Bradyarrhythmias

Symptomatic bradyarrhythmias · SND + AV block · complete reference · all doses + pacing protocols · Full Card

Symptoms / Associated Sx

• Fatigue (most common — often chronic and attributed to aging); lightheadedness; presyncope; syncope (Adams-Stokes attacks in complete heart block — sudden loss of consciousness without prodrome at onset of ventricular standstill); dyspnea; reduced exercise tolerance (chronotropic incompetence — inability to increase HR with exertion); palpitations (tachycardia-bradycardia syndrome)

• Hemodynamically unstable bradycardia: SBP <90 + AMS + chest pain + APE + signs of poor perfusion → transcutaneous pacing immediately — do NOT spend time trying medications

• AV block classification by ECG: 1° AV block = PR >200 ms, every P conducts, benign; 2° Mobitz I (Wenckebach) = progressive PR lengthening until one P wave fails to conduct (footprint: PR gets longer + longer + QRS drops + repeat cycle; narrow QRS usually; AV nodal level; vagal or medication-related; often benign); 2° Mobitz II = fixed PR interval → sudden P wave fails to conduct without warning (infranodal: below AV node in bundle of His or branches; wide QRS usually; dangerous; often progresses to complete heart block); 2:1 AV block = cannot classify as Mobitz I or II from 2:1 ratio alone → treat as Mobitz II; 3° (complete) AV block = complete AV dissociation; P waves march at regular rate independent of QRS; escape rhythm (junctional = narrow QRS 40–60 bpm; ventricular = wide QRS 20–40 bpm = very dangerous)

• Sick sinus syndrome (SSS): sinus node dysfunction manifesting as inappropriate sinus bradycardia, sinus pauses, sinus arrest, sino-atrial exit block; tachycardia-bradycardia variant = paroxysmal tachyarrhythmia (AF) followed by prolonged sinus pause (symptomatic) upon termination

Neg

• Pt denies regular slow wide bizarre QRS complexes without discernible P waves at 20–40 bpm in the setting of complete AV block — argues against effective atropine response (ventricular escape rhythm below the bundle of His = infranodal; atropine speeds atrial rate but does NOT improve infranodal conduction; may worsen by increasing atrial rate without ventricular response; transcutaneous or transvenous pacing is the correct treatment, not escalating atropine)

• Pt denies progressively widening QRS + peaked tall T-waves + loss of P waves + sine wave pattern in a bradycardic patient — argues against intrinsic conduction system disease (hyperkalemia — pseudoAV block; can produce any degree of AV block; check K+ immediately in any atypical bradyarrhythmia; treat with calcium gluconate 1 g IV to stabilize membrane)

• Pt denies asymptomatic HR 40–50 bpm with appropriate HR increase to >100 bpm with exercise in a trained athlete without any structural heart disease — argues against pathologic sinus bradycardia (physiologic sinus bradycardia in athletes: ↑vagal tone + ↑stroke volume; no symptoms; appropriate chronotropic response; no PM needed)

• Pt denies regular 2:1 pattern capable of being classified as Mobitz I vs Mobitz II — argues against confident classification (2:1 AV block requires seeing ≥3 consecutive P waves to distinguish PR behavior; treat 2:1 block as Mobitz II [infranodal] until 3:1 run or adenosine challenge demonstrates Wenckebach pattern; conservative approach prevents missing dangerous infranodal block)

Social History (SHx)

• Complete medication review (most important — BB dose and timing; CCB type [diltiazem (Cardizem) and verapamil (Calan) are AV-nodal; amlodipine (Norvasc) is vascular-selective — does NOT cause bradycardia]; digoxin [Lanoxin] dose and level; amiodarone [Pacerone] dose and duration; ivabradine [Corlanor]; clonidine [Catapres]); prior PM or ICD interrogation data (prior pauses documented?); prior syncope history

• Recent tick exposure or residence in Lyme-endemic area (northeastern US, upper Midwest, parts of Europe — Ixodes scapularis; Borrelia burgdorferi); recent viral illness (myocarditis); known infiltrative disease (sarcoidosis — bilateral hilar adenopathy; ↑ACE; amyloidosis — thick walls on echo); prior cardiac surgery (valve replacement near conduction system)

• Athletic training history (physiologic bradycardia — benign); family history of sudden cardiac death or cardiomyopathy (laminopathies — LMNA; conduction disease + DCM)

Main Etiology

• Intrinsic: degenerative fibrosis of conduction system (Lenègre disease — isolated conduction fibrosis; Lev disease — calcific AV annulus extending to conduction system; most common intrinsic cause in elderly); acute inferior MI (RCA → AV nodal artery occlusion — Mobitz I or complete block; usually transient, resolves with reperfusion; inferior MI AV block = transient in >90%; anterior MI AV block = infranodal, permanent, poor prognosis); cardiac sarcoidosis (AV block in 20–30% — may be presenting feature; FDG-PET diagnostic); amyloidosis (thick walls + AV block); genetic (SCN5A mutations — Brugada + conduction disease; LMNA — DCM + AV block + SCD); Lyme carditis (B. burgdorferi — AV block in 5% of disseminated Lyme)

• Extrinsic/reversible: medication-induced (BB, diltiazem [Cardizem]/verapamil [Calan], digoxin [Lanoxin], amiodarone [Pacerone], ivabradine [Corlanor] — most common reversible cause; drug-drug interactions ↑effect); hyperkalemia (K+ >6.5 — pseudo-AV block; K+ >8 — sine wave + cardiac arrest); hypothyroidism (sinus bradycardia; TSH >10); hypoxia; vagal surges (vasovagal, carotid sinus hypersensitivity, Bezold-Jarisch from inferior MI); post-cardiac surgery (valve surgery + PM lead manipulation)

RF

• Intrinsic conduction disease RF: older age (degenerative fibrosis ↑prevalence); prior inferior MI; cardiac sarcoidosis; amyloidosis; genetic conduction disease (LMNA, SCN5A); prior cardiac surgery or ablation near conduction system

• Reversible/extrinsic RF: AV nodal-blocking medications (BB + non-DHP CCB + digoxin + amiodarone); CKD (↑digoxin [Lanoxin] toxicity; ↑hyperkalemia); hypothyroidism; tick exposure in Lyme-endemic area; electrolyte abnormalities (↓K+/↓Mg2+ enhance digoxin toxicity; ↑K+ directly impairs conduction)

Data

• 12-lead ECG + long rhythm strip — immediate and serial (classify block type precisely: PR interval [normal <200 ms]; QRS width [narrow = nodal escape ≤120 ms; wide = ventricular escape or infranodal ≥120 ms]; P-QRS relationship — every P conducts = 1°; some P waves fail = 2°; no relationship = 3°; 2:1 = treat as Mobitz II until proven otherwise; measure PR in ALL conducted beats for Wenckebach pattern; compare to prior ECGs)

• BMP — STAT (K+ — hyperkalemia: any K+ >6.5 in bradycardia = treat immediately before further workup; K+ >5.5 + ECG changes = calcium gluconate now; Mg2+ — hypomagnesemia enhances digoxin toxicity; Cr — drug dose adjustment; glucose — hypoglycemia can cause sinus bradycardia)

• Digoxin (Lanoxin) level — if on digoxin (goal 0.5–0.9 ng/mL; toxic >2.0 ng/mL; draw 6h post-last dose; toxicity enhanced by ↓K+, ↓Mg2+, ↑Ca2+, renal failure, amiodarone [Pacerone] [doubles level], quinidine, verapamil [Calan]; classic toxicity: GI symptoms first, then visual [yellow-green halos], then cardiac [junctional tachycardia, bidirectional VT, AV block])

• TSH + free T4 (hypothyroidism: TSH >10 = overt hypothyroidism; sinus bradycardia, prolonged QT, reduced cardiac output, constipation, weight gain, fatigue — frequently missed; start levothyroxine [Synthroid] 12.5–25 mcg PO daily and titrate)

• Troponin I/T serial (acute inferior MI — AV block from RCA territory ischemia; Mobitz I → complete block pattern; dynamic ECG changes; usually transient with successful reperfusion; anterior MI AV block = infranodal, worse prognosis)

• Lyme serology (IgG + IgM) if clinically suspected (ELISA screen → Western blot confirm; Lyme carditis: 3rd-degree AV block in 5% of disseminated Lyme; young patient + endemic area + recent tick exposure/erythema migrans + AV block → empiric ceftriaxone [Rocephin] 2 g IV daily ×14–21 days; most AV block resolves with treatment; PM if block persists >1 week despite antibiotics)

• Echo (TTE) (structural heart disease; cardiomyopathy — sarcoid [restrictive + thickened walls]; amyloid [sparkling granular myocardium + biatrial enlargement]; LV hypokinesis [inferior MI]; EF assessment before PM implant; valvular disease)

• CXR (bilateral hilar adenopathy — sarcoidosis; cardiomegaly; pulmonary edema from hemodynamic compromise; PP lead position if pacemaker)

• Holter monitor (24–48h) or implantable loop recorder (for intermittent unexplained syncope) (document: sinus pauses >3 sec; PR prolongation; Mobitz I/II sequences; complete AV block; tachycardia-bradycardia; correlate with symptoms; ILR for unexplained syncope — monitor up to 3 years)

• Electrophysiology study (HV interval) (His-to-ventricle interval >70 ms = infranodal disease at high risk for complete AV block → prophylactic PM; HV >100 ms = immediate PM; used when non-invasive testing inconclusive and suspicion for infranodal disease high)

DDx

Hyperkalemia (K+ >6.5 → peaked T-waves → wide QRS → sine wave → PEA; ECG mimics AV block; calcium gluconate 1 g IV + insulin 10 U IV + D50 + NaHCO3 — treat before any antiarrhythmic) · Digoxin (Lanoxin) toxicity (bradycardia + junctional tachycardia + bidirectional VT + GI/visual sx; level >2.0; DigiFab/Digibind; DO NOT cardiovert) · Hypothyroidism (sinus brady + fatigue + weight gain + constipation + cold intolerance + TSH >10 — levothyroxine [Synthroid]) · Acute inferior MI (AV block from RCA ischemia — usually Wenckebach/complete; troponin + inferior STE; reperfusion → block resolves) · Lyme carditis (AV block in young patient + endemic area + tick exposure — ceftriaxone [Rocephin] 2 g IV daily + temporary pacing if 3°) · Cardiac sarcoidosis (AV block + young + bilateral hilar adenopathy + restrictive CM — FDG-PET; prednisolone 40–60 mg PO daily) · Vagal/carotid sinus hypersensitivity (positional + triggered; carotid sinus massage (CSM) test; tilt table; dual-chamber PM if cardioinhibitory type)

Home Meds

• Hold immediately (if symptomatic bradycardia): all beta-blockers (carvedilol [Coreg]/metoprolol tartrate [Lopressor]/bisoprolol [Zebeta]/atenolol [Tenormin]); non-DHP CCBs (diltiazem [Cardizem]/verapamil [Calan] — hold; amlodipine [Norvasc] is vascular-selective and does NOT cause bradycardia — continue); digoxin (Lanoxin) — hold if symptomatic bradycardia; check level; digoxin immune Fab (Digibind/DigiFab) if toxic; amiodarone (Pacerone) — half-life 40–55 days — holding has delayed effect; ivabradine (Corlanor) — sinus node current blocker; clonidine (Catapres) — centrally-acting sympatholytic

• Do NOT hold amlodipine (Norvasc) for bradycardia — it is a vascular-selective CCB and does not affect AV conduction; a common unnecessary hold

• Hold immunosuppressants carefully: sarcoid patients on corticosteroids — do NOT abruptly stop; taper with rheumatology if PM implant planned (↑infection risk peri-procedure)

Plan

• Step 1 — Hemodynamic assessment and stabilization:

  • Hemodynamically stable → proceed with workup; continuous monitoring; treat reversible causes

  • Hemodynamically unstable (SBP <90, AMS, chest pain, APE) → transcutaneous pacing IMMEDIATELY (do not delay for medications; pads anterior/posterior; set demand rate 60–80 bpm; start at 70 mA → increase 10 mA at a time until capture confirmed: QRS complex after each spike + palpable pulse; check for mechanical capture by palpating femoral/radial pulse — not just ECG spike)

  • Atropine 0.5–1 mg IV q3–5 min (max 3 mg total) while setting up transcutaneous pacing — may temporize for sinus bradycardia and Mobitz I; INEFFECTIVE in Mobitz II and complete heart block with wide escape (infranodal block — atropine speeds atrial rate without helping ventricular rate; may worsen hemodynamics)

• Step 2 — Identify and reverse all treatable causes:

  • Stop AV nodal blockers: BB, diltiazem (Cardizem), verapamil (Calan), digoxin (Lanoxin), amiodarone (Pacerone), ivabradine (Corlanor)

  • Hyperkalemia: calcium gluconate 1 g IV over 5–10 min (membrane stabilization — immediate; does NOT lower K+; repeat in 5 min if no ECG improvement); insulin 10 units IV + D50 25 g IV (K+ shift intracellular; onset 15–30 min; ↓K+ 0.5–1.5 mEq/L); sodium bicarbonate (NaHCO3) 50 mEq IV (acidosis + hyperkalemia); albuterol (Proventil) nebulized 10–20 mg (shifts K+ intracellular; onset 15–30 min; ↓K+ 0.5–1 mEq/L); furosemide (Lasix) IV or Kayexalate or patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma) for definitive K+ removal; hemodialysis if refractory

  • Hypothyroidism: levothyroxine (Synthroid) 12.5–25 mcg PO daily (start LOW in elderly and cardiac patients — risk of ↑myocardial O2 demand + arrhythmia with too-rapid replacement; increase dose q4–6 weeks; target TSH 0.5–2.5)

  • Digoxin (Lanoxin) toxicity: hold digoxin; correct K+ to ≥4.0 and Mg2+ to ≥2.0; digoxin immune Fab (Digibind/DigiFab) for: hemodynamically unstable bradycardia or AV block; serum level >10 ng/mL; life-threatening arrhythmia; dose: empiric 10 vials IV in cardiac arrest; calculated: (serum level [ng/mL] × weight [kg]) / 100 = number of vials; infuse over 30 min; do NOT cardiovert digoxin-toxic bradycardia (↑VF risk)

  • Acute inferior MI + AV block: emergent PCI → AV block usually resolves with reperfusion; temporary pacing bridge if hemodynamically compromised; permanent PM only if block persists >14 days post-reperfusion

  • Lyme carditis + AV block: ceftriaxone (Rocephin) 2 g IV daily ×14–21 days; continuous telemetry; temporary pacing if complete heart block; most resolve with antibiotics; PM if persists >1 week despite therapy

  • Cardiac sarcoidosis + AV block: prednisolone 40–60 mg PO daily (may reverse AV block if caught early in active inflammatory phase); FDG-PET to document activity; PM/ICD — most sarcoid AV block patients need PM; ICD often preferred over PM given ↑SCD risk in cardiac sarcoidosis

• Step 3 — Transvenous temporary pacing (if transcutaneous inadequate or need expected to last >hours):

  • Access: internal jugular (preferred — more stable lead position) or subclavian; femoral is less stable and limits patient mobility

  • Balloon-tipped pacing catheter floated to RV apex (fluoroscopy or echo guidance preferred; bedside ECG-guided acceptable)

  • Settings: VVI mode; demand rate 60 bpm; sensitivity 2–3 mV (sense native QRS); output at 2× threshold (usually 2–4 mA; threshold = minimum mA for consistent capture)

  • Confirm RV capture: LBBB morphology paced QRS (RV pacing → initial activation from RV → LBBB pattern); palpable pulse with each pacing spike; SBP >90

  • Complications: lead dislodgement (hiccups = diaphragm pacing = lead too far); pneumothorax; cardiac perforation; infection (>72h ↑risk; change site if >5–7 days); failure to sense (can be fixed by ↑sensitivity setting)

• Step 4 — Permanent pacemaker (PM) decision:

  • Class I indications (2023 ACC/AHA guidelines): symptomatic bradycardia or sinus pauses >3 sec from SND or AV block not from reversible cause; 2° Mobitz II regardless of symptoms; 3° (complete) AV block regardless of symptoms; alternating LBBB + RBBB; persistent AV block post-cardiac surgery >14 days; post-TAVR with complete AV block >24–48h; HV interval >100 ms on EP study; tachycardia-bradycardia SSS with symptomatic pauses

  • Class IIa: chronotropic incompetence (failure to increase HR to 85% of max predicted with exercise) with exertional symptoms; carotid sinus hypersensitivity — cardioinhibitory type with syncope + >3 sec asystole on carotid sinus massage

  • Mode: DDD (preferred — dual chamber; preserves AV synchrony; rate-responsive [DDDR] if chronotropic incompetence); VVI (single-chamber ventricular; use in AF + complete block); SSI/AAI (single-chamber atrial; SND without AV block — rarely used alone); consider His-bundle pacing or left bundle branch area pacing to maintain physiologic conduction pattern (reduces pacemaker-induced CMP from long-term RV pacing)

• Specific bridge therapies:

  • Dopamine (Intropin) 5–20 mcg/kg/min IV: chronotropic + inotropic; bridge to pacing if hemodynamically unstable; second-line after atropine; arrhythmogenic at high doses

  • Isoproterenol (Isuprel) 2–10 mcg/min IV (start low; titrate to HR): pure beta-1/beta-2 agonist; increases HR and conduction velocity; useful for: bradycardia-dependent torsades de pointes; symptomatic drug-induced bradycardia refractory to atropine; bridge to pacing; avoid in ischemic heart disease (↑O2 demand)

  • Theophylline 200 mg PO q8–12h: adenosine antagonist; used in denervated transplant hearts (atropine ineffective); rare use in reversible SND

• PT/OT eval and treat — restrict ambulation during active bradycardia until stable; mobilize once rate controlled or paced; functional capacity evaluation post-PM; driving restrictions; fall precautions during bradycardic episodes

• Trend daily: continuous telemetry (pause detection; pacing capture verification — failure to capture [spike without QRS] = lead dislodgement or threshold rise; failure to sense [pacing despite native QRS] = sensitivity too low or lead issue); ECG daily (PR interval; QRS width; pacing spikes + morphology); BMP daily (K+ and Mg2+ to targets; Cr — drug dose adjustment); digoxin (Lanoxin) level q48h if toxicity suspected; TSH weekly if hypothyroid treatment; troponin if MI suspected; vitals q4h

• Escalation triggers: hemodynamic instability (SBP <90 + AMS) at any time → transcutaneous pacing immediately — do not wait · transcutaneous failure to capture or patient intolerance → transvenous temporary pacing via EP/cath lab urgently · digoxin (Lanoxin) toxicity + hemodynamic instability → digoxin immune Fab (Digibind/DigiFab); NEVER cardiovert digoxin-toxic patient · hyperkalemia + AV block → calcium gluconate 1 g IV immediately; emergent nephrology if refractory · complete heart block post-inferior MI not resolving at 14 days → permanent pacemaker implant · cardiac sarcoidosis refractory to corticosteroids → ICD (↑SCD risk) · failure to capture on transvenous pacing → lead dislodgement → reposition urgently; check mA threshold; increase to 3× threshold

• Discharge: PM check before discharge (sensing, pacing, battery); patient education on: PM pocket care (no submersion; no vigorous ipsilateral arm activity ×4–6 weeks; keep incision dry ×48h; no strong magnetic fields [MRI only if MRI-conditional device documented]); no driving for 1 week post-uncomplicated PM implant (varies by state — check local regulations; longer if syncope was presenting symptom — typically 6 months); PM device card (always carry); device clinic f/u 2–4 weeks post-implant; resume medications as tolerated (review AV nodal blocker dose reduction — often reduced dose tolerated post-PM); ICD evaluation if EF ≤35% (cardiomyopathy + conduction disease = ↑SCD risk); return precautions: recurrent syncope + chest pain + PM alarm sounding + swelling/redness at implant site → ED immediately; avoid strong electromagnetic interference sources (arc welders, MRI without MRI-conditional PM, anti-theft systems for prolonged contact)

⚠ Red Flags

• Atropine in infranodal (Mobitz II or complete heart block with wide escape) bradycardia → speeds atrial rate without improving ventricular conduction → ↑AV nodal demand → paradoxical worsening of ventricular rate → hemodynamic collapse; transcutaneous pacing is the correct treatment for infranodal block, not atropine escalation

• Hyperkalemia mimicking complete AV block — any atypical bradyarrhythmia + widened QRS → check K+ immediately; calcium gluconate 1 g IV if K+ >6.0 on clinical suspicion even before lab result (membrane stabilization); giving pacemaker to a hyperkalemic patient without treating K+ = dangerous and will not help

• Digoxin (Lanoxin) toxicity cardioversion — DO NOT cardiovert bradycardia or junctional arrhythmias in digoxin toxicity; ↑VF risk; treat with digoxin immune Fab (Digibind/DigiFab); correct electrolytes (K+, Mg2+)

• 2:1 AV block treated as Mobitz I (benign) — 2:1 block cannot be classified without seeing ≥3 consecutive P waves; always treat as Mobitz II (dangerous, infranodal) until proven otherwise; admit for monitoring + consider PM referral

• Lyme carditis missed in young patient with complete heart block — Lyme carditis is the most common cause of 3rd-degree AV block in patients under 40 in endemic areas; ask about tick exposure, erythema migrans; ELISA + Western blot; empiric ceftriaxone (Rocephin) 2 g IV daily while awaiting serology; most resolve completely with antibiotics

• Holding amlodipine (Norvasc) for bradycardia — amlodipine is vascular-selective; does NOT affect sinus node or AV conduction; holding it is unnecessary and may cause rebound hypertension; only diltiazem (Cardizem) and verapamil (Calan) significantly slow AV conduction among CCBs

• Post-inferior MI complete AV block treated with permanent PM on Day 2 — inferior MI AV block is transient in >90% of cases and resolves with reperfusion within 5–14 days; wait 14 days before committing to permanent PM; temporary pacing bridge in the interim

Senior IM Resident Pearls

• AV block classification — infranodal vs nodal is the critical distinction: nodal (AV node level): Mobitz I / Wenckebach — usually narrow QRS escape; often vagal/medication/inferior MI; responds to atropine; often benign; infranodal (bundle of His/branches): Mobitz II — usually wide QRS escape; degenerative fibrosis or anterior MI; does NOT respond to atropine; dangerous; almost always needs PM; complete AV block with narrow escape = nodal/junctional (more stable, rate 40–60); complete AV block with wide escape = ventricular (unstable, rate 20–40, rate <40 usually incompatible with life)

• Atropine rule — memorize it: atropine works for NODAL block (Mobitz I, sinus bradycardia, vagal); atropine does NOT work for INFRANODAL block (Mobitz II, complete heart block with wide escape); in infranodal block atropine may speed atrial rate without ventricular response → worsening hemodynamics; transcutaneous pacing is the ONLY treatment for hemodynamically unstable infranodal block

• 2:1 AV block — cannot classify, must treat as Mobitz II: 2:1 ratio prevents seeing progressive PR lengthening vs constant PR before drop; only way to distinguish is with longer sequences (3:1 run) or adenosine challenge (speeds AV conduction → if Mobitz I [nodal], temporarily resolves to 1:1; if Mobitz II [infranodal], block worsens or stays same); treat conservatively — PM referral appropriate for symptomatic 2:1 block

• Lyme carditis — the reversible complete heart block: most common cause of 3rd-degree AV block in young patients (under 40) in northeastern US; B. burgdorferi disseminated hematogenously to myocardium; 3rd-degree block in 5%; temporary pacing if hemodynamically unstable; ceftriaxone (Rocephin) 2 g IV daily ×14–21 days; most AV block resolves completely within 1–3 weeks; permanent PM only if persistent; always ask about tick exposure in young patient with otherwise unexplained AV block

• Digoxin (Lanoxin) toxicity management — AUC-guided and Fab dosing: goal 0.5–0.9 ng/mL (post-hoc DIG trial data); toxic >2.0; drug interactions that ↑levels: amiodarone (Pacerone) ×2, quinidine ×2, verapamil (Calan) ×1.5; toxicity enhanced by hypokalemia + hypomagnesemia + hypercalcemia + renal failure; Fab dosing: vials = serum level × weight (kg) / 100; empiric 10 vials if unknown level + hemodynamic instability; do NOT cardiovert; correct K+/Mg2+; monitor for precipitous hypokalemia after Fab (K+ shifts)

• Post-TAVR AV block: complete AV block in 15–25% post-TAVR (most common with self-expanding Evolut valves due to radial force on membranous septum/conduction system); most resolve within 24–48h; permanent PM if persists >48h (center-specific protocols vary); new LBBB post-TAVR alone does NOT mandate PM; HV interval >100 ms on EP study warrants PM; continued telemetry ×48–72h post-TAVR standard

• Cardiac sarcoidosis — the masquerader: can present as unexplained AV block, VT, DCM, or restrictive CM in patients under 60; bilateral hilar adenopathy on CXR; ↑ACE and ↑calcium; FDG-PET is the most sensitive for myocardial inflammation; endomyocardial biopsy often falsely negative (patchy disease); prednisolone 40–60 mg daily may reverse inflammatory AV block; ICD often preferred over PM (↑SCD risk from VT); cardiology + pulmonology co-management

• Common mistake — attributing bradycardia to AV nodal blocker without checking level/dose: always quantify: exact beta-blocker dose + timing of last dose; digoxin (Lanoxin) level (6h post-dose); amiodarone (Pacerone) dose + duration (half-life 40–55 days — stopping has delayed benefit); drug-drug interactions (amiodarone + digoxin = digoxin level doubles); medication reconciliation is the most important first action in drug-induced bradycardia