for equipment logic, not as a substitute for device-specific training or current protocols.

Link checked 2026-07-16
Visual learning unitsSelf-paced

Marion-Arnsdorf ECG Project

University of Chicago Medicine

Before opening
Choose one mechanism—automaticity, triggered activity, or re-entry—and sketch it first.
Afterward
Explain how that mechanism predicts onset, regularity, response to AV-nodal blockade, and recurrence.

Access: JavaScript is required. Learning units combine electrophysiology diagrams with rhythm examples.

Boundary: No reuse license was visible; link to the original rather than copying its images.

Link checked 2026-07-16
Image-based quiz10 cases

Arrhythmia Quiz

University of Utah ECG Learning Center

Before opening
Use the same sequence every time: rate → regularity → P–QRS relation → width → patient context.
Afterward
Record one morphology clue you over-weighted and one clinical clue you under-weighted.

Access: Image-based questions include AVNRT, AF, flutter, VT, and a ladder diagram.

Boundary: Licensed CC BY-ND-NC; link-only avoids creating an unauthorized derivative.

Link checked 2026-07-16
Visual algorithmOne-page reference

2025 Electrical Cardioversion Algorithm

American Heart Association

Before opening
Predict the starting-energy rows and the point at which synchronization no longer applies.
Afterward
Turn the algorithm into a bedside preparation checklist rather than memorizing one number.

Access: Graphic PDF plus a linked long-description companion.

Boundary: Confirm the specific defibrillator’s recommended energy and local protocol.

Link checked 2026-07-16

Baseline assessment · six decisions

Explain the answer you choose.

Score is secondary. Every item exposes why each alternative fails and when it would become appropriate.

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 medication 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.

Evidence dossier

Hierarchy is only one axis.

A meta-analysis is not automatically more useful than a direct trial, and a guideline is not a study design. Each source is judged by question, risk of bias, directness, precision, applicability, recency, and corrections.

Evidence design
  1. SynthesisSystematic review / meta-analysis
  2. ExperimentRandomized trial
  3. ObservationCohort / case-control
  4. SignalsCase series / reports / pharmacovigilance
  5. MechanismHuman physiology / translational evidence
Recommendation authority
  1. GuidelineMethods, evidence review, classes/levels
  2. ConsensusExpert integration where evidence is incomplete
  3. RegulatoryLabel, safety communication, approval review
  4. InstitutionalLocal formulary, workflow, resources
  5. Our synthesisExplicit inference, never disguised as guidance
17

seed records · verified links and identifiers

Scope: initial guideline spine and practice-shaping studies. This is a documented scoping set, not yet a completed systematic review.

1 Part 9: Adult Advanced Life Support — 2025 AHA Guidelines for CPR and ECCGuideline · current emergency algorithm · Recommendation-specific

Acute tachyarrhythmia, bradycardia, cardioversion, polymorphic VT, and arrest pathways.

Citation
Wigginton JG, et al. Circulation. 2025;152(suppl 2):S538–S577.
DOI / identifier
10.1161/CIR.0000000000001376
Open primary record
2 Part 10: Adult and Pediatric Special Circumstances of Resuscitation — 2025 AHA GuidelinesGuideline · toxicology/special circumstances · Recommendation-specific

Hyperkalemia, pregnancy, pulmonary embolism, and arrhythmogenic drug/toxin emergencies.

Citation
Cao D, et al. Circulation. 2025;152(suppl 2):S578–S672.
DOI / identifier
10.1161/CIR.0000000000001380
Open primary record
3 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial FibrillationGuideline · multidisciplinary synthesis · Recommendation-specific

US framework for AF staging, stroke prevention, rate/rhythm control, acute illness, and ablation.

Citation
Joglar JA, et al. Circulation. 2024;149:e1–e156.
DOI / identifier
10.1161/CIR.0000000000001193
Correction / erratum
Correction DOI 10.1161/CIR.0000000000001207; PMID 38153996.
Open primary record
4 2024 ESC Guidelines for the management of atrial fibrillationGuideline · international synthesis · Recommendation-specific

AF-CARE framework and an explicit international comparison to US recommendations.

Citation
Van Gelder IC, et al. Eur Heart J. 2024;45:3314–3414.
DOI / identifier
10.1093/eurheartj/ehae176
Correction / erratum
Later correction indexed as PMID 40622753.
Open primary record
5 2018 ACC/AHA/HRS Bradycardia and Cardiac Conduction Delay Guideline — Executive SummaryGuideline · bradycardia/conduction · Recommendation-specific

Sinus node disease, AV block, pacing decisions, and reversible causes.

Citation
Kusumoto FM, et al. Circulation. 2019;140:e333–e381.
DOI / identifier
10.1161/CIR.0000000000000627
Open primary record
6 2015 ACC/AHA/HRS Guideline for Adult Supraventricular TachycardiaGuideline · supraventricular tachycardia · Recommendation-specific

AVNRT/AVRT, focal atrial tachycardia, pre-excitation, acute therapy, and ablation.

Citation
Page RL, et al. Circulation. 2016;133:e506–e574.
DOI / identifier
10.1161/CIR.0000000000000311
Open primary record
7 2019 ESC Guidelines for Supraventricular TachycardiaGuideline · international comparison · Recommendation-specific

Updated SVT diagnosis, acute treatment, ablation, pregnancy, and special contexts.

Citation
Brugada J, et al. Eur Heart J. 2020;41:655–720.
DOI / identifier
10.1093/eurheartj/ehz467
Open primary record
8 2022 ESC Guidelines for Ventricular Arrhythmias and Prevention of Sudden Cardiac DeathGuideline · ventricular arrhythmias · Recommendation-specific

Ventricular arrhythmias, electrical storm, structural disease, genetic evaluation, devices, and ablation.

Citation
Zeppenfeld K, et al. Eur Heart J. 2022;43:3997–4126.
DOI / identifier
10.1093/eurheartj/ehac262
Open primary record
9 REVERT: modified versus standard Valsalva for supraventricular tachycardiaRandomized controlled trial · Moderate · direct for stable SVT

Shows why the postural modification belongs before medication in a stable regular narrow-complex pathway.

Citation
Appelboam A, et al. Lancet. 2015;386:1747–1753.
DOI / identifier
10.1016/S0140-6736(15)61485-4
Open primary record
10 PROCAMIO: procainamide versus amiodarone for tolerated wide-QRS tachycardiaRandomized controlled trial · Low–moderate · small open-label trial

Practice-shaping comparative evidence, taught with its small sample and setting limitations visible.

Citation
Ortiz M, et al. Eur Heart J. 2017;38:1329–1335.
DOI / identifier
10.1093/eurheartj/ehw230
Open primary record
11 RAFF2: electrical versus drug–shock cardioversion for acute atrial fibrillationRandomized controlled trial · Moderate · ED acute AF population

ED rhythm-control strategy, procainamide, and electrical cardioversion in selected recent-onset AF.

Citation
Stiell IG, et al. Lancet. 2020;395:339–349.
DOI / identifier
10.1016/S0140-6736(19)32994-0
Open primary record
12 EAST-AFNET 4: early rhythm-control therapy in atrial fibrillationRandomized controlled trial · High for enrolled early-AF population

Changes the longitudinal frame from symptom rescue alone to selected early rhythm control.

Citation
Kirchhof P, et al. N Engl J Med. 2020;383:1305–1316.
DOI / identifier
10.1056/NEJMoa2019422
Open primary record
13 EHRA Practical Compendium of Antiarrhythmic DrugsExpert consensus · pharmacology compendium · Consensus plus drug-specific evidence

Current drug-mechanism, selection, safety, interaction, and monitoring backbone; paired with correction DOI 10.1093/europace/euag041.

Citation
Merino JL, et al. Europace. 2025;27:euaf076; corrected March 2026.
DOI / identifier
10.1093/europace/euaf076
Correction / erratum
March 2026 correction DOI 10.1093/europace/euag041.
Open primary record
14 FDA approval of intranasal etripamil (Cardamyst) for adult PSVT self-treatmentRegulatory review + randomized trials · Approved indication; post-guideline

A living-evidence example: contemporary approved therapy that is not integrated into the older US/ESC SVT guidelines.

Citation
US Food and Drug Administration. Drug Trials Snapshot: Cardamyst. December 2025.
DOI / identifier
FDA approval record; RAPID trial DOI 10.1016/S0140-6736(23)00776-6
Open primary record
15 Effectiveness of the Valsalva manoeuvre for reversion of SVTSystematic review · Limited by heterogeneous, older studies

Evidence-synthesis layer used alongside, not as a substitute for, the later REVERT trial.

Citation
Smith GD, et al. Cochrane Database Syst Rev. 2015;CD009502.
DOI / identifier
10.1002/14651858.CD009502.pub3
Open primary record
16 Wide QRS Complex TachycardiaTertiary clinical review · Orientation layer · verify management claims

Open-access scaffold for WCT definitions, mechanisms, differential diagnosis, and initial evaluation.

Citation
Obando MA, Marra EM. StatPearls [Internet]. Updated June 26, 2023.
DOI / identifier
Bookshelf ID NBK559054; PMID 32644480
Open primary record
17 Modified versus standard Valsalva for PSVT in an Indian emergency departmentRandomized controlled trial · new evidence · Low–moderate · small single-center trial

A current, imprecise replication signal used to teach confidence intervals, external context, and why one small trial does not erase REVERT.

Citation
Arora S, et al. Indian Heart J. 2026. Online ahead of print.
DOI / identifier
10.1016/j.ihj.2026.02.004
Open primary record

Arrhythmias release map

One hard decision every 4–5 days.

The module grows in focused releases, then recombines into cumulative capstones. Older material resurfaces at 2, 7, 21, 45, and 90 days.

  1. ARR-00

    Baseline diagnostic assessment

    Find the exact gaps in recognition, ECG logic, pharmacology, and bedside decisions.

    available
  2. ARR-01

    Electrical foundations & rhythm classification

    Conduction, action potentials, re-entry, automaticity, ECG intervals, and the pulse–stability–width–regularity framework.

    active
  3. ARR-02

    The unstable rhythm & electrical therapies

    Causal instability, synchronized versus unsynchronized energy, pacing, reversible causes, and post-conversion care.

    next
  4. ARR-03

    Atrial fibrillation & flutter

    Acute rate/rhythm control, cardioversion, stroke prevention, precipitants, HF, sepsis, and pre-excitation.

    queued
  5. ARR-04

    Regular narrow-complex tachycardia

    Sinus tachycardia, AVNRT, AVRT, atrial tachycardia, vagal maneuvers, adenosine, and AV nodal drugs.

    queued
  6. ARR-05

    Wide-complex tachycardia & monomorphic VT

    Safe presumptive management, electrical therapy, antiarrhythmics, ischemia, and structural heart disease.

    queued
  7. ARR-06

    Polymorphic VT, torsades & QT

    QT measurement, congenital versus acquired causes, drug stacks, electrolytes, magnesium, and recurrence prevention.

    queued
  8. ARR-07

    Bradyarrhythmias & AV block

    Localization, reversible causes, atropine, vasoactive support, pacing, poisoning, and post-MI contexts.

    queued
  9. ARR-08

    Antiarrhythmic pharmacology atlas

    Ion-channel mechanisms, state/use dependence, PK/PD, metabolites, interactions, organ dysfunction, and proarrhythmia.

    queued
  10. ARR-09

    Complex contexts

    ACS, HF, shock, sepsis, renal/hepatic failure, pregnancy, older adults, postoperative states, and toxicology.

    queued
  11. ARR-10

    Four-lens capstone

    A patient moving from ED to ICU to medicine to discharge, followed by unseen transfer cases and teach-back.

    queued