7/6/23, 11:17 AM Sinus bradycardia - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Sinus bradycardia : Munther K Homoud, MD : Jonathan Piccini, MD, MHS, FACC, FAHA, FHRS : Susan B Yeon, MD, JD, FACC All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Apr 25, 2022. INTRODUCTION Sinus bradycardia is a rhythm in which the rate of impulses arising from the sinoatrial (SA) node is lower than expected. The normal adult heart rate, arising from the SA node, has been considered historically to range from 60 to 100 beats per minute, with sinus bradycardia being defined as a sinus rhythm with a rate below 60 beats per minute. The heart rate reflects a complex interplay between the sympathetic and parasympathetic nervous systems. It is affected by numerous factors, including age and physical conditioning ( table 1) [1,2]. Sinus arrhythmia, the fluctuation in sinus rate with respiratory cycles, often accompanies sinus bradycardia. (See "Normal sinus rhythm and sinus arrhythmia".) The etiology, clinical presentation, evaluation, and management of sinus bradycardia will be reviewed here. Primary sinus node dysfunction (ie, sinus node dysfunction) is discussed in detail separately. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation" and "Sinus node dysfunction: Treatment".) DEFINITION AND ECG FEATURES Normal sinus rhythm (NSR) is the characteristic rhythm of the healthy heart. NSR is considered to be present in adults if the heart rate is between 60 and 100 beats per minute, the P wave vector on the electrocardiogram (ECG) is normal (ie, consistent with SA nodal impulse origin), https://www.uptodate.com/contents/sinus-bradycardia/print 1/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate and the rate is largely regular ( waveform 1). The normal sinus P wave demonstrates right atrial followed by left atrial depolarization and high to low atrial activation giving rise to an upright P wave in leads I, II, and aVL, and a negative P wave in lead aVR. By conventional definition, bradycardia indicates a heart rate less than 60 beats per minute with a normal P wave vector on the surface ECG. As such, sinus bradycardia is typically thought of as sinus rhythm occurring at a rate of less than 60 beats per minute, although one professional society has advocated a rate of less than 50 beats per minute ( waveform 2) [3]. A rate less than 50 beats per minute may be a more pragmatic definition, as most patients with sinus rates in the 50s are asymptomatic. It is important to note that the rate at which a patient is labeled as having bradycardia is somewhat age dependent. ETIOLOGY Sinus bradycardia occurs in healthy patients as an adaptive response, particularly in well- conditioned persons or while sleeping, but it can also occur as a pathologic response in a variety of conditions. It is very important to recognize that in normal healthy children and adults, sinus bradycardia is a frequent and normal finding, particularly during sleep when rates may transiently drop as low as 30 beats per minute, and pauses of up to two seconds are not uncommon [4-7]. Sinus bradycardia may also be seen in the absence of heart disease in the following settings: Well-conditioned athletes, particularly in endurance athletic activities, where bradycardia is generally attributed to increased vagal tone induced by exercise conditioning [8-12]. Some older adult patients, although this may represent an early manifestation of sinus node dysfunction (SND) [13]. Sinus bradycardia may represent a manifestation of rare familial forms of SND that have been described. Mutations in two genes, HCN4 and SCN5A, have been associated with sinoatrial (SA) node dysfunction as well as other hereditary arrhythmic disorders such as the Brugada syndrome, atrial fibrillation, and progressive cardiac conduction disease [14- 16]. Sinus bradycardia can be seen in a variety of pathophysiologic settings ( table 2), including: Sinus node dysfunction Sinus bradycardia may be the first manifestation of SA node dysfunction [17,18]. Primary disease of the SA node is discussed in detail separately. (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation".) https://www.uptodate.com/contents/sinus-bradycardia/print 2/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate Medications A number of drugs can depress the SA node and slow the heart rate as either an expected response to or side effect of therapy, or as a toxicity related to overdose. These include: Parasympathomimetic agents (eg, acetylcholine, carbachol, acetylcholinesterase inhibitors) Sympatholytic drugs (eg, beta blockers, methyldopa, clonidine) Opioids and sedatives Cimetidine Digitalis Non-dihydropyridine calcium channel blockers (diltiazem and verapamil) Ivabradine Amiodarone and other antiarrhythmic drugs The chronic hepatitis C drugs sofosbuvir and daclatasvir in patients receiving amiodarone [19] Lithium Chemotherapeutic agents (eg, thalidomide, lenalidomide, paclitaxel) Organophosphate compounds [20] A 2020 scientific statement from the American Heart Association details drugs associated with bradycardia [21]. Acute myocardial infarction Sinus bradycardia occurs in 15 to 25 percent of patients with acute myocardial infarction, particularly those involving the right coronary artery as it supplies the SA node in approximately 60 percent of people. Increased vagal activity is primarily responsible, and the bradycardia is typically transient. If treatment is necessary because of hemodynamic compromise or ischemia, sinus bradycardia usually responds well to intravenous atropine (0.6 to 1.0 mg in the majority of cases). (See "Supraventricular arrhythmias after myocardial infarction", section on 'Sinus bradycardia'.) Obstructive sleep apnea Individuals with obstructive sleep apnea frequently have sinus bradycardia that may be severe (<30 beats per minute) during apneic episodes [22]. Therapies to improve the apnea frequently alleviate the bradycardia [23]. (See "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Other arrhythmias'.) Exaggerated vagal activity Vasovagal responses may be associated with a profound bradycardia due to heightened parasympathetic activity and sympathetic withdrawal on the SA node. There are a variety of stimuli for vagal activation, including carotid sinus stimulation, vomiting, coughing, and Valsalva maneuver. The combination of the slow https://www.uptodate.com/contents/sinus-bradycardia/print 3/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate heart rate and an associated decline in peripheral vascular resistance is often sufficient to produce presyncope or syncope. (See "Reflex syncope in adults and adolescents: Clinical presentation and diagnostic evaluation".) Increased intracranial pressure and other central nervous system conditions Increased intracranial pressure should be excluded when sinus bradycardia occurs in a patient with neurologic dysfunction. Stroke is another neurological condition that can display sinus bradycardia. Sinus bradycardia is also seen with trauma to the cervical or thoracic spine where sympathetic denervation of the heart leaves an unopposed parasympathetic tone [24]. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Clinical manifestations'.) Infectious causes Infectious agents associated with relative sinus bradycardia include Lyme disease, Chagas disease, legionella, psittacosis, Q fever, typhoid fever, typhus, babesiosis, malaria, leptospirosis, yellow fever, dengue fever, viral hemorrhagic fevers, trichinosis, and Rocky Mountain Spotted fever [25,26]. Other causes Other causes of sinus bradycardia include hypothyroidism, anorexia nervosa, hypothermia, and severe prolonged hypoxia. Sinus bradycardia is also seen in the long QT syndrome and in the catecholaminergic polymorphic ventricular tachycardia syndrome, two forms of genetic channelopathies. CLINICAL PRESENTATION In the vast majority of patients, sinus bradycardia itself does not directly cause symptoms, although a patient with comorbid conditions that might be exacerbated by reduced cardiac output (eg, angina, heart failure) may present with worsening symptoms related to the comorbidity. Symptoms related to the slow heart rate itself can occur, including lightheadedness, presyncope or syncope, worsening of angina pectoris or heart failure, cognitive slowing, and exercise intolerance. Symptoms may be subtle, with many patients noting only fatigue, which is frequently ascribed to aging rather than bradycardia. There is no specific heart rate below which all patients develop symptoms, as cardiac output will vary depending upon the ability to increase stroke volume related to underlying conditioning or comorbidities. Sinus bradycardia associated with pathology of the sinoatrial node is part of the sinus node dysfunction (SND). SND often does not respond appropriately to exercise (chronotropic incompetence), and fatigue or dyspnea on exertion may be the presenting feature. SND and https://www.uptodate.com/contents/sinus-bradycardia/print 4/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate chronotropic incompetence are discussed in detail separately. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and "Prognostic features of stress testing in patients with known or suspected coronary disease", section on 'Heart rate response to exercise'.) EVALUATION Confirm sinus bradycardia Sinus bradycardia is generally confirmed by ECG after a slow pulse is identified on physical examination, with the diagnosis usually being easy to establish from the surface ECG. An upright P wave in leads I, II, and aVL, and a negative P wave in lead aVR, indicates a sinus origin of the bradycardia. It is vital to exclude other causes of bradyarrhythmias such as atrioventricular (AV) block. Differential diagnosis Sinus bradycardia should be distinguished from other bradyarrhythmias ( table 3) resulting in a reduced heart rate (ie, second- or third-degree AV block, junctional escape rhythm, ventricular escape rhythm). This is easily done by establishing the 1:1 relationship between P waves and QRS complexes on the surface ECG. Patients with more than one P wave for every QRS complex have second- or third-degree AV block, while patients with no discernible P waves will have an escape rhythm (either junctional or ventricular in origin). The heart rate is often clinically assessed by detection of the pulse with a plethysmograph system, and conditions other than sinus bradycardia can cause a reduction in measured pulse rate (for example, ventricular bigeminy, in which the premature ventricular complex beats result in diminished pulse pressure, which may not be detected). In such cases of ineffective bigeminy, a falsely low heart rate can be recorded. Thus, it is important to always obtain an ECG when new or unexpected bradycardia is identified. Further evaluation For the majority of patients with sinus bradycardia, the underlying cause can usually be determined from history and physical examination alone. In addition to the measurement of a full set of vital signs, including temperature and pulse oximetry, important features to elicit in a history and examination include: Quantity of exercise performed and level of fitness Exposure to medications and toxins Signs of infectious exposure (eg, tick or insect bites) or other systemic conditions (eg, eating disorders, hypothyroidism) The evaluation of a patient who presents with sinus bradycardia requires a comprehensive evaluation where the history is probably the most important component of the evaluation https://www.uptodate.com/contents/sinus-bradycardia/print 5/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate ( algorithm 1). The aim of the initial evaluation is to establish the presence or absence of symptoms, and any evidence of hemodynamic compromise as a result of the bradycardia. This may include hypotension, chest discomfort, altered mental status, or shortness of breath. The presence of hemodynamic compromise demands immediate attention to the cause of the bradycardia and its amelioration. Once hemodynamic compromise has been excluded, the clinician will have to exclude diseases, cardiovascular or other, associated with sinus bradycardia and, most importantly, drugs associated with sinus bradycardia ( algorithm 1). The list of medications, cardiovascular and otherwise, that suppress the sinus node is extensive. Symptoms may be subtle such as lightheadedness, unexplained falls, or exertional dyspnea due to chronotropic incompetence, or they may be pronounced such as syncope. These symptoms point to underlying sinus node disease, which may or may not be exacerbated by drugs that suppress the sinus node. Sinus bradycardia in a healthy, athletic individual requires no further evaluation or intervention. On the other hand, sinus bradycardia in an older individual may indicate sinus node dysfunction (SND) [27]. Sinus bradycardia may be associated with ischemic heart disease if the blood supply to the sinus node (right coronary artery or, in some patients, the left circumflex artery) is compromised. Patients with congestive heart failure have slower heart rates than their healthy counterparts [28]. Sinus bradycardia in an individual with a history of atrial fibrillation and/or conduction disease, especially if associated with a family history of sinoatrial node dysfunction, should raise the possibility of a hereditary form of SND [15]. MANAGEMENT For asymptomatic patients with sinus bradycardia, treatment is neither indicated nor required. The following approach should be followed when symptoms occur ( algorithm 1): For patients with symptoms who have evidence of hemodynamic instability, we administer atropine (1.0 mg intravenous [IV] push, which can be repeated every three to five minutes, if needed, to a total dose of 3 mg) [29-31]. If symptoms do not improve following atropine, proceed with temporary cardiac pacing and/or IV dopamine or epinephrine infusion [29-31]. (See "Temporary cardiac pacing" and "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia'.) If beta adrenergic or calcium channel blocker overdose is suspected, administer IV glucagon. The glucagon dose is 3 to 10 mg IV bolus given over three to five minutes; the bolus may repeat once if no response (increase in heart rate). If there is a response to https://www.uptodate.com/contents/sinus-bradycardia/print 6/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate bolus glucagon therapy, start a continuous infusion at 3 to 5 mg per hour titrated according to response [30]. If symptoms improve, the patient should be monitored with continuous cardiac telemetry. For patients who are hemodynamically stable, the following should be considered: Patients with signs or symptoms of acute myocardial ischemia or infarction should be treated accordingly. (See "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Overview of the acute management of ST-elevation myocardial infarction".) Patients with evidence of another systemic condition associated with sinus bradycardia (eg, hypothyroidism, infection, etc) should be treated accordingly. (See "Treatment of primary hypothyroidism in adults" and "Lyme carditis".) Patients in whom a medication is suspected to be causing the symptomatic bradycardia should have the medication withheld. If the medication is mandatory for the treatment of a comorbid condition (eg, beta blockers for severe angina), a permanent pacemaker may be required [30]. If the symptoms resolve and heart rate improves following the withdrawal of the suspected offending agent, no additional immediate treatment is required. Patients with no other evidence of a potential cause should be evaluated for SND. (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation".) PROGNOSIS There is no adverse prognostic significance to sinus bradycardia in otherwise healthy subjects. In subjects over the age of 40, for example, there is no adverse effect on longevity [32]. INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." th th The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more https://www.uptodate.com/contents/sinus-bradycardia/print 7/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Basics topics (see "Patient education: Bradycardia (The Basics)") SUMMARY AND RECOMMENDATIONS Definition Sinus bradycardia, most commonly defined as sinus rhythm with a rate below 60 beats per minute ( waveform 2), occurs in normal children and adults, particularly during sleep or at rest, in well-conditioned athletes, and in some older adult patients. Sinus bradycardia can also be seen in a variety of pathophysiologic settings, most commonly due to medication effects/toxicities or primary sinoatrial disease ( table 2). (See 'Definition and ECG features' above and 'Etiology' above.) Symptoms In the vast majority of patients, sinus bradycardia itself does not cause symptoms. However, a slow heart rate can cause symptoms such as fatigue, lightheadedness, and presyncope or syncope. Patients with comorbid conditions that might be exacerbated by reduced cardiac output (eg, angina, heart failure) may present with worsening symptoms related to the comorbidity. (See 'Clinical presentation' above.) Evaluation The aim of the initial evaluation is to establish the presence or absence of symptoms, and any evidence of hemodynamic compromise as a result of the bradycardia ( algorithm 1). Once hemodynamic compromise has been excluded, the clinician will have to exclude diseases, cardiovascular or other, associated with sinus bradycardia and, most importantly, drugs associated with sinus bradycardia. (See 'Further evaluation' above.) Management For asymptomatic patients with sinus bradycardia, treatment is neither indicated nor required. The approach to the treatment of patients with symptomatic sinus bradycardia is presented within the text and the adjoining algorithm ( algorithm 1). (See 'Management' above.) Prognosis There is no adverse prognostic significance to asymptomatic sinus bradycardia in otherwise healthy subjects. (See 'Prognosis' above.) https://www.uptodate.com/contents/sinus-bradycardia/print 8/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate ACKNOWLEDGMENT The UpToDate editorial staff acknowledges Leonard Ganz, MD, who contributed to an earlier version of this topic review. Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Spodick DH. Normal sinus heart rate: sinus tachycardia and sinus bradycardia redefined. Am Heart J 1992; 124:1119. 2. Spodick DH, Raju P, Bishop RL, Rifkin RD. Operational definition of normal sinus heart rate. Am J Cardiol 1992; 69:1245. 3. Kadish AH, Buxton AE, Kennedy HL, et al. ACC/AHA clinical competence statement on electrocardiography and ambulatory electrocardiography. A report of the ACC/AHA/ACP- ASIM Task Force on Clinical Competence (ACC/AHA Committee to Develop a Clinical Competence Statement on Electrocardiography and Ambulatory Electrocardiography). J Am Coll Cardiol 2001; 38:2091. 4. Scott O, Williams GJ, Fiddler GI. Results of 24 hour ambulatory monitoring of electrocardiogram in 131 healthy boys aged 10 to 13 years. Br Heart J 1980; 44:304. 5. Brodsky M, Wu D, Denes P, et al. Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol 1977; 39:390. 6. Bjerregaard P. Mean 24 hour heart rate, minimal heart rate and pauses in healthy subjects 40-79 years of age. Eur Heart J 1983; 4:44. 7. Hilgard J, Ezri MD, Denes P. Significance of ventricular pauses of three seconds or more detected on twenty-four-hour Holter recordings. Am J Cardiol 1985; 55:1005. 8. Talan DA, Bauernfeind RA, Ashley WW, et al. Twenty-four hour continuous ECG recordings in long-distance runners. Chest 1982; 82:19. 9. Abdon NJ, Landin K, Johansson BW. Athlete's bradycardia as an embolising disorder? Symptomatic arrhythmias in patients aged less than 50 years. Br Heart J 1984; 52:660. 10. Balady GJ, Cadigan JB, Ryan TJ. Electrocardiogram of the athlete: an analysis of 289 professional football players. Am J Cardiol 1984; 53:1339. 11. Northcote RJ, Canning GP, Ballantyne D. Electrocardiographic findings in male veteran endurance athletes. Br Heart J 1989; 61:155. https://www.uptodate.com/contents/sinus-bradycardia/print 9/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate 12. Corrado D, Basso C, Schiavon M, Thiene G. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med 1998; 339:364. 13. Agruss NS, Rosin EY, Adolph RJ, Fowler NO. Significance of chronic sinus bradycardia in elderly people. Circulation 1972; 46:924. 14. Milanesi R, Baruscotti M, Gnecchi-Ruscone T, DiFrancesco D. Familial sinus bradycardia associated with a mutation in the cardiac pacemaker channel. N Engl J Med 2006; 354:151. 15. Ruan Y, Liu N, Priori SG. Sodium channel mutations and arrhythmias. Nat Rev Cardiol 2009; 6:337. 16. Hao X, Zhang Y, Zhang X, et al. TGF- 1-mediated fibrosis and ion channel remodeling are key mechanisms in producing the sinus node dysfunction associated with SCN5A deficiency and aging. Circ Arrhythm Electrophysiol 2011; 4:397. 17. Alpert MA, Flaker GC. Arrhythmias associated with sinus node dysfunction. Pathogenesis, recognition, and management. JAMA 1983; 250:2160. 18. Eraut D, Shaw DB. Sinus bradycardia. Br Heart J 1971; 33:742. 19. Renet S, Chaumais MC, Antonini T, et al. Extreme bradycardia after first doses of sofosbuvir and daclatasvir in patients receiving amiodarone: 2 cases including a rechallenge. Gastroenterology 2015; 149:1378. 20. Ludomirsky A, Klein HO, Sarelli P, et al. Q-T prolongation and polymorphous ("torsade de pointes") ventricular arrhythmias associated with organophosphorus insecticide poisoning. Am J Cardiol 1982; 49:1654. 21. Tisdale JE, Chung MK, Campbell KB, et al. Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association. Circulation 2020; 142:e214. 22. Caples SM, Rosen CL, Shen WK, et al. The scoring of cardiac events during sleep. J Clin Sleep Med 2007; 3:147. 23. Becker H, Brandenburg U, Peter JH, Von Wichert P. Reversal of sinus arrest and atrioventricular conduction block in patients with sleep apnea during nasal continuous positive airway pressure. Am J Respir Crit Care Med 1995; 151:215. 24. Gilson GJ, Miller AC, Clevenger FW, Curet LB. Acute spinal cord injury and neurogenic shock in pregnancy. Obstet Gynecol Surv 1995; 50:556. 25. Cunha BA. The diagnostic significance of relative bradycardia in infectious disease. Clin Microbiol Infect 2000; 6:633. 26. Puljiz I, Beus A, Kuzman I, Seiwerth S. Electrocardiographic changes and myocarditis in trichinellosis: a retrospective study of 154 patients. Ann Trop Med Parasitol 2005; 99:403. https://www.uptodate.com/contents/sinus-bradycardia/print 10/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate 27. Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. Circulation 2007; 115:1921. 28. Sanders P, Kistler PM, Morton JB, et al. Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve. Circulation 2004; 110:897. 29. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122:S729. 30. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 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. 31. https://cpr.heart.org/-/media/CPR-Files/CPR-Guidelines-Files/Algorithms/AlgorithmACLS_Bra dycardia_200612.pdf (Accessed on January 06, 2022). 32. Tresch DD, Fleg JL. Unexplained sinus bradycardia: clinical significance and long-term prognosis in apparently healthy persons older than 40 years. Am J Cardiol 1986; 58:1009. Topic 1075 Version 31.0 https://www.uptodate.com/contents/sinus-bradycardia/print 11/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate GRAPHICS Normal heart rates in adults based on age and sex HR (beats per minute) Age All Male Female (years) N Mean 1%-99% N Mean 1%-99% N Mean 1%-99% 20-29 6086 67 43-98 3127 64 42-99 2959 69 46-99 30-39 9569 69 46-100 4605 67 44-99 4964 70 48-100 40-49 15,392 69 46-101 7104 68 45-101 8288 70 48-102 50-59 18,578 68 46-102 9936 68 45-102 8642 69 47-102 60-69 16,585 67 44-102 9457 65 42-102 7128 68 46-101 70-79 8432 65 43-101 4509 64 42-102 3923 67 44-101 80-89 2259 65 44-101 1001 63 41-98 1258 67 46-102 90-99 119 70 43-146 58 64 43-95 81 72 44-147 Normal heart rate values (with range from 1st to 99th percentile) for heart rate (beats/minute) in 77,276 healthy adults according to age and gender. %: percent; HR: heart rate. Data from: Mason JW, Ramseth DJ, Chanter DO, et al. Electrocardiographic reference ranges derived from 79,743 ambulatory subjects. J Electrocardiol 2007; 40:228. Graphic 77746 Version 4.0 https://www.uptodate.com/contents/sinus-bradycardia/print 12/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate ECG of sinus rhythm to Normal electrocardiogram (ECG) Normal sinus rhythm at a rate of 71 beats/minute, a P wave axis of 45 , and a PR interval of 0.15 seconds. ECG: electrocardiogram. Courtesy of Morton Arnsdorf, MD. Graphic 58149 Version 5.0 https://www.uptodate.com/contents/sinus-bradycardia/print 13/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate Single lead electrocardiogram (ECG) showing sinus bradycardia Marked sinus bradycardia at a rate of 25 to 30 beats/min. The normal P waves (upright in lead II) and PR interval are consistent with a sinus mechanism with normal atrioventricular (AV) conduction. Courtesy of Ary Goldberger, MD. Graphic 52675 Version 4.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/sinus-bradycardia/print 14/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate Causes of bradycardia Intrinsic Extrinsic Idiopathic degenerative disorder Drugs Ischemic heart disease Antiarrhythmic agents Chronic ischemia Class IA - quinidine, procainamide Acute myocardial infarction Class IC - propafenone, flecainide Hypertensive heart disease Class II - -blockers Cardiomyopathy Class III - sotalol, amiodarone, dronedarone Trauma Class IV - diltiazem, verapamil Surgery for congenital heart disease Cardiac glycosides Heart transplant Antihypertensive agents Inflammation Clonidine, reserpine, methyldopa Collagen vascular disease Antipsychotic agents Rheumatic fever Lithium, phenothiazines, amitriptyline Pericarditis Autonomically mediated Infection Vasovagal syncope (cardioinhibitory) Viral myocarditis Carotid sinus hypersensitivity Lyme disease (Borrelia burgdorfer I) Hypothyroidism Neuromuscular disorder Intracranial hypertension Friedreich ataxia Hypothermia X-linked muscular dystrophy Hyperkalemia Familial disorder Hypoxia Anorexia nervosa Reproduced with permission from: Fuster V, Walsh R, Harrington R. Hurst's the Heart, 13th ed, McGraw-Hill Professional, New York 2010. Copyright 2010 The McGraw-Hill Companies, Inc. Graphic 65521 Version 11.0 https://www.uptodate.com/contents/sinus-bradycardia/print 15/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate Major etiologies of bradyarrhythmias Sinus bradycardia and its variants - including sinoatrial block Atrioventricular heart block or dissociation - can occur with sinus rhythm or atrial fibrillation or flutter Second or third degree AV block Isorhythmic AV dissociation and related variants Wandering atrial pacemaker Junctional (AV nodal) escape rhythms - can occur with sinus rhythm or atrial fibrillation or flutter Ventricular escape (idioventricular) rhythms Graphic 50037 Version 1.0 https://www.uptodate.com/contents/sinus-bradycardia/print 16/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate Algorithm for the diagnosis and management of sinus bradycardia https://www.uptodate.com/contents/sinus-bradycardia/print 17/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate https://www.uptodate.com/contents/sinus-bradycardia/print 18/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate ECG: electrocardiogram; ETT: exercise tolerance test; TSH: thyroid stimulating hormone; IV: intravenous; MI: myocardial infarction; HR: heart rate; ILR: implantable loop recorder; SSS: sick sinus syndrome; PPM: permanent pacemaker. If atropine is ineffective, IV infusion of dopamine (5 to 20 mcg/kg/minute) or epinephrine (2 to 10 mcg/minute) may also be considered prior to temporary pacing. Graphic 103718 Version 2.0 https://www.uptodate.com/contents/sinus-bradycardia/print 19/20 7/6/23, 11:17 AM Sinus bradycardia - UpToDate Contributor Disclosures Munther K Homoud, MD Speaker's Bureau: Abbott [Live heart dissection]. All of the relevant financial relationships listed have been mitigated. Jonathan Piccini, MD, MHS, FACC, FAHA, FHRS Grant/Research/Clinical Trial Support: Abbott [Atrial fibrillation, catheter ablation]; AHA [Atrial fibrillation, cardiovascular disease]; Bayer [Atrial fibrillation]; Boston Scientific [Cardiac mapping, pacemaker/ICD, atrial fibrillation care]; iRhythm [Atrial fibrillation]; NIA [Atrial fibrillation]; Philips [Lead management]. Consultant/Advisory Boards: Abbott [Atrial fibrillation, catheter ablation]; Abbvie [Atrial fibrillation]; Bayer [Atrial fibrillation]; Boston Scientific [Cardiac mapping, atrial fibrillation, pacemaker/ICD]; ElectroPhysiology Frontiers [Atrial fibrillation, catheter ablation]; Element Science [DSMB]; Medtronic [Atrial fibrillation, pacemaker/ICDs]; Milestone [Supraventricular tachycardia]; Pacira [Atrial fibrillation]; Philips [Lead extraction]; ReCor [Cardiac arrhythmias]; Sanofi [Atrial fibrillation]. All of the relevant financial relationships listed have been mitigated. Susan B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy https://www.uptodate.com/contents/sinus-bradycardia/print 20/20