ATRIO-VENTRICULAR BLOCK Background

Atrioventricular (AV) block occurs when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. Three degrees of AV block are recognized. First-degree AV block consists of prolongation of the PR interval on the electrocardiogram (ECG) (> 200 msec in adults and > 160 msec in young children). The upper limit of the reference range for the PR interval is agedependent in children. All atrial impulses reach the ventricles in first-degree AV block; however, conduction is delayed within the AV node (see the image below).

First-degree atrioventricular block. PR interval is constant and is 280 msec.

Second-degree AV block is characterized by atrial impulses (generally occurring at a regular rate) that fail to conduct to the ventricles in 1 of the following 4 ways. The first form of second-degree AV block is Mobitz I second-degree AV block (Wenckebach block), which consists of progressive prolongation of the PR interval with the subsequent occurrence of a single nonconducted P wave that results in a pause. The pause is shorter than the sum of any 2 consecutive conducted beats (R-R interval). An episode of Mobitz I AV block usually consists of 3-5 beats, with a ratio of nonconducted to conducted beats of 4:3, 3:2, and so on (see the image below). The block is generally in the AV node but can occasionally occur in the His-Purkinje system and is termed infrahisian Wenckebach.

Second-degree atrioventricular block, Mobitz type I (Wenckebach). Note prolongation of PR interval preceding dropped beat and shortened PR interval following dropped beat.

The second form is Mobitz II second-degree AV block, which is characterized by a constant PR interval followed by sudden failure of a P wave to be conducted to the ventricles, so that either an occasional dropped P wave or a regular conduction pattern of 2:1 (2 conducted and 1 blocked), 3:1 (3 conducted and 1 blocked), and so on is observed (see the image below).

Second-degree atrioventricular block, Mobitz type II. Constant PR interval in conducted beats is present. Intraventricular conduction delay also is present.

The third form is high-grade AV block, which consists of multiple P waves in a row that should conduct, but do not. The conduction ratio can be 3:1 or higher, and the PR interval of conducted beats is constant. This is a distinct form of complete AV block, in that the P waves that conduct to the QRS complexes occur at fixed intervals. For complete AV block, no relationship exists between the P waves and QRS complexes.

The fourth form is 2:1 AV block. This could be either Mobitz I or Mobitz II, but distinguishing one variety from the other is nearly impossible. Third-degree AV block is diagnosed when no supraventricular impulses are conducted to the ventricles. P waves on the rhythm strip reflect a sinus node rhythm independent from QRS wave complexes. The QRS complexes represent an escape rhythm, either junctional or ventricular. The escape rhythm originating from the junctional or high septal region is characterized by narrow QRS complexes at a rate of 40-50 beats/min, whereas escape rhythm from low ventricular sites is characterized by broad QRS complexes at a rate of 30-40 beats/min. No relationship exists between the rhythm of P waves and the rhythm of QRS complexes in third-degree AV block. The frequency of P waves (atrial rate) is higher than the frequency of QRS complexes (ventricular rate) (see the image below).

Third-degree atrioventricular block (complete heart block). Atrial rate is faster than ventricular rate, and no association exists between atrial and ventricular activity.

AV dissociation is a rhythm identified by atrial and ventricular activation occurring from different pacemakers. AV dissociation does not indicate the presence of AV block and is distinctly different. Ventricular activation may be from either junctional pacemakers or infranodal. AV dissociation can occur in the presence of intact AV conduction, especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate. Third-degree AV block can occur with AV dissociation. However, in AV dissociation without AV block, the ventricular rate can exceed the atrial rate and conduction can occasionally occur dependent on the timing between the P wave and the QRS complex. AV block may also occur in patients with atrial fibrillation (see the Atrial Fibrillation Center). Regular R-R intervals are possible in the presence of AV block (generally at slow regular rates).

Pathophysiology
The atrioventricular node (AVN) is part of the conduction system of the heart that allows electrical impulses to be transmitted from the sinus node via atrial tissue (intra-atrial fascicles) to the ventricles. This node consists of 3 partsatrionodal (transitional zone), nodal (compact portion), and nodal-His (penetrating His bundle). The nodal part causes the slowest conduction. The AVN is supplied by the right coronary artery (90%) or by the circumflex artery (10%) and is innervated by both sympathetic and parasympathetic fibers. It receives impulses anteriorly via the intra-atrial fibers in the septum and posteriorly via the crista terminalis. Impulses arriving at the AVN are transmitted to the ventricle in a 1:1 ratio. As faster impulses arrive, the conduction to the ventricles slows; this is called decremental conduction. The His-Purkinje system is composed of 2 bundles of Purkinje fibers (the left and right bundle) that conduct electrical impulses to allow rapid ventricular activation. The His-Purkinje system is yet another location where AV block may occur. First-degree AV block and second-degree Mobitz I AV block usually involve a delay at the level of the AVN, whereas second-degree Mobitz II AV block generally involves blockage in the His bundle or lower in the conduction system. Third-degree AV block involves conduction disturbances in the AV node or the His-Purkinje system. In most cases of complete AV block, an escape rhythm originates from the ventricles, with wide QRS complexes at a low regular rate of 30-40 beats/min. A higher anatomic location of the block results in a higher location of the escape rhythm pacemaker, a faster escape rhythm (40-60 beats/min in the region of His bundle), and a narrower QRS duration.

Etiology
Delay or lack of conduction through the AV node has multiple causes.

First-degree AV block and Mobitz I (Wenckebach) second-degree AV block may occur in healthy, wellconditioned people as a physiologic manifestation of high vagal tone. Mobitz I AV block also may occur physiologically at high heart rates (especially with pacing) as a result of increased refractoriness of the AVN, which protects against conducting a fast rhythm to the ventricles. AV block may be caused by acute myocardial ischemia or infarction. Inferior myocardial infarction may lead to third-degree block, usually at the AVN level; this may occur through by other mechanisms via the Bezold-Jarisch reflex. Anterior myocardial infarction usually is associated with third-degree block resulting from ischemia or infarction of bundle branches. Degenerative changes in the AVN or bundle branches (eg, fibrosis, calcification, or infiltration) are the most common cause of nonischemic AV block. Lenegre-Lev syndrome is an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. It is most commonly seen in the elderly and is often described as senile degeneration of the conduction system and may lead to third-degree AV block. In 1999, degenerative changes in the AV conduction system were linked to mutations of the SCN5A sodium channel gene (mutations of the same gene may lead to congenital long QT syndrome type 3 and to Brugada syndrome).[1] Infiltrative myocardial diseases resulting in AV block include sarcoidosis, myxedema, hemochromatosis, and progressive calcification related to mitral or aortic valve annular calcification. Endocarditis and other infections of the myocardium, such as Lyme disease with active infiltration of the AV conduction system, may lead to varying degrees of AV block. Systemic diseases, such as ankylosing spondylitis and Reiter syndrome, may affect the AV nodal conducting tissue. Surgical procedures (eg, aortic valve replacement and congenital defect repair) may cause AV block, as may other therapeutic procedures (eg, AV ablation in patients with supraventricular arrhythmias and alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy). Patients with corrected transposition of the great vessels have anterior displacement of the AVN and are prone to develop complete heart block during right heart catheterization or surgical manipulation. A variety of drugs may affect AV conduction. The most common of these include digitalis glycosides, betablockers, calcium channel blockers, and other antiarrhythmic agents.

Epidemiology
First-degree AV block can be found in healthy adults, and its incidence increases with age. At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5-2% of healthy people. At age 60 years, more than 5% of healthy individuals have PR intervals exceeding 0.20 seconds. Mobitz II second-degree AV block (Mobitz II) is rare in healthy individuals, whereas Mobitz I (Wenckebach) second-degree AV block is observed in 1-2% of healthy young people, especially during sleep. Congenital third-degree AV block is rare, at 1 case per 20,000 births. This form of heart block, in the absence of major structural abnormalities, is associated with maternal antibodies to Ro (SS-A) and La (SS-B) and secondary to maternal lupus. It is most commonly diagnosed between 18 and 24 weeks gestation and may be first, second, or third degree (complete). Mortality approaches approximately 20%; most surviving children require pacemakers. AV blocks occur more frequently in people older than 70 years, especially in those who have structural heart disease. Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block. The international incidence is the same as incidence in the United States.

Age-, sex-, and race-related demographics

The incidence of AV block increases with age. The incidence of third-degree AV block is highest in people older than 70 years (approximately 5-10% of patients with heart disease). A 60% female preponderance exists in congenital third-degree AV block. For acquired third-degree AV block, a 60% male preponderance exists. No racial proclivity exists in AV blocks.

History
First-degree atrioventricular (AV) block is generally not associated with any symptoms and is usually an incidental finding on electrocardiography (ECG). People with newly diagnosed first-degree AV block may be healthy individuals with high vagal tone (eg, well-conditioned athletes), or they may have a history of myocardial

infarction or myocarditis. First-degree AV block also may represent the first sign of a degenerative process of the AV conduction system. Second-degree AV block usually is asymptomatic. However, in some patients, sensed irregularities of the heartbeat, presyncope, or syncope may occur. The latter usually is observed in more advanced conduction disturbances, such as Mobitz II second-degree AV block. A history of medications that affect atrioventricular node (AVN) function (eg, digitalis, beta-blockers, and calcium channel blockers) may be contributory and should be obtained. Third-degree AV block frequently is symptomatic, with fatigue, dizziness, lightheadedness, presyncope, and syncope being reported most commonly. Syncopal episodes due to slow heart rates are called Morgagni-AdamsStokes (MAS) episodes, in recognition of the pioneering work of these researchers on syncope. Patients with third-degree AV block may have associated symptoms of acute myocardial infarction either causing the block or related to reduced cardiac output from bradycardia in the setting of advanced atherosclerotic coronary artery disease.

Physical Examination
Routine physical examination does not lead to the diagnosis of first-degree AV block. Second-degree AV block may manifest on physical examination as bradycardia (especially Mobitz II), irregularity of heart rate (especially Mobitz I [Wenckebach]), or both. Third-degree AV block is associated with profound bradycardia unless the site of the block is located in the proximal portion of the AVN. Exacerbation of ischemic heart disease or congestive heart failure caused by AV blockrelated bradycardia and reduced cardiac output may lead to specific clinically recognizable symptoms (eg, chest pain, dyspnea, confusion, and pulmonary edema). Cannon a waves may be observed intermittently in the jugular venous pulsation when the right atrium contracts against a closed tricuspid valve due to atrioventricular dissociation.

Complications
Complications include the following: Sudden death due to asystole or secondary to polymorphic ventricular tachyarrhythmias Cardiovascular collapse with syncope, aggravation of ischemic heart disease, congestive heart failure, and exacerbation of renal disease Head and musculoskeletal injuries during syncopal episodes

Diagnostic Considerations
In making the diagnosis, it is important to differentiate Mobitz I second-degree atrioventricular (AV) block from Mobitz II second-degree AV block, as well as to differentiate Mobitz II second-degree AV block from third-degree AV block. Both Mobitz I and Mobitz II AV block must be differentiated from sinus nodal dysfunction. Atrial fibrillation with a low heart rate may mask third-degree AV block. Third-degree block must be differentiated from AV dissociation, where the frequency of the ventricular rhythm exceeds the frequency of the atrial rhythm.

Differentials
Myocardial Infarction Syncope

Laboratory Studies
Laboratory testing is not usually indicated in patients with atrioventricular (AV) block. levels of electrolytes and drugs (eg, digitalis) can be checked in the case of second-degree or third-degree AV block when suspicion of increased potassium level or drug toxicity exists. In cases when second-degree and third-degree AV block might be a manifestation of acute myocardial infarction, cardiac enzymes should be measured. If clinical evaluation suggests systemic illness, appropriate directed laboratory studies for infection, myxedema, or connective tissue disease should be performed.

Electrocardiography
Routine electrocardiographic (ECG) recording and cardiac monitoring with careful evaluation of the relationship between P waves and QRS complexes are the standard tests leading to proper diagnosis of AV blocks.

Identifying episodes of transient AV block with sudden pauses and/or low heart rate causing syncopal episodes may require 24-hour Holter monitoring, multiple ECG recordings, event (loop) ECG recordings, or, in selected cases, monitoring with implantable loop recorders (Reveal, Medtronic, Inc).

Electrophysiologic Testing
Electrophysiologic testing is indicated in a patient with suspected AV block as the cause of syncope. The invasive recording of AH (atrium-His) and HV (His-ventricle) intervals may determine the degree of conduction abnormality and may guide decisions for pacemaker therapy. As noted, in selected cases, invasive diagnostic procedures may include implantation of loop recorders and electrophysiology testing.

Imaging Studies
In general, routine imaging studies are not helpful in diagnosing AV blocks. However, imaging studies (eg, echocardiography) might be useful in diagnosing underlying comorbid conditions, such as aortic valve stenosis with calcification, wall motion abnormalities in acute ischemia, cardiomyopathy, and congenital heart disease (eg, congenitally corrected transposition of the great vessels).

Exercise
Advanced heart block, such as Mobitz II or third-degree AV block, may become more symptomatic with increased activity, where an actual increase in block and decrease in effective heart rate may occur. Exercise may be used to evaluate 2:1 heart block and differentiate Mobitz I second-degree AV block (where the conducted rate increases) from Mobitz II AV block (where the block becomes more significant and often symptomatic).

Approach Considerations
Long-term medical therapy is not indicated in atrioventricular (AV) block. Permanent pacing is the therapy of choice in advanced AV block, and it does not require concomitant medical therapy. Sometimes AV nodal blocking medications that contribute to heart block can be discontinued if not necessary. Pacemaker implantation is a routine surgical procedure, generally performed with local anesthesia in the electrophysiology lab. The procedure usually requires an overnight observation period in the hospital. Temporary transcutaneous or transvenous pacing is the treatment of choice for an emergency involving a slow heart rate (and for asystole) caused by AV blocks. Transfer to a specialized medical center may be advisable. Atropine administration (0.5-1.0 mg) may improve AV conduction in emergencies where bradycardia is caused by a proximal AV block (located in the atrioventricular node [AVN]) but may worsen conduction if the block is in the His-Purkinje system.

Pacemaker Implantation
In general, the decision regarding implantation of a pacemaker must be considered with respect to whether or not AV block is permanent. Reversible causes of AV block, such as electrolyte abnormalities, if present, should be corrected first. Some diseases may follow a natural history to resolution (eg, Lyme disease), and some AV block can be expected to reverse (eg, hypervagotonia due to recognizable and avoidable physiologic factors, perioperative AV block due to hypothermia, or inflammation near the AV conduction system after surgery in this region). Conversely, some conditions may warrant pacemaker implantation owing to the possibility of disease progression even if the AV block reverses transiently (eg, sarcoidosis, amyloidosis, neuromuscular diseases). Finally, permanent pacing for AV block after valve surgery follows a variable natural history, and, therefore the decision for permanent pacing is at the physicians discretion. Types of cardiac pacemakers implanted in patients with heart block may include ventricular (usually VVI) or dual chamber (usually DDD) modes of pacing. The cardiologist or electrophysiologist should make the decision regarding the optimal mode of pacing.

ACC/AHA/NASPE guidelines
The following recommendations are based on the 2002 guidelines for implantation of cardiac pacemakers and antiarrhythmia devices formulated by the American College of Cardiology (ACC), the American Heart Association (AHA), and the North American Society for Pacing and Electrophysiology (NASPE).[4]

First-degree AV block and Mobitz I second-degree AV block do not generally require treatment unless they cause symptoms and are not due to a reversible cause. If a drug overdose is a possible cause, the drug must be withheld (and its future use or dosage subsequently should be decreased or reconsidered). Small, uncontrolled trials have suggested that some symptomatic and functional improvement may be achieved in pacing patients with PR intervals longer than 300 msec by decreasing the time for AV conduction. This is rare. Although echocardiographic or invasive techniques may be used to assess hemodynamic improvement before permanent pacemaker implantation, such studies are not required for evaluation of symptoms due to first-degree and Mobitz I second-degree AV block. Mobitz II second-degree AV block and third-degree AV block usually require temporary and/or permanent cardiac pacing. Mobitz II second-degree AV block and a wide QRS complex indicate diffuse conduction system disease and constitute an indication for pacing even in the absence of symptoms. Mobitz II with a wide QRS may degenerate into third-degree AV block, and this is another reason to consider permanent pacing. In the setting of acute anterior myocardial infarction, transcutaneous pacing initially and transvenous pacing subsequently are warranted. With inferior myocardial infarction, the block usually resolves spontaneously within several days, and only a small percentage of patients require temporary or permanent pacing. Patients with persistent bundle branch block and transient third-degree AV block may benefit from permanent pacing therapy, especially after anterior myocardial infarction. Nonrandomized studies strongly suggest that permanent pacing does improve survival in patients with third-degree AV block, especially if syncope has occurred. Indications for treatment may be summarized according to the ACC/AHA classifications I, II, and III as follows: Class I - Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective Class IIa - Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment, but the weight of evidence/opinion is in favor of usefulness/efficacy Class IIb - Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment, but usefulness/efficacy is less well established by evidence/opinion Class III - Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful. With respect to pacemaker implantation in the setting of AV block, class I is defined as third-degree and advanced second-degree AV block at any anatomic level, associated with any 1 of the following conditions: Bradycardia with symptoms (including heart failure) presumed to be due to AV block (level of evidence: C) Arrhythmias and other medical conditions that require drugs that result in symptomatic bradycardia (level of evidence: C) Documented periods of asystole greater than or equal to 3.0 sec or any escape rate less than 40 beats/min in awake, symptom-free patients (level of evidence: B, C) After catheter ablation of the AV junction (level of evidence: B, C) - No trials have assessed outcome without pacing, and pacing is virtually always planned in this situation unless the operative procedure is AV junction modification Postoperative AV block that is not expected to resolve after cardiac surgery (level of evidence: C) Neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limb-girdle), and peroneal muscular atrophy, with or without symptoms, because unpredictable progression of AV conduction disease may occur (level of evidence: B) Class IIa is defined as follows: Asymptomatic third-degree AV block at any anatomic site with average awake ventricular rates of 40 beats/min or faster, especially if cardiomegaly or left ventricular (LV) dysfunction is present (level of evidence: B, C) Asymptomatic type II second-degree AV block with a narrow QRS - When Mobitz II second-degree AV block occurs with a wide QRS, pacing becomes a class I recommendation(level of evidence: B). Asymptomatic Mobitz I second-degree AV block at intra- or infra-His levels found on electrophysiologic study performed for other indications (level of evidence: B) First- or second-degree AV block with symptoms similar 2 those of pacemaker syndrome (level of evidence: B)

Class IIb is defined as follows: Marked first-degree AV block (> 300 msec) in patients with LV dysfunction and symptoms of congestive heart failure in whom a shorter AV interval results in hemodynamic improvement, presumably by decreasing left atrial filling pressure (level of evidence: C) Neuromuscular diseases such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limbgirdle), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, bcoz unpredictable progression of AV conduction disease may occur (level of evidence: B)

Complications of pacing
Pacing therapy (temporary or permanent) may be complicated acutely by tamponade, hemothorax, or pneumothorax. Dysfunction of the pacemaker, lead fracture, and malfunction (eg, inappropriate capture or sensing) are infrequent complications of pacing therapy. Infection of the pacemaker or lead wires is a rare, but important, short-term and long-term complication of pacemaker implantation.

Activity Restriction
Restrictions after permanent pacemaker implantation include restricted weight lifting with the ipsilateral hand/arm to the pacemaker until healing occurs (approximately 6 wk). Contact sports are restricted unless a protective shield is worn over the implanted pacemaker. Electromagnetic interferencefrom power lines and arc welding, for examplemay cause inhibition of pacing. This is problematic for patients who are pacemaker dependent.

Consultations
Consultation with a cardiologist or cardiac electrophysiologist is indicated in the case of advanced heart block or unexplained syncope. An electrophysiologist must be consulted when invasive electrophysiology study is needed to determine the level and/or magnitude of conduction disturbance.

Long-Term Monitoring
Patients with first-degree and benign Mobitz I second-degree AV block do not require hospitalization. Patients with symptomatic second- or third-degree AV block require hospitalization with telemetry monitoring. Transcutaneous or transvenous pacing should be utilized, and indications for permanent pacing need to be determined. Patients with first- and second-degree Mobitz I AV block may require follow-up ECG or Holter monitoring to determine the likelihood and rate of progression of the AV conduction disorder. Patients with implanted pacemakers require routine follow-up to monitor pacemaker function.

Medication Summary
Long-term medical therapy is not indicated in atrioventricular (AV) block. Permanent pacing is the therapy of choice in advanced AV block, and it does not require concomitant medical therapy. Sometimes AV nodal blocking medications that contribute to heart block can be discontinued if not necessary. Atropine administration (0.5-1.0 mg) may improve AV conduction in emergencies where bradycardia is caused by a proximal AV block (located in the atrioventricular node [AVN]) but may worsen conduction if the block is in the His-Purkinje system.

Anticholinergic Agents
Class Summary
The goal of administering anticholinergic agents is to improve conduction through the AVN by reducing vagal tone via muscarinic receptor blockade. This is only effective if the site of block is within the AVN. For patients with suspected infranodal block, this therapy is ineffective and may make the level of the block worse if it is in the His bundle or below.

Atropine IV/IM (Atropair, Atropisol)

Atropine increases AV conduction. An insufficient dose may cause paradoxical slowing of the heart rate. View full
drug information

Isoproterenol (Isuprel)
Isoproterenol has beta1- and beta2-adrenergic receptor activity. It binds the beta-receptors of the heart, smooth muscle of bronchi, skeletal muscle, the vasculature, and the alimentary tract. It has positive inotropic and chronotropic actions. View full drug information

Prognosis
Patients treated with permanent pacing to treat AV blocks have an excellent prognosis. Patients with advanced AV blocks who are not treated with permanent pacing remain at high risk of sudden cardiac death. Although AV blocks generally are not associated with major morbidity, progressive degrees of AV block carry increasing morbidity and mortality. Cheng et al found that first-degree AV block (ie, PR interval > 200 msec) is associated with an increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality.[2] In a prospective, community-based cohort of 7,575 individuals from the Framingham Heart Study (mean age, 47 y; 54% women) who underwent routine 12lead ECG in 1968-1974, 124 individuals had PR intervals > 200 msec on the baseline examination. On follow-up of the cohort through 2007, individuals with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation, a 3-fold adjusted risk of pacemaker implantation, and a 1.4-fold adjusted risk of all-cause mortality.[2]For all 3 outcomes, each 20-msec increment in PR was associated with an increase in risk. A prospective cohort study of 938 patients with stable coronary artery disease were examined to assess if firstdegree AV block was associated with an increased risk of heart failure and mortality. Patients were classified as a PR interval of 220 ms or less. Patients with first-degree AV block were at increased risk for heart failure hospitalization (age-adjusted heart rate, 2.33; 95% CI, 1.49-3.65; P = 0.0002), mortality (age-adjusted heart rate, 1.58; 95% CI, 1.13-2.20; P = 0.008], cardiovascular mortality (age-adjusted heart rate 2.33; 95% CI, 1.284.22; P = 0.005], and the combined endpoint of heart failure hospitalization or cardiovascular mortality (ageadjusted heart rate, 2.43: 95% CI, 1.643.61; P 0.0001). These associations persisted after multivariable adjustment for heart rate, medication use, ischemic burden, and QRS duration. Despite adjusting for systolic and diastolic dysfunction, first-degree AV block wasassociated with an increased risk for heart failure or cardiovascular death (heart rate, 1.61; 95% CI, 1.022.54; P = 0.04).[3] The low heart rate observed in third-degree or Mobitz II second-degree AV block may lead to syncopal episodes with major injuries (eg, head trauma, hip fracture), exacerbation of congestive heart failure, or exacerbation of ischemic heart disease symptoms due to low cardiac output.

Patient Education
Patients with implanted pacemakers require additional education, with particular emphasis on situations involving exposure to magnetic and electrical fields (eg, airport security gates) and training regarding transtelephonic monitoring of pacemaker function.

http://emedicine.medscape.com/article/151597-overview#showall

Atrioventricular block
An atrioventricular block (or AV block) involves the impairment of the conduction between the atria and ventricles of the heart. Strong vagal stimulation may produce AV block. The cholinergic receptor types affected are the muscarinic receptors. There are three types:

First degree AV block - PR interval greater than 0.20sec. Second degree AV block - Type 1 (aka Mobitz 1, Wenckebach): Progressive prolongation of PR interval with dropped beats (the PR interval gets longer and longer; finally one beat drops) . Type 2 (aka Mobitz 2, Hay): PR interval remains unchanged prior to the P wave which suddenly fails to conduct to the ventricles.

Third degree AV block - No association between P waves and QRS complexes.

http://en.wikipedia.org/wiki/Atrioventricular_block

FIRST-DEGREE ATRIOVENTRICULAR BLOCK Background

First-degree atrioventricular (AV) block, or first-degree heart block, is defined as prolongation of the PR interval on an electrocardiogram (ECG) to more than 200 msec.[1] The PR interval of the surface ECG is measured from the onset of atrial depolarization (P wave) to the beginning of ventricular depolarization (QRS complex). Normally, this interval should be between 120 and 200 msec in the adult population. First-degree AV block is considered marked when the PR interval exceeds 300 msec. [2] Whereas conduction is slowed, there are no missed beats. In first-degree AV block, every atrial impulse is transmitted to the ventricles, resulting in a regular ventricular rate.

Pathophysiology
The atrioventricular node (AVN) is the only normal electrical connection between the atria and the ventricles. It is an oval or elliptical structure, measuring 7-8 mm in its longest (anteroposterior) axis, 3 mm in its vertical axis, and 1 mm transversely. The AVN is located beneath the right atrial endocardium, dorsal to the septal leaflet of the tricuspid valve, and about 1 cm superior to the orifice of the coronary sinus. The bundle of His originates from the anteroinferior pole of the AVN and travels through the central fibrous body to reach the dorsal edge of the membranous septum. It then divides into right and left bundle branches. The right bundle continues first intramyocardially, then subendocardially, toward the right ventricular apex. The left bundle continues distally along the membranous septum and then divides into anterior and posterior fascicles. Blood supply to the AVN is provided by the AVN artery, a branch of the right coronary artery in 90% of individuals and of the left circumflex coronary artery in the remaining 10%. The His bundle has a dual blood supply from branches of anterior and posterior descending coronary arteries. Likewise, the bundle branches are supplied by both left and right coronary arteries. The AVN has a rich autonomic innervation and is supplied by both sympathetic and parasympathetic nerve fibers. This autonomic innervation has a major role in the time required for the impulse to pass through the AVN. The PR interval represents the time needed for an electrical impulse from the sinoatrial (SA) node to conduct through the atria, the AVN, the bundle of His, the bundle branches, and the Purkinje fibers. Thus, as shown in electrophysiologic studies, PR interval prolongation (ie, first-degree AV block) may be due to conduction delay within the right atrium, the AVN, the His-Purkinje system, or a combination of these. Overall, dysfunction at the AVN is much more common than dysfunction at the His-Purkinje system. If the QRS complex is of normal width and morphology on the ECG, then the conduction delay is almost always at the level of the AVN. If, however, the QRS demonstrates a bundle-branch morphology, then the level of the conduction delay is often localized to the His-Purkinje system. Occasionally, the conduction delay can be the result of an intra-atrial conduction defect. Some causes of atrial disease resulting in a prolonged PR interval include endocardial cushion defects and Ebstein anomaly.[3]

Etiology
The following are the most common causes of first-degree AV block: Intrinsic AVN disease Enhanced vagal tone Acute myocardial infarction (MI), particularly acute inferior wall MI Myocarditis Electrolyte disturbances (eg, hypokalemia, hypomagnesemia) Drugs (especially those drugs that increase the refractory time of the AVN, thereby slowing conduction) A number of specific disorders and events have been implicated (see below).

Athletic training
Well-trained athletes can demonstrate first-degree (and occasionally higher degree) AV block owing to an increase in vagal tone.

Coronary artery disease

Coronary artery disease is a factor. First-degree AV block occurs in fewer than 15% of patients with acute MI admitted to coronary care units. His bundle electrocardiographic studies have shown that, in most of these patients, the AVN is the site of conduction block. AV block is more common in the setting of inferior MI. In the Thrombolysis in Myocardial Infarction (TIMI) II study, high-degree (second- or third-degree) AV block occurred in 6.3% of patients at the time of presentation and in 5.7% in the first 24 hours after thrombolytic therapy.[4] Patients with AV block at the time of presentation had a higher in-hospital mortality than patients without AV block; however, the 2 groups had similar mortalities during the following year. [4] Patients who developed AV block after thrombolytic therapy had higher mortalities both in hospital and during the following year than patients without AV block. The right coronary artery was more often the site of infarction in patients with heart block than in those without heart block. Patients with AV block are believed to have larger infarct size. However, the prevalence of multivessel disease is not higher in patients with AV block.

Idiopathic degenerative diseases of conduction system

Lev disease is due to progressive degenerative fibrosis and calcification of the neighboring cardiac structures, or sclerosis of the left side of cardiac skeleton (including the mitral annulus, central fibrous body, membranous septum, base of the aorta, and crest of the ventricular septum). Lev disease has an onset about the fourth decade and is believed to be secondary to wear and tear on these structures caused by the pull of the left ventricular musculature. It affects the proximal bundle branches and is manifested by bradycardia and varying degrees of AV block. Lengre disease is an idiopathic, fibrotic degenerative disease restricted to the His-Purkinje system. It is caused by fibrocalcareous changes in the mitral annulus, membranous septum, aortic valve, and crest of the ventricular septum. These degenerative and sclerotic changes are not attributed to inflammatory or ischemic involvement of adjacent myocardium. Lengre disease involves the middle and distal portions of both bundle branches and affects a younger population than Lev disease does.

Drugs
Drugs that most commonly cause first-degree AV block include the following: Class Ia antiarrhythmics (eg, quinidine, procainamide, disopyramide) Class Ic antiarrhythmics (eg, flecainide, encainide, propafenone) Class II antiarrhythmics (beta-blockers) Class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide, ibutilide) Class IV antiarrhythmics (calcium channel blockers) Digoxin or other cardiac glycosides Magnesium Although first-degree AV block is not an absolute contraindication for administration of drugs such as calcium channel blockers, beta-blockers, digoxin, and amiodarone, extreme caution should be exercised in the use of these medications in patients with first-degree AV block. Exposure to these drugs increases the risk of developing higher-degree AV block.

Mitral or aortic valve annulus calcification

The main penetrating bundle of His is located near the base of the anterior leaflet of the mitral valve and the noncoronary cusp of the aortic valve. Heavy calcium deposits in patients with aortic or mitral annular calcification is associated with increased risk of AV block.

Infectious disease
Infective endocarditis, diphtheria, rheumatic fever, Chagas disease, Lyme disease, and tuberculosis all may be associated with first-degree AV block. Extension of the infection to the adjacent myocardium in native or prosthetic valve infective endocarditis (ie, ring abscess) can cause AV block. Acute myocarditis caused by diphtheria, rheumatic fever, or Chagas disease can result in AV block.

Collagen vascular disease

Rheumatoid arthritis, systemic lupus erythematosus (SLE), and scleroderma all may be associated with firstdegree AV block. Rheumatoid nodules may occur in the central fibrous body and result in AV block. Fibrosis of the AVN or the adjacent myocardium in patients with SLE or scleroderma can cause first-degree AV block.

Doppler echocardiographic signs of first-degree AV block have been demonstrated in about 33% of fetuses of pregnant women who are anti-SSA/Ro 52-kd positive.[5] In most of these fetuses, the blocks resolved spontaneously. However, progression to a more severe degree of block was seen in 2 of the fetuses. Serial Doppler echocardiographic measurement of AV-time intervals can be used for surveillance of these high-risk pregnancies.

Iatrogenesis
First-degree AV block occurs in about 10% of patients who undergo adenosine stress testing and is usually hemodynamically insignificant. Patients with baseline first-degree AV block more often develop higher degrees of AV block during adenosine stress testing. These episodes, however, are generally well tolerated and do not require specific treatment or discontinuance of the adenosine infusion. [6] Marked first-degree AV block may occur after catheter ablation of the fast AVN pathway with resultant conduction of the impulse via the slow pathway. This may result in symptoms similar to those of the pacemaker syndrome. First-degree AV block (reversible or permanent) has been reported in about 2% of patients who undergo closure of an atrial septal defect using the Amplatzer septal occluder.[7] First-degree AV block can occur following cardiac surgery. Transient first-degree AV block may result from right heart catheterization.

Epidemiology
In the United States, the prevalence of first-degree AV block among young adults ranges from 0.65% to 1.6%. Higher prevalence (8.7%) is reported in studies of trained athletes. The prevalence of first-degree AV block increases with advancing age; first-degree AV block is reported in 5% of men older than 60 years.[8] The overall prevalence is 1.13 cases per 1000 lives. In a study of 2,123 patients aged 20-99 years, first-degree AV block was more prevalent among AfricanAmerican patients than among Caucasian patients in all age groups except for those in the 8th decade of life.[8] In this study, the prevalence of first-degree AV block increased at age 50 years in both ethnic groups and gradually increased with advancing age. The peak in African-American patients occurred in the 10th decade of life, whereas the peak in Caucasian patients was in the 9th decade of life.[8]

History
Patients with first-degree atrioventricular (AV) block are generally asymptomatic at rest. Markedly prolonged PR interval may reduce exercise tolerance in some patients with left ventricular systolic dysfunction. Syncope may result from transient high-degree AV block, especially in those with infranodal block and wide QRS complex. Patients may have a history of past heart disease, including myocarditis or myocardial infarction (MI). Patients may be highly conditioned athletes with a high degree of vagal tone, or they may be on medications that slow conduction through the atrioventricular node (AVN). A history of an infectious disease, such as Lyme disease, may be present. Asymptomatic first-degree heart block is part of the spectrum of presentation of Lyme carditis in children. Lyme carditis is most likely in children with Lyme disease who are older than 10 years of age, those with arthralgias, and those with cardiopulmonary symptoms.[10] Borderline first-degree AV block in patients with long-standing systemic lupus erythematosus (SLE) may be a clue to more significant cardiac disease, resulting from the progression of SLE; these patients require careful screening for underlying myocardial disease.[12] Conduction disturbances may also be secondary to drugs used to treat SLE. Patients who have undergone mitral valve replacement or mitral valve annuloplasty may have heart block postoperatively.[13]

Physical Examination
No findings on the physical examination are specifically associated with first-degree AV block; it is generally an incidental finding noted on an electrocardiogram (ECG). The intensity of the first heart sound (S1) is decreased in patients with first-degree AV block. Patients with firstdegree AV block may have a short, soft, blowing, diastolic murmur heard at the cardiac apex. This diastolic murmur is not caused by diastolic mitral regurgitation, because it reaches its peak before the onset of regurgitation. The diastolic murmur is thought to be related to antegrade flow through closing mitral valve leaflets that are stiffer than normal.[14] Administration of atropine may reduce the duration of this murmur by shortening the PR interval.

Differentials
Atrioventricular Block Atrioventricular Dissociation Second-Degree Atrioventricular Block Third-Degree Atrioventricular Block

Approach Considerations
First-degree atrioventricular (AV) block is frequently noted as an incidental finding on electrocardiography (ECG). Routine laboratory studies are usually not indicated in the evaluation of first-degree AV block. Electrolyte and drug screen can be obtained if a metabolic derangement or drug toxicity is suspected. Routine imaging studies are not indicated for first-degree AV block.

Electrocardiography
On a surface ECG, the PR interval exceeds 200 msec, and all P waves conduct to the ventricle with constant but prolonged PR interval (see the images below).

The PR interval is 0.24 seconds (240 ms) in this patient with asymptomatic first-degree atrioventricular block.

ECG in a patient with first-degree heart block.

ECG in patient with first-degree heart block.

His bundle ECG is necessary only in patients with symptomatic (ie, presyncope and syncope) first-degree AV block and a wide QRS complex, indicative of bundle-branch block. The study is used to locate the site of the block in these patients. As many as 50% of patients show an infranodal conduction delay. Follow-up ECGs may be indicated in patients who are treated with AV nodal agents while in the emergency department (ED), as well as for patients with a concomitant myocardial infarction (MI).

Ultrasonography
In patients with first-degree AV block and left ventricular systolic dysfunction, Doppler ultrasonography may be used to document an improvement in cardiac output during dual-chamber pacing at short AV delay. This may provide evidence for the appropriateness of implanting a permanent pacemaker for hemodynamic support in such patients. More recently, cardiac resynchronization therapy (ie, biventricular pacing) has been applied in patients with cardiomyopathy, congestive heart failure, or intraventricular conduction delay (IVCD). First-degree AV block is frequently present in these patients as well.

Histologic Findings
Under light microscopy, an atrioventricular node (AVN) is seen to be composed of a thick mesh of tiny pale cells, which anastomose with one another via short pluridirectional cytoplasmic projections. Under electron microscopy, 4 types of cells are observed in the AVN: transitional cells, P cells, common myocardial cells, and Purkinje cells. Three functional regions have been described in the AVN on the basis of their differing conductive properties: atrionodal (AV), nodal (N), and nodal-His (NH). Cells in the N region have slower conduction times than the other regions and have no automaticity properties. Cells of the AN and NH regions have faster conduction times and display spontaneous diastolic repolarization activity.

Approach Considerations
In general, no treatment is indicated for asymptomatic isolated first-degree atrioventricular (AV) heart block. For patients with marked first-degree AV block (PR interval > 300 msec), however, several uncontrolled trials have demonstrated symptomatic improvement with placement of a dual-chamber pacemaker, though there is little evidence suggesting improved survival.[2] in patients with severe bradycardia or those with the possibility of

progression to higher-degree AV block, medications (eg, atropine, isoproterenol) can be used in anticipation of insertion of a cardiac pacemaker. Any associated condition (eg, myocardial infarction [MI], digitalis intoxication) should be treated appropriately. Significant electrolyte abnormalities should be corrected. In patients with symptomatic first-degree AV block, discontinue medications with potential for AV block, if possible. Electrophysiology consultation may be indicated for patients with first-degree AV block and symptoms of syncope or heart failure. In general, hospitalization specifically for first-degree AV block is not indicated. However, admission may be indicated for associated conditions (eg, MI). Patients with a marked first-degree AV block can present with symptoms similar to the pacemaker syndrome.[2] In these individuals, admission may be indicated.

Pacemaker Implantation
According to guidelines from the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS), permanent pacemaker implantation is reasonable for first-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise (class IIa recommendation; level of evidence, B).[15] Additional ACC/AHA/HRS recommendations have been formulated for other patients with first-degree AV block, as follows. Patients with first-degree AV block, with or without symptoms, may be considered for permanent pacemaker implantation if the block occurs in the setting of neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), or peroneal muscular atrophy, because these patients may experience unpredictable progression of AV conduction disease ( class IIb recommendation, level of evidence, B). Permanent pacemaker implantation is not indicated for asymptomatic first-degree AV block (class III recommendation; level of evidence, B).

Long-Term Monitoring
In the absence of a disease process that requires admission, patients with first-degree AV block may be safely discharged and receive follow-up on an outpatient basis. Patients should get serial follow-up electrocardiograms (ECGs) to evaluate for progression to a higher-grade AV block. Patients with first-degree AV block started on atrioventricular node (AVN)-blocking drugs should be monitored to make sure that higher-grade AV block does not develop. Patients with first-degree AV block and coexistent bundle-branch block should be closely observed.

Medication Summary
Use of medication is not indicated for treatment of asymptomatic first-degree atrioventricular (AV) block. However, in patients with severe bradycardia or those with the possibility of progression to higher-degree AV block, medications (eg, atropine, isoproterenol) can be used in anticipation of insertion of a cardiac pacemaker.

Anticholinergic Agents
Class Summary
Parasympathetic blockade shortens the PR interval by improving AV nodal conduction.

Atropine IV/IM (AtroPen)

Atropine increases heart rate through vagolytic effects, causing increase in cardiac output. View full drug information

Sympathomimetics
Class Summary
Isoproterenol infusion can be used to shorten AV conduction time. Isoproterenol has chronotropic as well as inotropic effects, which result in an increase in cardiac output.

Isoproterenol (Isuprel)
Isoproterenol has beta1- and beta2-adrenergic receptor activity. It binds the beta-receptors of the heart, smooth muscle of bronchi, skeletal muscle, vasculature, and the alimentary tract. It has positive inotropic and chronotropic actions. View full drug information

Complications
Patients with first-degree AV block can occasionally progress to higher-grade AV blocks. Usually, such a progression is only to Mobitz I second-degree heart block, but occasionally, higher-grade block can occur. The later scenario is particularly seen in patients with an acute MI, myocarditis, or acute drug overdoses. Drugs that slow conduction through the AVN system increase the risk of progression to higher-grade heart blocks. Administering such agents to a person with a coexisting first-degree AV block should be done with caution. Other potential complications include the following: Reduction in left ventricular stroke volume and cardiac output Pacemaker syndrome

Prognosis
The prognosis for isolated first-degree AV block is very good. This condition carries no increased risk of mortality, and progression from isolated first-degree heart block to high-degree block is very uncommon.[9] Patients with first-degree AV block and infranodal blocks, however, are at increased risk for progression to complete AV block. Heart block in children with Lyme carditis tends to resolve spontaneously, with median recovery in 3 days (range, 1-7 days).[10] Cheng et al found that first-degree heart block is associated with increased long-term risks of atrial fibrillation, pacemaker implantation, and all-cause mortality.[11] Their community-based cohort included 7575 individuals from the Framingham Heart Study who underwent baseline routine 12-lead ECG in 1968-1974 and were followed prospectively through 2007. Compared with individuals whose PR intervals were 200 msec or shorter, those with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation, a 3-fold adjusted risk of pacemaker implantation, and a 1.4-fold adjusted risk of all-cause mortality.[11] Each 20-msec increment in PR interval was associated with an adjusted hazard ratio (HR) of 1.11 for atrial fibrillation, 1.22 for pacemaker implantation, and 1.08 for all-cause mortality. Although no significant mortality or morbidity is related to isolated first-degree AV block, first-degree AV block in the setting of acute inferior MI may herald higher degrees of AV block. Markedly prolonged PR interval in patients with left ventricular systolic dysfunction may impair ventricular filling and thus reduce cardiac output.

http://emedicine.medscape.com/article/161829-medication#showall

SECOND DEGREE ATRIOVENTRICULAR BLOCK Background

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.

Pathophysiology
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.

Etiology
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]

Epidemiology
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 seconddegree AV block is 1:1.

Prognosis
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.

History and Physical Examination

In patients with Mobitz I second-degree atrioventricular (AV) block, symptoms may vary substantially, ranging from an absence of symptoms in well-trained athletes and persons without structural heart disease to recurrent syncope, presyncope, and bradycardia in patients with heart disease. Most patients are asymptomatic. Patients may experience light-headedness, dizziness, or syncope, but these symptoms are uncommon. Patients may have chest pain if the heart block is related to myocarditis or ischemia. Patients may have a history of structural heart disease. In contrast to patients with Mobitz I AV block, those with Mobitz II AV block are more likely to experience lightheadedness, dizziness, or syncope, though they may be asymptomatic as well. Patients may have chest pain if the heart block is related to myocarditis or ischemia. Patients often have a regularly irregular heartbeat. Bradycardia may be present. Symptomatic patients may have signs of hypoperfusion, including hypotension.

Diagnostic Considerations
In addition to the conditions in the differential diagnosis, the following problems should be considered: Congenital heart block Sinoatrial exit block Nonconducted premature atrial contractions

Differentials
First-Degree Atrioventricular Block Myocardial Infarction Third-Degree Atrioventricular Block

Approach Considerations
Serum electrolytes, calcium, and magnesium levels should be checked. A digoxin level should be obtained for patients on digoxin. Cardiac biomarker testing is indicated for any patient with suspected myocardial ischemia. Myocarditis-related laboratory studies may be sent (eg, Lyme titers, HIV serologies, enterovirus polymerase chain reaction [PCR], adenovirus PCR, Chagas titers), if clinically relevant. Thyroid function studies may be obtained. Electrocardiography (ECG) is employed to determine the type of second-degree atrioventricular (AV) block present. Follow-up ECGs and cardiac monitoring are appropriate. Routine imaging studies are not required. However, if myocarditis is a concern, echocardiography may be indicated. If myocardial ischemia is a concern, a chest radiograph may be indicated.

Electrocardiography
It is important to try to distinguish between the different types of second-degree heart block. Mobitz I (Wenckebach) block is the most common form of second-degree AV block. The typical ECG findings of Mobitz I AV block (see the image below) are as follows.

Electrocardiogram of patient with Mobitz I (Wenckebach) second-degree atrioventricular block.

Gradually progressive PR interval prolongation occurs before the blocked sinus impulse, with the greatest PR increment typically occurring between the first and second beats of a cycle, gradually decreasing in subsequent beats. Shortening of the PR interval occurs after the blocked sinus impulse, provided that the P wave is conducted to the ventricle. A common situation is the occurrence of junctional escape beats along with nonconducted P waves. A pause occurs after the blocked P wave that is less than the sum of the 2 beats before the block (see the image below).

Typical Mobitz I atrioventricular block with progressive prolongation of PR interval before blocked P wave. Pauses are always less than sum of 2 preceding beats because PR interval after pause always shortens.

A Mobitz I block manifesting with atypical ECG findings that result in a misdiagnosis of Mobitz II block is not uncommon. During very long sequences (typically > 6:5), PR-interval prolongation may be minimal until the last beat of the cycle, when it abruptly becomes much greater. Postblock PR-interval shortening remains the cornerstone of the diagnosis of Mobitz I block, regardless of whether the periodicity has typical or atypical features. Occasionally, every other beat is dropped. In these cases, it is impossible to determine if there is prolongation of the PR interval. In this situation, if the rate changes, occasionally the number of beats before the QRS complex is dropped will change, thereby permitting differentiating Mobitz I from Mobitz II. In cases where every other beat is dropped, it is safest to assume it is a Mobitz II block, rather than a Mobitz I block. In Mobitz II block (see the images below), consecutively conducted beats with the same PR interval are followed by a blocked sinus P wave. A PR interval in the first beat occurs after the block, with the same PR interval as the previous beats. A pause encompassing the blocked P wave is equal to exactly twice the sinus cycle length.

Electrocardiogram of patient with Mobitz II second-degree atrioventricular block.

Mobitz II atrioventricular (AV) block with intermittent periods of 2:1 AV block. If only 2:1 block was seen in beginning of strip, site of block could not be localized with certainty; however, single dropped QRS complex at end of strip with constant PR interval indicates that this block is localized in one of the bundle branches.

Evaluating for stability of the sinus rate is important because conditions associated with increases in vagal tone may cause simultaneous sinus slowing and AV block and therefore, mimic a Mobitz II block. In addition, diagnosing Mobitz II block in the presence of a shortened postblock PR interval is impossible. This sequence can be secondary to enhanced conduction or a nonconducted P wave occurring with a junctional escape beat. Prolonged ECG recordings or intracardiac recordings may be needed to establish the correct site of block (ie, AV nodal or infranodal).

Mobitz II block is typically associated with significant underlying conduction system disease. Therefore, the QRS complex is usually wide, and the PR interval is usually normal. However, a long PR interval and a narrow QRS complex do not exclude Mobitz II block, because AV nodal conduction disease may coexist with an infranodal lesion. Another consideration in a Mobitz II block with narrow QRS is atypical Mobitz I block. A Mobitz I block with a narrow QRS complex is almost always located in the atrioventricular node (AVN) (see the image below). An exception is the rare occurrence of an infranodal Wenckebach block. A normal PR interval with miniscule increments in AV conduction delay should raise the suggestion of an infranodal Wenckebach block but is not a diagnostic finding. Larger increments in AV conduction do not necessarily exclude infranodal Wenckebach block.

Variable-ratio Mobitz I atrioventricular block. Note marked PR-interval prolongation in first beat of each cycle. Maximum prolongation of PR interval takes place in second beat of cycle, with much smaller increments in subsequent beats. Also, notice that R-R interval actually shortens with each beatparadox of shortening R-R interval when PR interval increases by diminishing increments.

In the presence of a wide QRS complex, a type I block is more often infranodal (see the image below). An invasive His bundle recording is required to make the diagnosis of an infranodal block.

Sinus rhythm with Mobitz I second-degree 3:2 infranodal atrioventricular (AV) block and bifascicular block. Note that AH interval (indicative of AV nodal conduction) remains constant. HV interval (indicative of His-Purkinje conduction) increases from 65 msec (after first P wave) to 185 msec (after second P wave). Third P wave is followed a His bundle deflection (H) but no QRS complex. AV block occurs in His-Purkinje system below site of recording of His bundle potential. Note shorter PR interval after nonconducted P wave, typical of Mobitz I AV block. HRA = high right atrial electrogram; A = atrial deflection; HB = His bundle electrogram, proximal and distal; H = His bundle deflection; RV = right ventricular electrogram; T = time line, 50 msec.

The incremental pattern of AV block may be helpful in determining the correct site of block. For example, an increment in PR interval of longer than 100 msec favors a block site in the AVN. A Mobitz II block is always infranodal. An infranodal block is associated with a wide QRS complex and accounts for the majority of Mobitz II blocks. Less commonly, the block is intranodal and, therefore, is associated with a narrow QRS complex. Sinus slowing with AV block is characteristic of vagal activation and effectively excludes a type II block. Among the conditions that may mimic Mobitz II block are atypical Mobitz I block, junctional parasystole, and concealed extrasystoles arising from the His-Purkinje system. A 2:1 block can be either in the AVN or in the His-Purkinje system (see the image below). If the QRS complex is narrow, the block is more likely located in the AVN. If a wide QRS complex is present, the block may be located either in the His-Purkinje system (80-85%) or, less commonly, in the AVN (15-20%). Observing for a narrow QRS, Mobitz IIlike block and a Mobitz I block in close temporal proximity can sometimes help determine the correct site of block. A true Mobitz II block almost never coexists with an intra-Hisian Mobitz I block.

Representative 12-lead electrocardiogram in asymptomatic 78-year-old woman during recent noncardiac surgery. Patient was referred for implantation of permanent pacemaker with diagnosis of sinus tachycardia with 2:1 atrioventricular (AV) block and narrow QRS complex. As sinus rate slowed, 1:1 AV conduction resumed. Intracardiac recordings confirmed diagnosis of infra-Hisian 2:1 AV block.

Autonomic manipulation (eg, carotid sinus massage, exercise) may help distinguish between an AV nodal and a His-Purkinje (infranodal) block. Improvement in the degree of block with exercise strongly favors an AV nodal location. Conversely, an increase in block with exercise or atropine more strongly favors a His-Purkinje (infranodal) block. Compared with exercise, vagal maneuvers have opposite effects on AV blocks, exacerbating the AV nodal blocks and improving infranodal blocks. AV block localized to the infranodal specialized conduction system occurs in as many as 5% of patients with acute anterior MI, giving rise to a wide-QRS Mobitz II block. A transient AV block of any degree in acute inferior MI almost always is AV nodal and not an indication for permanent pacing.

Electrophysiologic Testing
Diagnostic electrophysiologic testing can help determine the level of the block and the potential need for a permanent pacemaker.

Such testing is indicated for patients in whom His-Purkinje (infranodal) block is suspected but has not been confirmed, such as those with the following: Mobitz I second-degree AV block associated with a wide QRS complex in the absence of symptoms 2:1 second-degree AV block with a wide QRS complex in the absence of symptoms Mobitz I second-degree block with a history of unexplained syncope Electrophysiologic testing is also indicated for patients with pseudo-AV block and those with premature, concealed junctional depolarization, which may be the cause of second- or third-degree AV block. Finally, electrophysiologic testing is indicated for patients with second- or third-degree AV block in whom another arrhythmia is suspected as the cause of the symptoms (eg, those who remain symptomatic after pacemaker placement).

Approach Considerations
Second-degree atrioventricular (AV) block in the asymptomatic patient does not require any specific therapy in the prehospital setting. If the patient is symptomatic, standard advanced cardiac life support (ACLS) guidelines for bradycardia, including the use of atropine and transcutaneous pacing, are indicated. [6, 26] No specific therapy is required in the emergency department (ED) for Mobitz I (Wenckebach) second-degree AV block, unless the patient is symptomatic. Patients with suspected myocardial ischemia should be treated with an appropriate anti-ischemic regimen. Second-degree block at the level of the atrioventriocular node (AVN) may be due to digoxin, beta-blockers, or calcium channel blockers. Decreasing the dose and/or discontinuing these medications may restore normal AV conduction. Mobitz II block is more likely to progress to complete heart block and thus requires a different approach. As with Mobitz I block, AV nodal agents should be avoided, and an anti-ischemic regimen should be instituted if ischemia is suspected. Permanent pacing is considered in accordance with the relevant guidelines (see Pacemaker Implantation). Except for the use of atropine in selected cases of transient AV block, permanent cardiac pacing has replaced medical interventions in the treatment of patients with symptomatic, otherwise untreatable, AV block.

Atropine and Transcutaneous/Transvenous Pacing

Mobitz I block
Admit patients who have symptoms or who have concomitant acute myocardial ischemia or myocardial infarction (MI). Admission should be to a unit with telemetry monitoring, which has transcutaneous pacing capabilities. Symptomatic patients should be treated with atropine and transcutaneous pacing. However, atropine should be administered with caution in patients with suspected myocardial ischemia, as ventricular dysrhythmias can occur in this situation. The goal of atropine administration is to improve conduction through the AVN by reducing vagal tone via atropine-induced receptor blockade. However, this goal will only be effective if the level of the blockade is at the site of the AVN. Patients with infranodal second-degree AV block are unlikely to benefit from atropine. In addition, in patients who have denervated hearts (eg, patients who have undergone a cardiac transplant), atropine is also not likely to be effective.

Mobitz II block
Admit all patients to a unit with monitored beds, where transcutaneous and transvenous pacing capabilities are available. The admitting cardiologist should determine whether permanent pacemaker implantation is indicated. Transcutaneous pacing pads should be applied to all patients with Mobitz II second-degree AV block, including those who are asymptomatic patients, because such patients have a propensity to progress to complete heart block. The transcutaneous pacemaker should be tested to ensure capture. If capture is not able to be achieved, then insertion of a transvenous pacemaker is indicated, even in asymptomatic patients. Urgent cardiology consult is indicated for patients who have symptomatic type II block and for those asymptomatic patients who are unable to achieve capture with transcutaneous pacing. Some institutions recommend insertion of a transvenous pacemaker for all new Mobitz type II blocks, although this practice varies greatly from institution to institution.

Patients who are hemodynamically unstable for whom an emergency cardiology consult is not available should undergo placement of a temporary transvenous pacing wire in the ED. A chest radiograph is required to confirm position of the wire and to exclude complications, including hemothorax or pneumothorax.

2:1 block
In cases where there is a 2:1 block and one is unable to determine if there is a Mobitz I block or Mobitz II block, the patient should be admitted and cardiology consultation should be obtained. In such cases, it is safest to assume that a Mobitz II second-degree AV block exists.

Pacemaker Implantation
Indications for permanent pacing in second-degree AV block are explained in detail in the guidelines published by the American College of Cardiology (ACC), the American Heart Association (AHA), and the North American Society for Pacing and Electrophysiology (NASPE) in 2002[27] and by the ACC, the AHA, and the Heart Rhythm Society (HRS) in 2008.[28] A summary of indications is as follows. Second-degree AV block associated with signs such as bradycardia, heart failure, and asystole greater than or equal to 3 seconds Second-degree AV block with neuromuscular diseases, such as myotonic muscular dystrophy, Erb dystrophy, and peroneal muscular atrophy, even in asymptomatic patients (progression of the block is unpredictable in these patients); in some of these patients, an implantable cardioverter defibrillator (ICD) may be appropriate Mobitz II second-degree AV block with wide QRS complexes Asymptomatic Mobitz I second-degree AV block with the block at intra- or infra-His level found on electrophysiologic testing (level II recommendation) Second-degree AV block may occur after MI, and it may be transient or asymptomatic. In this case, pacemaker placement may not be needed. However, persistent and symptomatic second-degree AV block after MI, especially if it is associated with bundle-branch block, warrants permanent pacemaker placement. High-grade AV block after anterior MI, even if transient, may warrant permanent pacing. Second-degree AV block after cardiac surgery may be persistent and necessitate pacemaker placement. Second-degree AV block in patients with drug toxicity, Lyme disease, or hypoxia in sleep apnea is expected to resolve. In any situation where second-degree AV is expected to resolve as a result of correction of the underlying pathology, permanent pacemaker placement is not indicated.

Consultations
For symptomatic patients with Mobitz I AV block, a cardiology consultation is indicated. Asymptomatic patients with a Mobitz I block can be referred to a cardiologist on an outpatient basis. For any patient with a new Mobitz II AV block, cardiology consultation is indicated, regardless of symptoms.

Long-Term Monitoring
Patients who are discharged from the ED with a Mobitz II AV block should have prompt follow-up arranged with a cardiologist. If high-grade AV block and, possibly, symptoms due to AV block are present, consider monitoring the patient and then performing Holter monitoring or treadmill testing in the future. If the AV block occurs at night, consider sleep apnea as the cause.

Medication Summary
Atropine can be used for immediate treatment of symptomatic second-degree atrioventricular (AV) block in the atrioventricular node (AVN). For block in the His-Purkinje system, atropine does not improve conduction and can actually precipitate third-degree AV block by increasing the sinus rate and AVN conduction. Anticholinergic agents
Class Summary
Anticholinergic agents improve AV nodal conduction in second-degree block at the level of the AVN. Drug therapy in second-degree heart block is aimed at vagolysis; atropine is the only currently recommended agent.

Atropine IV/IM (AtroPen)

Atropine is used to increase heart rate through vagolytic effects, causing an increase in cardiac output. It enhances sinus node automaticity; in addition, it blocks the effects of acetylcholine at the AVN, thereby decreasing the refractory time and speeding conduction through the AVN. Insufficient doses of atropine can cause paradoxical effects, further slowing the heart rate. View full drug information

THIRD DEGREE ATRIOVENTRICULAR BLOCK / TOTAL AV BLOCK Background

Third-degree atrioventricular (AV) block, also referred to as third-degree heart block or complete heart block, is a disorder of the cardiac conduction system where there is no conduction through the atrioventricular node (AVN). Therefore, complete dissociation of the atrial and ventricular activity exists.[1]The ventricular escape mechanism can occur anywhere from the AVN to the bundle-branch Purkinje system.[2] It is important to realize that not all patients with AV dissociation have complete heart block. For example, patients with ventricular tachycardia have AV dissociation, but not complete heart block; in this example, AV dissociation is due to the ventricular rate being faster than the intrinsic sinus rate. On electrocardiography (ECG), complete heart block is represented by QRS complexes being conducted at their own rate and totally independent of the P waves (see the image below).

Electrocardiogram from patient in complete heart block.

AV block results from various pathologic states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Third-degree AV block can be either congenital or acquired. (See Etiology.) Initial triage of patients with complete heart block consists of determining symptoms, assessing vital signs, and looking for evidence of compromised peripheral perfusion. In particular, the physical examination findings of patients with third-degree AV block will be notable for bradycardia, which can be severe. (See Clinical.) Treatment of third-degree AV block is based on the level of the block. The first, and sometimes most important, medical treatment for heart block is the withdrawal of any potentially aggravating or causative medications. Medical treatment of complete heart block is limited to patients with conduction disease in the AVN. (See Treatment.) Initial treatment efforts should focus on assessing the need for temporary pacing and initiating the pacing. Most patients whose heart block is not otherwise treatable will require a permanent pacemaker or an implantable cardioverter defibrillator (ICD).

Pathophysiology

In the heart, normal impulse initiation begins in the sinoatrial node. The excitation wave then travels through the atrium. During this time, surface ECG recordings show the P wave. Following intra-atrial conduction to the area of the lower intra-atrial septum, this wavefront reaches the inputs to the AVN. The AVN then conducts the impulse to the His bundle. The His bundle divides into the right and left bundles, which distribute this impulse to the ventricles. During atrial, AVN, and His-Purkinje conduction, the PR segment is observed. Heart block occurs when slowing or complete block of this conduction occurs. Traditionally, AV block can be divided into first-, second-, and thirddegree block.

First-degree AV block
First-degree AV block is a condition in which a 1:1 relationship exists between P waves and QRS complexes, but the PR interval is longer than 200 msec. Thus, first-degree AV block represents delay or slowing of conduction. Occasionally, first-degree AV block may be associated with other conduction disturbances, including bundlebranch block and fascicular blocks (bifascicular or trifascicular block).

Second-degree AV block
Second-degree AV block exists when more P waves than QRS complexes are seen on the ECG, but a relationship between P waves and QRS complexes still exists. In other words, not all P waves are followed by QRS complexes (conducted). Traditionally, this type of AV block is divided into 2 main subcategories, Mobitz type I (Wenckebach) and Mobitz type II. In the Mobitz I second-degree AV block, the PR interval prolonging until the P wave is not followed by a QRS complex. In a typical Mobitz I block, the PR interval prolongation from beat to beat is greatest in the first interval and progressively less with subsequent intervals. This is reflected in shortening of the R-R interval and the overall PR interval increases. Also, the R-R interval enveloping the pause is less than twice the duration of the first R-R interval following the pause. On the ECG tracing, Mobitz I second-degree AV block results in the characteristic appearance of grouping beats; conversely, the presence of grouped beating should prompt a careful evaluation for Wenckebach conduction (though it should be noted that not all such conduction is pathologic). In Mobitz II second-degree AV block, the PR interval is constant, but occasional P waves are not followed by the QRS complexes (nonconducted). Occasionally, the first PR interval following nonconducted P waves may be shorter by as much as 20 msec. To differentiate between Mobitz I block and Mobitz II block, at least 3 consecutive P waves must be present in the tracing. If only every other P wave is conducted (2:1), a second-degree block cannot be classified into either of these categories and thus is best described as a 2:1 AV block, unless the mechanism can be inferred from surrounding patterns of atrial-to-ventricular conduction. An AV block resembling second-degree AV block has been reported with sudden surges of vagal tone associated with cough, hiccups, swallowing, carbonated beverages, pain, micturition, or airway manipulation in otherwise healthy subjects. The distinguishing feature is simultaneous slowing of the sinus rate. This condition is paroxysmal and benign but must be carefully differentiated from a true second-degree AV block because the prognosis is very different.

Third-degree AV block
Third-degree AV block (ie, complete heart block) exists when there are more P waves than QRS complexes and there is no relationship between them (ie, no conduction). The conduction block may be at the level of the AVN, the bundle of His, or the bundle-branch Purkinje system. In most cases (approximately 61%), the block occurs below the His bundle. Block within the AV node accounts for approximately one fifth of all cases, whereas block within the His bundle accounts for slightly fewer than one fifth of all cases. [2] The duration of the escape QRS complex depends on the site of the block and the site of the escape rhythm pacemaker. Pacemakers above the His bundle produce a narrow QRS complex escape rhythm, whereas those at or below the His bundle produce a wide QRS complex. When the block is at the level of the AVN, the escape rhythm generally arises from a junctional pacemaker with a rate of 45-60 beats/min. Patients with a junctional pacemaker frequently are hemodynamically stable, and their heart rate increases in response to exercise and atropine. When the block is below the AVN, the escape rhythm arises from the His bundle or the bundle-branch Purkinje system at rates slower than 45 beats/min. These patients generally are hemodynamically unstable, and their heart rate is unresponsive to exercise and atropine.

AV dissociation
AV dissociation is present when atrial and ventricular activation are independent of each other. It can result from complete heart block or from physiologic refractoriness of conduction tissue. It can also occur in a situation when the atrial/sinus rate is slower than the ventricular rate (eg, with accelerated junctional tachycardia and ventricular tachycardia). Occasionally, the atrial and ventricular rates are so close that the tracing would suggest normal AV conduction; only careful examination of the long rhythm strip may reveal a variation in PR interval. This form of AV dissociation is called isorhythmic AV dissociation. Maneuvers or medications resulting in acceleration of atrial/sinus rate will result in restoration of normal conduction.

Etiology
AV block results from various pathologic states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Third-degree AV block can be either congenital or acquired. The congenital form of complete heart block usually occurs at the level of the AVN. Patients are relatively asymptomatic at rest but later develop symptoms because the fixed heart rate is not able to adjust for exertion. In the absence of major structural abnormalities, congenital heart block is often associated with maternal antibodies to SS-A (Ro) and SS-B (La).[3] The common causes of acquired AV block are as follows: Drugs (see below) Degenerative diseases Lengre disease (sclerodegenerative process involving only the conduction system) and Lev disease (calcification of the conduction system and valves), noncompaction cardiomyopathy, nailpatella syndrome, mitochondrial myopathy[4] Infectious causes - Lyme borreliosis (particularly in endemic areas),Trypanosoma cruzi infection,[5] rheumatic fever, myocarditis, Chagas disease, Aspergillus myocarditis, varicella-zoster virus infection,[6] valve ring abscess Rheumatic diseases - Ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, scleroderma Infiltrative processes - Amyloidosis, sarcoidosis, tumors, Hodgkin disease, multiple myeloma Neuromuscular disorders - Becker muscular dystrophy, myotonic muscular dystrophy Ischemic or infarctive causes - AVN block associated with inferior wallmyocardial infarction (MI), His-Purkinje block associated with anterior wall MI (see below) Metabolic causes - Hypoxia, hyperkalemia, hypothyroidism Toxins Mad honey (grayanotoxin), cardiac glycosides (eg, oleandrin), and others Phase IV block (also known as bradycardia-related block) Iatrogenic causes (see below)

Drugs
Complete heart block can develop from isolated single-agent overdose oras is often the casefrom combined or iatrogenic coadministration of AV nodal, beta-adrenergic, and calcium channel blocking agents. Drugs or toxins associated with heart block include the following: Class Ia antiarrhythmics (eg, quinidine, procainamide, disopyramide) Class Ic antiarrhythmics (eg, flecainide, encainide, propafenone) Class II antiarrhythmics (beta-blockers) Class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide, ibutilide) Class IV antiarrhythmics (calcium channel blockers) Digoxin or other cardiac glycosides; patients who are on digoxin should be educated about possible early symptoms of digoxin toxicity

Myocardial infarction
Anterior wall MI can be associated with an infranodal complete AV block; this is an ominous finding. Complete heart block develops in slightly less than 10% of cases of acute inferior MI and is much less dangerous, often resolving within hours to a few days. Studies suggest that AV block rarely complicates MI.[7, 8] With an early revascularization strategy, the incidence of AV block decreased from 5.3 to 3.7%. Occlusion of each of the coronary arteries can result in development of conduction disease despite redundant vascular supply to the AVN from all coronary arteries.

Most commonly, occlusion of the right coronary artery (RCA) is accompanied by AV block. In particular, the proximal RCA occlusion has a high incidence of AV block (24%) because there is involvement not only of the AV nodal artery is involved but also of the right superior descending artery, which originates from the very proximal part of the RCA. In most cases, AV block resolves promptly after revascularization, but sometimes the course is prolonged. Overall, the prognosis is favorable. AV block in the setting of occlusion of the left anterior descending artery (particularly proximal to the first septal perforator) has a more ominous prognosis and usually calls for pacemaker implantation. Second-degree AV block associated with bundle-branch block and in particular with alternating bundle-branch block is an indication for permanent pacing.

Iatrogenesis
AV block may be associated with aortic valve surgery, septal alcohol ablation, percutaneous coronary intervention to the left anterior descending artery, or ablation of the slow or fast pathway of the AVN. Placement of catheters that mechanically interfere with one fascicle when conduction is already impaired in the remaining conduction system (eg, bumping the right bundle with a pulmonary artery catheter in a patient with existing left bundle-branch block) almost always resolves spontaneously. AV block after cardiac surgery is seen in 1-5.7% of patients.[9] Major risks factors identified for the need for permanent pacing are aortic valve surgery, preexisting conduction disease (either right or left bundle-branch block), bicuspid aortic valve, annular calcification, and female gender. The time course for recovery varies widely, with a significant portion of patients recovering during the 48 hours following surgery. Available evidence suggests that if no recovery in AV conduction is seen by postoperative day 4 or 5, a pacemaker should be implanted.

Epidemiology
In the United States, the prevalence of third-degree AV block is 0.02%. Worldwide, the prevalence of thirddegree AV block is 0.04%.[10] The incidence of AV conduction abnormalities increases with advancing age, resembling the age-related incidence of ischemic heart disease. An early peak in incidence occurs in infancy and early childhood due to congenital complete AV block, which is sometimes not recognized until childhood or even adolescence.

History
Third-degree atrioventricular (AV) block (ie, complete heart block) has a wide range of clinical presentations. Occasionally, patients are asymptomatic or have only minimal symptoms related to hypoperfusion. In these situations, symptoms include the following: Fatigue Dizziness Impaired exercise tolerance Chest pain

Patients with narrow complex escape rhythms (eg, those whose escape rhythm occurs above the His bundle) are more likely to have minimal symptoms. More commonly, however, patients are profoundly symptomatic, especially if a wide-complex escape rhythm is present, indicating that the origin of the pacemaker is below the His bundle. In such cases, symptoms can include the following: Syncope Confusion Dyspnea Severe chest pain Sudden death

Because an acute myocardial infarction (MI) can cause complete heart block, patients who concurrently experience an MI can have associated symptoms from the MI, including chest pain, dyspnea, nausea or vomiting, and diaphoresis. Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death. Patients who have a history of cardiac disease may be on medications that affect the conduction system through the atrioventricular node (AVN), including the following: Beta-blockers Calcium channel blockers Digitalis cardioglycosides

The patients history of cardiac interventions should be carefully investigated; aortic valve surgery, septal alcohol ablation, proximal anterior descending artery stenting (complicated by compromised flow in the first septal perforator branch), and ablation of the slow or fast pathway of the AVN all may result in third-degree AV block.

Physical Examination
Initial triage of patients with complete heart block consists of determining symptoms, assessing vital signs, and looking for evidence of compromised peripheral perfusion. In particular, the physical examination findings of patients with third-degree AV block will be notable for bradycardia, which can be severe. Careful examination of the neck veins can often show evidence of cannon a waves. A variable intensity S 1 may be heard. In addition, the pulse rate may be slow. If the slow rate or loss of atrial contraction prior to ventricular contraction has caused heart failure, then venous pressures will be elevated, including the jugular venous pressure. Any new murmurs or gallops should be noted because strong associations exist between cardiomyopathies, mitral calcification, aortic calcification, or endocarditis and complete AV block. If heart failure is present as evidenced by rales, an S3 gallop, peripheral edema, or hepatomegaly, then a more compelling need for immediate pacing exists. Because endocarditis, rheumatic fever, and Lyme disease cause heart block, pay attention to any signs of infection or skin rashes during the general examination. This is particularly true in endemic areas for Lyme disease. Neurologic examination may provide clues to the etiology of AV block because neuromuscular disease, especially myotonic dystrophy and Duchenne muscular dystrophy, can cause AV block. Signs of congestive heart failure as a result of decreased cardiac output may be present and may include the following: Tachypnea or respiratory distress Rales Jugular venous distention Patients may have signs of hypoperfusion, including the following: Altered mental status Hypotension Lethargy In patients with concomitant myocardial ischemia or MI, corresponding signs may be evident on examination: Signs of anxiety such as agitation or unease Diaphoresis Pale or pasty complexion Tachypnea Regularized atrial fibrillation is the classic sign of complete heart block due todigitalis toxicity. This rhythm occurs because of the junctional escape rhythm.

Diagnostic Considerations
Ischemia should always be in the differential for a patient with new-onset high-degree atrioventricular (AV) block. Take simple measures to rule out ischemia, such as 12-lead electrocardiography (ECG) and measurement of cardiac enzyme levels. If warranted, a more in-depth evaluation, including perfusion imaging, may be needed. Iatrogenic heart block due to medications is not uncommon and should always be considered. Other problems to be considered include the following: Bradycardia with a ventricular escape Bradycardia with a junctional escape Accelerated junctional escape rhythm

Differentials
Junctional Rhythm Myocardial Infarction Myocarditis Second-Degree Atrioventricular Block Sinus Bradycardia

Laboratory Studies
For most patients with illness serious enough to cause third-degree atrioventricular (AV) block (ie, complete heart block), a complete blood count (CBC) is indicated to screen for coincident problems (eg, anemia, infection) that may require emergency intervention. The presence of fever or an elevated white blood cell (WBC) count should be evaluated by using blood cultures because endocarditis can be complicated by heart block. Serum concentrations of electrolytes, including potassium and magnesium, should be measured to look for metabolic imbalance, indications of renal insufficiency or failure, and particularly for severe hyperkalemia. The prothrombin time and activated partial thromboplastin time should also be routinely obtained. A digoxin level should be obtained for patients on digoxin or in whom ingestion of digoxinlike compounds (eg, Lily of the Valley, Oleander, Foxglove, Bufonidae toads) is suspected. The same should be done for any other drugs the patient is taking that are capable of causing AV block. Note that the presence of a detectable digoxin level following a nondigoxin cardiac glycoside ingestion can only confirm the presence of such a toxin. The digoxin level does not correlate to the degree of cardiac glycoside toxicity following nondigoxin-induced cardiac glycoside ingestions. Myocarditis-related laboratory studies should be performed in patients suspected of having myocarditis. Such studies include Lyme titers, HIV serologies, enterovirus polymerase chain reaction (PCR), adenovirus PCR, and Chagas titers, as clinically appropriate. Lyme titers should be obtained from all patients who may have been exposed to Lyme disease. Because cardiac manifestations of Lyme disease are delayed, Lyme-induced heart block can occur during any season. The decision to perform serologic testing for Lyme disease or any of the collagen vascular diseases depends on other associated history and findings.

Imaging Studies
A chest radiograph should be obtained. If examination findings or history suggest cardiomyopathy or valvular disease, then transthoracic echocardiography should be performed. Specific etiologies (eg, valve ring abscess) may call for transesophageal echo imaging. A determination of left ventricular function by means of echocardiography or another technique can help in determining whether a pacemaker or defibrillator should be implanted for the treatment of the heart block.

Electrocardiography
The most important study is 12-lead electrocardiography (ECG). On 12-lead ECG, third-degree AV block is characterized by complete lack of conduction (no P waves cause a QRS complex). If complete AV block exists, then the R-R interval is very regular; therefore, before diagnosing third-degree AV block, the R-R interval should be either marched out or measured. If high-grade AV block exists without complete heart block, then some irregularity may occur during intervals following conducted P waves. Various pathologic conditions can cause conduction system disease and heart block (see Etiology). These systemic or myocardial diseases rarely present as conduction block, with the exception of Lyme disease, inferior myocardial infarction (MI), and some of the neuromuscular diseases. Unless suggested by history, examination findings, family history, risk factors, or 12-lead ECG findings, the authors do not screen for underlying pathology. Surface ECG and review of prior ECG data can provide important clues to the level of third-degree AV block. The assessment can begin with a review of the current QRS width and morphology, comparing the QRS during heart block to the QRS when conduction was occurring (see the image below).

ECG before and after complete heart block at the AV nodal level.

If the QRS is narrow (< 120 msec) during conducted beats and narrow with the same morphology during escape beats, then the block is in the AV junction. If the conducted QRS was narrow at baseline and is wide during the escape rhythm (see the image below), then this is likely a distal level of block located anatomically in the His bundle or in both right and left bundles.

Complete heart block with wide complex escape.

Other Studies
If history or 12-lead ECG findings suggest active coronary artery disease, then cardiac enzyme levels measurements and an evaluation of ischemia, including either cardiac catheterization or stress testing, are needed. Ambulatory monitoring may be performed to document heart-transient heart block or other bradyarrhythmias in patients presenting with symptoms suggestive of bradycardia. Diagnostic electrophysiologic studies can be performed to assess AV conduction and to discern the level of block (AV nodal or infranodal) when necessary.

Approach Considerations
New-onset third-degree atrioventricular (AV) block (ie, complete heart block) is a medical emergency. Treatment of third-degree AV block is based on the level of the block. A common misconception of an inexperienced clinician is to gauge a patients stability according to the heart rate and blood pressure rather than according to the symptoms and level of the block. An asymptomatic patient with inferior wall myocardial infarction (MI) causing complete heart block at the atrioventricular node (AVN) level and a heart rate of 35 beats/min is at very little immediate risk. A patient in the acute phase of an anterior wall MI with intermittent distal high-grade block is at immediate danger of impending asystole and requires immediate preparation for pacing of some kind, even though the heart rate between asystolic episodes might be 90 beats/min. The first, and sometimes most important, medical treatment for heart block is the withdrawal of any potentially aggravating or causative medications. Many antihypertensive, antianginal, antiarrhythmic, and heart failure medications cause AV block that resolves after withdrawal of the offending agent. Review patient medication lists upon presentation to help rule out medication-induced or medication-aggravated heart block. Common drugs that induce AV block include beta-blockers, calcium channel blockers, antiarrhythmics, and digoxin. Withdrawal of offending drugs is the first treatment for heart block. Cases in which complete heart block results from a calcium channel blocker should be managed in much the same fashion as cases involving other causes of third-degree block (eg, pacemaker) but should also receive appropriate treatment for calcium channel blockers. This therapy includes the administration of IV fluids, calcium, glucagons, vasopressors, and high-dose insulin (hyperinsulinemic euglycemia [HIE] therapy). (See Toxicity, Calcium Channel Blocker.) Overdoses of beta-blockers are managed similarly to overdoses of calcium channel blockers, although HIE therapy for beta-blocker overdoses is less well established. (See Toxicity, Beta-blocker.) Medical treatment of complete heart block is limited to patients with conduction disease in the AVN. Patients with block at the AVN level, in the absence of ischemia, can benefit from sympathomimetic agents or vagolytic agents. Initial efforts should focus on assessing the need for temporary pacing and initiating the pacing. Except in the case of AV block caused by medications that can be withdrawn or infections that can be treated, most patients with acquired complete heart block will require a permanent pacemaker or an implantable cardioverter defibrillator (ICD).

Initial Management Considerations

All patients should be rapidly transported to the nearest available facility, receiving advanced life support (ACLS) with continuous cardiac monitoring, as per local protocols. In all patients, oxygen should be administered and intravenous (IV) access established. Maneuvers likely to increase vagal tone (eg, Valsalva maneuvers, painful stimuli) should be avoided. Atropine can be administered but should be given cautiously. Treatment in the emergency department (ED) should continue that already established in the prehospital setting, which includes administering oxygen, maintenance of an IV line, frequent monitoring of blood pressure, and continuous cardiac monitoring. Transcutaneous pacing pads should be applied and tested, if this has not already been done. All patients with third-degree heart block need to be admitted to either a telemetry floor (if hemodynamically stable and transcutaneous pacing achieves capture) or an intensive care unit (ICU). The decision between the 2 should be made in conjunction with the cardiologist. Any patient who is hemodynamically unstable, has persistent complete heart block, has electrolyte abnormalities, or who is in complete heart block as a result of an overdose or myocardial infarction should be admitted to the ICU.

Patients may be transferred to a higher level of care if the hospital does not have intensive care capabilities or if appropriate consultation services (eg, cardiology) are not available.

Atropine and Transcutaneous/Transvenous Pacing

All patients who have complete heart block associated with repeated pauses, inadequate escape rhythm, or block below the AVN should be stabilized with temporary pacing. Although the transcutaneous pacer should be placed on all patients, this mode of pacing is not highly reliable and is extremely uncomfortable for the patient. When assessing capture with transcutaneous pacing, it is important to avoid the common mistake of looking for electrical capture on the monitor. The pacing artifact is usually large and that QRS complex can rarely be seen reliably. Instead, palpation for the pulse is the best indication of capture. Transcutaneous pacing is the treatment of choice for any symptomatic patient. Symptomatic patients in whom capture cannot be obtained with a transcutaneous pacemaker need urgent placement of a transvenous pacemaker. Placement of a transvenous pacemaker is also indicated for asymptomatic patients in whom capture cannot be obtained; the timing of this should be discussed with the consulting cardiologist. The decision to place a transvenous pacing wire depends on the availability of fully trained personnel and equipment for placing a transvenous wire. All patients with persistent block below the AVN should be prepared for temporary wire placement. Hemodynamically stable patients in whom transcutaneous pacing can be successfully performed can go to a telemetry unit or ICU at the discretion of the treating cardiologist. Hemodynamically unstable patients for whom timely cardiologic consultation is unavailable should undergo temporary transvenous pacemaker insertion in the ED. Hemodynamically unstable patients may be treated with atropine. This should be done with a degree of caution. The goal of atropine therapy is to improve conduction through the AVN by reducing vagal tone via receptor blockade. Atropine often improves the ventricular rate if the site of block is in the AVN. Peak increase in heart rate occurs in 2-4 minutes after IV administration; half-life is 2-3 hours. However, if the block is in the His bundle, atropine may lead to an increased atrial rate, and a greater degree of block can occur with a slower ventricular rate. Atropine is unlikely to be successful in wide-complex bradyarrhythmias where the level of the block is below the level of the AVN. In addition, care should be taken in administering atropine to a patient with a suspected acute MI, in that the resulting vagolysis leads to unopposed sympathetic stimulation, which can cause increased ventricular irritability and potentially dangerous ventricular arrhythmias. Furthermore, atropine is ineffective in patients with a denervated heart (eg, those patients who have undergone a cardiac transplant procedure). Similarly, isoproterenol may be attempted to accelerate a ventricular escape rhythm with a low probability for efficacy and the same concerns in patients with suspected acute MI. Isoproterenol is more likely to facilitate conduction with a distal level of block, but patients with a block at the distal level are more likely to have a contraindication, such as active ischemic heart disease. Isoproterenol should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged. Once the patient has been stabilized, a decision must be made regarding permanent pacemaker implantation. [11, 12, 13, 14] The admitting cardiologist will determine the need for and timing of permanent pacemaker implantation.

Pacemaker Implantation for Acquired AV Block in Adults

Unless the heart block is due to a medication that can be discontinued or an infectious process that can be effectively treated, most patients with acquired complete heart block should receive a permanent pacemaker or an ICD (if a high risk of sudden cardiac death exists on the basis of severe left ventricular dysfunction or other criteria). The ultimate decision whether to place a permanent pacemaker in patients with persistent heart block without a reversible cause depends on many factors. A clinical statement from the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS) was published in 2008. This paper outlined the indications for permanent pacing.[11]

Class I recommendations
Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block.

Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with arrhythmias and other medical conditions that require drug therapy that results in symptomatic bradycardia. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients in sinus rhythm with documented periods of asystole 3 seconds or longer or any escape rate less than 40 beats/min, or with an escape rhythm that is below the AVN. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level in awake, symptom-free patients with atrial fibrillation and bradycardia with 1 or more pauses of at least 5 seconds or longer. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level after catheter ablation of the AV junction. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with postoperative AV block that is not expected to resolve after cardiac surgery. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy, with or without symptoms. Permanent pacemaker implantation is indicated for second-degree AV block with associated symptomatic bradycardia, regardless of type or site of block. Permanent pacemaker implantation is indicated for asymptomatic persistent third-degree AV block at any anatomic site with average awake ventricular rates of 40 beats/min or faster if cardiomegaly or left ventricular dysfunction is present or if the site of block is below the AV node. Permanent pacemaker implantation is indicated for second- or third-degree AV block during exercise in the absence of myocardial ischemia.

Class IIa recommendations

Permanent pacemaker implantation is reasonable for persistent third-degree AV block with an escape rate faster than 40 beats/min in asymptomatic adult patients without cardiomegaly. Permanent pacemaker implantation is reasonable for asymptomatic second-degree AV block at intra- or infra-His levels found at electrophysiologic study. Permanent pacemaker implantation is reasonable for first- or second-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise. Permanent pacemaker implantation is reasonable for asymptomatic Mobitz II second-degree AV block with a narrow QRS. When Mobitz II second-degree AV block occurs with a wide QRS, including isolated right bundlebranch block, pacing becomes a class I recommendation.

Class IIb recommendations

Permanent pacemaker implantation may be considered for neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease. Permanent pacemaker implantation may be considered for AV block in the setting of drug use and/or drug toxicity when the block is expected to recur even after the drug is withdrawn.

Class III recommendations

Permanent pacemaker implantation is not indicated for asymptomatic first-degree AV block. Permanent pacemaker implantation is not indicated for asymptomatic Mobitz I second-degree AV block at the supra-His (AVN) level or that which is not known to be intra- or infra-Hisian. Permanent pacemaker implantation is not indicated for AV block that is expected to resolve and is unlikely to recur (eg, drug toxicity, Lyme disease, transient increases in vagal tone or during hypoxia in sleep apnea syndrome in the absence of symptoms).

Pacemaker Implantation for Chronic Bifascicular Block

ACC/AHA/HRS recommendations have also been formulated for permanent pacing in patients with chronic bifascicular block.[11]

Class I recommendations
Permanent pacemaker implantation is indicated for advanced second-degree AV block or intermittent thirddegree AV block. Permanent pacemaker implantation is indicated for Mobitz II second-degree AV block. Permanent pacemaker implantation is indicated for alternating bundle-branch block.

Class IIa recommendations

Permanent pacemaker implantation is reasonable for syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia (VT). Permanent pacemaker implantation is reasonable for an incidental finding at electrophysiological study of a markedly prolonged HV interval (100 ms) in asymptomatic patients. Permanent pacemaker implantation is reasonable for an incidental finding at electrophysiological study of pacing-induced infra-His block that is not physiological.

Class IIb recommendations

Permanent pacemaker implantation may be considered in the setting of neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with bifascicular block or any fascicular block, with or without symptoms.

Class III recommendations

Permanent pacemaker implantation is not indicated for fascicular block without AV block or symptoms. Permanent pacemaker implantation is not indicated for fascicular block with first-degree AV block without symptoms.

Pacemaker Implantation for AV Block After Acute MI

ACC/AHA/HRS recommendations have also been formulated for permanent pacing in patients with AV block associated with acute MI.[11]

Class I recommendations
Permanent ventricular pacing is indicated for persistent second-degree AV block in the His-Purkinje system with alternating bundle-branch block or third-degree AV block within or below the His-Purkinje system after STsegment elevation MI. Permanent ventricular pacing is indicated for transient advanced second- or third-degree infranodal AV block and associated bundle-branch block. If the site of block is uncertain, an electrophysiologic study may be necessary. Permanent ventricular pacing is indicated for persistent and symptomatic second- or third-degree AV block.

Class IIb recommendations

Permanent ventricular pacing may be considered for persistent second- or third-degree AV block at the AV node level, even in the absence of symptoms.

Class III recommendations

Permanent ventricular pacing is not indicated for transient AV block in the absence of intraventricular conduction defects.mPermanent ventricular pacing is not indicated for transient AV block in the presence of isolated left anterior fascicular block. Permanent ventricular pacing is not indicated for new bundle-branch block or fascicular block in the absence of AV block. Permanent ventricular pacing is not indicated for persistent asymptomatic firstdegree AV block in the presence of bundle-branch or fascicular block.

Activity Restriction
Bed rest is advisable for patients with new complete heart block. Bed rest minimizes the chance of significant injury if syncope occurs as a result of ventricular asystole and decreases hemodynamic demand. A temporary pacemaker may be required.

Because these patients have decreased cardiac output, assuming upright posture after prolonged periods in the supine position can lead to orthostatic hypotension with syncope or near-syncope.

Prevention
Patients with renal insufficiency or failure, dehydration, and certain electrolyte disturbances are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy. Patients on multiple nodal agents (eg, beta-blockers and calcium channel blockers) are at an increased risk for the development of complete heart block; the more nodal blockade that occurs, the higher the chance of developing complete heart block.

Consultations
Cardiologic consultation is indicated for all patients with third-degree AV block. The consultation is emergent in patients with concomitant acute MI, active myocardial ischemia, congestive heart failure, wide-complex escape rhythm, or symptoms of hypoperfusion. Patients in this group may require early placement of a permanent pacemaker, or assistance may be needed if difficulty is encountered obtaining capture from an external or transvenous pacer. The involvement of an electrophysiologist should also be considered when appropriate.

Long-Term Monitoring
Patients can be discharged from the hospital the following day after pacemaker implantation. Routinely, chest radiography is required before discharge. Routine postpacemaker care is necessary. This includes transtelephonic checks every 2 months and office visits for pacemaker interrogation every 6-12 months. In the initial postimplantation period, these visits are more frequent.

Medication Summary
Common drugs that induce atrioventricular (AV) block include beta-blockers, calcium channel blockers, antiarrhythmics, and digoxin. Withdrawal of offending drugs is the first treatment for heart block. Patients with block at the level of the atrioventricular node (AVN), in the absence of ischemia, can benefit from sympathomimetic agents or vagolytic agents. Medications that may be used in the management of third-degree AV block (complete heart block) include sympathomimetic or vagolytic agents, catecholamines, and antidotes.

Sympathomimetic agents or vagolytic agents

Class Summary
Sympathomimetic or vagolytic agents improve conduction through the AVN by reducing vagal tone via muscarinic receptor blockade. They increase heart rate through their vagolytic effects, causing an increase in cardiac output.

Atropine (AtroPen)

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Atropine is an antimuscarinic agent that enhances sinus node automaticity. It may enhance conduction and/or improve the rate of junctional escape. In addition, it blocks the effects of acetylcholine at the AVN, thereby decreasing the refractory time and speeding conduction through the AVN. At inefficient doses, atropine can have paradoxical effects, further slowing the heart rate (HR).

Isoproterenol hydrochloride (Isuprel)

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Isoproterenol is a synthetic sympathomimetic acting directly on beta-receptors. It should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged. Cardiac ischemia or a high cardiac risk profile suggesting possible coronary artery disease is a contraindication to its use. Telemetry monitoring should always accompany the use of this agent because of the risks of proarrhythmia.

Catecholamines
Class Summary

Catecholamines improve hemodynamics by acting on the beta-adrenergic receptors to increase the HR and contractility and by acting on the alpha-adrenergic receptors to increase the systemic vascular resistance.

Dopamine

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Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1- and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion; it also stimulates release of norepinephrine. In low doses (2-5 g/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 g/kg/min), it acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 g/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure (BP).

Norepinephrine (Levophed)

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Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, HR, and vasoconstriction. It increases BP and afterload. The increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Norepinephrine is generally reserved for patients with severe hypotension (eg, systolic BP < 70 mm Hg) or hypotension unresponsive to other medication.

Antidotes
Class Summary
Antidotes are used in select cases for patients with third-degree AV block secondary to digoxin toxicity. These patients should receive a digoxin-specific antidote.

Digoxin immune Fab (DigiFab)

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Digoxin immune Fab is an immunoglobulin fragment with a specific and high affinity for both digoxin and digitoxin molecules. It removes digoxin or digitoxin molecules from tissue-binding sites. Each vial contains 40 mg of purified digoxin-specific antibody fragments, which will bind approximately 0.6 mg of digoxin or digitoxin. The dose of the antidote depends on the total body load (TBL) of digoxin. The digoxin TBL can be estimated in the following 3 ways: 1. Estimate the quantity of digoxin ingested in the acute ingestion, and assume 80% bioavailability for digoxin or 100% for digitoxin (X mg ingested 0.8 = TBL) 2. Obtain a serum digoxin concentration (in ng/mL) and multiply it by the patient's weight in kilograms. Divide the result by 100 [number of vials = (digoxin concentration) x (patient's weight) / 100] 3. Use an empiric dose based on average requirements for an acute or chronic overdose in an adult or child If the quantity of ingestion cannot be estimated reliably, the antidote may be administered empirically (it is safest to use the largest calculated estimate). Alternatively, be prepared to increase dosing if resolution is incomplete.

Prognosis
Patients with complete heart block are frequently hemodynamically unstable, and as a result, they may experience syncope, hypotension, cardiovascular collapse, or death. Other patients can be relatively asymptomatic and have minimal symptoms other than dizziness, weakness, or malaise. Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death. The cause of death may often be tachyarrhythmias precipitated by the secondary changes in ventricular repolarization (QT prolongation) secondary to the abrupt changes in rate. Some patients may develop polymorphic ventricular tachycardia when significant bradycardia is present. This is related to prolongation of repolarization with extremely slow rates. This mechanism is also mostly responsible for death in these patients. When treated with permanent pacing, the prognosis is excellent. The complications related to pacemaker insertion are rare (< 1%). Ventricular arrhythmias from atropine or catecholamines may occur. Common complications include those related to line and/or transvenous pacemaker placement. These complications include arterial injury, hemothorax, pneumothorax, or cardiac tamponade. http://emedicine.medscape.com/article/162007-medication#showall

This picture shows an ECG (electrocardiogram, EKG) of a person with an abnormal rhythm (arrhythmia) called an atrioventricular (AV) block. P waves show that the top of the heart received electrical activity. Each P wave is usually followed by the tall (QRS) waves. QRS waves reflect the electrical activity that causes the heart to contract. When a P wave is present and not followed by a QRS wave (and heart contraction), there is an atrioventricular block, and a very slow pulse (bradycardia).

http://www.nlm.nih.gov/medlineplus/ency/imagepages/1429.htm