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Sinus Node Dysfunction

  • Author: Yingbo Yang, MD, PhD; Chief Editor: Jeffrey N Rottman, MD  more...
Updated: Dec 31, 2015


Sinus node dysfunction (SND) refers to abnormalities in SN impulse formation and propagation and includes sinus bradycardia, sinus pause/arrest, chronotropic incompetence, and sinoatrial exit block. (See Workup.)[1, 2, 3]

SND is frequently associated with conduction system disease in the heart and various supraventricular tachyarrhythmias, such as atrial fibrillation[3, 4] and atrial flutter. When associated with supraventricular tachyarrhythmias, SND is often termed tachy-brady syndrome. (See Pathophysiology and Etiology.)[2, 3]

SND is referred to as sick sinus syndrome when it is accompanied by symptoms such as dizziness or syncope. (See Etiology and Presentation.)

Although SND may occur at any age, it is primarily a disease of the elderly and, presumably, is related to the senescence of the SN, which is often accompanied with the senescence of the atrium and the conduction system in the heart.[3, 5] When SND occurs earlier in life, it is often secondary to other cardiac disease processes.[6] It constitutes an important cause of morbidity in patients who have undergone surgery for congenital heart disease (CHD). (See Etiology, Prognosis, and Epidemiology.)

The natural history of SND may be highly variable, although it tends to be progressive in nature. The only effective treatment for patients with chronic symptomatic SND is pacemaker therapy. Asymptomatic patients do not require therapy. (See Pathophysiology, Prognosis, Treatment, and Medication.)


The sinus node (SN) is a subepicardial structure normally located in the right atrial wall near the superior vena cava entrance on the upper end of the sulcus terminalis. It is formed by a cluster of cells capable of spontaneous depolarization. Normally, these pacemaker cells depolarize at faster rates than any other latent cardiac pacemaker cell inside the heart. Therefore, a healthy SN directs the rate at which the heart beats. Electrical impulses generated in the SN must then be conducted outside the SN in order to depolarize the rest of the heart.

SN activity is regulated by the autonomic nervous system. For example, parasympathetic stimulation causes sinus bradycardia, sinus pauses, or sinoatrial exit block. These actions decrease SN automaticity, thereby decreasing the heart rate.

Sympathetic stimulation, on the other hand, increases the slope of phase 4 spontaneous depolarizations. This increases the automaticity of the SN, thereby increasing the heart rate. Blood supply to the SN is provided by the right coronary artery in most cases.



SND involves abnormalities in SN impulse formation and propagation, which are often accompanied by similar abnormalities in the atrium and in the conduction system of the heart. Together, these abnormalities may result in inappropriately slow ventricular rates and long pauses at rest or during various stresses. When SND is mild, patients are usually asymptomatic. As SND becomes more severe, patients may develop symptoms due to organ hypoperfusion and pulse irregularity. Such symptoms include the following:

  • Fatigue
  • Dizziness
  • Confusion
  • Fall
  • Syncope
  • Angina
  • Heart failure symptoms and palpitations


Although the exact etiology of SND is usually not identified, most cases are believed to be attributable to a combination of various intrinsic and extrinsic factors. The most common intrinsic causes are cardiac age-related SN changes and coronary artery disease. The most common extrinsic causes are medications and autonomic hyperactivity.

The acquired form of SND may also occur after damage to the SN artery during cardiac surgery or may be due to occlusion, such as after myocardial infarction. In the pediatric population, SND and atrioventricular (AV) block have been found to occur more frequently in patients with Kawasaki disease with moderate to severe coronary artery disease than in the general population. This is believed to be secondary to myocarditis or abnormal microcirculation in the SN artery and the AV-node artery.[7]

The idiopathic form of SND is degenerative, with fibrosis and fatty infiltration of the SN and consequent decrease of functional nodal cells.

Intrinsic SND

Age-related changes

Age-related changes are believed to be the most common cause of SND and are related to fibrosis in the SN. These fibrotic changes also occur in the atrium and the conduction system of the heart and are believed to contribute to the association among SND, tachy-brady syndrome, conductive system disease, and an inappropriately slow escape rhythm.

The pacemaker activity in the SN has been found to be related to voltage and calcium clocks.[8] Age-related down-regulation of calcium channel expression in the SN has been suggested as a potential cause of SND with aging.[9]

Coronary artery disease

Coronary artery disease is believed to be a common contributory cause of SND, probably through atherosclerotic changes in the SN artery.

Genetic causes

SND may be familial; an autosomal dominant pattern of inheritance has been described. Several molecular defects in human hearts (defects in the sodium channel, calcium channel, hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel, ankyrin-B, and connexin 40) have been associated with familial sick sinus syndromes.[6]

In addition, SND is seen in children with congenital and acquired heart disease, particularly after corrective surgery. The cause of SND in these children is likely related to the underlying structural heart disease and surgical trauma to the SN and/or SN artery.

Emery-Dreifuss muscular dystrophy is an X-linked muscle disorder associated with SND and AV conduction defects. If AV conduction defects are present, sudden cardiac death may result unless the condition is treated with permanent pacing. Males and females may be affected with equal frequency.

In addition, sinus venosus atrial septal defect (ASD), Ebstein anomaly, and heterotaxy syndromes, particularly left atrial isomerism, can lead to SND.

Mechanisms in tachy-brady syndrome

Tachycardia-mediated remodeling of the SN is present in patients with atrial fibrillation/flutter and it may contribute to SND in these patients. In patients with tachy-brady syndrome, atrial fibrillation ablation can reverse SND, as evidenced by a reduction in SN recovery time, an increase in mean and maximal heart rates, and a lack of symptoms related to sinus bradycardia or pause.[10] The mechanism of SND in tachy-brady syndrome may involve the abnormal function of voltage and calcium clocks in the SN.[11, 12]

Other heart diseases

Other structural heart diseases are uncommon causes of SND. These include, but are not limited to, the following:

  • Various cardiomyopathies
  • Myocarditis
  • Pericarditis
  • Infiltrative heart diseases - Amyloidosis, hemochromatosis, neoplasm
  • Collagen vascular diseases - Systemic lupus, scleroderma
  • Neuromuscular diseases - Myotonic dystrophy, Friedreich ataxia

Extrinsic SND


Beta blockers, calcium channel blockers, digoxin, and various anti-arrhythmic drugs suppress SN function. Antiarrhythmic drugs that can lead to SND include the following:

  • Digitalis - Because of SN exit block
  • Propranolol
  • Verapamil
  • Quinidine
  • Procainamide
  • Lidocaine
  • Disopyramide
  • Reserpine

Autonomic dysfunction

SND can be secondary to autonomic nervous system dysfunction in patients with neurocardiogenic syncope, and carotid sinus hypersensitivity. Conditions associated with marked hypervagotonia, as in well-trained athletes, can also result in SND. However, evidence suggests that there may be some intrinsic factor as well in well-trained athletes who develop SND.[13]

Surgical causes, especially from operations involving the right atrium

Gradual loss of sinus rhythm occurs after the Mustard, Senning, and all varieties of the Fontan operation. This is thought to be secondary to direct injury to the SN during surgery and also due to later, chronic hemodynamic abnormalities. Paroxysmal atrial tachycardias are frequently associated with SND, and loss of sinus rhythm appears to increase the risk of sudden death. Patients with transposition of the great arteries now undergo the arterial switch operation, which avoids the extensive atrial suture lines that lead to SN damage.

SND was described in 15% of patients who had undergone the Ross operation for aortic valve disease or complex left-sided heart disease, 2.6-11 years earlier.[14] Other arrhythmias, such as complete AV block and ventricular tachycardia, were present as well after the Ross operation.

When repairing ASDs, especially sinus venosus ASDs, SND frequently occurs because of the proximity of the defect with SN tissue.

Other surgically related causes of SND include the following:

  • Patients who have undergone surgery for endocardial cushion defects (ECDs) may later develop SND
  • SND may be caused by a Blalock-Hanlon atrial septectomy
  • Cannulation of the superior vena cava (SVC), usually performed for cardiopulmonary bypass or extracorporeal membrane oxygenation (ECMO), may damage SN tissue.
  • Ischemic cardiac arrest may cause SND.


Rheumatic fever is another cause of SND. Such dysfunction may also result from CNS disease, which is usually secondary to increased intracranial pressure with subsequent increase in the parasympathetic tone.

Endocrine-metabolic diseases (hypothyroidism and hypothermia) and electrolyte imbalances (hypokalemia and hypocalcemia) are other conditions that can contribute to SND.

A study by Sunaga et al of 202 subjects indicated that in patients with persistent atrial fibrillation, those with low-amplitude fibrillatory waves and a large left atrial volume index are at increased risk for the appearance of concealed SND after catheter ablation has restored sinus rhythm.[15]



Occurrence in the United States

The exact incidence of SN dysfunction is unknown. The syndrome occurs in approximately 1 in 600 cardiac patients older than 65 years.[16]

International occurrence

Due to its relationship with advanced age, SND is more prevalent in countries where citizens have a longer life expectancy.

Age-related demographics

SND may develop at any age but it is primarily a disease of the elderly, with the average age of occurrence being about 68 years.[17] SND in young patients is often related to underlying heart disease.



The incidence of sudden cardiac death in patients with SND is very low.[18] Mortality in patients with SND is primarily determined by underlying heart disease. Pacemaker therapy does not appear to affect survival in patients with SND[19, 20, 21] and is, therefore, used primarily for the alleviation of symptoms. Symptomatic patients with normal systemic ventricular function and SND have an overall good prognosis with atrial (rate-responsive) pacing.

Patients with tachy-brady syndrome have a worse prognosis than do patients with isolated SND. The overall prognosis in patients with SND and additional systemic ventricular dysfunction (eg, numerous postoperative Mustard and Fontan patients) depends on their underlying ventricular dysfunction or degree of congestive heart failure (CHF).

A study has shown that in patients who have undergone a Fontan surgery and developed SND, endocardial atrial leads can be implanted relatively safely and can permit low-energy thresholds for as long as 5 years after implantation.[22]

Morbidity and mortality

The complications of SND include the following:

  • Sudden cardiac death (rare)
  • Syncope
  • Fall
  • Thromboembolic events, including stroke - Especially in patients with tachy-brady syndrome
  • CHF
  • Exercise intolerance
  • Cardiac dysfunction due to bradycardia and loss of AV synchrony
  • Atrial tachyarrhythmias - Such as atrial flutter or fibrillation

Symptoms of SN dysfunction almost invariably progress over time. The most dramatic symptom in patients with SND is syncope.

About 50% of patients with SND develop tachy-brady syndrome over a lifetime; such patients have a higher risk of stroke and death. However, the incidence of sudden death owing directly to SND is extremely low.[18]

The treatment of symptoms is achieved with the implant of an atrial pacemaker to provide atrial rate support. This prevents symptoms related to bradycardia from occurring. In patients with atrial tachyarrhythmias, it is a useful adjunct to antiarrhythmic therapy.


Patient Education

Educate patients to recognize symptoms of SND. Family members should learn cardiopulmonary resuscitation (CPR).

Because most pediatric patients with SND have already received surgery for CHD (eg, Mustard procedure, Fontan procedure), their education is focused on recognizing symptoms of CHF and tachyarrhythmias, such as atrial flutter/fibrillation, which are usually poorly tolerated.

Patients who are on antiarrhythmic medication for atrial flutter or fibrillation should be instructed to take their medication regularly and to visit the cardiologist as scheduled. They should also be cognizant of the adverse effects and toxicity of the medication.

In patents who have already received a Mustard or Fontan procedure, undergoing yearly echocardiography to monitor cardiac function is advisable. If cardiac function is decreased, anti-CHF management should be started and close follow-ups with the cardiologist are advisable.

Patients who have a pacemaker should be instructed on the means of obtaining regular checks. Such checks are usually achieved from home with a transtelephonic monitor that transmits to a central monitoring station, which, in turn, contacts the cardiologist in case a problem is detected (eg, device malfunction, arrhythmia).

Patients who have an intracardiac defibrillator (ICD) device should receive the same instructions that patients who have pacemakers receive. Because patients with ICDs often are placed on antiarrhythmic medication, they also should receive instruction regarding medication schedules and information about adverse effects and toxicity.

In addition, in patients with frequent atrial flutter or fibrillation episodes, which are followed by a shock from the ICD, patients are instructed to avoid activities that may pose a risk to themselves and/or other people (eg, driving). They also receive instruction on when to go to the cardiologist or the emergency department.

For patient education information, see the Heart Health Center, as well as Heart Rhythm Disorders.

Contributor Information and Disclosures

Yingbo Yang, MD, PhD Clinical Assistant Professor of Cardiovascular Medicine, Division of Cardiology, Lawrence J Ellison Ambulatory Care Center, University of California, Davis, Medical Center

Yingbo Yang, MD, PhD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society

Disclosure: Nothing to disclose.


Yasir Batres, MD Physician, Division of Cardiology, University of California, Davis, Medical Center

Yasir Batres, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.


Stuart Berger, MD Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Alan D Forker, MD Professor of Medicine, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research, MidAmerica Heart Institute of St Luke's Hospital

Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association , American Society of Hypertension, and Phi Beta Kappa

Disclosure: Nothing to disclose.

M Silvana Horenstein, MD Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association

Disclosure: Nothing to disclose.

Peter P Karpawich, MD Professor of Pediatric Medicine, Department of Pediatrics (Cardiology), Wayne State University School of Medicine; Director, Cardiac Electrophysiology and Pacemaker Services, Children's Hospital of Michigan

Peter P Karpawich, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, Michigan State Medical Society, and Pediatric Electrophysiology Society

Disclosure: Nothing to disclose.

Adrian W Messerli, MD Consulting Staff, Cardiology Associates of Kentucky

Disclosure: Nothing to disclose.

John W Moore, MD, MPH Professor of Clinical Pediatrics, Section of Pediatric Cardiology, Department of Pediatrics, University of California San Diego School of Medicine; Director of Cardiology, Rady Children's Hospital

John W Moore, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Brian Olshansky, MD Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Justin D Pearlman, MD, PhD, ME, MA Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center

Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

Disclosure: Nothing to disclose.

Paul M Seib, MD Associate Professor of Pediatrics, University of Arkansas for Medical Sciences; Medical Director, Cardiac Catheterization Laboratory, Co-Medical Director, Cardiovascular Intensive Care Unit, Arkansas Children's Hospital

Paul M Seib, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Arkansas Medical Society, International Society for Heart and Lung Transplantation, and Society for Cardiac Angiography and Interventions

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

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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This 12-lead electrocardiogram (ECG) is from an asymptomatic girl aged 10 years, which was brought to our attention because of the irregularity of the P-P intervals. This ECG shows sinus arrhythmia at a rate of 65-75 beats per minute. The P waves all originate from the sinus node (SN) because they have a positive axis (upright) in leads I, II, and aVF. The PR interval is 104ms, and the QRS is narrow at 86ms, with a normal axis of 64°. The corrected QT (QTc) interval measures 402ms. Therefore, this is a normal ECG.
Below is an electrocardiogram (ECG) of a girl aged 2 years who was referred to the clinic by a pediatrician for evaluation of a heart murmur. This ECG shows atrial rhythm originating most likely from the lower left atrium (P waves are inverted in lead I and are positive in II and aVF, with a frontal axis of 124°). The PR interval measures 113 ms, and the QRS is narrow at 90 ms. Right ventricular (RV) conduction delay is shown and is best seen in the precordial leads V1 and V2. The QRS frontal axis shows right axis deviation (reference range for a child aged 2 years is 0-110°). The patient does not have RV hypertrophy by voltage criteria. The inverted T waves in V1 are a normal finding at this age. An echocardiogram showed a moderately sized atrial septal defect. Nonsinus atrial rhythm is not a synonym of sinus node dysfunction.
This is a 12-lead electrocardiogram (ECG) from a boy aged 12 years with a history of syncope. This patient was healthy until 1 month earlier, when he started to experience episodes of lightheadedness. The ECG shows sinus arrhythmia (bradycardia) at a rate of 50-79 beats per minute, with a PR interval of 136 ms. Two junctional escape beats are present after a prolonged pause. The QRS is narrow at 85 ms, with a normal frontal axis of 70°. The corrected QT interval (QTc) is 411 ms. A later electrophysiologic study showed prolonged sinus node recovery time (SNRT) and sinoatrial conduction time (SACT). Because of the patient's symptoms and his sinus node (SN) dysfunction, he received an atrial pacemaker. If this 12-lead ECG had been recorded from an asymptomatic patient, the findings would be considered within normal limits and no further workup would be indicated. In this case, the lightheadedness and, ultimately, the syncope defined sick sinus syndrome, with the patient requiring pacemaker therapy.
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