eMedicine Specialties > Emergency Medicine > Cardiovascular

Sinus Bradycardia

Mark W Livingston, MD, Consulting Staff, Department of Emergency Medicine, Yakima Valley Memorial Hospital
David T Overton, MD, Professor, Chair, Program Director, Department of Emergency Medicine, Michigan State University, Kalamazoo Center for Medical Studies

Updated: Aug 4, 2009

Introduction

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, 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.

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.

• 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.

Clinical

History

• Sinus bradycardia is most often asymptomatic. However, symptoms may include the following:
  • Syncope
  • Dizziness
  • Lightheadedness
  • Chest pain
  • Shortness of breath
  • Exercise intolerance
• Pertinent elements of the history include the following:
  • Previous cardiac history (eg, myocardial infarction, congestive heart failure, valvular failure)
  • Medications
  • Toxic exposures
  • Prior illnesses

Physical

• Cardiac auscultation and palpation of peripheral pulses reveal a slow, regular heart rate.
• The physical examination is generally nonspecific, although it may reveal the following signs:
  • Decreased level of consciousness
  • Cyanosis
  • Peripheral edema
  • Pulmonary vascular congestion
  • Dyspnea
  • Poor perfusion
  • Syncope

Causes

• One of the most common pathologic causes of symptomatic sinus bradycardia is the sick sinus syndrome.
• The most common medications responsible include therapeutic and supratherapeutic doses of digitalis glycosides, beta-blockers, and calcium channel-blocking agents.
• Other cardiac drugs less commonly implicated include class I antiarrhythmic agents and amiodarone.
• A broad variety of other drugs and toxins have been reported to cause bradycardia, including lithium, paclitaxel, toluene, dimethyl sulfoxide (DMSO), topical ophthalmic acetylcholine, fentanyl, alfentanil, sufentanil, reserpine, and clonidine.
• Sinus bradycardia may be seen in hypothermia, hypoglycemia, and sleep apnea.
• Less commonly, the sinus node may be affected as a result of diphtheria, rheumatic fever, or viral myocarditis.

Differential Diagnoses

Hypoglycemia
Hypothermia
Hypothyroidism and Myxedema Coma

Other Problems to Be Considered

Obstructive sleep apnea

Workup

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:
  • Electrolyte levels
  • Glucose level
  • Calcium level
  • Magnesium level
  • Thyroid function tests
  • Toxicologic screen

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.

Treatment

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, and Heart Rhythm Society.¹
• 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.
• Sleep apnea is usually treated with weight loss, nasal bilevel positive airway pressure (BiPAP) and, occasionally, surgery.

Medication

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.²

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.

Anticholinergics

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.

Atropine (Atropair, Isopto)

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

Dosing

Adult

0.5-1 mg IV or ET q3-5min up to 3 mg total (0.04 mg/kg)

Pediatric

0.02 mg/kg/dose IV, minimum of 0.1 mg

Interactions

Other anticholinergics have additive effects; may increase pharmacologic effects of atenolol and digoxin; may decrease antipsychotic effects of phenothiazines; tricyclic antidepressants with anticholinergic activity may increase effects of atropine

Contraindications

Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in Down syndrome and/or in children with brain damage to prevent hyperreactive response; avoid in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; patients with prostatic hypertrophy or prostatism can have dysuria and may require urinary catheterization

Follow-up

Further Inpatient Care

• Once the patient's condition is stabilized, inpatient care must be tailored to the inciting cause of the dysrhythmia.

Further Outpatient Care

• Outpatient follow-up care is dependent on the underlying cause of the bradycardia.
• Most patients should be able to follow up with their primary care provider or obtain a referral for a follow-up visit.
• Some patients may require specialized referral to a cardiologist.
• Regular follow-up care is necessary for patients in whom a permanent pacemaker is placed.

Complications

• 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.

Miscellaneous

Medicolegal Pitfalls

• Failure to arrange prompt follow-up care in patients with symptomatic sinus bradycardia exposes the emergency medicine practitioner to considerable medicolegal risk.

References

1. [Guideline] Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. May 27 2008;51(21):e1-62. [Medline]. [Full Text].

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

3. Bharati S, Nordenberg A, Bauernfiend R, Varghese JP, Carvalho AG, Rosen K, et al. The anatomic substrate for the sick sinus syndrome in adolescence. Am J Cardiol. Jul 1980;46(1):163-72. [Medline].

4. Chokshi DS, Mascarenhas E, Samet P, Center S. Treatment of sinoatrial rhythm disturbances with permanent cardiac pacing. Am J Cardiol. Aug 1973;32(2):215-20. [Medline].

5. Davies MJ, Pomerance A. Quantitative study of ageing changes in the human sinoatrial node and internodal tracts. Br Heart J. Feb 1972;34(2):150-2. [Medline].

6. Ferrer MI. The sick sinus syndrome in atrial disease. JAMA. Oct 14 1968;206(3):645-6. [Medline].

7. Gann D, Tolentino A, Samet P. Electrophysiologic evaluation of elderly patients with sinus bradycardia: a long-term follow-up study. Ann Intern Med. Jan 1979;90(1):24-9. [Medline].

8. Krahn AD, Klein GJ, Norris C, Yee R. The etiology of syncope in patients with negative tilt table and electrophysiological testing. Circulation. Oct 1 1995;92(7):1819-24. [Medline].

9. Kulbertus HE, De Leval-Rutten F, Demoulin JC. Sino-atrial disease: a report on 13 cases. J Electrocardiol. 1973;6(4):303-12. [Medline].

10. Maisch B, Lotze U, Schneider J, Kochsiek K. Antibodies to human sinus node in sick sinus syndrome. Pacing Clin Electrophysiol. Nov 1986;9(6 Pt 2):1101-9. [Medline].

11. Margolis JR, Strauss HC, Miller HC, Gilbert M, Wallace AG. Digitalis and the sick sinus syndrome. Clinical and electrophysiologic documentation of severe toxic effect on sinus node function. Circulation. Jul 1975;52(1):162-9. [Medline].

12. Mills TA, Kawji MM, Cataldo VD, Pappas ND, O'Meallie LP, Breaux DM, et al. Profound sinus bradycardia due to diltiazem, verapamil, and/or beta-adrenergic blocking drugs. J La State Med Soc. Nov-Dec 2004;156(6):327-31. [Medline].

13. Pollock G, Brady WJ Jr, Hargarten S, DeSilvey D, Carner CT. Hypoglycemia manifested by sinus bradycardia: a report of three cases. Acad Emerg Med. Jul 1996;3(7):700-7. [Medline].

14. Rosenqvist M, Brandt J, Schüller H. Atrial versus ventricular pacing in sinus node disease: a treatment comparison study. Am Heart J. Feb 1986;111(2):292-7. [Medline].

15. Sasaki Y, Shimotori M, Akahane K, Yonekura H, Hirano K, Endoh R, et al. Long-term follow-up of patients with sick sinus syndrome: a comparison of clinical aspects among unpaced, ventricular inhibited paced, and physiologically paced groups. Pacing Clin Electrophysiol. Nov 1988;11(11 Pt 1):1575-83. [Medline].

16. Touboul P, Atallah G, Gressard A, Kirkorian G. Effects of amiodarone on sinus node in man. Br Heart J. Nov 1979;42(5):573-8. [Medline].

17. Watt AH. Sick sinus syndrome: an adenosine-mediated disease. Lancet. Apr 6 1985;1(8432):786-8. [Medline].

Keywords

sinus bradycardia, vagal tone, bradycardia, inferior wall myocardial infarction, electrolyte disorders, tachycardia, sinus arrest, first-degree block, second-degree block, third-degree block, complete SA block, hypothermia, hypoglycemia, sleep apnea, diphtheria, rheumatic fever, viral myocarditis, digitalis glycosides, beta-blockers, calcium channel-blocking agents, class I antiarrhythmic agents, amiodarone, increased vagal tone, infection, hypothyroidism, increased intracranial pressure, sick sinus syndrome, cerebral hypoperfusion, sinoatrial block, SA block, carotid hypersensitivity, syncope, dizziness, shortness of breath, lightheadedness, chest pain, myocardial infarction, congestive heart failure, valvular failure

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, Professor, Chair, Program Director, Department of Emergency Medicine, Michigan State University, Kalamazoo Center for Medical Studies
David T Overton, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physician Executives, and American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Professor, Department of Emergency Medicine, University of Texas-Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center, San Antonio, Texas
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Talecris Biotherapeutics Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

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
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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