Continuing Education Activity

Atrioventricular (AV) conduction is evaluated by assessing the relationship between the P waves and QRS complexes. Normally, there is a P wave that precedes each QRS complex by a fixed PR interval of 120 to 200 milliseconds. AV block represents a delay or disturbance in the transmission of an impulse from the atria to the ventricles. This can be due to an anatomical or functional impairment in the heart’s conduction system. This disruption in normal electrical activity can be transient or permanent, and then further characterized as delayed, intermittent, or absent. This activity describes the causes, pathophysiology, and diagnosis of atrioventricular block and highlights the role of the interprofessional team in the management of these patients.

Objectives:

• Recall the causes of AV block.
• Summarize the ECG features of atrioventricular block.
• List the treatment and management options available for atrioventicular block.
• Explain the interprofessional team strategies for improving care coordination and communication regarding the diagnosis and management of patients with atrioventricular block.

Introduction

Atrioventricular (AV) conduction is evaluated by assessing the relationship between the P waves and QRS complexes. Normally, there is a P wave that precedes each QRS complex by a fixed PR interval of 120 to 200 milliseconds. AV block represents a delay or disturbance in the transmission of an impulse from the atria to the ventricles. This can be due to an anatomical or functional impairment in the heart’s conduction system. This disruption in normal electrical activity can be transient or permanent, and then further characterized as delayed, intermittent, or absent. In general, there are three degrees of AV nodal blocks: first degree, second degree (Mobitz type 1 or 2), and third-degree.[1][2][3]

Etiology

Higher degrees of AV block than those seen from increased vagal tone often suggest some underlying pathology. This is known as a pathophysiologic AV block. About half of such cases are a result of chronic idiopathic fibrosis and sclerosis of the conduction system as seen in Lenegre’s disease[4] and Lev's disease [5]

Another common source is ischemic heart disease which is responsible for around 40 percent of cases of AV block [6]. 

AV block is also associated with cardiomyopathies, including hypertrophic obstructive cardiomyopathy and infiltrative conditions such as sarcoidosis and amyloidosis. Infectious causes such as Lyme disease, rheumatic fever, endocarditis, viruses as well as autoimmune disease such as systemic lupus erythematosus should also be explored [7][8][9][10].

Other potential triggers include cardiac surgery, medications, and inherited conditions [11].

Epidemiology

There have not been large population-based studies on the prevalence of AV blocks. One study suggested that First-degree AVblock was more prevalent in African-American patients compared with Caucasian patients in all age groups except in the eighth decade of life[12]. However, at this time, there is no well-characterized large study about the correlation between different types of AV block with age, racial, or gender. AV block is sometimes seen in athletes and in patients with congenital heart disorders.

Pathophysiology

First degree AV block can originate from various locations within the conduction system. The levels of conduction delay include the atrium, AV node (most common in first-degree heart block), Bundle of His, bundle branches, fascicles, Purkinje system. Mobitz type I second degree AV block usually occurs within the AV block while Mobitz type II second degree AV block mainly originates from conduction system disease below the level of the AV node (in the bundle of His and in the bundle branches). In third-degree AV block, no atrial impulses could reach the ventricle- it can occur in the AV node or in the infranodal specialized conduction system. [13] 

Toxicokinetics

 The following medications can affect different levels of conduction delay: 

• Increased parasympathetic tone, digoxin (which upgrades vagotonic action), calcium channel blockers (which obstructs the inward calcium current responsible for depolarization) and beta-blockers can affect the AV node 
• Medications such as procainamide, quinidine, and disopyramide can block sodium channels and delay conduction in the bundle of His
• Similarly though rarely, medications such as procainamide, quinidine, and disopyramide can also delay infra-Hisian conduction system 

History and Physical

History taking for patients with concerns for AV block should include: 

• History of heart disease, both congenital and acquired
• Full list of medications and dosing. Particular drugs of interest include beta-blockers, calcium channel blockers, antiarrhythmic drugs, digoxin
• Recent cardiac procedure 
• Signs and symptoms associated with other systemic diseases associated with heart block (amyloidosis, sarcoidosis) 
• Baseline exercise capacity 
• Potential expose to tick bites

 The following symptoms should raise concerns: 

• Dyspnea
• Fatigue
• Chest pain
• Presyncope or syncope
• Sudden cardiac arrest 

Evaluation

First degree. In first-degree AV block, the P waves always precede the QRS complexes, but there is a prolongation of the PR interval. That is, the PR interval will be greater than 200 milliseconds in duration without any dropped beats. There is a delay, without interruption, in conduction from the atrium to the ventricle. In other words, while the impulse is slowed, it is still able to get through to the ventricles. All atrial activation is eventually transmitted to the ventricles. The delay is typically due to a minor AV conduction defect occurring at or below the AV node. If the PR interval is more than 300 milliseconds, it is considered “marked” first-degree AV block and the P waves may be buried in the preceding T wave.

• Causes. There are multiple causes of first-degree AV block, including simply being a normal variant. Other causes include inferior myocardial infarction (MI), increased vagal tone (e.g., athletes), status post-cardiac surgery, myocarditis, hyperkalemia, or even medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).
• Clinical significance. This is a benign entity that does not result in any hemodynamic instability. No specific treatment is required.

Second degree (incomplete). Second-degree or incomplete AV block occurs when there is intermittent atrial to ventricle conduction. That is, the P waves are sometimes related to the QRS complexes. It often occurs in a regular P:QRS pattern with ratios of 2:1. 3:2, 4:3, 5:4, and so forth. Second-degree AV blocks can be further classified into Mobitz type 1 (Wenckebach) or Mobitz type 2, which can be distinguished by examining the PR interval.

Second degree, Mobitz type 1 (Wenckebach). In second-degree Mobitz type 1 AV block, there is a progressive prolongation of the PR interval, which eventually culminates in a non-conducted P wave. It is often evident by clustering of QRS complexes in groups that are separated by non-conducted P waves. The greatest increase in PR interval prolongation is often between the first two beats of the cycle. While the PR interval continues to prolong with each beat of the cycle, the subsequent PR lengthening is progressively shorter. Even though the PR interval is progressively increasing in duration, the PP interval remains relatively unchanged. One way to confirm the presence of this is by noticing that the PR interval after the dropped beat is shorter than the PR interval that came before the dropped beat. In other words, the PR interval before the dropped beat is the longest of the cycle, and the PR interval after the dropped beat is the shortest as the cycle starts over.

• Mechanism. This is usually a result of a reversible conduction block at the level of the AV node. In fact, studies have shown that the site of block is likely at the crest of the AV node, where the atrium and AV node meet. There is typically a functional suppression of AV conduction. The AV nodal cells seem to progressively fatigue until they fail to conduct an impulse to the ventricles and a dropped beat occurs.
• Causes. There are multiple causes of second-degree Mobitz type 1 (Wenckebach) AV block, including reversible ischemia, myocarditis, increased vagal tone, status post-cardiac surgery, or even medications that slow AV nodal conduction (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).
• Clinical significance. Differentiating between second-degree Mobitz type 1 (Wenckebach) and Mobitz type 2 AV blocks is important as the management and treatment is different. Mobitz type 1 is often a benign rhythm. Most patients are asymptomatic, and there is tends to be minimal hemodynamic disturbance. The risk of Mobitz type 1 (Wenckebach) progressing to third-degree (complete) heart block is much lower than Mobitz type 2. Patients that are asymptomatic do not require treatment and can be monitored on an outpatient basis. Patients that are symptomatic typically respond to atropine and rarely require permanent cardiac pacing. Medication-induced impairment of AV conduction is often reversible after stopping the offending agent.

Second degree, Mobitz type 2. In second-degree Mobitz type 2 AV block, there are intermittent non-conducted P waves without warning. Unlike Mobitz type 1 (Wenckebach), there is no progressive prolongation of the PR interval; instead, the PR interval remains constant, and the P waves occur at a constant rate with unchanged P-P intervals. Because the P waves continue to occur at normal intervals, the R-R interval surrounding the dropped beat is simply a multiple of the preceding R-R interval and remains unchanged.

• Mechanism. Whereas in Mobitz type 1 there was a reversible block at the level of the AV node, in Mobitz type 2 the block occurs further along the electrical conduction system below the AV node. It can occur at the level of the His Bundle, both bundles branches, or the three fascicles (i.e., the left anterior fascicle, left posterior fascicle, and right bundle branch).
• In this case, the cells don’t progressively fatigue, but rather abruptly and unpredictably fail to conduct a supraventricular impulse. This is often the result of structural damage to the conduction system, such as from MI, fibrosis, or necrosis. Many patients have a pre-existing left bundle branch or bifascicular block, and the remaining fascicle intermittently fails to conduct causing the second degree AV block.
• Because the defect occurs below the AV node and often times distal to the His Bundle, it produces wide, bizarre-appearing QRS complexes. In the remaining cases, the defect is located within the Bundle of His, resulting in the normal, narrow QRS complexes. There can be a fixed P:QRS relationship (e.g., 2:1, 3:1) or no pattern at all.
• Causes. Common causes of second-degree Mobitz type 2 AV block include anterior MI, causing septal infarction with necrosis of the bundle branches. Other causes include idiopathic fibrosis of the conducting system, autoimmune (e.g., systemic sclerosis or systemic lupus erythematosus) or inflammatory (e.g., myocarditis, Lyme disease, or rheumatic fever) conditions, infiltrative myocardial disease (hemochromatosis, sarcoidosis, or amyloidosis), electrolyte imbalance (e.g., hyperkalemia), medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blockers, digitalis, adenosine, or amiodarone), or status post-cardiac surgery (e.g., mitral valve repair).
• Clinical significance. Mobitz type 2 AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole. Because the onset of dropped beats can occur abruptly and unexpectedly, hemodynamic instability and the consequential syncope and potential sudden cardiac death can occur at any moment. Thus, patients require a permanent pacemaker. While Mobitz type 1 can improve with atropine, giving atropine in the setting of Mobitz type 2 can worsen the block and increase the risk of complete heart block or asystole.

Note in cases in which every other QRS complex is dropped, there are never two consecutive PR intervals. Therefore, there is not enough information to evaluate the PR interval to further classify it as either second-degree Mobitz type 1 (Wenckebach) or Mobitz type 2 AV block. The site of block is also indeterminate.

Second degree, high-grade. High-grade AV block is a form of second-degree (incomplete) heart block that can commonly be confused with third-degree (complete) heart block. It occurs when there are two or more consecutively blocked P waves. This conduction disturbance can be particularly dangerous as it can progress to complete heart block. The anatomic region involved is almost always below the AV node as in Mobitz type 2. The P:QRS is 3:1 or higher and the ventricular rate is typically very slow. What differentiates high-grade AV block from the third-degree (complete) heart block is that there remains some relationship between the P waves and QRS complexes. In other words, there is still some AV conduction taking place.

Third-degree (complete). In third-degree, or complete, heart block there is an absence of AV nodal conduction, and the P waves are never related to the QRS complexes. In other words, the supraventricular impulses generated do not conduct to the ventricles. Instead, if ventricular conduction occurs, it is maintained by a junctional or ventricular escape rhythm. There is a complete dissociation between the atria and ventricles. The atria and ventricles conduct independent of each other. The P waves (atrial activity) are said to “march through” the QRS complexes at their regular, faster rate. The QRS complexes (ventricular activity) also occur at a regular, but slower rate. There are two independent rhythms occurring simultaneously. 

• Mechanism. Third-degree heart block is the end result of progressively worsening second-degree AV block. It can be from Mobitz type 1 if the AV nodal cells fatigue to a point in which they no longer conduct impulses through to the ventricles; or from Mobitz type 2, where there can be an abrupt and complete conduction failure throughout the His-Purkinje system. Because third-degree heart block can occur above or below the AV node, two different rhythms can take over. If it occurs above or at the crest of the AV node, a junctional rhythm will take over and drive the ventricles. The resulting QRS complexes will be narrow and occur at the intrinsic rate of the AV node (40 to 55 beats/minute). Whereas if the block occurs below the AV node, a ventricular pacemaker must take over. In such cases, the QRS complexes will be wide and at the intrinsic rate of the ventricular pacemaker (20 to 40 beats/minute).
• Causes. Complete heart block is often the result of the same causes as Mobitz type 1 and Mobitz type 2. Other causes include inferior MI, degeneration of the conduction system, and AV-nodal blocking agents such as beta-blockers, non-dihydropyridine calcium channel blockers, adenosine, digitalis, and amiodarone.
• Clinical significance. Patients with complete heart block are at a greater risk of developing asystole, ventricular tachycardia, and sudden cardiac death. Insertion of a permanent pacemaker is required.

AV dissociation. AV dissociation occurs when there is no relationship between the P waves and QRS complexes; however, the QRS complexes occur at a faster rate than the P rate. Unlike AV block, in which failure of an intrinsically more rapid atrial rhythm to conduct antegrade and supersede a slower ventricular rhythm is abnormal, failure of a rapid ventricular rhythm to conduct retrograde and supersede a slower atrial rhythm does not necessarily imply damage to the conducting system. In fact, AV dissociation with more rapid ventricular rates is typically due to unusual ventricular irritability.

Treatment / Management

In general, patients that present with first-degree or second-degree Mobitz type 1 AV block do not require treatment. Any provoking medications can be removed, and patients can be monitored on an outpatient basis. However, patients with higher degrees of AV block (Mobitz type 2 AV block, 3rd degree) tend to have severe damage to the conduction system. They are usually at a much greater risk of progressing into asystole, ventricular tachycardia, or sudden cardiac death. Hence, they require urgent admission for cardiac monitoring, further evaluation, consideration of a backup temporary cardiac pacing on a case-to-case basis, and eventually the insertion of a permanent pacemaker.[14][15][16][17]. There is modest evidence and strong clinical consensus that patients with persistent second or third-degree AV block must receive permanent cardiac pacing therapy. The evidence is modest and the consensus is weak for patients who have persistent bifascicular block (with or without underlying first degree AV block) associated with transient AV block or with prolongation of PR interval.

Use of an urgent or emergent temporary transvenous pacemaker should not be a "knee jerk" reaction to the presence of a second-degree, high grade or third-degree AV block. It should be considered after a careful evaluation of the risk-benefit ratio in clinical settings, consideration of hemodynamic stability (as gauged by the evaluation of systolic blood pressure and the degree and duration of patient's clinical symptoms), level of AV block and presence of the type of escape rhythm. 

 Complications are very common in patients treated with placement of a temporary transvenous pacemaker. The complications are not just related to the implant itself but also related to the care post-implant including the change of position of the lead, change of capture threshold, pacer malfunction, faulty programming and/or battery depletion of the pacer box. Complications may also be related to accidental extraction of the lead by the patient. The use of a temporary pacer should be kept to the shortest duration possible in order to avoid patients' risk of immobility, infection, thromboembolism and risk of cardiac perforation. The potential complications must be kept in mind as sometimes the risk-benefit ratio may significantly outweigh justifying its potential use.  European Task force guidelines and other expert consensus usually strongly leans towards  the fact that temporary transvenous pacing should be avoided as far as possible and the treatment time should be kept as brief as possible [19].

Based on the European Guidelines and a Wide Expert Consensus

1. Temporary transvenous pacer should not be used routinely as a knee-jerk reaction in AV block and preferably used as a last resort when response to positive chronotropic drugs such as isoproteronol, epinephrine or low-dose dopamine is insufficient.2. Temporary transvenous pacing should be ideally limited to cases of : (i) high-degree AV block without a stable escape rhythm (ii) life-threatening bradyarrhythmias, that may occur during interventional procedures such as percutaneous coronary intervention, or, rarely, in acute settings such as acute myocardial infarction, drug toxicity or in a condition with a concomitant systemic infection where permanent pacing device should ideally be delayed until clearance of infection. For example, patients with a stable blood pressure and a persistent junctional escape rhythm or even a persistent ventricular escape rhythm or those with a subacute onset can be monitored carefully on telemetry. 3. If the indication for permanent pacing is definitely established, every effort should be made to implant a permanent pacer as soon as possible. The general expert notion is that routine implantation of a temporary pacer before a permanent pacer may increase the risk of complications such as device infection of a permanent implant, other risk of possible complications related to two invasive procedures instead of one and also potentially increases risk of cardiac perforation especially in cases with extended delay between temporary pacer and permanent pacer lead implantation. [18][19]

Differential Diagnosis

Once diagnosed, underlying causes should be evaluated that include ischemic workup, autoimmune diseases in young patients that can cause fibrosis of the conducting system, offending medications and electrolyte disturbances such as hyperkalemia. 

Prognosis

Prognosis depends on the various factors that include age and other chronic medical conditions such as diabetes mellitus, chronic kidney disease, underlying heart disease, and underlying types of AV block.  

Complications

Pacemaker infection is common in the elderly, especially with underlying medical conditions. Also, sometimes it can be challenging for pacemaker patients who need other studies like MRI for diagnosing other medical conditions such as stroke.

Deterrence and Patient Education

Patients with first-degree and asymptomatic Mobitz type 1 AV block usually can continue their usual activities but should be advised to avoid medications that can prolong PR interval Patients with Mobitz type 2 and third-degree AV block should discuss with their cardiologists about the need for pacemakers. All patients should be educated on alarming symptoms of hypoperfusion such as fatigue, lightheadedness, syncope, presyncope, or angina and seek timely medical treatment 

Enhancing Healthcare Team Outcomes

The management of heart block is best done with an interprofessional team because if the diagnosis is missed (esp higher degrees of heart block), the condition can have significant morbidity and mortality.

Patients with heart block may be encountered by the nurse practitioner, primary care provider, internist or the emergency department physician. Except for a first-degree heart block, the rest of the patients should be referred to a cardiologist for more definitive workup. Some of these patients may require a pacemaker which can be life-saving. Following treatment, the cardiology nurse should follow up on the patients to ensure that the heart rate has normalized and the patients have no symptoms.[20]

Anytime patients with a pacemaker undergo surgery, the cardiologist should be consulted first. In some cases, the pacemaker may have to be deactivated with a magnet to prevent interference from electrocautery. After surgery, the pacemaker has to be reprogrammed. Today, most centers have a pacemaker nurse who monitors these patients for complications. Only through a combined team approach can the morbidity of heart block be decreased.