Bradyarrhythmias & Heart Block
A board-focused walkthrough of bradyarrhythmias and heart block — from conduction anatomy and nodal-vs-infranodal localization through the ECG hallmarks of each AV block, classic vignettes (complete heart block, Lyme carditis), and the ACLS-to-pacemaker management pathway. Built around STEP 2 CK next-best-step decisions.
Pathophysiology & Anatomy
Bradyarrhythmia = HR <60 bpm from failure of impulse generation (sinus node) or conduction (AV node / His-Purkinje). The single most useful board concept is where the block sits.
Blood supply → localization:
- The AV node is supplied by the RCA in ~90% of people (right-dominant circulation); the SA node by the RCA in ~60% (left circumflex in the rest). An inferior MI (RCA) therefore causes AV-nodal block that is typically vagally mediated, transient, and atropine-responsive.
- The His-Purkinje system (infranodal) is fed largely by LAD septal perforators. Block here — e.g., during an anterior MI — is ominous, unresponsive to atropine, and needs pacing.
Nodal vs infranodal — the key distinction:
- Nodal block → narrow junctional escape (40–60 bpm), often benign/reversible.
- Infranodal block → wide, slow ventricular escape (20–40 bpm), unstable, high risk of asystole → pacemaker.
Sinus node dysfunction (sick sinus syndrome): sinus bradycardia, sinus pauses/arrest, and tachy-brady syndrome (alternating AFib and bradycardia) in the elderly — a common indication for a permanent pacemaker.
- Sinus bradycardia causes: athletic conditioning, high vagal tone, drugs (β-blockers, non-dihydropyridine CCBs, digoxin), hypothyroidism, ↑ICP (Cushing reflex), inferior MI, hypothermia.
- 1° AV block = PR >200 ms, every P conducts → benign, no treatment.
- Mobitz I (Wenckebach) = progressive PR prolongation until a dropped QRS → "grouped beating"; nodal, usually benign.
- Mobitz II = constant PR then a sudden non-conducted P, often with a wide QRS; infranodal → high risk of complete block → pacemaker.
- 3° (complete) block = AV dissociation with the atrial rate > ventricular rate; P–P and R–R march out independently.
- Physical signs of complete block: intermittent cannon A waves, variable-intensity S1, wide pulse pressure, syncope (Stokes–Adams attacks).
- Always exclude reversible causes (drugs, Lyme, ischemia, hyperkalemia, hypothyroidism) before committing to a permanent pacemaker.
AV Block Comparison
| Type | ECG hallmark | Block site | Treatment |
|---|---|---|---|
| 1° AV block | PR >200 ms, every P conducts | AV node | None — benign |
| Mobitz I (Wenckebach) | Progressive PR → dropped QRS; grouped beating | AV node | Observe; atropine if symptomatic |
| Mobitz II | Constant PR, sudden dropped QRS; often wide | His-Purkinje | Permanent pacemaker |
| High-grade | ≥2 consecutive non-conducted Ps | Usually infranodal | Pacemaker |
| 3° (complete) | AV dissociation, atrial rate > ventricular | Node or infranodal | Pacing → permanent PPM |
The most-quoted ECG mnemonic in medicine — read the P–QRS relationship in one line each:
- *"If the R is far from P, then you have a first degree."* — long PR, all conduct.
- *"Longer, longer, longer, drop — then you have a Wenckebach."* — Mobitz I.
- *"If some P's just don't get through, then you have a Mobitz II."*
- *"If P's and Q's don't agree, then you have a third degree."* — AV dissociation.
Vignette: A 72-year-old man presents with syncope. HR 38, BP 84/58. ECG shows P waves at ~90/min and QRS complexes at ~38/min that bear no relationship to each other, with a wide QRS. Exam reveals intermittent cannon A waves and variable S1.
- Diagnosis: Third-degree (complete) AV block with a slow ventricular (infranodal) escape.
- Next step (unstable): start transcutaneous pacing immediately while arranging a transvenous pacer; add a dopamine or epinephrine infusion as a bridge. Atropine is unlikely to help a wide infranodal escape (and may worsen it) — do not let it delay pacing.
- Definitive: permanent pacemaker once reversible causes are excluded.
Contrast: the same rhythm during an inferior STEMI with a narrow junctional escape is usually atropine-responsive and transient — reperfuse and support; permanent pacing is often unnecessary.
Vignette: A 24-year-old hiker from Connecticut reports fatigue and near-syncope. Weeks earlier he had a target-shaped (bull's-eye) rash. ECG now shows third-degree AV block with a narrow escape; an earlier strip showed a prolonged PR.
- Diagnosis: Lyme carditis (high-grade AV block from Borrelia burgdorferi).
- Next best step: admit + IV ceftriaxone; send Lyme serology (ELISA → confirmatory Western blot). Use temporary pacing if symptomatic/unstable.
- Key point: the block is reversible — no permanent pacemaker. Young patient + AV block + tick exposure / erythema migrans = Lyme until proven otherwise.
Other reversible mimics to screen for: digoxin toxicity, β-blocker / CCB overdose, hyperkalemia, and cardiac sarcoidosis (young patient, unexplained block ± VT → cardiac MRI/PET).
Management: Acute & Definitive
Acute symptomatic bradycardia (ACLS):
- Assess stability — hypotension, altered mentation, ischemic chest pain, signs of shock.
- Atropine 1 mg IV, repeat every 3–5 min to a maximum 3 mg.
- If atropine fails → transcutaneous pacing and/or an infusion of dopamine (5–20 µg/kg/min) or epinephrine (2–10 µg/min).
- Refractory → transvenous pacing; always treat the underlying cause.
Atropine caveats (high-yield): it is ineffective — and may worsen the block — in Mobitz II / complete block with a wide (infranodal) QRS; go straight to pacing. It is also ineffective in the transplanted (denervated) heart.
Toxin antidotes: glucagon for β-blocker overdose; IV calcium + high-dose insulin for CCB overdose; digoxin-specific Fab for dig toxicity.
Permanent pacemaker (Class I): symptomatic sinus node dysfunction; Mobitz II, high-grade, or third-degree AV block not due to a reversible cause — regardless of symptoms.
Reversible / Secondary Causes to Exclude First
| Cause | Vignette clue | Management |
|---|---|---|
| Drugs (β-blocker, CCB, digoxin) | Med list / overdose | Stop drug; antidote (glucagon / Ca + insulin / Fab) |
| Inferior MI | ST elevation II, III, aVF; nodal block | Reperfuse; atropine; usually transient |
| Lyme carditis | Young, tick / EM rash, endemic area | IV ceftriaxone; temporary pacing |
| Hyperkalemia | Peaked T waves, wide QRS, renal failure | Calcium gluconate, insulin + glucose |
| Hypothyroidism / myxedema | Cold intolerance, delayed reflexes | Levothyroxine |
| Cardiac sarcoidosis | Young, unexplained block ± VT | MRI/PET; immunosuppression ± ICD |
| Hypothermia | Osborn (J) waves, exposure | Rewarming |
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