Arrhythmias and Conduction Disorders: A High-Yield USMLE Review

Cardiac Electrophysiology and the Pacemaker Hierarchy

The conduction system fires in a hierarchy of decreasing intrinsic rates: SA node (60–100 bpm) is the primary pacemaker; the AV node delays the impulse to allow atrial contraction before the ventricles (40–60 bpm); the bundle of His and branches transmit to the ventricles; and Purkinje fibers (20–40 bpm) rapidly depolarize the ventricular myocardium. If the SA node fails, the AV node takes over; if the AV node fails, ventricular escape beats provide backup—each lower level is slower, which is why complete heart block causes profound bradycardia. The myocyte action potential has five phases: phase 0 rapid Na+ influx (QRS), phase 1 early K+ efflux (J point), phase 2 Ca2+/K+ plateau (ST segment), phase 3 K+ efflux repolarization (T wave), and phase 4 resting baseline. Pacemaker cells differ by having spontaneous diastolic depolarization—a non-flat phase 4 driven by the funny current (If), a mixed Na+/K+ current that fires them automatically. During late phase 2/early phase 3 (relative refractory period) a stronger-than-normal stimulus can trigger arrhythmia—the vulnerable window underlying R-on-T. Reentry, the most common mechanism, requires two pathways with different conduction velocities and refractory periods, plus unidirectional block.

The Five-Step Diagnostic Framework

Approach every arrhythmia identically. Step 1: Stable or unstable? Hypotension, altered mental status, or ischemia mandate immediate intervention—pacing for bradycardia, cardioversion for tachycardia. Step 2: Rate—bradycardia (<60), normal (60–100), or tachycardia (>100). Step 3: Regular or irregular? Regular rhythms include sinus, SVT, atrial flutter with fixed block, and VT; irregularly irregular means atrial fibrillation or MAT. Step 4: Narrow (<120 ms, supraventricular origin) or wide (≥120 ms, ventricular OR SVT with aberrancy/BBB) QRS. Step 5: P-wave analysis—normal P before each QRS is sinus; more P than QRS means AV block; more QRS than P (or dissociated) suggests VT; retrograde P after QRS suggests AVNRT/AVRT/junctional; sawtooth flutter waves and fibrillatory waves have their own signatures. Two overriding rules: for wide complex tachycardia, when in doubt treat as VT; and in every patient correct reversible causes (ischemia, electrolytes, drugs).

Bradyarrhythmias, AV Blocks, and Bundle Branch Blocks

First-degree AV block is a PR >200 ms with every P conducting—benign, no treatment. Mobitz Type I (Wenckebach) shows progressive PR prolongation with gradually shortening RR until a dropped beat (grouped beating), sits at the AV node, is usually benign, and rarely needs pacing. Mobitz Type II shows a constant PR with sudden, unpredictable dropped beats, is infranodal (His bundle or below), often has a wide QRS, and carries high risk of progressing to complete block—it requires a permanent pacemaker. Third-degree (complete) heart block shows AV dissociation: regular P waves at one rate and regular, slower QRS at another with no relationship; the escape rhythm sets tolerance (junctional 40–60 bpm narrow QRS is better tolerated than ventricular 20–40 bpm wide QRS). Complete block always requires permanent pacing unless the cause is reversible (e.g., Lyme disease). For bundle branch blocks (QRS ≥120 ms): LBBB gives a broad notched R in lateral leads and rS/QS in V1–V2 ('WiLLiaM') and usually indicates underlying heart disease. When a patient with LBBB and ischemic symptoms presents, do not assume LBBB alone equals a STEMI—apply the Sgarbossa (or modified Sgarbossa) criteria to detect concurrent infarction, since LBBB is frequently not truly new and is non-specific. RBBB gives an RSR' ('rabbit ears') in V1–V2 with a broad S laterally ('MaRRoW'), often benign in isolation. RBBB plus left anterior fascicular block is bifascicular block; adding first-degree AV block is often labeled a 'trifascicular' pattern as review shorthand, but this is imprecise—the prolonged PR may reflect AV nodal delay rather than true distal (infranodal) trifascicular disease, so correlate with symptoms before assuming high-grade conduction system disease.

Supraventricular Tachycardias and Atrial Fibrillation

AVNRT is the most common paroxysmal SVT—a reentrant circuit within the AV node (typically down slow, up fast) giving a regular narrow complex tachycardia at 150–250 bpm with P waves hidden in the QRS (pseudo-R' in V1, pseudo-S inferiorly) and abrupt onset/termination. AVRT uses an accessory pathway: orthodromic (down AV node, up pathway) is narrow-complex; antidromic is wide. WPW's baseline triad is short PR (<120 ms), delta wave, and wide QRS. For a regular narrow complex tachycardia: vagal maneuvers, then adenosine 6 mg then 12 mg rapid IV push, then a beta-blocker or diltiazem/verapamil; cardiovert if unstable. Atrial fibrillation shows irregularly irregular RR, no P waves (fibrillatory baseline), and narrow QRS unless BBB or pre-excitation, with rates often 110–180 untreated. Consequences: loss of atrial kick, rapid ventricular rate (tachycardia-mediated cardiomyopathy), and thromboembolism. Rate control (beta-blockers first-line, non-DHP CCBs, digoxin) suits older, asymptomatic patients; rhythm control (cardioversion, antiarrhythmics, ablation) suits younger, symptomatic, first-episode, or reversible-cause patients. Anticoagulate by CHA2DS2-VASc: score ≥2 (men) or ≥3 (women) → anticoagulate, DOAC preferred, warfarin for valvular AF. Atrial flutter gives sawtooth waves at ~300 bpm atrial rate with regular RR depending on block ratio; a regular tachycardia at ~150 bpm is flutter with 2:1 block until proven otherwise. MAT is an irregular rhythm with ≥3 distinct P-wave morphologies and a rate typically >100 bpm, is classically associated with COPD, and is treated by correcting the underlying cause rather than by anticoagulation.

Ventricular Arrhythmias and the WPW Emergency

VT is ≥3 consecutive ventricular beats at >100 bpm: wide (≥120 ms, often >160 ms), usually regular, with AV dissociation, fusion and capture beats, and concordance—all highly specific for VT. Monomorphic VT (uniform QRS) is usually scar-mediated reentry after MI; polymorphic VT arises from ischemia or long QT. Treat by status: pulseless VT → defibrillation and ACLS; unstable with pulse → synchronized cardioversion; stable sustained → amiodarone or procainamide (cardiovert if drugs fail); non-sustained → treat the cause. In a patient with prior MI, wide complex tachycardia is VT until proven otherwise—AV nodal blockers like diltiazem will not terminate it and can cause hemodynamic collapse. PVCs are wide, early beats with no preceding P and a compensatory pause; high burden (>10%) can cause reversible PVC-induced cardiomyopathy. Torsades de Pointes is polymorphic VT twisting around the baseline in the setting of a prolonged QT, often initiated by a short-long-short sequence; treat with IV magnesium (even if normal), remove offending drugs, correct electrolytes, and increase heart rate (isoproterenol or pacing) to eliminate pauses. The lethal WPW scenario is pre-excited AF: irregular, wide complex tachycardia at extremely rapid rates (up to ~280 bpm). AV nodal blockers—adenosine, beta-blockers, CCBs, digoxin—are absolutely contraindicated because they force conduction down the accessory pathway and can precipitate VF; treat with procainamide or immediate cardioversion.

Inherited Arrhythmia Syndromes and Devices

Suspect inherited channelopathies in young patients with syncope, exertional collapse, or a family history of sudden death. Long QT Syndrome: QTc >480 ms is diagnostic (>500 ms high risk); LQT1 (KCNQ1, IKs) is triggered by exercise/swimming with broad-based T waves; LQT2 (KCNH2/HERG, IKr) by emotion and auditory stimuli with bifid low-amplitude T waves; LQT3 (SCN5A, INa gain-of-function) during rest/sleep. Beta-blockers are first-line (most effective in LQT1/LQT2); mexiletine may help LQT3; avoid QT-prolonging drugs. Brugada syndrome (SCN5A in ~25%) affects men 30–50, is triggered by fever/rest, and shows coved ST elevation in V1–V3—treat fever aggressively and place an ICD if symptomatic. ARVC (desmosomal mutations) shows T-wave inversions V1–V3 and epsilon waves and presents with exertional VT of LBBB morphology in young patients; diagnosis is made using the multiparametric Task Force Criteria integrating ECG findings, imaging (echo or MRI), tissue characterization/histology, arrhythmias, family history, and genetics—no single test, including MRI, is confirmatory on its own. CPVT (RyR2/CASQ2) shows exercise-induced bidirectional VT with a normal resting ECG. Pacemaker indications: symptomatic sinus node dysfunction, Mobitz II second-degree AV block (regardless of symptoms, given its high risk of progression to complete block), third-degree block (always), tachy-brady syndrome, and post-MI persistent advanced AV block. ICD indications include survivors of VF or unstable VT (secondary prevention), LVEF ≤35% with NYHA II–III symptoms or LVEF ≤30% (primary prevention), high-risk HCM, Brugada with syncope, and high-risk LQTS.

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