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Third-degree atrioventricular block

Third-degree atrioventricular block, also known as complete heart block, is a severe cardiac conduction disorder characterized by the complete failure of electrical impulses to conduct from the atria to the ventricles, resulting in independent atrial and ventricular rhythms with no atrioventricular synchrony.^[1] This condition leads to a slowed ventricular rate, typically below 50 beats per minute, as the ventricles are driven by an escape rhythm originating from the AV junction or ventricles, often compromising cardiac output and hemodynamic stability.^[1] It represents the most advanced form of atrioventricular block and is considered a medical emergency due to the risk of syncope, heart failure, or sudden cardiac arrest if untreated.^[2] The etiology of third-degree AV block is diverse, encompassing degenerative processes such as idiopathic fibrosis of the conduction system, ischemic damage from myocardial infarction (particularly inferior wall involvement in 5-10% of cases), medication toxicity (e.g., beta-blockers, calcium channel blockers, or digoxin), infectious causes like Lyme disease, and iatrogenic factors including post-cardiac surgery complications.^[1] Epidemiologically, it has a low incidence in the general population of 0.02% to 0.04%, as low as approximately 0.001% in apparently healthy individuals but increasing significantly with comorbidities such as diabetes (up to 1.1%) or in the context of acute ST-elevation myocardial infarction (around 2.2%).^[1] Pathophysiologically, the block can occur at the level of the AV node, His bundle, or distal Purkinje fibers, leading to atrioventricular dissociation where P waves march through independently of QRS complexes on electrocardiography.^[1] Clinically, patients may present asymptomatically if the escape rhythm is stable, but symptomatic cases often manifest with fatigue, dizziness, dyspnea, chest pain, or syncope due to bradycardia and reduced cardiac output; physical examination may reveal bradycardia, variable jugular venous pulsations from cannon A-waves, and signs of heart failure.^[1] Diagnosis is primarily confirmed via 12-lead electrocardiogram (ECG) demonstrating complete AV dissociation with atrial rates exceeding ventricular rates and no consistent PR interval relationship.^[1] Additional evaluation may include echocardiography to assess structural heart disease, laboratory tests for reversible causes (e.g., electrolytes, Lyme serology), and sometimes electrophysiological studies.^[2] Management prioritizes stabilization, with atropine as an initial pharmacologic intervention though often ineffective in infranodal blocks; transcutaneous or transvenous pacing is urgently required for symptomatic bradycardia, and permanent pacemaker implantation is indicated for persistent third-degree AV block to restore atrioventricular synchrony and prevent recurrence.^[1] Reversible causes, such as medication-induced block or acute ischemia, should be addressed promptly to potentially avoid long-term pacing.^[2] Prognosis varies, with higher mortality in cases associated with anterior myocardial infarction compared to inferior, underscoring the need for rapid intervention.^[1]

Background

Definition

Third-degree atrioventricular block, also known as complete heart block or third-degree heart block, is defined as the complete interruption of electrical impulses from the atria to the ventricles via the atrioventricular (AV) node, leading to atrioventricular dissociation where the atria and ventricles beat independently.^[1]^[3]^[4] Under normal conditions, electrical impulses originating from the sinoatrial node pass through the AV node to the ventricles with a characteristic delay, corresponding to a PR interval of 0.12 to 0.20 seconds on electrocardiography, ensuring coordinated atrial and ventricular contraction. In third-degree AV block, this conduction pathway is entirely disrupted, preventing any atrial impulses from reaching the ventricles and requiring subsidiary pacemakers to generate ventricular beats.^[4]^[5] The atrial rhythm is typically driven by the sinoatrial node at a rate of 60 to 100 beats per minute, while the ventricular rhythm arises from an escape focus, resulting in a slower rate of 40 to 60 beats per minute if the escape is junctional or 20 to 40 beats per minute if ventricular in origin.^[4]^[6] This condition represents the most severe form of AV block, in contrast to first- and second-degree blocks where partial conduction persists.^[5]

Classification

Atrioventricular (AV) blocks are classified into three degrees based on the extent of conduction delay or interruption between the atria and ventricles. First-degree AV block is characterized by a prolonged PR interval greater than 0.20 seconds on electrocardiogram (ECG), with consistent 1:1 conduction of P waves to QRS complexes.^[5] Second-degree AV block involves intermittent failure of conduction, subdivided into Mobitz type I (Wenckebach), where the PR interval progressively lengthens until a P wave is non-conducted, and Mobitz type II, featuring constant PR intervals with abrupt non-conduction of P waves.^[5] Third-degree AV block, also known as complete heart block, represents total dissociation between atrial and ventricular activity, with no atrial impulses conducting to the ventricles; the atria are paced by the sinoatrial node, while the ventricles rely on an independent escape rhythm.^[5] In third-degree AV block, the anatomical site of the block further refines classification and influences clinical implications. Blocks at the level of the AV node typically result in a junctional escape rhythm with narrow QRS complexes (duration <0.12 seconds) and a relatively stable rate of 40-60 beats per minute.^[7] In contrast, infranodal blocks, occurring below the AV node in the His-Purkinje system, produce a ventricular escape rhythm with wide QRS complexes (>0.12 seconds) and slower rates (20-40 beats per minute), carrying a worse prognosis due to the potential for hemodynamic instability and higher risk of progression or sudden events without intervention.^[7]^[1] Third-degree AV block is distinct from other conduction abnormalities, such as sinoatrial (SA) block, which affects impulse generation or exit from the SA node without impacting AV conduction directly, and bundle branch blocks, which involve delayed intraventricular conduction but preserve AV synchrony.^[4] These entities may coexist but do not equate to the complete AV dissociation defining third-degree block.^[5] Third-degree AV block can be broadly categorized as congenital or acquired, with the former typically identified in utero, at birth, or within the first month of life, often associated with structural heart defects, while the latter develops later due to various insults.^[3] Lower-degree blocks, such as second-degree, may occasionally progress to third-degree, underscoring the importance of monitoring.^[5]

Pathophysiology

Conduction Disruption

In third-degree atrioventricular (AV) block, conduction disruption results in a complete failure of electrical impulses to propagate from the atria to the ventricles, despite normal atrial depolarization. Under normal conditions, the cardiac impulse originates in the sinoatrial (SA) node, spreads through the atria to the AV node, and then proceeds via the bundle of His and Purkinje fibers to activate the ventricles.^[7] In this condition, however, the block interrupts this pathway at a specific site, leading to atrioventricular dissociation where atrial and ventricular activities occur independently.^[6] The site of the conduction block is most commonly the AV node (nodal block), occurring in the majority of cases and often reversible upon addressing the underlying cause, while infranodal blocks in the His-Purkinje system account for a substantial portion and are frequently irreversible due to extensive fibrosis or ischemic damage.^[5]^[8] At the AV node, the block arises from progressive prolongation of the refractory period, extending beyond the atrial cycle length and preventing any supraventricular impulse from conducting to the ventricles, even as the atria continue to contract normally with regular P waves on electrocardiography.^[7] These P waves "march through" at their intrinsic rate, dissociated from the QRS complexes generated by a lower escape focus, reflecting total impulse failure at the block site.^[6] Contributing factors to this complete conduction halt include heightened vagal tone, which predominantly affects the AV node by enhancing its refractory period; inflammatory processes that impair nodal or infranodal tissue integrity; ischemic injury that disrupts cellular excitability in the conduction pathway; and pharmacological agents that depress conduction velocity to the point of zero propagation.^[7]^[8] In infranodal locations, structural degeneration from fibrosis or sclerosis more commonly leads to abrupt and persistent block, as the His-Purkinje system's rapid conduction properties are particularly vulnerable to such insults.^[5] This electrophysiological interruption underscores the condition's reliance on subsidiary pacemakers below the block for ventricular activation.

Escape Rhythms and Hemodynamics

In third-degree atrioventricular block, the complete interruption of conduction between the atria and ventricles leads to the emergence of escape rhythms as a compensatory mechanism to maintain ventricular depolarization. The type and rate of the escape rhythm depend on the level of the block within the conduction system. If the block occurs at the level of the AV node, a junctional escape rhythm typically arises from the AV junction or His bundle, exhibiting a rate of 40 to 60 beats per minute and narrow QRS complexes (duration less than 120 ms) due to conduction through the normal His-Purkinje system.^[1]^[5] In contrast, an infranodal block below the AV node, involving the His-Purkinje system, results in a ventricular escape rhythm originating from the distal Purkinje fibers or ventricular myocardium, characterized by a slower rate of 20 to 40 beats per minute and wide QRS complexes (duration greater than 120 ms) owing to abnormal ventricular activation.^[1]^[5] This conduction failure manifests as atrioventricular dissociation, where atrial and ventricular activities proceed independently. The atria continue to be driven by the sinoatrial node, producing P waves at their intrinsic rate (typically 60 to 100 beats per minute), while the ventricles rely on the slower escape rhythm, resulting in no fixed relationship between P waves and QRS complexes.^[9] The hemodynamic consequences of third-degree AV block stem primarily from the loss of atrioventricular synchrony and the bradycardic escape rates, profoundly impacting cardiac output. Cardiac output is determined by the product of heart rate and stroke volume (CO = HR × SV), and in this condition, the reduced heart rate—particularly when below 40 beats per minute—leads to a significant decline in CO, as the ventricles fail to receive the atrial "kick" that normally augments ventricular filling by 20-30%.^[5] This desynchronization also produces intermittent cannon A waves visible in the jugular venous pulse, arising from atrial contraction occurring against a closed tricuspid valve when ventricular systole coincides with atrial depolarization.^[1]^[5] If the escape rhythm fails entirely, the condition can progress to asystole, resulting in absent ventricular activity and immediate hemodynamic collapse.^[1]^[10]

Etiology

Acquired Causes

Acquired third-degree atrioventricular (AV) block refers to the complete interruption of electrical conduction between the atria and ventricles that develops during life, rather than from birth, and is most prevalent in adults over 60 years of age, with the incidence of third-degree AV block increasing with advancing age.^[1]^[11] These cases often stem from reversible factors such as metabolic derangements or iatrogenic influences, contrasted with irreversible structural changes from ischemia or degeneration, and account for the majority of third-degree AV blocks encountered in clinical practice.^[3] Ischemic heart disease, particularly acute myocardial infarction (MI), is a leading acquired cause, occurring in up to 10% of inferior wall MIs due to transient ischemia of the AV node supplied by the right coronary artery, while anterior wall MIs more commonly involve infranodal structures via left anterior descending artery occlusion, leading to persistent block with poorer prognosis.^[3] Early revascularization has reduced the overall incidence of such blocks from historical rates of 5-7% to approximately 3.7%.^[3]^[12] Degenerative processes, such as Lenègre's disease—an idiopathic sclerodegenerative fibrosis primarily affecting the bundle branches—and Lev's disease—involving calcific infiltration of the conduction system—are common in elderly patients over 70 years and result in progressive loss of conduction tissue integrity without myocardial involvement.^[3] These fibrotic changes disrupt the His-Purkinje system, often leading to irreversible third-degree AV block requiring permanent pacing.^[13] Inflammatory and infectious etiologies include Lyme disease caused by Borrelia burgdorferi, which infiltrates the AV node leading to reversible conduction block in up to 10% of untreated cases; viral or bacterial myocarditis; endocarditis; and rheumatic fever, where immune-mediated damage scars the conduction pathways.^[3] Other examples encompass Chagas disease from Trypanosoma cruzi and varicella-zoster virus infections, all of which can cause transient or permanent block through direct tissue inflammation or infiltration.^[3] Iatrogenic causes frequently arise from medications that depress AV nodal conduction, including beta-blockers, calcium channel blockers, digoxin, and antiarrhythmics like amiodarone, particularly in overdose or with underlying conduction disease, often resolving upon discontinuation.^[3] Procedural interventions, such as cardiac surgery (e.g., aortic valve replacement with 1-5.7% incidence of block) or catheter-based septal alcohol ablation and AV nodal ablation, can mechanically damage the conduction system, necessitating temporary pacing if the block persists beyond 4-5 days.^[3] Metabolic disturbances, such as hyperkalemia, induce third-degree AV block by elevating extracellular potassium levels, which stabilize cardiac cell membranes, reduce phase 0 depolarization, and depress AV nodal excitability and conduction velocity, typically reversible with correction.^[3]^[14] Hypermagnesemia similarly causes AV nodal depression through membrane stabilization and impaired excitability, often seen in renal failure or excessive magnesium administration.^[3]^[15] Hypothyroidism contributes via slowed metabolic and conduction rates in the AV node, with block improving after thyroid hormone replacement.^[3]

Congenital Causes

Third-degree atrioventricular block can occur congenitally, either in isolation or in association with other cardiac anomalies, with an estimated incidence of 1 in 15,000 to 20,000 live births.^[16] Isolated congenital cases are particularly rare and often remain asymptomatic, potentially going undetected until adulthood when symptoms such as fatigue or syncope arise due to progressive conduction slowing. In contrast, when associated with structural heart disease, the block frequently presents earlier and is linked to defects such as atrial septal defect (ASD), ventricular septal defect (VSD), or congenitally corrected transposition of the great arteries (ccTGA), where abnormal anatomy disrupts the atrioventricular conduction pathway during fetal development.^[17] A major etiology of congenital third-degree AV block is maternal autoimmune disease, especially systemic lupus erythematosus (SLE), mediated by transplacental passage of anti-Ro/SSA antibodies that trigger inflammation and fibrosis in the fetal conduction system.^[18] Offspring of mothers with these antibodies face approximately a 2% risk of developing the block, with cases often clustered in families due to recurrent antibody exposure in subsequent pregnancies.^[19] Genetic factors also contribute, notably mutations in the SCN5A gene, which encodes the alpha subunit of the cardiac voltage-gated sodium channel; these loss-of-function variants impair impulse propagation and underlie progressive familial heart block type IA, manifesting as early or progressive AV conduction defects from infancy.^[20] Clinically, congenital third-degree AV block is frequently identified in utero via fetal echocardiography or in neonates who present with bradycardia, sometimes accompanied by signs of low cardiac output such as poor feeding or lethargy.^[21] The condition's course varies: some cases, particularly those tied to transient autoimmune inflammation, may partially resolve with recovery of conduction, while others progress inexorably, necessitating lifelong monitoring or intervention to prevent hemodynamic compromise.^[22] Overall, congenital forms are uncommon, comprising a small fraction of pediatric arrhythmias, with autoimmune-mediated instances showing a predisposition linked to maternal factors.^[23]

Clinical Presentation

Symptoms

Third-degree atrioventricular block often manifests with symptoms that depend on the ventricular escape rate and the duration of the block. Patients with an adequate escape rhythm exceeding 50 beats per minute are frequently asymptomatic at rest, as the heart maintains sufficient cardiac output.^[1] However, when the escape rate falls below 40 beats per minute, individuals commonly report fatigue, dizziness, and dyspnea due to inadequate perfusion and reduced cardiac output from bradycardia and atrioventricular dissociation.^[4]^[1] In acute presentations, such as those associated with myocardial infarction, symptoms can be more severe and include syncope, known as Stokes-Adams attacks, triggered by transient asystole or profound bradycardia leading to cerebral hypoperfusion.^[24]^[1] Additional acute symptoms may encompass chest pain and signs of heart failure, such as shortness of breath, reflecting ischemic or hemodynamic compromise.^[2]^[1] Chronic third-degree block typically presents with exercise intolerance, as the fixed ventricular rate fails to increase appropriately with physical demand, limiting cardiac output augmentation.^[3] Palpitations may also occur due to atrioventricular dissociation, where atrial contractions against closed mitral and tricuspid valves create irregular sensations.^[2] In special populations, infants with congenital complete heart block often exhibit poor feeding and failure to thrive secondary to fatigue during suckling and overall low cardiac output.^[25] Among the elderly, confusion can arise from cerebral hypoperfusion, particularly when escape rhythms are slow.^[26]

Physical Findings

Patients with third-degree atrioventricular block typically present with bradycardia on vital signs assessment, with heart rates often ranging from 30 to 50 beats per minute, reflecting the independent ventricular escape rhythm.^[1] Hypotension may accompany this finding in symptomatic cases, particularly when the heart rate falls below 40 beats per minute, leading to reduced cardiac output.^[1] Examination of the neck veins commonly reveals intermittent cannon A waves in the jugular venous pulse, resulting from atrial contraction against closed tricuspid and mitral valves due to atrioventricular dissociation.^[1]^[27] Auscultation of the heart often discloses variable intensity of the first heart sound (S1), attributable to the inconsistent timing between atrial and ventricular contractions.^[27] An S3 gallop may be present if concomitant heart failure has developed, and murmurs related to bradycardia-induced hemodynamic changes or underlying structural issues can occasionally be heard.^[1] In acute presentations, general inspection may show pallor, cool extremities, diaphoresis, and prolonged capillary refill time, indicative of hypoperfusion from hemodynamic instability.^[1] In cases of congenital third-degree atrioventricular block, physical findings may include signs of associated congenital heart defects, such as murmurs from atrioventricular canal defects or other structural anomalies.^[5]

Diagnosis

Electrocardiographic Features

Third-degree atrioventricular (AV) block is diagnosed primarily through electrocardiographic (ECG) findings demonstrating complete AV dissociation, in which atrial and ventricular activities are entirely independent. This manifests as regular P waves occurring at the atrial rate, typically 60 to 100 beats per minute in sinus rhythm, alongside regular QRS complexes at a slower ventricular escape rate, usually less than the atrial rate and often 20 to 50 beats per minute. There is no consistent relationship between P waves and QRS complexes, resulting in variable or absent PR intervals, as no atrial impulses conduct to the ventricles. The PP intervals remain constant, reflecting uninterrupted atrial depolarization, while the RR intervals are also constant, indicating a stable escape rhythm.^[1]^[4]^[3] The morphology of the QRS complexes further characterizes the level of conduction block. Narrow QRS complexes (duration <0.12 seconds) are observed in cases of AV nodal block, where the escape rhythm originates from the junctional tissue above the His bundle, producing a supraventricular-like waveform. In contrast, wide QRS complexes (>0.12 seconds) signify infranodal block, with the escape rhythm arising from the ventricles below the His-Purkinje system, often resulting in aberrant conduction and a slower rate (typically 20 to 40 beats per minute). This distinction is crucial for assessing hemodynamic stability, as junctional escapes are generally faster and narrower, while ventricular escapes are slower and wider.^[1]^[4]^[3] In rare instances, isoelectric AV dissociation may complicate ECG interpretation, where P waves are obscured or hidden within QRS complexes or T waves due to superimposition, potentially masking the full extent of dissociation. Careful measurement of PP and RR intervals, often using calipers, is essential to identify the underlying independent rhythms in such cases. Additionally, a diagnostic hint distinguishing third-degree AV block from other forms of AV dissociation, such as those seen in ventricular tachycardia, is the absence of ventricular capture during incremental atrial pacing; in complete block, increasing the atrial rate fails to conduct impulses to the ventricles, confirming the lack of AV nodal or infranodal conduction. This reflects the underlying pathophysiologic complete interruption of atrioventricular conduction.^[28]^[29]

Supporting Tests

Laboratory investigations are crucial for identifying reversible causes of third-degree atrioventricular block, such as electrolyte disturbances or ischemia. Serum electrolytes, particularly potassium and magnesium, should be measured, as hyperkalemia or hypomagnesemia can impair conduction and precipitate the block.^[1] Troponin levels are evaluated to detect myocardial ischemia or infarction as an underlying etiology.^[1] In patients with suspected autoimmune conditions, such as systemic lupus erythematosus or Sjögren's syndrome, antinuclear antibody (ANA) and anti-Ro/SSA antibody testing is recommended to identify immune-mediated contributions to the conduction abnormality.^[30] Imaging modalities provide insight into structural heart disease and ischemic causes. Transthoracic echocardiography is indicated to assess for cardiomyopathy, valvular abnormalities, or other structural issues that may contribute to the block, guiding further management decisions.^[8] Coronary angiography is performed in cases suggestive of acute coronary syndrome to evaluate for obstructive lesions responsible for the conduction disturbance.^[1] Advanced electrophysiologic evaluation via an invasive electrophysiology study (EPS) helps localize the site of the block within the conduction system. During EPS, measurement of the HV interval (from His bundle deflection to ventricular activation) exceeding 70 ms signifies infranodal involvement, which carries a higher risk of progression and influences prognosis.^[31] Ambulatory monitoring, such as Holter electrocardiography, is useful for detecting intermittent or paroxysmal third-degree AV block and correlating episodes with symptoms in stable patients.^[8] Exercise testing can evaluate conduction behavior under physiologic stress but is contraindicated in symptomatic or hemodynamically unstable individuals due to the risk of worsening bradycardia.^[8] Cardiac magnetic resonance imaging is not routinely employed but may be considered if sarcoidosis or infiltrative myocardial disease is suspected based on clinical features.^[8]

Management

Acute Interventions

The initial management of third-degree atrioventricular (AV) block focuses on stabilizing the patient and addressing hemodynamic instability, following the advanced cardiovascular life support (ACLS) bradycardia algorithm for unstable patients. This begins with ensuring airway, breathing, and circulation (ABCs), including maintenance of a patent airway, assisted ventilation if necessary, and supplemental oxygen for hypoxemia. Continuous cardiac monitoring, blood pressure assessment, pulse oximetry, and establishment of intravenous (IV) access are essential, along with obtaining a 12-lead electrocardiogram (ECG) to confirm the diagnosis without delaying therapy. Identification of underlying causes, such as myocardial ischemia, drug toxicity, or electrolyte imbalances, should occur concurrently.^[32]^[8] Pharmacologic interventions serve as a bridge to pacing in symptomatic bradycardia. Atropine, a first-line agent, is administered as 1 mg IV bolus, repeated every 3-5 minutes up to a maximum of 3 mg, to increase sinus node rate and potentially enhance AV nodal conduction; however, it is often ineffective in infranodal blocks due to its primary action at the AV node. If atropine fails, isoproterenol (1-20 mcg/min IV infusion) may be used as a beta-adrenergic agonist to augment heart rate and AV conduction, particularly when pacing is unavailable. Alternative infusions include dopamine (5-20 mcg/kg/min IV) or epinephrine (2-10 mcg/min IV), titrated to response for temporary hemodynamic support in unstable cases.^[32]^[8]^[1] Reversible causes must be promptly identified and treated to potentially restore conduction and avoid unnecessary pacing. For hyperkalemia-induced block, IV calcium gluconate (10 mL of 10% solution over 2-5 minutes) is given to stabilize cardiac membranes and counteract arrhythmogenic effects, followed by measures like insulin-glucose infusion to shift potassium intracellularly. Hypermagnesemia, often in renal failure, requires urgent dialysis if severe (>5 mEq/L) and symptomatic, as it prolongs AV conduction. Drug toxicity, such as from beta-blockers, is managed with glucagon (3-10 mg IV bolus, followed by infusion if needed) to enhance myocardial contractility and rate via non-adrenergic pathways. Discontinuation of offending agents, like calcium channel blockers or digoxin, is critical, with specific antidotes (e.g., digoxin immune Fab for digoxin toxicity) used as indicated.^[8]^[1]^[33] For persistent symptomatic bradycardia (e.g., heart rate <40 bpm) or hemodynamic compromise unresponsive to pharmacology, temporary pacing is indicated per ACLS guidelines. Transcutaneous pacing provides immediate noninvasive support, with pads applied in anterior-posterior positions and energy titrated to achieve electrical and mechanical capture, often starting at 40-80 mA. If ineffective or intolerable, transvenous pacing is pursued within hours via femoral or internal jugular access for more reliable ventricular capture. These measures are prioritized in unstable patients with signs of shock, altered mental status, ischemia, or heart failure.^[32]^[8]^[1]

Definitive Therapy

The definitive therapy for third-degree atrioventricular (AV) block primarily involves permanent pacemaker implantation to restore effective cardiac rhythm and prevent life-threatening complications. According to the 2018 ACC/AHA/HRS guidelines, permanent pacing is indicated (Class I, Level of Evidence B-NR) for third-degree AV block not attributable to reversible or physiologic causes, regardless of symptoms, including asymptomatic cases with documented asystole greater than or equal to 3 seconds or an escape rate below 40 beats per minute.^[34] The 2021 ESC guidelines similarly recommend permanent pacing (Class I, Level C) for symptomatic third-degree AV block, such as syncope or heart failure, as well as asymptomatic cases with pauses exceeding 3 seconds or escape rates below 40 beats per minute, and for blocks persisting more than 5 days after myocardial infarction or cardiac surgery. In post-myocardial infarction settings, particularly infranodal blocks, pacing is essential due to the high risk of hemodynamic instability, while symptomatic blocks in any location warrant intervention to alleviate bradycardia-related symptoms.^[1] Permanent pacemakers are selected based on patient anatomy, sinus node function, and comorbidities, with dual-chamber (DDD) devices preferred to maintain atrioventricular synchrony and reduce risks like pacemaker syndrome. The ACC/AHA guidelines endorse dual-chamber pacing over single-chamber ventricular pacing (VVI) (Class I, Level A) in patients with intact sinus node function, as it improves quality of life and hemodynamic performance by preserving atrial contribution to ventricular filling.^[34] VVI pacing is reserved for cases with chronic atrial fibrillation or limited life expectancy (Class IIa, Level B-R), providing reliable ventricular rate support without atrial leads.^[34] Emerging physiologic pacing options, such as conduction system pacing (CSP) including His-bundle pacing (HBP) and left bundle branch area pacing (LBBAP), are recommended by the 2025 ESC/EHRA consensus (Class I in select cases) for patients with AV block and reduced left ventricular ejection fraction (≤40%) to mimic natural conduction and prevent pacing-induced cardiomyopathy, showing comparable efficacy to biventricular pacing with lower thresholds and complication rates.^[35] Emerging leadless options, such as the Micra AV pacemaker, offer an alternative for select patients with high infection risk, venous access issues, or those requiring single-chamber pacing; the ESC guidelines support their use (Class IIa, Level B) in such scenarios, with real-world data showing high implantation success and low complication rates in AV block patients.^[36] In congenital third-degree AV block, surgical interventions are rare and typically limited to open-heart procedures addressing associated structural heart defects, with permanent pacing indicated if the block persists postoperatively or causes symptoms like bradycardia below 50 beats per minute or ventricular dysfunction. The ACC/AHA guidelines recommend pacing (Class I, Level C-LD) for congenital complete AV block with significant symptoms or dysfunction, often following initial surgical repair of anomalies such as ventricular septal defects.^[34] Permanent pacing is preferred over prolonged observation in high-risk congenital cases, though epicardial leads may be placed during concomitant cardiac surgery to avoid transvenous complications (ESC Class IIa, Level C). For reversible causes of third-degree AV block, such as Lyme carditis or electrolyte imbalances, definitive therapy shifts to monitoring after targeted treatment, with pacing deferred if conduction recovers. The ESC guidelines advise against permanent pacing (Class III, Level B) for blocks resolving after cause correction, exemplified by Lyme disease where antibiotics often restore AV conduction within weeks, allowing close observation rather than implantation. An observation period of 5-10 days post-myocardial infarction or 3-7 days post-surgery is recommended to assess reversibility before committing to permanent devices (Class I, Level C). Long-term follow-up after pacemaker implantation includes regular device interrogation to monitor lead function, battery life, and thresholds, typically every 6-12 months or via remote monitoring to enable early detection of issues. The ACC/AHA guidelines emphasize routine follow-up (Class I, Level B-NR) to ensure optimal device performance and patient safety.^[34] In patients with third-degree AV block and high risk for ventricular tachycardia, such as those with cardiomyopathy or prior arrhythmias, an implantable cardioverter-defibrillator (ICD) may be combined with pacing (ESC Class IIa, Level C), particularly if left ventricular ejection fraction is below 50% or fibrosis is evident on imaging.

Prognosis

Outcomes

The prognosis for third-degree atrioventricular block varies significantly based on the underlying cause, the site of the block, patient age, and whether pacing therapy is implemented. With permanent pacemaker implantation, long-term survival is favorable, particularly in patients with isolated AV block, where observed 5-year survival rates have been reported as approximately 52% in older cohorts, though more recent data indicate improvements exceeding 80% at 3 years in patients with a mean age of 64 years.^[37]^[38] Untreated symptomatic cases carry a high risk of mortality, with 1-year survival rates as low as 68% and 5-year rates around 37% in historical untreated cohorts.^[39] Outcomes differ markedly by etiology. Reversible causes, such as drug-induced blocks (e.g., from beta-blockers or calcium channel blockers), often lead to full recovery upon discontinuation of the offending agent, with AV conduction resolving in 41% of cases within 48 hours and spontaneous improvement in an additional 23%.^[40] In contrast, ischemic third-degree AV block associated with anterior myocardial infarction portends a poor prognosis, with in-hospital mortality rates up to 20-33% even in the reperfusion era, reflecting extensive myocardial damage; blocks associated with inferior myocardial infarction generally have better outcomes as they are often transient and nodal in location.^[12] For congenital third-degree AV block, pacemaker therapy yields highly favorable long-term outcomes, with very low overall mortality in paced children and adults despite a risk of disease progression requiring pacing upgrades.^[41] Prognostic factors include age and the type of escape rhythm. Patients over 70 years often experience worse outcomes due to comorbidities, with higher mortality risks compared to younger individuals.^[42] A junctional escape rhythm confers a better prognosis than a ventricular escape rhythm, as the former typically provides a more reliable and faster rate (40-60 bpm), reducing the likelihood of hemodynamic instability.^[6]^[43] Recent advancements up to 2025 have further improved outcomes through leadless pacemakers, which reduce infection risks compared to traditional transvenous devices; studies report 90% freedom from major complications at 90 days and lower revision rates (3.2% at 5 years), enhancing quality of life in AV block patients.^[44]^[45]

Complications

If left untreated, third-degree atrioventricular block can lead to sudden cardiac death due to asystole or ventricular tachyarrhythmias triggered by bradycardia-induced QT prolongation.^[3] Chronic bradycardia and reduced cardiac output may precipitate heart failure through sustained low perfusion and neuroendocrine activation.^[1] Blood stasis from diminished ventricular filling increases the risk of thromboembolism.^[1] Syncope from hemodynamic instability often results in falls, causing musculoskeletal injuries or head trauma.^[3] Pacemaker implantation, the primary management strategy, carries procedural and long-term risks. Lead infection occurs in 1-2% of cases, with higher rates (up to 7%) in patients with prior temporary pacing.^[8] Cardiac perforation affects 0.1-0.8% of implantations, potentially leading to tamponade or hemothorax.^[46] Single-chamber ventricular pacing can cause pacemaker syndrome in over 18-20% of patients, manifesting as fatigue, dyspnea, and hypotension from atrioventricular dyssynchrony.^[8] Battery depletion requires periodic device replacement, with failure risks escalating after 5-10 years depending on usage.^[8] The underlying etiology may contribute additional sequelae. In congenital cases, particularly autoimmune-mediated, progression to dilated cardiomyopathy develops in 5-30% of patients.^[23] Post-myocardial infarction, the block heightens vulnerability to further ventricular arrhythmias.^[3] Rarely, association with sick sinus syndrome can result in tachy-brady syndrome, featuring paroxysmal tachycardia alternating with profound bradycardia.^[8] Early pacemaker implantation mitigates these risks, improving survival and reducing heart failure incidence compared to conservative management.^[8]

References

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Complete Heart Block Complicating ST-Segment Elevation ... - JACC
Oct 17, 2015 · In the pre-thrombolytic era, second- or third-degree AV block was recorded in 5% to 7% of patients presenting with acute MI (2,3), and reached ...
[13]
Lenègre-Lev disease • LITFL • Medical Eponym Library
Jun 30, 2025 · Acquired fibrous degeneration of the left and right bundle branches; permanent complete atrioventricular (AV) dissociation.Missing: degree | Show results with:degree
[14]
Hyperkalaemia induced complete atrioventricular block with a ... - NIH
In general, hyperkalaemia produces a gradual depression of the excitability, conduction velocity of the specialised pacemaker cells and conducting tissues ...Missing: mechanism | Show results with:mechanism
[15]
A case report of complete atrioventricular heart block due...
The metabolic causes of AV blocks are hyperkalemia and hypermagnesemia. Hyponatraemia is the commonest electrolyte disturbance seen in intensive care patients, ...
[16]
Pediatric Congenital Atrioventricular Block - Medscape Reference
May 16, 2025 · Autoimmune AV block occurs in approximately 1 per 15,000-20,000 live births, and 1-2% of newborns whose mothers have positive anti-SSA-Ro ...Background · Etiology · Epidemiology · Prognosis
[17]
Congenital Heart Block - Symptoms, Causes, Treatment | NORD
CHB can happen at any age but is termed congenital when it occurs in the fetus or newborn up to 28 days of life. Individuals may progress from one type of heart ...Missing: epidemiology | Show results with:epidemiology
[18]
Early Diagnosis and Treatment of Atrioventricular Block in the Fetus ...
Mar 30, 2009 · Fetal exposure to maternal anti-SSA/Ro or anti-SSB/La antibodies (or both) results in a 2% to 5% risk of complete AV block, with up to 30% risk ...
[19]
Autoimmune congenital heart block: a case report and review of the ...
Jan 2, 2024 · ACHB occurs in 2% of women with positive anti-Ro/SSA and anti-La/SSB antibodies and causes a high risk of intrauterine fetal death, neonatal ...
[20]
Clinical, Genetic, and Biophysical Characterization of SCN5A ...
We present clinical, genetic, and biophysical features of 2 new SCN5A mutations that result in atrioventricular (AV) conduction block.
[21]
Pediatric Congenital Atrioventricular Block Clinical Presentation
May 16, 2025 · Congenital atrioventricular block (CAVB) may be associated with findings of low cardiac output or congestive heart failure.Missing: progress | Show results with:progress
[22]
Perinatal Outcome of Fetal Atrioventricular Block | Circulation
Sep 16, 2008 · This long-term study confirms that fetal AV block has a poor outcome when associated with structural heart disease and that spontaneous regression of AV block ...<|control11|><|separator|>
[23]
Congenital and childhood atrioventricular blocks: pathophysiology ...
Jun 28, 2016 · Atrioventricular block is classified as congenital if diagnosed in utero, at birth, or within the first month of life.
[24]
Stokes-Adams Syndrome: Symptoms, Causes & Treatment
Jan 25, 2023 · Stokes-Adams syndrome is a condition in which you faint because of an abnormal heart rhythm. It's a type of cardiac (heart) syncope (fainting).
[25]
Outcome and Growth of Infants Fetally Exposed to Heart Block ...
Apr 1, 2008 · Based on our clinical observation of feeding problems and failure to thrive in infants affected by complete heart block, we initiated this ...
[26]
Third-Degree Atrioventricular Block (Complete Heart Block) Clinical ...
Jul 29, 2022 · Confusion. Dyspnea. Severe chest pain. Sudden death. Because an acute ... Patients may have signs of hypoperfusion, including the following:.
[27]
ACC/AHA/ESC Guidelines for the Management of Patients With ...
Therefore, one should also look for evidence of VA dissociation on physical examination: irregular cannon A waves in the jugular venous pulse and variability in ...Missing: variable | Show results with:variable
[28]
Third-degree (complete) heart block - Example 1 - teachIM
Some P's may be hidden under a QRS complex or T wave and may be difficult to identify. However, your P-P interval should remain constant. Calipers are helpful ...
[29]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5430927/
[30]
Autoimmunity and Atrioventricular Block of Unknown Etiology in Adults
Jan 29, 2014 · Recent data suggest a likely role of anti-Ro/SSA antibodies in the development of complete heart block in these patients.
[31]
Third-Degree Atrioventricular Block (Complete Heart Block) Workup
Jul 29, 2022 · The most important study in patients with suspected third-degree atrioventricular (AV) block (complete heart block) is 12-lead electrocardiography (ECG).Missing: EPS | Show results with:EPS
[32]
[PDF] Adult Bradycardia Algorithm
Atropine IV dose: First dose: 1 mg bolus. Repeat every 3-5 minutes. Maximum: 3 mg. Dopamine IV infusion: Usual infusion rate is. 5-20 mcg/kg per minute.Missing: third- | Show results with:third-
[33]
Third-Degree Atrioventricular Block (Complete Heart Block ...
Jul 29, 2022 · Class IIb recommendations. Permanent ventricular pacing may be considered for persistent second- or third-degree AV block at the AV node level, ...
[34]
2018 ACC/AHA/HRS Guideline on the Evaluation and Management ...
Nov 6, 2018 · In patients with a left ventricular ejection fraction between 36% to 50% and atrioventricular block, who have an indication for permanent pacing ...
[35]
12-Month results from the Micra AV post-approval registry
Jun 13, 2024 · The Micra AV leadless pacemaker was implanted with a high rate of success in patients with multiple comorbidities, with a significantly lower ...
[36]
Long-term survival after pacemaker implantation for heart block in ...
Observed survival at 1, 3, 5, and 10 years was 85%, 68%, 52%, 21%, and 72%, 50%, 31%, 11% for patients with isolated AV block and patients with coexisting heart ...
[37]
Risk Factors for Mortality in Patients Undergoing Permanent ...
Jun 20, 2025 · In our study, the average age at which patients received implantation was 64.3 years, with a 3-year survival rate of 83.9%. For instance, a ...Missing: third- degree
[38]
Prognosis of patients with complete heart block or ... - PubMed
Prognosis of patients with complete heart block or arrhythmic syncope who were not treated with artificial pacemakers. A long-term follow-up study of 101 ...
[39]
Drug-induced atrioventricular block: prognosis after discontinuation ...
Jul 7, 2004 · Drug discontinuation was followed by resolution of AV block in 41% of cases, whereas spontaneous improvement of AV conduction occurred in 23% of patients.Missing: recovery | Show results with:recovery
[40]
Risk Stratification of Patients With Acute Anterior Myocardial ...
Aug 14, 2006 · The 30-day mortality rate was 31.6% in the 415 patients with RBBB and anterior AMI at randomization and 33% in the 100 patients who developed ...
[41]
Pathophysiology, clinical course, and management of congenital ...
The estimated overall mortality of nonpaced patients with isolated complete congenital AV block is 8%–16% in infants and 4%–8% in children and adults.
[42]
Long term clinical outcomes in patients requiring cardiac pacing due ...
Conclusion. Long-term outcomes for patients with congenital complete heart block who undergo pacemaker insertion are highly favourable. Despite high pacing ...
[43]
The prevalence and prognosis of third‐degree atrioventricular ...
Dec 25, 2001 · Third-degree atrioventricular block was found in 11 persons, seven male and four female, an overall prevalence of 0.04%. All of these ...Missing: common | Show results with:common
[44]
Third-degree AV block (3rd degree AV block, AV block 3, AV block III)
Third-degree AV block is a very serious condition because escape rhythms may (1) not occur, (2) occur transiently, or (3) occur but generate insufficient ...Missing: source | Show results with:source
[45]
Leadless Pacemakers: The “Leading Edge” of Quality of Life in ... - NIH
Mar 31, 2025 · Knops (2023) reported that 90.3% of patients experienced freedom from complications at 90 days, with 90.2% achieving adequate atrial capture ...Missing: degree | Show results with:degree
[46]
12-Month results from the Micra AV post-approval registry
More recently, long-term observational data reported a major complication rate of 4.5% and a revision rate of 3.2% at 5-year follow-up and a reduction of 53% ...
[47]
Right heart perforation by pacemaker leads - PMC - NIH
Feb 29, 2012 · Studies have reported overall lead perforation rates after pacemaker implantation to be 0.1–0.8%, and after ICD placement-0.6–5.2%.