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Sinus Bradycardia

  • Author: Mark W Livingston, MD; Chief Editor: Erik D Schraga, MD  more...
 
Updated: Dec 18, 2014
 

Background

Sinus bradycardia can be defined as a sinus rhythm with a resting heart rate of 60 beats per minute or less. However, few patients actually become symptomatic until their heart rate drops to less than 50 beats per minute. The action potential responsible for this rhythm arises from the sinus node and causes a P wave on the surface ECG that is normal in terms of both amplitude and vector. These P waves are typically followed by a normal QRS complex and T wave.

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Pathophysiology

The pathophysiology of sinus bradycardia is dependent on the underlying cause. Commonly, sinus bradycardia is an incidental finding in otherwise healthy individuals, particularly in young adults or sleeping patients. Other causes of sinus bradycardia are related to increased vagal tone.

Physiologic causes of increased vagal tone include the bradycardia seen in athletes. Pathologic causes include, but are not limited to, inferior wall myocardial infarction, toxic or environmental exposure, electrolyte disorders, infection, sleep apnea, drug effects, hypoglycemia, hypothyroidism, and increased intracranial pressure.

Sinus bradycardia may also be caused by the sick sinus syndrome,[1] which involves a dysfunction in the ability of the sinus node to generate or transmit an action potential to the atria. Sick sinus syndrome includes a variety of disorders and pathologic processes that are grouped within one loosely defined clinical syndrome. The syndrome includes signs and symptoms related to cerebral hypoperfusion in association with sinus bradycardia, sinus arrest, sinoatrial (SA) block, carotid hypersensitivity, or alternating episodes of bradycardia and tachycardia.

Sick sinus syndrome most commonly occurs in elderly patients with concomitant cardiovascular disease and follows an unpredictable course. Some studies have shown that these patients have a functional decrease in the number of nodal cells, while others have demonstrated the presence of antinodal antibodies. Although these and other developments are beginning to focus our understanding of this syndrome, most cases remain idiopathic.

SA block occurs when the SA node fails to excite the atria uniformly. SA block may be associated with abnormal intrinsic nodal function, a failure of the SA junction, or a failure of propagation in the surrounding tissue. The 3 forms of SA block are first-, second-, and third-degree block.

Both first- and third-degree SA blocks are essentially undiagnosable on the surface ECG. First-degree SA block is characterized by a delay in the propagation of the action potential from the SA node to the atria. Unlike first-degree atrioventricular (AV) block, this delay is not reflected in the surface ECG. In third-degree, or complete, SA block, the surface ECG is identical to that of sinus arrest, with absent P waves. Second-degree SA block is characterized by an occasional dropped P wave (analogous to the dropped QRS complex of second-degree AV block), reflecting the inability of the SA node to consistently transmit an action potential to the surrounding myocardium.

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Epidemiology

Frequency

United States

Frequency of sinus bradycardia is unknown, given that most cases represent normal variants. Although the frequency of sick sinus syndrome is unknown in the general population, in cardiac patients it has been estimated to be 3 in 5000.

Mortality/Morbidity

Sequelae of sinus bradycardia are related to its underlying etiology, including the following:

  • In patients who present with toxic exposure, the prognosis is good once the offending agent has been removed.
  • Patients with sick sinus syndrome have a relatively poor prognosis, with 5-year survival rates in the range of 47-69%. However, whether this mortality rate is due to factors intrinsic to the sinus node itself or the concomitant heart disease is unclear.

Patients with sick sinus syndrome may convert to atrial fibrillation, a rhythm that is amenable to medical therapy and may eliminate the need for pacemaker placement.

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Contributor Information and Disclosures
Author

Mark W Livingston, MD Consulting Staff, Department of Emergency Medicine, Yakima Valley Memorial Hospital

Disclosure: Nothing to disclose.

Coauthor(s)

David T Overton, MD, MBA Professor and Chairman, Department of Emergency Medicine, Associate Dean for Educational Affairs, Western Michigan University School of Medicine

David T Overton, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Michigan College of Emergency Physicians, Association of Academic Chairs of Emergency Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Department of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, National Association of EMS Physicians

Disclosure: Medical Director for: SironaHealth.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, American Academy of Emergency Medicine, American College of Emergency Physicians, Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

References
  1. Semelka M, Gera J, Usman S. Sick sinus syndrome: a review. Am Fam Physician. 2013 May 15. 87(10):691-6. [Medline].

  2. [Guideline] Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA 3rd, et al. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. [corrected]. Circulation. 2012 Oct 2. 126(14):1784-800. [Medline].

  3. [Guideline] Brignole M, Auricchio A, Baron-Esquivias G, Bordachar P, Boriani G, Breithardt OA, et al. 2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy: the Task Force on cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA). Eur Heart J. 2013 Aug. 34(29):2281-329. [Medline].

  4. [Guideline] Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW, Kloeck WG, Billi J, et al. Therapeutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation. Circulation. 2003 Jul 8. 108(1):118-21. [Medline].

  5. [Guideline] Field JM, Hazinski MF, Sayre MR, Chameides L, Schexnayder SM, Hemphill R, et al. Part 1: executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 2. 122(18 Suppl 3):S640-56. [Medline].

  6. Grantham HJ. Emergency management of acute cardiac arrhythmias. Aust Fam Physician. 2007 Jul. 36(7):492-7. [Medline]. [Full Text].

 
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