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Heart block
This image shows bundle branch block where the beating rhythm is hindered, but not stopped. A blockage in Site A in the left ventricle blocks electrical signals from the atrium, causing the heart to rely on the right ventricle to maintain the correct rhythm. A:obstruction B:sinus node C:atrioventricular (AV) node 1:right atrium 2:left atrium 3:left ventricle 4:right ventricle
SpecialtyCardiology

Heart block (HB)[1] is a disorder in the heart's rhythm due to a fault in the natural pacemaker.[2] This is caused by an obstruction – a block – in the electrical conduction system of the heart. Sometimes a disorder can be inherited. Despite the severe-sounding name, heart block may cause no symptoms at all or mere occasional missed heartbeats and ensuing light-headedness, syncope (fainting), and palpitations. However, depending upon exactly where in the heart conduction is impaired and how significantly, the disorder may require the implantation of an artificial pacemaker, a medical device that provides correct electrical impulses to trigger heartbeats, compensating for the natural pacemaker's unreliability, so making heart block usually treatable in more serious cases.

Heart block should not be confused with other conditions, which may or may not be co-occurring, relating to the heart and/or other nearby organs that are or can be serious, including angina (heart-related chest pain), heart attack (myocardial infarction), any heart failure, cardiogenic shock or other types of shock, different types of abnormal heart rhythms (arrhythmias), cardiac arrest, or respiratory arrest.

The human heart uses electrical signals to maintain and initiate the regular heartbeat in a living person. Conduction is initiated by the sinoatrial node ("sinus node" or "SA node"), and then travels to the atrioventricular node ("AV node") which also contains a secondary "pacemaker" that acts as a backup for the SA nodes, then to the bundle of His and then via the bundle branches to the point of the apex of the fascicular branches. Blockages are therefore classified based on where the blockage occurs – namely the SA node ("Sinoatrial block"), AV node ("AV block" or AVB), and at or below the bundle of His ("Intra-Hisian" or "Infra-Hisian block" respectively). Infra-Hisian blocks may occur at the left or right bundle branches ("bundle branch block") or the fascicles of the left bundle branch ("fascicular block" or "Hemiblock"). SA and AV node blocks are each divided into three degrees, with second-degree blocks being divided into two types (written either "type I" or "II" or "type 1" or "2"). The term "Wenckebach block" is also used for second-degree type 1 blocks of either the SA or AV node; in addition, second-degree blocks type 1 and 2 are also sometimes known as " Mobitz 1" and "Mobitz 2".

Clinically speaking, the blocks tend to have more serious potential the closer they are to the "end" of the electrical path (the muscles of the heart regulated by the heartbeat), and less serious effects the closer they are to the "start" (at the SA node), because the potential disruption becomes greater as more of the "path" is "blocked" from its "end" point. Therefore, most of the important heart blocks are AV nodal blocks and infra-Hisian blocks. SA blocks are usually of lesser clinical significance, since, in the event of an SA node block, the AV node contains a secondary pacemaker which would still maintain a heart rate of around 40–60 beats per minute, sufficient for consciousness and much of daily life in most cases.

Types

[edit]
Conduction system of the heart
Sinus rhythm with acute inferior infarction complicated by Type I AV block manifest in the form of 5:4 Wenckebach periods; R-P/P-R reciprocity.
Sinus rhythm (rate = 100/min) with 3:2 and 2:1 Type II AV block; right bundle branch block
Sinus tachycardia with complete AV block and resulting junctional escape

Following the path of the electrical signals, the places where conduction can be blocked give rise to different kinds of heart blocks:

Location Name
Within the sinoatrial node (SA node or Sinus node), where the heart's signals originate Sinoatrial nodal blocks (often abbreviated "SA nodal block" or "SA block", sometimes written "Sinuatrial block")
Within the atrioventricular node (AV node) Atrioventricular block (often abbreviated "AV nodal block", "AV block" or AVB).
At and below the bundle of His Intra-Hisian blocks and Infra-Hisian blocks respectively.
Within the left or right bundle branches Bundle branch blocks.
Within the fascicles of the left bundle branch "Fascicular block" or hemiblocks.

SA and AV node blocks are each divided into three degrees, with second-degree blocks being divided into two types (written either "type I or II" or "type 1 or 2"). In an SA block, the electrical impulse is delayed or blocked on the way to the atria, thus delaying atrial depolarization. By contrast, an AV block occurs in the AV node and delays ventricular depolarization. The term "Wenckebach block" is also used for some heart blocks, and can refer to a second-degree type I block in either the SA node or the AV node; however, the ECG features of the two are quite distinctly different.

SA nodal blocks

[edit]

SA blocks rarely give severe symptoms, because even if an individual had complete block at this level of the conduction system (which is uncommon), the secondary pacemaker of the heart would be at the AV node, which would fire at 40 to 60 beats a minute, which is enough to retain consciousness in the resting state. However, SA block is capable of causing problematic symptoms even so, and may also hint at conduction issues elsewhere in the heart, and therefore SA blocks are – despite their lower level of life-threatening risk – still "the most common indication for pacemaker implantation in the US".[3]

Types of SA nodal blocks include:

  • SA node Wenckebach (Mobitz I)[4]
  • SA node Mobitz II
  • SA node exit block

In addition to the above blocks, the SA node can be suppressed by any other arrhythmia that reaches it. This includes retrograde conduction from the ventricles, ectopic atrial beats, atrial fibrillation, and atrial flutter.[citation needed]

The difference between SA node block and SA node suppression is that in SA node block, an electrical impulse is generated by the SA node that does not make the atria contract. In SA node suppression, on the other hand, the SA node does not generate an electrical impulse because it is reset by the electrical impulse that enters the SA node.[citation needed]

AV nodal blocks

[edit]

There are three basic types of AV nodal block:

Infra-Hisian block

[edit]

An infra-Hisian block is that of the distal conduction system. Types of infra-Hisian block include:

Of these types of infra-Hisian block, Mobitz II heart block is considered most important because of the possible progression to complete heart block.[citation needed]

Epidemiology

[edit]

Data on the incidence and prevalence of heart block are relatively scarce. A recent study from the United Kingdom reported the incidence of heart block to have approximately doubled over the past two decades, now lying at 149 per 100 000 person-years.[6] At the same age, men are about two-times more likely to develop heart block.[6] Median age at heart block diagnosis is 75 years in men and 78 years in women.[6]

References

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Heart block

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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 . 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. 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 longer than 200 milliseconds on an electrocardiogram (ECG), but all signals eventually reach the ventricles. Second-degree heart block is characterized by intermittent failure of signals to conduct, subdivided into Mobitz type I (with progressive lengthening before a dropped beat) and Mobitz type II (sudden dropped beats without prior lengthening), which carries a higher of progression. 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. These types can occur congenitally or be acquired later in life. Common causes of heart block include age-related degeneration of the conduction system, , certain medications (such as beta-blockers or ), electrolyte imbalances, and congenital factors like maternal . Risk factors encompass older age, family history of cardiac conditions, and underlying heart diseases such as or valvular disorders. Symptoms vary by degree but may include fatigue, dizziness, fainting (syncope), , and , with complete block potentially causing hemodynamic instability or sudden cardiac arrest. 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. may assess structural heart issues contributing to the block. Treatment depends on severity and symptoms: suffices for 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. In acute settings, temporary pacing or medications may stabilize the patient. Early management improves prognosis, particularly for complete heart block, where untreated five-year survival is approximately 37%.

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. 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. Histologically, the SA node is insulated by dense connective tissue that separates it from surrounding atrial myocardium, ensuring directed impulse propagation. 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 , and the ostium. 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 , which delays conduction to allow atrial contraction completion. The AV node's histology includes transitional cells connecting to atrial myocardium and penetrating fibers that form the initial segment of the His bundle. 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. It comprises Purkinje-type cells and slender transitional cells, with minimal fibrous encapsulation to facilitate rapid signal transmission. 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. These branches distribute into an extensive network of , which ramify subendocardially through the ventricular myocardium from apex to base, consisting of large, pale-staining cells with abundant , few myofibrils, and peripheral nuclei for swift impulse conduction.

Physiology

The sinoatrial (SA) node, the heart's primary pacemaker, exhibits through spontaneous generation of action potentials at a rate of 60 to 100 beats per minute, initiating the normal . This stems from phase 4 diastolic depolarization, where the slowly rises due to decaying outward currents and inward currents via ion channels, including the hyperpolarization-activated funny current (I_f, primarily sodium influx) and T-type calcium channels. 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. 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. 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. This delay coordinates atrial emptying prior to ventricular activation. From the AV node, the impulse proceeds through the penetrating , 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 from to epicardium and apex to base. After , cardiac cells enter periods that enforce sequential activation and prevent premature excitations. The absolute 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. The following relative period, during late phase 3, partially restores excitability but requires a stronger stimulus for as efflux continues. Collectively, these periods promote unidirectional impulse travel and inhibit re-entrant loops by allowing full recovery before subsequent impulses. This orderly propagation synchronizes atrial and ventricular contractions, with atrial preceding ventricular to maximize filling. The atrial contribution, known as the "atrial kick," boosts ventricular by 20-30% at rest, thereby increasing and without excessive energy expenditure.

Pathophysiology

Mechanisms of Block

Heart block encompasses impaired electrical conduction within the atrioventricular (AV) conduction , occurring at the AV junction or infranodal regions below the His bundle, which leads to delayed or absent activation of the ventricles. This disruption prevents normal propagation of impulses from the atria to the ventricles, potentially causing or if uncompensated. The normal conduction pathway, originating from the sinoatrial (SA) node through the atria to the AV node and His-Purkinje , serves as the baseline for these impairments. Various mechanisms underlie heart block, including prolongation of the refractory period in conduction tissues, structural damage to the pathways, and influences. Increased refractory periods can arise from electrolyte imbalances, such as , where elevated extracellular potassium depolarizes the resting , slowing conduction velocity and extending the in atrial, nodal, and ventricular tissues. Structural damage, often involving 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. influences, such as heightened , selectively prolong refractoriness in the AV node by enhancing acetylcholine-mediated hyperpolarization, thereby delaying AV conduction without necessarily affecting the infranodal regions. 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. Infra-Hisian block, occurring distal to the His bundle in the , 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. When higher-order pacemakers fail, subsidiary escape rhythms emerge to maintain . 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. 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 , which provides less reliable and hemodynamically suboptimal pacing. These escape mechanisms highlight the of the conduction system, where lower pacemakers activate only after prolonged suppression of superior sites.

Classification

Heart block is classified primarily by anatomical location within the AV conduction system and by the degree of conduction impairment, which determines 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 ) 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. Atrioventricular blocks are subdivided by degree of impairment in atrial-to-ventricular impulse transmission. First-degree AV block is characterized by a prolonged 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 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 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 () activity, with no conducted impulses and independent rhythms in each chamber, necessitating an escape rhythm for ventricular . 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 , and propensity for rapid progression to complete AV block, frequently requiring permanent pacing.

Epidemiology

Prevalence

Heart block, encompassing atrioventricular (AV) and sinoatrial (SA) blocks, exhibits low overall in the general population, with advanced forms being particularly rare. The of third-degree (complete) AV block is estimated at 0.02% in the United States and 0.04% worldwide. 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. Second- and third-degree AV blocks together have a of 0.2-1.2% in screened populations. 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. For high-grade AV block (second- or third-degree), prevalence is elevated in the elderly. SA block, a component of , is less frequently reported but contributes to the broader category of bradyarrhythmias, with affecting approximately 0.2% of people over age 65. 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 and , report higher rates of age-related AV block compared to , where younger populations predominate.

Risk Factors

Age is the strongest for developing heart block, with incidence increasing markedly due to age-related degenerative changes in the , such as idiopathic fibrosis and sclerosis of the and bundle branches. The risk of atrioventricular block rises with advancing age, with a of 1.34 per 5-year increment in a large population-based . This age-related progression contributes to higher prevalence in older adults, where alone affects approximately 5.3% of individuals, particularly males. Comorbid cardiovascular conditions significantly predispose individuals to heart block by promoting structural and functional damage to the conduction pathways. Ischemic heart disease, particularly following , elevates the risk by approximately 3.5-fold (hazard ratio 3.54, 95% CI 1.33-9.42). Similarly, congestive increases the risk by about 3.3-fold (hazard ratio 3.33, 95% CI 1.10-10.09). and further amplify vulnerability; elevated systolic (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 , with population-attributable risks of 47% and 11%, respectively. Certain medications commonly used for cardiovascular conditions can induce reversible atrioventricular block by slowing conduction through the . Beta-blockers, non-dihydropyridine (such as verapamil and ), and 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. These effects are dose-dependent and more pronounced in individuals with underlying conduction abnormalities. 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 gene encoding the cardiac , results in idiopathic progressive cardiac conduction defect and is a notable example of such syndromes. This autosomal dominant disorder predisposes affected families to requiring pacemaker implantation at relatively early ages.

Etiology

Acquired Causes

Acquired heart block refers to disruptions in the that develop after birth due to various pathological processes, distinct from congenital origins. These causes often involve ischemia, , 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. Ischemic heart disease, particularly acute (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 supplying the AV node, ischemia leads to transient or persistent nodal block due to heightened 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 . Inflammatory and infectious conditions can infiltrate or inflame the conduction system, producing blocks that range from first-degree to complete AV dissociation. , caused by , frequently manifests as AV block in early disseminated stages, with approximately 80-90% of cases showing conduction abnormalities; these are typically transient, resolving with antibiotics, though rare permanent damage occurs. , often viral in origin, induces 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. , an autoimmune response to , classically prolongs the via inflammation in the conduction tissues, but higher-degree blocks are uncommon and usually resolve with anti-inflammatory therapy. Iatrogenic causes arise from therapeutic interventions that mechanically or pharmacologically disrupt conduction. Post-cardiac surgery, particularly aortic or replacement, complete AV block develops in 3-6% of cases due to , , 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 (e.g., verapamil), , and class I/III antiarrhythmics (e.g., , ), prolong the or induce higher-grade blocks by slowing nodal recovery or enhancing refractoriness, often reversible upon discontinuation but with recurrence risk in susceptible patients. Metabolic imbalances further contribute to acquired conduction delays by altering membrane potentials or myocardial excitability. , typically at levels exceeding 6.5 mEq/L, depresses phase 0 of the action potential in 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 , and bradycardic effects, manifesting as first- or second-degree block in severe cases, which generally improves with thyroid hormone replacement.

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. 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 or other 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. 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. Genetic mutations also contribute to congenital heart block, particularly in familial forms. Mutations in the gene, which encodes the cardiac 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 or early childhood.

Clinical Features

Symptoms

First-degree atrioventricular (AV) block is typically asymptomatic, as the conduction delay does not significantly impair cardiac output or heart rate. 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. 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. 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. These symptoms arise from inadequate perfusion to vital organs during periods of slowed or irregular ventricular response. Overall, symptom severity correlates with the degree of block, as higher-grade AV blocks more frequently result in and heart failure-like presentations, including dyspnea on exertion and easy fatigability.

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. , defined as a 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. In third-degree (complete) heart block, atrioventricular dissociation may produce intermittent in the jugular venous pulse, resulting from atrial contraction against a closed when atria and ventricles contract simultaneously. These waves appear as prominent, irregular pulsations in the neck veins and are a key bedside clue to complete dissociation. 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 , while Mobitz type II features sudden dropped beats without prior prolongation. In cases of varying conduction ratios, such as 2:1 or 3:2 , the may exhibit alternating strong and weak beats due to differences in ventricular filling and . The overall rate remains bradycardic, and regularity is preserved in third-degree block at the escape rhythm rate, though intensity may vary slightly with hemodynamic effects. In symptomatic patients with significant heart block, signs of reduced are evident, including from inadequate and cool, clammy extremities reflecting peripheral and hypoperfusion. These findings are more pronounced in acute or severe cases where compromises systemic . If heart block is associated with underlying structural heart disease, such as valvular or , auscultation may reveal murmurs, including systolic or diastolic types depending on the lesion. 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 , though these are uncommon and nonspecific. 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. Overall, the provides vital clues to hemodynamic stability but requires electrocardiographic confirmation for definitive .

Diagnosis

Electrocardiography

is the primary diagnostic tool for identifying heart block, revealing characteristic patterns of atrioventricular (AV) conduction delays or dissociations through analysis of , , and . Standard 12-lead ECG recordings at 25 mm/s speed allow measurement of intervals, with the defined as the time from the onset of the to the onset of the . First-degree AV block is diagnosed when the PR interval is prolonged beyond 200 ms, yet every atrial impulse () conducts to the ventricles, resulting in 1:1 AV conduction without dropped beats. This prolongation reflects delayed conduction through the AV node or His-Purkinje system but does not impair overall rhythm regularity. 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 behavior. In Mobitz type I (Wenckebach), there is progressive lengthening of the across consecutive beats until a P wave is not followed by a QRS complex, producing a pattern of grouped beating; the following the dropped beat shortens, and atrial rate remains constant below 100 bpm. This type typically originates in the AV node and is associated with narrow QRS complexes. In Mobitz type II, the 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. 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. 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.

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%. 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. Invasive 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 . Echocardiography is routinely performed to evaluate for structural causes of heart block, carrying a Class I recommendation for identifying conditions such as 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. Blood tests target reversible causes and are selected based on clinical suspicion, with Class I recommendation for electrolytes and to detect imbalances like or acute ischemia. and serology for receive Class IIa support, while autoimmune markers may be pursued in suspected inflammatory conditions. Directed testing avoids unnecessary comprehensive panels, focusing on etiologies like or .

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 type I second-degree (Mobitz I) AV block. For 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. 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. Correction of reversible causes is a of conservative management, focusing on discontinuing offending medications such as beta-blockers, , or that may exacerbate AV conduction delays, as well as treating electrolyte imbalances (e.g., or ) or infections like . Identifying and resolving these factors through patient history, tests, and vital sign monitoring can often restore normal conduction without further intervention, preventing progression to higher-degree blocks. 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. Lifestyle modifications play a supportive role, particularly in individuals with high 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 intake to support overall cardiac stability.02560-8/fulltext)

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. 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. Pacemaker selection depends on anatomy, comorbidities, and the need for atrioventricular synchrony. Dual-chamber pacemakers (DDD mode) are preferred (Class I, Level of Evidence B-R) for most s with AV block, as they maintain physiologic timing between atrial and ventricular contractions, reducing the risk of pacemaker syndrome and compared to single-chamber ventricular pacing (VVI mode). VVI pacing is reasonable (Class IIa, Level of Evidence B-R) in frail elderly s or those with chronic , where atrial synchronization is not feasible, offering simplicity and lower procedural complexity. Implantation timing is critical; for instance, in postoperative settings after , permanent pacing is advised if high-grade AV block persists beyond 7-14 days, with earlier intervention considered for symptomatic cases. 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. 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. 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 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 where rate control is needed, intentionally creating complete AV block to prevent rapid ventricular rates. 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.

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. 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 (adjusted 2.06). 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. 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 , and rarely progresses to complete heart block in asymptomatic individuals without structural heart disease. It often resolves when the underlying cause is addressed, such as during recovery from acute or electrolyte correction. In contrast, Mobitz type II block carries a higher , 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. 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. Third-degree (complete) AV block represents the most severe form, with poor if untreated due to profound and risk of ; untreated cases have high mortality, with approximately 37% five-year survival, heavily influenced by comorbidities and etiology, such as lower rates in acute settings. 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. Prompt pacing is essential, as it significantly reduces mortality and restores near-normal in otherwise healthy individuals. varies by block location; AV nodal blocks generally have better outcomes than infranodal blocks, which are more likely to progress.

Complications

Untreated infra-Hisian heart block carries a significant of sudden cardiac due to episodes of or associated ventricular arrhythmias, with studies indicating an annual incidence of approximately 1-2% in the absence of pacing. This is particularly elevated in conditions involving bifascicular or complete infra-Hisian conduction delay, where unreliable escape rhythms can lead to hemodynamic collapse. Pacemaker implantation substantially mitigates this danger by maintaining atrioventricular synchrony and preventing bradycardic pauses. Chronic from can precipitate through reduced and ventricular dyssynchrony, with up to 23% of patients with high-degree block presenting with decompensated , often linked to impaired left ventricular compliance and diastolic rather than systolic dysfunction alone. This progression underscores the need for timely intervention to restore physiologic heart rates and preserve myocardial function. Pacemaker therapy, while effective, introduces device-related complications in approximately 5% of implants, including lead fractures and mechanical failures that may necessitate revision. 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. Inappropriate pacing or shocks, though less common in pure pacemakers, can arise from lead dislodgement or sensing errors, contributing to overall morbidity.

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