Sinus Bradycardia

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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.

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.

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.

History

Physical

Causes

Laboratory Studies

Laboratory studies may be helpful if the cause of the bradycardia is thought to be related to electrolytes, drug, or toxins. In cases of sick sinus syndrome, routine laboratory studies are rarely of specific value.

Reasonable screening studies, especially if the patient is symptomatic and this is the initial presentation, include the following:

Imaging Studies

Routine imaging studies are rarely of value in the absence of specific indications.

Other Tests

12-lead ECG may be performed to confirm the diagnosis.

Prehospital Care

Intravenous access, supplemental oxygen, and cardiac monitoring should be initiated in the field.

In symptomatic patients, intravenous atropine may be used.

In rare cases, transcutaneous pacing may need to be initiated in the field.

Emergency Department Care

Care in the ED should first rapidly ensure the stability of the patient's condition. This is followed by an investigation into the underlying cause of the bradycardia.

Patients in unstable condition may require immediate endotracheal intubation and transcutaneous or transvenous pacing.

Patients should have continuous cardiac monitoring and intravenous access.

In hemodynamically stable patients, attention should be directed at the underlying cause of the bradycardia.

In sick sinus syndrome, drug therapy approaches have been relatively disappointing. While atropine has aided some patients transiently, most patients ultimately require placement of a pacemaker. Guidelines on permanent pacing are available from the American College of Cardiology/American Heart Association/Heart Rhythm Society,[2] as well as from the European Society of Cardiology (ESC), in association with the European Heart Rhythm Association.[3]

The ESC guidelines state that in adults with acquired persistent bradycardia, pacing is indicated if a patient displays symptoms that are clearly caused by sinus bradycardia; moreover, pacing may be indicated in the presence of symptoms that, despite inconclusive evidence, are probably the result of sinus bradycardia. If sinus bradycardia is asymptomatic or produced by a reversible cause, according to the guidelines, pacing is not indicated.[3]

In patients with sinus bradycardia secondary to therapeutic use of digitalis, beta-blockers, or calcium channel blockers, simple discontinuation of the drug, along with monitored observation, are often all that is necessary. Occasionally, intravenous atropine and temporary pacing are required.

Treatment of postinfectious bradycardia usually requires permanent pacing.

In patients with hypothermia who have confirmed sinus bradycardia with a pulse, atropine and pacing are usually not recommended because of myocardial irritability. Rewarming and supportive measures are the mainstays of therapy.

Sinus bradycardia may be seen in patients undergoing therapeutic hypothermia.[4] These patients are likely to develop sinus bradycardia sometime during their course that will require close monitoring of perfusion status. If they show signs of adequate perfusion, no treatment is necessary. Treatment of inadequate perfusion would include pressors, atropine, and pacing.[5]

Sleep apnea is usually treated with weight loss, nasal bilevel positive airway pressure (BiPAP) and, occasionally, surgery.

Medication Summary

Drug treatment of sinus bradycardia is usually not indicated for asymptomatic patients. In symptomatic patients, underlying electrolyte or acid-base disorders or hypoxia should be corrected. Intravenous atropine may provide temporary improvement in symptomatic patients, although its use should be balanced by an appreciation of the increase in myocardial oxygen demand this agent causes.[6]

Although in the past, isoproterenol was used quite commonly in patients with bradycardia, further appreciation of its substantial risks has diminished its role. Temporary pacing is recommended in symptomatic patients who are unresponsive or only temporarily responsive to atropine, or in whom atropine therapy is contraindicated. Transcutaneous pacing, where available, is the initial procedure of choice.

Atropine IV/IM

Clinical Context:  Used to increase heart rate through vagolytic effects, causing increase in cardiac output.

Class Summary

These agents are indicated when symptoms of hypoperfusion exist. They are thought to work centrally by suppressing conduction in the vestibular cerebellar pathways. They may have an inhibitory effect on the parasympathetic nervous system.

Further Inpatient Care

Further Outpatient Care

Complications

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

Disclosure: Nothing to disclose.

Specialty Editors

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

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

References

  1. Semelka M, Gera J, Usman S. Sick sinus syndrome: a review. Am Fam Physician. May 15 2013;87(10):691-6. [View Abstract]
  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. Oct 2 2012;126(14):1784-800. [View Abstract]
  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. Aug 2013;34(29):2281-329. [View Abstract]
  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. Jul 8 2003;108(1):118-21. [View Abstract]
  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. Nov 2 2010;122(18 Suppl 3):S640-56. [View Abstract]
  6. Grantham HJ. Emergency management of acute cardiac arrhythmias. Aust Fam Physician. Jul 2007;36(7):492-7. [View Abstract]