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Atrial Fibrillation & Arrhythmias

Name: Atrial Fibrillation & Arrhythmias
Creator: Veli Bakalov, MD

Read the rhythm, score the stroke risk, and know which drugs can kill

Cardiology·Arrhythmias & Conduction·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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AF is irregularly irregular with no P waves; AFFIRM showed rate control (β-blocker or diltiazem/verapamil, digoxin as add-on) is non-inferior to rhythm control for mortality.
Anticoagulate AF at CHA2DS2-VASc ≥2 in men or ≥3 in women; DOACs are preferred, but a mechanical valve or moderate-to-severe mitral stenosis requires warfarin (INR 2–3).
AF ≥48 h or of unknown duration: 3 weeks of anticoagulation or a TEE before cardioversion, then at least 4 weeks after; unstable AF gets immediate synchronized cardioversion.
Stable regular narrow-complex SVT (usually AVNRT): vagal maneuvers, then adenosine 6 mg rapid IV push, then 12 mg; use diltiazem instead in asthma.
WPW = short PR, delta wave, wide QRS; in pre-excited AF avoid adenosine, β-blockers, CCBs, and digoxin, and give procainamide or ibutilide; ablation is definitive.
Pulseless VT/VF: unsynchronized defibrillation, CPR, epinephrine 1 mg every 3–5 min, amiodarone 300 mg; unstable VT with a pulse gets synchronized cardioversion.
Torsades de pointes (polymorphic VT with long QT): IV magnesium first even if the level is normal; stop QT-prolonging drugs and correct K and Mg.
Mobitz II (fixed PR, sudden dropped QRS) and complete heart block need a pacemaker; Mobitz I and first-degree block are usually benign.
Symptomatic bradycardia: atropine first, then transcutaneous pacing or dopamine/epinephrine infusion if refractory.

Atrial fibrillation: recognition, rate, and rhythm

ECG. Atrial fibrillation is an irregularly irregular rhythm with no discrete P waves and a variable ventricular response. It is the most common sustained arrhythmia; hypertension, age, valve disease, alcohol, hyperthyroidism, and sleep apnea predispose, so new AF warrants a TSH and an echocardiogram.

Unstable AF. Hypotension, ischemic chest pain, pulmonary edema, or altered mental status call for immediate synchronized cardioversion regardless of how long AF has been present; do not delay for anticoagulation.

Rate vs rhythm control. The AFFIRM trial showed rate control is non-inferior to rhythm control for mortality, so rate control is first-line for stable, older, minimally symptomatic patients.

Rate control: β-blockers (metoprolol) or non-dihydropyridine calcium channel blockers (diltiazem, verapamil) first-line. Digoxin is an add-on, useful in HFrEF but slow. Avoid non-DHP CCBs in decompensated HFrEF.
Rhythm control (persistent symptoms, younger patients): cardioversion, antiarrhythmic drugs such as amiodarone or flecainide (only without structural heart disease), or catheter ablation isolating the pulmonary veins, where AF triggers usually arise.

Stroke prevention and cardioversion

CHA₂DS₂-VASc score

Letter	Risk factor	Points
C	Congestive heart failure	1
H	Hypertension	1
A₂	Age ≥75	2
D	Diabetes	1
S₂	Prior stroke or TIA	2
V	Vascular disease (prior MI, peripheral artery disease, aortic plaque)	1
A	Age 65–74	1
Sc	Sex category female	1

Anticoagulate at ≥2 in men or ≥3 in women; 0 in men or 1 in women needs none. Female sex adds risk only alongside another factor.

Choice of anticoagulant. DOACs (apixaban, rivaroxaban, dabigatran) are preferred over warfarin in nonvalvular AF. Warfarin (INR 2–3) is required with a mechanical heart valve or moderate-to-severe mitral stenosis. HAS-BLED estimates bleeding risk but does not by itself justify withholding anticoagulation; use it to find modifiable bleeding risks.

The 48-hour rule. Once AF has lasted 48 hours or more, left atrial appendage thrombus becomes a real risk, and restoring organized contraction can dislodge it.

AF ≥48 h or of unknown durationGive 3 weeks of therapeutic anticoagulation, or perform a TEE to exclude left atrial appendage thrombus.
CardiovertElectrical or pharmacologic.
Anticoagulate at least 4 weeks afterwardRegardless of the score, because the stunned atrium contracts poorly after conversion.

SVT, adenosine, and Wolff-Parkinson-White

Paroxysmal SVT, usually AV nodal reentrant tachycardia (AVNRT), is a regular narrow-complex tachycardia at 150–250 bpm, often with no visible P waves. If stable, try vagal maneuvers (Valsalva, carotid sinus massage) first; if they fail, give adenosine 6 mg by rapid IV push, then 12 mg. An unstable narrow-complex tachycardia gets synchronized cardioversion. Catheter ablation prevents recurrences.

Adenosine blocks the AV node transiently, with a half-life under 10 seconds. Expect flushing, chest tightness, transient asystole, and a fleeting sense of impending doom. It can cause bronchospasm, so in asthma or COPD use diltiazem instead. Theophylline and caffeine block adenosine receptors and blunt its effect.

Wolff-Parkinson-White. An accessory pathway (bundle of Kent) bypasses the AV node, giving a short PR interval, a slurred upstroke (delta wave), and a wide QRS. Regular narrow-complex reentry that uses the AV node can be treated like other SVT, but AF with pre-excitation (an irregular, very fast, wide-complex rhythm) is different.

In AF with WPW, avoid all AV-nodal blockers: Adenosine, β-Blockers, Calcium channel blockers, Digoxin. Blocking the node diverts impulses down the accessory pathway, which can conduct at extreme rates and degenerate into VF. Give procainamide or ibutilide, or cardiovert if unstable; catheter ablation of the pathway is definitive.

Ventricular arrhythmias

Ventricular rhythms and first actions

Rhythm	Treatment
Pulseless VT or VF	Immediate unsynchronized defibrillation plus CPR; epinephrine 1 mg every 3–5 min; amiodarone 300 mg (lidocaine is an alternative)
Unstable VT with a pulse	Synchronized cardioversion
Stable monomorphic VT	Amiodarone or procainamide
Torsades de pointes	IV magnesium sulfate first, even with a normal serum magnesium; correct potassium and magnesium; stop QT-prolonging drugs; defibrillate if unstable

Torsades de pointes is polymorphic VT with a twisting QRS axis on a background of a prolonged QT interval. Common culprits are antipsychotics such as haloperidol, antiemetics such as ondansetron, macrolides, fluoroquinolones, methadone, and class IA and III antiarrhythmics, plus hypokalemia and hypomagnesemia. Do not treat it with a QT-prolonging antiarrhythmic such as procainamide.

Bradycardia and heart block

AV blocks

Block	ECG	Significance
First-degree	PR >200 ms, every P conducted	Benign
Mobitz I (Wenckebach)	PR lengthens progressively until a QRS drops	Usually benign; AV node level, often high vagal tone or nodal-blocking drugs
Mobitz II	Sudden dropped QRS with a fixed PR	His-Purkinje level; can progress to complete block, so pace
Third-degree (complete)	Complete AV dissociation: P waves and a slow escape rhythm march independently	Pacemaker

Symptomatic bradycardia. Give atropine first: current ACLS uses 1 mg IV, repeated every 3–5 minutes to a maximum of 3 mg (older protocols started at 0.5 mg). If bradycardia persists, use transcutaneous pacing or a dopamine or epinephrine infusion. Atropine often fails in infranodal block (Mobitz II, complete block), so move quickly to pacing.

Permanent pacemaker indications include symptomatic sinus bradycardia, Mobitz II, and third-degree (complete) heart block. Mobitz I and first-degree block usually need only observation and removal of nodal-blocking drugs.