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Sinus node dysfunction: Treatment

Sinus node dysfunction: Treatment
Literature review current through: Aug 2023.
This topic last updated: Jun 16, 2022.

INTRODUCTION — Sinus node dysfunction (SND), also historically referred to as sick sinus syndrome, is characterized by dysfunction of the sinoatrial (SA) node that is often secondary to senescence of the SA node and surrounding atrial myocardium. The initial clues to the diagnosis of SND are often derived from taking the history and obtaining a routine electrocardiogram (ECG), though the symptoms (eg, fatigue, lightheadedness, palpitations, presyncope, and/or syncope) and ECG findings are frequently vague and nonspecific. The occasional patient may be identified during a standard ECG or ambulatory ECG monitoring performed for another indication. Different forms of SND exist electrophysiologically from inappropriate sinus bradycardia, chronotropic incompetence, sinus pauses, SA exit block and the tachycardia-bradycardia syndrome. Treatment of SND is directed at symptoms and typically involves the implantation of a permanent pacemaker. (See "Permanent cardiac pacing: Overview of devices and indications".)

The treatment of SND will be reviewed here. The etiologies, clinical manifestations, diagnosis, evaluation, and natural history are discussed in detail separately. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation" and "Arrhythmia management for the primary care clinician", section on 'Referral to a specialist'.)

DEFINITION — SND is a clinical syndrome characterized by chronic sinoatrial (SA) node dysfunction, a sluggish or absent SA nodal pacemaker after electrical cardioversion, and/or depressed escape pacemakers in the presence or absence of atrioventricular (AV) nodal conduction disturbances [1-3]. SND may also manifest as chronotropic incompetence with inappropriate heart rate responses to physiologic demands during activity. SND can also be accompanied by AV nodal conduction disturbances and by atrial tachyarrhythmias as part of the tachycardia-bradycardia syndrome. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history", section on 'Definition'.)

TREATMENT — Treatment of SND is directed at ameliorating symptoms, which may include lightheadedness, presyncope, syncope, and, less often, dyspnea on exertion or worsening angina. In addition, patients with tachycardia-bradycardia syndrome may present with palpitations and other symptoms associated with a rapid heart rate. While some individuals present with frank syncope, patients more commonly report progressive development of symptoms and often equate this with natural aging. Specific treatment for the control of symptomatic SND usually involves the implantation of a pacemaker. There is a limited role for pharmacologic intervention in symptomatic and/or hemodynamically unstable sinoatrial (SA) node dysfunction. Definitive therapy of irreversible SA node dysfunction requires the implantation of a permanent pacemaker. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" and 'Long-term management' below.)

It is important to recognize that there may be an "extrinsic" component to SND compounding the "intrinsic" component inherent to the dysfunctional SA node. The most common of these extrinsic agents are pharmacologic agents. The higher prevalence of hypertension, coronary artery disease, and atrial fibrillation (AF) in the same group of patients with SND would make it more likely that the pharmacologic regimen of such patients may include beta adrenergic blockers, non-dihydropyridine calcium channel blockers, and antiarrhythmic agents, all of which would potentially exacerbate any underlying SA node dysfunction.

Initial management — The initial management of the patient with symptomatic SND depends on the presence and severity of any signs and symptoms (eg, lightheadedness, presyncope, syncope, dyspnea on exertion or worsening angina) related to the ventricular rate. Unstable patients require immediate pharmacologic therapy and, in most instances, should also receive temporary pacing to increase heart rate and cardiac output. Once the patient is hemodynamically stable, assessment and treatment for any potentially reversible causes should occur, followed by placement of a permanent pacemaker for patients without an identifiable reversible etiology.

The evaluation and management of patients with symptomatic SND should include a review of the patient's medical regimen. Identifying pharmacologic agents with the potential to exacerbate SND (extrinsic component) is critical. If possible, discontinuing or modifying the dose of the implicated agent may help stave off the need for permanent pacing. (See 'Stable patients' below.)

In order to treat patients with apparent SND appropriately, it is important to try to correlate symptoms with bradycardia or, less commonly, the associated tachycardia. Some patients have episodic symptoms suggestive of an arrhythmia (eg, lightheadedness or palpitations) but are found to have a relatively normal heart rhythm during an episode. Due to the intermittent nature of symptomatic arrhythmias, ambulatory monitoring or an event recorder is often required to establish this correlation. Bradyarrhythmias and pauses during sleep are not taken into consideration when deciding on implantation of a pacemaker. (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation".)

Unstable patients — Patients with SND are rarely hemodynamically unstable for a prolonged period; however, those who are should be urgently treated (algorithm 1) using the Advanced Cardiac Life Support (ACLS) protocol with atropine, dopamine, or epinephrine as well as temporary cardiac pacing (either with transcutaneous or, if immediately available, transvenous pacing) [4]. (See "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia'.)

The most important clinical determination in a patient presenting with SND is whether or not the patient is hemodynamically stable or not due to the resulting bradycardia and the ensuing reduced cardiac output. Signs and symptoms of hemodynamic instability include hypotension, altered mental status, signs of shock, ongoing ischemic chest pain, and evidence of acute pulmonary edema. Such patients should be treated according to the ACLS protocol for patients with symptomatic bradycardia (algorithm 2) [4]:

Except in a transplanted (ie, denervated) heart, the first line of therapy in symptomatic bradycardia is atropine. Atropine should be promptly administered if intravenous (IV) access is available, but treatment with atropine should not delay treatment with transcutaneous pacing or a chronotropic agent. The initial dose of atropine is 0.5 mg IV. This dose may be repeated every three to five minutes to a total dose of 3 mg.

If the patient remains unstable, temporary cardiac pacing should be provided, although the need for this is rare in this patient population. The duration of temporary cardiac pacing should be as brief as possible, with discontinuation following treatment of reversible causes or implantation of a permanent pacemaker if no reversible cause is identified.

In the absence of central venous access, the most immediate way to provide temporary cardiac pacing is via transcutaneous pacing. Transcutaneous pacing is uncomfortable for the patient and may have variable efficacy depending on how well the impulses are transmitted to the myocardium; as such, transcutaneous pacing should be viewed as a temporizing measure until temporary transvenous pacing can be provided. (See "Temporary cardiac pacing".)

In patients with hypotension associated with SND following atropine therapy, we administer dopamine, epinephrine, or isoproterenol via IV infusion for heart rate and blood pressure augmentation.

If dopamine is chosen, we begin at a dose of 2 mcg/kg/minute and titrate up to 20 mcg/kg/minute if needed.

If epinephrine is chosen, we begin at a dose of 2 mcg/minute and titrate up to 10 mcg/minute if needed.

If isoproterenol is chosen, we begin at a dose of 2 mcg/minute and titrate up to 10 mcg/minute if needed.

Once a hemodynamically unstable patient has been stabilized, the approach to further management is the same as for patients who were initially stable. (See 'Stable patients' below.)

Stable patients — Patients with SND who are hemodynamically stable do not require urgent therapy with atropine or temporary cardiac pacing (algorithm 1). However, many patients can have recurrent prolonged pauses or periods of bradycardia, so patients should be continuously monitored with transcutaneous pacing pads in place in the event of clinical deterioration.

While stable patients are being monitored, evaluation and treatment should focus on a search for reversible causes of SA nodal depression, such as drugs (eg, beta blockers, calcium channel blockers, digoxin), ischemia, and autonomic imbalance. Not infrequently, a symptomatic bradyarrhythmia is induced by medications. The management of patients with suspected beta blocker or calcium channel blocker toxicity/overdose (either accidental or intentional) is discussed in detail separately. (See "Beta blocker poisoning" and "Calcium channel blocker poisoning".)

In patients taking a beta blocker or calcium channel blocker for certain indications (ie, hypertension), there are alternative medications that can be equally effective without slowing the heart rate. However, for adequate medical treatment of atrial or ventricular tachyarrhythmias, or angina related to coronary artery disease, beta blockers or calcium channel blockers may be required.

Patients with SND felt to be medication-induced should be observed while the offending agent or agents are withdrawn, if clinically feasible. Such patients will often have improvement or resolution of symptoms following removal of the medication(s). For patients with drug-induced bradycardia in whom the risk/benefit ratio favors the continuation of the offending agent, pacemaker insertion is indicated. (See 'Long-term management' below.)

A discussion of possible reversible causes and the approach to evaluation is presented separately. (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation", section on 'Approach to the diagnosis'.)

Long-term management — The long-term management of the patient with symptomatic SND depends on the extent of symptoms and conduction abnormalities (algorithm 1), as well as the likelihood of recurrence or progression leading to subsequent problems (eg, syncope, cardiac arrest, etc).

Asymptomatic patients — Persons with bradycardia and no symptoms attributable to the bradycardia do not require placement of a permanent pacemaker. Instead, these patients may be followed with intermittent examinations and deferral of pacemaker placement. Professional society guidelines do not generally recommend implanting a pacemaker in asymptomatic individuals with bradycardia or pauses [5]. (See "Permanent cardiac pacing: Overview of devices and indications", section on 'Class III: Pacing not indicated'.)

Symptomatic patients — For patients with symptomatic SND and documented symptomatic bradycardia, we recommend implantation of a permanent pacemaker rather than medical therapy or observation alone [5]. Pacemaker placement is indicated in patients with SND and a documented correlation between symptoms and sinus bradycardia or sinus pauses [5]. Symptoms of syncope and lightheadedness are reversed in virtually all patients following pacemaker placement, but there does not appear to be a survival benefit [6-10].

Temporary pacing — Due to the complications associated with the use of temporary pacing wires, this therapy should be reserved for patients who fail to respond to medical therapy and for the shortest amount of time possible [11]. The use of externalized permanent pacemakers utilizing active fixation leads allows the patient greater mobility and fewer complications if the interval until the insertion of a permanent pacemaker is prolonged [12]. (See "Temporary cardiac pacing".)

Permanent pacing — Selection of the type of pacemaker and appropriate programming for a specific patient depends upon the presence or absence of atrioventricular (AV) conduction abnormalities, the presence or absence of atrial arrhythmias, the desire to maintain AV synchrony, and the need for rate-responsiveness (algorithm 3). (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation".)

Pacing within the atrium (utilizing either AAI or DDD) is required. Single chamber atrial-based pacing (AAI) can be used in selected cases when AV conduction is considered to be normal and when the expectation of developing impaired AV conduction is minimal [5,13].

While there is an advantage in minimizing the number of leads used in a pacemaker (AAI versus DDD), the fear of the future development and progression of atrioventricular conduction disease has led to the widespread adoption of dual chamber (DDD) versus single chamber (AAI) pacing. The guidelines recommend DDD for symptomatic SND with extension of the AV interval to minimize ventricular pacing [5,13].

When it is anticipated that the patient will require frequent pacing, physiologic pacing is preferred. Physiologic pacing refers to pacing modes that most closely approximate normal cardiac behavior by maintaining AV synchrony (ie, AAI or DDD systems, in contrast to VVI systems). Promoting intrinsic AV conduction and minimizing right ventricular pacing has been shown to reduce the likelihood of developing AF, heart failure, hospitalization, and pacemaker syndrome. (See "Modes of cardiac pacing: Nomenclature and selection" and "Modes of cardiac pacing: Nomenclature and selection", section on 'Pacemaker syndrome'.)

Given that patients with SND will often have chronotropic incompetence, programming rate response should be considered. This allows the pacemaker's lower rate to increase commensurate with the patient's physical activity.

Several randomized trials and a subsequent 2006 meta-analysis have compared physiologic (DDD) and nonphysiologic (VVI) pacing in various settings [14-18]. While some trials were limited to patients with SND, others included patients with both SND and AV block. Among the more than 7000 patients included in the meta-analysis, some clinical benefits were seen with physiologic pacing, primarily a reduction in the development of AF and stroke, but there was no significant difference in all-cause mortality with physiologic pacing when compared with VVI pacing. Approximately one-half of patients in the meta-analysis had SND, and a subgroup analysis demonstrated a greater benefit from physiologic pacing in patients with SND compared with those with AV block, including a possible reduction in the combined endpoint of cardiovascular death and stroke [14]. (See "Modes of cardiac pacing: Nomenclature and selection", section on 'Potential advantages'.)

For patients without a baseline bundle branch block, the incidence of high-grade AV block requiring ventricular pacing has been estimated to be between 0.6 and 1.8 percent per year [19-22]. However, the risk of high-grade AV block is greater in patients with a complete bundle branch block or bifascicular block at presentation (7 percent per year) [22]. This observation suggests that AAI pacing may be safe in patients with SND who do not have baseline AV conduction abnormalities or bundle branch block. The largest randomized trial evaluating AAI pacing and DDD pacing in patients with SND is the DANPACE trial, a multicenter, randomized study of 1415 patients with SND and apparently normal AV conduction (baseline PR 0.22 seconds or less, baseline QRS less than 0.12 seconds) who were followed for a mean 5.4 years after initial pacemaker insertion [23]. There was no significant difference in the primary outcome of death from any cause in the AAI group versus the DDD group (hazard ratio [HR] 1.06, 95% CI 0.88-1.29). Among the prespecified secondary outcomes, patients with an AAI pacemaker were significantly more likely to undergo pacemaker reoperation (22 versus 12 percent in the DDD group), although less than half of the AAI patients undergoing pacemaker reoperation did so because of a need for DDD pacing (9.3 percent). The annualized rate of developing the need for DDD pacing was 1.7 percent, which is consistent with the previously published rates.

A more detailed discussion of various pacemaker modalities and functions is presented separately. (See "Modes of cardiac pacing: Nomenclature and selection".)

Pharmacologic therapy — There are no recommended pharmacologic therapies for patients with symptomatic SND; however, withdrawal of pharmacologic agents with the potential to exacerbate SND is frequently beneficial. Many patients with SND have an SA node that is unresponsive or has a blunted response to pharmacologic agents. In a trial of 107 patients with symptomatic SND who were randomly assigned to no therapy, a rate-responsive pacemaker, or oral theophylline (which can increase heart rate by stimulation of the sympathetic nervous system) and followed for an average of 19 months, patients assigned to pacemaker therapy had a significantly lower incidence of syncope compared with those assigned to no therapy (6 versus 23 percent respectively) and a trend towards less syncope when compared with those receiving theophylline (6 versus 17 percent) [24]. Implantation of a pacemaker and theophylline had an equivalent benefit on the incidence of heart failure compared with controls (3 versus 17 percent).

Anticoagulation — Patients with SND who require pacemaker therapy have a high incidence of AF [25]. A known history of AF prior to pacemaker implantation as well as the duration of time since pacemaker implantation are the two most important determinants of the development of AF [25]. Thromboembolism may occur in patients with SND, particularly those with the tachycardia-bradycardia syndrome and associated AF [18,26,27]. Tachycardia-bradycardia syndrome, with periods of alternating atrial tachyarrhythmias and bradycardia, occurs in over 50 percent of cases of SND, with AF being the most common tachyarrhythmia [15,28]. Thromboembolism is most likely related to the associated AF. Thus, decisions surrounding anticoagulation of patients with tachycardia-bradycardia SND with documented episodes of AF should be guided by a discussion of the potential benefits and risks of anticoagulation (table 1 and table 2) [29]. (See "Atrial fibrillation in adults: Use of oral anticoagulants".)

Patients with pacemakers may be less likely to be aware of the development of AF, particularly if AV conduction abnormalities prevent a rapid ventricular response [30]. Due to the thromboembolic risks associated with unrecognized AF, patients with pacemakers should be closely observed, by means of routine pacemaker interrogation, for the development of AF. Contemporary pacemakers are able to detect and record brief episodes of AF, which may be clinically significant [31]. Nevertheless, determining the duration of atrial tachyarrhythmias that should mandate consideration of systemic anticoagulation remains a topic of controversy and investigation with no clear guidelines [29,32]. Unless there are contraindications, patients with AF should be risk stratified on their need for anticoagulant therapy (table 1). Most patients with SND are older adults, and older adult patients have both increased sensitivity to warfarin and an increased risk of bleeding complications (table 2). Thus, careful monitoring is required. Other newer anticoagulants are now available and may be considered in select patients who require anticoagulation. These issues are discussed in detail separately. (See "Atrial fibrillation in adults: Use of oral anticoagulants".)

Catheter ablation — Patients with symptomatic sinus node dysfunction and paroxysmal AF can have significant post-conversion pauses that would mandate the implantation of a permanent pacemaker (PPM). PPMs allow for antiarrhythmic agents and/or more aggressive rate control with higher doses of rate-controlling agents without exacerbating the pauses that ensue upon reversion to sinus rhythm. In a select group of patients, implantation of a pacemaker can be averted by eliminating AF through catheter ablation [33]. The clinician should be mindful that, following ablation, AF may continue for three to six months before the full effect of the ablation is realized or that the long-term result of the ablation is not the complete but rather the partial elimination of AF, leaving them vulnerable to the consequences of post-conversion pauses/bradyarrhythmias.

In rare instances, patients may be symptomatic due to profound sinus bradycardia alone, without evidence of AF or other tachyarrhythmias. In a pilot study involving 62 patients (40 patients <50 years of age, 22 patients ≥50 years of age) with symptomatic sinus bradycardia, catheter ablation of the atrial ganglionated plexus, thereby modifying autonomic input to the sinus node, resulted in significantly increased resting heart rate and attenuation of symptoms in all patients, although the effect was greater in patients <50 years of age (19.3 versus 10.8 beats per minute) and was attenuated at one year in patients ≥50 years of age [34]. Though thought-provoking as a means of improving symptoms without implantation of a permanent pacemaker, these data should be replicated in additional studies with longer-term follow-up to determine if the benefit is sustained or attenuated with time.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline links: Syncope" and "Society guideline links: Atrial fibrillation" and "Society guideline links: Cardiac implantable electronic devices".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Sinus node dysfunction (The Basics)" and "Patient education: Pacemakers (The Basics)" and "Patient education: Bradycardia (The Basics)")

Beyond the Basics topic (see "Patient education: Pacemakers (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Definition and clinical presentation – Sinus node dysfunction (SND) is a clinical syndrome characterized by sinoatrial (SA) node dysfunction (not due to a reversible cause), a sluggish or absent SA nodal pacemaker after electrical cardioversion, and/or depressed escape pacemakers. These abnormalities can result in profound sinus bradycardia, sinus pauses, sinus arrest, SA nodal exit block, and inappropriate responses to physiologic demands during exercise or stress. (See 'Definition' above.)

Initial management – The initial management of the patient with symptomatic SND depends on the presence and severity of any signs and symptoms (eg, lightheadedness, presyncope, syncope, dyspnea on exertion or worsening angina) related to the ventricular rate (algorithm 1).

Unstable patients – Patients with SND are rarely hemodynamically unstable for a prolonged period; however, those who are should be urgently treated using the Advanced Cardiac Life Support protocol with atropine, dopamine, or epinephrine as well as temporary cardiac pacing (either with transcutaneous or, if immediately available, transvenous pacing) (algorithm 2). (See 'Unstable patients' above and "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia'.)

Stable patients

-Monitor – Patients with SND who are hemodynamically stable do not require urgent therapy with atropine or temporary cardiac pacing. However, many patients can have recurrent prolonged pauses or periods of bradycardia, so patients should be continuously monitored with transcutaneous pacing pads in place in the event of clinical deterioration. (See 'Stable patients' above.)

-Avoid drugs exacerbating SND – The evaluation and management of patients with symptomatic SND should include a review of the patient's medical regimen. Identifying pharmacologic agents with the potential to exacerbate SND (extrinsic component) is critical. If possible, discontinuing or modifying the dose of the implicated agent may help stave off the need for permanent pacing.

Long-term management – The long-term management of the patient with symptomatic SND depends on the extent of symptoms and conduction abnormalities (algorithm 1), as well as the likelihood of recurrence or progression leading to subsequent problems (eg, syncope, cardiac arrest, etc).

Asymptomatic patients – Persons with bradycardia and no symptoms attributable to the bradycardia do not require placement of a permanent pacemaker. Instead, these patients may be followed with intermittent examinations and deferral of pacemaker placement. (See 'Asymptomatic patients' above.)

Symptomatic patients – For patients with symptomatic SND and documented symptomatic bradycardia, we recommend implantation of a permanent pacemaker rather than medical therapy or observation alone (Grade 1A). Selection of the type of pacemaker and appropriate programming for a specific patient depends upon the presence or absence of atrioventricular (AV) conduction abnormalities, the presence or absence of atrial arrhythmias, the desire to maintain AV synchrony, and the need for rate-responsiveness (algorithm 3). (See 'Symptomatic patients' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Alan Cheng, MD, and Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.

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