Sinus node dysfunction

Last updated: July 11, 2023

Summarytoggle arrow icon

Sinus node dysfunction (SND), previously called sick sinus syndrome, is an abnormality in sinoatrial (SA) node action potential generation or conduction. It can be caused by factors intrinsic to the SA node (e.g., fibrosis of the SA node, infiltrative diseases) or extrinsic factors (e.g., pharmacotherapy with negative chronotropes, hypothyroidism) and most commonly results in bradycardia. Patients typically present with symptoms of end-organ hypoperfusion due to bradycardia (e.g., fatigue, presyncope, syncope, dyspnea on exertion). Establishing a temporal correlation between symptoms of bradycardia and rhythm abnormalities of SND (e.g., on ECG, stress testing, cardiac monitoring) confirms the diagnosis. Unstable bradycardia requires immediate implementation of advanced cardiac life support (ACLS) measures. Reversible causes of SND should be identified and managed. If reversible causes are not present, permanent pacemaker placement is preferred for long-term management of symptomatic patients. Tachycardia-bradycardia syndrome is a subtype of SND that manifests as alternating episodes of tachycardia and bradycardia and is associated with increased risk of cardiovascular events and mortality.

See also “Management of bradycardia” for related information.

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

Intrinsic factors [2]

Conditions that alter the structure or function of the SA node

Idiopathic degeneration of the SA node is the most common cause of SND. [1][2]

Extrinsic factors [2][3]

Factors external to the SA node that affect sinoatrial conduction

Reversible causes of sinus node dysfunction [3]

Clinical featurestoggle arrow icon

The identification of a temporal correlation between symptoms of bradycardia and rhythm abnormalities of SND is considered the gold standard for diagnosing SND. In some individuals, SND may be asymptomatic in the early stages; symptomatic patients have a higher risk of cardiovascular events. [2][3]

Initial managementtoggle arrow icon

Diagnosticstoggle arrow icon

Approach [2][3]

In hemodynamically unstable patients, start immediate treatment for unstable bradycardia without waiting for diagnostic confirmation.

ECG studies [2][3]

Rhythm abnormalities of SND [2][3]

Inappropriate or absent impulse generation by the SA node pacemaker cells
Inappropriate impulse transmission by the SA node transitional cells
Tachycardia-bradycardia syndrome
Chronotropic incompetence [2][3]
  • Heart rate does not increase sufficiently in response to increased activity or demand.

Evaluation for an underlying cause [2]

Laboratory studies

Evaluate all patients for common reversible causes of SND as clinically indicated (i.e., based on history and physical examination). [3]

Additional studies [2][3][4]

Advanced diagnostics [3][4]

  • Indications: diagnostic uncertainty in symptomatic patients
  • Modalities

Electrophysiology studies are not recommended in asymptomatic patients, as it is an invasive modality and the risks outweigh the potential benefits. [3]

Differential diagnosestoggle arrow icon

Up to 50% of patients with SND eventually develop atrioventricular block, as fibrosis of pacemaker cells often occurs in both nodes. [4]

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

The long-term management of SND is detailed here. See “Management of unstable bradycardia” for initial management of SND causing hemodynamic compromise or severe symptoms.

General principles [2][3]

Permanent pacing should not be performed based on ECG findings alone. Permanent pacing is not recommended for asymptomatic patients. [3]

Oral anticoagulation is not routinely recommended for patients with SND unless another indication for anticoagulation is present. [2]

Management of the underlying cause [3]

Permanent pacemaker placement [3][4]

Permanent pacing decreases symptom frequency and improves quality of life. [2][3]

  • Indications
    • First-line management for symptomatic SND caused by intrinsic or irreversible extrinsic factors
    • Symptomatic SND caused by essential medications that cannot be stopped
    • Symptomatic SND with chronotropic incompetence
  • Important considerations: Permanent pacing is not routinely recommended in the following circumstances [3]

Establishing a temporal correlation between symptoms and rhythm abnormalities aids patient selection for permanent pacing, as permanent pacing is most effective in these patients. [3][4]

Rule out reversible causes of SND before considering permanent pacemaker placement. [3]

Phosphodiesterase inhibitors [2][3]

  • Indication: second-line option for patients in whom permanent pacing is indicated but cannot be performed
  • Agents: theophylline, cilostazol

Subtypes and variantstoggle arrow icon

Tachycardia-bradycardia syndrome

Definition [3]

  • A subtype of SND in which there are alternating periods of bradyarrhythmia and atrial tachyarrhythmias (typically atrial fibrillation)
  • Present in 40–50% of patients with SND [2][8]
  • Associated with increased risk of cardiovascular events and mortality. [2]

Clinical features [2][3]


Treatment [3]

Arrhythmia control

Pharmacotherapy for tachyarrhythmia can trigger complete heart block, asystole, and bradyarrhythmias in patients without a pacemaker. [3]

Ablation for atrial tachyarrhythmias may be sufficient for the management of both tachycardia and bradycardia in patients with tachycardia-bradycardia syndrome. [3]

Thromboembolism prophylaxis

Referencestoggle arrow icon

  1. 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. J Am Coll Cardiol. 2019; 74 (7): p.e51-e156.doi: 10.1016/j.jacc.2018.10.044 . | Open in Read by QxMD
  2. Teva Amir, Michael Ilan, Euvgeny Fishman, Yoav Michowitz, Vladimir Khalameizer, Amos Katz, Michael Glikson, Aharon Medina, Moshe Rav Acha. "Preventive" pacing in patients with tachy‐brady syndrome (TBS): Confirming a common practice. Int J Clin Pract. 2020; 74 (10).doi: 10.1111/ijcp.13583 . | Open in Read by QxMD
  3. Hawks MK, Paul MLB, Malu OO. Sinus Node Dysfunction. Am Fam Physician. 2021; 104 (2): p.179-185.
  4. John RM, Kumar S. Sinus Node and Atrial Arrhythmias. Circulation. 2016; 133 (19): p.1892-1900.doi: 10.1161/circulationaha.116.018011 . | Open in Read by QxMD
  5. Semelka M, et. al. Sick sinus syndrome: a review. Am Fam Physician. 2013; 87 (10): p.691-6.
  6. Jensen PN, Gronroos NN, Chen LY, et al. Incidence of and Risk Factors for Sick Sinus Syndrome in the General Population. J Am Coll Cardiol. 2014; 64 (6): p.531-538.doi: 10.1016/j.jacc.2014.03.056 . | Open in Read by QxMD
  7. 2018 Guidelines Made Simple: Bradycardia and Cardiac Conduction Dela. . Accessed: January 14, 2020.
  8. 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 (18_suppl_3): p.S729-S767.doi: 10.1161/circulationaha.110.970988 . | Open in Read by QxMD
  9. Brubaker PH, Kitzman DW. Chronotropic Incompetence: Causes, Consequences, and Management. Circulation. 2011; 123 (9): p.1010-1020.doi: 10.1161/circulationaha.110.940577 . | Open in Read by QxMD
  10. Dakkak W, Doukky R. Sick Sinus Syndrome. StatPearls. 2019.
  11. Issa ZF, Miller JM, Zipes DP. Clinical Arrhythmology and Electrophysiology. Elsevier Health Sciences ; 2012

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