Cardiac conduction disorder

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cardiac conduction disorders classification pathophysiology ECG findings

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heart block bundle branch block diagnosis management treatment

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cardiac conduction system ECG heart block bundle branch block

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Cardiac Conduction Disorders

Cardiac conduction disorders encompass a spectrum of abnormalities in the generation or propagation of electrical impulses through the heart's specialized conduction system. They range from benign incidental findings to life-threatening emergencies requiring urgent intervention.

Anatomy of the Conduction System

The normal cardiac conduction pathway:
SA NodeAV NodeBundle of HisRight & Left Bundle BranchesPurkinje FibersVentricular myocardium
Disruption at any level produces a characteristic conduction disorder.

Classification

I. Sinoatrial (SA) Node Disorders

DisorderDescription
Sinus bradycardiaRate < 60 bpm; can be physiologic (athletes) or pathologic
Sick Sinus Syndrome (SSS)Dysfunction of SA node: bradycardia, sinus arrest, sinoatrial block, tachy-brady syndrome
Sinus arrest / SA blockFailure of SA node to fire or conduct to atria

II. Atrioventricular (AV) Block

DegreeECG FindingClinical Significance
1st DegreePR interval > 200 ms; all P waves conductUsually benign; can be drug-induced
2nd Degree – Mobitz I (Wenckebach)Progressive PR prolongation until a QRS is droppedOften at AV node level; usually benign; may be vagally mediated
2nd Degree – Mobitz IIConstant PR interval with sudden dropped QRSInfranodal (His-Purkinje); unpredictable — high risk of progression to complete block
3rd Degree (Complete)No relationship between P waves and QRS; AV dissociationLife-threatening; requires pacemaker

III. Bundle Branch & Fascicular Blocks

BlockKey ECG FeaturesCommon Associations
RBBBrsR' in V1; wide slurred S in I, V6; QRS ≥ 120 msASD, PE, RV strain; also seen in normal hearts
LBBBBroad monophasic R in I, aVL, V6; no septal Q waves; QRS ≥ 120 msCoronary artery disease, hypertensive heart disease, aortic valve disease, dilated cardiomyopathy
Left Anterior Fascicular Block (LAFB)Left axis deviation (−45° to −90°); qR in I, aVL; rS in II, III, aVFMost common fascicular block; often isolated
Left Posterior Fascicular Block (LPFB)Right axis deviation; rS in I, aVL; qR in III, aVFLess common; diagnosis of exclusion
Bifascicular blockRBBB + LAFB (most common) or RBBB + LPFBCarries risk of progression to complete block
Trifascicular blockBifascicular block + 1st/2nd degree AV blockHigh risk; pacemaker often indicated
Per Harrison's Principles (p. 6801), LBBB specifically is a marker of one of four high-risk underlying conditions: coronary heart disease (often with impaired LV function), hypertensive heart disease, aortic valve disease, and dilated cardiomyopathy.

ECG Example: Multilevel Conduction Disease

Alternating Bundle Branch Block with Second-Degree AV Block (Wenckebach)
This 12-lead ECG shows alternating RBBB and LBBB on a beat-to-beat basis with concomitant Mobitz I (Wenckebach) AV block — representing extensive multilevel His-Purkinje disease with high risk of progression to complete heart block.

Etiology

  • Ischemic heart disease (most common cause of acquired block)
  • Degenerative/fibrotic disease (Lev's disease, Lenègre's disease — progressive fibrosis of the conduction system)
  • Infectious: Lyme disease, Chagas disease, myocarditis, infective endocarditis with abscess
  • Infiltrative: Sarcoidosis, amyloidosis, hemochromatosis
  • Metabolic: Hyperkalemia, hypothyroidism
  • Autoimmune: SLE (neonatal lupus → congenital complete heart block)
  • Iatrogenic: Drug toxicity (digoxin, beta-blockers, calcium channel blockers, antiarrhythmics), post-cardiac surgery, catheter ablation
  • Congenital: Congenitally corrected TGA, ASD, Ebstein's anomaly
  • Neuromuscular disorders: Myotonic dystrophy, Kearns-Sayre syndrome

Clinical Presentation

SymptomUnderlying Mechanism
Fatigue, exercise intoleranceReduced cardiac output
Presyncope / syncope (Stokes-Adams attacks)Sudden complete heart block or pause
PalpitationsEscape rhythms, compensatory changes
DyspneaLow output, especially with LBBB + LV dysfunction
AsymptomaticMany BBBs and 1st-degree blocks

Diagnosis

  1. 12-lead ECG — cornerstone of diagnosis
  2. Ambulatory monitoring (Holter, event recorder, implantable loop recorder) — for intermittent/paroxysmal blocks
  3. Exercise stress testing — to unmask rate-dependent blocks or exercise-induced AV block
  4. Electrophysiology (EP) study — measures HV interval; HV > 70 ms suggests infranodal disease; HV > 100 ms strongly predicts progression to complete block
  5. Echocardiography — assess structural heart disease, LV dysfunction (especially with LBBB)
  6. Cardiac MRI — evaluate myocardial scar, infiltrative disease (sarcoid, amyloid)
  7. Lab work — electrolytes, thyroid function, Lyme serology, iron studies, ANA/anti-Ro in appropriate context

Management

Acute / Reversible Causes

  • Correct underlying cause first: treat hyperkalemia, withhold offending drugs, antibiotics for Lyme disease
  • Atropine (0.5–1 mg IV) for symptomatic vagally mediated bradycardia/AV block
  • Transcutaneous pacing — for hemodynamically unstable patients
  • Transvenous temporary pacing — bridge for high-degree blocks pending definitive therapy

Permanent Pacemaker Indications (ACC/AHA Guidelines)

IndicationClass
Symptomatic complete (3rd-degree) AV blockI (mandatory)
Symptomatic Mobitz II 2nd-degree AV blockI
Asymptomatic complete AV block with documented pauses > 3 s or escape rate < 40 bpmI
Asymptomatic Mobitz II with wide QRSIIa
Bifascicular or trifascicular block with syncope and suspected advanced AV blockI
HV interval ≥ 100 ms on EP study (non-physiologic)IIa
SSS with symptomatic bradycardiaI

Device Therapy Considerations

  • CRT (Cardiac Resynchronization Therapy): Indicated in LBBB with QRS ≥ 150 ms, EF ≤ 35%, NYHA Class II–IV despite optimal medical therapy — restores ventricular synchrony and improves outcomes
  • His-bundle pacing / Left bundle branch area pacing (LBBAP): Emerging alternatives to conventional RV pacing that preserve physiologic conduction and avoid pacing-induced cardiomyopathy

Complications

  • Progression to complete heart block (especially Mobitz II, trifascicular block)
  • Sudden cardiac death
  • Pacing-induced cardiomyopathy from chronic RV apical pacing (dyssynchrony → LV dysfunction)
  • Syncope and trauma
  • Reduced quality of life from fatigue and exercise intolerance

Key Clinical Pearls

  • RBBB alone in an otherwise healthy person is generally benign and does not require workup beyond baseline ECG.
  • New LBBB warrants urgent evaluation to exclude acute MI (STEMI equivalent if new with chest pain — Sgarbossa criteria apply).
  • Alternating bundle branch block (beat-to-beat RBBB/LBBB alternation) signals extensive His-Purkinje disease and is a near-absolute indication for permanent pacemaker.
  • Lyme carditis is a reversible cause of high-degree AV block — always check Lyme serology in endemic areas with unexplained AV block, especially in young patients.
  • Mobitz I in inferior MI reflects ischemia to the AV node (RCA territory) — usually transient. Mobitz II in anterior MI indicates massive infranodal ischemia — carries poor prognosis and requires pacing.
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