Sick Sinus Syndrome


Article Author:
Wael Dakkak


Article Editor:
Rami Doukky


Editors In Chief:
Sherri Murrell


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
6/3/2019 5:07:13 PM

Introduction

Sick sinus syndrome, also known as sinus node dysfunction (SND), is a disorder of the sinoatrial (SA) node caused by impaired pacemaker function and impulse transmission producing a constellation of abnormal rhythms. These include atrial bradyarrhythmias, atrial tachyarrhythmias and, sometimes, bradycardia alternating with tachycardia often referred to as “tachy-brady syndrome.” These arrhythmias may result in palpitations and tissue under-perfusion leading to fatigue, lightheadedness, pre-syncope, and syncope.

Etiology

The etiologic factors leading to sinus node dysfunction can be classified into two categories: intrinsic pathology to the sinus node itself, typically results from fibrosis of the nodal tissue and external causes that affect the SA node function.

While the most common intrinsic factor leading to sinus node dysfunction is age-related degeneration of the SA node [1], sinus node dysfunction can be a result of congenital disorders, arrhythmias, infiltrative disorders and surgery. Recent studies have identified several mutations in the ion channels explaining familial and congenital forms of sick sinus syndrome. Heart failure and atrial tachyarrhythmias have been shown to induce cellular remodeling of the sinus node in animal models [2]. Infiltration of the SA node by sarcoidosis, amyloidosis, hemochromatosis, collagen vascular disease or metastatic cancer results in SA node dysfunction. Damage to SA node or the sinus nodal artery may occur after cardiothoracic surgery from valve replacement, correction of congenital heart disease or heart transplant. Infectious agents such as bacterial endocarditis and Chagas disease commonly result in atrioventricular conduction problems rather than sinus node dysfunction. Because the SA node is located within the atrial wall, ischemic injury by atherosclerosis of the arteries feeding the SA node is unusual [3]

Several external causes that can affect the pacing function of the SA node. These can occur in conditions where there is abnormally increased vagal tone such as carotid sinus hypersensitivity, vasovagal syncope, and autonomic dysfunction. Furthermore, metabolic derangements such as hypothyroidism, hyperkalemia, hypokalemia, hypocalcemia, hypoxia, and hypothermia can lead to depression of the pacing function of the SA node. Obstructive sleep apnea may cause bradycardia by profound hypoxia during episodes of apnea. Increased intracranial pressure (Cushing’s reflex) also causes bradycardia. Several pharmacologic and toxic substances can produce a similar effect on the SA node; these include class I to IV antiarrhythmic medications, digoxin, lithium and sympatholytic medications.

Epidemiology

Sinus node dysfunction is a disease of older adults, although it can occur at any age. The mean age of a patient with sinus node dysfunction is 68 years. Sinus node dysfunction develops in one of every 600 cardiac patients of 65 years of age or older. Males and females are equally affected. Sinus node dysfunction accounted for more than 50% of the pacemaker implantations in the United States in the 1990s [4].

Pathophysiology

The sinoatrial (SA) node is composed of a collection of atrial myocytes that are specialized into two different functional cells. Pacemaker “P cells” with intrinsic pacemaker function and transitional “T cells” which are responsible for propagating the impulse into the right atrium. Dysfunction of these cells leads to the several arrhythmias:

  1. Abrupt, inappropriate, severe sinus bradycardia.
  2. Sinus pause or arrest where there are pauses of 3 seconds or more without atrial activity. This is often rescued by an escape rhythm which can be atrial, junctional and ventricular in origin. It usually reflects a failure of P cells to generate the action potential.
  3. Sinoatrial (SA) exit block which is caused by the failure of the T cells to transmit the impulse. Three degrees of sinoatrial (SA) block parallel atrioventricular (AV) block: (1) First-degree SA block is usually subclinical and undetectable on the surface electrocardiogram (ECG); (2) Second-degree-type 1 SA block is characterized by progressive shortening of PP interval prior to the dropped P wave, and Second-degree-type 2 SA block refers to a dropped P wave without any preceding change in the PP interval; (3) Third-degree SA block refers to complete failure of the SA node to conduct impulses to the atrial tissue and is reflected by the absence of P waves on surface ECG. Third-degree SA exit block is clinically identical to sinus arrest.
  4. Tachy-brady syndrome is identified by bradycardia alternating with paroxysmal supraventricular arrhythmias, most frequently atrial fibrillation (AF). This results from abnormal automaticity and conduction within the atrial tissue. It affects at least 50% of patients with SND.
  5. Failure to resume sinus rhythm after cardioversion, manifesting as a prolonged sinus pause.
  6. Atrial fibrillation with slow ventricular response in the absence of AV node blocking agents. This is likely due to the simultaneous degeneration in the AV node. In these patients, spontaneous or therapeutic termination of AF (cardioversion) results in a sinus pause due to concomitant SND. The annual incidence of complete AV block ranges from (0% to 4.5% with a median of 0.6% [5][6].
  7. Chronotropic incompetence is defined as inappropriate bradycardia resulting in an inability to meet the metabolic demands. It is estimated to occur in 20% to 60% of patients.

History and Physical

The natural history of sinus node dysfunction is usually a slow progression over decades. In the early stages, most patients are asymptomatic. When symptoms do develop, they are usually attributed to hypo-perfusion to vital organs with high oxygen demand. Sinus pauses or severe bradycardia results in central nervous system (CNS) underperfusion which manifests in paroxysmal presyncope or syncope. The sudden termination of AF in tachy-brady syndrome typically results in a prolonged sinus pause and failure to return to sinus rhythm which can manifest in syncope. Renal and gastrointestinal hypoperfusion may result in oliguria and abdominal pain, respectively. Rhythms with AF or atrial flutter pose a significant increased risk of thromboembolism, manifesting as transient ischemic attack or cardioembolic stroke, thus carrying the worst prognosis. Chronotropic incompetence results in fatigue and exercise intolerance. Palpitations are usually felt during episodes of tachycardia, after termination of tachyarrhythmias or due to prolonged pauses. Worsening of angina pectoris or congestive heart failure are also reported.

Evaluation

The first step in evaluating sinus node dysfunction is to exclude reversible causes such as electrolyte abnormalities, metabolic abnormalities, or uncontrolled sleep apnea, and removal of possible offending medications (e.g., beta-blockers, calcium channel blockers). There should be clear documentation of bradycardia that correlates with patient’s symptoms to make a diagnosis of sinus node dysfunction. Given the episodic nature of the disease, diagnosis on 12 lead ECG is unusual and prolonged monitoring to detect and document bradycardic episodes is often indicated. This is achieved by 24-48 Holter monitor or telemonitoring, depending on the severity of the symptoms. If telemetry or Holter monitoring fails to demonstrate bradycardia, then an external or implantable long-term event monitor or a loop recorder is warranted. If the diagnosis of sinus node dysfunction is strongly suspected, but no arrhythmias were detected, then the electrophysiologic study is suggested. Autonomic modulation testing such as prolonged sinus pause more than 3 seconds after carotid sinus massage is suggestive of sinus node dysfunction but not by itself diagnostic. Testing for chronotropic incompetence is usually done by treadmill exercise test especially in those who experience fatigue and exertional symptoms. Chronotropic incompetence is diagnosed when the patient achieves less than 80% of maximal predicted heart rate; however, this has not been clinically validated [6].

Treatment / Management

The management of sinus node dysfunction includes identifying and correcting reversible factors, as an initial step. After treating reversible causes, the treatment of sinus node dysfunction can include the placement of a permanent pacemaker. A permanent pacemaker is indicated in symptomatic patients who have documented bradycardia responsible for their symptoms or in those who have demonstrated chronotropic incompetence. A permanent pacemaker is also indicated in sinus node dysfunction secondary to medications necessitated by another medical condition. This is commonly encountered in tachy-brady syndrome where beta-adrenergic blockers are required for treatment of AF, but they suppress the SA node causing prolonged sinus pauses and syncope upon the cessation of tachyarrhythmia episodes. Moreover, it is reasonable to consider a permanent pacemaker in symptomatic patients who have bradycardia less than 40 beats per minute that were not documented to be associated with their symptoms. A permanent pacemaker is also reasonable in patients who have had a diagnostic electrophysiologic study.

When considering the type of pacemaker, the dual-chamber pacing is usually preferred due to the increased risk of AV block in sinus node dysfunction. Anticoagulation should be addressed in patients with paroxysmal atrial tachyarrhythmias since these patients are at increased risk of stroke. Dual-chamber pacemaker is recommended in patients with sinus node dysfunction due to increased risk of AV block. Moreover, atrial pacing, attained with a dual-chamber pacemaker, may reduce the incidence of AF and subsequent risk of systemic thromboembolism and stroke compared to patients who receive ventricular pacing only [7]. Importantly, sinus node dysfunction follows a benign course and the risk of sudden cardiac death is low, as sinus node dysfunction has not been shown to impact survival whether treated with a pacemaker or not.[8][9][10][11]

Pearls and Other Issues

Sick sinus syndrome or sinus node dysfunction is primarily a disease of the elderly population. It results from the degeneration of the SA node affecting its ability to generate or transmit impulses to the atrial tissue. Sinus node dysfunction has several characteristic rhythm disturbances manifesting in symptoms of organ hypo-perfusion. The main treatment of sick sinus syndrome is permanent pacemaker; it is usually done after secondary causes are ruled out. The risk of sudden cardiac death with sinus node dysfunction is low.

Enhancing Healthcare Team Outcomes

Sick sinus syndrome is best managed by an interprofessional team that includes cardiology nurses. To improve patient outcomes, clinicians should consider the dual-chamber pacing due to the increased risk of AV block in sinus node dysfunction. Anticoagulation should be addressed in patients with paroxysmal atrial tachyarrhythmias since these patients are at increased risk of stroke. Dual-chamber pacemaker is recommended in patients with sinus node dysfunction due to increased risk of AV block. Moreover, atrial pacing, attained with a dual-chamber pacemaker, may reduce the incidence of AF and subsequent risk of systemic thromboembolism and stroke compared to patients who receive ventricular pacing only.

The outcomes for most patients with sick sinus syndrome are guarded because of advanced aged and other comorbidities. Failure to anticoagulate in the presence of atrial arrhythmias is another reason for high morbidity of the disorder.


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Sick Sinus Syndrome - Questions

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Sick sinus syndrome is frequently associated with which of the following conditions?

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    Contributed by McGill University, Micheal Rosengarten, BEng, MD
Attributed To: Contributed by McGill University, Micheal Rosengarten, BEng, MD



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What is the best treatment plan for an elderly female with a history of three recent syncopal episodes who is diagnosed with tachycardia-bradycardia syndrome?



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A 69-year-old male with tachy-brady syndrome has had a single lead pacemaker for three years. He presents for follow up without complaint. His past medical history includes diabetes mellitus and a stroke two years ago without residual deficits. An echocardiogram shows an ejection fraction of 35 percent, left atrial enlargement, and nonvalvular abnormalities. Medications include aspirin, simvastatin, metoprolol, enalapril, furosemide, and glipizide. Which of the following is most appropriate?



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A 73 year old male is brought to the emergency department after a syncopal episode and is admitted in atrial flutter that converts spontaneously to sinus bradycardia at 45 bpm. There are intermittent episodes of atrial flutter without symptoms. Which of the following would be the best therapy?



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A 77-year-old male presented to the clinic complaining of fatigue and exertional dyspnea. He has hypertension treated with hydrochlorothiazide 25 mg daily. He used to smoke cigarettes but stopped 3 years ago and denies drinking alcohol or illicit drug use. His blood pressure is 134/88 mmHg and heart rate is 44 beats/min. Blood chemistry and complete blood count are within normal limits, and his thyroid stimulating hormone is 1.5 mlU/L. His 12-lead ECG shows sinus bradycardia with first degree AV block. On a treadmill exercise test, he achieved only 75% of the maximal predicted heart rate. What is the next step in the management of this patient?



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A 68-year-old black female with past medical history of diabetes mellitus, hypertension, bilateral presbyacusis, and osteoarthritis of both knees presents to the emergency department with episodes of dizziness and pre-syncope. She takes all of her medications regularly; these include aspirin 81 mg daily, atorvastatin 40 mg daily, metformin 1000 mg twice a day, carvedilol 25 mg twice a day, gabapentin 300 mg three times a day, and ibuprofen as needed for her joint pain. She reported snoring at night which is bothering her husband, in addition to daytime sleepiness. Physical examination revealed blood pressure of 154/95 mmHg, heart rate of 39 beats per minute, and a body mass index of 33 kg/m2. Her lungs were clear to auscultation; no heart murmurs were appreciated, and orthostatic blood pressure was normal. Her labs were unremarkable including thyroid stimulating hormone. ECG was only significant for sinus bradycardia. Tele-monitoring demonstrated one episode of lightheadedness that corresponded with bradycardia. What is the next step in the management of this patient?



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A 68 year-old-female presented to the office after she had a stroke last month with residual aphasia and right-sided hemiparesis. She has a past medical history of degenerative joint disease, congestive heart failure due to idiopathic dilated cardiomyopathy, and paroxysmal atrial fibrillation. She was hospitalized 2 years ago with an episode of atrial fibrillation that resulted in hypotension and hemodynamic instability requiring direct-current cardioversion. Following cardioversion, she had prolonged pause, after which sinus rhythm was restored. At that time, she was not started on oral anticoagulation. Her medications include metoprolol XL 25 mg daily, enalapril 20 mg twice daily, and furosemide 40 mg twice daily. She has baseline bradycardia, preventing maximizing the dose of metoprolol. Her left ventricular ejection fraction by transthoracic echocardiography is 40%. ECG shows baseline bradycardia with QRS duration of 100 milliseconds. What is the correct statement about this patient?



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Which of the following rhythms is not a manifestation of sick sinus syndrome?



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Sick Sinus Syndrome - References

References

Sick sinus syndrome: a review., Semelka M,Gera J,Usman S,, American family physician, 2013 May 15     [PubMed]
New insights into pacemaker activity: promoting understanding of sick sinus syndrome., Dobrzynski H,Boyett MR,Anderson RH,, Circulation, 2007 Apr 10     [PubMed]
The evaluation and management of bradycardia., Mangrum JM,DiMarco JP,, The New England journal of medicine, 2000 Mar 9     [PubMed]
Atrial pacing and the risk for AV block: is there a time for change in attitude?, Rosenqvist M,Obel IW,, Pacing and clinical electrophysiology : PACE, 1989 Jan     [PubMed]
Diagnosis and treatment of sick sinus syndrome., Adán V,Crown LA,, American family physician, 2003 Apr 15     [PubMed]
Pacing therapy for prevention of atrial fibrillation., Ellenbogen KA,, Heart rhythm, 2007 Mar     [PubMed]
Epstein AE,DiMarco JP,Ellenbogen KA,Estes NA 3rd,Freedman RA,Gettes LS,Gillinov AM,Gregoratos G,Hammill SC,Hayes DL,Hlatky MA,Newby LK,Page RL,Schoenfeld MH,Silka MJ,Stevenson LW,Sweeney MO,Tracy CM,Epstein AE,Darbar D,DiMarco JP,Dunbar SB,Estes NA 3rd,Ferguson TB Jr,Hammill SC,Karasik PE,Link MS,Marine JE,Schoenfeld MH,Shanker AJ,Silka MJ,Stevenson LW,Stevenson WG,Varosy PD, 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 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. Journal of the American College of Cardiology. 2013 Jan 22;     [PubMed]
Proclemer A,Zecchin M,D'Onofrio A,Boriani G,Facchin D,Rebellato L,Ghidina M,Bianco G,Bernardelli E,Pucher E,Gregori D, [The Pacemaker and Implantable Cardioverter-Defibrillator Registry of the Italian Association of Arrhythmology and Cardiac Pacing - Annual report 2016]. Giornale italiano di cardiologia (2006). 2018 Feb;     [PubMed]
Kutarski A,Polewczyk A, [Sinus node disease and atrio-ventricular disorders in pregnant women. When temporary or permanent pacing is necessary?]. Przeglad lekarski. 2015;     [PubMed]
Boriani G,Padeletti L, Management of atrial fibrillation in bradyarrhythmias. Nature reviews. Cardiology. 2015 Jun;     [PubMed]
Kuniewicz M,Rydlewska A,Karkowski G,Lelakowska-Pieła M,Majewski J,Lelakowski J, Effectiveness of atrial versus atrioventricular pacing for sick sinus syndrome during long-term follow-up. Kardiologia polska. 2015;     [PubMed]

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