Arrhythmias, Channelopathies & Conduction Blocks — USMLE Step 2 CK Notes

Narrow-complex tachycardias (QRS <120 ms — supraventricular)

• Atrial fibrillation: chaotic atrial re-entry → irregularly irregular rhythm with no discernible P waves. Causes: hypertension, valve disease, thyrotoxicosis, alcohol, sepsis. Risk of atrial thrombus and stroke. Manage with rate control (beta-blocker, diltiazem), rhythm control if appropriate, and anticoagulation by CHA2DS2-VASc.
• Atrial flutter: a single re-entrant atrial circuit → regular "sawtooth" flutter waves at ~300/min, often conducted 2:1 (ventricular rate ~150). Definitive treatment is catheter ablation of the cavotricuspid isthmus; anticoagulate as for AF.
• Multifocal atrial tachycardia: multiple ectopic atrial foci → irregular rhythm with ≥3 distinct P-wave morphologies; classically in COPD. Treat the lung disease; avoid non-selective beta-blockers (calcium channel blockers if needed).
• Paroxysmal supraventricular tachycardia: usually AV nodal re-entry — abrupt onset regular narrow-complex tachycardia ~150-250, P waves buried in the QRS. Terminate with vagal manoeuvres then adenosine.
• Wolff-Parkinson-White: an accessory pathway (bundle of Kent) pre-excites the ventricle — short PR with a delta wave and widened QRS. Re-entry causes tachycardia. In WPW with atrial fibrillation, avoid AV nodal blockers (adenosine, verapamil, digoxin) — they can drive conduction down the accessory pathway into VF; use procainamide or cardioversion. Definitive treatment is ablation.

Wide-complex tachycardias (QRS ≥120 ms)

• Ventricular tachycardia: regular wide-complex rhythm from a ventricular focus; assume VT until proven otherwise in anyone with structural heart disease. Unstable → synchronised cardioversion; stable → amiodarone/procainamide.
• Torsades de pointes: polymorphic VT with a twisting axis, arising from a prolonged QT. Causes: congenital long QT, hypokalaemia, hypomagnesaemia, hypocalcaemia, and QT-prolonging drugs (class IA/III antiarrhythmics, macrolides, antipsychotics, ondansetron, methadone). Treat with IV magnesium, correct electrolytes, stop the offending drug.
• Ventricular fibrillation: chaotic disorganised activity with no output — the usual rhythm in sudden cardiac death. Treat with immediate defibrillation and CPR.

Hereditary channelopathies

• Congenital long QT syndrome: mutations in potassium (KCNQ1, KCNH2) or sodium channels prolong repolarisation → syncope and torsades. Romano-Ward is autosomal dominant, cardiac only; Jervell and Lange-Nielsen is autosomal recessive with sensorineural deafness. Treat with beta-blockers, avoid QT-prolonging drugs, ICD if high risk.
• Brugada syndrome: autosomal dominant sodium channel (SCN5A) mutation, commonest in Asian men — pseudo-right bundle branch block with coved ST elevation in V1-V3, unmasked by fever. Risk of sudden death during sleep; only an ICD prevents it.
• Catecholaminergic polymorphic VT: ryanodine receptor mutation; exercise- or stress-induced VT in children/young adults; treat with beta-blockers.

Sick sinus syndrome

• Fibrosis or degeneration of the sinus node causes inappropriate bradycardia, sinus pauses/arrest, and often a tachy-brady pattern alternating with atrial fibrillation.
• Presents with fatigue, dizziness and syncope in older adults. Treatment is a permanent pacemaker (with rate control for the tachycardic phases).

Conduction blocks

• First degree: PR >200 ms, every P conducts. Benign, no treatment.
• Second degree Mobitz type I (Wenckebach): progressive PR lengthening until a beat drops; block is within the AV node, usually benign; treat only if symptomatic (atropine).
• Second degree Mobitz type II: constant PR with sudden dropped beats; block is below the node (His-Purkinje) and may progress abruptly to complete block — needs a pacemaker.
• Third degree (complete): AV dissociation — P waves and QRS complexes march independently; escape rhythm is slow. Causes include inferior MI and Lyme carditis. Needs a pacemaker.
• Right bundle branch block: wide QRS with RSR' ("rabbit ears") in V1-V2 and slurred S in I/V6; may be normal or from right heart strain/pulmonary embolism.
• Left bundle branch block: wide QRS with a broad notched R in I/V5-V6; new LBBB with chest pain is treated as a STEMI equivalent and obscures usual ischaemia criteria.

Premature beats

• Premature atrial contraction: early abnormal P wave with a narrow QRS and a non-compensatory pause; usually benign.
• Premature ventricular contraction: early wide QRS with no preceding P wave, followed by a full compensatory pause; benign in isolation, but frequent PVCs can cause cardiomyopathy.

Antiarrhythmic pharmacology (Vaughan-Williams)

• Class I — sodium channel blockers (slow phase 0): IA (quinidine, procainamide, disopyramide) also prolong QT — risk of torsades and drug-induced lupus with procainamide; IB (lidocaine, mexiletine) shorten the action potential and work best in ischaemic ventricular arrhythmias; IC (flecainide, propafenone) are strong blockers used in structurally normal hearts only — contraindicated after MI.
• Class II — beta-blockers: slow AV conduction and the sinus rate; used for rate control and after MI.
• Class III — potassium channel blockers (amiodarone, sotalol, dofetilide): prolong repolarisation and QT. Amiodarone is broadly effective but causes thyroid, pulmonary, hepatic, corneal and skin toxicity — monitor thyroid, liver and lung function.
• Class IV — non-dihydropyridine calcium channel blockers (verapamil, diltiazem): slow AV nodal conduction for rate control.
• Others: adenosine transiently blocks the AV node (very short half-life; causes flushing and chest discomfort) and is diagnostic/therapeutic in SVT; digoxin increases vagal tone; magnesium treats torsades.

High-yield revision notes; verify against a primary source before clinical use.