Bradycardias: Sinus Node Dysfunction and Atrioventricular Conduction Disturbances



Bradycardias: Sinus Node Dysfunction and Atrioventricular Conduction Disturbances


Osamu Fujimura

Houman Khakpour


Deceased author.



INTRODUCTION

Bradycardia is generally defined as a heart rate less than 60 beats per minute (bpm) and is caused by sinus node dysfunction, disturbances of the atrioventricular (AV) conduction system, or both. Causes can be reversible or irreversible. In the absence of reversible causes, permanent pacing is the only reliable treatment for patients with symptomatic bradycardia and asymptomatic type II second-degree and third-degree AV block.


SINUS NODE DYSFUNCTION


Epidemiology and Etiology

The precise prevalence of sinus node dysfunction is difficult to study because of its wide range of presentations including asymptomatic patients. Studies on sick sinus syndrome have shown an incidence rate of 0.5 to 3.5 per 1000 person-years.1

Analysis of two large epidemiologic studies comprised of more than 20,000 patients showed a sick sinus syndrome incidence of 0.8 cases per 1000 person-years during a mean follow-up of 17 years.2,3,4 Advanced age was the most significant risk factor among several identified variables, with most patients presenting in their 70s and 80s.2

Sinus node dysfunction is classified as intrinsic or extrinsic (Table 54.1). The differentiation is crucial because the extrinsic causes of sinus node dysfunction are often reversible, and permanent pacing can largely be avoided.


Intrinsic Bradycardia

Sinus node dysfunction is most often seen in the elderly population as a result of age-related progressive fibrosis in the sinus node and its adjacent atrial tissue. This may result in abnormalities of impulse formation, conduction, or both and manifest as a variety of clinical abnormalities (Figure 54.1A).5 Patients with sinus node dysfunction often have underlying cardiac conditions, including ischemic heart disease, infiltrative disorders (amyloidosis, hemochromatosis, and sarcoidosis), collagen vascular disease, musculoskeletal disorders,6 and prior cardiac surgeries including orthotopic heart transplantation and congenital heart surgery.7 Familial forms of sinus node dysfunction related to autosomal dominance and recessive inheritance have been reported.8


Extrinsic (Functional) Bradycardia

Extrinsic factors include medications and perturbances in the autonomic nervous system leading to an increase in the parasympathetic tone. Medications that directly suppress sinoatrial nodal tissue or indirectly affect it via the autonomic nervous system include digoxin, beta-blockers, non-dihydropyridine calcium channel blockers (verapamil and diltiazem), clonidine, and antiarrhythmic drugs (type IA, IC, and III).9,10 Increase in parasympathetic tone is seen in carotid sinus hypersensitivity (Figure 54.1B), neurally mediated syncope (vasovagal syncope), and situational syncope.11 Sleep apnea can cause a variety of arrhythmias including significant sinus bradycardia and AV block, primarily because of an increase in vagal tone.12 Significant bradycardia is well documented in patients with grand mal seizure and anorexia nervosa.13 Well-trained athletes can have a resting heart rate of less than 40 bpm and a type I AV block.14 Hypothyroidism may also lead to sinus bradycardia.


Clinical Presentation of Sinus Node Dysfunction


Common Signs and Symptoms

Abnormalities in sinus node can be persistent or intermittent. Bradycardia produces a wide variety of symptoms such as fatigue, shortness of breath, light-headedness, and syncope, whereas some patients experience little to no symptoms. It is often difficult to determine if vague symptoms, such as lack of energy, are in fact caused by bradycardia. Thus, it is crucial to correlate the presenting symptoms with electrocardiographic (ECG) findings. Sinus node dysfunction is generally considered significant when sinus pause is greater than 3 seconds while awake and sinus rate less than 40 bpm, although significant overlap exists between asymptomatic and symptomatic individuals.


Diagnosis of Sinus Node Dysfunction


History and Physical Examination

Comprehensive history taking is crucial and should focus on duration, frequency, and severity of symptoms. Evaluation for extrinsic causes should include symptoms provoked or preceded by cough, defecation, urination, food swallowing, shaving, prolonged standing, dehydration, and unpleasant experiences. Medications, family and surgical history should be carefully reviewed.

Physical examination includes vital signs (ie, heart rate and blood pressure) and orthostatic changes in vital signs. Carotid sinus massage can be performed at the bedside by
applying gentle pressure over the carotid sinus with the patient in the supine position. It is contraindicated if there is an ipsilateral carotid bruit.














Noninvasive Testing

A 12-lead ECG is important to evaluate the overall electrical activation of the heart but is often insufficient unless the symptomatic episode is present during the ECG recording. A variety of extended ambulatory ECG monitors are available and can continuously record the cardiac rhythm up to 30 days. US Food and Drug Administration (FDA)-cleared portable ECG devices with one- or six-lead capability also are commercially available. An echocardiogram may be performed to evaluate for any underlying cardiac pathology. Exercise testing is used not only to evaluate stress-induced ischemia but importantly for its effects on sinus rate. For example, a normal chronotropic response is present in well-trained athletes with resting sinus bradycardia.14 Patients with chronotropic incompetence show a variety of abnormalities in response to exercise.9,10 Screening for sleep apnea can be performed with a sleep study.12 Genetic testing and counseling may be required in select cases.15


Electrocardiographic Features

Sinus node dysfunction manifests as sinus bradycardia, sinus pause—caused by sinus arrest, sinoatrial conduction block, or overdrive suppression (tachycardia-bradycardia)—and chronotropic incompetence.

Patients with chronotropic incompetence are not able to adequately increase their heart rate during exercise to meet metabolic demands. There is no uniformly acceptable definition, as a variety of heart rate responses to exercise have been reported.9,10 Inability to achieve a sinus rate to 100 to 120 bpm or 70% to 75% of the predicted maximum heart rate for age (220-age) is a commonly used target.10


Sick sinus syndrome is defined by symptoms directly caused by bradycardia. A pause greater than 3 seconds and heart rate less than 40 bpm while awake are generally considered to be diagnostic once extrinsic bradycardia is excluded. Upon gentle carotid sinus massage, a pause greater than 3 seconds during carotid massage is diagnostic for carotid sinus hypersensitivity when associated with symptoms, but this can be seen in asymptomatic elderly individuals.9,10


Electrophysiologic Features

An electrophysiologic study (EPS) is beneficial in select patients suspected of sick sinus syndrome.16 The test involves placement of a pacing catheter in the high right atrium. Atrial pacing is performed at multiple constant rates (usually from 100 to 200 bpm) for at least 30 seconds. Sinus node recovery time (SNRT) is measured from the last atrial pacing beat to the first spontaneous sinus beat. The SNRT is abnormal when greater than 1500 ms and diagnostic of sick sinus syndrome if it is greater than 3000 ms especially if associated with symptoms. SNRTs have about 80% sensitivity and 90% specificity for the diagnosis of sick sinus syndrome. The sinoatrial conduction time (ie, the time in milliseconds that it takes for a high-rate atrial paced beat to enter and reset the sinus node) may be prolonged in patients with sick sinus syndrome. It can be measured directly or indirectly, with normal being 45 to 125 ms. It is, however, a less sensitive method than SNRTs for detecting sick sinus syndrome.10,16


Management 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).









  • 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


ATRIOVENTRICULAR CONDUCTION DISTURBANCES


Epidemiology

Although AV conduction abnormalities are common, advanced degree of AV block is relatively infrequent. Analysis of a cohort of greater than 6000 individuals with a follow-up of 25 years revealed an incidence of hospitalization because of second- or third-degree AV block of 0.9%.17 Older age, male gender, a history of myocardial infarction, a history of heart failure, elevated blood pressure, and elevated glucose levels were individually linked to AV block.17 Patients with sick sinus syndrome also have a higher incidence of development of AV block. Analysis of the collected data from 28 studies on atrial pacing used for sick sinus syndrome disclosed a median annual incidence of complete AV block of 0.6% (0%-4.5%).18 The DANPACE trial comprised of 1384 patients with a mean follow-up of 8.9 years showed the annual rate of mode change from atrial pacing to dual-chamber pacing was 4.5%.19


Pathogenesis

Disturbances in the AV conduction system can be defined as a delayed or interrupted electric signal transmission from the atrium to the ventricle. They can be caused by a variety of factors and can be transient or permanent.



Congenital Atrioventricular Block

Congenital complete heart block (CHB) is considered to be a result of embryonic maldevelopment of the AV node and less frequently the His-Purkinje system.20 The incidence is reported to be about 1 in 22,000 live births. Neonatal lupus is associated with 60% to 90% of these cases, and 50% of diagnosed patients have other cardiac malformations, such as congenitally corrected transposition of the great vessels, ventricular septal defects, AV canal defects, and Ebstein anomaly.20


Acquired Atrioventricular Block

The following causes are associated with development of acquired AV block (Table 54.3).21



  • 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

    Only gold members can continue reading. Log In or Register to continue

May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Bradycardias: Sinus Node Dysfunction and Atrioventricular Conduction Disturbances
Premium Wordpress Themes by UFO Themes