applying gentle pressure over the carotid sinus with the patient in the supine position. It is contraindicated if there is an ipsilateral carotid bruit.
TABLE 54.1 Intrinsic and Extrinsic Causes of Sinus Node Dysfunction
Immediate management: No immediate therapy is generally required with the exception of the patient with frequent and profound symptomatic sinus pauses or bradycardia in whom medication (such as atropine, or beta-agonists such as isoproterenol or dopamine) or temporary pacing may be required. A search for reversible causes should simultaneously be undertaken (see management for AV conduction disturbances for detail).
TABLE 54.2 Indications for Permanent Pacemaker in SND
Indications for Permanent Pacemaker in SND
In patients with symptoms that are directly attributable to SND, permanent pacing is indicated to increase heart rate and improve symptoms.
In patients who develop symptomatic sinus bradycardia as a consequence of guideline-directed therapy for which there is no alternative treatment and continued treatment is clinically necessary, permanent pacing is recommended to increase heart rate and improve symptoms.
For patients with tachy-brady syndrome and symptoms attributable to bradycardia, permanent pacing is reasonable to increase heart rate and reduce symptoms.
In patients with symptomatic chronotropic incompetence, permanent pacing with rate-responsive programming is reasonable to increase exertional heart rates and improve symptoms.
COR, class of recommendation; SND, sinus node dysfunction.
Adapted from 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: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2019;140(8):e382-e482.
Long-term management: Because sinus node dysfunction is not a life-threatening condition, the search for a reversible cause can generally be performed in the outpatient setting and, if present, stopped. Occasionally, medications identified to be the culprit cannot be stopped because of the lack of alternative therapy. In the absence of a reversible cause, the only effective therapy for sick sinus syndrome is permanent pacing (Table 54.2).9
Degenerative diseases of the conduction system. This is the most common cause of acquired AV block accounting for approximately 50% of cases and is attributed to fibrosis and sclerosis of the conduction system.
Medications. Beta-blockers and digoxin impair or block the AV node indirectly via the autonomic nervous system. Calcium channel blockers and amiodarone directly slow or block the AV node. Class I and III antiarrhythmic medications can affect conduction in the His-Purkinje system, which leads to block within or below the His bundle, especially in the presence of preexisting disease of the conduction system.22
Acute myocardial infarction. Before reperfusion interventions became widely available, the incidence of AV block was 12% to 25% in patients with acute myocardial infarction. First-degree AV block occurred in 2% to 12%, second-degree AV block in 3% to 10%, and third-degree AV block in 3% to 7%.21 It is unclear whether reperfusion therapy has altered the incidence of AV block. First- and second-degree type I AV block occurs more commonly with inferior myocardial infarction than anterior or lateral infarctions. In patients with CHB as a complication of acute inferior myocardial infarction, the site of the AV block is usually the AV node with a junctional escape beat of 40 to 60 bpm. It generally responds to atropine and resolves spontaneously within several days. Some patients with AV block occurring during the early phase of acute inferior wall myocardial infarction are resistant to atropine. Small series showed reversal of atropine-resistant AV block with aminophylline, a competitive adenosine antagonist. The release of adenosine during myocardial infarction may be responsible in such cases.23 In the setting of acute anterior wall myocardial infarction, CHB is associated with a large amount of myocardial damage that involves the His-Purkinje system. The escape beat stems from the His-Purkinje system with a rate of 30 to 40 bpm. The AV block is less likely transient and should be treated with permanent pacing. Conversely, current guidelines recommend against permanent pacing in patients with acute myocardial infarction and transient second- or third-degree AV block that subsequently resolves.10
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