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Heart block

Heart block, also known as atrioventricular (AV) block, is a conduction disorder in which the electrical signals that regulate the heartbeat are delayed or completely blocked as they travel from the heart's upper chambers (atria) to the lower chambers (ventricles), potentially leading to an irregular or slowed heart rate.^[1] This condition disrupts the normal synchronization between atrial and ventricular contractions, which can range from mild and asymptomatic to severe and life-threatening if untreated.^[2] Heart block is classified into three main degrees based on the severity of the conduction impairment. First-degree heart block involves a prolonged delay in signal transmission, typically manifesting as a PR interval longer than 200 milliseconds on an electrocardiogram (ECG), but all signals eventually reach the ventricles.^[2] Second-degree heart block is characterized by intermittent failure of signals to conduct, subdivided into Mobitz type I (with progressive PR interval lengthening before a dropped beat) and Mobitz type II (sudden dropped beats without prior lengthening), which carries a higher risk of progression.^[2] Third-degree, or complete, heart block represents total dissociation between atrial and ventricular activity, where no atrial impulses reach the ventricles, resulting in independent rhythms and often requiring urgent intervention.^[2] These types can occur congenitally or be acquired later in life.^[2] Common causes of heart block include age-related degeneration of the conduction system, myocardial infarction, certain medications (such as beta-blockers or calcium channel blockers), electrolyte imbalances, and congenital factors like maternal lupus erythematosus.^[2] Risk factors encompass older age, family history of cardiac conditions, and underlying heart diseases such as cardiomyopathy or valvular disorders.^[1] Symptoms vary by degree but may include fatigue, dizziness, fainting (syncope), shortness of breath, and palpitations, with complete block potentially causing hemodynamic instability or sudden cardiac arrest.^[1] Diagnosis primarily relies on a 12-lead ECG to identify characteristic patterns, supplemented by ambulatory monitoring (e.g., Holter), exercise testing, or electrophysiological studies for confirmation.^[2] Echocardiography may assess structural heart issues contributing to the block.^[2] Treatment depends on severity and symptoms: observation suffices for asymptomatic first-degree block, while second- and third-degree blocks often necessitate permanent pacemaker implantation to restore coordinated heartbeats, alongside addressing reversible causes like medication adjustments.^[1] In acute settings, temporary pacing or medications may stabilize the patient.^[2] Early management improves prognosis, particularly for complete heart block, where untreated five-year survival is approximately 37%.^[2]

Cardiac Conduction System

Anatomy

The sinoatrial (SA) node, the heart's primary pacemaker, is a small, elongated structure located at the junction of the superior vena cava and the right atrium, typically measuring about 10-20 mm in length and embedded within the atrial wall.^[3] It consists of specialized autorhythmic cells, including nodal (P) cells and transitional (T) cells, which have fewer myofibrils than typical cardiomyocytes and are rich in glycogen, enabling spontaneous depolarization.^[4] Histologically, the SA node is insulated by dense connective tissue that separates it from surrounding atrial myocardium, ensuring directed impulse propagation.^[4] The atrioventricular (AV) node serves as the electrical gateway between the atria and ventricles and is positioned in the lower right atrium within the triangle of Koch, bounded by the tendon of Todaro, the septal leaflet of the tricuspid valve, and the coronary sinus ostium.^[5] This compact structure, approximately 1-5 mm in size, features specialized nodal cells with sparse myofibrils and prominent fibrous insulation provided by the central fibrous body of the cardiac skeleton, which delays conduction to allow atrial contraction completion.^[4] The AV node's histology includes transitional cells connecting to atrial myocardium and penetrating fibers that form the initial segment of the His bundle.^[4] Distal to the AV node, the bundle of His (or AV bundle) emerges as an elongated cord of specialized conduction fibers, about 1-2 cm long, penetrating the fibrous cardiac skeleton at the top of the interventricular septum to connect with the bundle branches.^[6] It comprises Purkinje-type cells and slender transitional cells, with minimal fibrous encapsulation to facilitate rapid signal transmission.^[6] The His bundle bifurcates into the left and right bundle branches: the right branch courses along the right interventricular septum toward the apex, while the left branch, thicker and divided into anterior and posterior fascicles, traverses the left septum.^[7] These branches distribute into an extensive network of Purkinje fibers, which ramify subendocardially through the ventricular myocardium from apex to base, consisting of large, pale-staining cells with abundant glycogen, few myofibrils, and peripheral nuclei for swift impulse conduction.^[4]

Physiology

The sinoatrial (SA) node, the heart's primary pacemaker, exhibits automaticity through spontaneous generation of action potentials at a rate of 60 to 100 beats per minute, initiating the normal sinus rhythm.^[3] This automaticity stems from phase 4 diastolic depolarization, where the membrane potential slowly rises due to decaying outward potassium currents and inward currents via ion channels, including the hyperpolarization-activated funny current (I_f, primarily sodium influx) and T-type calcium channels.^[8] Upon reaching threshold (around -40 mV), phase 0 depolarization occurs through rapid activation of L-type voltage-gated calcium channels, allowing calcium influx to propagate the impulse, distinct from the sodium-driven phase 0 in contractile myocytes.^[8] The generated impulse spreads rapidly across the atrial myocardium via gap junctions at conduction velocities of 0.5 to 1 m/s, reaching the atrioventricular (AV) node within about 90 milliseconds.^[9] At the AV node, physiological conduction is intentionally slowed, introducing a delay of approximately 0.1 seconds due to reliance on slower calcium-dependent action potentials and fewer gap junctions in nodal cells.^[9] This delay coordinates atrial emptying prior to ventricular activation.^[10] From the AV node, the impulse proceeds through the penetrating bundle of His, dividing into left and right bundle branches, and then into the Purkinje fiber network, which facilitates rapid conduction at velocities up to 2 m/s to ensure near-simultaneous ventricular depolarization from endocardium to epicardium and apex to base.^[9] After depolarization, cardiac cells enter refractory periods that enforce sequential activation and prevent premature excitations. The absolute refractory period, spanning phases 0 through most of phase 3 (lasting 200-250 ms in ventricular myocytes), inactivates sodium channels, rendering the tissue inexcitable to maintain the heart's rhythm.^[11] The following relative refractory period, during late phase 3, partially restores excitability but requires a stronger stimulus for propagation as potassium efflux continues.^[11] Collectively, these periods promote unidirectional impulse travel and inhibit re-entrant loops by allowing full recovery before subsequent impulses.^[11] This orderly propagation synchronizes atrial and ventricular contractions, with atrial systole preceding ventricular systole to maximize filling. The atrial contribution, known as the "atrial kick," boosts ventricular end-diastolic volume by 20-30% at rest, thereby increasing stroke volume and cardiac output without excessive energy expenditure.^[12]

Pathophysiology

Mechanisms of Block

Heart block encompasses impaired electrical conduction within the atrioventricular (AV) conduction system, occurring at the AV junction or infranodal regions below the His bundle, which leads to delayed or absent activation of the ventricles.^[2] This disruption prevents normal propagation of impulses from the atria to the ventricles, potentially causing bradycardia or asystole if uncompensated.^[13] The normal conduction pathway, originating from the sinoatrial (SA) node through the atria to the AV node and His-Purkinje system, serves as the baseline for these impairments.^[3] Various mechanisms underlie heart block, including prolongation of the refractory period in conduction tissues, structural damage to the pathways, and autonomic nervous system influences. Increased refractory periods can arise from electrolyte imbalances, such as hyperkalemia, where elevated extracellular potassium depolarizes the resting membrane potential, slowing conduction velocity and extending the effective refractory period in atrial, nodal, and ventricular tissues.^[14] Structural damage, often involving fibrosis or degeneration of the conduction fibers, physically interrupts impulse transmission, particularly in aging or ischemic hearts where sclerotic changes accumulate in the AV node or His-Purkinje system.^[13] Autonomic influences, such as heightened vagal tone, selectively prolong refractoriness in the AV node by enhancing acetylcholine-mediated hyperpolarization, thereby delaying AV conduction without necessarily affecting the infranodal regions.^[2] The location of the block determines its specific physiological impact. AV junctional block interrupts transmission from atria to ventricles, compromising atrioventricular synchrony and leading to dissociated atrial and ventricular rhythms where atrial contractions may not effectively preload the ventricles.^[2] Infra-Hisian block, occurring distal to the His bundle in the Purkinje fibers, more severely affects ventricular activation, often producing wide QRS complexes and predisposing to unstable ventricular escape rhythms due to the slower intrinsic rates and broader conduction delays in these distal tissues.^[13] When higher-order pacemakers fail, subsidiary escape rhythms emerge to maintain cardiac output. The AV junctional pacemaker, with an intrinsic rate of 40-60 beats per minute, can assume control in proximal AV blocks, generating narrow QRS complexes if the His-Purkinje system is intact.^[13] In more distal infra-Hisian blocks, ventricular escape rhythms predominate at slower rates of 20-40 beats per minute, often with wide QRS morphology due to reliance on Purkinje or myocardial automaticity, which provides less reliable and hemodynamically suboptimal pacing.^[2] These escape mechanisms highlight the hierarchical organization of the conduction system, where lower pacemakers activate only after prolonged suppression of superior sites.^[15]

Classification

Heart block is classified primarily by anatomical location within the AV conduction system and by the degree of conduction impairment, which determines clinical significance and management implications. Blocks at the AV node, intra-Hisian (within the His bundle), and infra-Hisian regions (below the His bundle, involving the bundle branches and Purkinje fibers) represent distinct subtypes, with degrees ranging from partial delays to complete interruption. This taxonomic approach distinguishes benign, often reversible forms from those prone to progression and hemodynamic instability.^[16] Atrioventricular blocks are subdivided by degree of impairment in atrial-to-ventricular impulse transmission. First-degree AV block is characterized by a prolonged PR interval exceeding 200 milliseconds with consistent 1:1 conduction, representing a uniform delay usually at the AV nodal level without dropped beats. Second-degree AV block encompasses intermittent failure of conduction: Type I (Wenckebach) involves progressive PR interval prolongation culminating in a non-conducted P wave and dropped QRS complex, often supranodal in location and associated with vagal influences; Type II features a constant PR interval with sudden, intermittent non-conducted P waves, typically infra-nodal and signaling higher risk of progression. Third-degree, or complete, AV block entails total dissociation between atrial (P waves) and ventricular (QRS) activity, with no conducted impulses and independent rhythms in each chamber, necessitating an escape rhythm for ventricular depolarization.^[2]^[16] Infra-Hisian blocks involve conduction disturbances distal to the His bundle, affecting the bundle branches or Purkinje system, and often result in wide QRS escape rhythms due to slowed ventricular activation via myocardial fibers rather than the specialized conduction pathway. These blocks are distinguished from more proximal forms by their association with structural degeneration, poor response to atropine, and propensity for rapid progression to complete AV block, frequently requiring permanent pacing.^[2]^[16]

Epidemiology

Prevalence

Heart block, encompassing atrioventricular (AV) and sinoatrial (SA) blocks, exhibits low overall prevalence in the general population, with advanced forms being particularly rare. The prevalence of third-degree (complete) AV block is estimated at 0.02% in the United States and 0.04% worldwide.^[17]^[18] First-degree AV block is more common, occurring in approximately 1-1.5% of individuals under age 60 and up to 5% in men over age 60.^[19]^[20]^[21] Second- and third-degree AV blocks together have a prevalence of 0.2-1.2% in screened populations.^[21] Prevalence increases significantly with age, reflecting degenerative changes in the conduction system, and is generally higher in males. In individuals aged 60 and older, the overall prevalence of any AV block rises to about 1.8%, compared to 0.27% in those aged 18-39.^[22] For high-grade AV block (second- or third-degree), prevalence is elevated in the elderly. SA block, a component of sinus node dysfunction, is less frequently reported but contributes to the broader category of bradyarrhythmias, with sinus node dysfunction affecting approximately 0.2% of people over age 65.^[23] SA block is often underdiagnosed due to its intermittent nature and overlap with other sinus pauses. Global variations in heart block prevalence are influenced by differences in population aging and underlying cardiovascular disease burdens. Regions with older demographics, such as Europe and North America, report higher rates of age-related AV block compared to Asia, where younger populations predominate.^[24]

Risk Factors

Age is the strongest risk factor for developing heart block, with incidence increasing markedly due to age-related degenerative changes in the cardiac conduction system, such as idiopathic fibrosis and sclerosis of the atrioventricular node and bundle branches.^[25] The risk of atrioventricular block rises with advancing age, with a hazard ratio of 1.34 per 5-year increment in a large population-based cohort study.^[26] This age-related progression contributes to higher prevalence in older adults, where first-degree atrioventricular block alone affects approximately 5.3% of individuals, particularly males.^[21] Comorbid cardiovascular conditions significantly predispose individuals to heart block by promoting structural and functional damage to the conduction pathways. Ischemic heart disease, particularly following myocardial infarction, elevates the risk by approximately 3.5-fold (hazard ratio 3.54, 95% CI 1.33-9.42).^[26] Similarly, congestive heart failure increases the risk by about 3.3-fold (hazard ratio 3.33, 95% CI 1.10-10.09).^[26] Hypertension and diabetes further amplify vulnerability; elevated systolic blood pressure (hazard ratio 1.22 per 10-mm Hg increase) and fasting glucose levels (hazard ratio 1.22 per 20-mg/dL increase) are independently associated with atrioventricular block, with population-attributable risks of 47% and 11%, respectively.^[26] Certain medications commonly used for cardiovascular conditions can induce reversible atrioventricular block by slowing conduction through the atrioventricular node. Beta-blockers, non-dihydropyridine calcium channel blockers (such as verapamil and diltiazem), and digoxin are frequent culprits, accounting for up to 54% of drug-related atrioventricular block cases in clinical series, with resolution often occurring upon discontinuation in a majority of patients.^[27] These effects are dose-dependent and more pronounced in individuals with underlying conduction abnormalities.^[28] Genetic predispositions, though rare, can lead to progressive forms of heart block, particularly in younger individuals. Lev-Lenègre disease, an inherited condition caused by mutations in the SCN5A gene encoding the cardiac sodium channel, results in idiopathic progressive cardiac conduction defect and is a notable example of such syndromes.^[17] This autosomal dominant disorder predisposes affected families to atrioventricular block requiring pacemaker implantation at relatively early ages.^[29]

Etiology

Acquired Causes

Acquired heart block refers to disruptions in the cardiac conduction system that develop after birth due to various pathological processes, distinct from congenital origins. These causes often involve ischemia, inflammation, iatrogenic factors, or metabolic derangements that impair atrioventricular (AV) node function or infranodal conduction pathways. While some acquired blocks are transient and reversible upon addressing the underlying trigger, others may progress to permanent conduction defects requiring intervention.^[2] Ischemic heart disease, particularly acute myocardial infarction (MI), is a leading cause of acquired AV block, accounting for approximately 5-13% of third-degree blocks in affected patients. In inferior wall MI, which often involves the right coronary artery supplying the AV node, ischemia leads to transient or persistent nodal block due to heightened vagal tone and direct ischemic damage. Anterior wall MI, by contrast, more commonly affects the bundle branches below the AV node, resulting in wider QRS complexes and higher mortality risk from extensive septal necrosis.^[30]^[31]^[32] Inflammatory and infectious conditions can infiltrate or inflame the conduction system, producing blocks that range from first-degree to complete AV dissociation. Lyme disease, caused by Borrelia burgdorferi, frequently manifests as AV block in early disseminated stages, with approximately 80-90% of carditis cases showing conduction abnormalities; these are typically transient, resolving with antibiotics, though rare permanent damage occurs. Myocarditis, often viral in origin, induces edema and lymphocytic infiltration around the AV node or His-Purkinje system, leading to high-grade blocks in up to 10-20% of severe cases, with potential for reversibility if inflammation subsides promptly. Rheumatic fever, an autoimmune response to group A streptococcal infection, classically prolongs the PR interval via Aschoff body inflammation in the conduction tissues, but higher-degree blocks are uncommon and usually resolve with anti-inflammatory therapy.^[33]^[34]^[35]^[36] Iatrogenic causes arise from therapeutic interventions that mechanically or pharmacologically disrupt conduction. Post-cardiac surgery, particularly aortic or mitral valve replacement, complete AV block develops in 3-6% of cases due to edema, hematoma, or direct trauma to the perivalvular conduction tissues, with higher rates (up to 10%) in combined procedures. Drug toxicities, especially from AV nodal blocking agents like beta-blockers, non-dihydropyridine calcium channel blockers (e.g., verapamil), digoxin, and class I/III antiarrhythmics (e.g., flecainide, amiodarone), prolong the PR interval or induce higher-grade blocks by slowing nodal recovery or enhancing refractoriness, often reversible upon discontinuation but with recurrence risk in susceptible patients.^[37]^[38]^[28] Metabolic imbalances further contribute to acquired conduction delays by altering membrane potentials or myocardial excitability. Hyperkalemia, typically at levels exceeding 6.5 mEq/L, depresses phase 0 of the action potential in Purkinje fibers and ventricular myocytes, leading to PR prolongation, widened QRS, and progression to complete heart block; this is often seen in renal failure and reverses with potassium correction. Hypothyroidism slows AV conduction through reduced sympathetic tone, myocardial hypothyroidism-induced fibrosis, and bradycardic effects, manifesting as first- or second-degree block in severe cases, which generally improves with thyroid hormone replacement.^[39]^[40]^[41]

Congenital Causes

Congenital heart block, also known as congenital atrioventricular (AV) block, is a rare condition with an incidence of approximately 1 in 15,000 to 20,000 live births, most cases presenting as isolated complete AV block without other cardiac anomalies.^[42] This form of heart block arises during fetal development and is typically diagnosed prenatally or shortly after birth through fetal echocardiography or electrocardiography. A primary congenital cause is autoimmune-mediated heart block linked to maternal systemic lupus erythematosus or other connective tissue diseases, where transplacental passage of anti-Ro/SSA antibodies targets fetal cardiac conduction tissue, leading to inflammation and fibrosis of the AV node. Fetuses exposed to these maternal autoantibodies face a 2-5% risk of developing congenital AV block, with the majority of affected cases manifesting as irreversible third-degree (complete) block by 16-24 weeks of gestation.^[43]^[44] Structural congenital heart defects are associated with 30-50% of congenital heart block cases, often involving abnormalities that disrupt the normal development of the conduction system, such as atrial septal defects (ASD), ventricular septal defects (VSD), or more complex lesions like atrioventricular septal defects. In these instances, the heart block may result from malalignment or hypoplasia of the AV node during embryogenesis, exacerbating the conduction delay.^[45] Genetic mutations also contribute to congenital heart block, particularly in familial forms. Mutations in the SCN5A gene, which encodes the cardiac sodium channel Nav1.5, are implicated in progressive familial heart block type IA, where heterozygous loss-of-function variants lead to impaired conduction velocity and progressive AV block starting in utero or early childhood.^[17]^[46]

Clinical Features

Symptoms

First-degree atrioventricular (AV) block is typically asymptomatic, as the conduction delay does not significantly impair cardiac output or heart rate.^[47] Similarly, many cases of second-degree type I (Mobitz I or Wenckebach) AV block remain asymptomatic, particularly when the block is intermittent and does not lead to substantial bradycardia.^[2] In contrast, second-degree type II (Mobitz II) AV block and third-degree (complete) AV block often produce noticeable symptoms due to more pronounced conduction failure and resultant bradycardia, typically with ventricular rates below 50 beats per minute.^[48] Patients commonly report fatigue, dizziness, and syncope, with the latter manifesting as sudden fainting episodes known as Stokes-Adams attacks, triggered by transient drops in cardiac output.^[2]^[49] These symptoms arise from inadequate perfusion to vital organs during periods of slowed or irregular ventricular response.^[50] Overall, symptom severity correlates with the degree of block, as higher-grade AV blocks more frequently result in exercise intolerance and heart failure-like presentations, including dyspnea on exertion and easy fatigability.^[47]^[2]

Physical Examination

Physical examination in patients with heart block often reveals signs related to impaired atrioventricular conduction, particularly in second- and third-degree blocks, where objective findings can indicate the severity of the conduction disturbance. Bradycardia, defined as a heart rate less than 60 beats per minute, is a hallmark finding in advanced heart block due to delayed or blocked impulse transmission from the atria to the ventricles, leading to a slow ventricular response.^[2] In third-degree (complete) heart block, atrioventricular dissociation may produce intermittent cannon A waves in the jugular venous pulse, resulting from atrial contraction against a closed tricuspid valve when atria and ventricles contract simultaneously.^[51] These waves appear as prominent, irregular pulsations in the neck veins and are a key bedside clue to complete dissociation.^[52] Pulse examination typically shows irregularities in second-degree heart block, characterized by periodic pauses corresponding to non-conducted P waves, creating a pattern of grouped beating; for instance, in Mobitz type I (Wenckebach), the pauses follow progressive lengthening of the PR interval, while Mobitz type II features sudden dropped beats without prior prolongation.^[53] In cases of varying conduction ratios, such as 2:1 or 3:2 atrioventricular block, the pulse may exhibit alternating strong and weak beats due to differences in ventricular filling and stroke volume.^[52] The overall pulse rate remains bradycardic, and regularity is preserved in third-degree block at the escape rhythm rate, though intensity may vary slightly with hemodynamic effects.^[2] In symptomatic patients with significant heart block, signs of reduced cardiac output are evident, including hypotension from inadequate stroke volume and cool, clammy extremities reflecting peripheral vasoconstriction and hypoperfusion.^[52] These findings are more pronounced in acute or severe cases where bradycardia compromises systemic perfusion.^[53] If heart block is associated with underlying structural heart disease, such as valvular calcification or cardiomyopathy, auscultation may reveal murmurs, including systolic or diastolic types depending on the lesion.^[52] Auscultation of heart sounds occasionally uncovers rare additional findings, such as an S3 or S4 gallop, attributable to ventricular dyssynchrony in blocks with wide QRS complexes or concurrent heart failure, though these are uncommon and nonspecific.^[52] Variable intensity of the first heart sound (S1) may also be noted in complete heart block due to differing atrioventricular valve positions at ventricular contraction.^[2] Overall, the physical examination provides vital clues to hemodynamic stability but requires electrocardiographic confirmation for definitive diagnosis.

Diagnosis

Electrocardiography

Electrocardiography is the primary diagnostic tool for identifying heart block, revealing characteristic patterns of atrioventricular (AV) conduction delays or dissociations through analysis of P waves, PR intervals, and QRS complexes.^[54] Standard 12-lead ECG recordings at 25 mm/s speed allow measurement of intervals, with the PR interval defined as the time from the onset of the P wave to the onset of the QRS complex.^[2] First-degree AV block is diagnosed when the PR interval is prolonged beyond 200 ms, yet every atrial impulse (P wave) conducts to the ventricles, resulting in 1:1 AV conduction without dropped beats.^[55] This prolongation reflects delayed conduction through the AV node or His-Purkinje system but does not impair overall rhythm regularity.^[2] Second-degree AV block manifests as intermittent failure of atrial impulses to conduct to the ventricles and is subclassified into Mobitz type I and type II based on PR interval behavior. In Mobitz type I (Wenckebach), there is progressive lengthening of the PR interval across consecutive beats until a P wave is not followed by a QRS complex, producing a pattern of grouped beating; the PR interval following the dropped beat shortens, and atrial rate remains constant below 100 bpm.^[55]^[56] This type typically originates in the AV node and is associated with narrow QRS complexes. In Mobitz type II, the PR interval remains fixed before and after the nonconducted P wave, with sudden drops of QRS complexes; it often features wide QRS complexes (>120 ms) indicating infranodal involvement.^[55]^[53] Third-degree AV block, also known as complete heart block, shows complete dissociation between P waves and QRS complexes, with no atrial impulses conducting to the ventricles.^[55] P waves march independently at the atrial rate (typically 60-100 bpm), while the ventricular rate is slower, driven by an escape rhythm from the AV junction (40-60 bpm) or ventricles (30-40 bpm), often with wide QRS if ventricular escape predominates.^[48]^[57]

Additional Tests

Additional tests beyond electrocardiography are essential for evaluating the extent of heart block, correlating symptoms with arrhythmias, localizing conduction abnormalities, identifying structural heart disease, and detecting reversible etiologies. These supplementary investigations help guide management decisions, particularly in cases of intermittent or symptomatic blocks. Ambulatory electrocardiographic monitoring, such as 24- to 48-hour Holter monitoring, is recommended to capture intermittent heart block episodes that may be missed on a resting ECG, especially in patients with daily symptoms. For less frequent events, extended monitoring with event recorders (up to 30-90 days) or implantable loop recorders (beyond 2 years) increases diagnostic yield, though overall detection of significant bradyarrhythmias remains below 15%.^[16]^[2] Exercise testing is useful for assessing atrioventricular conduction during stress, particularly in patients with suspected exercise-induced block or symptoms provoked by exertion (Class IIa recommendation). It can reveal progression to higher-degree AV block with increased heart rates, helping differentiate infranodal from nodal conduction issues, though it should be performed cautiously in symptomatic or high-risk patients.^[54] Invasive electrophysiology studies are indicated to map the site of conduction delay in symptomatic patients where non-invasive tests are inconclusive, providing Class I recommendation for assessing atrioventricular conduction. These studies measure intervals such as the HV interval, where a value exceeding 55 ms suggests infra-Hisian block, and prolongation to 70 ms or greater indicates high risk for progression to complete heart block. Diagnostic yield varies from 12% to 80%, making them particularly useful in syncope with suspected conduction disease or post-procedural scenarios like transcatheter aortic valve replacement.^[16] Echocardiography is routinely performed to evaluate for structural causes of heart block, carrying a Class I recommendation for identifying conditions such as cardiomyopathy or valvular disease that may contribute to conduction abnormalities. Transthoracic or transesophageal approaches assess left ventricular function and valvular integrity, offering prognostic insights in conduction disorders.^[16]^[2] Blood tests target reversible causes and are selected based on clinical suspicion, with Class I recommendation for electrolytes and troponin to detect imbalances like hyperkalemia or acute ischemia. Thyroid function tests and serology for Lyme disease receive Class IIa support, while autoimmune markers may be pursued in suspected inflammatory conditions. Directed testing avoids unnecessary comprehensive panels, focusing on etiologies like hypothyroidism or Lyme carditis.^[16]

Management

Conservative Approaches

Conservative approaches to managing heart block primarily involve non-invasive strategies aimed at monitoring, addressing underlying reversible factors, and providing temporary symptomatic relief, particularly for first-degree atrioventricular (AV) block and asymptomatic type I second-degree (Mobitz I) AV block.^[16] For asymptomatic patients with first-degree AV block or type I second-degree AV block, observation with regular follow-up electrocardiograms (ECGs) is recommended to monitor for progression, as these conditions often do not require intervention and permanent pacing is not indicated.^[16]^[58] Routine clinical follow-up every 3 to 6 months, including annual 12-lead ECGs and possibly 24- to 48-hour Holter monitoring if symptoms arise, helps ensure stability without unnecessary treatment.^[16] Correction of reversible causes is a cornerstone of conservative management, focusing on discontinuing offending medications such as beta-blockers, calcium channel blockers, or digoxin that may exacerbate AV conduction delays, as well as treating electrolyte imbalances (e.g., hyperkalemia or hypokalemia) or infections like Lyme disease.^[59]^[60]^[16] Identifying and resolving these factors through patient history, laboratory tests, and vital sign monitoring can often restore normal conduction without further intervention, preventing progression to higher-degree blocks.^[59] In acute settings with symptomatic vagally mediated AV block at the nodal level, atropine administered intravenously at a dose of 1 mg (repeatable every 3 to 5 minutes up to a total of 3 mg) can temporarily enhance sinoatrial and AV nodal rates by blocking vagal effects, providing short-term relief while addressing the underlying cause.^[16]^[61] Lifestyle modifications play a supportive role, particularly in individuals with high vagal tone such as athletes, where avoiding excessive vagal triggers like prolonged Valsalva maneuvers or high-intensity endurance activities that heighten parasympathetic activity may reduce episode frequency; general advice includes minimizing stress, alcohol, and caffeine intake to support overall cardiac stability.02560-8/fulltext)^[62]^[62]

Interventional Therapies

Interventional therapies for heart block primarily involve device-based and invasive procedures to restore effective cardiac conduction or rhythm when conservative measures are insufficient. Pacemaker implantation is the cornerstone treatment for advanced forms of atrioventricular (AV) block, particularly when symptoms such as syncope, fatigue, or hemodynamic instability are present. According to the 2018 ACC/AHA/HRS Guideline, permanent pacing is recommended (Class I, Level of Evidence B) for symptomatic second-degree AV block Mobitz type II, third-degree AV block, or infra-Hisian block, as these conditions carry a high risk of progression to complete heart block and sudden cardiac events.^[16] In asymptomatic cases of third-degree or advanced second-degree AV block with documented infra-Hisian conduction delay, implantation is also indicated (Class I, Level of Evidence B-NR) due to the potential for asystole or ventricular arrhythmias.^[16] Pacemaker selection depends on patient anatomy, comorbidities, and the need for atrioventricular synchrony. Dual-chamber pacemakers (DDD mode) are preferred (Class I, Level of Evidence B-R) for most patients with AV block, as they maintain physiologic timing between atrial and ventricular contractions, reducing the risk of pacemaker syndrome and atrial fibrillation compared to single-chamber ventricular pacing (VVI mode).^[16] VVI pacing is reasonable (Class IIa, Level of Evidence B-R) in frail elderly patients or those with chronic atrial fibrillation, where atrial synchronization is not feasible, offering simplicity and lower procedural complexity.^[16] Implantation timing is critical; for instance, in postoperative settings after cardiac surgery, permanent pacing is advised if high-grade AV block persists beyond 7-14 days, with earlier intervention considered for symptomatic cases.^[16] Temporary pacing serves as a bridge in acute scenarios, such as hemodynamic instability from drug-induced or ischemic AV block, prior to permanent device placement. Transvenous temporary pacing is recommended (Class I, Level of Evidence B-NR) for urgent management of acute high-degree AV block, providing reliable ventricular capture while minimizing infection risk through short-term use.^[16] External (transcutaneous) pacing may be employed (Class IIa, Level of Evidence B-NR) as an immediate, non-invasive option in emergencies when vascular access is delayed, though its use is limited by patient discomfort and lower efficacy for prolonged support.^[16] Catheter ablation is infrequently utilized for heart block but may address rare focal etiologies, such as post-surgical injury to conduction pathways or accessory tracts causing intermittent block. In select cases of symptomatic AV block due to a ventricular nodal pathway, radiofrequency catheter ablation can alleviate the conduction abnormality (success rate >90% in reported series), potentially avoiding pacemaker dependency.30998-0/fulltext) Surgical interventions are reserved for refractory or complex scenarios; AV node ablation combined with permanent pacing is indicated (Class I, Level of Evidence B-NR) for patients with tachycardia-bradycardia syndrome or refractory atrial fibrillation where rate control is needed, intentionally creating complete AV block to prevent rapid ventricular rates.^[16] In congenital heart block associated with structural defects, surgical repair of the underlying anomaly (e.g., during correction of atrioventricular septal defects) may resolve or prevent progression of block, with epicardial pacemaker leads placed intraoperatively if persistent conduction issues arise.^[63]

Prognosis

Outcomes by Type

First-degree atrioventricular (AV) block is generally considered benign, with the majority of patients remaining asymptomatic and experiencing no increased mortality when isolated from other cardiac conditions.^[58] Studies indicate that while most cases do not progress to higher-degree blocks, prolonged PR intervals (>200 ms) are associated with a 1.44-fold adjusted risk of all-cause mortality and a higher incidence of atrial fibrillation (adjusted hazard ratio 2.06).^[64] In the absence of symptoms or underlying heart disease, long-term outcomes are favorable, with rare need for intervention. Prognosis varies by block location; AV nodal blocks generally have better outcomes than infranodal blocks, which are more likely to progress.^[20] Second-degree AV block encompasses two subtypes with distinct prognoses. Mobitz type I (Wenckebach) block typically has an excellent prognosis, particularly when reversible due to factors like medications or increased vagal tone, and rarely progresses to complete heart block in asymptomatic individuals without structural heart disease.^[53] It often resolves when the underlying cause is addressed, such as during recovery from acute myocardial infarction or electrolyte correction.^[65] In contrast, Mobitz type II block carries a higher risk, with progression to third-degree AV block occurring in more than 50% of cases, especially if infranodal in location, leading to increased morbidity and potential sudden cardiac events without pacing.^[66] Outcomes improve substantially with permanent pacemaker implantation, mitigating the risk of hemodynamic compromise. Prognosis varies by block location; AV nodal blocks generally have better outcomes than infranodal blocks, which are more likely to progress.^[53] Third-degree (complete) AV block represents the most severe form, with poor prognosis if untreated due to profound bradycardia and risk of asystole; untreated cases have high mortality, with approximately 37% five-year survival, heavily influenced by comorbidities and etiology, such as lower rates in acute myocardial infarction settings.^[2] With permanent pacemaker therapy, survival improves markedly, achieving 85% at one year and 52% at five years for isolated cases, though rates vary by patient age and coexisting conditions.^[67] Prompt pacing is essential, as it significantly reduces mortality and restores near-normal life expectancy in otherwise healthy individuals. Prognosis varies by block location; AV nodal blocks generally have better outcomes than infranodal blocks, which are more likely to progress.^[68]

Complications

Untreated infra-Hisian heart block carries a significant risk of sudden cardiac death due to episodes of asystole or associated ventricular arrhythmias, with studies indicating an annual incidence of approximately 1-2% in the absence of pacing.^[69] This risk is particularly elevated in conditions involving bifascicular or complete infra-Hisian conduction delay, where unreliable escape rhythms can lead to hemodynamic collapse.^[16] Pacemaker implantation substantially mitigates this danger by maintaining atrioventricular synchrony and preventing bradycardic pauses.^[16] Chronic bradycardia from third-degree atrioventricular block can precipitate heart failure through reduced cardiac output and ventricular dyssynchrony, with up to 23% of patients with high-degree block presenting with decompensated heart failure, often linked to impaired left ventricular compliance and diastolic mitral regurgitation rather than systolic dysfunction alone.^[70] This progression underscores the need for timely intervention to restore physiologic heart rates and preserve myocardial function.^[16] Pacemaker therapy, while effective, introduces device-related complications in approximately 5% of implants, including lead fractures and mechanical failures that may necessitate revision.^[71] Infection remains a critical concern, occurring in 1-2% of procedures, with rates reaching 2.2% within 90 days post-implantation and potentially leading to systemic involvement or device explantation.^[72] Inappropriate pacing or shocks, though less common in pure pacemakers, can arise from lead dislodgement or sensing errors, contributing to overall morbidity.^[71]

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