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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
© 2019 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION,
THE AMERICAN HEART ASSOCIATION, INC., AND THE HEART RHYTHM SOCIETY.
PUBLISHED BY ELSEVIER
VOL. 74, NO. 7, 2019
CLINICAL PRACTICE GUIDELINE
2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay
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 Committee Members*
Fred M. Kusumoto, MD, FACC, FAHA, FHRS, Chair
Mark H. Schoenfeld, MD, FACC, FAHA, FHRS, Vice Chair
Coletta Barrett, RN, FAHA†
James R. Edgerton, MD, FACC, FHRS‡
Kenneth A. Ellenbogen, MD, FACC, FAHA, FHRS*†
Michael R. Gold, MD, PhD, FACC*§
Nora F. Goldschlager, MD, FACC, FAHA, FHRS \( ^{\dagger} \)
Robert M. Hamilton, MD ||
José A. Joglar, MD, FACC, FAHA, FHRS¶
Robert J. Kim, MD†
Richard Lee, MD, MBA#
Joseph E. Marine, MD, MBA, FACC, FHRS
Christopher J. McLeod, MB, ChB, PhD, FACC,
FAHA, FHRS†
Keith R. Oken, MD, FACC†
Kristen K. Patton, MD, FACC, FAHA, FHRS†
Cara N. Pellegrini, MD, FHRS*§**
Kimberly A. Selzman, MD, MPH, FACC, FHRS†
Annemarie Thompson, MD†
Paul D. Varosy, MD, FACC, FAHA, FHRS††
*Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry may apply; see Appendix 1 for detailed information. †ACC/AHA Representative. ‡STS Representative. §HRS Representative. ||PACES Representative. ¶ACC/AHA Task Force on Clinical Practice Guidelines Liaison. #AATS Representative. **Dr. Pellegrini contributed to this article in her personal capacity. The views expressed are her own and do not necessarily represent the views of the U.S. Department of Veterans Affairs or the U.S. government. ††ACC/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 American Heart Association Executive Committee in October 2018, and the Heart Rhythm Society in August 2018.
The American College of Cardiology requests that this document be cited as follows: Kusumoto FM, Schoenfeld MH, Barrett CN, 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: 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:e51-156.
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 (https://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 (reprints@elsevier.com).
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American College of Cardiology. Requests may be completed online via the Elsevier site (https://www.elsevier.com/about/policies/copyright/permissions).
ISSN 0735-1097/$36.00
https://doi.org/10.1016/j.jacc.2018.10.044
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ACC/AHA Task Glenn N. Levine, MD, FACC, FAHA, Chair
Force Members Patrick T. O'Gara, MD, MACC, FAHA, Chair-Elect Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair‡‡
Sana M. Al-Khatib, MD, MHS, FACC, FAHA
Joshua A. Beckman, MD, MS, FAHA
Kim K. Birtcher, PHARM D, MS, AACC
Biykem Bozkurt, MD, PhD, FACC, FAHA‡‡
Ralph G. Brindis, MD, MPH, MACC‡‡
Joaquin E. Cigarroa, MD, FACC
Lesley H. Curtis, PhD, FAHA‡‡
Anita Deswal, MD, MPH, FACC, FAHA
Lee A. Fleisher, MD, FACC, FAHA
Federico Gentile, MD, FACC
Samuel Gidding, MD, FAHA‡‡
Zachary D. Goldberger, MD, MSc, FACC, FAHA
Mark A. Hlatky, MD, FACC, FAHA
John Ikonomidis, MD, PhD, FAHA‡‡
José A. Joglar, MD, FACC, FAHA
Laura Mauri, MD, MSc, FAHA‡‡
Mariann R. Piano, RN, PhD, FAHA
Susan J. Pressler, PhD, RN, FAHA‡‡
Barbara Riegel, PhD, RN, FAHA‡‡
Duminda N. Wijesundera, MD, PhD
‡Former Task Force member; current member during the writing effort.
TABLE OF CONTENTS
TOP 10 TAKE-HOME MESSAGES FOR THE
MANAGEMENT OF BRADYCARDIA AND
CARDIAC CONDUCTION DELAY e53
PREAMBLE e54
1. INTRODUCTION e55
1.1. Methodology and Evidence Review e55
1.2. Organization of the Writing Committee e55
1.3. Document Review and Approval e55
1.4. Scope of the Guideline e56
1.5. Class of Recommendation and Level of Evidence e56
1.6.Abbreviations e56
2. EPIDEMIOLOGY AND DEFINITIONS e57
2.1. Bradycardia and Conduction Disorders e57
2.2. Definitions e59
3. CLINICAL MANIFESTATION OF BRADYCARDIA AND CONDUCTION DISORDERS e59
3.1. Clinical Manifestations of Bradycardia e59
3.2. Clinical Manifestations of Conduction Disorders . e61
4. GENERAL EVALUATION OF PATIENTS WITH DOCUMENTED OR SUSPECTED BRADYCARDIA OR CONDUCTION DISORDERS e61
4.1. History and Physical Examination of Patients With Documented or Suspected Bradycardia or Conduction Disorders e61
4.2. Noninvasive Evaluation e66
4.2.1. Resting ECG in Patients With Documented or Suspected Bradycardia or Conduction Disorders e66
4.2.2. Exercise Electrocardiographic Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorders . . . . e66
4.2.3. Ambulatory Electrocardiography in Patients With Documented or Suspected Bradycardia or Conduction Disorders . . . . e67
4.2.4. Imaging in Patients With Documented or Suspected Bradycardia or Conduction Disorders e69
4.2.5. Laboratory Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorders e70
4.2.6. Genetic Testing in Patients With Documented or Suspected Bradycardia or Conduction Disorders e71
4.2.7. Sleep Apnea Evaluation and Treatment in Patients With Documented or Suspected Bradycardia or Conduction Disorders . . . e72
4.3. Invasive Testing e73
4.3.1. Implantable Cardiac Monitor in Patients With Documented or Suspected Bradycardia or Conduction Disorders . . . e73
4.3.2. Electrophysiology Study in Patients With Documented or Suspected Bradycardia or Conduction Disorders e74
5. BRADYCARDIA ATTRIBUTABLE TO SND e74
5.1. Pathology/Pathophysiology/Etiology of SND . e74
5.2. Clinical Presentation of SND e75
5.3. Acute Management of SND e75
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5.3.1. Acute Management of Reversible Causes of SND e75
5.3.2. Acute Medical Therapy for Bradycardia . e77
5.3.3. Temporary Pacing for Bradycardia
Attributable to SND e82
5.4. Chronic Therapy/Management of Bradycardia Attributable to SND e84
5.4.1. General Principles of Chronic Therapy/Management of Bradycardia Attributable to SND e84
5.4.2. Transient/Reversible Causes (Including Medications) of Bradycardia Attributable to SND e85
5.4.3. Additional Testing of Bradycardia Attributable to SND e85
5.4.4. Permanent Pacing for Chronic Therapy/Management of Bradycardia Attributable to SND e86
6. BRADYCARDIA ATTRIBUTABLE TO
ATRIOVENTRICULAR BLOCK e90
6.1. Pathophysiology, Etiology, and Classification of Bradycardia Attributable to Atrioventricular Block e90
6.2. Clinical Presentation e91
6.3. Acute Management e92
6.3.1. Acute Management of Reversible Causes of Bradycardia Attributable to Atrioventricular Block e92
6.3.2. Acute Medical Therapy for Bradycardia Attributable to Atrioventricular Block e93
6.3.3. Temporary Pacing for Atrioventricular Block e94
6.4. Chronic Therapy/Management of Bradycardia Attributable to Atrioventricular Block e95
6.4.1. General Principles of Chronic Therapy/Management of Bradycardia Attributable to Atrioventricular Block e97
6.4.2. Transient/Potentially Reversible Causes of Atrioventricular Block e98
6.4.3. Additional Testing for Chronic Therapy/Management of Bradycardia Attributable to Atrioventricular Block e99
6.4.4. Permanent Pacing e100
7. CONDUCTION DISORDERS
(WITH 1:1 ATRIOVENTRICULAR CONDUCTION) e106
7.1. Pathophysiology e106
7.2. Etiology/Classification e106
7.3. Clinical Presentation e106
7.4. Evaluation of Conduction Disorders e106
7.5. Management of Conduction Disorders (With 1:1 Atrioventricular Conduction) e109
8. SPECIAL POPULATIONS e111
8.1. Perioperative Management e111
8.1.1. Patients at Risk for Bradycardia During Noncardiac Surgery or Procedures ..... e111
8.1.2. Postoperative Bradycardia and Conduction Disorders After Cardiac Surgery e112
8.2. Bradycardia Management for Adult Congenital Heart Disease ..... e120
8.3. Management of Bradycardia in Patients With an Acute MI e122
8.4. Neurologic Disorders e123
8.4.1. Epilepsy e124
9. EVALUATION OF THE RISKS FOR VENTRICULAR ARRHYTHMIAS IN PATIENTS WHO REQUIRE PERMANENT PACING e124
10. COST AND VALUE CONSIDERATIONS ..... e125
11. SHARED DECISION-MAKING e125
12. QUALITY OF LIFE e126
13. DISCONTINUATION OF PACEMAKER THERAPY ..... e126
14. END-OF-LIFE CONSIDERATIONS ..... e127
15. KNOWLEDGE GAPS AND FUTURE RESEARCH ... e128
REFERENCES e129
APPENDIX 1
Author Relationships With Industry and Other Entities (Relevant) e153
APPENDIX 2
Abbreviated Reviewer Relationships With Industry and Other Entities e155
TOP 10 TAKE-HOME MESSAGES FOR THE MANAGEMENT OF BRADYCARDIA AND CARDIAC CONDUCTION DELAY
1. Sinus node dysfunction is most often related to age-dependent progressive fibrosis of the sinus nodal tissue and surrounding atrial myocardium leading to abnormalities of sinus node and atrial impulse formation and propagation and will therefore result in various bradycardic or pause-related syndromes.
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2. Both sleep disorders of breathing and nocturnal bradycardias are relatively common, and treatment of sleep apnea not only reduces the frequency of these arrhythmias but also may offer cardiovascular benefits. The presence of nocturnal bradycardias should prompt consideration for screening for sleep apnea, beginning with solicitation of suspicious symptoms. However, nocturnal bradycardia is not in itself an indication for permanent pacing.
3. The presence of left bundle branch block on electrocardiogram markedly increases the likelihood of underlying structural heart disease and of diagnosing left ventricular systolic dysfunction. Echocardiography is usually the most appropriate initial screening test for structural heart disease, including left ventricular systolic dysfunction.
4. In sinus node dysfunction, there is no established minimum heart rate or pause duration where permanent pacing is recommended. Establishing temporal correlation between symptoms and bradycardia is important when determining whether permanent pacing is needed.
5. In patients with acquired second-degree Mobitz type II atrioventricular block, high-grade atrioventricular block, or third-degree atrioventricular block not caused by reversible or physiologic causes, permanent pacing is recommended regardless of symptoms. For all other types of atrioventricular block, in the absence of conditions associated with progressive atrioventricular conduction abnormalities, permanent pacing should generally be considered only in the presence of symptoms that correlate with atrioventricular block.
6. In patients with a left ventricular ejection fraction between 36% to 50% and atrioventricular block, who have an indication for permanent pacing and are expected to require ventricular pacing >40% of the time, techniques that provide more physiologic ventricular activation (e.g., cardiac resynchronization therapy, His bundle pacing) are preferred to right ventricular pacing to prevent heart failure.
7. Because conduction system abnormalities are common after transcatheter aortic valve replacement, recommendations on postprocedure surveillance and pacemaker implantation are made in this guideline.
8. In patients with bradycardia who have indications for pacemaker implantation, shared decision-making and patient-centered care are endorsed and emphasized in this guideline. Treatment decisions are based on the best available evidence and on the patient's goals of care and preferences.
9. Using the principles of shared decision-making and informed consent/refusal, patients with decision-making capacity or his/her legally defined surrogate has the right to refuse or request withdrawal of pacemaker therapy, even if the patient is pacemaker dependent, which should be considered palliative, end-of-life care, and not physician-assisted suicide. However, any decision is complex, should involve all stakeholders, and will always be patient specific.
10. Identifying patient populations that will benefit the most from emerging pacing technologies (e.g., His bundle pacing, transcatheter leadless pacing systems) will require further investigation as these modalities are incorporated into clinical practice.
PREAMBLE
Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a foundation for the delivery of quality cardiovascular care. The ACC and AHA sponsor the development and publication of clinical practice guidelines without commercial support, and members volunteer their time to the writing and review efforts.
Clinical practice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease. The focus is on medical practice in the United States, but these guidelines are relevant to patients throughout the world. Although guidelines may be used to inform regulatory or payer decisions, the intent is to improve quality of care and align with patients' interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances, and should not replace clinical judgment.
Recommendations for guideline-directed management and therapy, which encompasses clinical evaluation, diagnostic testing, and both pharmacological and procedural treatments, are effective only when followed by both practitioners and patients. Adherence to recommendations can be enhanced by shared decision-making between clinicians and patients, with patient engagement in selecting interventions on the basis of individual values, preferences, and associated conditions and comorbidities.
The ACC/AHA Task Force on Clinical Practice Guidelines strives to ensure that the guideline writing committee both contains requisite expertise and is
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representative of the broader medical community by selecting experts from a broad array of backgrounds representing different geographic regions, sexes, races, ethnicities, intellectual perspectives/biases, and scopes of clinical practice, and by inviting organizations and professional societies with related interests and expertise to participate as partners or collaborators. The ACC and AHA have rigorous policies and methods to ensure that documents are developed without bias or improper influence. The complete policy on relationships with industry and other entities (RWI) can be found online.
Beginning in 2017, numerous modifications to the guidelines have been and continue to be implemented to make guidelines shorter and enhance “user friendliness.” Guidelines are written and presented in a modular knowledge chunk format, in which each chunk includes a table of recommendations, a brief synopsis, recommendation-specific supportive text and, when appropriate, flow diagrams or additional tables. Hyperlinked references are provided for each modular knowledge chunk to facilitate quick access and review. More structured guidelines—including word limits (“targets”) and a web guideline supplement for useful but noncritical tables and figures—are 2 such changes. This Preamble is an abbreviated version, with the detailed version available online.
Glenn N. Levine, MD, FACC, FAHA
Chair, ACC/AHA Task Force on Clinical Practice Guidelines
1. INTRODUCTION
1.1. Methodology and Evidence Review
The recommendations listed in this guideline are, whenever possible, evidence based. An initial extensive evidence review, which included literature derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline, was conducted from January 2017 to September 2017. Key search words included but were not limited to the following: AV block, bradycardia, bundle branch block, conduction disturbance, left bundle branch block, loop recorder, pauses, permanent pacemaker, sick sinus syndrome, sinus node dysfunction, and temporary pacemaker. Additional relevant studies, published through January 2018 during the guideline writing process, were also considered by the writing committee and added to the evidence tables when appropriate. The final evidence tables are included in the Online Data Supplement and summarize the evidence used by the writing committee to
formulate recommendations. References selected and published in the present document are representative and not all-inclusive.
As noted in the detailed version of the Preamble, an independent evidence review committee was commissioned to perform a formal systematic review of 1 critical clinical question related to bradycardia, the results of which were considered by the writing committee for incorporation into this guideline. Concurrent with this process, writing committee members evaluated study data relevant to the rest of the guideline. The findings of the evidence review committee and the writing committee members were formally presented and discussed, and then recommendations were developed. The systematic review, titled “Impact of Physiologic Versus Right Ventricular Pacing Among Patients With Left Ventricular Ejection Fraction Greater Than 35%: A Systematic Review for the 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay,” is published in conjunction with this guideline (S1.1-1) and its respective data supplements are available online. The evidence review committee report informed recommendations in Section 6.4.4.1.
1.2. Organization of the Writing Committee
The writing committee consisted of cardiac electrophysiologists, clinicians, cardiologists, surgeons, an anesthesiologist, and a lay/patient representative. The writing committee included representatives from the ACC, AHA, Heart Rhythm Society (HRS), American Association for Thoracic Surgery (AATS), Pediatric & Congenital Electrophysiology Society (PACES), and the Society of Thoracic Surgeons (STS). Appendix 1 of the present document lists writing committee members' relevant RWI. For the purposes of full transparency, the writing committee members' comprehensive disclosure information is available online).
1.3. Document Review and Approval
This document was reviewed by 2 official reviewers each nominated by the ACC, AHA, and HRS; 1 official lay reviewer nominated by the AHA; 1 organizational reviewer each from the AATS, PACES, and STS; and 31 individual content reviewers. Reviewers' RWI information was distributed to the writing committee and is published as an abbreviated table in this document (Appendix 2). The reviewers' detailed RWI information is available online.
This document was approved for publication by the governing bodies of the ACC, the AHA, and the HRS; and was endorsed by the American Association for Thoracic Surgery, the Pediatric & Congenital Electrophysiology Society, and the Society of Thoracic Surgeons.
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1.4. Scope of the Guideline
The purpose of this ACC/AHA/HRS guideline is to provide guidance to clinicians for the management of patients with bradycardia, or symptoms thought to be associated with bradycardia or cardiac conduction system disorders. This guideline supersedes the pacemaker recommendations made in the “ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities” (S1.4-1, S1.4-2) and “2012 ACCF/AHA/HRS Focused Update Incorporated Into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities” (S1.4-2). The guideline will be useful to general internists, family physicians, emergency physicians, anesthesiologists, surgeons, cardiologists, and arrhythmia specialists. This document is aimed at the adult population (>18 years of age) and offers no specific recommendations in pediatric patients, although some of the evidence review included pediatric patients. Although background on the pathophysiology and epidemiology of bradycardia and cardiac conduction disorders is summarized, this guideline is not intended to be an exhaustive review. Rather, it focuses on practical clinical evaluation and management. Specific objectives and goals include:
■ Describe the clinical significance of bradycardia with respect to mortality, symptoms (e.g., syncope, impaired functional capacity), and exacerbations of associated disorders (e.g., ischemia, heart failure, provoked tachyarrhythmias).
■ Address inherited and acquired disorders of the sinus node, atrioventricular node, His-Purkinje fibers, and intramyocardial conducting tissue, including the effects of medications, aging, metabolic derangements, trauma, radiation, infiltrative, ischemic, and inflammatory disorders, infectious and toxic agents, and iatrogenic factors.
■ Delineate the clinical presentation and general approach to clinical evaluation of patients with overt or suspected bradycardias or conduction diseases.
■ Comprehensively evaluate the evidence supporting recommendations for the selection and timing of available diagnostic testing modalities, including monitoring devices and electrophysiologic testing.
■ Define the evidence base supporting recommendations for the use of available treatment modalities, including lifestyle interventions, pharmacotherapy, and external and implanted device-based therapies, with particular attention to indications for temporary and permanent pacing.
■ Address special considerations that may be applicable to distinct populations based on age (>18 years of age), comorbidities or other relevant factors.
■ Identify knowledge gaps, pertinent trials in progress and directions for future research.
Table 1 lists other guidelines and pertinent documents that the writing committee considered for this guideline. The listed documents contain relevant information for the management of patients with bradycardia or cardiac conduction system disorder.
1.5. Class of Recommendation and Level of Evidence
Recommendations are designated with both a class of recommendation (COR) and a level of evidence (LOE). The class of recommendation indicates the strength of recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk. The level of evidence rates the quality of scientific evidence supporting the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 2) (S1.5-1).
1.6. Abbreviations
<table><tr><td>Abbreviation</td><td>Meaning/Phrase</td></tr><tr><td>ACHD</td><td>adult congenital heart disease</td></tr><tr><td>AF</td><td>atrial fibrillation</td></tr><tr><td>CIED</td><td>cardiovascular implantable electronic devices</td></tr><tr><td>CRT</td><td>cardiac resynchronization therapy</td></tr><tr><td>HV</td><td>His-ventricular</td></tr><tr><td>ICD</td><td>implantable cardioverter defibrillator</td></tr><tr><td>ICM</td><td>implantable cardiac monitor</td></tr><tr><td>ECG</td><td>electrocardiogram</td></tr><tr><td>EPS</td><td>electrophysiology study</td></tr><tr><td>LBBB</td><td>left bundle branch block</td></tr><tr><td>LVEF</td><td>left ventricular ejection fraction</td></tr><tr><td>MI</td><td>myocardial infarction</td></tr><tr><td>MRI</td><td>magnetic resonance imaging</td></tr><tr><td>PPM</td><td>permanent pacemaker</td></tr><tr><td>QOL</td><td>quality of life</td></tr><tr><td>RBBB</td><td>right bundle branch block</td></tr><tr><td>RCT</td><td>randomized controlled trial</td></tr><tr><td>RV</td><td>right ventricle</td></tr><tr><td>SACT</td><td>sinoatrial conduction time</td></tr><tr><td>SND</td><td>sinus node dysfunction</td></tr><tr><td>SNRT</td><td>sinus node recovery time</td></tr><tr><td>TAVR</td><td>transcatheter aortic valve replacement</td></tr></table>
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TABLE 1 Associated Guidelines and Related References
<table><tr><td>Title</td><td>Organization</td><td>Publication Year (Reference)</td></tr><tr><td colspan="3">Guidelines</td></tr><tr><td>Ventricular arrhythmias and sudden cardiac death</td><td>ACC/AHA/HRS</td><td>2017 (S1.4-3)</td></tr><tr><td>Syncope</td><td>ACC/AHA/HRS</td><td>2017 (S1.4-4)</td></tr><tr><td>Stable ischemic heart disease</td><td>ACC/AHA/AATS/PCNA/SCAI/STS</td><td>2014* (S1.4-5)2012 (S1.4-6)</td></tr><tr><td>Atrial fibrillation</td><td>AHA/ACC/HRS</td><td>2014 (S1.4-7)</td></tr><tr><td>Perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery</td><td>ACC/AHA</td><td>2014 (S1.4-8)</td></tr><tr><td>Non-ST-elevation acute coronary syndromes</td><td>AHA/ACC</td><td>2014 (S1.4-9)</td></tr><tr><td>Heart failure</td><td>ACC/AHA</td><td>2013 (S1.4-10)</td></tr><tr><td>ST-elevation myocardial infarction</td><td>ACC/AHA</td><td>2013 (S1.4-11)</td></tr><tr><td>Device-based therapy for cardiac rhythm abnormalities</td><td>ACC/AHA/HRS</td><td>2013 (S1.4-2)</td></tr><tr><td>Coronary artery bypass graft surgery</td><td>ACC/AHA</td><td>2011 (S1.4-12)</td></tr><tr><td>Hypertrophic cardiomyopathy</td><td>ACC/AHA</td><td>2011 (S1.4-13)</td></tr><tr><td>Percutaneous coronary intervention</td><td>ACC/AHA/SCAI</td><td>2011 (S1.4-14)</td></tr><tr><td>Guidelines for CPR and emergency cardiovascular care-part 9: post-cardiac arrest care</td><td>AHA</td><td>2010 (S1.4-15)</td></tr><tr><td colspan="3">Other related references</td></tr><tr><td>Expert consensus statement on cardiovascular implantable electronic device lead management and extraction</td><td>HRS</td><td>2017 (S1.4-16)</td></tr><tr><td>Management of cardiac involvement associated with neuromuscular diseases</td><td>AHA</td><td>2017 (S1.4-17)</td></tr><tr><td>Expert consensus statement on magnetic resonance imaging</td><td>HRS</td><td>2017 (S1.4-18)</td></tr><tr><td>Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 9: arrhythmias and conduction defects</td><td>ACC/AHA</td><td>2015 (S1.4-19)</td></tr><tr><td>Expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope</td><td>HRS</td><td>2015 (S1.4-20)</td></tr><tr><td>Expert consensus statement on the recognition and management of arrhythmias in adult congenital heart disease</td><td>PACES/HRS</td><td>2014 (S1.4-21)</td></tr><tr><td>Expert consensus statement on the use of implantable cardioverter-defibrillator therapy in patients who are not included or not well represented in clinical trials</td><td>HRS/ACC/AHA</td><td>2014 (S1.4-22)</td></tr><tr><td>Expert consensus statement on the diagnosis and management of arrhythmias associated with cardiac sarcoidosis</td><td>HRS</td><td>2014 (S1.4-23)</td></tr><tr><td>Cardiac pacing and cardiac resynchronization therapy</td><td>ESC</td><td>2013 (S1.4-24)</td></tr><tr><td>Expert consensus statement on pacemaker device and mode selection</td><td>HRS/ACCF</td><td>2012 (S1.4-25)</td></tr><tr><td>Expert consensus statement on the state of genetic testing for the channelopathies and cardiomyopathies</td><td>HRS/EHRA</td><td>2011 (S1.4-26)</td></tr><tr><td>Expert consensus statement on the management of cardiovascular implantable electronic devices (CIEDs) in patients nearing end of life or requesting withdrawal of therapy</td><td>HRS</td><td>2010 (S1.4-27)</td></tr><tr><td>Recommendations for the standardization and interpretation of the electrocardiogram: part III: intraventricular conduction disturbances: a scientific statement</td><td>AHA/ACCF/HRS</td><td>2009 (S1.4-28)</td></tr><tr><td>Recommendations for the standardization and interpretation of the electrocardiogram: part V: electrocardiogram changes associated with cardiac chamber hypertrophy: a scientific statement</td><td>AHA/ACCF/HRS</td><td>2009 (S1.4-29)</td></tr></table>
*Focused Update.
AATS indicates American Association for Thoracic Surgery; ACC, American College of Cardiology; ACCF, American College of Cardiology Foundation; AHA, American Heart Association; CPR, cardiopulmonary resuscitation; 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.
2. EPIDEMIOLOGY AND DEFINITIONS
2.1. Bradycardia and Conduction Disorders
Because slower heart rates and changes in intercellular conduction can be observed as both part of normal aging and disease progression, bradycardia and conduction abnormalities are more commonly identified in the elderly. Abnormalities of the sinus node, atrial tissue, atrioventricular nodal tissue, and the specialized conduction
system can all contribute to bradycardia, discordant timing of atrial and ventricular depolarization, and abnormal ventricular depolarization.
Sinus node dysfunction (SND), historically referred to as sick sinus syndrome, is most often related to age-dependent, progressive, degenerative fibrosis of the sinus nodal tissue and surrounding atrial myocardium (S2.1-1–S2.1-3). This can result in abnormalities of sinus node and atrial impulse formation and propagation and
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TABLE 2
Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)
CLASS (STRENGTH) OF RECOMMENDATION
CLASS I (STRONG)
Benefit >>> Risk
Suggested phrases for writing recommendations:
■ Is recommended
■ Is indicated/useful/effective/beneficial
■ Should be performed/administered/other
■ Comparative-Effectiveness Phrases†:
- Treatment/Strategy A is recommended/indicated in preference to treatment B
- Treatment A should be chosen over treatment B
CLASS IIa (MODERATE)
Benefit >> Risk
Suggested phrases for writing recommendations:
■ Is reasonable
■ Can be useful/effective/beneficial
■ Comparative-Effectiveness Phrases†:
- Treatment/strategy A is probably recommended/indicated in preference to treatment B
- It is reasonable to choose treatment A over treatment B
CLASS IIb (WEAK)
Benefit ≥ Risk
Suggested phrases for writing recommendations:
■ May/might be reasonable
■ May/might be considered
■ Usefulness/effectiveness is unknown/unelec/uncertain or not well established
CLASS III: No Benefit (MODERATE)
Benefit = Risk
(Generally, LOE A or B use only)
Suggested phrases for writing recommendations:
■ Is not recommended
■ Is not indicated/useful/effective/beneficial
■ Should not be performed/administered/other
CLASS III: Harm (STRONG)
Risk > Benefit
Suggested phrases for writing recommendations:
■ Potentially harmful
■ Causes harm
■ Associated with excess morbidity/mortality
■ Should not be performed/ administered/other
can be associated with various bradycardia or pause-related syndromes. In addition, the same milieu of degenerative fibrosis is also responsible for the development of atrial arrhythmias, which can coexist with sinus node disease and the combination often called “tachy-brady syndrome.” There is evidence that heart block occurs in a portion of patients who have required permanent atrial pacing for SND, suggesting that, in some patients, a similar fibrotic process likely involves the specialized atrioventricular conduction system (S2.1-3, S2.1-4). Data gathered from permanent pacemaker (PPM) studies and the large cohort studies of ARIC
(Atherosclerosis Risk In Communities) and CHS (Cardiovascular Health Study) suggest that SND is most common in individuals who are in their 70s or 80s (S2.1-5–S2.1-7). SND appears to mirror the incidence of pacemaker implantation for atrioventricular nodal disease because both are age related (S2.1-7). In these analyses, ischemic heart disease, heart failure, valvular heart disease, cerebrovascular disease, and atrial fibrillation (AF) were found to be common concurrent issues in this subgroup of patients who require treatment for their atrioventricular nodal disease (S2.1-5–S2.1-7). The intrinsic sinus and atrioventricular nodal diseases present in a similar clinical manner
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to extrinsic/secondary processes that can injure the sinus node, atrioventricular node or conduction system tissues. Multiple pathophysiologic processes (e.g., myocardial ischemia or infarction, infiltrative diseases, collagen vascular disease, surgical trauma, endocrine abnormalities, autonomic effects, neuromuscular disorders (S2.1-2, S2.1-8–S2.1-10), individually or in combination, can compromise impulse initiation and propagation. Whether intrinsic or extrinsic, the clinical manifestations of these pathologies can be identical.
2.2. Definitions
The National Institutes of Health defines bradycardia as a heart rate <60 bpm in adults other than well trained athletes (S2.2-1). However, population studies frequently use a lower cutoff of 50 bpm (S2.2-2, S2.2-3). In an analysis of 4 population studies from the Netherlands, in adults from 20 to 90 years of age, the lowest second percentile for heart rate ranged from 40 to 55 bpm depending on sex and age (S2.2-3). Sinus pauses of 2 seconds and 3 seconds have been described during 24-hour ambulatory electrocardiographic monitoring in healthy elderly patients and long-distance runners, respectively (S2.2-4, S2.2-5). On the basis of the available evidence, for the purposes of this document, we have chosen a sinus rate <50 bpm and/or a sinus pause >3 seconds as potential components of the definitions of SND. However, the presence of sinus bradycardia or a pause >3 seconds alone should not be used for the diagnosis of SND; multiple factors should be recognized and be taken into consideration for the individual patient (Table 3). With rare exceptions, the sole reason for considering any treatment for SND is the presence of symptoms.
Chronotropic incompetence represents failure to reach a target heart rate with exertion relative to expected for age that is inadequate to meet metabolic demand. Because the incremental heart rate achieved with exercise will be dependent on resting heart rate, the most commonly used definition in the literature has been failure to reach 80% of the expected heart rate reserve. Expected heart rate reserve is defined as the difference between the age-predicted maximal heart rate (220 - age) and the resting heart rate. Percentage of expected heart rate reserve is the ratio of demonstrated and predicted heart rate reserve. Although this definition has been used in literature, in practice, specifically defining chronotropic incompetence is difficult (S2.2-8–S2.2-11). Other investigators suggest that another age-related equation (220 - 0.7 × age) is a better predictor for heart rate, while others stress the importance of sex and the presence of comorbidities (S2.2-8–S2.2-10). Collectively, the data suggest that the diagnosis of chronotropic incompetence in a patient requires careful individualized clinical assessment and probably cannot be determined by age
alone. The definitions for atrioventricular block and conduction tissue disorders have been adopted from the 2009 AHA/ACCF/HRS recommendations for the standardization of electrocardiographic measurements (both intraventricular conduction disorders and chamber hypertrophy) (S2.2-7, S2.2-12), although some have argued that stricter criteria are required for left bundle branch block (LBBB) (S2.2-13).
3. CLINICAL MANIFESTATION OF BRADYCARDIA AND CONDUCTION DISORDERS
3.1. Clinical Manifestations of Bradycardia
The clinical manifestations of bradycardia can vary widely from insidious symptoms to episodes of frank syncope. Bradycardia can be broadly classified into 2 general categories: SND and atrioventricular block. The associated wide range of clinical presentations can be explained by the disparate electrophysiologic manifestations, ventricular rates, transience of these abnormalities, overall medical conditions, and medications.
The electrocardiographic findings in patients with SND are varied and the diagnosis may be considered in patients with sinus bradycardia or atrial depolarization from a subsidiary pacemaker other than the sinus node (i.e., ectopic atrial rhythm, junctional rhythm, or ventricular escape), intermittent sinus pauses, or a blunted heart rate response with exercise (chronotropic incompetence) (S3.1-1). The clinical manifestations of atrioventricular block will also depend on whether the atrioventricular block is fixed or intermittent and the ventricular rate or duration of ventricular asystole associated with atrioventricular block. In addition, symptoms will vary depending on underlying cause and timing. For example, patients with vagally mediated atrioventricular block can be asymptomatic if the periods of atrioventricular block occur at night while sleeping when parasympathetic tone is increased. Vagally mediated atrioventricular block during sleep can be recognized by the presence of concomitant sinus node slowing (P-P prolongation). Conversely the sudden increase in parasympathetic tone with vasovagal syncope can cause bradycardia (usually sinus node slowing or sinus arrest, but sometimes with atrioventricular block) (S3.1-2).
Regardless of whether the bradycardia is caused by SND or atrioventricular block, the term “symptomatic bradycardia” is used throughout this document and has been defined as a “documented bradyarrhythmia that is directly responsible for development of the clinical manifestations of syncope or presyncope, transient dizziness or lightheadedness, heart failure symptoms, or confusional states resulting from cerebral hypoperfusion attributable to slow heart rate” (S3.1-3). Direct attribution
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TABLE 3 Table of Definitions
<table><tr><td>Term</td><td>Definition or Description</td></tr><tr><td>Sinus node dysfunction (with accompanying symptoms)</td><td>■ Sinus bradycardia: Sinus rate <50 bpm■ Ectopic atrial bradycardia: Atrial depolarization attributable to an atrial pacemaker other than the sinus node with a rate <50 bpm■ 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.■ Sinus pause: Sinus node depolarizes >3 s after the last atrial depolarization■ Sinus node arrest: No evidence of sinus node depolarization■ Tachycardia-bradycardia ("tachy-brady") syndrome: Sinus bradycardia, ectopic atrial bradycardia, or sinus pause alternating with periods of abnormal atrial tachycardia, atrial flutter, or AF (S2.2-6). The tachycardia may be associated with suppression of sinus node automaticity and a sinus pause of variable duration when the tachycardia terminates.■ 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.■ 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).</td></tr><tr><td>Atrioventricular block (S2.2-7)</td><td>■ 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)■ Second-degree atrioventricular block: P waves with a constant rate (<100 bpm) where atrioventricular conduction is present but not 1:1■ 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■ 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)■ 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■ 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■ Third-degree atrioventricular block (complete heart block): No evidence of atrioventricular conduction■ Vagally mediated atrioventricular block: Any type of atrioventricular block mediated by heightened parasympathetic tone■ Infranodal block: Atrioventricular conduction block where clinical evidence or electrophysiologic evidence suggests that the conduction block occurs distal to the atrioventricular node</td></tr><tr><td>Conduction tissue disease (S2.2-7)</td><td>■ RBBB (as defined in adults):■ Complete RBBB:1. QRS duration ≥120 ms2. rsr', rsR', rSR', or rarey a qR in leads \( V_1 \) or \( V_2 \). The R' or r' 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 \( V_2 \).3. S wave of greater duration than R wave or >40 ms in leads I and \( V_6 \) in adults4. Normal R peak time in leads \( V_5 \) and \( V_6 \) but >50 ms in lead \( V_1 \)Incomplete RBBB: Same QRS morphology criteria as complete RBBB but with a QRS duration between 110 and 119 ms</td></tr><tr><td>■ LBBB (as defined in adults):Complete LBBB:1. QRS duration ≥120 ms in adults2. 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 complex3. Absent Q waves in leads I, \( V_5 \), and \( V_6 \), but in the lead aVL, a narrow Q wave may be present in the absence of myocardial pathology4. R peak time >60 ms in leads \( V_5 \) and \( V_6 \) but normal in leads \( V_1 \), \( V_2 \), and \( V_3 \), when small initial R waves can be discerned in the precordial leads5. ST and T waves usually opposite in direction to QRS</td></tr><tr><td>■ Incomplete LBBB:1. QRS duration between 110 and 119 ms in adults2. Presence of left ventricular hypertrophy pattern3. R peak time >60 ms in leads \( V_4 \), \( V_5 \), and \( V_6 \)4. Absence of Q wave in leads I, \( V_5 \), and \( V_6 \)</td></tr><tr><td>■ Nonspecific intraventricular conduction delay (as defined in adults): QRS duration >110 ms where morphology criteria for RBBB or LBBB are not present■ Left anterior fascicular block:■ QRS duration <120 ms■ Frontal plane axis between -45° and -90°■ qR (small r, tall R) pattern in lead aVL■ R-peak time in lead aVL of ≥45 ms■ rS pattern (small r, deep S) in leads II, III, and aVF</td></tr></table>
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TABLE 3 Continued
<table><tr><td>Term</td><td>Definition or Description</td></tr><tr><td>■ Left posterior fascicular block:</td><td></td></tr><tr><td>■ QRS duration <120 ms</td><td></td></tr><tr><td>■ 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.</td><td></td></tr><tr><td>■ rS (small r, deep S) pattern in leads I and aVL</td><td></td></tr><tr><td>■ qR (small q, tall R) pattern in leads III and aVF</td><td></td></tr></table>
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.
of bradycardia as the sole source of symptoms is challenging. For example, in patients with vasovagal syncope, bradycardia is often accompanied by a significant vaso-depressor effect. In addition, nonspecific symptoms such as fatigue can be multifactorial and therefore difficult to correlate with bradycardia particularly in the setting of modest resting sinus bradycardia or with exercise (S3.1-4).
3.2. Clinical Manifestations of Conduction Disorders
The clinical manifestations of conduction tissue disease primarily will depend on the underlying cause of the conduction tissue disorder. Patients may often be asymptomatic, particularly in the setting of isolated right bundle branch block (RBBB) or fascicular block. However, patients with LBBB may present with heart failure that may be attributable to cardiac dyssynchrony or because
of an underlying cardiomyopathy. The definitions outlined in the “AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram: Part III: Intraventricular Conduction Disturbances” (S3.2-1) are used for this document, although it is acknowledged that these recommendations are not without controversy (S3.2-1).
4. GENERAL EVALUATION OF PATIENTS WITH DOCUMENTED OR SUSPECTED BRADYCARDIA OR CONDUCTION DISORDERS
4.1. History and Physical Examination of Patients With Documented or Suspected Bradycardia or Conduction Disorders
Recommendation for History and Physical Examination in Patients With Documented or Suspected Bradycardia or Conduction Disorders
<table><tr><td>COR</td><td>LOE</td><td>RECOMMENDATION</td></tr><tr><td>I</td><td>C-EO</td><td>1. In patients with suspected bradycardia or conduction disorders a comprehensive history and physical examination should be performed.</td></tr></table>
Synopsis
The history and physical examination remains the foundation for the medical evaluation of any patient and is particularly helpful for the patient with possible arrhythmias (Figures 1, 2, and 3). The 2017 ACC/AHA/HRS guideline for the evaluation of syncope and the 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death emphasize the importance of the history and physical examination in the initial evaluation particularly for identifying those patients with structural heart disease (S4.1-1, S4.1-2).
Recommendation-Specific Supportive Text
1. The history should outline the frequency, timing, duration, severity, longevity, circumstances, triggers and alleviating factors of symptoms suspicious for bradycardia or conduction disorders. The relationship
of the symptoms to medications, meals, medical interventions, emotional distress, physical exertion, positional changes, and triggers (e.g., urination, defecation, cough, prolonged standing, shaving, tight collars, and head turning) can help narrow the broad differential diagnosis. Because of the propensity of some commonly prescribed medications (and nutraceuticals) to elicit or exacerbate bradyarrhythmias, a thorough review of both prescription and over-the-counter medications is essential (Table 4 and Table S1 in the Web Supplement). Bradycardia and conduction tissue disorders can be the first manifestation of a systemic illness or heart disease (Table 5). A complete history should include comprehensive cardiovascular risk assessment, family history, travel history, and review of systems. Like the medical history, the physical examination should not only focus on manifestations of bradycardia but also signs of underlying structural heart
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FIGURE 1 Evaluation of Bradycardia and Conduction Disease Algorithm
Colors correspond to Class of Recommendation in Table 2. See Section 4 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 4.3.2., Figure 2. ‡Refer to Section 4.3.2., Figure 3. § Refer to Section 7.4., Figure 8. || Monitor choice based on the frequency of symptoms. AV indicates atrioventricular; and ECG, electrocardiogram/electrocardiographic.
disease and systemic disorders. Care should be taken to correlate slow radial pulses with precordial auscultation or carotid pulse assessment as some rhythms (e.g., ventricular or conducted atrial bigeminy) can be misinterpreted as bradycardia if premature beats generate inadequate stroke volume to be palpable peripherally. As disorders of autonomic regulation figure prominently in the differential diagnosis of syncope and near syncope, orthostatic changes in heart rate and blood pressure can be helpful. Carotid sinus massage can be helpful in patients with symptoms suggestive of carotid
sinus hypersensitivity syndrome (syncope or near syncope elicited by tight collars, shaving, or turning the head). Carotid sinus massage should be performed in both the supine and upright position in a safe environment with careful blood pressure and electrocardiographic monitoring. Careful carotid auscultation (and/or carotid ultrasound) to exclude an ipsilateral carotid bruit (or significant abnormalities) is mandatory before performing this maneuver as strokes precipitated by carotid sinus massage have been reported (S4.1-5).
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FIGURE 2 Initial Evaluation of Suspected or Documented SND Algorithm
Colors correspond to Class of Recommendation in Table 2. See Section 4 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 5.5.4.1., Figure 6. ACHD indicates adult congenital heart disease; CM, cardiomyopathy; and ECG, electrocardiogram/electrocardiographic.
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FIGURE 3 Initial Evaluation of Suspected Atrioventricular Block Algorithm
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 6.4., 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.
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TABLE 4 Medications That Can Induce/Exacerbate Bradycardia or Conduction Disorders
<table><tr><td>Antihypertensive</td><td>Antiarrhythmic</td><td>Psychoactive</td><td>Other</td></tr><tr><td>Beta-adrenergic receptor blockers (including beta-adrenergic blocking eye drops used for glaucoma)</td><td>Adenosine ■ Diltramine ■ Dronedarone ■ Propactinamide ■ Propafenone ■ Quinidine ■ Sotalol</td><td>Donepezil ■ Lithium ■ Opioid analgesics ■ Phenothiazine antiemetics and antipsychotics ■ Phentizine ■ Selective serotonin reuptake inhibitors ■ Tricyclic antidepressants</td><td>Anesthetic drugs (propofol) ■ Cannabis ■ Digoxin ■ Ivabradine ■ Muscle relaxants (e.g., succinylcholine)</td></tr></table>
TABLE 5 Conditions Associated With Bradycardia and Conduction Disorders
Intrinsic
Cardiomyopathy (ischemic or nonischemic)
Congenital heart disease
Degenerative fibrosis
Infection/inflammation
Chagas disease
Diphtheria
■ Infectious endocarditis
Lyme disease
Myocarditis
Sarcoidosis
Toxoplasmosis
Infiltrative disorders
Amyloidosis
Hemochromatosis
Lymphoma
Ischemia/infarction
Rheumatological conditions
■ Rheumatoid arthritis
Scleroderma
■ Systemic lupus erythematosus
Surgical or procedural trauma
■ Cardiac procedures such as ablation or cardiac catheterization
■ Congenital heart disease surgery
■ Septal myomectomy for hypertrophic obstructive cardiomyopathy
■ Valve surgery (including percutaneous valve replacement)
Extrinsic
Autonomic perturbation
■ Carotid sinus hypersensitivity
■ Neurally-mediated syncope/presyncope
■ Physical conditioning
■ Situational syncope
Cough
Defecation
■ Glottic stimulation
■ Medical procedures
■ Micturition
■ Vomiting
■ Sleep (with or without sleep apnea)
Metabolic
Acidosis
■ Hyperkalemia
■ Hypokalemia
■ Hypothermia
■ Hypothyroidism
Hypoxia
Adapted with permission from Mangrum and DiMarco (S4.1-3) and Vogler et al. (S4.1-4).
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4.2. Noninvasive Evaluation
4.2.1. Resting ECG in Patients With Documented or Suspected Bradycardia or Conduction Disorders
Recommendation for Electrocardiogram (ECG) in Patients With Documented or Suspected Bradycardia or Conduction Disorders Referenced studies that the support recommendation are summarized in Online Data Supplement 1.
<table><tr><td>COR</td><td>LOE</td><td>RECOMMENDATION</td></tr><tr><td>1</td><td>B-NR</td><td>1. In patients with suspected bradycardia or conduction disorder, a 12-lead ECG is recommended to document rhythm, rate, and conduction, and to screen for structural heart disease or systemic illness (S4.2.1-1-S4.2.1-4).</td></tr></table>
Synopsis
The resting ECG is an essential component of the initial evaluation of those with known or suspected bradycardia or conduction disorder. An appropriately timed ECG during a symptomatic episode may provide a definitive diagnosis. For those in whom physical examination or telemetry monitoring suggest bradycardia or conduction disturbance, a 12-lead ECG is useful to confirm the rhythm and rate, the nature and extent of conduction disturbance, and to document other abnormalities suggestive of structural heart or systemic disease (e.g., left ventricular hypertrophy, diagnostic Q waves, prolonged corrected QT interval, findings suggestive of hyperkalemia).
Recommendation-Specific Supportive Text
1. Unless a patient with suspected bradycardia or conduction disorder is symptomatic or bradycardic at the time of the recording, the 12-lead ECG will not provide a rhythm correlation with symptoms. In patients presenting with syncope, the initial ECG provides a diagnosis in only approximately 5% (S4.2.1-2, S4.2.1-4) and in those with less well-defined clinical presentations and nonspecific symptoms, the diagnostic yield is probably lower. However, an abnormal initial ECG is predictive of adverse outcomes in patients presenting
with syncope and near syncope, in large part as an indicator of underlying structural heart disease or the presence of systemic disease. A multicenter, prospective observational study of syncope evaluated in the emergency department concluded that a broad range of electrocardiographic abnormalities was associated with increased all-cause mortality at 1 year (S4.2.1-1). The prognostic value of an abnormal initial ECG in those with syncope and near syncope is reflected in its inclusion in most published multivariate risk scores used to predict adverse outcomes in this population (S4.2.1-5). This risk does not necessarily correlate with pathological bradycardia as the mechanism of syncope, as only approximately 10% of syncope can be attributed to bradycardia or a conduction disorder at the time of initial presentation. An additional 18% can be attributed to neurally mediated syncope which frequently is manifest by both bradycardia and hypotension (S4.2.1-2).
4.2.2. 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.
<table><tr><td>COR</td><td>LOE</td><td>RECOMMENDATIONS</td></tr><tr><td>Ila</td><td>B-NR</td><td>1. In patients with suspected chronotropic incompetence, exercise electrocardiographic testing is reasonable to ascertain the diagnosis and provide information on prognosis (S4.2.2-1, S4.2.2-2).</td></tr><tr><td>Ila</td><td>C-LD</td><td>2. In patients with exercise-related symptoms suspicious for bradycardia or conduction disorders, or in patients with 2:1 atrioventricular block of unknown level, exercise electrocardiographic testing is reasonable (S4.2.2-3, S4.2.2-4).</td></tr></table>
Synopsis
Although there is no routine role for exercise electrocardiographic testing in the evaluation of patients with suspected or documented bradycardia/conduction disorder, it may be useful in selected patients. Limited
observational data suggest that it can be useful in evaluating those whose symptoms occur during or immediately after exercise, including those suspected of chronotropic incompetence and exercise-induced, neurally mediated syncope. Occasionally, patients manifest conduction
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disorders precipitated by myocardial ischemia during exercise electrocardiographic testing. Exercise testing can be helpful in evaluating
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