2018 ACC/AHA/HRS Bradycardia and Cardiac Conduction Delay Guideline

Authors, Journal, Affiliations, Type, DOI

• Chair: Fred M. Kusumoto MD; Vice Chair: Mark H. Schoenfeld MD
• Multi-society writing committee: ACC, AHA, HRS; collaborating: AATS, PACES, STS
• Journal: Journal of the American College of Cardiology 2019;74:e51–156 (approved Oct 2018; co-published in Circulation and HeartRhythm)
• Type: Multi-society clinical practice guideline
• DOI: https://doi.org/10.1016/j.jacc.2018.10.044

Overview

The 2018 ACC/AHA/HRS Bradycardia Guideline is the definitive multi-society clinical practice guideline superseding the 2008 device-based therapy document. It covers evaluation and management of bradycardia and cardiac conduction delay across all mechanisms — sinus node dysfunction (SND), atrioventricular (AV) block, and conduction tissue disorders — with recommendations graded by Class of Recommendation (COR) and Level of Evidence (LOE). Key advances include: establishing symptom–bradycardia temporal correlation as the clinical standard for SND pacing decisions (no minimum HR or pause threshold); recognizing that Mobitz II/high-grade/third-degree AV block from irreversible causes requires permanent pacing regardless of symptoms; introducing the LVEF 36–50% category as a threshold for preferring physiologic pacing over RV pacing; and providing the first systematic recommendations for conduction disturbances after TAVR.

Keywords

Bradycardia, sinus node dysfunction, sick sinus syndrome, atrioventricular block, cardiac conduction delay, permanent pacemaker, chronotropic incompetence, His bundle pacing, cardiac resynchronization therapy, TAVR, temporary pacing, tachy-brady syndrome

Key Takeaways

Epidemiology and Definitions (Section 2)

• SND is most common in individuals in their 70s–80s; driven by age-dependent degenerative fibrosis of sinoatrial nodal tissue and surrounding atrial myocardium
• Same fibrotic process underlies both SND and atrial arrhythmias → tachy-brady syndrome
• SND mirrors pacemaker implantation rates for AV nodal disease (both age-related)
• Comorbidities in patients requiring AV nodal pacing: ischemic heart disease, HF, valvular disease, cerebrovascular disease, AF
• Bradycardia definition: NIH defines as <60 bpm; practical cutoffs for SND diagnosis: sinus rate <50 bpm and/or sinus pause >3 seconds
• Chronotropic incompetence: failure to reach 80% of expected heart rate reserve (HR reserve = [220 − age] − resting HR); difficult to diagnose by age formula alone
• SND definitions include: sinus bradycardia, ectopic atrial bradycardia, sinoatrial exit block, sinus pause >3 s, sinus node arrest, tachy-brady syndrome, chronotropic incompetence

Clinical Manifestations (Section 3)

• Symptomatic bradycardia defined as documented bradyarrhythmia directly causing syncope/presyncope, transient dizziness, HF symptoms, or confusional states from cerebral hypoperfusion
• In SND: symptoms range from fatigue to syncope; severity generally correlates with heart rate or pause duration; syncope present in 50% of patients receiving PPM for SND
• AV block symptoms depend on whether block is fixed or intermittent, the ventricular rate, and the cause
• Vagally mediated AV block at night (identified by concomitant sinus slowing = P-P prolongation) may be asymptomatic
• LBBB may present with HF attributable to cardiac dyssynchrony or underlying cardiomyopathy; isolated RBBB/fascicular block often asymptomatic

General Evaluation (Section 4)

• Class I (C-EO): Comprehensive history and physical examination in all suspected bradycardia
• History should document symptom frequency, timing, triggers, positional changes, medications (bradycardia can be first manifestation of systemic illness)
• Class I (C-EO): Resting 12-lead ECG
• LBBB on ECG markedly increases likelihood of structural heart disease and LV systolic dysfunction → echocardiography is the initial screening test
• Ambulatory ECG: for symptom–bradycardia correlation; duration depends on symptom frequency (24–48h Holter → extended monitoring → ICM)
• Sleep apnea evaluation: both sleep-disordered breathing and nocturnal bradycardias are common; treating sleep apnea reduces frequency of nocturnal bradycardia; nocturnal bradycardia is NOT in itself an indication for permanent pacing
• ICM (implantable cardiac monitor): for infrequent/unexplained syncope undiagnosed by non-invasive means
• EPS (electrophysiology study): Class IIa for symptomatic patients with BBB where HV interval ≥70 ms or frank infranodal block may prompt pacing

Sinus Node Dysfunction — Pathophysiology (Section 5.1)

• SNA node comprises pacemaker cells, transitional cells, endothelial cells, fibroblasts, and extracellular scaffold with unique ion channel/connexin expression
• Collagen content increases with age → fibrosis → slower heart rate and longer SACT; histopathology shows more extensive fibrosis in SND and tachy-brady syndrome
• Fibrosis of the sinus node is associated with fibrosis in the AV node → patients with SND can develop AV block
• Asymptomatic sinus bradycardia: not associated with adverse outcomes
• Symptomatic SND: high risk of syncope, AF, and HF; chronotropic incompetence with age associated with increased CV death and overall mortality

SND — Acute Management (Section 5.3)

• Class I (C-EO): Evaluate and treat reversible causes (acute MI, atrial tachyarrhythmias, electrolytes, hypothyroidism, medications, infections, metabolic abnormalities)
• Atropine (Class IIa, B-NR): for symptomatic or hemodynamically significant bradycardia; not effective in patients with cardiac transplantation (no vagal innervation)
• Beta-agonists (dopamine, isoproterenol, epinephrine): Class IIa for refractory symptomatic bradycardia unresponsive to atropine
• Beta-blocker/calcium channel blocker toxicity: supportive care; Class IIa: high-dose insulin/glucose; Class IIb: calcium chloride/gluconate, glucagon; no role for atropine in infranodal block
• Digoxin toxicity: Digibind (Fab) for life-threatening bradycardia; Class IIa; Class III Harm: atropine not recommended as sole therapy for digoxin-mediated bradycardia
• Temporary pacing (Class I): for symptomatic SND unresponsive to medical therapy; transcutaneous → transvenous as bridge to permanent pacing

SND — Chronic Management / Permanent Pacing (Section 5.4)

• Class I (C-LD): Permanent pacing when symptoms directly attributable to SND
• Class I (C-EO): PPM when symptomatic sinus bradycardia is a consequence of essential GDMT with no alternative treatment
• Class IIa (C-EO): PPM for tachy-brady syndrome with symptoms attributable to bradycardia
• Class IIa (C-EO): PPM with rate-responsive programming for symptomatic chronotropic incompetence
• Class IIb (C-LD): Trial of oral theophylline may be considered to test potential effects of pacing
• No established minimum heart rate or pause duration for PPM in SND; temporal correlation between symptoms and bradycardia is the key determinant
• Primary benefit of pacing in SND: quality of life improvement (not mortality)
• Reversible causes (medications) should be addressed before PPM: stopping offending drug may be appropriate vs. maintaining essential therapy and adding PPM

SND — Pacing Mode (Section 5.4.4.1)

• Class I (B-R): Atrial-based pacing (AAI or DDD) recommended over single-chamber ventricular (VVI) pacing — reduces new-onset AF
• Class I (B-R): Dual chamber or single-chamber atrial pacing in patients with intact AV conduction without conduction abnormalities
• Class IIa (B-R): In patients with DDD and intact AV conduction, program to minimize ventricular pacing
• Class IIa (C-EO): Single-chamber ventricular pacing reasonable if frequent ventricular pacing not expected or significant comorbidities limit benefit
• Four RCTs compared atrial-based vs VVI pacing (PASE, MOST, CTOPP, UKPACE): most consistent benefit = reduction in AF; impact on HF, stroke, QOL less clear; no mortality difference
• Risk of AV block after atrial PPM: 3–35% at 5 years (DDD preferred over AAI in most patients to avoid need for lead addition later)
• Single-chamber ventricular pacing can cause pacemaker syndrome (uncoupled AV depolarization, valvular regurgitation, HF-type symptoms)

AV Block — Pathophysiology and Classification (Section 6.1)

• Etiology of AV block: congenital, infectious (Lyme carditis — reversible), inflammatory/infiltrative (sarcoidosis, amyloidosis, myocarditis), ischemic, degenerative (most common in clinical practice — age, hypertension, diabetes), iatrogenic
• AV block classification: anatomical level = AV nodal, intra-Hisian, infra-Hisian
  • AV nodal block: slower progression, faster/more reliable junctional escape, responsive to atropine and catecholamines
  • Infranodal block: may progress rapidly/unexpectedly, slow/unpredictable ventricular escape, does NOT respond to atropine but may respond to catecholamines
• First-degree "AV block" (PR >200 ms) is more accurately AV delay — every P wave conducts
• Second-degree: Mobitz I (Wenckebach — gradual PR prolongation before dropped QRS, usually AV nodal); Mobitz II (constant PR before dropped QRS, usually infranodal)
• 2:1 AV block: cannot be classified as Mobitz I or II → EPS may be needed to determine level of block
• High-grade/advanced AV block: ≥2 consecutive non-conducted P waves with some AV conduction preserved
• Third-degree (complete) AV block: no AV conduction; paroxysmal or persistent; junctional or ventricular escape
• Complete AV block in AF: suspected when ventricular response is slow (<50 bpm) and regular

AV Block — Acute Management (Section 6.3)

• Class I (C-EO): Evaluate and treat reversible causes (Lyme carditis, medication, AMI, electrolytes)
• Class IIa (C-LD): Atropine for symptomatic/hemodynamically significant AV nodal block; NOT effective for infranodal block
• Class IIa (B-NR): Beta-agonists (dopamine, epinephrine, isoproterenol) for refractory AV nodal block unresponsive to atropine; may be useful for infranodal block
• Class I: Temporary pacing for medically refractory, hemodynamically significant AV block

AV Block — Chronic Management / Permanent Pacing (Section 6.4.4)

• Class I (B-NR): PPM for acquired Mobitz type II, high-grade AV block, or third-degree AV block NOT from reversible/physiologic causes — regardless of symptoms
• Class I (B-NR): PPM (± ICD if needed, if survival >1 year expected) for neuromuscular diseases (myotonic dystrophy type 1, Kearns-Sayre syndrome) with second-degree, third-degree AV block, or HV interval ≥70 ms — regardless of symptoms
• Class I (C-LD): PPM for permanent AF + symptomatic bradycardia
• Class I (C-LD): PPM when symptomatic AV block is consequence of essential GDMT with no alternative
• Class IIa (B-NR): PPM (± ICD) for infiltrative cardiomyopathy (cardiac sarcoidosis, amyloidosis) + Mobitz II/high-grade/third-degree AV block
• Class IIa (B-NR): PPM (± ICD) for lamin A/C gene mutations (incl. limb-girdle, Emery-Dreifuss muscular dystrophies) with PR >240 ms AND LBBB
• Class IIa (C-LD): PPM for marked first-degree or Wenckebach AV block with symptoms clearly attributable to AV block
• Class IIb (C-LD): PPM (± ICD) for myotonic dystrophy type 1 with PR >240 ms, QRS >120 ms, or fascicular block
• Key principle: Unlike SND, infranodal AV block regardless of symptoms warrants pacemaker (risk of sudden onset complete AV block → syncope/harm)

AV Block — Pacing Mode (Section 6.4.4.1)

• Class I (A): Dual chamber pacing recommended over VVI in patients with SND and AV block requiring PPM
• Class I (A): In select patients where frequent ventricular pacing not expected or significant comorbidities — single-chamber VVI effective
• Class I (B-R): Develop pacemaker syndrome on VVI → upgrade to dual chamber
• Class IIa (B-R [SR]): LVEF 36–50% + indication for PPM + expected ventricular pacing >40%: prefer physiologic activation (CRT or His bundle pacing) over RV pacing
• Class IIa (B-R): LVEF 36–50% + expected ventricular pacing <40%: RV pacing reasonable over CRT/His
• Class IIb (B-R [SR]): AV block at level of AV node: His bundle pacing may be considered for physiologic activation
• Class III Harm (C-LD): Permanent/persistent AF without rhythm control strategy: no atrial lead implantation
• Evidence: PASE, MOST, CTOPP, UKPACE — RCTs of dual vs single-chamber pacing; no reduction in all-cause/CV mortality; benefits include reduced pacemaker syndrome and AF reduction

Conduction Disorders with 1:1 AV Conduction (Section 7)

• Class I (C-LD): PPM for syncope + BBB + HV ≥70 ms or infranodal block at EPS
• Class I (C-LD): PPM for alternating bundle branch block (alternating LBBB/RBBB morphologies) — implies unstable infranodal disease, high risk of sudden complete AV block
• Class IIa (C-LD): PPM (± ICD) for Kearns-Sayre syndrome + conduction disorders
• Class IIb (C-LD): PPM (± ICD) for Anderson-Fabry disease + QRS >110 ms
• Class IIb (C-LD): LVEF 36–50% + HF + LBBB (QRS ≥150 ms): CRT may be considered
• Class III Harm (B-NR): Asymptomatic isolated conduction disease with 1:1 AV conduction: PPM NOT indicated (absence of other indications)

Special Populations — Perioperative (Section 8.1)

• Noncardiac surgery: existing PPM/ICD should be assessed and reprogrammed; Class I (C-EO)
• Post-CABG: temporary epicardial pacing wires routine; permanent pacing rarely needed for isolated sinus bradycardia; Class IIa (C-LD) for complete AV block persisting ≥5 days after CABG
• Post-TAVR conduction disturbances:
  • New LBBB: 19–55% of TAVR cases; new high-degree AV block: ~10%
  • Up to half of new BBB and CHB can resolve before discharge
  • Class I (B-NR): PPM before discharge for new persistent AV block with symptoms or hemodynamic instability after TAVR
  • Class IIa (B-NR): New persistent BBB after TAVR → surveillance for bradycardia (reasonable)
  • Class IIb (B-NR): New persistent LBBB after TAVR → PPM may be considered (early PPM not protective against increased mortality from new LBBB)
  • Pre-TAVR predictors of PPM: preexisting RBBB, increased prosthesis-to-LVOT ratio, increased LV end-diastolic diameter

Special Populations — Acute MI (Section 8.3)

• Class I (B-NR): Temporary pacing for medically refractory symptomatic/hemodynamically significant bradycardia (SND or AV block) in AMI
• Class I (B-NR): Waiting period before determining need for PPM in AMI
• Class I (B-NR): PPM (after waiting period) for AMI + Mobitz II/high-grade AV block/alternating BBB/persistent or infranodal third-degree AV block
• Class IIa (B-NR): Atropine for symptomatic SND or AV block at AV node level in AMI
• Class III Harm (B-NR): No PPM for transient AV block that resolves in AMI
• Class III Harm (B-NR): No PPM for new BBB or isolated fascicular block without second/third-degree AV block in AMI
• Inferior wall MI → AV block often transient (vagal tone or AV nodal ischemia); anterior MI + AV block → extensive myocardial damage, worse prognosis
• Long-term prognosis of MI survivors with AV block related primarily to extent of myocardial injury, not the AV block itself

Shared Decision-Making, QOL, and End-of-Life (Sections 11–14)

• Shared decision-making and patient-centered care endorsed and emphasized
• Patients with decision-making capacity have the right to refuse or request withdrawal of pacemaker therapy, even if pacemaker-dependent → considered palliative/end-of-life care, NOT physician-assisted suicide
• Benefits of pacing: primarily QOL improvement for SND; some evidence for mortality benefit in complete AV block

Emerging Technologies (Section 15)

• His bundle pacing (HBP): provides physiologic ventricular activation; indicated in Class IIa (AV block at AV node level, LVEF 36–50%, >40% ventricular pacing expected); Class IIb (AV node level block, regardless of EF)
• Transcatheter leadless pacing systems: further investigation needed to define optimal patient populations
• Gene therapy: genome-wide association has identified multiple loci for heart rate control → future therapeutic targets for SND

Limitations of the Document

• No randomized controlled trials specifically for tachy-brady syndrome pacing
• No RCTs comparing pacing approaches in AV block complicating acute MI
• Evidence for TAVR-associated conduction disturbances consists of observational studies and registries only; no prospective RCTs for PPM implantation timing post-TAVR
• Guideline targets adult population (>18 years); limited applicability to pediatric patients
• Most evidence for pacing mode selection (PASE, MOST, CTOPP, UKPACE) predates current physiologic pacing modalities (His bundle pacing, LBBAP)
• LVEF 36–50% CRT/His pacing recommendations based on systematic review but limited RCT data

Key Concepts Mentioned

• concepts/Sinus-Node-Dysfunction — primary clinical entity covered (SND diagnosis, management, pacing indications)
• concepts/Atrioventricular-Block — second major clinical entity covered (classification, management, pacing indications)
• concepts/Permanent-Pacing-Indications — comprehensive pacing indications across all mechanisms
• concepts/Conduction-System-Pacing — His bundle pacing Class IIa/IIb recommendations
• concepts/ECG-Conduction-Disturbances — ECG definitions, AV block classification, BBB criteria
• concepts/Cardiac-Resynchronization-Therapy — CRT in LVEF 36–50% + high ventricular pacing
• concepts/Tachycardia-Induced-Cardiomyopathy — mentioned in tachy-brady context

Key Entities Mentioned

• entities/Atrial-Fibrillation — tachy-brady syndrome; AF + symptomatic bradycardia → PPM indication
• entities/CRT — physiologic pacing option for LVEF 36–50% with high ventricular pacing burden
• entities/Anderson-Fabry-Disease — PPM consideration for QRS >110 ms
• entities/ARVC — mentioned in context of neuromuscular disease conduction disorders

Wiki Pages Updated

• wiki/sources/bradycardia-acc-aha-hrs-2018.md — created
• wiki/concepts/Sinus-Node-Dysfunction.md — created
• wiki/concepts/Atrioventricular-Block.md — created
• wiki/concepts/Permanent-Pacing-Indications.md — created
• wiki/concepts/Conduction-System-Pacing.md — updated (His bundle pacing Class IIa/IIb)
• wiki/concepts/ECG-Conduction-Disturbances.md — updated (LBBB + structural disease, alternating BBB)
• wiki/wikiindex.md — updated
• wiki/sourceindex.md — updated