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Atrial fibrillation with RVR

Updated Oct 17, 2026Adults · ED management18 sources · 12 checked in PubMed2 figuresACC/AHA/ACCP/HRS 2023

Bottom line

  • Unstable because of the AF? Synchronized cardioversion now. That means hypotension or shock, ongoing ischemia, or pulmonary edema. Unstable pre-excited AF gets the same shock.1,2
  • Ask whether the fast rate is primary or secondary. When sepsis, bleeding, PE, heart failure or ACS is driving it, treat that cause. Cardioversion may harm these patients, and aggressive rate control should be avoided.2
  • Stable: a beta-blocker or diltiazem. Use diltiazem only when the EF is above 40%. In pooled data, diltiazem worked faster, while metoprolol caused fewer adverse events (10% vs 19%).1,3,4
  • Stable recent-onset AF does not have to be shocked today. In RAFF2, drug-then-shock converted 96% and shock alone 92%. In RACE 7, rate control and waiting was noninferior at 4 weeks: 69% converted on their own within 48 hours.5,6
  • Weigh clot risk before any cardioversion. At 48 hours or more, give 3 weeks of anticoagulation or image for thrombus first. Under 48 hours, risk still rises with CHA₂DS₂-VASc. Anticoagulate before cardioversion and for at least 4 weeks after.1,7

First steps

  1. Monitor and get a 12-lead ECG. The ECG confirms AF and screens for pre-excitation (WPW), other atrial arrhythmias, bradycardia and a long QT.1
  2. Decide whether the AF is causing instability. Look for hypotension (SBP < 90 mm Hg or shock), ongoing ischemia, or pulmonary edema. If any is present, cardiovert (next section).2,1
  3. Decide whether the rate is primary or secondary. Secondary rates are usually in patients who already have AF. Sepsis, bleeding, PE, heart failure and ACS are common drivers. Treat the cause first.2
  4. Wide, irregular, and over 200 bpm? Suspect pre-excited AF. Do not give AV nodal blockers.8,1
  5. Stable primary AF: choose rate or rhythm control. The choice rests on time since onset, anticoagulation status, stroke risk and the patient's preference.1,2
  6. Labs: electrolytes, renal and liver function, and thyroid function. Without symptoms or signs pointing to them, AF alone is not a reason to test for ACS, ischemia or PE.1

ECG

AF shows irregular R-R intervals, no distinct P waves, and chaotic fibrillatory atrial activity.1

12-lead ECG of atrial fibrillation with a rapid ventricular rate of about 150, showing irregularly spaced narrow QRS complexes without P waves
FIG 1Rapid atrial fibrillation, about 150 bpm. Narrow QRS complexes at irregular intervals, with no clear P waves. Look at the long lead II strip along the bottom.James Heilman, MD · Wikimedia Commons · CC BY-SA 3.0

Pre-excited AF (WPW)

  • Clues: a rate over 200 bpm, with some beats at nearly 300. The rhythm is irregular and the QRS is wide, with small beat-to-beat changes in QRS shape. The axis stays stable, which helps separate it from polymorphic VT.8
  • About 15% of people with WPW develop AF. Conduction down the accessory pathway can degenerate into VF.1
  • Before giving diltiazem, the label says to tell AF with bundle branch block apart from pre-excited AF. Diltiazem is contraindicated in AF or flutter with an accessory pathway.9

Unstable vs stable

Sign of instabilityWhat counts
HypotensionSBP < 90 mm Hg, or signs of shock such as altered mental status
Cardiac ischemiaOngoing severe chest pain, or marked ST depression (> 2 mm) despite treatment
Pulmonary edemaMarked dyspnea, crackles and hypoxia

Criteria from the 2021 CAEP checklist. Acute primary AF rarely causes instability on its own, except pre-excited AF.2

  • Instability caused by AF: immediate electrical cardioversion (class 1, level C-LD). Direct data in unstable patients are limited.1
  • Synchronize every shock. A shock that lands on the T wave can cause VF. When repeat shocks are needed, turn sync back on and check it before each one.1
  • Hypotensive, but the AF has lasted over 48 hours? CAEP suggests considering a trial of rate control first. For onset under 48 hours or WPW, it advises urgent cardioversion.2
  • Rate control with hypotension or acute heart failure: CAEP suggests digoxin may be first line.2 The US guideline allows IV amiodarone (class 2b) for critically ill or decompensated patients when beta-blockers and calcium channel blockers fail or can't be used. Amiodarone can convert the rhythm, so think about stroke risk first.1

Rate control

AgentAdult doseOnsetNotes
First line (stable, no pre-excitation)
Diltiazem IV0.25 mg/kg actual body weight over 2 min (20 mg is typical). If response is inadequate at 15 min: 0.35 mg/kg over 2 min (25 mg is typical). Infusion 5–15 mg/h~3 min; peak 2–7 min; bolus effect lasts 1–3 hOnly if EF > 40%. Contraindicated with IV beta-blockers, severe hypotension, cardiogenic shock, or AF with an accessory pathway.1,9
Metoprolol tartrate IV2.5–5 mg over 2 min, up to 3 doses—CAEP repeats every 15–20 min.1,2
Esmolol IV500 µg/kg over 1 min, then 50–300 µg/kg/min—Half-life 9 min.1
Second line or add-on
Digoxin IV0.25–0.5 mg, then 0.25 mg every 6 h, max 1.5 mg in 24 h5–30 min; peak 1–4 hWhen first-line agents fail or can't be used. Cleared by the kidneys. Higher mortality above 1.2 ng/mL.1,10
Magnesium IVDose per institutional protocol and label—Add-on (class 2a). Pooled rate control 63% vs 40% with standard care alone.1
Amiodarone IV150–300 mg over 1 h, then 10–50 mg/h over 24 h—For critically ill or decompensated HF when first-line drugs fail or can't be used (class 2b). It may convert the rhythm.1
Avoid
IV diltiazem or verapamilDo not give—Known moderate or severe LV systolic dysfunction (class 3: harm).1
All AV nodal blockersDo not give—Pre-excited AF: beta-blockers, diltiazem, verapamil, digoxin, adenosine, amiodarone (class 3: harm).1

Unreviewed doses. Verify against the current label and your institution's protocol before giving anything.

IV doses from the guideline's rate-control table1 and, for diltiazem, the FDA label.9 Onset times are from the diltiazem and digoxin labels.9,10 If the patient already takes an oral beta-blocker or calcium channel blocker, CAEP suggests starting with the same class. Once IV control works, it starts the oral form within 30 minutes.2

FIG 2How fast IV drugs act in AF. Drawn for this page. Rate-control times come from the diltiazem and digoxin labels.9,10 Times to conversion come from the guideline's cardioversion drug table.1 No label or guideline we read gives an onset time for IV metoprolol, so it is not shown. Times are approximate.

Diltiazem or metoprolol?

  • ED randomized trial (Fromm): heart rate < 100 at 5 minutes in 50.0% on diltiazem vs 10.7% on metoprolol. At 30 minutes, 95.8% vs 46.4%. Rates of hypotension and bradycardia did not differ.11
  • ED randomized trial (Demircan, n = 40): diltiazem 0.25 mg/kg vs metoprolol 0.15 mg/kg. Success at 20 minutes was 90% vs 80%. Diltiazem acted earlier, and no patient became hypotensive.12
  • Meta-analysis (17 studies, 1,214 patients): diltiazem was more effective (RR 1.11) and acted sooner. Adverse events did not differ.3
  • Adverse-event meta-analysis (13 studies, 1,660 patients): adverse events were 10% with metoprolol vs 19% with diltiazem (RR 0.74). Hypotension and bradycardia did not differ significantly when counted separately. Higher starting heart rates went with more adverse events.4
  • Guideline: both are class 1 for stable AF with RVR. Calcium channel blockers only if the EF is above 40%.1
Sources disagree

Diltiazem in reduced EF. The guideline calls IV diltiazem harmful in known moderate or severe LV dysfunction. Part of its evidence is a retrospective study where worsening heart failure was more common with diltiazem (33% vs 15%).1,13 Another retrospective study (n = 48) found similar rate control (62% metoprolol vs 50% diltiazem) and similar signs of worsening heart failure.14 A systematic review found no high-level evidence either way.13

How low to go

  • RACE II (614 outpatients with permanent AF, 2–3 years): lenient control (resting rate < 110) was noninferior to strict control (< 80). The primary outcome occurred in 12.9% vs 14.9%. More patients reached the lenient target (97.7% vs 67.0%).15
  • Guideline: let symptoms guide the target, generally a resting rate under 100–110 bpm, in patients without heart failure (class 2a).1
  • CAEP target: under 100 bpm at rest and under 110 bpm walking.2

Rhythm control and cardioversion

For stable patients, electrical and drug cardioversion are both acceptable. Electrical cardioversion works better but needs sedation. It is favored when the patient can tolerate sedation, wants conversion now, or a drug has failed or isn't suitable.1 First check that cardioversion is safe from a clot standpoint (anticoagulation section).

  • RACE 7 ACWAS (stable, symptomatic AF under 36 hours, ED patients): rate control with delayed cardioversion at 48 hours if needed was noninferior to early cardioversion. Sinus rhythm at 4 weeks: 91% vs 94%. In the wait-and-see arm, 69% converted on their own within 48 hours and 28% after delayed cardioversion. Recurrence by 4 weeks was about 30% in both arms.6
  • RAFF2 (396 ED patients with acute AF): procainamide followed by shocks if needed converted 96%, vs 92% with shocks alone. Procainamide alone converted 52%. Discharge home: 97% vs 95%. Anterolateral and anteroposterior pads worked equally well (94% vs 92%).5
  • Ottawa Aggressive Protocol (660 ED visits): IV procainamide converted 58.3%. Electrical cardioversion then worked in 91.7% of those who needed it. 96.8% went home, with a median ED stay of 4.9 hours. Adverse events occurred in 7.6% (mostly hypotension, 6.7%), with no strokes or deaths.16
  • Don't pre-treat with rate-control drugs before cardioversion. CAEP says it doesn't help and delays care.2

Electrical cardioversion

  • Synchronize to the QRS (class 1).1
  • For elective cardioversion, an initial biphasic shock of at least 200 J is reasonable (class 2a). In RAFF2, a strategy starting at 200 J (up to 3 shocks) converted 92% of the shock-only group.1
  • CAEP suggests starting at 150–200 J and not starting low. Either pad position is fine. If a shock fails, press on the pads or switch position.2
  • Obesity lowers success. Manual pressure and higher energy can help.1

Drug cardioversion

DrugAdult doseTime to conversionCautions
Procainamide IV1 g over 30 min, then 2 mg/min for 1 h30–60 minHypotension in 5–12%. Can worsen HFrEF. Class 2b for routine AF; class 1 for stable pre-excited AF.1
Ibutilide IV≥ 60 kg: 1 mg over 10 min. < 60 kg: 0.01 mg/kg. May repeat once if no conversion 10 min after the first dose ends30–90 minConverts about 30% of AF. Risk of torsades. Avoid if LVEF ≤ 40%.1
Amiodarone IV5–7 mg/kg or 300 mg load8–12 hSlow. Class 2a for conversion.1

Unreviewed doses. Verify against the current label and your institution's protocol before giving anything.

Sources disagree

Procainamide dose: the US guideline lists 1 g over 30 minutes.1 CAEP gives 15 mg/kg over 60 minutes (max 1,500 mg). It advises against procainamide if SBP < 100 mm Hg or QTc > 500 ms, and to stop the infusion if BP drops or the QRS widens (for example by more than 30%).2 RAFF2 gave 15 mg/kg over 30 minutes.5 Amiodarone: the US guideline calls it reasonable for conversion, though slow.1 CAEP advises against it as slow and not very effective.2

Pre-excited AF

  • Unstable: electrical cardioversion (class 1).1
  • Stable: IV ibutilide or IV procainamide (class 1). They slow conduction down the pathway and can end the AF.1 LITFL notes procainamide is the most widely available choice.8
  • Never give verapamil, diltiazem, amiodarone, digoxin, adenosine or beta-blockers. They can speed pathway conduction and trigger VF (class 3: harm).1
  • Refer for accessory pathway ablation (class 1). Large case series report 93–95% success.1

Anticoagulation and stroke risk

CHA₂DS₂-VASc itemPoints
Congestive heart failure1
Hypertension1
Age ≥ 752
Diabetes1
Prior stroke, TIA or thromboembolism2
Vascular disease (prior MI, PCI, CABG, peripheral arterial disease)1
Age 65–741
Female sex1

Points as listed in the guideline.1 The score was derived in 1,084 patients from the Euro Heart Survey. It predicted events only modestly (C-statistic 0.606), but patients it called low risk had no events.17 The same score can mean very different absolute risk in different populations.1

  • Long-term anticoagulation: recommended when annual risk is ≥ 2% (e.g. a score of ≥ 2 in men or ≥ 3 in women), class 1. It is reasonable at a score of 1 in men or 2 in women (class 2a). Prefer a DOAC over warfarin, unless the patient has moderate to severe rheumatic mitral stenosis or a mechanical valve.1
  • From the ED: CAEP advises starting an oral anticoagulant before discharge if any CHADS-65 criterion is present (age ≥ 65, diabetes, hypertension, heart failure, stroke/TIA). This includes patients who convert on their own.2
  • AF during sepsis: the benefit of anticoagulation during the illness is uncertain (class 2b). In 38,582 patients, parenteral anticoagulation didn't lower stroke (1.3% vs 1.4%) but raised significant bleeding (8.6% vs 7.2%).1

Is it safe to cardiovert?

SituationUS guideline (2023)CAEP (2021)
Anticoagulated ≥ 3 weeksCardioversion can proceedSafe to cardiovert
AF ≥ 48 h, not anticoagulated3 weeks of uninterrupted anticoagulation, or imaging to exclude thrombus, first (class 1)Only with a negative TEE
AF < 48 h, higher riskConsider imaging first if CHA₂DS₂-VASc ≥ 2 (class 2b)12–48 h: only if fewer than 2 CHADS-65 criteria (age ≥ 65, diabetes, hypertension, heart failure)
AF < 12 h, low riskCHA₂DS₂-VASc 0–1: benefit of imaging or anticoagulation is uncertain (class 2b)Safe if under 12 h
After any cardioversionAnticoagulate before and for at least 4 weeks after (class 1)TEE-guided: start a DOAC right away for 4 weeks

From the guideline1 and the CAEP checklist.2 CAEP's short-onset pathway also requires no prior stroke or TIA and no valvular heart disease.2

  • FinCV (5,116 cardioversions of AF < 48 h without anticoagulation): 0.7% had a definite thromboembolic event within 30 days, 31 of them strokes, at a median of 2 days. Risk was highest (9.8%) with heart failure plus diabetes and lowest (0.2%) with no heart failure and age under 60. Age, female sex, heart failure and diabetes were independent predictors.7
  • In FinCV data cited by the guideline, the 30-day event rate was 0.4% with CHA₂DS₂-VASc 0–1 and 0.3% when AF had lasted under 12 hours. Waiting more than 12 hours to cardiovert has been linked to more events.1
Sources disagree

The 48-hour rule is softening. The US guideline points out that patients often underestimate how long they've been in AF, and that risk under 48 hours is not uniformly low. It asks clinicians to weigh each patient's clot risk rather than rely on a strict 48-hour cutoff.1 CAEP keeps a time-based rule but tightens it to 12 hours for patients with CHADS-65 risk factors.2

Disposition

  • Most patients with uncomplicated acute AF can go home. CAEP advises admission only for patients who stay highly symptomatic despite treatment, have ACS (significant chest pain, a troponin rise and ECG changes), or have acute heart failure that doesn't improve in the ED.2
  • Troponin: not needed routinely. Expect a small demand rise.2
  • After conversion with procainamide or a shock, many patients can leave as soon as 30 minutes later.2 Discharge rates were 95–97% in RAFF2 and 96.8% in the Ottawa cohort.5,16
  • Follow-up: see a physician within 7 days if warfarin or a rate-control drug was started. See cardiology or internal medicine in 4–6 weeks. Don't start amiodarone or propafenone in the ED. If sinus rhythm returns, rate-control drugs are generally not needed.2
  • AF found during an acute illness: warn the patient it often comes back (42–68% over 5 years). Arrange outpatient follow-up for stroke risk and anticoagulation decisions.1

Pitfalls

  • Giving an AV nodal blocker to a wide, irregular tachycardia over 200 bpm. It may be pre-excited AF.8,1
  • Pushing down a compensatory rate in sepsis, bleeding or PE instead of treating the cause.2
  • Giving IV diltiazem to a patient with known moderate or severe LV dysfunction.1
  • Giving IV diltiazem on top of an IV beta-blocker. The label lists this as a contraindication.9
  • Forgetting to re-enable sync before a repeat shock.1
  • Trusting a reported onset under 48 hours. Patients may not notice AF, and clot risk under 48 hours varies with stroke risk factors.1,7
  • Cardioverting without a plan for 4 weeks of anticoagulation afterward.1
  • Using amiodarone for rate control without remembering it can convert the rhythm.1

How strong is the evidence?

The rate-control recommendations rest mostly on small randomized trials and observational data (level B). Immediate cardioversion for instability is level C-LD, because unstable patients are hard to study.1 The diltiazem vs metoprolol trials are small and short-term. The pooled data vary in dosing and leave out important subgroups.4,11,12 Data on AF with RVR in acute decompensated heart failure carry serious to critical risk of bias.13 The strongest ED evidence covers stable, recent-onset AF: RACE 7 and RAFF2 are multicenter randomized trials.5,6 The rules for anticoagulation around cardioversion rest largely on registry and cohort data such as FinCV.1,7

On-shift teaching

Questions to ask a learner at the bedside. Tap a question to see the answer. Every answer uses facts cited above.

Q1A stable patient has a wide, irregular tachycardia at about 250 bpm with changing QRS shapes. What should you avoid, and what can you give?
Suspect pre-excited AF.8 Avoid beta-blockers, diltiazem, verapamil, digoxin, adenosine and amiodarone (class 3: harm). Give IV procainamide or ibutilide, or cardiovert electrically if the patient becomes unstable.1
Q2What did RACE 7 ACWAS show about waiting instead of cardioverting early?
In stable AF under 36 hours, rate control with delayed cardioversion was noninferior: sinus rhythm at 4 weeks was 91% vs 94%. In the waiting group, 69% converted on their own within 48 hours.6
Q3Diltiazem or metoprolol: which is faster, and which is gentler?
In an ED trial, diltiazem brought 95.8% under 100 bpm by 30 minutes, vs 46.4% with metoprolol.11 In pooled data, metoprolol had fewer adverse events (10% vs 19%), though hypotension and bradycardia did not differ significantly when counted separately.4
Q4How strict does the heart rate target need to be?
Lenient is usually enough. In RACE II, a resting target under 110 was noninferior to under 80 (12.9% vs 14.9% primary outcome).15 The guideline suggests a resting rate under 100–110, guided by symptoms.1
Q5In FinCV, which patients with AF under 48 hours had the highest and lowest clot risk after cardioversion without anticoagulation?
Highest: 9.8% with heart failure plus diabetes. Lowest: 0.2% with no heart failure and age under 60. Overall, 0.7% had a thromboembolic event within 30 days.7
Q6A patient with an EF of 25% is in AF at 150 and is hypotensive. Why not diltiazem, and what are the options?
IV diltiazem is harmful in moderate or severe LV dysfunction (class 3).1 If the AF is causing the instability, cardiovert.1 For rate control, CAEP suggests digoxin first with hypotension or acute heart failure.2 IV amiodarone is a class 2b option in decompensated HF, but it may convert the rhythm.1

References

  1. 1
    Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Circulation. 2024;149(1):e1–e156.GuidelinePMID 38033089PMCFull text read
  2. 2
    Stiell IG, de Wit K, Scheuermeyer FX, et al. 2021 CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist. CJEM. 2021;23(5):604–610.GuidelinePMID 34383280PMCFull text read
  3. 3
    Lan Q, Wu F, Han B, et al. Intravenous diltiazem versus metoprolol for atrial fibrillation with rapid ventricular rate: a meta-analysis. Am J Emerg Med. 2022;51:248–256.Meta-analysisPMID 34781150PubMed
  4. 4
    Hintze TD, Downing JV, Acquisto NM, et al. Metoprolol vs diltiazem for atrial fibrillation with rapid ventricular rate: systematic review and meta-analysis of adverse events. Am J Emerg Med. 2025;89:230–240.Meta-analysisPMID 39764905PubMed
  5. 5
    Stiell IG, Sivilotti MLA, Taljaard M, et al. Electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2): a partial factorial randomised trial. Lancet. 2020;395(10221):339–349.RCTPMID 32007169PubMed
  6. 6
    Pluymaekers NAHA, Dudink EAMP, Luermans JGLM, et al.; RACE 7 ACWAS Investigators. Early or delayed cardioversion in recent-onset atrial fibrillation. N Engl J Med. 2019;380(16):1499–1508.RCTPMID 30883054PubMed
  7. 7
    Airaksinen KE, Grönberg T, Nuotio I, et al. Thromboembolic complications after cardioversion of acute atrial fibrillation: the FinCV (Finnish CardioVersion) study. J Am Coll Cardiol. 2013;62(13):1187–1192.CohortPMID 23850908PubMed
  8. 8
    Life in the Fast Lane. Atrial fibrillation/flutter in pre-excitation. ECG library.FOAMlitfl.comPage read
  9. 9
    Diltiazem hydrochloride in sodium chloride injection. FDA prescribing information (WG Critical Care). DailyMed.Drug labeldailymed.nlm.nih.govLabel text read
  10. 10
    Lanoxin (digoxin) injection. FDA prescribing information (Covis Pharma). DailyMed.Drug labeldailymed.nlm.nih.govLabel text read
  11. 11
    Fromm C, Suau SJ, Cohen V, et al. Diltiazem vs. metoprolol in the management of atrial fibrillation or flutter with rapid ventricular rate in the emergency department. J Emerg Med. 2015;49(2):175–182.RCTPMID 25913166PubMed
  12. 12
    Demircan C, Cikriklar HI, Engindeniz Z, et al. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Emerg Med J. 2005;22(6):411–414.RCTPMID 15911947PMCPubMed
  13. 13
    Niforatos JD, Ehmann MR, Balhara KS, et al. Management of atrial flutter and atrial fibrillation with rapid ventricular response in patients with acute decompensated heart failure: a systematic review. Acad Emerg Med. 2023;30(2):124–132.Meta-analysisPMID 36326565PubMed
  14. 14
    Hirschy R, Ackerbauer KA, Peksa GD, et al. Metoprolol vs. diltiazem in the acute management of atrial fibrillation in patients with heart failure with reduced ejection fraction. Am J Emerg Med. 2019;37(1):80–84.CohortPMID 29731345PubMed
  15. 15
    Van Gelder IC, Groenveld HF, Crijns HJ, et al.; RACE II Investigators. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010;362(15):1363–1373.RCTPMID 20231232PubMed
  16. 16
    Stiell IG, Clement CM, Perry JJ, et al. Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM. 2010;12(3):181–191.CohortPMID 20522282PubMed
  17. 17
    Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the Euro Heart Survey on atrial fibrillation. Chest. 2010;137(2):263–272.CohortPMID 19762550PubMed
  18. 18
    Farkas J. Atrial fibrillation. Internet Book of Critical Care, EMCrit. Further reading; not used for any claim above.FOAMemcrit.orgLink checked
How this page was made
  • Written from scratch. No source text was copied; facts are restated and cited.
  • The 2023 ACC/AHA/ACCP/HRS guideline and the 2021 CAEP checklist were read in full through PubMed Central. Trial and meta-analysis results were checked against their PubMed abstracts. Diltiazem and digoxin details come from FDA label text on DailyMed.
  • No ACEP clinical policy on atrial fibrillation was found. The 2024 ESC guideline was not openly accessible and is not used. No FDA label for IV metoprolol was found, so its dose comes from the guideline only and no onset time is given. The JAMA FinCV research letter on time to cardioversion has no abstract, so that finding is cited only as the guideline reports it.
  • No source we read gives a magnesium dose for AF, so none is given. Energy levels are given only for elective cardioversion, as the guideline and CAEP state them.
  • Adults only. Figure 1 is an openly licensed ECG from Wikimedia Commons, credited under the image. Figure 2 was drawn for this page from label and guideline data.
  • Not for clinical use until physician review.
Not for clinical use

AI-generated draft. Not reviewed by a physician. This page is for education only and may contain errors, including in doses. Do not use it to diagnose, treat or make decisions about any patient. Rely on your own clinical judgment, your institution's protocols and current drug labeling. Reading this page does not create a physician-patient relationship. Full terms