Evaluation and Treatment of AV Block and Intraventricular Conduction Disturbances

I. AV Block and Intraventricular Conduction Disturbances. What every physician needs to know.

AV block, or atrioventricular block, is a major cause of significant bradyarrhythmias. To diagnose and manage AV block, it is important to have a basic understanding of the anatomy of the conduction system of the heart.

The AV node lies at the AV junctional area. At the distal end of the AV node, the penetrating portion is known as the His-bundle, which lies on the left side of the interventricular septum in most cases. The conduction fibers then continue in the left septum, and divide into the left bundle branch and right bundle branch.

Clinically, we think of the left bundle branch dividing into bifascicular subdivisions of anterosuperior and posteroinferior branches. However, anatomically there is much individual variability. The bundle branches end in the Purkinje fibers, which form a network over the surface of the endocardium of the ventricles.

Slowed conduction, or blocked conduction, can occur anywhere along the path of conduction fibers, and can generally be identified by EKG analysis. Infra-Hisian block is the most important to identify, since it is the cause of most cases of symptomatic complete heart block.

Acquired AV block is most commonly caused by idiopathic fibrosis, acute myocardial infarction, or drug effects. AV block can also be congenital. If AV block is symptomatic, and determined to be permanent, pacing is the only effective long-term therapy.

Conduction Terminology

Type I second-degree AV block = Mobitz I block = Wenckebach block

Type II second-degree AV block = Mobitz II block

Third-degree AV block = complete heart block

Left anterior fascicular block = left anterior hemiblock

Left posterior fascicular block = left posterior hemiblock

II. Diagnostic Confirmation: Are you sure your patient has AV Block?

Clinical criteria for confirming significant AV clock

• Complete heart block or advanced AV block seen on an EKG or ambulatory monitoring in the presence of symptoms.

• Block below the His-bundle or an HV internal >100 ms found during an invasive electrophysiology study in a patient with intermittent symptoms.

• Causes of temporary or reversible AV block have been ruled out.

A. History Part I: Pattern Recognition:

Hemodynamically important signs of AV block

• Hypotension

• Syncope or near-syncope

• New or worsening heart failure

• Dyspnea

• Angina

• Ventricular tachycardia (due to long Q–T)

• Change in mental status

• Worsening renal function

• Fatigue, or decrease in exercise tolerance

Patients with acquired complete heart block or high-grade AV block with two or more nonconducted P waves in a row, are usually symptomatic. Children with congenital complete heart block are generally asymptomatic, but tend to develop symptoms as adults. Concomitant structural heart disease, a wide QRS complex, or long Q–T interval increases the risk of symptoms in the congenital group.

Flectrocardiogram (EKG) shows a constant P–nckebach) block, bundle branch blocks or fascicular blocks rarely produce symptoms.

B. History Part 2: Prevalence:

First-degree AV block, with a P–R interval greater than 200 ms, is rarely found in young, healthy adults during activity. However, a longer P–R interval, and even Mobitz I (Wenckebach) block can be seen in young, well-conditioned individuals at rest and during sleep. The P–R interval decreases and the Wenckebach block disappears with increased activity, and is considered normal vagal influence on the AV node.

Acquired complete heart block is rarely seen in young adults without heart disease. The highest incidence of complete heart block is seen in the seventh decade, with a 60% male predominance. Congenital complete heart block has an incidence of one in 15,000 to 25,000 live births, with a 60% female predominance.

Left anterior fascicular block, or hemiblock, is the most commonly seen conduction abnormality of the intraventricular system with up to a 6% prevalence in the normal population. After left anterior hemiblock, the next most common abnormality of the intraventricular conduction system is right bundle branch block, followed by left bundle branch block and left posterior fascicular block, or hemiblock.

Causes of AV block

• Ischemic heart disease

• Antiarrhythmic drug effects

• Idiopathic fibrosis of the conduction system

• Valvular calcification or endocarditis

• Trauma to the conduction system

• Infiltrative cardiomyopathies

• Collagen vascular diseases

• Infectious or inflammatory diseases

• Metabolic

• Neurally mediated

• Endocrine

• Tumors that infiltrate the heart

• Neuromuscular diseases

• Congenital heart disease

There are many causes of AV block. Acute myocardial infarction (MI) is associated with varying degrees of AV block, and is the most common cause of acquired AV block.

The blood supply to the AV node is from the AV nodal artery, a branch of the right coronary artery in 90% of hearts, with the remaining 10% arising from the left circumflex coronary artery. The His-bundle has a dual blood supply from branches of the anterior and posterior descending coronary arteries. The bundle branches also have a dual blood supply from the left and right coronary arteries.

Complete heart block can occur with either an anterior or inferior acute MI. The site of block in an inferior wall MI is usually at the level of the AV node, resulting in a junctional escape rhythm with a ventricular rate of 50 to 60 bpm and a narrow QRS complex. By contrast, complete heart block in the setting of an acute anterior MI is usually due to infarction of the bundle branches. A ventricular escape rhythm of 30 to 40 bpm is seen with a wide QRS complex.

Antiarrhythmic drug effects are a common cause of acquired AV block. Calcium channel blockers and other antiarrhythmic drugs, such as amiodarone and dronedarone, slow conduction in the AV node.

Through their effect on the autonomic nervous system, digoxin and beta-blocking agents act indirectly on the AV node. Drugs that have significant sodium channel blocking effect, such as flecainide, slow conduction in the His-Purkinje system. This can result in infranodal block. When AV block occurs due to antiarrhythmic drug therapy, it is usually in patients with pre-existing conduction abnormalities.

The most common cause of acquired conduction system disease is idiopathic fibrosis. In the elderly population, Lev’s disease results in sclerosis of the left side of the cardiac skeleton, and affects the branching His bundle. Lenegre’s disease is thought to be a genetic hereditary disorder that can affect middle-aged people.

This degenerative process involves the more distal portions of the bundle branches. Both Lev’s and Lenegre’s diseases cause right bundle branch block and left anterior hemiblock in people without other cardiac abnormalities, and can eventually progress to complete heart block.

Mitral or aortic valve disease can cause AV block. In cases of valvular calcification, infective endocarditis, or valve replacement surgery, the frequency of AV block is greater with aortic than with mitral valve involvement.

Trauma to the conduction system can occur as a result of cardiac surgery. AV block is most frequently associated with aortic valve replacement, and is rarely seen post coronary artery bypass grafting, in the absence of concomitant MI or prolonged ischemia. Transcatheter aortic valve replacement (TAVR) carries a risk of producing AV block. The need for post procedural permanent pacemaker placement is higher (37.6%) with the self-expandable valve, compared to the balloon-expandable valve (17.3%).

Surgical repair of congenital heart defects in the region of the conduction system, such as endocardial cushion malformations, ventricular septal defects, and tricuspid valve abnormalities, can lead to transient or persistent AV block.

AV block is a complication in 1% to 2% of radiofrequency catheter ablations used to cure AV nodal reentrant tachycardia, or accessory pathways near the AV node.

Infiltrative cardiomyopathies and collagen-vascular diseases can also cause AV block. A variety of viral bacterial and parasitic etiologies of myocarditis can result in varying degrees of AV block. In the case of Lyme disease, transient complete heart block is commonly seen in patients with cardiac involvement.

Hyperkalemia and hypermagnesemia are reversible causes of AV block. Transient AV block can be seen with carotid sinus hypersensitivity and vasovagal syncope.

Other causes of acquired AV block include Addison’s disease and tumors that infiltrate the heart. Patients with neuromuscular diseases, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy, and peroneal muscle atrophy, can develop any degree of AV block which can unpredictably progress to complete heart block.

Congenital complete AV block can result from abnormal embryonic development of the AV node. The defect usually occurs proximal to the His-bundle, resulting in a narrow QRS complex.

In 50% of cases of congenital complete heart block, no other structural cardiac abnormalities are present. The other 50% have concurrent congenital heart disease, including corrected transposition of the great vessels, ventricular septal defects, ostium primum atrial septal defects, and Ebstein’s anomaly of the tricuspid valve. Congenital complete heart block can also be a result of maternal systemic lupus erythematosis.

C. History Part 3: Competing diagnoses that can mimic AV Block.

• Mobitz II, or Type II, second degree AV block, can be confused with a nonconducted premature atrial complex. In Mobitz II block, the electrocardiogram (EKG) shows a constant P–R interval, followed by a sudden failure of a P wave to be conducted to the ventricles.

  The P to P intervals remain constant and the pause, including the blocked P wave, equals two P to P intervals. In the case of a nonconducted premature atrial complex, the nonconducted P wave will be premature.

• Mobitz II can be difficult to differentiate from Mobitz I, or Wenckebach block, with only minimal P–R variation. Wenckebach block is usually due to block within the AV node, with a narrow QRS complex. On the other hand, Mobitz II is generally associated with a wide QRS complex, due to infranodal disease.

• If the nonconducted P waves are obscured by the T wave of the preceding conducted beat, 2:1 AV block can go unrecognized (Figure 1).

  Figure 1.

  Wenckebach block with a narrow QRS complex.

• Fixed 2:1 AV block makes the diagnosis of Mobitz I (Wenckebach) versus Mobitz II block difficult to confirm by surface EKG alone. If a narrow QRS is present, and Wenckebach block has also been recently seen, block at the level of the AV node is probably present. On the other hand, if 2:1 AV block is seen with a wide QRS complex, infranodal block is the most likely diagnosis.

• When complete heart block is seen, it is important to determine whether loss of conduction will be persistent, or whether the block is temporary. Reversible causes of complete heart block can be due to metabolic abnormalities, drug effects, Lyme disease, or vasovagal episodes. In these cases, the complete heart block resolves once the abnormality has been treated.

• In true complete heart block, the sinus rate is faster than the ventricular rate. If AV dissociation is seen, but the ventricular rate is faster than the sinus rate, a competing AV junctional or idioventricular rhythm may be present. This is due to slowing or failure of the sinus node, allowing a faster subsidiary escape focus to take over from the AV junction or ventricle.

• Left anterior or posterior fascicular blocks, or hemiblocks, can mimic or mask the EKG signs of a myocardial infarction, ischemia, or ventricular hypertrophy. It may be difficult to distinguish between left axis deviation caused by left anterior hemiblock, and left axis deviation due to other causes. Left anterior hemiblock can mimic left ventricular hypertrophy in leads I and AVL, while hiding signs of left ventricular hypertrophy in the left precordial leads.

The diagnosis of myocardial infarction is difficult in the setting of a bundle branch block. Left bundle branch block is especially problematic, including hemiblocks.

A left anterior hemiblock can produce an initial R wave in the inferior leads, concealing an inferior infarction. Likewise, a left anterior hemiblock can hide an anterior infarction by causing small R waves in the anterior precordial leads, if the heart is horizontal or the chest leads are positioned too low.

On the other hand, a left anterior hemiblock may show a small Q wave in the leads V2 and V3, leading to the assumption of a previous anterior myocardial infarction, or can produce Q waves in leads I and AVL, mimicking a lateral infarct. A left posterior hemiblock can hide the signs of an inferior myocardial infarction. This is particularly important since left posterior hemiblock can occur as a result of inferior wall ischemia.

D. Physical Examination Findings.

When AV block is present, the physical exam should focus on establishing the hemodynamic significance of the conduction abnormality. An evaluation of the patient’s mental status and level of consciousness is important.

The patient’s blood pressure, heart rate, respiratory rate, and overall appearance helps determine the urgency of treatment for the AV block. If the patient is febrile, this may suggest an infectious etiology of the conduction abnormality.

On the other hand, if the patient has an unrelated infection, this will need to be treated prior to implanting a permanent pacemaker. Physical signs of congestive heart failure should be evaluated, since their presence would prompt initiation of early therapy. One should listen for mitral or aortic regurgitant murmurs, since valvular disease can result in AV block. A target lesion resulting from a tick bite suggests Lyme disease as the cause of AV block.

E. What diagnostic tests should be performed?

EKG (interpretation)/Monitors/EPS

The surface EKG is our most important tool for the diagnosis of AV block and intraventricular conduction disturbances. First-degree AV block is seen as a P–R interval >200 ms and each P wave is followed by a QRS complex with a constant, prolonged interval (Figure 2).

Figure 2.

The conduction delay is usually within the AV node, but can be anywhere in the system. When first-degree AV block is associated with a narrow QRS complex, the delay is within the AV node a majority of the time. However, when bundle branch block is present, an intracardiac electrogram is needed to localize the site of the block.

Second-degree Mobitz I block is also known as Wenckebach block. The classic features on the surface EKG are progressive lengthening of the P–R interval until an atrial impulse fails to be conducted to the ventricles. The P–R interval immediately post block returns to its baseline interval, which is shorter than the last conducted P–R interval.

Wenckebach block is almost always within the AV node when a narrow QRS complex is present (Figure 3). In the setting of a bundle branch block, the Mobitz I block could be below the His-bundle, but is still more likely to be in the AV node. An intracardiac electrogram would be needed to accurately localize the level of block.

Figure 3.

When Wenckebach block is in the AV node, progressive prolongation of the A-H interval is seen until an atrial deflection is not followed by a His-bundle or ventricular deflection. In the case of Wenckebach, due to block below the His-bundle, progressive prolongation of the H-V interval is followed by a His-bundle deflection without an associated ventricular depolarization.

Second-degree, or Mobitz II, AV block is seen on the surface EKG as constant P–R intervals, followed by a sudden failure of conduction of the P wave to the ventricles. The P–P intervals remain constant and the pause, including the blocked P wave, equals two P–P intervals.

Mobitz II block is usually associated with bundle branch block or bifascicular block. In most cases the block is within or below the His-bundle. It is rare to see Mobitz II with a narrow QRS interval (Figure 4). When present, the block is intra-Hisian.

Figure 4.

An intracardiac electrogram can help confirm the site of block as infranodal. The blocked cycle will show atrial and His-bundle deflections without a ventricular depolarization. The conducted beats usually show infranodal conduction system disease, with a prolonged H-V interval or a split His-bundle potential.

When fixed 2:1 AV block is seen on a surface EKG, it can represent either Mobitz I or Mobitz II block. If a narrow QRS complex is present, Mobitz I is suspected. If a wide QRS complex is seen, the block is likely infranodal. An intracardiac electrogram at the region of the His-bundle would be needed to make a definitive diagnosis.

High degree, or advanced AV block, is characterized by two or more nonconducted consecutive P waves on the surface EKG. When the QRS complexes of the adjacent conducted beats are narrow, the block is usually at the AV node.

When the block is at this level, atropine can improve the block and produce 1:1 AV conduction. If the adjacent beats are conducted with a bundle branch block, and no improvement in the advanced AV block is seen with atropine, this points toward a block in the His-Purkinje system.

When third-degree AV block, or complete AV block is seen on the surface EKG, the P waves are completely dissociated from the QRS complexes. The atrial rate is faster than the ventricular rate, and the atrial impulse is never conducted to the ventricles.

Different levels of block are possible with complete heart block, and the level of the block determines the QRS morphology along with the rate of the escape rhythm. When the block is within the AV node, the QRS complex is narrow with an escape rate of 40 to 60 bpm.

In the intracardiac tracings, the His-bundle potential consistently precedes each ventricular electrogram. The atrial electrograms are completely dissociated from the H-V complexes.

Block in the His-Purkinje system results in a wide QRS complex and a ventricular escape rate between 20 and 40 bpm (Figure 5). The corresponding intracardiac electrogram shows a His-bundle deflection after each atrial signal, but the ventricular electrogram is completely dissociated from these.

Figure 5.

When conduction abnormalities are intermittent, they may require more prolonged monitoring to document the rhythm present with symptoms. Holter monitors or loop recorders may then be useful. When syncopal episodes are months apart, and conduction abnormalities are considered a possible etiology, an implantable loop recorder may help in the diagnosis.

Determining the site of AV block is important, since prognosis and treatment depends on whether AV block is at the level of the AV node or His-Purkinje system. As described above, the EKG is a valuable tool. However, other noninvasive diagnostic techniques can also be helpful, such as vagal maneuvers, exercise, or administration of atropine.

These methods take advantage of the differences in autonomic innervation of the AV node versus the His-Purkinje system. The AV node is well innervated by both the sympathetic and parasympathetic nervous systems, but the His-Purkinje system is minimally influenced by the autonomic nervous system.

Carotid sinus massage increases vagal tone, which worsens the block at the AV node. In contrast, carotid sinus massage improves infranodal block due to slowing of atrial impulses conducted through the AV node.

Exercise or atropine improves AV nodal conduction due to sympathetic stimulation. On the other hand, these maneuvers worsen infranodal block by increasing the rate of atrial impulses conducted through the AV node.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Laboratory studies should be aimed at revealing possible reversible causes of AV block. Hyperkalemia, usually associated with acute renal failure, should not be overlooked.

Once the potassium level is corrected, the AV block should resolve. If the patient is taking an antiarrhythmic drug while being found to have AV block, a drug level can be obtained.

However, laboratory testing is not available for every drug, and when it is an option, there may be a delay of days before the results are known. A digoxin level can be obtained, and the results can be available on the same day.

It should be noted that digoxin can cause AV block even when the level is not in the toxic range. Levels of flecainide or amiodarone can take over a week to be processed. In a patient with AV block where Lyme disease is a possibility, Lyme titers can be obtained.

Preliminary results will be available in 3 to 4 days. If other infectious processes are suspected, the appropriate cultures should be obtained, as well as a white blood count with differential.

In all patients where temporary or permanent pacing is being considered, coagulation studies consisting of a platelet count, protime, and INR (international normalized ratio) should be evaluated. Additionally, a hemoglobin and hematocrit should be obtained to check for the presence of anemia. Significant abnormalities would need to be corrected prior to an invasive procedure being planned.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

When a patient presents with AV block, a chest radiograph can provide information regarding possible pulmonary or cardiac problems. Pneumonia or pulmonary edema can be seen, as well as evidence of cardiac chamber enlargement. Also, a baseline chest radiograph is recommended prior to proceeding with placement of a permanent pacemaker.

A cardiac echo is useful in patients with AV block to look for possible structural abnormalities and to evaluate heart function. Evidence of ischemic heart disease or valvular disease can be seen.

If a cardiomyopathy is present with a low ejection fraction, a patient needing a permanent pacemaker may need a device with defibrillation capability. In a patient with a congenital heart defect, the echo is essential to knowing whether transvenous pacing leads can be successfully placed.

III. Management.

Determine if the heart block is symptomatic. Once the diagnosis of the type of heart block is made, it is important to assess how symptomatic the patient is.

Symptoms are important in determining whether permanent pacing is needed. Many times patients are asymptomatic at rest, but have significant symptoms with exertion. The risk of syncope with trauma should be assessed. The patient with hemodynamic compromise requires more immediate urgent therapy.

Determine if the heart block is reversible. Before implanting a permanent pacemaker, it is important to look for potential reversible causes of heart block.AV nodal blocking agents and antiarrhythmic drugs should be stopped, if possible, to see if the block improves.

Electrolytes and renal function should be evaluated. Heart block can occur in the setting of acute renal failure with hyperkalemia. Once the electrolytes are corrected and the patient is dialyzed, the heart block resolves.

Lyme disease should be suspected, especially in a young person with sudden onset of complete heart block, who has been in an endemic area. In these patients, the heart block may be impressive, but always resolves within several days to 2 weeks.

Varying degrees of AV block occur in the majority of patients who develop myocarditis from Lyme disease. If Lyme disease is suspected, the placement of a permanent pacemaker should be delayed until the laboratory data is known, which takes several days.

A. Immediate management.

Immediate management

Once it has been determined that the patient has symptomatic AV block that is not reversible, pacing should be established as soon as possible. If a permanent pacemaker can be placed within a reasonable period of time, this is ideal.

If the patient is too hemodynamically unstable to wait for the permanent implant, a temporary pacing wire should be placed. At times drug therapy is needed if temporary pacing is delayed or cannot be accomplished.

Medical therapy

There is no effective long-term medical therapy for symptomatic AV block. However, drug therapy is sometimes useful as a short-term emergency measure, until either temporary or permanent pacing can be initiated.

Atropine 1 mg IV can temporarily improve symptomatic AV block. However, when a wide QRS escape rhythm is present, infranodal block should be suspected.

Atropine will either not be effective in this setting or will worsen the block. As an alternative to atropine, dopamine infusion can be used. Epinephrine or isoproterenol infusions can also be used when there is not a potential for ischemia. When using any of these drugs, external pacing should be available in case the drug worsens the AV block or is ineffective.

Temporary pacing

In the presence of symptomatic second- or third-degree AV block, placement of a temporary pacing wire is usually required if infranodal block is present.

Indications for Temporary Pacing

• Symptomatic complete heart block (congenital or acquired)

• Symptomatic second-degree AV block

• Acute MI (regardless of symptoms)

  Complete heart block

  Alternating bundle branch block

  New bundle branch block with transient complete heart block

• Complete heart block with long Q–T and resulting ventricular tachycardia (VT)

In the case of symptomatic congenital or acquired complete heart block, permanent pacing should be instituted as soon as feasible. Some patients with newly acquired complete heart block will have a long Q–T interval and a resulting ventricular tachycardia. Temporary pacing at a rate above 85 bpm is then required to shorten the Q–T interval and prevent the ventricular tachycardia.

Temporary pacing should also be used in patients with symptomatic heart block that is expected to be temporary, as in drug toxicity, electrolyte abnormalities, or Lyme disease.

AV block can occur in the setting of an acute MI. Patients with complete heart block, alternating bundle branch block, or new bundle branch block with transient complete heart block should be temporarily paced, even if they are asymptomatic.

Heart block associated with an inferior wall MI is usually proximal to the His-bundle and transient, whereas AV block secondary to an anterior wall MI is more distal to the His-bundle and often persists. Many times when the patient presents with an acute MI, they are taken to the cardiac catheterization lab. If heart block is noted while in the lab, a temporary pacing wire can be placed at that time.

Heart block can be temporarily or persistently seen post valve surgery, especially aortic valve replacement. If the patient will be at risk for heart block postoperatively, the surgeon generally places temporary epicardial pacing wires.

Risks of Temporary Pacing

In patients with asymptomatic complete heart block, with the exception of those post-MI or postoperative complete heart block, the risks of a temporary wire can be greater than the benefit. The hemodynamic significance of the complete heart block should be fully assessed.

Not only is blood pressure an issue, but whether the patient shows signs of altered mental status, hypoxia, congestive heart failure, ischemia, or poor renal perfusion. If none of these signs are present, the patient can usually tolerate ventricular rates down to the 30s overnight until the permanent pacemaker can be placed the next day.

External transcutaneous pacing can be used as a backup for temporary pacing if the patient’s condition were to suddenly worsen. Although external pacing can be uncomfortable in a nonsedated patient, it can be used briefly until a transvenous pacing wire is placed. The safest approach is to briefly test the external pacing system on the patient to confirm capture, before pacing is needed.

There are risks associated with a temporary pacing wire. Dislodgement is the most common complication, since they are not active fixation leads. This can result in loss of capture and possible asystole. However, at our institution, we sometimes place an active fixation lead under fluoroscopy and use it as a temporary lead.

Perforation of the lead through the thin right ventricular wall is another potential complication. The risk increases with stiffer leads and decreases with balloon-tipped leads. Perforation can be suspected due to loss of pacing, diaphragmatic stimulation, or a right bundle branch block pacing pattern. Pericardial tamponade is the most serious consequence from perforation, and requires emergent pericardiocentesis.

When the access used is the subclavian or jugular vein, a pneumothorax can occur, which would require placement of a chest tube. Accidental access into the adjacent artery while trying to obtain venous access, can lead to bleeding complications, especially if the patient is on anticoagulants.

Bacteremia is another potential risk, and can lead to delay of the placement of a permanent pacing system. Even if a temporary wire is placed emergently, every effort must be made to maintain sterility. The risk of infection is significant if the wire is left in place for greater than a week. In the case of femoral access, the wire should be in place no longer than 2 to 3 days.

Venous Access Sites

When it is determined that a temporary pacing lead is required, it is important to not use the access site that would be preferred for permanent pacing leads. In a right-handed patient, permanent leads are usually placed via the left subclavian or axillary vein.

The right internal jugular vein provides the most direct approach for placement of the temporary pacing lead. It is best to avoid the subclavian veins if there is uncertainty as to which side will be used for permanent pacing, or if there is a history of subclavian occlusion in the past.

Femoral vein access generally requires fluoroscopy for lead placement. This access may be used when the temporary lead is placed at the time of cardiac catheterization. The patient must be immobilized while a femoral lead is in place.

In general, permanent pacing is indicated for AV block if symptoms are present. In some disease states, prophylactic pacing is recommended in asymptomatic patients due to the high risk of progression to complete heart block. These include patients post-MI, those with congenital heart disease, or with certain neuromuscular diseases.

Indication for Pacing in AV Block

Class I (general agreement in need for pacing)

• Symptomatic complete heart block (CHB)

• Asystole >3 seconds, or escape rhythm <40 BPM in awake, asymptomatic patient with CHB

• Symptomatic second-degree AV block (regardless of site of block)

• CHB with neuromuscular disease (with or without symptoms)

• Alternating bundle branch block

• Bifascicular block with intermittent CHB

• Bifascicular or trifascicular block with Mobitz II AV block

• Persistent second-degree AV block with bilateral bundle branch block, or CHB that is infranodal, after acute MI

• Transient advanced infranodal AV block with bundle branch block

• Congenital CHB with wide QRS, and complex ventricular ectopy or ventricular dysfunction

• Advanced AV block with symptoms, ventricular dysfunction or low cardiac output in patients with congenital heart disease

Device & Mode Selection for AV Block

Dual chamber pacing (DDD) is recommended for patients predominantly in sinus rhythm. Single chamber ventricular pacing (VVI) is used in patients with persistent atrial fibrillation. A single lead dual chamber VDD device is an option for a young patient with congenital AV block, who has normal sinus nodal function. Patients with chronotropic incompetence should also have the rate responsive feature programmed on.

B. Physical Examination Tips to Guide Management.

Once pacing is instituted, symptoms of AV block should resolve quickly. Refer to Section II. A. for hemodynamically important signs of AV block, and section II. D. for physical exam findings. Refer to section III. E. for possible complications of therapy.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Immediately postpacemaker placement an EKG should be performed, with and without magnet application. This documents proper sensing and capture of the pacing leads. A chest radiograph should also be done to document proper position of the leads and generator. A pneumothorax or lead perforation through the myocardium can also be identified.

D. Long-term management.

Patients with permanent pacemakers require routine follow-up of their device (see schedule below). Most implanting centers see patients in the device clinic 2 weeks postimplant. This allows assessment of the wound for proper healing, signs of infection, or hematoma. The function of the leads is also evaluated for possible dislodgement or acute rise in pacing threshold.

At this visit, the patient can be given a transtelephonic monitoring unit, or arrangements can be made for remote monitoring. At the 3-month post-op visit, the pacing threshold should be at the chronic level. Many times the output can be reprogrammed at this time to a lower voltage to help prolong battery life.

Patients will then receive periodic monitoring at home, transtelephonically or via remote transmission, and be seen in device clinic only once or twice a year. Transtelephonic monitoring gives limited information regarding the function of the leads, and is mainly used to detect battery end of life by the magnet rate.

Remote monitoring units can give as much information as an interrogation at a clinic visit. Both remote and transtelephonic monitoring can also be used to check the rhythm of patients’ experiencing a sudden change in symptoms.

The frequency of monitoring increases when the battery life reaches the final 18-month period. The pacemaker may also need more frequent monitoring if the generator or one of the leads is under an advisory by the manufacturer or FDA, and could experience earlier than expected failure.

Pacemaker follow-up schedule

Device Clinic Visits

2-weeks post-op:

• 3 months post-op

• Dual chamber: every 6 months

• Single chamber: every year

Plus: Transtelephonic Monitoring

Alternative Monitoring:

• 1-month post-op

• Every 3 months

• Monthly (starting when 18 months battery life reached)

Remote Monitoring (single and dual chamber)

• 3-month intervals

• Monthly (starting when 18 months battery life reached)

Plus:

• Yearly device clinic visits

E. Common Pitfalls and Side-Effects of Management

Permanent pacing is the only effective long-term therapy for symptomatic AV block. While the majority of patients enjoy a significant improvement in symptoms and lifestyle, there are adverse side effects that can occur from pacing. Many of these are unavoidable, but there are preventative measures that can be taken to reduce the incidence of problems.

Lead dislodgement is usually an early complication of pacemaker implantation. Most commonly this involves the atrial lead, since it lies in a “J” curve in the right atrium.

If evidence of an “injury current” is seen on the intracardiac electrogram of the atrial lead at the time of implant, there is more assurance the lead has good tissue fixation to the endocardium. Care should be taken to leave an ample amount of lead in the heart, since this “slack” will be needed when the patient is upright, and the diaphragm and chest structures drop.

It is also important to securely anchor the proximal end of the leads to the fascia in the pocket to prevent lead migration. Likewise, the pacemaker generator should be sutured to the pectoral fascia.

If it were to track downward in the prepectoral plane, the generator could pull the leads out of position in the heart. During the first month after implant, patients should be instructed to refrain from raising their arm (on the same side as the pacemaker) above shoulder level, as this could result in lead dislodgement.

Infection of the pacemaker system can occur early after implantation, or later as a result of bacteremia from another source. Meticulous attention to sterile technique is the best way to reduce the risk of infection at implant.

Additionally, intravenous antibiotic is given just prior to implant, and for the 24 hours postimplant.

A superficial skin infection at the pocket site may clear with antibiotic therapy. However, once the infection involves the internal pocket, or leads, the whole system will need to be explanted.

Erosion of the skin over the pacemaker pocket site can occur in patients with very little subcutaneous adipose tissue, or when the generator is not placed down to the prepectoral fascial plane. Early erosion is seen as thinning and erythema of the skin over the generator. If action is taken while the skin is still intact, the generator can be moved to a subpectoral position and the system can be saved. Once the generator is in contact with the open air, the entire system must be explanted.

Lead fracture, or a break in the insulation, is most frequently seen at the suture sleeve or at the point where the lead goes under the clavicle. To help reduce this risk, the implanter can obtain lead access via the axillary vein to avoid subclavian crush.

The implanter should also be careful to not suture the lead too tightly in the pocket. Patients should be advised to not perform frequent repetitive arm exercises, as this puts added stress on leads at the access site and can cause the lead to fracture.

In some cases, a lead fracture can be seen on a chest radiograph. A more definitive diagnosis can be made by interrogating the pacemaker.

A low impedance is consistent with an insulation break, and a high impedance points to a lead fracture. Prompt diagnosis is important, since loss of lead integrity can lead to lack of pacing in a pacemaker-dependent patient. The system can see noise on the fractured lead, and interpret it as intrinsic rhythm.

Thrombosis of the subclavian vein can occur after placement of pacing leads. The physical signs are swelling in arm and neck on the side of the implant. The definitive diagnosis is made by a vascular duplex study. Generally, the only therapy required is oral anticoagulant.

Pacemaker syndrome has become an uncommon problem now that most patients receive dual-chamber pacemakers. Single lead systems with only a ventricular lead should be reserved for patients in persistent atrial fibrillation, or those in sinus rhythm with no VA conduction. Loss of AV synchrony, or VA retrograde conduction, can produce hypotension or a variety of adverse symptoms. The problem can be resolved by adding an atrial lead, or reprogramming a dual-chamber system to restore AV synchrony.

Chronic pacing from the right ventricular apex can worsen left ventricular function in patients with existing structural heart disease. If this occurs, the patient’s pacemaker may need to be upgraded to a biventricular device. Additionally, patients with a right ventricular pacing lead can develop new or worsening tricuspid regurgitation.

IV. Management with Co-Morbidities

Anticoagulation

Patients on anticoagulants who need temporary or permanent pacemaker placement are at increased risk of bleeding complications. If the procedure is not emergent, and the patient is on warfarin for atrial fibrillation, the drug can be withheld for 3 to 5 days, and restarted postprocedure when the risk of bleeding is acceptable.

However, if the procedure is urgent, the warfarin effect can be reversed with vitamin K or fresh frozen plasma. The bleeding risk is usually acceptable with an INR <1.6.

For patients with a mechanical valve, or otherwise at high risk of thrombosis off anticoagulation drugs, implanting leads with an INR around 2.0 has been found to carry an acceptable bleeding risk. This practice poses a lower risk for post procedural pocket hematoma than if bridging with heparin is required. Alternatively, if warfarin has been withheld preprocedure, and bridging anticoagulation is required postprocedure, heparin infusion without boluses poses a lower post operative bleeding risk than subcutaneous low molecular weight heparin.

Our practice is to restart Coumadin at the patient’s usual dose the night of the procedure, and initiate heparin infusion 12 to 24 hours postprocedure at 500 to 600 units per hour. The prothrombin time is then checked every 6 hours, and the heparin dose can be increased by 100 unit increments as needed until the prothrombin time is in the desired range. Heparin should be continued until the INR is therapeutic.

The new oral anticoagulants are now being used in place of warfarin in many patients with atrial fibrillation. They have not been studied in patients with mechanical valves or rheumatic mitral stenosis. An advantage of these newer agents is their shorter half-life. Depending on the drug, the pacemaker implant can be done without a significant bleeding risk in 1-2 days. However, these drugs should be held several days post-procedure, since full anticoagulation is achieved within 2 hours of giving the first dose. An antidote for dabigatran is currently available, and a single antidote is being developed for the factor X inhibitors. It is anticipated that these antidotes will only be needed on rare occasions.

If a patient on clopidogrel has a nonurgent need for a pacemaker, and the clopidogrel can be safely stopped, 2 weeks is needed to allow full reversal of the drug’s effect on coagulation. Withholding clopidogrel at least 5 days can reduce the bleeding risk.

In some cases, clopidogrel cannot be safely stopped, or the procedure is considered urgent. The bleeding risk must then be accepted, as there is no drug to reverse the effects of clopidogrel.

Infection

If a patient with symptomatic heart block also has a known or suspected bacterial infection, ideally this should be adequately treated prior to implantation of a permanent pacemaker. Bacteremia could result in infection of the pacing leads and generator, necessitating removal of the entire system.

The patient with hemodynamically stable heart block can wait for pacemaker implantation until after their infection has resolved with antibiotic therapy. On the other hand, a very symptomatic patient may require temporary pacing while being stabilized from an infection standpoint.

The course of antibiotics may not be completed when the permanent pacemaker is implanted, but the risk of recurrent or ongoing bacteremia should be low. The patient should be afebrile with improving white blood count and negative blood cultures.

Prognosis

Once appropriately paced, the prognosis for patients with symptomatic complete heart block depends on their underlying disease process. Patients with acquired AV block secondary to idiopathic fibrosis have a prognosis similar to those of the same age without heart block.

By contrast, patients with complete heart block due to an extensive myocardial infarction will have a poor prognosis despite pacing. Congenital complete heart block without additional structural heart disease carries a good prognosis. In patients with bifascicular or trifascicular block, their prognosis depends on the extent of their underlying heart disease.

Patient counseling

Patients who have received a pacemaker for symptomatic AV block need to be cautioned about potential electromagnetic interference (EMI). The most concern is with pacemaker-dependent patients, where EMI can create noise which inhibits pacing. Most of the sources of EMI that cause clinical problems are hospital-based.

Hospital-based EMI sources

• Electrocautery

• Magnetic resonance imaging (MRI)

• Radiofrequency ablation

• Cardioversion and defibrillation

• Radiation therapy

• Transcutaneous electrical nerve stimulation (TENS)

• Electroconvulsive therapy

Patients need to inform medical personnel that they have a pacemaker to avoid being exposed to EMI without the proper precautions being taken. For surgical procedures above the umbilicus where electrocautery is to be used, pacemaker-dependent patients should have their device reprogrammed to an asynchronous mode (VOO or DOO) to avoid sensing noise. Alternatively, a magnet can be placed over the generator, which causes the pacemaker to temporarily pace asynchronously while in place.

Due to its strong magnetic fields, MRI should be avoided in patients with pacemakers, unless they have a MRI compatible pacemaker generator and leads.

Transcutaneous electrical nerve stimulation (TENS) is not recommended for patients who are pacemaker-dependent. Electroconvulsive therapy can be used in these patients if the device is reprogrammed to the asynchronous mode. Radiation therapy, radiofrequency ablation, cardioversion, and defibrillation can all be performed if the proper precautions are taken, and the device is tested after completion of the procedure.

Pacemaker patients should be advised prior to leaving the hospital that they should not drive for the first 2 weeks postimplant. They should also refrain from activities requiring raising the arm on the side of the pacemaker above shoulder level in the first month after implant.

This would apply to golfing or fly fishing. After the first month, there are no activity restrictions, except for participation in contact sports.

Trauma to the generator or leads could damage the system. Additionally, the patient should not shoot a rifle on the side of the pacemaker generator, as this can also damage the system.

Patients should be advised to carry their pacemaker identification card with them at all times. It can then be shown to medical personnel when required, and to security personnel at airports.

Patients should be aware their pacemaker will activate the metal detector, but this should not interfere with the device functionality. Patients should also be advised to not store cell phones in a shirt pocket over the pacemaker generator.

When talking on a cell phone, they should use the ear opposite the generator. Finally, it should be stressed to patients the importance of keeping appointments in the device clinic and being compliant with transtelephonic or remote monitoring.

V. Patient Safety and Quality Measures

A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Patient instructions (to prevent readmission postpacemaker implant):

• Keep incision dry for 5 days

• Do not raise arm on side of implant above shoulder level for first month

• Do not pick up objects over 15 lb for first month

• Report redness, swelling, or drainage at pacemaker pocket site

• Keep pacemaker clinic appointments

B. What's the Evidence for specific management and treatment recommendations?

Wolbrette, DL, Naccarelli, GV. “Bradycardias: sinus nodal dysfunction and atrioventricular conduction disturbances”. Cardiovascular Medicine. 2007. pp. 1038(This book chapter provides a more in-depth text on bradycardias.)

Josephson, ME. “Electrophysiologic investigation: general concepts”. Clin Cardiac Electrophysiol. 2002. pp. 19(This is an excellent text for understanding basic electrophysiology.)

Elizari, MV, Acunzo, RS, Ferreiro, M. “Hemiblocks revisited”. Circulation. vol. 115. 2007. pp. 1154-63. (This paper is a good review of the complicated anatomy of the bundle branches.)

Gregoratos, G. “ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and arrhythmia devices”. J Am Coll Cardiol. vol. 40. 2002. pp. 1703-19. (This paper provides expert opinion on which patients should be considered for pacemaker implant.)

Hayes, DL, Lloyd, MA, Friedman, PA. “Cardiac pacing and defibrillation: a clinical approach”. 2000. (This is a comprehensive book on pacing.)

“Perioperative management of patients with devices; consensus statement from Heart Rhythm Society & American Society of Anesthesia”. Heart Rhythm. vol. 8. 2011. pp. 1114(This long-awaited paper proves the consensus opinion between the electrophysiology and anesthesiology experts regarding the optimal perioperative management of patients with devices.)

Abdel-Wahab, M, Mehilli, J, Frerker, C. “Comparison of balloon-expandable vs. self-expandable valves in patients undergoing transcatheter aortic valve replacement: the CHOICE randomized clinical trial”. JAMA. vol. 311. 2014 Apr 16. pp. 1503-14.

Gillis, AM, Russo, AM, Ellenbogen, KA. “HRS/ACCF expert consensus statement on pacemaker device and mode selection”. J Am Coll Cardiol. vol. 60. 2012 Aug 14. pp. 682-703.

Expected Length of Stay

Length of stay for a pacemaker implant is 24 hours. A patient can be discharged to home the morning after implant.

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