Second-Degree Atrioventricular Block 

Second-degree atrioventricular (AV) block, or second-degree heart block, is a disorder characterized by disturbance, delay, or interruption of atrial impulse conduction to the ventricles through the atrioventricular node (AVN). Electrocardiographically, some P waves are not followed by a QRS complex. The AV block can be permanent or transient, depending on the anatomic or functional impairment in the conduction system.

Second-degree AV block is mostly classified as either Mobitz I (Wenckebach) or Mobitz II AV block. The diagnosis of Mobitz I and II second-degree AV block is based on electrocardiographic (ECG) patterns, not on the anatomic site of the block. Precise localization of the site of the block within the specialized conduction system is, however, critical to the appropriate treatment of individuals with second-degree AV block.

Mobitz I second-degree AV block is characterized by a progressive prolongation of the PR interval. Ultimately, the atrial impulse fails to conduct, a QRS complex is not generated, and there is no ventricular contraction. The PR interval is the shortest in the first beat in the cycle.

Mobitz II second-degree AV block is characterized by an unexpected nonconducted atrial impulse, without prior measurable lengthening of the conduction time. Thus, the PR and R-R intervals between conducted beats are constant.^{[1, 2]}

Besides Mobitz I and II, other classifications used to describe forms of second-degree AV block are 2:1 AV block and high-grade AV block. By itself, a 2:1 AV block cannot be classified as either Mobitz I or Mobitz II, because only 1 PR interval is available for analysis before the block. Both a 2:1 AV block and a block involving 2 or more consecutive sinus P waves are sometimes referred to as high-grade AV block. In high-grade AV block, some beats are conducted, in contrast to what is seen with third-degree AV block.

Mobitz I second-degree AV block most often results from conduction disturbances in the AVN (~70% of cases); however, in a minority of cases (~30%), it may be due to infranodal block.

Mobitz I block is rarely secondary to AVN structural abnormalities when the QRS complex is narrow in width and no underlying cardiac disease is present. In this setting, Mobitz I block can be vagally mediated and may be observed in conditions associated with relative activation of the parasympathetic nervous system, such as in well-trained athletes, cardiac glycoside (ie, digoxin) excess, or neurally mediated syncope syndromes.

A vagally mediated AV block occurs in the AVN when vagal discharge is enhanced (eg, as a result of pain, carotid sinus massage, or hypersensitive carotid sinus syndrome). Accordingly, vagally mediated AV block can be associated with ECG evidence of sinus slowing. High vagal tone can occur in young patients or athletes at rest.^[1] Mobitz type I AV block has been described in 2-10% of long distance runners.^[3]

A vagally mediated AV block improves with exercise and may occur more commonly during sleep, when parasympathetic tone dominates. If an increase in sympathetic tone (eg, exercise) initiates or exacerbates a type I block, infranodal block should be considered.

Infrequently, Mobitz I AV block can occur with a block localized to the His bundle or distal to the His bundle. In this situation, the QRS complex may be wide, and the baseline PR interval is usually shorter with smaller PR increments preceding the block. The presence of a narrow QRS complex suggests the site of the delay is more likely to be in the AVN; however, a wide QRS complex may be observed with either AVN or infranodal conduction delay.^[1] Mobitz I block with infranodal block carries a worse prognosis than AVN block.

In Mobitz type II block, the conduction delay generally occurs infranodally. The QRS complex is likely to be wide, except in patients where the delay is localized to the bundle of His. The typical infranodal location of a Mobitz II block is associated with a higher risk to the patient.

Cardioactive drugs are an important cause of AV block.^{[4, 5, 6]} They may exert negative (ie, dromotropic) effects on the AVN directly, indirectly via the autonomic nervous system, or both. Digoxin, beta-blockers, calcium channel blockers, and certain antiarrhythmic drugs have been implicated in second-degree AV block.

Of the antiarrhythmic medications that may cause second-degree AV block, sodium channel blockers, such as procainamide, cause more distal block in the His-Purkinje system. Persistent second-degree AV block following adenosine infusion for nuclear stress testing has been reported.^[7]

The AV block may not resolve in many of the patients who take cardioactive medications. This suggests an underlying conduction disturbance in addition to the medications as the etiology of the AV block. At toxic levels, other pharmacologic agents, such as lithium, may be associated with AV block. Benzathine penicillin has been associated with second-degree AV block.^[8] Presynaptic alpha agonists (eg, clonidine) may rarely be associated with, or exacerbate, AV block.

Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders have been associated with AVN block, as follows.

• Inflammatory diseases -Endocarditis, myocarditis, Lyme disease,^[9] acute rheumatic fever
• Infiltrative diseases -Amyloidosis, hemochromatosis, sarcoidosis (AV conduction abnormalities can be the first sign of sarcoidosis^[10] )
• Infiltrative malignancies, such as Hodgkin lymphoma and other lymphomas, and multiple myeloma^[11]
• Metabolic and endocrine disorders – Hyperkalemia, hypermagnesemia, Addison disease, hyperthyroidism, myxedema, thyrotoxic periodic paralysis^[12]
• Collagen vascular diseases -Ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, lupus erythematosus, Reiter syndrome, mixed connective tissue disease^[13]

Other conditions or procedures associated with AV block are as follows.

• Cardiac tumors
• Trauma (including catheter-related, especially in the setting of preexisting left bundle-branch block)
• Following transcatheter valve replacement
• Myocardial bridging^[14]
• Ethanol septal reduction (also called transcoronary ablation of septal hypertrophy for the treatment of obstructive hypertrophic cardiomyopathy)
• Transcatheter closure of atrial and ventricular septal defects^{[15, 16]}
• Corrective congenital heart surgery, especially those near the septum
• Progressive (age-related) idiopathic fibrosis of the cardiac skeleton
• Valvular heart disease complications, especially aortic stenosis and aortic valve replacement surgery
• Following some catheter ablation procedures
• Obstructive sleep apnea^[17]
• Muscular dystrophies
• Acute ethanol poisoning
• Acute myocardial infarction (MI)

Any cardiac tumor has the potential for affecting the AVN if it will be in close anatomic relation with the node. Myxoma is the most common primary cardiac tumor, but a variety of secondary tumors may also be found in the heart. Cho et al reported a patient with primary cardiac lymphoma who presented with unexplained dyspnea and a progressive AV block.^[4]

Erkapic and colleagues studied the incidence of AV block after transcatheter aortic valve replacement and found that up to 34% of patients (mean age, 80 ± 6 years) experienced second- and third-degree AV block, mainly within the first 24 hours of the procedure.^[18] They did not observe any improvement in the AV block within the next 14 days, and most of these patients required permanent pacemaker implantation.

In this report, preoperative right bundle-branch block and CoreValve prosthesis were associated with higher rate of AV block and subsequent pacemaker implantation.^[18] On the basis of this report, the rate of postoperative AV block seems significantly higher in transcatheter valve replacement than a traditional surgical approach.

Nardi and colleagues reported pacemaker implantation in only 3% of patients undergoing isolated aortic valve replacement.^[19] Nevertheless, patients who undergo transcatheter valve replacement are much sicker and older than those who undergo a traditional surgical valve replacement (80 ± 6 years in the Erkapic study compared with 69 ± 12 years in the Nardi study).

Catheter ablation of any structure close to the AVN can be associated with AV block as an adverse effect of this procedure. In particular, AV block may be seen following ablation for AV nodal reentrant tachycardia (AVNRT) and some accessory pathways. Bastani and colleagues suggest that cryoablation of superoparaseptal and septal accessory pathways may be a safer alternative to radiofrequency ablation in this regard.^[20]

The conduction defects in patients with muscular dystrophy are progressive; therefore, these patients should undergo careful workup and follow-up, even if they present with a benign conduction defect such as first-degree AV block.^[21]

Acute ethanol poisoning has been reported to be associated with transient first-degree AV block; however, a few case reports have shown occasional association with Mobitz I AV block and high-degree AV block.^[22]

Genetic factors

In some patients, AV block may be an autosomal dominant trait and a familial disease. Several mutations in the SCN5A gene have been linked to familial AV block. Different mutations in the same gene have been reported in other dysrhythmias such as long QT syndrome (LQTS) and Brugada syndrome. In LQTS, a pseudo 2:1 AV block may be seen as a result of a very prolonged ventricular refractory period. Nevertheless, a true 2:1 AV block with possible primary pathology in the AVN and conduction system has also been reported in LQTS.^[23]

In the United States, the prevalence of second-degree AV block in young adults is reported to be 0.003%. However, the rate is significantly higher among trained athletes.^[24] Nearly 3% of patients with underlying structural heart disease develop some form of second-degree AV block. The male-to-female ratio of second-degree AV block is 1:1.

The level of the block determines the prognosis. AV nodal blocks, which are the vast majority of Mobitz I blocks, carry a favorable prognosis, whereas infranodal blocks, whether Mobitz I or Mobitz II, may progress to complete block with a worse prognosis. However, Mobitz I AV block may be significantly symptomatic. When a Mobitz I block occurs during an acute MI, mortality is increased. Vagally mediated AV block is typically benign from a mortality standpoint but may lead to dizziness and syncope.

Mobitz I second-degree AV block is localized to the AVN and thus is not associated with any increased risk of morbidity or death, in the absence of organic heart disease. In addition, when the block is localized to the AVN, no risk of progression to a Mobitz II block or a complete heart block exists.^[25] However, the risk of progression to complete heart block is significant when the level of block is in the specialized His-Purkinje conduction system (infranodal).

Mobitz type II blocks do carry a risk of progressing to complete heart block, and thus are associated with an increased risk of mortality.^{[25, 1]} In addition, they are associated with MI and all its attendant risks. Mobitz II block may produce Stokes-Adams syncopal attacks. Mobitz I blocks localized to the His-Purkinje system are associated with the same risks as type II blocks.