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Atrioventricular block

Atrioventricular (AV) block is a cardiac conduction disorder characterized by a delay, partial interruption, or complete blockage of electrical impulses traveling from the atria to the ventricles via the atrioventricular node and surrounding conduction pathways.^[1] This condition disrupts the normal synchronized heartbeat, potentially leading to slowed or irregular ventricular rates depending on the severity.^[2] AV block is classified into three main degrees—first, second, and third—based on the extent of conduction impairment, with first-degree being the mildest and third-degree representing complete dissociation between atrial and ventricular activity.^[1] The etiology of AV block includes both congenital and acquired factors. Congenital forms are rare, occurring in approximately 1 in 15,000 live births, often linked to maternal autoimmune diseases like systemic lupus erythematosus or structural heart defects.^[1] Acquired causes predominate in adults and encompass degenerative fibrosis of the conduction system (Lenegre-Lev disease), ischemic heart disease such as myocardial infarction, inflammatory conditions like sarcoidosis or Lyme disease, and iatrogenic factors including medications (e.g., beta-blockers, digoxin, or calcium channel blockers).^[2]^[3] Pathophysiologically, these lead to fibrosis or inflammation in the AV node or His-Purkinje system, impairing impulse propagation.^[1] Clinically, symptoms vary by degree and underlying escape rhythms. First-degree AV block (prolonged PR interval >200 ms on ECG) is often asymptomatic and benign, though it may cause exercise intolerance if severe.^[2] Second-degree block, subdivided into Mobitz type I (progressive PR prolongation with dropped beats, often benign) and Mobitz type II (sudden dropped beats without PR change, higher risk), can present with fatigue, dizziness, or palpitations.^[1] Third-degree (complete) AV block typically manifests with profound symptoms such as syncope, dyspnea, heart failure, or sudden cardiac arrest due to ventricular rates of 20-50 beats per minute from junctional or ventricular escape rhythms.^[2]^[3] Diagnosis relies primarily on electrocardiography (ECG), which reveals characteristic PR interval abnormalities, dropped QRS complexes, or AV dissociation.^[1] Additional evaluations include ambulatory Holter monitoring for intermittent cases, echocardiography to assess structural heart disease, and electrophysiological studies if needed to localize the block site.^[2] Laboratory tests may identify reversible causes, such as electrolyte imbalances or drug toxicity.^[3] Management focuses on addressing reversible causes and symptom relief. Asymptomatic first-degree or Mobitz type I blocks often require only observation and medication adjustment if implicated.^[1] Symptomatic second-degree (especially Mobitz type II) or third-degree blocks necessitate permanent pacemaker implantation, which significantly improves survival—untreated third-degree block carries a 5-year survival rate of about 37%, but pacemaker implantation significantly improves survival and quality of life.^[2]^[1] Acute interventions like atropine or temporary pacing may be used in emergencies.^[2] Prevention involves managing cardiovascular risk factors and monitoring high-risk patients.^[3]

Anatomy and Physiology

Normal Cardiac Conduction System

The sinoatrial (SA) node, situated at the junction of the superior vena cava and the right atrium, functions as the heart's primary pacemaker by spontaneously generating electrical impulses that initiate each heartbeat.^[4] These specialized pacemaker cells in the SA node depolarize at an intrinsic rate of 60 to 100 beats per minute under resting conditions, establishing the normal sinus rhythm.^[4] The impulse from the SA node spreads rapidly across the atria via internodal pathways, causing atrial contraction, before reaching the atrioventricular (AV) node.^[5] The AV node is located within the triangle of Koch, a triangular region in the lower right atrium bounded by the tendon of Todaro, the septal leaflet of the tricuspid valve, and the coronary sinus ostium, positioned near the interatrial septum.^[6] From the AV node, the electrical signal travels to the bundle of His, a compact group of fibers that penetrates the fibrous skeleton of the heart and runs along the crest of the interventricular septum.^[7] The bundle of His then divides into the left and right bundle branches, which course through the interventricular septum toward the ventricular apex.^[8] The left bundle branch further subdivides into anterior and posterior fascicles, while the right bundle branch remains a single tract; both branches distribute the impulse via a network of Purkinje fibers that ramify across the endocardial surfaces of the ventricles, ensuring synchronized ventricular contraction from apex to base.^[9] On an electrocardiogram (ECG), the normal conduction from the SA node through the atria to the ventricles is reflected in the PR interval, which measures 120 to 200 milliseconds and represents the time from the onset of atrial depolarization (P wave) to the start of ventricular depolarization (QRS complex).^[1]

Function of the Atrioventricular Node

The atrioventricular (AV) node serves as a critical gatekeeper in the cardiac conduction system, receiving electrical impulses from the sinoatrial node and delaying their transmission to the ventricles to ensure coordinated atrial and ventricular contraction. This delay, typically lasting 80-120 milliseconds, allows sufficient time for atrial systole to complete, thereby optimizing ventricular filling and preventing backflow of blood into the atria during ventricular contraction.^[10]^[11] The AV node's conduction properties are characterized by its decremental response and refractory periods, which prevent excessive ventricular rates during rapid atrial activity. Specifically, the effective refractory period of the AV node ranges from 200-300 milliseconds, enabling rate-dependent conduction that adapts to varying heart rates while maintaining rhythm stability.^[12]^[13] Autonomic nervous system modulation finely tunes AV nodal function to meet physiological demands. Sympathetic stimulation accelerates conduction through beta-1 adrenergic receptors, reducing the delay and enhancing atrioventricular synchrony during increased cardiac output needs, such as exercise. Conversely, parasympathetic input via vagal tone acts on muscarinic receptors to slow conduction, promoting a more deliberate impulse propagation that conserves energy during rest.^[14]^[15] In the event of sinoatrial node failure, the AV node functions as a subsidiary pacemaker, initiating a junctional escape rhythm at an intrinsic rate of 40-60 beats per minute to sustain basic cardiac output until the primary pacemaker resumes.^[16]^[17]

Classification

First-Degree AV Block

First-degree atrioventricular (AV) block is defined as a prolongation of the PR interval greater than 0.20 seconds on electrocardiogram (ECG) without any disruption in the conduction of atrial impulses to the ventricles, ensuring that every P wave is followed by a QRS complex.^[18] This condition represents the mildest form of AV block, where the delay occurs primarily at the level of the AV node due to slowed conduction.^[18] On ECG, first-degree AV block is characterized by a consistently prolonged PR interval exceeding 200 milliseconds, with a normal QRS complex unless complicated by an associated bundle branch block; there is no evidence of P-wave dissociation or non-conducted beats.^[18] The prolongation is fixed across all cardiac cycles, distinguishing it from higher-degree blocks, and it may be classified as "marked" if the PR interval surpasses 0.30 seconds.^[18] In some cases, P waves can appear embedded within the preceding T wave due to the extended interval.^[18] Common associations include increased vagal tone, particularly in younger individuals or athletes, as well as medications such as beta-blockers, calcium channel blockers, and digoxin, which exert negative dromotropic effects on the AV node.^[18]^[19] Other frequent links involve age-related fibrotic changes in the conduction system, electrolyte imbalances like hypokalemia or hypomagnesemia, and acute conditions such as myocardial infarction, especially inferior wall involvement due to ischemia affecting the AV nodal blood supply.^[18]^[20] Clinically, first-degree AV block is often asymptomatic and discovered incidentally on routine ECG, carrying a generally benign prognosis in otherwise healthy individuals, with a prevalence of about 1-1.5% in those under 60 years and up to 6% in older adults.^[18] However, it may signal underlying pathology and is associated with an increased risk of progression to higher-degree AV block or atrial fibrillation, particularly when the PR interval exceeds 0.30 seconds, potentially leading to symptoms like fatigue or palpitations from suboptimal atrioventricular synchrony.^[18] In the context of acute myocardial infarction, its presence correlates with higher morbidity and mortality, warranting close monitoring.^[20]

Mobitz Type I Second-Degree AV Block

Mobitz Type I second-degree atrioventricular (AV) block, also known as Wenckebach block, is characterized by progressive prolongation of the PR interval on the electrocardiogram (ECG) until a P wave fails to conduct to the ventricles, resulting in a non-conducted atrial impulse and a subsequent pause.^[21] This pattern repeats in cycles, often manifesting as grouped beating, where the PR interval is longest immediately before the dropped beat and shortest following the pause.^[22] The conduction ratio typically presents as 3:2, 4:3, or higher, reflecting intermittent failure of AV nodal conduction without complete block.^[22] On ECG, the hallmark features include a constant P-P interval with progressive PR lengthening across conducted beats, culminating in a P wave not followed by a QRS complex, after which the cycle resets.^[22] The QRS complex is usually narrow, indicating an origin at the AV node rather than infranodal structures, and the RR interval shortens progressively within each cycle before the pause.^[22] This subtype differs from other AV blocks by its incremental conduction delay, often resolving spontaneously or with interventions that enhance nodal function.^[21] Pathophysiologically, Mobitz Type I arises from reversible fatigue in AV nodal cells, where successive depolarizations extend the node's refractory period, eventually blocking an impulse during its absolute refractory phase and allowing reset.^[21] It commonly occurs at the AV nodal level due to increased vagal tone or physiological stress, and is responsive to atropine, which accelerates sinus rate and improves nodal conduction.^[22] This mechanism contrasts with more fixed blocks and underscores its typically benign nature.^[23] Common scenarios include inferior myocardial infarction, where AV nodal ischemia triggers the block via the Bezold-Jarisch reflex; elevated vagal tone in athletes, often asymptomatic and nocturnal; and conditions like obstructive sleep apnea, where hypoxemia exacerbates conduction delays.^[22] It may also appear in medication toxicity (e.g., beta-blockers or digoxin), hyperkalemia, or post-cardiac surgery, but rarely progresses to higher-degree blocks, particularly when nodal in origin.^[21]^[23]^[24]

Mobitz Type II Second-Degree AV Block

Mobitz type II second-degree atrioventricular (AV) block is characterized by intermittent non-conduction of atrial impulses, where the PR interval remains constant for all conducted beats, followed by a sudden dropped QRS complex without preceding PR prolongation.^[21] This pattern reflects an "all-or-none" conduction failure, distinguishing it from progressive delays in other AV block subtypes.^[25] On electrocardiography (ECG), the key features include a fixed PR interval (which may exceed 200 ms) for conducted P waves, abrupt non-conduction of a P wave leading to a pause typically equal to two P-P intervals, and often a 2:1 AV conduction ratio, though higher ratios like 3:2 can occur.^[21] The QRS complex is frequently widened (>120 ms), indicating involvement of the infranodal conduction system, such as bundle branch or fascicular blocks.^[1] At least two consecutive conducted beats are required to confirm the diagnosis, ensuring the PR stability is not confounded by rate changes.^[25] Pathophysiologically, Mobitz type II AV block arises from structural damage in the infranodal region, particularly the His-Purkinje system, due to fibrosis, ischemia, or degeneration, rather than the AV node itself.^[1] This location renders the block less responsive to vagal maneuvers or medications that affect nodal tissue, as the conduction failure is abrupt and indicative of underlying His-Purkinje impairment.^[25] In 70-80% of cases, it coexists with bundle branch blocks, underscoring the diffuse conduction system pathology.^[25] Clinically, this block carries significant implications, often presenting with symptoms such as fatigue, dyspnea, presyncope, syncope, or hemodynamic instability due to bradycardia and reduced cardiac output.^[21] It has a high risk of progression to third-degree (complete) AV block, asystole, or sudden cardiac death, necessitating prompt intervention.^[1] According to ACC/AHA/HRS guidelines, permanent pacemaker implantation is a class I recommendation for Mobitz type II AV block, even if asymptomatic, to prevent adverse outcomes, with temporary pacing used in unstable cases.^[26]

Third-Degree AV Block

Third-degree atrioventricular (AV) block, also known as complete heart block, is characterized by a complete failure of conduction from the atria to the ventricles, resulting in total atrioventricular dissociation where the atria and ventricles beat independently of each other.^[27]^[26] In this condition, no atrial impulses generated by the sinoatrial node reach the ventricles through the AV node, leading to reliance on subsidiary pacemaker sites for ventricular depolarization.^[27]^[28] On electrocardiography (ECG), third-degree AV block is identified by regular P waves that march independently of QRS complexes, with no consistent relationship between them, and the atrial rate exceeding the ventricular rate.^[27]^[28] The ventricular rhythm arises from an escape focus, typically exhibiting a rate of 40 to 60 beats per minute if junctional (with narrow QRS complexes) or 20 to 40 beats per minute if ventricular (with wide QRS complexes), reflecting the location of the escape pacemaker below the AV node.^[26]^[28] This dissociation can sometimes appear as isorhythmic if the atrial and ventricular rates are similar, but the absence of conducted P waves preceding QRS complexes confirms the diagnosis.^[26] Pathophysiologically, third-degree AV block results from a complete interruption in the cardiac conduction system, most commonly at the level of the AV node, His bundle, or distal Purkinje fibers, preventing any supraventricular impulses from activating the ventricles.^[27]^[26] The block at the AV nodal level often produces a more stable junctional escape rhythm due to higher inherent automaticity, whereas infranodal blocks (e.g., in the His-Purkinje system) lead to slower, less reliable ventricular escapes, increasing the risk of hemodynamic compromise.^[26] Escape rhythms originate from latent pacemakers in the AV junction or ventricles, but their rates are insufficient to meet normal circulatory demands, potentially causing reduced cardiac output.^[27]^[28] Third-degree AV block can manifest as an acute or chronic condition, with acute forms often reversible and linked to transient insults such as myocardial ischemia (e.g., in 5-10% of inferior myocardial infarctions), drug toxicities (e.g., beta-blockers or digoxin), or electrolyte imbalances, while chronic cases typically stem from irreversible degenerative changes like Lenègre's disease or fibrosis of the conduction system.^[27]^[26] In acute settings, such as post-myocardial infarction, the block may resolve with treatment of the underlying cause, but chronic progressive fibrosis often requires permanent intervention.^[27] Clinically, patients may experience symptoms ranging from fatigue, dizziness, and dyspnea to severe manifestations like syncope due to abrupt pauses in ventricular activity, known as Stokes-Adams attacks, which arise from unreliable escape rhythms leading to transient cerebral hypoperfusion.^[27]^[29] In severe cases, especially with infranodal block and slow ventricular rates below 40 beats per minute, patients can develop heart failure symptoms or sudden cardiac arrest if the escape rhythm fails.^[26] Asymptomatic chronic presentations are possible but warrant evaluation due to the risk of progression to symptomatic bradycardia.^[27]

Causes

Acquired Causes

Acquired causes of atrioventricular (AV) block encompass a range of environmental, pathological, and iatrogenic factors that disrupt the cardiac conduction system in adulthood, often leading to reversible or progressive impairment depending on the underlying mechanism. These etiologies are distinct from congenital or genetic origins and frequently manifest in the context of acute illness, chronic disease, or therapeutic interventions. Common acquired causes include ischemic events, inflammatory or infectious processes, medication effects, surgical complications, degenerative changes, and metabolic disturbances, each targeting the AV node or infranodal structures to varying degrees.^[1] Ischemic causes, particularly acute myocardial infarction (MI), represent a major precipitant of AV block, with the location of infarction determining the site of conduction disturbance. In inferior MI, which often involves the right coronary artery supplying the AV node, first- or second-degree AV block occurs in up to 20% of cases due to transient nodal ischemia, typically resolving with reperfusion.^[30] In contrast, anterior MI affecting the left anterior descending artery can cause more severe infranodal block, such as complete AV block below the bundle of His, with a poorer prognosis and higher mortality rate due to extensive septal necrosis.^[31] Chronic coronary artery disease may also contribute to progressive ischemia of the conduction pathways, exacerbating block over time.^[1] Inflammatory and infectious conditions can infiltrate or inflame the conduction system, leading to AV block that is often reversible with targeted therapy. Lyme disease, caused by Borrelia burgdorferi, frequently presents with high-degree AV block in up to 90% of Lyme carditis cases, resulting from myocardial inflammation and direct spirochetal invasion of the AV node; this typically resolves within weeks of antibiotic treatment.^[32] Viral or bacterial myocarditis, rheumatic fever, and endocarditis similarly disrupt conduction through edema and cellular damage, while sarcoidosis causes granulomatous infiltration of the AV node or His-Purkinje system, potentially leading to permanent block if untreated.^[1]^[33] Iatrogenic causes arise from therapeutic interventions that inadvertently impair conduction. Medications such as beta-blockers, non-dihydropyridine calcium channel blockers (e.g., verapamil, diltiazem), and digoxin commonly induce AV block by suppressing AV nodal function, with resolution often occurring upon discontinuation in 41% of cases, though pacemaker implantation may be required in persistent instances.^[34] Post-cardiac surgery, particularly aortic or mitral valve procedures and transcatheter aortic valve replacement, damages the perivalvular conduction tissue in 5-10% of patients, with higher risk in those with preexisting bundle branch block.^[1] Degenerative processes account for many idiopathic cases of progressive AV block in older adults. Lenègre's disease involves idiopathic fibrosis and sclerosis of the His-Purkinje system, leading to bilateral bundle branch block and eventual complete AV block, often necessitating pacemaker placement.^[35] Lev's disease, conversely, features calcification and degeneration of the central fibrous skeleton, including the AV node and proximal His bundle, predominantly in the elderly and resulting in infranodal block.^[1] These age-related changes, affecting up to 1% of the population over 70, stem from fibrotic replacement of conductive tissue without an identifiable inflammatory trigger.^[36] Electrolyte and metabolic imbalances can acutely precipitate AV block by altering membrane potentials and conduction velocity. Hyperkalemia, often from renal failure or medications, impairs Purkinje fiber excitability, causing progressive AV block that may advance to complete heart block; correction of potassium levels typically restores conduction.^[37] Hypothyroidism slows AV nodal conduction through reduced sympathetic tone and myocardial metabolic changes, manifesting as bradycardia or first-degree block in severe cases, which improves with thyroid hormone replacement.^[1]

Congenital and Genetic Causes

Congenital atrioventricular (AV) block refers to conduction abnormalities present at birth or detected in utero, distinct from acquired forms by their developmental origins. It encompasses a spectrum from first-degree to complete (third-degree) block and can occur in isolation or alongside structural heart defects. The condition arises from disruptions in the formation or function of the AV node during embryogenesis, often linked to maternal autoantibodies or genetic factors. Isolated congenital AV block without structural anomalies accounts for the majority of cases, while associated forms may involve complex cardiac malformations. The most common etiology of congenital AV block is autoimmune-mediated, resulting from transplacental passage of maternal anti-Ro/SSA and anti-La/SSB autoantibodies, typically in mothers with systemic lupus erythematosus or Sjögren's syndrome. These antibodies target fetal cardiac tissues, particularly the AV node, leading to inflammation and fibrosis that impair conduction; the risk to the fetus is approximately 2% if the mother is antibody-positive. This form often manifests as complete AV block in utero or at birth, with a fetal mortality rate of 14-34% if untreated, and survivors facing a 5-30% risk of developing dilated cardiomyopathy. Diagnosis is frequently made via fetal echocardiography, revealing bradycardia or blocked atrial impulses. Congenital AV block may also occur in conjunction with structural heart defects, such as atrioventricular septal defects (AVSD), which combine atrial septal defects (ASD) and ventricular septal defects (VSD) with a common AV valve. In these cases, the block stems from abnormal development of the endocardial cushions, affecting both septation and conduction pathways; associations with heterotaxy syndromes, including left atrial isomerism and ASD, further highlight the embryologic overlap. Approximately 30-50% of congenital AV block cases involve such structural anomalies, contrasting with the isolated autoimmune form. Genetic causes of congenital AV block include mutations in ion channel genes and mitochondrial disorders. Mutations in SCN5A, encoding the cardiac sodium channel Nav1.5, lead to progressive cardiac conduction disease, manifesting as isolated AV block from infancy; these loss-of-function variants reduce sodium current, slowing conduction and predisposing to complete block. Mitochondrial syndromes like Kearns-Sayre syndrome, caused by large-scale deletions in mitochondrial DNA, frequently feature AV conduction defects due to energy failure in cardiac myocytes, often progressing to complete block by adolescence. Similarly, Emery-Dreifuss muscular dystrophy, linked to mutations in EMD (emerin) or FHL1 genes, involves conduction system fibrosis resulting in AV block in over 90% of patients, typically emerging in early adulthood but detectable congenitally in familial cases. The estimated incidence of congenital AV block is 1 per 15,000-20,000 live births, with higher recurrence risk (up to 16-20%) in subsequent pregnancies of mothers with anti-Ro/SSA antibodies. Progression is common: many cases begin as first- or second-degree block at birth and advance to complete block within years, with 68% of incomplete forms progressing over a decade. Symptomatic neonates often require permanent pacing, as ventricular rates below 50-55 bpm increase mortality risk.

Clinical Presentation

Symptoms

Many cases of atrioventricular (AV) block, particularly first-degree and Mobitz type I second-degree, are asymptomatic and discovered incidentally during routine evaluation.^[18]^[21] In these mild forms, patients experience no noticeable manifestations due to minimal impact on cardiac output.^[38] Symptoms typically emerge in more advanced blocks, such as Mobitz type II second-degree and third-degree AV block, where intermittent or complete conduction failure leads to bradycardia and reduced cardiac output. Common patient-reported complaints include fatigue, dizziness, and dyspnea on exertion, resulting from inadequate perfusion during daily activities.^[1]^[27] These manifestations often worsen with physical demand, contributing to exercise intolerance, especially in infranodal blocks where escape rhythms are slower.^[21]^[38] Syncope or presyncope, known as Stokes-Adams attacks, is a hallmark of intermittent higher-degree blocks, occurring due to prolonged pauses that cause sudden hypotension.^[1] In rare chronic cases of severe bradycardia, patients may develop heart failure symptoms such as persistent shortness of breath or edema from cardiomyopathy secondary to chronic bradycardia.^[27] Symptom severity correlates with ventricular rate; rates above 50 beats per minute may remain tolerable, while slower rates exacerbate hemodynamic instability.^[1]

Physical Examination Findings

In patients with atrioventricular (AV) block, physical examination often reveals bradycardia, defined as a heart rate less than 60 beats per minute, which is particularly prominent in second-degree Mobitz type II and third-degree blocks due to impaired ventricular depolarization.^[1] The pulse may be irregular in cases of variable conduction, such as in second-degree blocks, reflecting intermittent failure of atrial impulses to reach the ventricles.^[1] In first-degree AV block, physical findings are typically absent or nonspecific, as the conduction delay does not usually affect hemodynamics significantly.^[39] Auscultation of the heart may disclose variable intensity of the first heart sound (S1) in second- and third-degree AV blocks, resulting from fluctuating atrioventricular synchrony that alters the timing of mitral and tricuspid valve closure.^[2] In third-degree AV block, cannon A waves can be observed in the jugular venous pulse, occurring when the atria contract against a closed tricuspid valve during ventricular systole due to complete atrioventricular dissociation.^[27] These findings are intermittent and more evident during episodes of hemodynamic instability.^[40] Signs of reduced cardiac output may manifest in severe cases, particularly with third-degree block, including hypotension, cool extremities, and weak peripheral pulses indicative of peripheral hypoperfusion.^[41] Altered mental status or lethargy can also appear if cerebral perfusion is compromised by profound bradycardia.^[41] Associated auscultatory findings, such as murmurs, may be present if underlying structural heart disease contributes to the AV block, though these are not specific to the conduction abnormality itself.^[1]

Diagnosis

Electrocardiographic Features

Electrocardiographic diagnosis of atrioventricular (AV) block relies on identifying delays or interruptions in the conduction from atrial depolarization (P waves) to ventricular depolarization (QRS complexes) on a 12-lead ECG. The normal PR interval, measured from the onset of the P wave to the onset of the QRS complex, ranges from 120 to 200 milliseconds; deviations from this establish the degree of block. Careful assessment of P wave-QRS relationships, PR interval variations, and QRS morphology is essential, as narrow QRS complexes often indicate AV nodal involvement, while wide QRS suggests infranodal block.^[42]^[26] First-degree AV block is characterized by a prolonged PR interval exceeding 200 milliseconds (or 0.20 seconds) on every beat, with each P wave consistently followed by a QRS complex, indicating delayed but complete conduction through the AV node or His-Purkinje system. This prolongation does not result in dropped beats, and the rhythm remains regular. QRS complexes are typically narrow unless preexisting bundle branch block is present.^[42]^[26] Second-degree AV block manifests as intermittent failure of atrial impulses to conduct to the ventricles and is subclassified into Mobitz type I (Wenckebach) and Mobitz type II based on PR interval behavior. In Mobitz type I, the PR interval progressively lengthens with each successive beat until a P wave is not followed by a QRS complex (dropped beat), after which the cycle resets with a shorter PR interval; this pattern forms characteristic Wenckebach cycles, often grouped as 3:2 or 4:3 conduction. The site is usually the AV node, reflected by narrow QRS complexes. In Mobitz type II, the PR interval remains constant for conducted beats, but non-conducted P waves occur suddenly without prior prolongation, leading to intermittent dropped QRS complexes; 2:1 AV conduction (every other P wave conducted) is common and may mimic sinus bradycardia. Wide QRS complexes are typical, indicating infranodal involvement.^[42]^[26] Third-degree (complete) AV block features complete dissociation between P waves and QRS complexes, with no atrial impulses conducting to the ventricles; P waves march out regularly at the atrial rate, independent of the slower ventricular escape rhythm. The ventricular rate is typically 30 to 50 beats per minute if junctional escape or slower if ventricular escape, resulting in more P waves than QRS complexes. QRS morphology depends on the escape focus: narrow for junctional, wide for ventricular. AV dissociation is confirmed by varying PR intervals across beats and no consistent relationship between P waves and QRS complexes.^[42]^[26] Advanced or high-grade second-degree AV block involves multiple consecutive non-conducted P waves (e.g., 3:1 or higher ratios), progressing toward complete block and sharing features of both Mobitz types depending on the pattern. Ladder diagrams, schematic illustrations depicting parallel atrial (P waves) and ventricular (QRS) lines with conduction pathways, aid in visualizing these complex ratios and dissociation; for instance, they highlight progressive delays in Mobitz I or abrupt blocks in Mobitz II leading to multiple drops. For intermittent or paroxysmal blocks not captured on standard ECG, ambulatory ECG monitoring such as 24- to 48-hour Holter recording is recommended to document episodes correlating with symptoms like syncope.^[26]

Additional Diagnostic Tests

While the electrocardiogram (ECG) remains the cornerstone for diagnosing atrioventricular (AV) block, additional tests are essential to identify underlying etiologies, assess structural heart involvement, and evaluate the functional impact of the conduction abnormality.^[1] Echocardiography is routinely recommended in all patients with AV block to detect structural cardiac diseases that may contribute to conduction disturbances, such as valvular abnormalities, cardiomyopathy, or reduced ejection fraction indicating systolic dysfunction. Transthoracic echocardiography provides non-invasive visualization of chamber sizes, wall motion, and valvular function, helping to rule out ischemic or infiltrative processes affecting the conduction system.^[1]^[43] An electrophysiology study (EPS) is an invasive procedure indicated for symptomatic patients or those with ambiguous ECG findings to precisely localize the site of block, distinguishing between nodal (AV junctional) and infranodal (infranodal or His-Purkinje) involvement through His bundle electrogram recordings. During EPS, catheters are positioned in the heart to measure conduction intervals, such as the HV interval, which if prolonged (>55 ms) suggests infranodal disease and higher risk for progression. This test is particularly useful in cases of second-degree Mobitz type II or 2:1 AV block with bundle branch block, guiding decisions on pacemaker necessity.^[43]^[1] Blood tests play a critical role in uncovering reversible causes of AV block, including electrolyte imbalances like hyperkalemia or hypocalcemia, which can prolong AV conduction. Elevated troponin levels indicate myocardial ischemia or infarction as a potential trigger, while serologic testing for Lyme disease (Borrelia burgdorferi IgM and IgG antibodies) is essential in endemic areas due to its association with Lyme carditis causing high-degree AV block. Additionally, screening for autoantibodies, such as anti-Ro/SSA and anti-La/SSB in suspected autoimmune etiologies, helps identify immune-mediated conduction issues, particularly in younger patients without structural disease.^[43]^[44]^[45] Exercise testing, often performed via treadmill or bicycle ergometry, is used to provoke or unmask intermittent AV block under physiological stress, assessing whether the block worsens with increased heart rate, which may indicate infranodal involvement and poorer prognosis. This test monitors PR interval prolongation or progression to higher-degree block, providing insights into chronotropic competence and risk stratification, though it is contraindicated in unstable patients.^[43]^[1] Ambulatory monitoring with Holter recorders or telemetry is indicated for patients with suspected paroxysmal or intermittent AV block to correlate symptoms like syncope with rhythm disturbances over 24-48 hours or longer periods. These devices detect asymptomatic pauses, bradycardia, or transient high-grade block not captured on resting ECG, offering higher diagnostic yield for episodic events and informing the need for intervention. Event monitors or implantable loop recorders may extend monitoring for infrequent symptoms.^[1]^[43]

Management

Initial Assessment and Monitoring

Initial assessment of atrioventricular (AV) block begins with a thorough history and physical examination to identify symptoms, potential reversible causes, and the need for immediate intervention. Patients presenting with suspected AV block should undergo a 12-lead electrocardiogram (ECG) as the cornerstone of evaluation to confirm the type and severity of the block. Risk stratification is essential: asymptomatic first-degree AV block typically requires no immediate intervention and can be managed with routine monitoring, as it is often benign and associated with low risk of progression. In contrast, symptomatic second- or third-degree AV block demands urgent attention due to the potential for hemodynamic instability, with symptoms such as syncope, dizziness, or fatigue correlating directly with bradycardia.^[26] Addressing reversible causes is a priority in the initial phase to potentially resolve the block without further escalation. Offending medications, such as beta-blockers, calcium channel blockers, or digoxin, should be discontinued or dose-adjusted promptly, as they commonly contribute to AV conduction delays. Electrolyte imbalances, particularly hyperkalemia or hypokalemia, must be corrected through targeted therapy, as these can exacerbate or induce AV block. For acute bradycardia due to AV nodal involvement, vagal maneuvers (e.g., carotid sinus massage) or intravenous atropine may be employed as first-line measures to temporarily improve conduction and stabilize heart rate.^[26] Observation strategies depend on clinical stability and block type. Stable patients with Mobitz type I (Wenckebach) second-degree AV block may be suitable for inpatient telemetry monitoring to assess for progression, while asymptomatic or low-risk cases can transition to outpatient follow-up with periodic ECGs or ambulatory event monitoring over 30 to 90 days to capture intermittent episodes. According to the 2018 ACC/AHA/HRS guidelines, temporary pacing is indicated for symptomatic bradycardia refractory to medical therapy, particularly in cases of hemodynamic compromise or when reversible causes cannot be adequately managed.^[26] Patient education plays a crucial role in initial management to empower individuals to recognize worsening symptoms. Patients should be instructed to seek emergency care for signs such as presyncope, chest pain, shortness of breath, or confusion, which may indicate advancing block or complications like heart failure. This education, combined with clear follow-up plans, helps mitigate risks during the monitoring period.^[26]

Interventional Therapies

Interventional therapies for atrioventricular (AV) block primarily involve device-based and invasive procedures aimed at restoring effective cardiac conduction in cases of persistent or high-risk block. Permanent pacemaker implantation is the cornerstone treatment for advanced second- or third-degree AV block that does not resolve with conservative measures.^[46] Permanent pacemaker implantation is indicated for symptomatic second-degree or third-degree AV block, as well as for asymptomatic Mobitz type II second-degree AV block or third-degree AV block when the block is infranodal, associated with a wide QRS complex, or accompanied by periods of asystole greater than 3 seconds or an escape rate below 40 beats per minute.^[46] Dual-chamber pacemakers (DDD mode) are generally preferred to maintain atrioventricular synchrony and reduce the risk of pacemaker syndrome or heart failure in patients with intact sinus node function.^[46] Single-chamber ventricular pacemakers (VVI mode) may be appropriate in cases of chronic atrial fibrillation or when atrial lead placement is not feasible, providing ventricular rate support without AV coordination.^[46] Leadless pacemakers, such as the Micra transcatheter pacing system, represent an alternative to traditional transvenous devices for patients with high-degree AV block, particularly those at higher risk for infection or with limited vascular access. These single-chamber devices are implanted directly into the right ventricle and have demonstrated efficacy in maintaining appropriate heart rates while reducing complications like lead dislodgement and infection.^[26]^[47] In acute settings, such as during myocardial infarction or post-cardiac surgery, temporary pacing is employed to stabilize hemodynamics when AV block causes symptomatic bradycardia refractory to pharmacological interventions like atropine.^[46] Transvenous temporary pacing, using active-fixation leads or balloon-flotation catheters inserted via the femoral or subclavian vein, is the preferred method for reliable capture in high-degree AV block.^[46] External (transcutaneous) pacing serves as a noninvasive bridge in emergencies, delivering stimuli via skin electrodes to achieve ventricular capture until invasive access is available.^[46] Catheter ablation is rarely indicated for AV block and is reserved for focal or reversible causes, such as intra-Hisian block due to a ventricular nodal accessory pathway or post-surgical injury to conduction tissue.^[48] In select cases, radiofrequency or cryoablation targeting the aberrant pathway can restore normal AV conduction, avoiding the need for lifelong pacing.^[48] Surgical interventions are primarily relevant in congenital AV block associated with structural heart defects, where pacemaker leads may be placed epicardially during corrective procedures for conditions like atrioventricular septal defects to minimize risks such as thromboembolism.^[49] In postoperative scenarios following congenital heart surgery, persistent complete AV block beyond 7-14 days often necessitates permanent pacing integrated with the surgical repair.^[49] Long-term management after device implantation includes regular follow-up with device interrogation to assess battery life, lead integrity, and pacing thresholds, typically every 3-12 months via in-person visits or remote monitoring depending on device type and patient factors.^[50] Complications such as lead dislodgement, fracture, or infection require vigilant monitoring; infection rates for initial implants are estimated at 0.5-2%, often managed by lead extraction and reimplantation.^[51] Patients are advised to avoid electromagnetic interference sources and report symptoms like dizziness or swelling at the implant site promptly.^[50]

Prognosis

Outcomes by Block Type

First-degree atrioventricular (AV) block is associated with an excellent prognosis in the absence of underlying structural heart disease, with patients typically experiencing no symptoms and a very low risk of progression to higher-degree block.^[18] Mortality rates in these individuals are comparable to those in the general population, though the presence of comorbidities such as ischemic heart disease or hypertrophic cardiomyopathy can elevate risks of adverse events like atrial fibrillation or heart failure hospitalization.^[52] Second-degree AV block manifests differently by subtype, influencing outcomes. Mobitz type I (Wenckebach) is generally benign, with minimal hemodynamic impact and a low progression rate to third-degree block, particularly in asymptomatic cases without structural disease.^[22] In contrast, Mobitz type II carries a higher risk, with 20-50% of cases progressing to complete heart block within several years, often necessitating pacemaker implantation to prevent sudden deterioration.^[53] Third-degree (complete) AV block portends a poor prognosis without intervention, especially in symptomatic patients, where untreated mortality can reach 20-50% due to bradycardia-induced complications like syncope or asystole.^[27] Following permanent pacemaker implantation, survival improves substantially, with 5-year rates of approximately 50-70% depending on comorbidities and patient selection.^[54]^[55] Several factors modulate outcomes across AV block types, including patient age, where older individuals face higher mortality risks independent of block degree, and comorbidities such as congestive heart failure, which worsen prognosis by exacerbating hemodynamic instability and increasing hospitalization rates.^[56] Congenital AV block generally carries a better long-term outlook than acquired forms, with neonatal survival rates up to 94% in treated cases and lower rates of progression to dilated cardiomyopathy compared to acquired blocks linked to degenerative or ischemic etiologies.^[57] Recent studies underscore the benefits of pacing in AV block, demonstrating that dual-chamber pacemaker implantation reduces syncope recurrence by approximately 70-95% in patients with documented high-grade block and reflex mechanisms, thereby improving quality of life and preventing falls.^[58]

Complications and Long-Term Risks

Untreated second-degree Mobitz type II and third-degree atrioventricular (AV) block carry a significant risk of sudden death due to episodes of asystole, where the ventricles fail to generate an escape rhythm, leading to cardiac arrest.^[59]^[3] In these advanced forms, the complete dissociation between atrial and ventricular activity can result in profound bradycardia or pauses exceeding several seconds, precipitating hemodynamic collapse without intervention.^[27] Heart failure may develop in patients with AV block, particularly through overlap with tachy-brady syndrome in sick sinus syndrome, where alternating bradycardia and tachycardia exacerbates ventricular remodeling and systolic dysfunction.^[60] Additionally, chronic right ventricular pacing in treated AV block can induce dyssynchrony, mimicking left bundle branch block and leading to pacing-induced cardiomyopathy, with reduced left ventricular ejection fraction over time.^[61] This dyssynchrony impairs coordinated contraction, increasing the risk of heart failure hospitalization in high-burden pacing patients.^[62] Pacemaker implantation, the primary treatment for symptomatic AV block, introduces several long-term complications. Lead fracture occurs at a rate of approximately 0.2-1.0% per year, often requiring surgical revision due to failure in signal transmission.^[63] Pocket or systemic infections affect about 1% of patients, potentially necessitating device explantation and prolonged antibiotic therapy.^[64] Battery depletion typically necessitates replacement every 5-15 years, depending on pacing dependency, and can lead to abrupt loss of function if not monitored.^[65] Thromboembolism is a rare but serious risk in complete AV block associated with atrial standstill, where absent atrial mechanical activity promotes blood stasis and thrombus formation in the atria.^[66] This condition heightens the likelihood of embolic stroke or systemic events, comparable to that in atrial fibrillation, warranting anticoagulation in affected patients.^[67] Patients with pacemakers for AV block may experience psychological complications, including anxiety stemming from device dependence and fear of malfunction or sudden failure.^[68] This can manifest as reduced quality of life, with up to 20-40% reporting heightened emotional distress post-implantation.^[69] Long-term, the development of ventricular tachycardia in these patients may necessitate upgrading to an implantable cardioverter-defibrillator for secondary prevention of arrhythmic events.^[70]

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