Kusumoto Et Al 2018 2018 Acc Aha Hrs Guideline On The Evaluation and Management of Patients With Bradycardia and

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY VOL. 74, NO.
7, 2019
ª 2019 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION,
THE AMERICAN HEART ASSOCIATION, INC., AND THE HEART RHYTHM SOCIETY
PUBLISHED BY ELSEVIER
CLINICAL PRACTICE GUIDELINE: EXECUTIVE SUMMARY
2018 ACC/AHA/HRS Guideline on

the Evaluation and Management of
Patients With Bradycardia and Cardiac
Conduction Delay: Executive Summary
A Report of the American College of Cardiology/American Heart Association
Task Force on Clinical Practice Guidelines, and the Heart Rhythm Society
Developed in Collaboration With the American Association for Thoracic Surgery,

the Pediatric & Congenital Electrophysiology Society, and the Society of Thoracic Surgeons
Endorsed by the American Association for Thoracic Surgery, the Pediatric & Congenital
Electrophysiology Society, and the Society of Thoracic Surgeons
Writing Fred M. Kusumoto, MD, FACC, FAHA, FHRS, Chair Keith R. Oken, MD, FACCy
Committee Mark H. Schoenfeld, MD, FACC, FAHA, FHRS, Vice Chair Kristen K. Patton, MD, FACC, FAHA, FHRSy
Members* Cara N. Pellegrini, MD, FHRS*x**
Coletta Barrett, RN, FAHAy Kimberly A. Selzman, MD, MPH, FACC, FHRSy
James R. Edgerton, MD, FACC, FHRSz Annemarie Thompson, MDy
Kenneth A. Ellenbogen, MD, FACC, FAHA, FHRS*y Paul D. Varosy, MD, FACC, FAHA, FHRSyy
Michael R. Gold, MD, PHD, FACC*x
Nora F. Goldschlager, MD, FACC, FAHA, FHRSy
*Writing committee members are required to recuse themselves from
Robert M. Hamilton, MDk
voting on sections to which their specific relationships with industry may
José A. Joglar, MD, FACC, FAHA, FHRS{ apply; see Appendix 1 for detailed information. yACC/AHA Representative.
Robert J. Kim, MDy zSTS Representative. xHRS Representative. kPACES Representative.
Richard Lee, MD, MBA# {ACC/AHA Task Force on Clinical Practice Guidelines Liaison. #AATS
Representative. **Dr. Pellegrini contributed to this article in her personal
Joseph E. Marine, MD, MBA, FACC, FHRSx
capacity. The views expressed are her own and do not necessarily
Christopher J. McLeod, MB, CHB, PHD, FACC, FAHA, represent the views of the U.S. Department of Veterans Affairs or the
FHRSy U.S. government. yyACC/AHA Performance Measures Representative.
This document was approved by the American College of Cardiology Clinical Policy Approval Committee, the American Heart Association Science
Advisory and Coordinating Committee, and the Heart Rhythm Society in August 2018, and the American Heart Association Executive Committee in
October 2018.
The American College of Cardiology requests that this document be cited as follows: Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR,
Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA,
Thompson A, Varosy PD. 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay:
executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines, and the
Heart Rhythm Society. J Am Coll Cardiol 2019;74:932-87.
This article has been copublished in Circulation and HeartRhythm.
Copies: This document is available on the websites of the American College of Cardiology (www.acc.org), the American Heart Association
(professional.heart.org), and the Heart Rhythm Society (www.hrsonline.org). For copies of this document, please contact the Elsevier Inc. Reprint
Department via fax (212-633-3820) or e-mail ([email protected]).
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
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ISSN 0735-1097/$36.00 https://doi.org/10.1016/j.jacc.2018.10.043

JACC VOL. 74, NO. 7, 2019 Kusumoto et al. 933
AUGUST 20, 2019:932–87 2018 Bradycardia Guideline: Executive Summary
ACC/AHA Task Glenn N. Levine, MD, FACC, FAHA, Chair Samuel Gidding, MD, FAHAzz
Force Members Patrick T. O’Gara, MD, MACC, FAHA, Chair-Elect Zachary D. Goldberger, MD, MSc, FACC, FAHA
Jonathan L. Halperin, MD, FACC, FAHA, Immediate Mark A. Hlatky, MD, FACC, FAHA
Past Chairzz John Ikonomidis, MD, PHD, FAHAzz
José A. Joglar, MD, FACC, FAHA
Sana M. Al-Khatib, MD, MHS, FACC, FAHA Laura Mauri, MD, MSc, FAHAzz
Joshua A. Beckman, MD, MS, FAHA Mariann R. Piano, RN, PHD, FAHA
Kim K. Birtcher, PharmD, MS, AACC Susan J. Pressler, PHD, RN, FAHAzz
Biykem Bozkurt, MD, PHD, FACC, FAHAzz Barbara Riegel, PHD, RN, FAHAzz
Ralph G. Brindis, MD, MPH, MACCzz Duminda N. Wijeysundera, MD, PHD
Joaquin E. Cigarroa, MD, FACC
Lesley H. Curtis, PHD, FAHAzz
zzFormer Task Force member; current member during the
Anita Deswal, MD, MPH, FACC, FAHA
writing effort.
Lee A. Fleisher, MD, FACC, FAHA
Federico Gentile, MD, FACC
TABLE OF CONTENTS
TOP 10 TAKE-HOME MESSAGES . . . . . . . . . . . . . . . . . . 934 3.2.3. Ambulatory Electrocardiography

in Patients With Documented or
Suspected Bradycardia or Conduction
PREAMBLE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 935
Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . 946
3.2.4. Imaging in Patients With Documented or
1. INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 936
Suspected Bradycardia or Conduction
1.1. Methodology and Evidence Review . . . . . . . . . . 936 Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . 947
3.2.5. Laboratory Testing in Patients With
1.2. Organization of the Writing Committee . . . . . . . 936
Documented or Suspected Bradycardia
1.3. Document Review and Approval . . . . . . . . . . . . . 936 or Conduction Disorders . . . . . . . . . . . . . . 947
3.2.6. Genetic Testing in Patients With
1.4. Scope of the Guideline . . . . . . . . . . . . . . . . . . . . . 936
Documented or Suspected Bradycardia or
1.5. Class of Recommendation and Level of Conduction Disorders . . . . . . . . . . . . . . . . 948
Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 937 3.2.7. Sleep Apnea Evaluation and Treatment in
Patients With Documented or Suspected
1.6. Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . 937
Bradycardia or Conduction Disorders . . . . 948
2. EPIDEMIOLOGY AND DEFINITIONS . . . . . . . . . . . . 940 3.3. Invasive Testing . . . . . . . . . . . . . . . . . . . . . . . . . . 948

2.1. Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 940 3.3.1. Implantable Cardiac Monitor in Patients
With Documented or Suspected
Bradycardia or Conduction Disorders . . . . 948
3. GENERAL EVALUATION OF PATIENTS WITH
DOCUMENTED OR SUSPECTED BRADYCARDIA 3.3.2. Electrophysiology Study in Patients With
OR CONDUCTION DISORDERS . . . . . . . . . . . . . . . . 941
Conduction Disorders . . . . . . . . . . . . . . . . . 948
3.1. History and Physical Examination of Patients
With Documented or Suspected Bradycardia or
4. BRADYCARDIA ATTRIBUTABLE TO SINUS NODE
Conduction Disorders . . . . . . . . . . . . . . . . . . . . . . 941
DYSFUNCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 949
3.2. Noninvasive Evaluation . . . . . . . . . . . . . . . . . . . . 941
4.1. Acute Management of Sinus Node Dysfunction . 949
3.2.1. Resting ECG in Patients With
Documented or Suspected Bradycardia 4.1.1. Acute Management of Reversible Causes
or Conduction Disorders . . . . . . . . . . . . . . 941 of Sinus Node Dysfunction . . . . . . . . . . . . 950
3.2.2. Exercise Electrocardiographic Testing in 4.1.2. Acute Medical Therapy for Bradycardia . . 950
Patients With Documented or Suspected 4.1.3. Temporary Pacing for Bradycardia
Bradycardia or Conduction Disorders . . . . 946 Attributable to SND . . . . . . . . . . . . . . . . . . 952
934 Kusumoto et al. JACC VOL. 74, NO. 7, 2019
2018 Bradycardia Guideline: Executive Summary AUGUST 20, 2019:932–87
4.2. Chronic Therapy/Management of Bradycardia 7.3. Management of Bradycardia in Patients With

Attributable to SND . . . . . . . . . . . . . . . . . . . . . . . 954 an Acute MI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 969
4.2.1. General Principles of Chronic Therapy/ 7.4. Neurologic Disorders . . . . . . . . . . . . . . . . . . . . . . 969
Management of Bradycardia Attributable
to SND . . . . . . . . . . . . . . . . . . . . . . . . . . . . 954 7.4.1. Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 969
4.2.2. Transient/Reversible Causes (Including

Medications) of Bradycardia Attributable 8. EVALUATION OF THE RISKS FOR VENTRICULAR
to SND . . . . . . . . . . . . . . . . . . . . . . . . . . . . 954 ARRHYTHMIAS IN PATIENTS WHO REQUIRE
4.2.3. Additional Testing of Bradycardia PERMANENT PACING . . . . . . . . . . . . . . . . . . . . . . . . 969

Attributable to SND . . . . . . . . . . . . . . . . . . 954
4.3.4. Permanent Pacing for Chronic Therapy/ 9. SHARED DECISION-MAKING . . . . . . . . . . . . . . . . . . 970
Management of Bradycardia Attributable
to SND . . . . . . . . . . . . . . . . . . . . . . . . . . . . 955 10. DISCONTINUATION OF PACEMAKER THERAPY . . 970
5. BRADYCARDIA ATTRIBUTABLE TO PRESIDENTS AND STAFF . . . . . . . . . . . . . . . . . . . . . . . . 970
ATRIOVENTRICULAR BLOCK . . . . . . . . . . . . . . . . . . 957

REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 971
5.1. Pathophysiology, Etiology, and Classification of
Bradycardia Attributable to Atrioventricular
Block . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 957 APPENDIX 1
5.2. Acute Management . . . . . . . . . . . . . . . . . . . . . . . . 958 Author Relationships With Industry and

Other Entities (Relevant) . . . . . . . . . . . . . . . . . . . . . . . 984
5.2.1. Acute Management of Reversible Causes of
Block . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 958 APPENDIX 2
5.2.2. Acute Medical Therapy for Bradycardia Abbreviated Reviewer Relationships With Industry
Attributable to Atrioventricular Block . . . . 958 and Other Entities . . . . . . . . . . . . . . . . . . . . . . . . . . . . 986
5.2.3. Temporary Pacing for Atrioventricular
Block . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 958
TOP 10 TAKE-HOME MESSAGES
5.3. Chronic Therapy/Management of Bradycardia
Attributable to Atrioventricular Block . . . . . . . . . 959 1. Sinus node dysfunction is most often related to age-
5.3.1. General Principles of Chronic Therapy/ dependent progressive fibrosis of the sinus nodal tis-
Management of Bradycardia Attributable to sue and surrounding atrial myocardium leading to
Atrioventricular Block . . . . . . . . . . . . . . . . 960 abnormalities of sinus node and atrial impulse for-
5.3.2. Transient/Potentially Reversible Causes of mation and propagation and will therefore result in
Atrioventricular Block . . . . . . . . . . . . . . . . 960 various bradycardic or pause-related syndromes.
5.3.3. Additional Testing for Chronic Therapy/ 2. Both sleep disorders of breathing and nocturnal bra-
Management of Bradycardia Attributable to dycardias are relatively common, and treatment of
Atrioventricular Block . . . . . . . . . . . . . . . . 960
sleep apnea not only reduces the frequency of these
5.3.4. Permanent Pacing . . . . . . . . . . . . . . . . . . . 961 arrhythmias but also may offer cardiovascular bene-
fits. The presence of nocturnal bradycardias should
6. CONDUCTION DISORDERS (WITH 1:1
prompt consideration for screening for sleep apnea,
ATRIOVENTRICULAR CONDUCTION) . . . . . . . . . . . 962 beginning with solicitation of suspicious symptoms.
6.1. Evaluation of Conduction Disorders . . . . . . . . . . 962 However, nocturnal bradycardia is not in itself an
indication for permanent pacing.
6.2. Management of Conduction Disorders (With 1:1
Atrioventricular Conduction) . . . . . . . . . . . . . . . . 964 3. The presence of left bundle branch block on electro-
cardiogram markedly increases the likelihood of un-
7. SPECIAL POPULATIONS . . . . . . . . . . . . . . . . . . . . . . 965

derlying structural heart disease and of diagnosing
left ventricular systolic dysfunction. Echocardiogra-
7.1. Perioperative Management . . . . . . . . . . . . . . . . . 965 phy is usually the most appropriate initial screening
7.1.1. Patients at Risk for Bradycardia During test for structural heart disease, including left ven-
Noncardiac Surgery or Procedures . . . . . . 965
tricular systolic dysfunction.
7.1.2. Postoperative Bradycardia and Conduction 4. In sinus node dysfunction, there is no established
Disorders After Cardiac Surgery . . . . . . . . . 965
minimum heart rate or pause duration where perma-
7.2. Bradycardia Management for Adult Congenital nent pacing is recommended. Establishing temporal
Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 968 correlation between symptoms and bradycardia is
important when determining whether permanent scientific evidence into clinical practice guidelines with
pacing is needed. recommendations to improve cardiovascular health.
5. In patients with acquired second-degree Mobitz type These guidelines, which are based on systematic methods
II atrioventricular block, high-grade atrioventricular to evaluate and classify evidence, provide a foundation
block, or third-degree atrioventricular block not for the delivery of quality cardiovascular care. The ACC
caused by reversible or physiologic causes, permanent and AHA sponsor the development and publication of
pacing is recommended regardless of symptoms. For clinical practice guidelines without commercial support,
all other types of atrioventricular block, in the and members volunteer their time to the writing and re-
absence of conditions associated with progressive view efforts.
atrioventricular conduction abnormalities, permanent Clinical practice guidelines provide recommendations
pacing should generally be considered only in the applicable to patients with or at risk of developing
presence of symptoms that correlate with atrioven- cardiovascular disease. The focus is on medical practice
tricular block. in the United States, but these guidelines are relevant
6. In patients with a left ventricular ejection fraction to patients throughout the world. Although guidelines
between 36% to 50% and atrioventricular block, who may be used to inform regulatory or payer decisions,
have an indication for permanent pacing and are ex- the intent is to improve quality of care and align with
pected to require ventricular pacing >40% of the time, patients’ interests. Guidelines are intended to define
techniques that provide more physiologic ventricular practices meeting the needs of patients in most, but not
activation (e.g., cardiac resynchronization therapy, all, circumstances, and should not replace clinical
His bundle pacing) are preferred to right ventricular judgment.
pacing to prevent heart failure. Recommendations for guideline-directed management
7. Because conduction system abnormalities are com- and therapy, which encompasses clinical evaluation,
mon after transcatheter aortic valve replacement, diagnostic testing, and both pharmacological and proce-
recommendations on postprocedure surveillance and dural treatments, are effective only when followed by
pacemaker implantation are made in this guideline. both practitioners and patients. Adherence to recom-
8. In patients with bradycardia who have indications for mendations can be enhanced by shared decision-making
pacemaker implantation, shared decision-making and between clinicians and patients, with patient engage-
patient-centered care are endorsed and emphasized in ment in selecting interventions on the basis of individual
this guideline. Treatment decisions are based on the values, preferences, and associated conditions and
best available evidence and on the patient’s goals of comorbidities.
care and preferences. The ACC/AHA Task Force on Clinical Practice Guide-
9. Using the principles of shared decision-making and lines strives to ensure that the guideline writing com-
informed consent/refusal, patients with decision- mittee both contains requisite expertise and is
making capacity or his/her legally defined surrogate representative of the broader medical community by
has the right to refuse or request withdrawal of selecting experts from a broad array of backgrounds rep-
pacemaker therapy, even if the patient is pacemaker resenting different geographic regions, sexes, races, eth-
dependent, which should be considered palliative, nicities, intellectual perspectives/biases, and scopes of
end-of-life care, and not physician-assisted suicide. clinical practice, and by inviting organizations and pro-
However, any decision is complex, should involve all fessional societies with related interests and expertise to
stakeholders, and will always be patient specific. participate as partners or collaborators. The ACC and AHA
10. Identifying patient populations that will benefit the have rigorous policies and methods to ensure that docu-
most from emerging pacing technologies (e.g., His ments are developed without bias or improper influence.
bundle pacing, transcatheter leadless pacing systems) The complete policy on relationships with industry
will require further investigation as these modalities and other entities (RWI) can be found online.
are incorporated into clinical practice. Beginning in 2017, numerous modifications to the
guidelines have been and continue to be implemented to
PREAMBLE make guidelines shorter and enhance “user friendliness.”
Guidelines are written and presented in a modular
Since 1980, the American College of Cardiology (ACC) and knowledge chunk format, in which each chunk
American Heart Association (AHA) have translated includes a table of recommendations, a brief synopsis,
recommendation-specific supportive text and, when the evidence review committee and the writing commit-
appropriate, flow diagrams or additional tables. Hyper- tee members were formally presented and discussed, and
linked references are provided for each modular knowl- then recommendations were developed. The systematic
edge chunk to facilitate quick access and review. More review, titled “Impact of Physiologic Versus Right Ven-
structured guidelines—including word limits (“targets”) tricular Pacing Among Patients With Left Ventricular
and a web guideline supplement for useful but noncritical Ejection Fraction Greater Than 35%: A Systematic Review
tables and figures—are 2 such changes. This Preamble is for the 2018 ACC/AHA/HRS Guideline on the Evaluation
an abbreviated version, with the detailed version and Management of Patients With Bradycardia and Car-
available online. diac Conduction Delay” is published in conjunction with
The reader is encouraged to consult the full-text guide- this guideline (S1-1) and its respective data supplements
line (P-1) for additional guidance and details about brady- are available online. The evidence review committee
cardia and cardiac conduction delay, because the executive report informed recommendations in Section 6.4.4.1.
summary contains mainly the recommendations.
Glenn N. Levine, MD, FACC, FAHA 1.2. Organization of the Writing Committee
Chair, ACC/AHA Task Force on The writing committee consisted of cardiac electrophysi-
Clinical Practice Guidelines ologists, clinicians, cardiologists, surgeons, an anesthe-
siologist, and a lay/patient representative. The writing
1. INTRODUCTION committee included representatives from the ACC, AHA,

Heart Rhythm Society (HRS), American Association for
1.1. Methodology and Evidence Review Thoracic Surgery (AATS), Pediatric & Congenital Electro-
physiology Society (PACES), and the Society of Thoracic
The recommendations listed in this guideline are, when-
Surgeons (STS). Appendix 1 of the present document
ever possible, evidence based. An initial extensive evi-
lists writing committee members’ relevant RWI. For the
dence review, which included literature derived from
purposes of full transparency, the writing committee
research involving human subjects, published in English,
members’ comprehensive disclosure information is
and indexed in MEDLINE (through PubMed), EMBASE,
available online.
the Cochrane Library, the Agency for Healthcare Research
and Quality, and other selected databases relevant to this
1.3. Document Review and Approval
guideline, was conducted from January 2017 to September
2017. Key search words included but were not limited to This document was reviewed by 2 official reviewers each
the following: AV block, bradycardia, bundle branch block, nominated by the ACC, AHA, and HRS; 1 official lay
conduction disturbance, left bundle branch block, loop reviewer nominated by the AHA; 1 organizational
recorder, pauses, permanent pacemaker, sick sinus syn- reviewer each from the AATS, PACES, and STS; and 31 in-
drome, sinus node dysfunction, and temporary pacemaker. dividual content reviewers. Reviewers’ RWI information
Additional relevant studies published through January was distributed to the writing committee and is published
2018, during the guideline writing process, were also as an abbreviated table in this document (Appendix 2). The
considered by the writing committee and added to reviewers’ detailed RWI information is available online.
the evidence tables when appropriate. The final evidence This document was approved for publication by the
tables are included in the Online Data Supplement and governing bodies of the ACC, the AHA, and the HRS; and
summarize the evidence used by the writing committee to was endorsed by the American Association for Thoracic
formulate recommendations. References selected and Surgery, the Pediatric & Congenital Electrophysiology
published in the present document are representative and Society, and the Society of Thoracic Surgeons.
not all-inclusive.
As noted in the detailed version of the Preamble, an 1.4. Scope of the Guideline
independent evidence review committee was commis- The purpose of this ACC/AHA/HRS guideline is to provide
sioned to perform a formal systematic review of 1 critical guidance to clinicians for the management of patients
clinical question related to bradycardia, the results of with bradycardia, or symptoms thought to be associated
which were considered by the writing committee for with bradycardia or cardiac conduction system disorders.
incorporation into this guideline. Concurrent with this This guideline supersedes the pacemaker recommenda-
process, writing committee members evaluated study tions made in the “ACC/AHA/HRS 2008 Guidelines
data relevant to the rest of the guideline. The findings of for Device-Based Therapy of Cardiac Rhythm
Abnormalities” (S1.4-1, S1.4-2) and “2012 ACCF/AHA/HRS and implanted device-based therapies, with particular
Focused Update Incorporated Into the ACCG/AHA/HRS attention to indications for temporary and permanent
2008 Guidelines for Device-Based Therapy of Cardiac pacing.
Rhythm Abnormalities (S1.4-2). The guideline will be n Address special considerations that may be applicable
useful to general internists, family physicians, emergency to distinct populations based on age (>18 years of age),
physicians, anesthesiologists, surgeons, cardiologists, comorbidities or other relevant factors.
and arrhythmia specialists. This document is aimed at the n Identify knowledge gaps, pertinent trials in progress
adult population (>18 years of age) and offers no specific and directions for future research.
recommendations in pediatric patients, although some
Table 1 lists other guidelines and pertinent documents
of the evidence review included pediatric patients.
that the writing committee considered for this guideline.
Although background on the pathophysiology and
The listed documents contain relevant information for
epidemiology of bradycardia and cardiac conduction dis-
the management of patients with bradycardia or cardiac
orders is summarized, this guideline is not intended to be
conduction system disorder.
an exhaustive review. Rather, it focuses on practical
clinical evaluation and management. Specific objectives
and goals include: 1.5. Class of Recommendation and Level of Evidence
Recommendations are designated with both a class of
n Describe the clinical significance of bradycardia with recommendation (COR) and a level of evidence (LOE). The
respect to mortality, symptoms (e.g., syncope, class of recommendation indicates the strength of
impaired functional capacity), and exacerbations of recommendation, encompassing the estimated magni-
associated disorders (e.g., ischemia, heart failure, tude and certainty of benefit in proportion to risk. The
provoked tachyarrhythmias). level of evidence rates the quality of scientific evidence
n Address inherited and acquired disorders of the supporting the intervention on the basis of the type,
sinus node, atrioventricular node, His-Purkinje quantity, and consistency of data from clinical trials and
fibers, and intramyocardial conducting tissue, other sources (Table 2) (S1.5-1).
including the effects of medications, aging, metabolic
derangements, trauma, radiation, infiltrative,
1.6. Abbreviations
ischemic, and inflammatory disorders, infectious and
toxic agents and iatrogenic factors.
n Delineate the clinical presentation and general Abbreviation Meaning/Phrase
approach to clinical evaluation of patients with overt ACHD adult congenital heart disease
or suspected bradycardias or conduction diseases. AF atrial fibrillation
n Comprehensively evaluate the evidence supporting CRT cardiac resynchronization therapy
recommendations for the selection and timing of
ECG electrocardiogram
available diagnostic testing modalities, including
EPS electrophysiology study
monitoring devices and electrophysiologic testing.
LBBB left bundle branch block
n Define the evidence base supporting recommendations
MI myocardial infarction
for the use of available treatment modalities, including
SND sinus node dysfunction
lifestyle interventions, pharmacotherapy and external
TABLE 1 Associated Guidelines and Related References
Publication Year
Title Organization (Reference)
Guidelines
Ventricular arrhythmias and sudden cardiac death ACC/AHA/HRS 2017 (S1.4-3)
Syncope ACC/AHA/HRS 2017 (S1.4-4)
Stable ischemic heart disease ACC/AHA/AATS/PCNA/SCAI/STS 2014* (S1.4-5)

2012 (S1.4-6)
Atrial fibrillation AHA/ACC/HRS 2014 (S1.4-7)
Perioperative cardiovascular evaluation and management of patients undergoing ACC/AHA 2014 (S1.4-8)
non-cardiac surgery
Non–ST-elevation acute coronary syndromes AHA/ACC 2014 (S1.4-9)
Heart failure ACC/AHA 2013 (S1.4-10)
ST-elevation myocardial infarction ACC/AHA 2013 (S1.4-11)
Device-based therapy for cardiac rhythm abnormalities ACC/AHA/HRS 2013 (S1.4-2)
Coronary artery bypass graft surgery ACC/AHA 2011 (S1.4-12)
Hypertrophic cardiomyopathy ACC/AHA 2011 (S1.4-13)
Percutaneous coronary intervention ACC/AHA/SCAI 2011 (S1.4-14)
Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care—Part 9: AHA 2010 (S1.4-15)
post-cardiac arrest care
Other related references
Expert consensus statement on cardiovascular implantable electronic device lead HRS 2017 (S1.4-16)
management and extraction
Management of cardiac involvement associated with neuromuscular diseases AHA 2017 (S1.4-17)
Expert consensus statement on magnetic resonance imaging HRS 2017 (S1.4-18)
Eligibility and disqualification recommendations for competitive athletes with ACC/AHA 2015 (S1.4-19)
cardiovascular abnormalities: Task Force 9: arrhythmias and conduction defects
Expert consensus statement on the diagnosis and treatment of postural tachycardia HRS 2015 (S1.4-20)
syndrome, inappropriate sinus tachycardia, and vasovagal syncope
Expert consensus statement on the recognition and management of arrhythmias PACES/HRS 2014 (S1.4-21)
in adult congenital heart disease
Expert consensus statement on the use of implantable cardioverter-defibrillator HRS/ACC/AHA 2014 (S1.4-22)
therapy in patients who are not included or not well represented in clinical trials
Expert consensus statement on the diagnosis and management of arrhythmias HRS 2014 (S1.4-23)
associated with cardiac sarcoidosis
Cardiac pacing and cardiac resynchronization therapy ESC 2013 (S1.4-24)
Expert consensus statement on pacemaker device and mode selection HRS/ACCF 2012 (S1.4-25)
Expert consensus statement on the state of genetic testing for the channelopathies HRS/EHRA 2011 (S1.4-26)
and cardiomyopathies
Expert consensus statement on the management of cardiovascular implantable electronic HRS 2010 (S1.4-27)
devices (CIEDs) in patients nearing end of life or requesting withdrawal of therapy
Recommendations for the standardization and interpretation of the electrocardiogram: AHA/ACCF/HRS 2009 (S1.4-28)
part III: intraventricular conduction disturbances: a scientific statement
Recommendations for the standardization and interpretation of the electrocardiogram: AHA/ACCF/HRS 2009 (S1.4-29)
part V: electrocardiogram changes associated with cardiac chamber hypertrophy:
a scientific statement
*Focused Update.
AATS indicates American Association for Thoracic Surgery; ACC, American College of Cardiology; ACCF, American College of Cardiology Foundation; AHA, American Heart Asso-
ciation; EHRA, European Heart Rhythm Association; ESC, European Society of Cardiology; HRS, Heart Rhythm Society; PACES, Pediatric & Congenital Electrophysiology Society; PCNA,
Preventive Cardiovascular Nurses Association; SCAI, Society for Cardiovascular Angiography and Interventions; and STS, Society of Thoracic Surgeons.
Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or
TABLE 2
Diagnostic Testing in Patient Care* (Updated August 2015)
2. EPIDEMIOLOGY AND DEFINITIONS
2.1. Definitions
See Table 3.
TABLE 3 Table of Definitions
Term Definition or Description
Sinus node dysfunction (with n Sinus bradycardia: Sinus rate <50 bpm
accompanying symptoms)
n Ectopic atrial bradycardia: Atrial depolarization attributable to an atrial pacemaker other than the sinus node with a
rate <50 bpm
n Sinoatrial exit block: Evidence that blocked conduction between the sinus node and adjacent atrial tissue is present.
Multiple electrocardiographic manifestations including “group beating” of atrial depolarization and sinus pauses.
n Sinus pause: Sinus node depolarizes >3 s after the last atrial depolarization
n Sinus node arrest: No evidence of sinus node depolarization
n Tachycardia-bradycardia (“tachy-brady”) syndrome: Sinus bradycardia, ectopic atrial bradycardia, or sinus pause
alternating with periods of abnormal atrial tachycardia, atrial flutter, or AF (S2.1-1). The tachycardia may be
associated with suppression of sinus node automaticity and a sinus pause of variable duration when the tachycardia
terminates.
n Chronotropic incompetence: Broadly defined as the inability of the heart to increase its rate commensurate with
increased activity or demand, in many studies translates to failure to attain 80% of expected heart rate reserve
during exercise.
n Isorhythmic dissociation: Atrial depolarization (from either the sinus node or ectopic atrial site) is slower than
ventricular depolarization (from an atrioventricular nodal, His bundle, or ventricular site).
Atrioventricular block (S2.1-2) n First-degree atrioventricular block: P waves associated with 1:1 atrioventricular conduction and a PR interval >200
ms (this is more accurately defined as atrioventricular delay because no P waves are blocked)
n Second-degree atrioventricular block: P waves with a constant rate (<100 bpm) where atrioventricular conduction is
present but not 1:1
n Mobitz type I: P waves with a constant rate (<100 bpm) with a periodic single nonconducted P wave associated
with P waves before and after the nonconducted P wave with inconstant PR intervals
n Mobitz type II: P waves with a constant rate (< 100 bpm) with a periodic single nonconducted P wave associated
with other P waves before and after the nonconducted P wave with constant PR intervals (excluding 2:1
atrioventricular block)
n 2:1 atrioventricular block: P waves with a constant rate (or near constant rate because of ventriculophasic sinus
arrhythmia) rate (<100 bpm) where every other P wave conducts to the ventricles
n Advanced, high-grade or high-degree atrioventricular block: $2 consecutive P waves at a constant physiologic
rate that do not conduct to the ventricles with evidence for some atrioventricular conduction
n Third-degree atrioventricular block (complete heart block): No evidence of atrioventricular conduction
n Vagally mediated atrioventricular block: Any type of atrioventricular block mediated by heightened para-
sympathetic tone
n Infranodal block: atrioventricular conduction block where clinical evidence or electrophysiologic evidence suggests
that the conduction block occurs distal to the atrioventricular node
Conduction tissue disease (S2.1-2) n RBBB (as defined in adults):
n Complete RBBB
1. QRS duration $120 ms
2. rsr0 , rsR0 , rSR 0 , or rarely a qR in leads V1 or V2 . The R0 or r0 deflection is usually wider than the initial R wave. In
a minority of patients, a wide and often notched R wave pattern may be seen in lead V 1 and/or V2 .
3. S wave of greater duration than R wave or >40 ms in leads I and V 6 in adults
4. Normal R peak time in leads V 5 and V 6 but >50 ms in lead V 1
n Incomplete RBBB: Same QRS morphology criteria as complete RBBB but with a QRS duration between 110 and
119 ms
n LBBB (as defined in adults):
n Complete LBBB:
1. QRS duration $120 ms in adults
2. Broad notched or slurred R wave in leads I, aVL, V 5 , and V 6 and an occasional RS pattern in V 5 and V 6
attributed to displaced transition of QRS complex
3. Absent Q waves in leads I, V5 , and V 6 , but in the lead aVL, a narrow Q wave may be present in the absence of
myocardial pathology
4. R peak time >60 ms in leads V5 and V 6 but normal in leads V 1 , V 2 , and V3, when small initial R waves can be
discerned in the precordial leads
5. ST and T waves usually opposite in direction to QRS
n Incomplete LBBB:
1. QRS duration between 110 and 119 ms in adults
2. Presence of left ventricular hypertrophy pattern
3. R peak time >60 ms in leads V4, V 5 , and V6
4. Absence of Q wave in leads I, V 5 , and V6
Continued on the next page

TABLE 3 Continued
Term Definition or Description
n Nonspecific intraventricular conduction delay (as defined in adults): QRS duration >110 ms where morphology
criteria for RBBB or LBBB are not present
n Left anterior fascicular block:
n QRS duration <120 ms
n Frontal plane axis between 45 and 90
n qR (small r, tall R) pattern in lead aVL
n R-peak time in lead aVL of $45 ms
n rS pattern (small r, deep S) in leads II, III, and aVF
n Left posterior fascicular block:
n QRS duration <120 ms
n Frontal plane axis between 90 and 180 in adults. Because of the more rightward axis in children up to 16 years
of age, this criterion should only be applied to them when a distinct rightward change in axis is documented.
n rS (small r, deep S) pattern in leads I and aVL
n qR (small q, tall R) pattern in leads III and aVF
Maximum predicted heart rate for age calculated as 220 – age (y).
AF indicates atrial fibrillation; bpm, beats per minute; LBBB, left bundle branch block; and RBBB, right bundle branch block.
3. GENERAL EVALUATION OF PATIENTS WITH

DOCUMENTED OR SUSPECTED BRADYCARDIA
OR CONDUCTION DISORDERS
3.1. History and Physical Examination of Patients With

Conduction Disorders
Recommendation for History and Physical Examination in Patients With Documented or Suspected Bradycardia or
COR LOE RECOMMENDATION
1. In patients with suspected bradycardia or conduction disorders a comprehensive history and physical
I C-EO examination should be performed.
See Figure 1 for the evaluation of bradycardia and conduction disorders in Table 4, and conditions associated
conduction disease algorithm, Figure 2 for the initial with bradycardia and conduction disorders in Table 5.
evaluation of suspected or documented sinus node
dysfunction algorithm, Figure 3 for the initial evaluation of 3.2. Noninvasive Evaluation
suspected atrioventricular block algorithm, a list of 3.2.1. Resting ECG in Patients With Documented or
medications that can induce/exacerbate bradycardia or Suspected Bradycardia or Conduction Disorders
Recommendation for Electrocardiogram (ECG) in Patients With Documented or Suspected Bradycardia or Conduction Disorders
Referenced studies that support the recommendation are summarized in Online Data Supplement 1.
1. In patients with suspected bradycardia or conduction disorder, a 12-lead ECG is recommended to docu-
I B-NR ment rhythm, rate, and conduction, and to screen for structural heart disease or systemic illness (S3.2.1-1–
S3.2.1-4).
F I G U R E 1 Evaluation of Bradycardia and Conduction Disease Algorithm
Patient with symptoms suggestive of

or consistent with bradycardia or
conduction disorder
Comprehensive history
and physical examination Sleep apnea?
(Class I)
ECG Directed blood testing

(Class I) (Class IIa)
Conduction disorder with

SND* AV Block Nondiagnostic
1:1 AV conduction
Echocardiography
SND Diagnostic AV Block Conduction disorder
if structural heart
algorithm† Diagnostic algorithm‡ Diagnostic algorithm §
disease suspected
Exercise-related
symptoms
Yes
No Infrequent
Exercise ECG testing Symptoms ICM
(Class IIa) (>30 days) (Class IIa)
Abnormal Normal
Ambulatory ECG
monitoring║
(Class I)
Significant arrythmias
No significant
arrhythmias
Conduction disorder
SND AV Block with 1:1 AV conduction Observation
Continued
SND Diagnostic AV Block Conduction disorder concern for
algorithm† Diagnostic algorithm‡ Diagnostic algorithm§ bradycardia?
Colors correspond to Class of Recommendation in Table 2. See Section 4 in the full-text guideline for discussion. Dashed lines indicate possible optional
strategies based on the specific clinical situation. *Sinus bradycardia, ectopic atrial rhythm, junctional rhythm, sinus pause. †Refer to Section 3.3.2. Figure 2.
‡Refer to Section 3.3.2. Figure 3. §Refer to Section 6.1. Figure 8. kMonitor choice based on the frequency of symptoms. AV indicates atrioventricular; and
ECG, electrocardiogram/electrocardiographic.
F I G U R E 2 Initial Evaluation of Suspected or Documented Sinus Node Dysfunction Algorithm
Evidence for sinus

node dysfunction*
Reversible or
physiologic cause
Treat underlying cause as
needed, e.g., sleep apnea Yes No
(Class I)
Treatment
effective or
unnecessary
Suspicion for
Yes structural heart
No disease
Observe
Yes
Transthoracic
echocardiography
(Class IIa)
No
Suspicion
for infiltrative CM,
endocarditis,
ACHD
Yes
No
Advanced imaging†
(Class IIa)
Treat identified
abnormalities
Symptoms
No Observe
Yes
Exercise
related
Yes No
If not already performed:
Exercise ECG testing
(Class IIa)
Diagnostic
If not already performed:
No Ambulatory ECG monitoring
(Class I)
Yes
Electrophysiology study†
(if performed for other reasons)
(Class IIb)
Sinus node dysfunction

treatment algorithm‡
Colors correspond to Class of Recommendation in Table 2. See Section 4 in the full-text guideline for discussion. *Sinus pauses, sinus bradycardia, junctional
rhythm, ectopic atrial rhythm (all with heart rates <50 bpm) while awake. †The electrophysiology test should not be done primarily for sinus node
dysfunction. If electrophysiology testing is being performed for another reason (e.g. risk stratification for sudden cardiac death), evaluation of sinus node
function may be useful to help inform whether an atrial lead for atrial pacing would have potential benefits. ‡Refer to Section 4.3.4.1., Figure 6. ACHD
indicates adult congenital heart disease; CM, cardiomyopathy; and ECG, electrocardiogram/electrocardiographic.
F I G U R E 3 Initial Evaluation of Suspected Atrioventricular Block Algorithm
Evidence for AV
Block
Reversible or
Physiologic cause
Yes No
Treat underlying cause as
needed, e.g., sleep apnea
(Class I)
Treatment
effective or not
necessary
Mobitz
type II 2° AV Block,
No Advanced AV Block,
Yes complete heart
block
Observe
Yes No
Transthoracic
echocardiography Suspicion for
(Class I) structural heart
disease
Suspicion Yes
for infiltrative CM,
endocarditis, ACHD,
etc. Suspicion
for infiltrative CM, No
Yes endocarditis, ACHD,
Advanced No etc.
imaging*
(Class IIa) Yes No
AV block
treatment Advanced Transthoracic
algorithm† imaging* echocardiography
(Class IIa) (Class IIa)
Treat identified
abnormalities
Determine
site of AV
AV node‡ Block
Unclear
Infranodal (Mobitz Type I)
e.g. 2:1 AV Block
Symptoms Symptoms
Exercise testing
Yes No Infranodal No
(Class IIa) Yes
Electrophysiology
study Infranodal
(Class IIb)
AV block AV block AV node AV block AV block

treatment treatment treatment treatment
algorithm† algorithm† Observe algorithm† algorithm† Observe
Colors correspond to Class of Recommendation in Table 2. *Targeted Advanced Imaging—Magnetic Resonance Imaging (MRI): Amyloidosis, myocarditis,
hemochromatosis, sarcoidosis, CHD, sinus of Valsalva aneurysm, aortic dissection, arrhythmogenic right ventricular cardiomyopathy; fluoro-deoxy-glucose
(fludeoxyglucose)-positron emission tomography (FDG PET): sarcoidosis; 99m technetium pyrophosphate (Tc PYP) or 99m technetium 3,3-diphosphono-1,2-
propanodicarboxylic acid (TC-DPD): Transthyretin (TTR) amyloidosis; cardiac computed tomography (CT): CHD, sinus of Valsalva aneurysm, aortic dissection,
arrhythmogenic right ventricular cardiomyopathy; echo longitudinal strain: Amyloidosis; transesophageal echocardiogram (TEE): Endocarditis, sinus of
Valsalva aneurysm, aortic dissection, CHD. †Refer to Section 5.3., Figure 7. ‡The atrioventricular node is more likely the site of block with second-degree
Mobitz type I atrioventricular block and a narrow QRS complex or severe first-degree atrioventricular block (>0.30 s) with a narrow QRS complex. AV
indicates atrioventricular; ACHD, adult congenital heart disease; CHD, congenital heart disease; and CM, cardiomyopathy.
TABLE 4 Medications That Can Induce/Exacerbate Bradycardia or Conduction Disorders
Antihypertensive Antiarrhythmic Psychoactive Other
n Beta adrenergic receptor blockers (including beta n Adenosine n Donepezil n Anesthetic drugs
adrenergic blocking eye drops used for glaucoma) n Amiodarone n Lithium (propofol)
n Clonidine n n n Cannabis
Dronedarone Opioid analgesics
n Methyldopa n n n Digoxin
Flecainide Phenothiazine antiemetics and antipsychotics
n Non-dihydropyridine calcium channel blockers n n n Ivabradine
Procainamide Phenytoin
n Reserpine n n n Muscle relaxants (e.g.,
Propafenone Selective serotonin reuptake inhibitors
succinylcholine)
n Quinidine n Tricyclic antidepressants
n Sotalol
TABLE 5 Conditions Associated With Bradycardia and Conduction Disorders
Intrinsic
Cardiomyopathy (ischemic or nonischemic)
Congenital heart disease
Degenerative fibrosis
Infection/inflammation
n Chagas disease
n Diphtheria
n Infectious endocarditis
n Lyme disease
n Myocarditis
n Sarcoidosis
n Toxoplasmosis
Infiltrative disorders
n Amyloidosis
n Hemochromatosis
n Lymphoma
Ischemia/infarction
Rheumatological conditions
n Rheumatoid arthritis
n Scleroderma
n Systemic lupus erythematosus
Surgical or procedural trauma

n Cardiac procedures such as ablation or cardiac catheterization
n Congenital heart disease surgery
n Septal myomectomy for hypertrophic obstructive cardiomyopathy
n Valve surgery (including percutaneous valve replacement)
Extrinsic
Autonomic perturbation
n Carotid sinus hypersensitivity
n Neurally-mediated syncope/presyncope
n Physical conditioning
n Situational syncope
n Cough
n Defecation
n Glottic stimulation
n Medical procedures
n Micturition
n Vomiting
n Sleep (with or without sleep apnea)
Metabolic
n Acidosis
n Hyperkalemia
n Hypokalemia
n Hypothermia
n Hypothyroidism
n Hypoxia
Adapted with permission from Mangrum and DiMarco (S3.1-1) and Vogler et al. (S3.1-2).
3.2.2. Exercise Electrocardiographic Testing in Patients With

Documented or Suspected Bradycardia or Conduction
Disorders
Recommendations for Exercise Electrocardiographic Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorders
Referenced studies that support recommendations are summarized in Online Data Supplement 2.
COR LOE RECOMMENDATIONS
1. In patients with suspected chronotropic incompetence, exercise electrocardiographic testing is reasonable

IIa B-NR to ascertain the diagnosis and provide information on prognosis (S3.2.2-1, S3.2.2-2).
2. In patients with exercise-related symptoms suspicious for bradycardia or conduction disorders, or in

IIa C-LD patients with 2:1 atrioventricular block of unknown level, exercise electrocardiographic testing is
reasonable (S3.2.2-3, S3.2.2-4).
3.2.3. Ambulatory Electrocardiography in Patients With

Documented or Suspected Bradycardia or Conduction
Disorders
Recommendation for Ambulatory Electrocardiography in Patients With Documented or Suspected Bradycardia or Conduction Disorders
1. In the evaluation of patients with documented or suspected bradycardia or conduction disorders, cardiac
I B-NR rhythm monitoring is useful to establish correlation between heart rate or conduction abnormalities with
symptoms, with the specific type of cardiac monitor chosen based on the frequency and nature of
symptoms, as well as patient preferences (S3.2.3-1–S3.2.3-12).
See Table 6, cardiac rhythm monitors, for monitor types,

descriptions, and patient selection.
TABLE 6 Cardiac Rhythm Monitors
Types of Monitor Device Description Patient Selection
Nonphysician prescribed n Commercially available smartphone–based systems Patient access to the technology
smartphone-based
n Can record a rhythm strip when the patient has symptoms or
systems
continuously depending on the technology
Holter monitor n Continuous recording for 24–72 h; up to 2 wk with newer models Symptoms frequent enough to be detected within a short period (24–
72 h) of monitoring
n Symptom rhythm correlation can be achieved through a patient
event diary and patient-activated annotations
Patient-activated, A recording device that transmits patient-activated data (live or stored) n Frequent, spontaneous symptoms likely to recur within 2–6
transtelephonic via an analog telephone line to a central remote monitoring station wk
monitor (event (e.g., physician office)
n Limited use in patients with incapacitating symptoms
monitor)
External loop recorder n A device that continuously records and stores rhythm data over Frequent, spontaneous symptoms potentially related to bradycardia
(patient or auto weeks to months or conduction disorder, likely to recur within 2–6 wk
triggered)*
n Patient activated, or auto triggered (e.g., to record asymptomatic
arrhythmias) to provide a recording of events antecedent to (3–14
min), during, and after (1–4 min) the triggered event
n Newer models are equipped with a cellular telephone, which
transmits triggered data automatically over a wireless network to
a remote monitoring system

TABLE 6 Continued
Types of Monitor Device Description Patient Selection
External patch n Patch device that continuously records and stores rhythm data, n Can be considered as an alternative to external loop recorder
recorders with patient-trigger capability to allow for symptom-rhythm n Given that it is leadless, can be accurately self-applied, and is
correlation largely water resistant, it may be more comfortable and less
n No leads or wires, and adhesive to chest wall/sternum cumbersome than an external loop recorder, potentially
n Various models record from 2–14 d improving compliance
n n Unlike Holter monitors and other external monitors, it offers
Offers accurate means of assessing burden of AF
only 1-lead recording
n Patient activated, or auto triggered (e.g., to record asymptomatic
arrhythmias) to provide a recording of events antecedent to,
during, and after the triggered event
Mobile cardiac n Device that records and transmits data (up to 30 d) from pre- n Spontaneous symptoms, potentially related to bradycardia or
outpatient programmed arrhythmias or patient activation to a communica- conduction disorder, that are too brief, too subtle, or too
telemetry tion hub at the patient’s home infrequent to be readily documented with patient activated
n Significant arrhythmias are detected; the monitor automatically monitors
transmits the patient’s electrocardiographic data through a n In high-risk patients whose rhythm requires real-time
wireless network to the central monitoring station, which is monitoring
attended by trained technicians 24 h/d
Implantable cardiac monitor n Subcutaneously implanted device, with a battery life of 2-3 y n Recurrent, infrequent, unexplained symptoms, potentially
n Triggered by the patient (or often family member witness) to related to bradycardia or conduction disorder after a non-
store the event diagnostic initial workup, with or without structural heart
disease
n Models allow for transtelephonic transmission, as well as auto-
mated detection of significant arrhythmias with remote
monitoring
*Higher yield in patients who are able to record a diary to correlate with possible arrhythmia. Adapted with permission from Shen et al. (S3.2.3-13).
AF indicates atrial fibrillation.
3.2.4. Imaging in Patients With Documented or

Suspected Bradycardia or Conduction Disorders
Recommendations for Cardiac Imaging in Bradycardia or Conduction Disorders

Referenced studies that support recommendations are summarized in Online Data Supplements 3 and 4.
1. In patients with newly identified left bundle branch block (LBBB), second-degree Mobitz type II atrioventricular
I B-NR block, high-grade atrioventricular block, or third-degree atrioventricular block with or without apparent structural
heart disease or coronary artery disease, transthoracic echocardiography is recommended (S3.2.4-1–S3.2.4-10).
2. In selected patients presenting with bradycardia or conduction disorders other than LBBB, second-degree Mobitz
IIa B-NR type II atrioventricular block, high-grade atrioventricular block, or third-degree atrioventricular block, trans-
thoracic echocardiography is reasonable if structural heart disease is suspected (S3.2.4-3, S3.2.4-11–S3.2.4-13).
3. In selected patients with bradycardia or bundle branch block, disease-specific advanced imaging (e.g., trans-
IIa C-LD esophageal echocardiography, computed tomography, cardiac magnetic resonance imaging, or nuclear imaging) is
reasonable if structural heart disease is suspected yet not confirmed by other diagnostic modalities (S3.2.4-14–
S3.2.4-22).
4. In the evaluation of patients with asymptomatic sinus bradycardia or first-degree atrioventricular block and no
III: No B-NR
Benefit clinical evidence of structural heart disease, routine cardiac imaging is not indicated (S3.2.4-22–S3.2.4-24).
3.2.5. Laboratory Testing in Patients With Documented or

Recommendation for Laboratory Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorders
1. In patients with bradycardia, laboratory tests (e.g., thyroid function tests, Lyme titer, potassium, pH)
IIa C-LD based on clinical suspicion for a potential underlying cause are reasonable (S3.2.5-1–S3.2.5-4).
3.2.6. Genetic Testing in Patients With Documented or

Recommendations for Genetic Testing in Documented or Suspected Bradycardia or Conduction Disorders
1. In patients in whom a conduction disorder-causative mutation has been identified, genetic counseling and
I C-EO mutation-specific genetic testing of first-degree relatives is recommended to identify similarly affected
individuals.
2. In patients with inherited conduction disease, genetic counseling and targeted testing may be considered
IIb C-EO to facilitate cascade screening of relatives as part of the diagnostic evaluation.
3.2.7. Sleep Apnea Evaluation and Treatment in Patients

With Documented or Suspected Bradycardia or
Recommendation for Sleep Apnea Evaluation and Treatment in Patients With Documented or Suspected Bradycardia or Conduction Disorders
1. In patients with documented or suspected bradycardia or conduction disorder during sleep, screening for
I B-NR symptoms of sleep apnea syndrome is recommended with subsequent confirmatory testing directed by
clinical suspicion (S3.2.7-1–S3.2.7-11).
2. In patients with sleep-related bradycardia or conduction disorder and documented obstructive sleep
I B-NR apnea, treatment directed specifically at the sleep apnea (e.g. continuous positive airway pressure and
weight loss) is recommended (S3.2.7-12–S3.2.7-16).
3. In patients who have previously received or are being considered for a permanent pacemaker for bradycardia or
IIa B-NR conduction disorder, screening for sleep apnea syndrome is reasonable (S3.2.7-10, S3.2.7-11).
3.3. Invasive Testing

3.3.1. Implantable Cardiac Monitor in Patients With Documented
or Suspected Bradycardia or Conduction Disorders
Recommendation for Implantable Cardiac Monitor in Patients With Documented or Suspected Bradycardia or Conduction Disorders
1. In patients with infrequent symptoms (>30 days between symptoms) suspected to be caused by brady-
IIa C-LD cardia, long-term ambulatory monitoring with an implantable cardiac monitor is reasonable if initial
noninvasive evaluation is nondiagnostic (S3.3.1-1–S3.3.1-3).
3.3.2. Electrophysiology Study in Patients With Documented or

Recommendation for Electrophysiology Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorders
1. In patients with symptoms suspected to be attributable to bradycardia, an electrophysiology study (EPS)

IIb C-LD may be considered in selected patients for diagnosis of, and elucidation of bradycardia mechanism, if
initial non-invasive evaluation is nondiagnostic (S3.3.2-1–S3.3.2-5).
4. BRADYCARDIA ATTRIBUTABLE TO
SINUS NODE DYSFUNCTION
4.1. Acute Management of Sinus Node Dysfunction

See Figure 4 for an acute bradycardia algorithm.
F I G U R E 4 Acute Bradycardia Algorithm
Acute
Bradycardia
VS, H+P, ECG

Assessment of stability
Assess for and treat

reversible causes
(COR I)
Moderate Evaluation and

or severe symptoms No
observation
Yes
Atropine*
(Class IIa)
Drug
Type? Yes
Toxicity?†
Calcium channel Beta Digoxin

blocker blocker
No
IV Calcium Anti-digoxin Fab
(COR IIa) (COR IIa)
IV Glucagon
(COR IIa)
High dose Insulin Continued

(COR IIa) symptoms?
Yes
Acute Pacing Severe symptoms/

Yes hemodynamically
Algorithm‡
unstable
No
MI with Aminophylline
Yes
AV Block? (COR IIb)
No
Beta-agonists
(COR IIb)
Yes
Continued
symptoms?
Yes
Acute Pacing
Algorithm‡
Colors correspond to Class of Recommendation in Table 2. See Sections 5.3. and 6.3. in the full-text guideline for discussion. *Atropine should not be given in
patients after heart transplant. †In patients with drug toxicity and severe symptoms, preparation for pacing should proceed simultaneously with pharma-
cologic treatment of drug toxicity. ‡Refer to Section 4.1.3., Figure 5. AADs indicates anti-arrhythmic drugs; AV, atrioventricular; BB, beta blocker; CCB,
calcium channel blocker; COR, Class of Recommendation; ECG, electrocardiographic; HþP, history and physical examination; IMI, inferior myocardial
infarction; IV, intravenous; PM, pacemaker; S/P, status post; and VS, vital signs.
4.1.1. Acute Management of Reversible Causes of

Sinus Node Dysfunction
See Table 7 for common potentially reversible or treatable
causes of SND.
Recommendation for Acute Management of Reversible Causes for Bradycardia Attributable to Sinus Node Dysfunction
1. In symptomatic patients presenting with sinus node dysfunction (SND), evaluation and treatment of
I C-EO reversible causes is recommended.
TABLE 7 Common Potentially Reversible or Treatable Causes of SND (S4.1.1-1)
Acute myocardial ischemia or infarction (S4.1.1-2–S4.1.1-4)
Athletic training (S4.1.1-5)
Atrial fibrillation (S4.1.1-6)
Cardiac surgery
n Valve replacement (S4.1.1-7, S4.1.1-8), maze procedure (S4.1.1-7), coronary artery bypass graft (S4.1.1-9, S4.1.1-10)
Drugs or toxins*
n Toluene, organophosphates, tetrodotoxin, cocaine (S4.1.1-11)
Electrolyte abnormality
n Hyperkalemia (S4.1.1-12), hypokalemia (S4.1.1-13), hypoglycemia (S4.1.1-14)
Heart transplant (S4.1.1-15): Acute rejection, chronic rejection, remodeling (S4.1.1-16, S4.1.1-17)
Hypervagotonia (S4.1.1-18, S4.1.1-19)
Hypothermia
n Therapeutic (post-cardiac arrest cooling (S4.1.1-20)) or environmental exposure (S4.1.1-21)
Hypothyroidism (S4.1.1-22)
Hypovolemic shock (S4.1.1-23)
Hypoxemia, hypercarbia, acidosis (S4.1.1-24)

n Sleep apnea, respiratory insufficiency (suffocation, drowning (S4.1.1-25), stroke (S4.1.1-26), drug overdose)
Infection (S4.1.1-27)
n Lyme disease (S4.1.1-28), legionella, psittacosis, typhoid fever, typhus, listeria (S4.1.1-29), malaria, leptospirosis, Dengue fever, viral hemorrhagic fevers,
Guillain-Barre (S4.1.1-30)
Medications*
n Beta blockers, non-dihydropyridine calcium channel blockers, digoxin (S4.1.1-31), antiarrhythmic drugs, lithium (S4.1.1-32), methyldopa, risperidone,
cisplatin, interferon
*Partial list.
SND indicates sinus node dysfunction.
4.1.2. Acute Medical Therapy for Bradycardia

4.1.2.1. Atropine and Beta-Agonists for Bradycardia
Attributable to SND
See Table 8 for acute medical management of bradycardia
attributable to SND or atrioventricular block.
Recommendations for Atropine and Beta-Agonists for Bradycardia Attributable to SND

Referenced studies that support recommendations are summarized in Online Data Supplements 8, 9, 10, and 11.
1. In patients with SND associated with symptoms or hemodynamic compromise, atropine is reasonable to
IIa C-LD increase sinus rate (S4.1.2.1-1–S4.1.2.1-4).
2. In patients with SND associated with symptoms or hemodynamic compromise who are at low likelihood of
IIb C-LD coronary ischemia, isoproterenol, dopamine, dobutamine, or epinephrine may be considered to increase
heart rate and improve symptoms (S4.1.2.1-5–S4.1.2.1-11).
3. In patients who have undergone heart transplant without evidence for autonomic reinnervation, atropine
III: Harm C-LD should not be used to treat sinus bradycardia (S4.1.2.1-12, S4.1.2.1-13).
TABLE 8 Acute Medical Management of Bradycardia Attributable to SND or Atrioventricular Block
Medication Dosage Comments
Symptomatic sinus bradycardia or atrioventricular block
Atropine 0.5-1 mg IV (may be repeated every 3-5 min to a maximum dose

of 3 mg) (S4.1.2.4-8–S4.1.2.4-12)
Dopamine 5 to 20 mcg/kg/min IV. starting at 5 mcg/kg/min and increasing Dosages of >20 mcg/kg/min may result in vasoconstriction or
by 5 mcg/kg/min every 2 min (S4.1.2.4-13) arrhythmias
Isoproterenol 20-60 mcg IV bolus followed doses of 10-20 mcg, or infusion of Monitor for potential development of ischemic chest pain
1-20 mcg/min based on heart rate response (S4.1.2.4-14–
S4.1.2.4-20)
Epinephrine 2-10 mcg/min IV or 0.1-0.5 mcg/kg/min IV titrated to desired

effect (S4.1.2.4-19, S4.1.2.4-21)
Second- or third-degree atrioventricular block associated with acute inferior MI
Aminophylline 250-mg IV bolus
Calcium channel blocker overdose
10% calcium chloride 1-2 g IV every 10-20 min or an infusion of 0.2-0.4 mL/kg/h
(S4.1.2.4-22–S4.1.2.4-24)
10% calcium gluconate 3-6 g IV every 10-20 min or an infusion at 0.6-1.2 mL/kg/h
(S4.1.2.4-22–S4.1.2.4-24)
Beta-blocker or calcium channel blocker overdose
Glucagon 3-10 mg IV with infusion of 3-5 mg/h (S4.1.2.4-25, S4.1.2.4-26)
High dose insulin IV bolus of 1 unit/kg followed by an infusion of 0.5 units/kg/h Follow glucose and potassium levels
therapy (S4.1.2.4-24, S4.1.2.4-27, S4.1.2.4-28).
Digoxin overdose
Digoxin antibody Dosage is dependent on amount ingested or known digoxin n One vial binds approximately 0.5 mg of digoxin.
fragment concentration (S4.1.2.4-29–S4.1.2.4-36) n Administer over at least 30 min
n May be repeated
Post-heart transplant
Aminophylline 6 mg/kg in 100-200 mL of IV fluid over 20-30 min
Theophylline 300 mg IV, followed by oral dose of 5-10 mg/kg/d titrated to effect n Therapeutic serum levels range from 10-20 mcg/mL
n Usual posttransplant dosages average 450 mg100 mg/d
Spinal cord injury
Aminophylline 6 mg/kg in 100-200 mL of IV fluid over 20-30 min (S4.1.2.4-7)
Theophylline Oral dose of 5-10 mg/kg/d titrated to effect (S4.1.2.4-6) Effective dosages often result in serum levels below the usual
effective range of 10-20 mcg/mL
IV indicates intravenous; MI, myocardial infarction; and SND, sinus node dysfunction.
4.1.2.2. Therapy of Beta Blocker and Calcium Channel Blocker

Mediated Bradycardia Attributable to SND or
Atrioventricular Block
Recommendations for Therapy of Beta Blocker and Calcium Channel Blocker Mediated Bradycardia
1. In patients with bradycardia associated with symptoms or hemodynamic compromise because of calcium
IIa C-LD channel blocker overdose, intravenous calcium is reasonable to increase heart rate and improve symptoms
(S4.1.2.2-1–S4.1.2.2-3).
2. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta-
IIa C-LD blocker or calcium channel blocker overdose, glucagon is reasonable to increase heart rate and improve
symptoms (S4.1.2.2-4, S4.1.2.2-5).
3. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta-
IIa C-LD blocker or calcium channel blocker overdose, high dose insulin therapy is reasonable to increase heart rate
and improve symptoms (S4.1.2.2-6, S4.1.2.2-7).
4.1.2.3. Therapy of Digoxin Mediated Bradycardia

Attributable to Either SND or Atrioventricular Block
Recommendations for Therapy of Digoxin Mediated Bradycardia Attributable to SND or Atrioventricular Block
Referenced studies that support recommendations are summarized in Online Data Supplements 13, 14, and 15.
1. In patients with bradycardia associated with symptoms or hemodynamic compromise in the setting of
IIa C-LD digoxin toxicity, digoxin Fab antibody fragment is reasonable to increase heart rate and improve symp-
toms (S4.1.2.3-1–S4.1.2.3-8).
2. In patients with bradycardia associated with symptoms or hemodynamic compromise attributable to

III: No Benefit C-LD digoxin toxicity, dialysis is not recommended for removal of digoxin (S4.1.2.3-9).
4.1.2.4. Aminophylline or Theophylline for Bradycardia

Attributable to SND
Recommendations for Theophylline/Aminophylline for Bradycardia Attributable to SND

1. In post-heart transplant patients, aminophylline or theophylline is reasonable to increase heart rate if

IIa C-LD clinically indicated (S4.1.2.4-1–S4.1.2.4-4).
2. In patients with SND associated with symptoms or hemodynamic compromise in the setting of acute
IIa C-LD spinal cord injury, aminophylline or theophylline is reasonable to increase heart rate and improve
symptoms (S4.1.2.4-5–S4.1.2.4-7).
4.1.3. Temporary Pacing for Bradycardia Attributable to SND

See Figure 5 for an acute pacing algorithm.
Recommendations for Temporary Pacing for Bradycardia Attributable to SND

1. In patients with persistent hemodynamically unstable SND refractory to medical therapy, temporary
IIa C-LD transvenous pacing is reasonable to increase heart rate and improve symptoms until a permanent pace-
maker is placed or the bradycardia resolves (S4.1.3-1–S4.1.3-15).
2. In patients with SND with severe symptoms or hemodynamic compromise, temporary transcutaneous
IIb C-LD pacing may be considered to increase heart rate and improve symptoms until a temporary transvenous or
permanent pacemaker is placed or the bradycardia resolves (S4.1.3-16–S4.1.3-21).
3. In patients with SND with minimal and/or infrequent symptoms without hemodynamic compromise,
III: Harm C-LD temporary transcutaneous or transvenous pacing should not be performed (S4.1.3-1, S4.1.3-2, S4.1.3-8,
S4.1.3-9, S4.1.3-11, S4.1.3-12, S4.1.3-14, S4.1.3-22).
F I G U R E 5 Acute Pacing Algorithm
Hemodynamic instability
despite medical therapy
Critically
ill due to
bradycardia
Yes No
Permanent
Transcutaneous pacemaker indicated and
pacing (Class IIb) capability immediately
available
Yes No
Implant Permanent Prolonged

pacemaker*† temporary pacing
needed
Yes No
Externalized Temporary
permanent transvenous
pacing lead pacing wire
(Class IIa) (Class IIa)
Colors correspond to Class of Recommendation in Table 2. See Sections 5.4. and 6.3. in the full-text guideline for discussion. *Refer to Section 4.3.4.1.,
Figure 6 for chronic SND and Section 5.3., Figure 7 for chronic atrioventricular block †Careful management of anesthesia to avoid or minimize the use of
drugs associated with bradycardia is required.
4.2. Chronic Therapy/Management of Bradycardia Attributable

to SND
4.2.1. General Principles of Chronic Therapy/Management of
Bradycardia Attributable to SND
Referenced studies that support recommendations are
summarized in Online Data Supplements 22 and 23.
Recommendations for General Principles of Chronic Therapy/Management of Bradycardia Attributable to SND
1. In asymptomatic individuals with sinus bradycardia or sinus pauses that are secondary to physiologically
III: Harm C-LD elevated parasympathetic tone, permanent pacing should not be performed (S4.2.1-1–S4.2.1-7).
2. In patients with sleep-related sinus bradycardia or transient sinus pauses occurring during sleep,
III: Harm C-LD permanent pacing should not be performed unless other indications for pacing are present
(S4.2.1-1–S4.2.1-7).
3. In patients with asymptomatic SND, or in those in whom the symptoms have been documented to occur in
III: Harm C-LD the absence of bradycardia or chronotropic incompetence, permanent pacing should not be performed
(S4.2.1-5–S4.2.1-7).
4.2.2. Transient/Reversible Causes (Including Medications) of

Recommendation for Transient/Reversible Causes of Sinus Bradycardia
1. Patients presenting with symptomatic SND secondary to a reversible cause should first be managed by
I C-EO directing the therapy at eliminating or mitigating the offending condition.
4.2.3. Additional Testing of Bradycardia Attributable to SND
Recommendations for Additional Testing of Bradycardia Attributable to SND
1. In patients with symptoms suggestive of bradycardia (e.g., syncope, lightheadedness) who are also un-
IIb C-EO dergoing an EPS for another indication, evaluation of sinus node function as part of the EPS may be
considered.
2. In symptomatic patients with suspected SND, EPS for the assessment of sinus node function may be
IIb C-EO considered when the diagnosis remains uncertain after initial noninvasive evaluations (S4.2.3-1–S4.2.3-5).
3. In patients with asymptomatic sinus bradycardia, an EPS should not be performed unless other indications
III: No Benefit C-LD for electrophysiological testing exist (S4.2.3-6, S4.2.3-7).
4.3.4. Permanent Pacing for Chronic Therapy/Management of

Recommendations for Permanent Pacing for Chronic Therapy/Management of Bradycardia Attributable to SND
1. In patients with symptoms that are directly attributable to SND, permanent pacing is indicated to increase
I C-LD heart rate and improve symptoms (S4.3.4-1, S4.3.4-2).
2. In patients who develop symptomatic sinus bradycardia as a consequence of guideline-directed man-

I C-EO agement and therapy for which there is no alternative treatment and continued treatment is clinically
necessary, permanent pacing is recommended to increase heart rate and improve symptoms.
3. For patients with tachy-brady syndrome and symptoms attributable to bradycardia, permanent pacing is
IIa C-EO reasonable to increase heart rate and reduce symptoms attributable to hypoperfusion.
4. In patients with symptomatic chronotropic incompetence, permanent pacing with rate-responsive pro-
IIa C-EO gramming is reasonable to increase exertional heart rates and improve symptoms.
5. In patients with symptoms that are likely attributable to SND, a trial of oral theophylline may be
IIb C-LD considered to increase heart rate, improve symptoms, and help determine the potential effects of
permanent pacing (S4.3.4-3, S4.3.4-4).
4.3.4.1. Permanent Pacing Techniques and Methods for

Chronic Therapy/Management of Bradycardia
Attributable to SND
See Figure 6 for the chronic SND management algorithm.
Recommendations for Permanent Pacing Techniques and Methods for Chronic Therapy/Management of Bradycardia
Attributable to SND Referenced studies that support recommendations are summarized in Online Data Supplement 25.
1. In symptomatic patients with SND, atrial-based pacing is recommended over single chamber ventricular
I B-R pacing (S4.3.4.1-1–S4.3.4.1-4).
2. In symptomatic patients with SND and intact atrioventricular conduction without evidence of conduction
I B-R abnormalities, dual chamber or single chamber atrial pacing is recommended (S4.3.4.1-5).
3. In symptomatic patients with SND who have dual chamber pacemakers and intact atrioventricular conduction, it
IIa B-R is reasonable to program the dual chamber pacemaker to minimize ventricular pacing (S4.3.4.1-6).
4. In symptomatic patients with SND in which frequent ventricular pacing is not expected or the patient has
IIa C-EO significant comorbidities that are otherwise likely to determine the survival and clinical outcomes, single
chamber ventricular pacing is reasonable.
F I G U R E 6 Chronic SND Management Algorithm
Sinus node dysfunction
Confirm symptoms
Rule out reversible
causes
Due
to required GDMT
(no reasonable
alternative)
Symptoms
No correlate with
bradycardia
Yes
Yes No (or asymptomatic)

Likely/uncertain
Observation
Permanent pacing Oral theophylline Permanent pacing

(Class I) (Class IIb) (Class III: Harm)
Response
*Infrequent
suggests symptomatic
pacing? Significant
sinus node
comorbidities?
dysfunction?
Yes No No
Yes
Single chamber
Willing to
ventricular pacing
have a PPM?
(Class IIa)
Normal
AV conduction Yes No
and reason to
avoid an RV Oral theophylline
lead? (Class IIb)
Yes No
Single chamber Dual chamber pacing

atrial pacing (Class I)
(Class I)
Program to minimize
ventricular pacing
(Class IIa)
Colors correspond to Class of Recommendation in Table 2. See Sections 4.3. and 5.5. in the full text guideline for discussion. Dashed lines indicate possible
optional strategies based on the specific clinical situation. *Symptomatic patients with very infrequent need for pacing for rate support or patients with
significant comorbidities. AV indicates atrioventricular; GDMT, guideline-directed management and therapy; PPM, permanent pacemaker; and RV, right
ventricular.
5. BRADYCARDIA ATTRIBUTABLE TO
ATRIOVENTRICULAR BLOCK
5.1. Pathophysiology, Etiology, and Classification of

Bradycardia Attributable to Atrioventricular Block
See Table 9 for the etiology of atrioventricular block.
TABLE 9 Etiology of Atrioventricular Block
Congenital/genetic
n Congenital AV block (associated with maternal systemic lupus erythematosus)

n Congenital heart defects (e.g., L-TGA)
n Genetic (e.g., SCN5A mutations)
Infectious
n Lyme carditis
n Bacterial endocarditis with perivalvar abscess
n Acute rheumatic fever
n Chagas disease
n Toxoplasmosis
Inflammatory/infiltrative
n Myocarditis
n Amyloidosis
n Cardiac sarcoidosis
n Rheumatologic disease: Systemic sclerosis, SLE, RA, reactive arthritis (Reiter’s syndrome)
n Other cardiomyopathy—idiopathic, valvular
Ischemic
n Acute MI
n Coronary ischemia without infarction—unstable angina, variant angina
n Chronic ischemic cardiomyopathy
Degenerative
n Lev’s and Lenegre’s diseases
Vagotonic-associated with increased vagal tone
n Sleep, obstructive sleep apnea

n High-level athletic conditioning
n Neurocardiogenic
Metabolic/endocrine
n Acid-base disorders
n Poisoning/overdose (e.g., mercury, cyanide, carbon monoxide, mad honey)
n Thyroid disease (both hypothyroidism and hyperthyroidism)
n Adrenal disease (e.g., pheochromocytoma, hypoaldosteronism)
Other diseases
n Neuromuscular diseases (e.g., myotonic dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy)

n Lymphoma
Iatrogenic
n Medication related
n Beta blockers, verapamil, diltiazem, digoxin
n Antiarrhythmic drugs
n Neutraceuticals
n Catheter ablation
n Cardiac surgery, especially valve surgery
n TAVR, alcohol septal ablation
RA indicates rheumatoid arthritis; MI, myocardial infarction; SLE, systemic lupus erythematosus; and TAVR, transcatheter aortic valve replacement.
5.2. Acute Management

5.2.1. Acute Management of Reversible Causes of Bradycardia
Attributable to Atrioventricular Block
Recommendations for Acute Management of Reversible Causes of Bradycardia Attributable to Atrioventricular Block
1. Patients with transient or reversible causes of atrioventricular block, such as Lyme carditis or drug toxicity,
I B-NR should have medical therapy and supportive care, including temporary transvenous pacing if necessary, before
determination of need for permanent pacing (S5.2.1-1–S5.2.1-5).
2. In selected patients with symptomatic second-degree or third-degree atrioventricular block who are on chronic
IIa B-NR stable doses of medically necessary antiarrhythmic or beta-blocker therapy, it is reasonable to proceed to
permanent pacing without further observation for drug washout or reversibility (S5.2.1-6–S5.2.1-9).
3. In patients with second-degree or third-degree atrioventricular block associated with cardiac sarcoidosis, per-
IIa B-NR manent pacing, with additional defibrillator capability if needed and meaningful survival of greater than 1 year is
expected, without further observation for reversibility is reasonable (S5.2.1-10, S5.2.1-11).
4. In patients with symptomatic second-degree or third-degree atrioventricular block associated with thyroid
IIb C-LD function abnormalities but without clinical myxedema, permanent pacing without further observation for
reversibility may be considered (S5.2.1-12).
5.2.2. Acute Medical Therapy for Bradycardia Attributable to

Atrioventricular Block
Recommendations for Acute Medical Therapy for Bradycardia Attributable to Atrioventricular Block
1. For patients with second-degree or third-degree atrioventricular block believed to be at the atrioventricular nodal
IIa C-LD level associated with symptoms or hemodynamic compromise, atropine is reasonable to improve atrioventricular
conduction, increase ventricular rate, and improve symptoms (S5.2.2-1–S5.2.2-3).
2. For patients with second-degree or third-degree atrioventricular block associated with symptoms or hemody-
IIb B-NR namic compromise and who have low likelihood for coronary ischemia, beta-adrenergic agonists, such as
isoproterenol, dopamine, dobutamine, or epinephrine, may be considered to improve atrioventricular conduction,
increase ventricular rate, and improve symptoms (S5.2.2-3–S5.2.2-7).
3. For patients with second-degree or third-degree atrioventricular block associated with symptoms or hemodynamic
IIb C-LD compromise in the setting of acute inferior myocardial infarction (MI), intravenous aminophylline may be considered to
improve atrioventricular conduction, increase ventricular rate, and improve symptoms (S5.2.2-8–S5.2.2-11).
5.2.3. Temporary Pacing for Atrioventricular Block
Recommendations for Temporary Pacing for Bradycardia Attributable to Atrioventricular Block

1. For patients with second-degree or third-degree atrioventricular block associated with symptoms or hemody-
IIa B-NR namic compromise that is refractory to medical therapy, temporary transvenous pacing is reasonable to increase
heart rate and improve symptoms (S5.2.3-1–S5.2.3-7).
2. For patients who require prolonged temporary transvenous pacing, it is reasonable to choose an externalized
IIa B-NR permanent active fixation lead over a standard passive fixation temporary pacing lead (S5.2.3-8–S5.2.3-14).
3. For patients with second-degree or third-degree atrioventricular block and hemodynamic compromise refractory
IIb B-R to antibradycardic medical therapy, temporary transcutaneous pacing may be considered until a temporary
transvenous or permanent pacemaker is placed or the bradyarrhythmia resolves (S5.2.3-15–S5.2.3-20).
5.3. Chronic Therapy/Management of Bradycardia Attributable

to Atrioventricular Block
See Figure 7 for management of bradycardia or pauses
attributable to chronic atrioventricular block algorithm.
F I G U R E 7 Management of Bradycardia or Pauses Attributable to Chronic Atrioventricular Block Algorithm
Colors correspond to Class of Recommendation in Table 2. Refer to Section 6.4. in the full-text guideline for discussion. *Symptoms correlate with atrio-
ventricular block. †PR interval >240 ms, LBBB. ‡PR interval >240 ms, QRS >120 ms or fascicular block. §Refer to heart failure guidelines (S5.3-1, S5.3-2). AV
indicates atrioventricular; GDMT, guideline directed management and therapy; HF, heart failure; LBBB, left bundle branch block; and LVEF, left ventricular
ejection fraction.
5.3.1. General Principles of Chronic Therapy/Management of

Recommendations for General Principles of Chronic Therapy/Management of Bradycardia Attributable to Atrioventricular Block
1. In patients with first-degree atrioventricular block or second-degree Mobitz type I (Wenckebach) or 2:1
III: Harm C-LD atrioventricular block which is believed to be at the level of the atrioventricular node, with symptoms that
do not temporally correspond to the atrioventricular block, permanent pacing should not be performed
(S5.3-1–S5.3-7).
2. In asymptomatic patients with first-degree atrioventricular block or second-degree Mobitz type I

III: Harm C-LD (Wenckebach) or 2:1 atrioventricular block which is believed to be at the level of the atrioventricular
node, permanent pacing should not be performed (S5.3-4–S5.3-10).
5.3.2. Transient/Potentially Reversible Causes of Atrioventricular

Block
Recommendations for Potentially Reversible or Transient Causes of Atrioventricular Block

1. In patients with symptomatic atrioventricular block attributable to a known reversible cause in whom the
I C-LD atrioventricular block does not resolve despite treatment of the underlying cause, permanent pacing is
recommended (S5.3.2-1–S5.3.2-3).
2. In patients who had acute atrioventricular block attributable to a known reversible and non-recurrent
III: Harm C-LD cause, and have had complete resolution of the atrioventricular block with treatment of the underlying
cause, permanent pacing should not be performed (S5.3.2-1, S5.3.2-4–S5.3.2-9).
3. In patients with asymptomatic vagally mediated atrioventricular block, permanent pacing should not be
III: Harm C-LD performed (S5.3.2-6–S5.3.2-10).
5.3.3. Additional Testing for Chronic Therapy/Management of

Recommendations for Additional Testing for Chronic Therapy/Management of Bradycardia Attributable to Atrioventricular Block
1. In patients with symptoms (e.g., lightheadedness, dizziness) of unclear etiology who have first-degree
IIa B-R atrioventricular block or second-degree Mobitz type I atrioventricular block on ECG, ambulatory
electrocardiographic monitoring is reasonable to establish correlation between symptoms and rhythm
abnormalities (S5.3.3-1–S5.3.3-4).
2. In patients with exertional symptoms (e.g., chest pain, shortness of breath) who have first-degree or
IIa C-LD second-degree Mobitz type I atrioventricular block at rest, an exercise treadmill test is reasonable to
determine whether they may benefit from permanent pacing (S5.3.3-5, S5.3.3-6).
3. In selected patients with second-degree atrioventricular block, an EPS may be considered to determine the level of
IIb B-NR the block and to determine whether they may benefit from permanent pacing (S5.3.3-7–S5.3.3-9).
4. In selected patients with second-degree atrioventricular block, carotid sinus massage and/or pharmacological
IIb C-LD challenge with atropine, isoproterenol, or procainamide may be considered to determine the level of the block and
to determine whether they may benefit from permanent pacing (S5.3.3-10–S5.3.3-12).
5.3.4. Permanent Pacing
Recommendations for Permanent Pacing for Chronic Therapy/Management of Bradycardia Attributable to Atrioventricular Block
1. In patients with acquired second-degree Mobitz type II atrioventricular block, high-grade atrioventricular
I B-NR block, or third-degree atrioventricular block not attributable to reversible or physiologic causes, per-
manent pacing is recommended regardless of symptoms (S5.3.4-1–S5.3.4-7).
2. In patients with neuromuscular diseases associated with conduction disorders, including muscular dys-
I B-NR trophy (such as myotonic dystrophy type 1) or Kearns-Sayre syndrome, who have evidence of second-
degree atrioventricular block, third-degree atrioventricular block, or an HV interval of 70 ms or greater,
regardless of symptoms, permanent pacing, with additional defibrillator capability if needed and mean-
ingful survival of greater than 1 year is expected, is recommended (S5.3.4-8–S5.3.4-15).
3. In patients with permanent atrial fibrillation (AF) and symptomatic bradycardia, permanent pacing is
I C-LD recommended (S5.3.4-2, S5.3.4-16, S5.3.4-17).
4. In patients who develop symptomatic atrioventricular block as a consequence of guideline-directed

I C-LD management and therapy for which there is no alternative treatment and continued treatment is clinically
necessary, permanent pacing is recommended to increase heart rate and improve symptoms (S5.3.4-18–
S5.3.4-24).
5. In patients with an infiltrative cardiomyopathy, such as cardiac sarcoidosis or amyloidosis, and second-
IIa B-NR degree Mobitz type II atrioventricular block, high-grade atrioventricular block, or third-degree atrio-
ventricular block, permanent pacing, with additional defibrillator capability if needed and meaningful
survival of greater than 1 year is expected, is reasonable (S5.3.4-25–S5.3.4-30).
6. In patients with lamin A/C gene mutations, including limb-girdle and Emery-Dreifuss muscular dystro-
IIa B-NR phies, with a PR interval greater than 240 ms and LBBB, permanent pacing, with additional defibrillator
capability if needed and meaningful survival of greater than 1 year is expected, is reasonable (S5.3.4-31–
S5.3.4-33).
7. In patients with marked first-degree or second-degree Mobitz type I (Wenckebach) atrioventricular block
IIa C-LD with symptoms that are clearly attributable to the atrioventricular block, permanent pacing is reasonable
(S5.3.4-34–S5.3.4-37).
8. In patients with neuromuscular diseases, such as myotonic dystrophy type 1, with a PR interval greater
IIb C-LD than 240 ms, a QRS duration greater than 120 ms, or fascicular block, permanent pacing, with additional
defibrillator capability if needed and meaningful survival of greater than 1 year is expected, may be
considered (S5.3.4-9–S5.3.4-13, S5.3.4-15).
5.3.4.1. Permanent Pacing Techniques and Methods for

Chronic Therapy/Management of Bradycardia
Attributable to Atrioventricular Block
Recommendations for Permanent Pacing Techniques and Methods for Chronic Therapy/Management of Bradycardia Attributable to
Atrioventricular Block Referenced studies that support recommendations are summarized in Online Data Supplements 39 and 40 and the
Systematic Review.
1. In patients with SND and atrioventricular block who require permanent pacing, dual chamber pacing is
I A recommended over single chamber ventricular pacing (S5.3.4.1-1–S5.3.4.1-7).
2. In select patients with atrioventricular block who require permanent pacing in whom frequent ventricular
I A pacing is not expected, or who have significant comorbidities that are likely to determine clinical out-
comes and that may limit the benefit of dual chamber pacing, single chamber ventricular pacing is
effective (S5.3.4.1-1–S5.3.4.1-6, S5.3.4.1-8–S5.3.4.1-10).
(continued)
3. For patients in sinus rhythm with a single chamber ventricular pacemaker who develop pacemaker syn-
I B-R drome, revising to a dual chamber pacemaker is recommended (S5.3.4.1-1, S5.3.4.1-2, S5.3.4.1-5,
S5.3.4.1-8–S5.3.4.1-10).
4. In patients with atrioventricular block who have an indication for permanent pacing with a left ventricular
IIa B-RSR ejection fraction between 36% and 50% and are expected to require ventricular pacing more than 40% of
the time, it is reasonable to choose pacing methods that maintain physiologic ventricular activation (e.g.,
cardiac resynchronization therapy [CRT] or His bundle pacing) over right ventricular pacing (S5.3.4.1-7,
S5.3.4.1-11–S5.3.4.1-19)
5. In patients with atrioventricular block who have an indication for permanent pacing with a left ventricular
IIa B-R ejection fraction between 36% and 50% and are expected to require ventricular pacing less than 40% of
the time, it is reasonable to choose right ventricular pacing over pacing methods that maintain physiologic
ventricular activation (e.g., CRT or His bundle pacing) (S5.3.4.1-15, S5.3.4.1-16, S5.3.4.1-20, S5.3.4.1-21).
6. In patients with atrioventricular block at the level of the atrioventricular node who have an indication for
IIb B-RSR permanent pacing, His bundle pacing may be considered to maintain physiologic ventricular activation
(S5.3.4.1-19, S5.3.4.1-22–S5.3.4.1-25).
7. In patients with permanent or persistent AF in whom a rhythm control strategy is not planned, implan-
III: Harm C-LD tation of an atrial lead should not be performed (S5.3.4.1-26, S5.3.4.1-27).
SR indicates systematic review.
6. CONDUCTION DISORDERS (WITH 1:1

ATRIOVENTRICULAR CONDUCTION)
6.1. Evaluation of Conduction Disorders

See Figure 8 for evaluation of conduction disorders algorithm.
Recommendations for Evaluation of Conduction Disorders (With 1:1 Atrioventricular Conduction and Normal PR Interval)
1. In patients with newly detected LBBB, a transthoracic echocardiogram to exclude structural heart disease
I B-NR is recommended (S6.1-1–S6.1-3).
2. In symptomatic patients with conduction system disease, in whom atrioventricular block is suspected,
I C-LD ambulatory electrocardiographic monitoring is useful (S6.1-4–S6.1-11).
3. In selected patients presenting with intraventricular conduction disorders other than LBBB, transthoracic
IIa B-NR echocardiography is reasonable if structural heart disease is suspected (S6.1-3, S6.1-12, S6.1-13).
4. In patients with symptoms suggestive of intermittent bradycardia (e.g., lightheadedness, syncope), with
IIa B-NR conduction system disease identified by ECG and no demonstrated atrioventricular block, EPS is
reasonable (S6.1-14).
5. In selected patients with LBBB in whom structural heart disease is suspected and echocardiogram is
IIa C-LD unrevealing, advanced imaging (e.g., cardiac MRI, computed tomography, or nuclear studies) is reason-
able (S6.1-15).
6. In selected asymptomatic patients with extensive conduction system disease (bifascicular or trifascicular
IIb C-LD block), ambulatory electrocardiographic recording may be considered to document suspected higher
degree of atrioventricular block (S6.1-4, S6.1-6).
7. In selected asymptomatic patients with LBBB in whom ischemic heart disease is suspected, stress testing
IIb C-LD with imaging may be considered (S6.1-2).
F I G U R E 8 Evaluation of Conduction Disorders Algorithm
Evidence for
conduction disorder
Reversible
or Physiologic
cause
Yes
Treat underlying cause as No
needed, e.g., ischemia
Treatment
effective or not
necessary
Genetic
disorder associated
Yes No with conduction
Observe disease
Yes
Y No
o
Conduction disorders Suspicion

treatment algorithm* for infiltrative CM,
endocarditis, ACHD,
etc.
Advanced imaging† Yes
(Class IIb) No
Type
of conduction
disorder
RBBB or fascicular
LBBB
block
Transthoracic Transthoracic
echocardiography echocardiography
(Class I) (Class IIa)
Treat identified
abnormalities
Symptoms
suggestive of intermittent
bradycardia
Y
Yes No
Ambulatory ECG Monitoring‡ Ambulatory ECG Monitoring§

(Class I) (Class IIb)
Electrophysiology study
Observe
(Class IIa)
Colors correspond to Class of Recommendation in Table 2. See Section 7.4. in the full-text guideline for discussion. *Refer to Section 6.2., Figure 9.
†Advanced imaging could include magnetic resonance imaging, computed tomography, or transesophageal echocardiography. ‡Monitor choice based on the
frequency of symptoms. §Extensive conduction disease (e.g., first degree atrioventricular block combined with LBBB). ACHD indicates adult congenital heart
disease; CM, cardiomyopathy; ECG, electrocardiogram/electrocardiographic; LBBB, left bundle branch block; and RBBB, right bundle branch block.
6.2. Management of Conduction Disorders

(With 1:1 Atrioventricular Conduction)
See Figure 9 for management of conduction disorders
algorithm.
Recommendations for Management of Conduction Disorders (With 1:1 Atrioventricular Conduction and Normal PR Intervals)
1. In patients with syncope and bundle branch block who are found to have an HV interval 70 ms or greater
I C-LD or evidence of infranodal block at EPS, permanent pacing is recommended (S6.2-1, S6.2-2)
2. In patients with alternating bundle branch block, permanent pacing is recommended (S6.2-3).
I C-LD
3. In patients with Kearns-Sayre syndrome and conduction disorders, permanent pacing is reasonable, with
IIa C-LD additional defibrillator capability if appropriate and meaningful survival of greater than 1 year is expected
(S6.2-4, S6.2-5).
4. In patients with Anderson-Fabry disease and QRS prolongation greater than 110 ms, permanent pacing,
IIb C-LD with additional defibrillator capability if needed and meaningful survival of greater than 1 year is
expected, may be considered (S6.2-6, S6.2-7).
5. In patients with heart failure, a mildly to moderately reduced left ventricular ejection fraction (36%–
IIb C-LD 50%), and LBBB (QRS ‡150 ms), CRT therapy may be considered (S6.2-8, S6.2-9).
6. In asymptomatic patients with isolated conduction disease and 1:1 atrioventricular conduction, permanent
III: Harm B-NR pacing is not indicated (in the absence of other indications for pacing) (S6.2-10–S6.2-15).
F I G U R E 9 Management of Conduction Disorders Algorithm
Conduction disorder:
BBB or fascicular block with
1:1 AV conduction*
Syncope,
BBB, and
HV >70ms
Permanent pacing
Yes
(Class I)
No
Alternating
BBB
Permanent pacing
Yes
No (Class I)
LVEF 36-50%, LBBB,

QRS >150 ms, and Class II or
greater HF symptoms
Cardiac resynchronization
Yes therapy
No
(Class IIb)
Symptoms
suggest intermittent
AV block?
Yes No
AV block diagnostic
Observation
algorithm†
Colors correspond to Class of Recommendation in Table 2. *For severe first-degree atrioventricular block or first-degree atrioventricular block with an
accompanying neuromuscular disease, also refer to Section 5.3., Figure 7, the atrioventricular block algorithm. †See Section 3.3.2., Figure 3. AV indicates
atrioventricular; BBB, bundle branch block; HF, heart failure; LBBB, left bundle branch block; and LVEF, left ventricular ejection fraction.
7. SPECIAL POPULATIONS
7.1. Perioperative Management

7.1.1. Patients at Risk for Bradycardia During Noncardiac Surgery
or Procedures
Recommendations for Patients at Risk for Bradycardia During Noncardiac Surgery or Procedures
1. In patients who are thought to be at high risk for the development of intraoperative or periprocedural
IIa B-NR bradycardia because of patient characteristics or procedure type, placement of transcutaneous pacing
pads is reasonable (S7.1.1-1–S7.1.1-3).
2. In patients with LBBB who require pulmonary artery catheterization for intraoperative monitoring, routine
III: Harm B-NR prophylactic temporary transvenous pacing should not be performed (S7.1.1-4, S7.1.1-5).
7.1.2. Postoperative Bradycardia and Conduction Disorders After

Cardiac Surgery
7.1.2.1. Coronary Artery Bypass
Recommendations for Pacing After Isolated Coronary Artery Bypass Surgery

1. In patients who have new postoperative SND or atrioventricular block associated with persistent symp-
I B-NR toms or hemodynamic instability that does not resolve after isolated coronary artery bypass surgery,
permanent pacing is recommended before discharge (S7.1.2.1-1–S7.1.2.1-9).
2. In patients undergoing isolated coronary artery bypass surgery, routine placement of temporary
IIa B-NR epicardial pacing wires is reasonable (S7.1.2.1-5, S7.1.2.1-10, S7.1.2.1-11).
3. In patients undergoing coronary artery bypass surgery who will likely require future CRT or ventricular
IIb C-EO pacing, intraoperative placement of a permanent epicardial left ventricular lead may be considered.
7.1.2.2. Surgery for Atrial Fibrillation
Recommendations for Pacing After Surgery for Atrial Fibrillation

1. In patients undergoing surgery for AF, routine placement of temporary epicardial pacing wires is rec-
I B-NR ommended (S7.1.2.2-1–S7.1.2.2-4).
2. In patients who have new postoperative SND or atrioventricular block associated with symptoms or he-
I B-NR modynamic instability that does not resolve after surgery for AF, permanent pacing is recommended
before discharge (S7.1.2.2-1–S7.1.2.2-4).
3. In patients undergoing surgery for AF who will likely require future CRT or ventricular pacing, intra-
IIb C-EO operative placement of a permanent epicardial left ventricular lead may be considered.
7.1.2.3. Valvular Surgery

7.1.2.3.1. Surgical Aortic Valve Replacement or Repair
Recommendations for Pacing After Aortic Valve Surgery

1. In patients undergoing surgical aortic valve replacement or repair, routine placement of temporary
I C-LD epicardial pacing wires is recommended (S7.1.2.3.1-1–S7.1.2.3.1-3).
I B-NR toms or hemodynamic instability that does not resolve after aortic valve replacement, permanent pacing
is recommended before discharge (S7.1.2.3.1-1–S7.1.2.3.1-5).
3. In patients undergoing aortic valve surgery who will likely require future CRT or ventricular pacing,
IIb C-EO intraoperative placement of a permanent epicardial left ventricular lead may be considered.
7.1.2.3.2. Mitral Valve Surgery
Recommendations for Pacing After Mitral Valve Surgery

I B-NR toms or hemodynamic instability that does not resolve after mitral valve repair or replacement surgery,
permanent pacing is recommended before discharge (S7.1.2.3.2-1, S7.1.2.3.2-2).
2. In patients undergoing mitral valve surgery, routine placement of temporary epicardial pacing wires is
IIa C-LD reasonable ( S7.1.2.3.2-1–S7.1.2.3.2-3).
3. In patients undergoing surgical mitral valve repair or replacement who will likely require future CRT or
IIb C-EO ventricular pacing, intraoperative placement of a permanent epicardial left ventricular lead may be
considered.
7.1.2.3.3. Tricuspid Valve Surgery
Recommendations for Pacing After Tricuspid Valve Surgery

1. In patients undergoing tricuspid valve surgery, routine placement of temporary epicardial pacing wires is
I C-LD recommended (S7.1.2.3.3-1–S7.1.2.3.3-4).
2. In patients who have new postoperative SND or atrioventricular block associated with symptoms or
I B-NR hemodynamic instability that does not resolve after tricuspid valve surgery, permanent pacing is
recommended before discharge (S7.1.2.3.3-1–S7.1.2.3.3-4).
3. In patients who are undergoing tricuspid valve replacement or tricuspid repair with high risk for post-
IIa C-LD operative atrioventricular block, intraoperative placement of permanent epicardial leads at the time of
cardiac surgery is reasonable (S7.1.2.3.3-1–S7.1.2.3.3-5).
7.1.2.4. Transcatheter Aortic Valve Replacement
Recommendations for Conduction Disturbances After Transcatheter Aortic Valve Replacement

1. In patients who have new atrioventricular block after transcatheter aortic valve replacement associated
I B-NR with symptoms or hemodynamic instability that does not resolve, permanent pacing is recommended
before discharge (S7.1.2.4-1–S7.1.2.4-4).
2. In patients with new persistent bundle branch block after transcatheter aortic valve replacement, careful
IIa B-NR surveillance for bradycardia is reasonable (S7.1.2.4-5, S7.1.2.4-6).
3. In patients with new persistent LBBB after transcatheter aortic valve replacement, implantation of a
IIb B-NR permanent pacemaker may be considered (S7.1.2.4-4, S7.1.2.4-7–S7.1.2.4-10).
7.1.2.5. Heart Transplant, Surgical Myectomy, and Alcohol

Septal Ablation
7.1.2.5.1. Surgical Myectomy and Alcohol Septal Ablation for
Hypertrophic Cardiomyopathy
Recommendations for Patients Undergoing Surgical Myectomy or Alcohol Septal Ablation for Hypertrophic Cardiomyopathy
1. In patients with second-degree Mobitz type II atrioventricular block, high-grade atrioventricular block, or
I B-NR persistent complete atrioventricular block after alcohol septal ablation or surgical myectomy, permanent
pacing is recommended before discharge (S7.1.2.5.1-1–S7.1.2.5.1-4).
2. In selected patients with hypertrophic cardiomyopathy who require permanent pacing for rate support
IIa B-NR after alcohol septal ablation or surgical myectomy and are at high risk for sudden cardiac death and
meaningful survival of greater than 1 year is expected, selecting a device with defibrillator capabilities is
reasonable (S7.1.2.5.1-5–S7.1.2.5.1-7).
3. In patients with hypertrophic cardiomyopathy who undergo alcohol septal ablation and who are at risk for
IIb C-LD developing late atrioventricular block, prolonged ambulatory electrocardiographic monitoring may be
considered (S7.1.2.5.1-1, S7.1.2.5.1-2, S7.1.2.5.1-4, S7.1.2.5.1-7, S7.1.2.5.1-8).
4. In patients with hypertrophic cardiomyopathy, evaluation of ventriculoatrial conduction by EPS at the

IIb C-LD time of alcohol septal ablation may be considered for identifying future risk of atrioventricular block
(S7.1.2.5.1-9).
7.2. Bradycardia Management for Adult Congenital

Heart Disease
Recommendations for Management of Bradycardia in Adults With Adult Congenital Heart Disease
1. In adults with adult congenital heart disease (ACHD )and symptomatic SND or chronotropic incompetence,
I B-NR atrial based permanent pacing is recommended (S7.2-1–S7.2-6).
2. In adults with ACHD and symptomatic bradycardia related to atrioventricular block, permanent pacing is
I B-NR recommended (S7.2-7–S7.2-9).
3. In adults with congenital complete atrioventricular block with any symptomatic bradycardia, a wide QRS
I B-NR escape rhythm, mean daytime heart rate below 50 bpm, complex ventricular ectopy, or ventricular
dysfunction, permanent pacing is recommended (S7.2-10, S7.2-11).
4. In adults with ACHD and postoperative second-degree Mobitz type II atrioventricular block, high-grade
I B-NR atrioventricular block, or third-degree atrioventricular block that is not expected to resolve, permanent
pacing is recommended (S7.2-12, S7.2-13).
5. In asymptomatic adults with congenital complete atrioventricular block, permanent pacing is reasonable
IIa B-NR (S7.2-7–S7.2-11).
6. In adults with repaired ACHD who require permanent pacing for bradycardic indications, a bradycardia
IIa B-NR device with atrial antitachycardia pacing capabilities is reasonable (S7.2-14, S7.2-15).
7. In adults with ACHD with preexisting sinus node and/or atrioventricular conduction disease who are
IIa C-EO undergoing cardiac surgery, intraoperative placement of epicardial permanent pacing leads is reasonable.
8. In adults with ACHD and pacemakers, atrial-based permanent pacing for the prevention of atrial
IIb B-NR arrhythmias may be considered (S7.2-3–S7.2-5, S7.2-16).
9. In selected adults with ACHD and venous to systemic intracardiac shunts, placement of endocardial
III: Harm B-NR pacing leads is potentially harmful (S7.2-17, S7.2-18).
7.3. Management of Bradycardia in Patients With an Acute MI
Recommendations for Management of Bradycardia in the Context of Acute MI

1. In patients presenting with an acute MI, temporary pacing is indicated for medically refractory
I B-NR symptomatic or hemodynamically significant bradycardia related to SND or atrioventricular
block (S7.3-1–S7.3-4).
2. Patients who present with SND or atrioventricular block in the setting of an acute MI should undergo a
I B-NR waiting period before determining the need for permanent pacing (S7.3-1, S7.3-4–S7.3-7).
3. In patients presenting with an acute MI with second-degree Mobitz type II atrioventricular block, high-
I B-NR grade atrioventricular block, alternating bundle branch block, or third-degree atrioventricular block
(persistent or infranodal), permanent pacing is indicated after a waiting period (S7.3-7, S7.3-8).
4. In patients with an acute MI with symptomatic or hemodynamically significant sinus bradycardia or

IIa B-NR atrioventricular block at the level of the atrioventricular node, the administration of atropine is
reasonable (S7.3-9–S7.3-11).
5. In patients with an acute MI and transient atrioventricular block that resolves, permanent pacing should
III: Harm B-NR not be performed (S7.3-1, S7.3-4, S7.3-7, S7.3-12–S7.3-16).
6. In patients with an acute MI and a new bundle branch block or isolated fascicular block in the absence
III: Harm B-NR of second-degree or third-degree atrioventricular block, permanent pacing should not be performed
(S7.3-17–S7.3-19).
7.4. Neurologic Disorders

7.4.1. Epilepsy
Recommendation for Patients With Epilepsy and Symptomatic Bradycardia

1. In patients with epilepsy associated with severe symptomatic bradycardia (ictal bradycardia) where
IIa C-LD antiepileptic medications are ineffective, permanent pacing is reasonable for reducing the severity of
symptoms (S7.4.1-1–S7.4.1-4).
8. EVALUATION OF THE RISKS FOR VENTRICULAR

ARRHYTHMIAS IN PATIENTS WHO REQUIRE
PERMANENT PACING
Recommendation for Management of Bradycardia and Conduction Tissue Disease in Patients Who Require Pacing Therapy and
May Also Be at Risk for Ventricular Arrhythmias Referenced studies that support the recommendation are summarized in
Online Data Supplement 56.
1. In patients who require permanent pacing therapy, before implantation, an assessment of the risk of
I B-NR future ventricular arrhythmias and need for an implantable cardioverter defibrillator should be performed
(S8-1–S8-7).
9. SHARED DECISION-MAKING
Recommendations for Shared Decision-Making for Pacemaker Implantation in the Setting of Guideline-Based Indications for Brady-
cardia Pacing
1. In patients with symptomatic bradycardia or conduction disorder, clinicians and patients should engage in
I C-LD a shared decision-making approach in which treatment decisions are based not only on the best available
evidence, but also on the patient’s goals of care, preferences, and values (S9-1–S9-6).
2. Patients considering implantation of a pacemaker or with a pacemaker that requires lead revision or
I C-LD generator change should be informed of procedural benefits and risks, including the potential short- and
long-term complications and possible alternative therapy, if any, in light of their goals of care, prefer-
ences, and values (S9-1–S9-6).
3. In patients with indications for permanent pacing but also with significant comorbidities such that pacing
III: No Benefit C-LD therapy is unlikely to provide meaningful clinical benefit, or if patient goals of care strongly preclude
pacemaker therapy, implantation or replacement of a pacemaker should not be performed (S9-1–S9-6).
10. DISCONTINUATION OF PACEMAKER THERAPY
Recommendation for Discontinuation of Pacemaker Therapy
1. In patients who present for pacemaker pulse generator replacement, or for management of pacemaker
IIa C-LD related complications, in whom the original pacing indication has resolved or is in question, discontinu-
ation of pacemaker therapy is reasonable after evaluation of symptoms during a period of monitoring
while pacing therapy is off (S10-1, S10-2).
PRESIDENTS AND STAFF Sam Shahid, MBBS, MPH, Associate Science and Medicine
Advisor
American College of Cardiology Zainab Shipchandler, MPH, Associate Guideline Advisor,
C. Michael Valentine, MD, FACC, President Clinical Practice Guidelines
Timothy W. Attebery, MBA, FACHE, Chief Executive Officer American Heart Association
William J. Oetgen, MD, MBA, FACC, Executive Vice Ivor J. Benjamin, MD, FAHA, President
President, Science, Education, Quality, and Publishing Nancy Brown, Chief Executive Officer
MaryAnne Elma, MPH, Senior Director, Science, Rose Marie Robertson, MD, FAHA, Chief Science and
Education, Quality, and Publishing Medical Officer
Amelia Scholtz, PhD, Publications Manager, Science, Gayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice
Education, Quality, and Publishing President, Office of Science Operations
American College of Cardiology/American Heart Association Paul St. Laurent, DNP, APRN, Science and
Katherine A. Sheehan, PhD, Director, Guideline Strategy Medicine Advisor
and Operations Jody Hundley, Production and Operations Manager,
Abdul R. Abdullah, MD, Science and Medicine Advisor Scientific Publications, Office of Science
Thomas S. D. Getchius, Manager, Guideline Science Operations
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culation. 2013;128:1433–41. e503–51.
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adults with congenital heart disease. J Am Coll Cardiol. S7.2-18. Khairy P, Landzberg MJ, Gatzoulis MA, et al. S7.3-16. Lee JZ, Ling J, Diehl NN, et al. Mortality and
2006;48:1250–6. Transvenous pacing leads and systemic thromboem- cerebrovascular events after heart rhythm disorder
boli in patients with intracardiac shunts: a multicenter management procedures. Circulation. 2018;137:24–33.
S7.2-3. Fishberger SB, Wernovsky G, Gentles TL, et al.
study. Circulation. 2006;113:2391–7.
Factors that influence the development of atrial flutter S7.3-17. Col JJ, Weinberg SL. The incidence and mor-
after the Fontan operation. J Thorac Cardiovasc Surg. 7.3. Management of Bradycardia in Patients tality of intraventricular conduction defects in acute
1997;113:80–6. With an Acute MI myocardial infarction. Am J Cardiol. 1972;29:344–50.
S7.2-4. Gelatt M, Hamilton RM, McCrindle BW, et al. S7.3-1. Auffret V, Loirat A, Leurent G, et al. High-de- S7.3-18. Hindman MC, Wagner GS, JaRo M, et al. The
Arrhythmia and mortality after the Mustard procedure: gree atrioventricular block complicating ST segment clinical significance of bundle branch block
complicating acute myocardial infarction. 2. In- Devices Registry: population, device utilization, and S9-5. Yuhas J, Mattocks K, Gravelin L, et al. Patients’
dications for temporary and permanent pacemaker outcomes. J Am Heart Assoc. 2016;5:e002798. attitudes and perceptions of implantable cardioverter-
insertion. Circulation. 1978;58:689–99. defibrillators: potential barriers to appropriate primary
S8-4. Kirkfeldt RE, Johansen JB, Nohr EA, et al.
prophylaxis. Pacing Clin Electrophysiol. 2012;35:1179–
S7.3-19. Hindman MC, Wagner GS, JaRo M, et al. The Complications after cardiac implantable electronic
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clinical significance of bundle branch block compli- device implantations: an analysis of a complete,
cating acute myocardial infarction. 1. Clinical charac- nationwide cohort in Denmark. Eur Heart J. 2014;35: S9-6. Elwyn G, Edwards A, Kinnersley P, et al. Shared
teristics, hospital mortality, and one-year follow-up. 1186–94. decision making and the concept of equipoise: the
Circulation. 1978;58:679–88. competences of involving patients in healthcare
S8-5. Maron BJ, Spirito P, Shen WK, et al. Implantable
choices. Br J Gen Pract. 2000;50:892–9.
cardioverter-defibrillators and prevention of sudden
7.4. Neurologic Disorders
cardiac death in hypertrophic cardiomyopathy. JAMA.
7.4.1. Epilepsy 2007;298:405–12. 10. DISCONTINUATION OF
S7.4.1-1. Bestawros M, Darbar D, Arain A, et al. Ictal PACEMAKER THERAPY
S8-6. Sochala M, Wahbi K, Sorbets E, et al. Risk for
asystole and ictal syncope: insights into clinical man-
complications after pacemaker or cardioverter defi-
agement. Circ Arrhythm Electrophysiol. 2015;8:159–64.
brillator implantations in patients with myotonic dys- S10-1. Iskos D, Lurie KG, Sakaguchi S, et al. Termina-
S7.4.1-2. Lanz M, Oehl B, Brandt A, et al. Seizure trophy type 1. J Neuromuscul Dis. 2017;4:175–81. tion of implantable pacemaker therapy: experience in
induced cardiac asystole in epilepsy patients under- S8-7. Takaya Y, Kusano KF, Nakamura K, et al. Out- five patients. Ann Intern Med. 1997;126:787–90.
going long term video-EEG monitoring. Seizure. 2011; comes in patients with high-degree atrioventricular S10-2. Martinelli M, Costa R, Nishioka S, et al. Criteria
20:167–72. block as the initial manifestation of cardiac sarcoidosis. for pacemaker explant in patients without a precise
Am J Cardiol. 2015;115:505–9. indication for pacemaker implantation. Pacing Clin
S7.4.1-3. Schuele SU, Bermeo AC, Alexopoulos AV, et al.
Video-electrographic and clinical features in patients Electrophysiol. 2002;25:272–7.
with ictal asystole. Neurology. 2007;69:434–41.
S7.4.1-4. Tenyi D, Gyimesi C, Kupo P, et al. Ictal asys- 9. SHARED DECISION-MAKING

KEY WORDS ACC/AHA Clinical Practice
tole: a systematic review. Epilepsia. 2017;58:356–62. Guidelines, ablation, ambulatory
S9-1. Ottenberg AL, Mueller PS, Topazian RJ, et al. electrocardiography, aminophylline,
“It’s not broke, so let’s not try to fix it”: why patients atrioventricular block, atropine, AV block,
8. EVALUATION OF THE RISKS FOR
decline a cardiovascular implantable electronic device. beta-adrenergic agonist, bradyarrhythmia,
VENTRICULAR ARRHYTHMIAS IN
Pacing Clin Electrophysiol. 2014;37:1306–14. bradycardia, bundle branch block, cardiac
PATIENTS WHO REQUIRE
S9-2. Lewis KB, Stacey D, Matlock DD. Making pacing, cardiac resynchronization therapy,
PERMANENT PACING
decisions about implantable cardioverter- cardiac sinus pause, cardiac surgery, congenital
defibrillators from implantation to end of life: an heart disease, digoxin antibodies Fab fragments,
S8-1. Anselme F, Moubarak G, Savoure A, et al. electrocardiogram, glucagon, heart block, Holter
integrative review of patients’ perspectives. Patient.
Implantable cardioverter-defibrillators in lamin A/C monitoring, intraoperative, isoproterenol, lamin
2014;7:243–60.
mutation carriers with cardiac conduction disorders. A-C, left bundle branch block, muscular
Heart Rhythm. 2013;10:1492–8. S9-3. Stewart GC, Weintraub JR, Pratibhu PP, et al.
dystrophies, myocardial infarction, myotonic
Patient expectations from implantable defibrillators to
dystrophy, pacemaker, pacing, preoperative,
S8-2. Gadler F, Valzania C, Linde C. Current use of prevent death in heart failure. J Card Fail. 2010;16:
quality of life, right bundle branch block,
implantable electrical devices in Sweden: data from 106–13.
sarcoidosis, shared decision making, sick sinus
S9-4. Hauptman PJ, Chibnall JT, Guild C, et al. Patient syndrome, sinus arrest, sinus bradycardia
perceptions, physician communication, and the syndrome, sinus node dysfunction, spinal cord
S8-3. Gupta N, Kiley ML, Anthony F, et al. Multi-Cen- implantable cardioverter-defibrillator. JAMA Intern injuries, syncope, theophylline, transcatheter
ter, Community-Based Cardiac Implantable Electronic Med. 2013;173:571–7. aortic valve replacement
984
APPENDIX 1. AUTHOR RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES (RELEVANT)—2018 ACC/AHA/HRS GUIDELINE ON THE
EVALUATION AND MANAGEMENT OF PATIENTS WITH BRADYCARDIA AND CARDIAC CONDUCTION DELAY (JULY 2018)
2018 Bradycardia Guideline: Executive Summary

Kusumoto et al.
Institutional,
Ownership/ Organizational,
Speakers Partnership/ or Other Expert Voting Recusals
Committee Member Employment Consultant Bureau Principal Personal Research Financial Benefit Witness by Section*
Fred M. Kusumoto (Chair) Mayo Clinic—Professor of Medicine None None None None None None None
Mark H. Schoenfeld (Vice Yale University School of Medicine— None None None None None None None
Chair) Clinical Professor of Medicine
Coletta C. Barrett American Heart Association—Chairman None None None None None None None
of the Board
James R. Edgerton The Heart Hospital Baylor—Director of None None None None None None None
Education
Kenneth A. Ellenbogen VCU Medical Center—Director, Clinical n Biotronik† n Biosense Webster† None n Biosense Webster† n Biosense Webster† None 4.3.1, 4.3.2, 5, 6, 7, 8,
Electrophysiology 9, 11, 13
n Boston Scientific† n Biotronik† n Boston Scientific† n Boston Scientific†
n Janssen Pharmaceuticals n Boston Scientific† n Medtronic† n Medtronic†
n Medtronic† n Medtronic† n Sanofi-Aventis† n Sanofi-Aventis
n Pfizer† n St. Jude Medical† n Medtronic (DSMB)†
n St. Jude Medical†
Michael R. Gold Medical University of South Carolina— n Boston Scientific† None None n Boston Scientific‡ None None 4.3.1, 5, 6, 7, 8, 9, 11,
Director, Division of Cardiology and 13
n Medtronic n St. Jude Medical‡
Professor of Medicine
n St. Jude Medical
Nora F. Goldschlager University of California San Francisco— None None None None None None None
Professor of Clinical Medicine
Robert M. Hamilton University of Toronto—Professor of None None None None None None None
Pediatrics
José A. Joglar UT Southwestern Medical Center None None None None None None None
University—Associate Professor of
Internal Medicine
Robert J. Kim University of Florida College of None None None None None None None
Medicine—Assistant Professor
Richard Lee St. Louis University Hospital—Co– None None None None None None None
Director, Center for Comprehensive
Cardiovascular Care
Joseph E. Marine Johns Hopkins University—Associate None None None None None None None
Professor of Medicine
Christopher J. McLeod Mayo Clinic—Co–Director, Division of None None None None None None None
Cardiovascular Diseases
JACC VOL. 74, NO. 7, 2019

AUGUST 20, 2019:932–87
Keith R. Oken Mayo Clinic—Program Director, None None None None None None None
Cardiovascular Diseases Fellowship
and Assistant Professor of Medicine
Kristen K. Patton University of Washington—Professor of None None None None None None None
Medicine

APPENDIX 1. CONTINUED
AUGUST 20, 2019:932–87
JACC VOL. 74, NO. 7, 2019

Institutional,
Ownership/ Organizational,
Speakers Partnership/ or Other Expert Voting Recusals
Committee Member Employment Consultant Bureau Principal Personal Research Financial Benefit Witness by Section*
Cara Pellegrini University of California San Francisco n Abbott None None None None None 4.3.1, 5, 6, 7, 8, 9, 11,
School of Medicine—Associate 13
n Medtronic
Professor
Kimberly A. Selzman University of Utah School of Medicine— None None None None None None None
Associate Professor of Medicine
Annemarie Thompson Duke University School of Medicine— None None None None None None None
Professor of Anesthesiology and
Medicine
Paul D. Varosy VA Eastern Colorado Health Care None None None None None None None
System—Director, Cardiac
Electrophysiology; University of
Colorado—Associate Professor of
Medicine
This table represents the relationships of committee members with industry and other entities that were determined to be relevant to this document. These relationships were reviewed and updated in conjunction with all meetings and/or conference calls
of the writing committee during the document development process. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents
ownership of $5% of the voting stock or share of the business entity, or ownership of $$5,000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person’s gross income for the
previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted.
According to the ACC/AHA, a person has a relevant relationship IF: a) the relationship or interest relates to the same or similar subject matter, intellectual property or asset, topic, or issue addressed in the document; or b) the company/entity (with whom
the relationship exists) makes a drug, drug class, or device addressed in the document or makes a competing drug or device addressed in the document; or c) the person or a member of the person’s household, has a reasonable potential for financial,
professional or other personal gain or loss as a result of the issues/content addressed in the document.
CMS reported payments from Cardiofocus to Dr. Kusumoto in 2016 and 2017. Dr. Kusumoto has established that the study he participated in ended in 2014 and was published in 2015.
CMS reported consulting payments to Dr. Lee from Abbott, Cryolife and Maquet in 2016. Dr. Lee has established that his participation with the companies ended in January 2015.
CMS reported research payments from Medtronic to Dr. McLeod in 2016 and 2017. Dr. McLeod is disputing the payments.
*Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry and other entities may apply. Section numbers pertain to those in the full-text guideline.
†Significant relationship.
‡No financial benefit.
ACC indicates American College of Cardiology; AHA, American Heart Association; DSMB, data safety monitoring board; HRS, Heart Rhythm Society; UT, University of Texas; VA, Veterans Affairs; and VCU, Virginia Commonwealth University.
2018 Bradycardia Guideline: Executive Summary

Kusumoto et al.
985
APPENDIX 2. ABBREVIATED REVIEWER RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES—2018

ACC/AHA/HRS GUIDELINE ON THE EVALUATION AND MANAGEMENT OF PATIENTS WITH BRADYCARDIA
AND CARDIAC CONDUCTION DELAY (AUGUST 2018)*
Comprehensive
Reviewer Representation Employment RWI?
Yong-Mei Cha Official Reviewer—AHA Mayo Clinic, Division of Cardiovascular Diseases No
Zachary D. Goldberger Official Reviewer—ACC/AHA Task Force University of Washington School of Medicine—Assistant Professor of No
on Clinical Practice Guidelines Medicine; Division of Cardiology, Harborview Medical Center
Richard J. Kovacs Official Reviewer—ACC Science and Indiana University School of Medicine, Krannert Institute of Cardiology— Yes
Quality Committee Professor of Clinical Medicine
Kevin F. Kwaku Official Reviewer—AHA Dartmouth-Hitchcock Medical No
Daniel M. Philbin Jr Official Reviewer—ACC Board of New England Heart Institute Yes
Governors
Peter A. Brady Organizational Reviewer—HRS Mayo Clinic, Mayo Foundation No
Ratika Parkash Organizational Reviewer—HRS Dalhousie University and Nova Scotia Health Authority—Professor of Yes
Medicine, Division of Cardiology (Arrhythmia); Director of Research,
Division of Cardiology
Jonathan Philpott Organizational Reviewer—STS Mid-Atlantic Cardiothoracic Surgeons Yes
Kevin Shannon Organizational Reviewer—PACES Mattel Children’s Hospital at UCLA—Clinical Professor, Division of Yes
Pediatric Cardiology
Gus J. Vlahakes Organizational Reviewer—AATS Harvard Medical School and Massachusetts General Hospital—Professor of No
Surgery
Nazem Akoum Content Reviewer University of Washington No
Sana M. Al-Khatib Content Reviewer—ACC/AHA Task Duke Clinical Research Institute— Professor of Medicine Yes
Force on Clinical Practice Guidelines
Joshua A. Beckman Content Reviewer—ACC/AHA Task Vanderbilt University Medical Center— Director, Section of Vascular Yes
Force on Clinical Practice Guidelines Medicine
Kim K. Birtcher Content Reviewer—ACC/AHA Task University of Houston College of Pharmacy—Clinical Professor Yes
Mitchell I. Cohen Content Reviewer—PACES Pediatric Cardiology Associates No
Freddy Del-Carpio Content Reviewer—ERC Member Mayo Clinic No

Munoz
Bernard Dennis Content Reviewer—ACC/AHA Lay Dennis Associates, LLC No

Reviewer
Anita Deswal Content Reviewer—ACC/AHA Task Michael E. DeBakey VA Medical Center—Chief, Cardiology; Baylor College Yes
Force on Clinical Practice Guidelines of Medicine—Professor of Medicine
Andrew E. Epstein Content Reviewer The Hospital of the University of Pennsylvania—Professor of Medicine Yes
Michael E. Field Content Reviewer University of Wisconsin School of Medicine and Public Health—Director, No
Clinical Electrophysiology and Cardiac Arrhythmia Service
Michael S. Firstenberg Content Reviewer—ACC Surgeons The Medical Center of Aurora—Chair, Cardiovascular and Cardiothoracic Yes
Member Section and Leadership Surgery
Council
John D. Fisher Content Reviewer—ACC Montefiore Medical Center— Program Director CCEP Yes
Electrophysiology Member Section
Chair
Federico Gentile Content Reviewer—ACC/AHA Task Centro Cardiologico Gentile No

Anne M. Gillis Content Reviewer University of Calgary Yes
Bulent Gorenek Content Reviewer Eskisehir Osmangazi University Cardiology Department— Professor of Yes
Cardiology
Mohamed H. Hamdan Content Reviewer University of Wisconsin-Madison— Chief of Cardiovascular Medicine Yes
Glenn N. Levine Content Reviewer—ACC/AHA Task Baylor College of Medicine— Professor of Medicine; Michael E. DeBakey Yes
Force on Clinical Practice Guidelines Medical Center—Director, Cardiac Care Unit
Mark S. Link Content Reviewer UT Southwestern Medical Center Yes
Daniel L. Lustgarten Content Reviewer University of Vermont School of Medicine Yes

Siva K. Mulpuru Content Reviewer—ERC Member Mayo Clinic—Associate Professor Yes

APPENDIX 2. CONTINUED
Comprehensive
Reviewer Representation Employment RWI?
Patrick T. O’Gara Content Reviewer—ACC/AHA Task Harvard Medical School—Professor of Medicine; Brigham and Women’s Yes
Force on Clinical Practice Guidelines Hospital—Director, Strategic Planning
Brian Olshansky Content Reviewer Professor of Medicine Yes
David S. Park Content Reviewer—AHA NYU Langone Health—Assistant Professor, Department of Medicine No
Mariann Piano Content Reviewer—ACC/AHA Task Vanderbilt University School of Nursing—Nancy and Hilliard Travis Yes
Force on Clinical Practice Guidelines Professor of Nursing; Senior Associate Dean for Research
Merritt H. Raitt Content Reviewer—ERC Vice Chair Oregon Heath & Science University; VA Portland Health Care System— No
Cardiologist
Satish R. Raj Content Reviewer University of Calgary Yes
Win-Kuang Shen Content Reviewer Mayo Clinic Arizona, Phoenix Campus—Professor of Medicine; Chair, No
Department of Cardiovascular Diseases
David J. Slotwiner Content Reviewer—ERC Chair Weill Cornell Medical College—Chief, Division of Cardiology; Assistant No
Professor of Clinical Medicine
Cynthia M. Tracy Content Reviewer The George Washington University School of Medicine & Health Sciences— Yes
Professor of Medicine; Associate Director of Cardiology
Richard G. Trohman Content Reviewer Rush University Medical Center Yes
Gaurav A. Upadhyay Content Reviewer—ACC The University of Chicago Medicine—Assistant Professor of Medicine; Yes
Electrophysiology Member Section Director, Heart Station
This table represents all relationships of reviewers with industry and other entities that were reported at the time of peer review, including those not deemed to be relevant to this
document, at the time this document was under review. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a
significant interest in a business if the interest represents ownership of $5% of the voting stock or share of the business entity, or ownership of $$5,000 of the fair market value of the
business entity; or if funds received by the person from the business entity exceed 5% of the person’s gross income for the previous year. Relationships that exist with no financial
benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. Names are listed in alphabetical order within each category of
review. Please refer to http://www.acc.org/guidelines/about-guidelines-and-clinical-documents/relationships-with-industry-policy for definitions of disclosure categories or addi-
tional information about the ACC/AHA Disclosure Policy for Writing Committees.
*Detailed reviewer disclosures can be found online.
AATS indicates American Association for Thoracic Surgery; ACC, American College of Cardiology; AHA, American Heart Association; CCEP, Clinical Cardiac Electrophysiology; ERC,
evidence review committee; HRS, Heart Rhythm Society; LLC, limited liability company, NYU, New York University; PACES, Pediatric & Congenital Electrophysiology Society; STS, the
Society of Thoracic Surgeons; UCLA, University of California, Los Angeles; UT, University of Texas; and VA, Veterans Affairs.

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY VOL. 74, NO.

CLINICAL PRACTICE GUIDELINE: EXECUTIVE SUMMARY

2018 ACC/AHA/HRS Guideline on

Developed in Collaboration With the American Association for Thoracic Surgery,

ISSN 0735-1097/$36.00 https://doi.org/10.1016/j.jacc.2018.10.043

TOP 10 TAKE-HOME MESSAGES . . . . . . . . . . . . . . . . . . 934 3.2.3. Ambulatory Electrocardiography

2. EPIDEMIOLOGY AND DEFINITIONS . . . . . . . . . . . . 940 3.3. Invasive Testing . . . . . . . . . . . . . . . . . . . . . . . . . . 948

2018 Bradycardia Guideline: Executive Summary AUGUST 20, 2019:932–87

4.2. Chronic Therapy/Management of Bradycardia 7.3. Management of Bradycardia in Patients With

4.2.2. Transient/Reversible Causes (Including

4.2.3. Additional Testing of Bradycardia PERMANENT PACING . . . . . . . . . . . . . . . . . . . . . . . . 969

5. BRADYCARDIA ATTRIBUTABLE TO PRESIDENTS AND STAFF . . . . . . . . . . . . . . . . . . . . . . . . 970

ATRIOVENTRICULAR BLOCK . . . . . . . . . . . . . . . . . . 957

5.2. Acute Management . . . . . . . . . . . . . . . . . . . . . . . . 958 Author Relationships With Industry and

7. SPECIAL POPULATIONS . . . . . . . . . . . . . . . . . . . . . . 965

2018 Bradycardia Guideline: Executive Summary AUGUST 20, 2019:932–87

1. INTRODUCTION committee included representatives from the ACC, AHA,

2018 Bradycardia Guideline: Executive Summary AUGUST 20, 2019:932–87

TABLE 1 Associated Guidelines and Related References

Ventricular arrhythmias and sudden cardiac death ACC/AHA/HRS 2017 (S1.4-3)

Syncope ACC/AHA/HRS 2017 (S1.4-4)

Stable ischemic heart disease ACC/AHA/AATS/PCNA/SCAI/STS 2014* (S1.4-5)

Atrial ﬁbrillation AHA/ACC/HRS 2014 (S1.4-7)

Non–ST-elevation acute coronary syndromes AHA/ACC 2014 (S1.4-9)

Heart failure ACC/AHA 2013 (S1.4-10)

ST-elevation myocardial infarction ACC/AHA 2013 (S1.4-11)

Device-based therapy for cardiac rhythm abnormalities ACC/AHA/HRS 2013 (S1.4-2)

Coronary artery bypass graft surgery ACC/AHA 2011 (S1.4-12)

Hypertrophic cardiomyopathy ACC/AHA 2011 (S1.4-13)

Percutaneous coronary intervention ACC/AHA/SCAI 2011 (S1.4-14)

Other related references

Expert consensus statement on magnetic resonance imaging HRS 2017 (S1.4-18)

Cardiac pacing and cardiac resynchronization therapy ESC 2013 (S1.4-24)

2018 Bradycardia Guideline: Executive Summary AUGUST 20, 2019:932–87

2. EPIDEMIOLOGY AND DEFINITIONS

TABLE 3 Table of Deﬁnitions

Term Deﬁnition or Description

Continued on the next page

Term Deﬁnition or Description

3. GENERAL EVALUATION OF PATIENTS WITH

3.1. History and Physical Examination of Patients With

COR LOE RECOMMENDATION

COR LOE RECOMMENDATION

2018 Bradycardia Guideline: Executive Summary AUGUST 20, 2019:932–87

F I G U R E 1 Evaluation of Bradycardia and Conduction Disease Algorithm

Patient with symptoms suggestive of

ECG Directed blood testing

Conduction disorder with

F I G U R E 2 Initial Evaluation of Suspected or Documented Sinus Node Dysfunction Algorithm

Evidence for sinus

Sinus node dysfunction

2018 Bradycardia Guideline: Executive Summary AUGUST 20, 2019:932–87

F I G U R E 3 Initial Evaluation of Suspected Atrioventricular Block Algorithm

AV block AV block AV node AV block AV block

TABLE 4 Medications That Can Induce/Exacerbate Bradycardia or Conduction Disorders

Antihypertensive Antiarrhythmic Psychoactive Other

TABLE 5 Conditions Associated With Bradycardia and Conduction Disorders

Cardiomyopathy (ischemic or nonischemic)

Congenital heart disease