Arrhythmias

Why it matters

• Hemodynamic: loss of atrioventricular synchrony (the atrial kick) and shortened diastolic filling drop cardiac output, causing syncope, angina, or pulmonary edema.
• Thromboembolic: fibrillating atria produce stasis in the left atrial appendage → cardioembolic stroke, the dominant morbidity of atrial fibrillation.
• Sudden death: ventricular fibrillation and pulseless ventricular tachycardia are the shockable rhythms of cardiac arrest; survival falls with every minute defibrillation is delayed.

Epidemiology worth recalling

• Atrial fibrillation is the most common sustained arrhythmia in adults, affecting several million people in the United States; prevalence rises steeply with age and is uncommon before 50. Lifetime risk is approximately 1 in 3 from index age 55 in individuals of European ancestry (about 1 in 4 from age 40 in earlier Framingham estimates).
• AVNRT is the most common paroxysmal SVT, typically in young to middle-aged patients with structurally normal hearts and a female predominance.
• Ventricular tachycardia clusters in patients with structural heart disease — prior myocardial infarction with scar, and cardiomyopathy with reduced ejection fraction.
• Ventricular pre-excitation (WPW pattern) is present in roughly 1–3 per 1,000 people; only a minority develop symptomatic arrhythmia, but AF conducted down the accessory pathway is the feared presentation.
• Out-of-hospital cardiac arrest occurs in the hundreds of thousands annually in the US (AHA surveillance), most often from ischemic ventricular arrhythmia.

Reentry (most common mechanism)

• Myocardial scar: prior MI, sarcoidosis, Chagas disease, arrhythmogenic right ventricular cardiomyopathy — fibrous tissue interdigitating with viable myocytes creates slow conduction and unidirectional block → monomorphic VT.
• Anatomic circuits: cavotricuspid isthmus (typical atrial flutter), dual AV nodal pathways (AVNRT), accessory pathway such as the bundle of Kent (AVRT/WPW).
• Atrial stretch and fibrosis: hypertension, mitral valve disease, heart failure, obstructive sleep apnea — dilated, fibrotic atria sustain the multiple wavelets of AF.

Enhanced automaticity

• Catecholamine excess: sepsis, pain, pheochromocytoma, cocaine/amphetamines, exogenous beta agonists.
• Metabolic drive: hyperthyroidism (classic new AF trigger), hypoxia and hypercapnia (multifocal atrial tachycardia in COPD), fever, anemia.

Triggered activity

• Early afterdepolarizations in the setting of a prolonged QT (hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, QT-prolonging drugs) → torsades de pointes.
• Delayed afterdepolarizations from calcium overload — digoxin toxicity, reperfusion, catecholaminergic polymorphic VT (RyR2 mutation).

Conduction system disease / bradyarrhythmia

• Idiopathic fibrosis (Lenègre/Lev disease), inferior MI (AV nodal ischemia), Lyme carditis, infiltrative disease, hypothyroidism, and AV nodal blocking drugs.

From insult to arrhythmia

• Reentry requires three ingredients: two limbs with differing conduction and refractoriness, unidirectional block in one limb, and slow conduction in the other so the initially blocked tissue has recovered excitability by the time the wavefront returns. Scar, ischemia, and fibrosis supply all three. A premature beat is the usual initiator — which is why a stem describes palpitations starting "suddenly."
• Automaticity: catecholamines and hypoxia steepen phase 4 diastolic depolarization in latent pacemaker tissue, letting an ectopic focus outrun the sinus node.
• Triggered activity: potassium channel blockade or hypokalemia prolongs phase 3 repolarization, allowing L-type calcium channels to reactivate → early afterdepolarization. If it reaches threshold in a heterogeneously repolarizing ventricle, a polymorphic R-on-T beat launches torsades. Intracellular calcium overload (digoxin, Na/K-ATPase inhibition) drives the Na/Ca exchanger to generate delayed afterdepolarizations.

Why the presentation looks the way it does

• Atrial fibrillation: ectopic firing from pulmonary vein sleeves plus a fibrotic atrium yields chaotic 400–600 bpm atrial activity. The AV node filters irregularly → irregularly irregular pulse with no discernible P waves. Loss of atrial kick removes a meaningful share of ventricular filling — devastating in stiff ventricles (HFpEF, hypertrophic cardiomyopathy, mitral stenosis). Appendage stasis completes Virchow's triad → cardioembolic stroke. Weak beats after short R–R intervals fail to open the aortic valve, producing a pulse deficit.
• WPW: the accessory pathway lacks the AV node's decremental, calcium-dependent conduction. Antegrade pre-excitation fuses with nodal conduction → short PR and delta wave. During AF the pathway lacks decremental conduction, so it can conduct at extremely short pre-excited R–R intervals (<250 ms), producing an irregular, wide, very rapid tachycardia that may degenerate to ventricular fibrillation.
• Ventricular tachycardia: impulses spread myocyte-to-myocyte rather than through the His-Purkinje system → wide QRS, and the atria continue independently → AV dissociation with intermittent cannon A waves, capture and fusion beats.

Symptoms driven by rate and filling

• Palpitations: awareness of forceful or irregular contraction. Sudden on/off ("like a switch") suggests reentrant AVNRT/AVRT; gradual acceleration and deceleration suggests sinus tachycardia.
• Dyspnea, fatigue, exercise intolerance: reduced cardiac output from tachycardia-shortened diastole and loss of atrial kick; most pronounced in mitral stenosis, HFpEF, and hypertrophic cardiomyopathy.
• Angina: shortened diastole cuts coronary perfusion time while increasing myocardial oxygen demand — chest pain even with normal coronaries.
• Presyncope/syncope: abrupt fall in cerebral perfusion. Syncope without prodrome, during exertion, or with a family history of sudden death is high-risk and points to VT or a channelopathy rather than vasovagal faint.
• Polyuria after an SVT episode: atrial stretch releases atrial natriuretic peptide.

Physical findings

• ***Irregularly irregular* pulse with a pulse deficit** (apical rate exceeds radial): atrial fibrillation.
• Cannon A waves: atrial contraction against a closed tricuspid valve — complete heart block, VT, or AVNRT (with the AVNRT variant producing regular frog sign neck pulsations).
• Variable-intensity S1 and intermittent cannon A waves: AV dissociation, supporting VT over SVT with aberrancy.
• Hypotension, altered mentation, cool extremities, pulmonary rales: the instability criteria that mandate immediate electrical therapy.

Demographics the stem names

• Elderly hypertensive or post-cardiac-surgery patient → AF.
• Young woman with abrupt palpitations and a normal heart → AVNRT.
• Young athlete with syncope and a delta wave → WPW.
• Patient days after an anterior MI, or with an ischemic cardiomyopathy and an ICD, with wide-complex tachycardia → VT.
• Hospitalized patient on a QT-prolonging antiemetic or antibiotic with hypokalemia and recurrent syncope → torsades.
• Binge drinker over a weekend with new AF → holiday heart.
• Asymptomatic athlete with resting bradycardia and Mobitz I → benign high vagal tone.

Initial evaluation

• 12-lead ECG during symptoms is the diagnostic gold standard — capture rhythm before treating anything stable. Read rate, QRS width, regularity, and P-wave relationship.
• Continuous telemetry for any unstable or high-risk patient.
• Labs: potassium, magnesium, calcium, TSH, troponin when ischemia is plausible, digoxin level if toxicity is suspected, and a toxicology screen in young patients.
• Transthoracic echocardiogram: ejection fraction, atrial size, valvular disease, scar — determines both arrhythmia mechanism and therapy (ICD candidacy, anticoagulation decisions in valvular AF).

Characteristic findings

• AF: absent organized P waves, irregularly irregular R–R.
• Atrial flutter: sawtooth flutter waves, atrial rate near 300 with 2:1 conduction giving a ventricular rate near 150.
• WPW: PR <120 ms, slurred delta wave, widened QRS with secondary repolarization change.
• Torsades: polymorphic VT with axis twisting about the baseline on a background of prolonged QTc; risk rises substantially once QTc exceeds roughly 500 ms.
• Complete heart block: AV dissociation with an atrial rate faster than and independent of a regular escape rhythm.

Named criteria

• Brugada criteria and the Vereckei aVR algorithm distinguish VT from SVT with aberrancy; AV dissociation, capture/fusion beats, and extreme axis favor VT.
• CHA₂DS₂-VASc estimates stroke risk and drives anticoagulation decisions; bleeding-risk scores such as HAS-BLED should be used to identify and modify reversible bleeding risk factors, not to withhold or discontinue anticoagulation (2023 ACC/AHA/ACCP/HRS Class 3: No Benefit).
• Exercise stress testing for exertional arrhythmia; electrophysiology study for mechanism definition, ablation mapping, and accessory-pathway risk stratification.

Atrial fibrillation (2023 ACC/AHA/ACCP/HRS)

• Anticoagulation is driven by stroke risk, not by rate-versus-rhythm strategy: a DOAC (apixaban, rivaroxaban) is preferred over warfarin except with a mechanical valve or moderate-to-severe rheumatic mitral stenosis, where warfarin is required.
• Rate control: beta blocker (metoprolol) or non-dihydropyridine calcium channel blocker (diltiazem); digoxin as an adjunct in heart failure or sedentary patients.
• Rhythm control: antiarrhythmics or cardioversion; catheter ablation is a Class 1 first-line option in selected younger patients with symptomatic paroxysmal AF and in AF with HFrEF. Cardioversion of AF >48 hours (or unknown duration) requires 3 weeks of anticoagulation or a TEE to exclude appendage thrombus, plus 4 weeks after. Left atrial appendage occlusion for patients with contraindications to long-term anticoagulation.

Of the arrhythmia

• Cardioembolic stroke and systemic embolism (AF, atrial flutter): appendage stasis → thrombus. Signals as sudden focal deficit; large-vessel occlusion is an emergency requiring immediate imaging and reperfusion assessment.
• Sudden cardiac death: degeneration of VT or pre-excited AF into ventricular fibrillation — an arrest emergency.
• Tachycardia-induced cardiomyopathy: months of poorly controlled ventricular rates cause calcium handling failure and chamber dilation; presents as new HFrEF that improves with rate/rhythm control.
• Acute decompensated heart failure and pulmonary edema: loss of atrial kick plus short diastole, worst in mitral stenosis and HFpEF.
• Syncope with traumatic injury, and demand ischemia (type 2 MI) from rate-related supply–demand mismatch.

Of therapy

• Anticoagulant bleeding: GI hemorrhage and intracranial hemorrhage (emergency). Reverse dabigatran with idarucizumab, factor Xa inhibitors with andexanet alfa, warfarin with 4-factor PCC plus vitamin K.
• Proarrhythmia: sotalol, dofetilide, and ibutilide prolong QT → torsades, which is why initiation is often inpatient with QT monitoring. Class IC agents can organize AF into flutter with 1:1 AV conduction and can increase mortality in post-MI patients (the CAST experience).
• Amiodarone toxicity: thyroid (both hypo- and hyperthyroidism), pulmonary fibrosis, hepatotoxicity, corneal microdeposits, blue-gray skin, and optic neuropathy — mandates periodic TSH, LFTs, chest imaging, and eye exams.
• Digoxin toxicity: nausea, yellow-green visual halos, and atrial tachycardia with block; treat with digoxin-specific Fab fragments.
• Ablation: cardiac tamponade (emergency), pulmonary vein stenosis, phrenic nerve palsy, and the rare but frequently fatal atrioesophageal fistula presenting days to weeks later with fever, dysphagia, and neurologic events.
• Device complications: pocket infection or lead endocarditis, lead perforation, pneumothorax, and inappropriate ICD shocks (usually triggered by AF with rapid rates).

• Instability decides everything. Hypotension, altered mentation, ischemic pain, or acute heart failure with a tachyarrhythmia → synchronized cardioversion now, not another drug. Pulseless VT and ventricular fibrillation → unsynchronized defibrillation.
• A wide-complex tachycardia is VT until proven otherwise, especially with prior MI. Do not "test" it with a calcium channel blocker — verapamil in VT can precipitate hemodynamic collapse. Look for AV dissociation, capture and fusion beats, and extreme axis deviation.
• Pre-excited AF (irregular, wide, very fast) forbids AV nodal blockade. Blocking the node shunts conduction down the accessory pathway → ventricular fibrillation. Use procainamide or ibutilide, or cardiovert.
• Adenosine is diagnostic as well as therapeutic: transient AV block unmasks sawtooth flutter waves. Warn the patient about chest pressure and flushing; effects are amplified by dipyridamole and blunted by caffeine/theophylline.
• Anticoagulate on stroke risk, not on rhythm strategy. Rate control and rhythm control confer the same stroke risk; the CHA₂DS₂-VASc score, not the rate, drives DOAC use (2023 ACC/AHA/ACCP/HRS). Warfarin — not a DOAC — is required for mechanical valves and rheumatic mitral stenosis.
• New AF? Check a TSH. Hyperthyroidism is the classic reversible driver, and thyroid storm must be treated alongside rate control.
• Torsades = magnesium. Give IV magnesium sulfate even when the serum magnesium is normal, replete potassium, stop every QT-prolonging drug, and use overdrive pacing or isoproterenol for pause-dependent recurrences.
• Common distractor: attributing a delta wave to bundle branch block, or calling a regular narrow-complex tachycardia at exactly 150 bpm "sinus tachycardia" — that rate should prompt a search for atrial flutter with 2:1 conduction.

• SVT and AFib are most common arrhythmias; VF/pulseless VT are most life-threatening
• ECG is diagnostic gold standard; Holter monitor for paroxysmal rhythms
• Acute hemodynamic instability → immediate synchronized cardioversion (except VF → defibrillation)
• Beta-blockers and calcium channel blockers are first-line for rate control in most supraventricular rhythms
• Wolff-Parkinson-White (WPW) presents with short PR interval + delta wave and risk of AFib with RVR

1. 1.AFib with RVR in WPW: AV nodal blockers paradoxically increase conduction down accessory pathway → VF. Use procainamide/ibutilide/amiodarone instead.

1. 1.Misdiagnosing SVT with aberrancy as VT: If narrow QRS → more likely SVT. VT distinguishers: AV dissociation, capture/fusion beats, extreme axis deviation, Brugada criteria. Always check for prior MI.

1. 1.Forgetting anticoagulation in AFib: CHA₂DS₂-VASc score ≥2 (or ≥1 if female/≥65yo) requires anticoagulation regardless of rate control strategy; major stroke risk.