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 , 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 and (e.g., on ECG, stress testing, cardiac monitoring) confirms the diagnosis. 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. 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.
- Incidence: 0.8 per 1000 person-years 
- Mean age: 68 years (although can occur at any age) 
- Sex: no specific predilection
- Risk factors 
Epidemiological data refers to the US, unless otherwise specified.
Intrinsic factors 
Conditions that alter the structure or function of the SA node
- Degeneration, ischemia, infiltration , or fibrosis of the SA node and surrounding myocardium
- Cardiac intervention (e.g., repair of a septal defect)
Extrinsic factors 
Factors external to the SA node that affect sinoatrial conduction
- Medications such as β-blockers, digoxin, and nondihydropyridine calcium channel blockers (verapamil, diltiazem)
- Excessive vagal tone (e.g., athletes)
- Electrolyte abnormalities
- See “ ” for details.
Reversible causes of sinus node dysfunction 
|Potentially reversible or treatable causes of sinus node dysfunction |
|Increased vagal tone|| |
- hypoperfusion)  (features of end-organ
- Patients with tachycardia-bradycardia syndrome will also present with symptoms of tachycardia, including palpitations.
The identification of a temporal correlation between and 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. 
- Assess patients for
- Hemodynamically unstable patients
- Initiate immediate treatment for atropine, ). (e.g., IV
- Admit for further management.
- Hemodynamically stable patients
- Hemodynamically unstable patients
- Identify and treat the underlying cause.
- Consult cardiology.
- Correlate symptoms with .
- Evaluate for an underlying cause.
- Refer for specialist evaluation for alternative diagnoses or advanced diagnostics if symptoms do not correlate with rhythm abnormalities.
In hemodynamically unstable patients, start immediate treatment for without waiting for diagnostic confirmation.
ECG studies 
- Preferred initial diagnostic study: 12-lead ECG
- Second line : (typically in the following order)
- Supportive findings: The presence of any of the following with accompanying symptoms of end-organ hypoperfusion is diagnostic of SND. 
Rhythm abnormalities of SND 
|Inappropriate or absent impulse generation by the SA node pacemaker cells|
|Inappropriate impulse transmission by the SA node transitional cells|
|Chronotropic incompetence |
Evaluation for an underlying cause 
- BMP with magnesium
- Hemoglobin A1C
- Consider genetic testing (e.g., for SCN5A, HCN4 mutations) in consultation with a specialist. 
Additional studies 
- Sleep-related symptoms: Consider nocturnal .
- Concern for structural heart disease : transthoracic echocardiogram (TTE)
- Suspected structural and/or infiltrative heart disease that cannot be confirmed with other diagnostic techniques: Consider advanced imaging
Advanced diagnostics 
- Indications: diagnostic uncertainty in symptomatic patients
Electrophysiology studies are not recommended in asymptomatic patients, as it is an invasive modality and the risks outweigh the potential benefits. 
The long-term management of SND is detailed here. See “” for initial management of SND causing hemodynamic compromise or severe symptoms.
General principles 
- Asymptomatic patients: observation
- Manage .
Severe and/or frequent due to irreversible causes
- First-line (after patient stabilization): permanent pacemaker placement
- Alternative: phosphodiesterase inhibitors
- Tachycardia-bradycardia syndrome: See “Subtypes and variants” for details.
Permanent pacing should not be performed based on ECG findings alone. Permanent pacing is not recommended for asymptomatic patients. 
Oral anticoagulation is not routinely recommended for patients with SND unless another indication for anticoagulation is present. 
Management of the underlying cause 
- Indication: first-line management of patients with
- Stop or decrease the dosage of nonessential medications; see “ ” for management of drug toxicity.
Permanent pacemaker placement 
Permanent pacing decreases symptom frequency and improves quality of life. 
- 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 
- Asymptomatic or minimally symptomatic SND
- Symptoms in the absence of rhythm abnormalities of SND
- Nocturnal SND
Establishing a temporal correlation between symptoms and rhythm abnormalities aids patient selection for permanent pacing, as permanent pacing is most effective in these patients. 
Rule out reversible causes of SND before considering permanent pacemaker placement. 
Phosphodiesterase inhibitors 
Subtypes and variants
- 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 
- Associated with increased risk of cardiovascular events and mortality. 
Clinical features 
- Symptoms vary in intensity depending on the extent of bradycardia and tachycardia.
- and , e.g.:
- Symptoms of atrial tachyarrhythmia-associated thromboembolic complications, e.g., stroke.
- Diagnostic studies and findings are similar to those for SND.
- Rhythm abnormalities: alternating atrial tachyarrhythmias (e.g., , , ) and bradycardia (e.g., sinus bradycardia, ectopic atrial bradycardia, sinus pause) 
- Bradycardia not triggered by atrial tachyarrhythmia
- Bradycardia triggered by atrial tachyarrhythmia