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Cardiology > Arrhythmias
Second-Degree Atrioventricular Block
Article Last Updated: Jun 29, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Ali A Sovari, MD, Research Fellow, Department of Medicine, Division of Cardiology, University of California at Los Angeles
Ali A Sovari is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Coauthor(s):
Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago;
Ryan L Cooley, MD, Consulting Staff, Heart Care Associates LLC, Wisconsin Electrophysiology Group; Assistant Professor, Department of Medicine, University of Wisconsin Medical School at Milwaukee
Editors: Robert E Fowles, MD, Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine; Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital; Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital
Author and Editor Disclosure
Synonyms and related keywords:
second-degree atrioventricular block, heart block, 2nd degree heart block, second-degree AV block, 2nd degree AV block, AV block, Mobitz AV block, Mobitz heart block, Mobitz type I, Mobitz type II, Wenckebach phenomenon, Wenckebach heart block, high-grade AV block, complete heart block, third-degree AV block, Stokes-Adams syncopal attack, heart failure, angina, acute myocardial infarction, sinus slowing, cardioactive drugs, endocarditis, myocarditis, Lyme disease, acute rheumatic fever, amyloidosis, hemochromatosis, sarcoidosis, hyperkalemia, hypermagnesemia, Addison disease, ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, lupus erythematosus, Reiter syndrome, progressive idiopathic fibrosis of the cardiac skeleton, aortic stenosis, aortic valve replacement surgery, muscular dystrophies, corrective congenital heart surgery
Background
Second-degree atrioventricular (AV) block is characterized by block of some, but not all, atrial beats. This excludes block due to premature atrial beats. Typically, it is divided into Mobitz type I block or Wenckebach block, Mobitz type II block, 2:1 block, and high-grade AV block. The diagnosis of type I and II second-degree AV block is based on electrocardiographic patterns, not on the anatomic site of the block. Precise localization of the site of the block within the specialized conduction system is critical to the appropriate treatment of individuals with second-degree AV block.
By itself, a 2:1 AV block cannot be classified as type I or II mechanism 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 advanced second-degree AV block.
Pathophysiology
Type I AV block most often results from conduction disturbances in the AV node; however, in rare cases, it may be due to intra- or infra-His bundle block. Type I block is rarely secondary to AV nodal structural abnormalities when the QRS complex is narrow in width and no underlying cardiac disease is present. In this setting, type I block can be vagally mediated and may be observed in conditions associated with relative activation of the parasympathetic nervous system, such as (1) well-trained athletes, (2) cardiac glycoside (ie, digoxin) excess, or (3) neurally mediated syncopal syndromes.
A vagally mediated AV block occurs in the AV node when vagal discharge is enhanced and often is associated with electrocardiographic evidence of sinus slowing. 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.
Cardioactive drugs are another important cause of AV block. They may exert negative (ie, dromotropic) effects on the AV node 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.
Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders have been associated with AV nodal block.
Less commonly, type I 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. Type I block with intra- or infra-His bundle block carries a worse prognosis compared with AV nodal block.
Type II block most often occurs in the His-Purkinje system. As such, this poses higher risk to the patient.
Frequency
United States
Nearly 3% of patients with underlying structural heart disease develop some form of second-degree AV block.
Mortality/Morbidity
The level of the block determines the prognosis. AV nodal blocks, which are the vast majority of type I blocks, carry a good prognosis while intra- or infra-His bundle blocks, whether type I or type II, may progress to complete block with a worse prognosis.
- Type I block (in the AV node) is often nonprogressive and benign from a mortality standpoint. The risk of progression to complete heart block is significant when the level of block is in the specialized His-Purkinje conduction system.
- Type II AV block often progresses to third-degree block and, as such, carries a more worrisome prognosis. Type II block may produce Stokes-Adams syncopal attacks.
- Vagally mediated AV block is typically benign from a mortality standpoint but may lead to dizziness and syncope.
Sex
- The male-to-female ratio is 1:1.
History
Symptoms related to type I block vary substantially, ranging from asymptomatic in well-trained athletes and those without structural heart disease, to recurrent syncope, presyncope, and bradycardia in patients with heart disease. AV block may provoke heart failure and angina.
Causes
Second-degree AV block may occur in the presence or absence of structural heart disease.
- Vagally mediated AV block occurs in the AV node when vagal activation is enhanced. It can be associated with electrocardiographic evidence of sinus slowing.
- Cardioactive drugs are another important cause of AV block. They may exert negative effects on the AV node 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. Several antiarrhythmic medications may cause second-degree AV block, and among them, Na channel blockers, such as procainamide, cause more distal block in the His-Purkinje system. 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.
- Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders that have been associated with AV nodal block are as follows:
- Inflammatory diseases
- Endocarditis
- Myocarditis
- Lyme disease
- Acute rheumatic fever
- Infiltrative diseases
- Amyloidosis
- Hemochromatosis
- Sarcoidosis
- Metabolic and endocrine disorders
- Hyperkalemia
- Hypermagnesemia
- Addison disease
- Collagen vascular diseases
- Ankylosing spondylitis
- Dermatomyositis
- Rheumatoid arthritis
- Scleroderma
- Lupus erythematosus
- Reiter syndrome
- Some of the more common causes of infranodal AV block (type II) include the following:
- Progressive (age-related) idiopathic fibrosis of the cardiac skeleton
- Valvular heart disease complications, especially aortic stenosis and aortic valve replacement surgery
- Infiltrative and inflammatory conditions listed above
- Muscular dystrophies
- Corrective congenital heart surgery, especially those in close proximity to the septum
- Acute myocardial infarction (MI) may cause second-degree AV block.
- 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 and Brugada syndrome.
Third-Degree Atrioventricular Block
Other Problems to be Considered
Sinoatrial exit block
Nonconducted premature atrial contractions
Lab Studies
- Serum electrolyte and magnesium levels
- Serum digoxin level
- Thyroid function studies
Other Tests
- Type I AV block is the most common form of second-degree AV block. The typical electrocardiographic findings of type I block (Wenckebach periodicity; see Image 1) include the following:
- Gradually progressive PR interval prolongation occurs prior to the blocked sinus impulse, with the greatest PR increment occurring typically between the first and second beat of a cycle, gradually decreasing in subsequent beats.
- Shortening of the PR interval occurs after the blocked sinus impulse, provided the P wave is conducted to the ventricle. A common situation after type I block 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.
- A type I block manifesting with atypical electrocardiographic findings that result in a misdiagnosis of type 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 prolongs abruptly, or the AV interval may shorten and then lengthen in the middle of the sequence. Postblock PR interval shortening remains the cornerstone of the diagnosis of type I block, regardless of whether the periodicity has typical or atypical features.
- Type II block (Image 2) is characterized by the following:
- 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.
- 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 type II block.
- In addition, diagnosing type 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 electrocardiographic recordings or intracardiac recordings may be needed to establish the correct site of block, ie, AV nodal versus infranodal.
- Type 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 (ie, block is infra-Hisian). However, a long PR interval and a narrow QRS complex does not exclude type II block because AV nodal conduction disease may coexist with an intra-Hisian lesion. Another consideration in a type II block with narrow QRS is atypical type I block.
- Determining the site of the block
- A type I block with a narrow QRS complex is almost always located in the AV node (Image 3).
- An exception is the rare occurrence of an intra-Hisian Wenckebach block. A normal PR interval with miniscule increments in AV conduction delay should raise the suggestion of an intra-Hisian Wenckebach block but is not a diagnostic finding. Larger increments in AV conduction do not necessarily exclude intra-Hisian Wenckebach block.
- In the presence of a wide QRS complex, a type I block is more often infranodal (Image 4). An invasive His bundle recording is required to make the diagnosis of an infranodal block.
- 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 milliseconds favors a site in the AV node.
- A type II block is always located in the His-Purkinje system.
- An infra-Hisian block is associated with a wide QRS complex and accounts for the majority of type II blocks.
- Less commonly, the block is intra-Hisian 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 type II block are atypical type I block, junctional parasystole, and concealed extrasystoles arising from the His-Purkinje system.
- A 2:1 block can be either in the AV node or in the His-Purkinje system (Image 5).
- If the QRS complex is narrow, the block is more likely located in the AV node.
- 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 AV node (15-20%).
- Observing for a narrow QRS, type II–like block, and a type I block in close temporal proximity can sometimes help determine the correct site of block.
- A true type II block almost never coexists with an intra-Hisian type I block.
- Autonomic manipulation (eg, carotid sinus massage, exercise) may help distinguish between an AV nodal and a His-Purkinje block.
- For example, improvement in the degree of block with exercise strongly favors an AV nodal location.
- Conversely, an increase in block with exercise more strongly favors a His-Purkinje block.
- Compared with exercise, vagal maneuvers have opposite effects on AV blocks, exacerbating the AV nodal blocks and improving infranodal blocks.
- Acute myocardial infarction
- 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 type 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 study may be indicated to establish the level of the block. The indications for electrophysiologic study may be as follows:
- In patients in whom His-Purkinje block is suspected but has not been confirmed, such as patients with the following:
- Type I AV block associated with a wide QRS complex in the absence of symptoms
- Second-degree AV block of the 2:1 form with a wide QRS complex in the absence of symptoms
- Type II block with a narrow QRS complex
- In patients with pseudo AV block and those with premature, concealed junctional depolarization, which may be the cause of second- or third-degree AV block
- In patients with second- or third-degree AV block in whom another arrhythmia is suspected as the etiology of the symptoms (eg, those who remain symptomatic after pacemaker placement)
Procedures
- Diagnostic electrophysiologic studies can help determine the site of block and the potential need for a permanent pacemaker.
Medical Care
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.
Surgical Care
- Indications for permanent pacing in second-degree AV block are explained in detail in ACC/AHA/NASPE guidelines. A summary of indications are as follows:
- Second-degree AV block associated with symptoms 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 (The progression of the block is unpredictable in these patients.)
- Type II second-degree AV block with wide QRS complexes
- Asymptomatic type I second-degree AV block with the block at intra- or infra-His level found at electrophysiologic study (level II recommendation)
- Second-degree AV block may occur following MI, and it may be transient or asymptomatic. In this case, it may not need pacemaker placement. However, persistent and symptomatic second-degree AV block after MI, especially if it is associated with bundle-branch block needs permanent pacemaker placement.
- Second-degree AV block following cardiac surgery may be persistent and require pacemaker placement.
- Second-degree AV block in drug toxicity, lyme disease, and hypoxia in sleep apnea are expected to resolve. In any situation that second-degree AV is expected to resolve by correction of the underlying pathology, permanent pacemaker placement is not indicated.
Consultations
Cardiac electrophysiologist
Atropine can be used for immediate treatment of symptomatic second-degree AV block in the AV node. 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 AV nodal conduction.
Drug Category: Anticholinergic agents
Improve AV nodal conduction in second-degree block at the AV nodal level.
| Drug Name | Atropine sulfate injection |
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| Description | Used to increase heart rate through vagolytic effects, causing an increase in cardiac output. |
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| Adult Dose | 0.5-1 mg IV or ET q3-5min; not to exceed 3 mg total (0.04 mg/kg) |
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| Pediatric Dose | 0.02 mg/kg/dose IV; use a minimum of 0.1 mg |
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| Contraindications | Documented hypersensitivity, thyrotoxicosis, narrow-angle glaucoma, tachycardia |
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| Interactions | Coadministration with other anticholinergics has additive effects; pharmacologic effects of atenolol and digoxin may increase; antipsychotic effects of phenothiazines may decrease; tricyclic antidepressants with anticholinergic activity may increase effects |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Caution in Down syndrome and/or children with brain damage to prevent hyperreactive response; caution in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, hypertension, peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can lead to dysuria and may require catheterization |
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Further Inpatient Care
- 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.
- Second-degree block at the AV nodal level may be due to digoxin, beta-blockers, or calcium channel blockers. Decreasing the dose and/or discontinuing these medications may restore normal AV conduction.
Medical/Legal Pitfalls
- Common pitfalls to avoid when diagnosing second-degree AV block are as follows:
- Failure to recognize nonconducted atrial premature beats as the apparent cause
- Failure to consider atypical type I block during an apparent narrow QRS type II block
- Failure to consider vagally induced AV block, ie, vomiting, sleep apnea
- Failure to realize that AV nodal and infranodal block almost never occur in the same electrocardiogram or Holter recording
- Belief that all type I blocks are AV nodal in nature
- Failure to consider concealed extrasystoles as a cause of pseudo-AV block (ie, observing for the common association of sudden PR-interval prolongation due to retrograde penetration of the extrasystole into the AV node and isolated retrograde P waves from retrograde conduction to the atrium)
- Relying solely on a computer-rendered ECG diagnosis: Computer interpretations are notoriously error-prone.
| Media file 1:
Typical Wenckebach atrioventricular block with progressive prolongation of the PR interval before the blocked P wave. The pauses are always less than the sum of the 2 preceding beats because the PR interval after the pause always shortens. |
 |  View Full Size Image | |
Media type: Rhythm Strip
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| Media file 2:
Mobitz II atrioventricular (AV) block with intermittent periods of 2:1 AV block. If only 2:1 block was seen in the beginning of the strip, then the site of block could not be localized with certainty; however, the single dropped QRS complex at the end of the strip with a constant PR interval indicates that this block is localized in one of the bundle branches. |
 | View Full Size Image | |
Media type: Rhythm Strip
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| Media file 3:
Variable-ratio type I atrioventricular (AV) block. Note the marked PR-interval prolongation in the first beat of each cycle. The maximum prolongation of the PR interval takes place in the second beat of the cycle, with much smaller increments in subsequent beats. Also, notice that the R-R interval actually shortens with each beat. This is the paradox of a shortening R-R interval when the PR interval increases by diminishing increments. |
 | View Full Size Image | |
Media type: Rhythm Strip
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| Media file 4:
Sinus rhythm with second-degree type I 3:2 infranodal atrioventricular (AV) block and bifascicular block. Note that the AH interval (indicative of AV nodal conduction) remains constant. The HV interval (indicative of His-Purkinje conduction) increases from 65 milliseconds (following the first P wave) to 185 milliseconds (following the second P wave). The third P wave is followed by a His bundle deflection (H) but no QRS complex. An AV block occurs in the His-Purkinje system below the site of recording of the His bundle potential. Note the shorter PR interval after the nonconducted P wave, a feature typical of type I AV block. HRA indicates 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 milliseconds. |
 | View Full Size Image | |
Media type: ECG
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| Media file 5:
Representative 12-lead ECG in an asymptomatic 78-year-old woman during recent noncardiac surgery. The patient was referred for implantation of a permanent pacemaker with a diagnosis of sinus tachycardia with 2:1 atrioventricular (AV) block and a narrow QRS complex. As the sinus rate slowed, 1:1 AV conduction resumed. Intracardiac recordings confirmed the diagnosis of an infra-Hisian 2:1 AV block. |
 | View Full Size Image | |
Media type: CT
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Second-Degree Atrioventricular Block excerpt Article Last Updated: Jun 29, 2006
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