Infra-Hisian Block
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Sara Mohsin, M.D.[2]
Overview
Infra-Hisian blocks are defined as impaired conduction in the electrical system of the heart that occur below the AV node.
Historical perspective
- In 1899, Dr. Wenckebach described progressive delay between atrial and ventricular contraction and the eventual failure of a P wave to reach the ventricles.
- Dr. Mobitz then divided the second degree AV block into two subtypes.
- In 1905, Dr. John Hay discovered the second degree of AV block.[1]
- Dr. Hay was examining a patient who complains of slow pulse and dyspnea on exertion for more than 2 years. Dr. Hay noticed the heart rate dropping from 80 beats to 40 beats per minute.
- Dr. Hay noted the a waves and the arterial pulse to remain stable in the beginning. However, recording pulsation for several times resulted in "a" waves that were not followed by c wave. The a-c jugular wave interval was used as a measurement of AV conduction.
- Dr. Hay figured out that the pause following a wave was due to failure of ventricular muscles to respond to a stimulus.
Classification
Infrahisian block describes block of the distal conduction system. Types of infrahisian block include:
Of these types of infrahisian block, Mobitz II heart block is considered most important because of the possible progression to complete heart block.
Pathophysiology
Mobitz type II second degree AV block Mobitz type II second degree AV block, in which the PR interval remains unchanged prior to a P wave that fails to conduct to the ventricles. It almost always results from conduction system disease below the level of the AV node, occurring in the bundle of His in approximately 20 percent of cases and in the bundle branches in the remainder. Patients with bundle branch involvement also have axis shifts and QRS widening depending upon the location of the block. In addition, at least two-thirds of patients with this disorder also have bifascicular or even trifascicular disease. Mobitz type I and Mobitz type II second degree AV block cannot be differentiated from the ECG when 2:1 AV block is present. In this situation, every other P wave is non-conducted and there is no opportunity to observe for the constant PR interval that is characteristic of Mobitz type II second degree AV block.
Mobitz Type II
Conduction delay in Mobitz type II second degree block is almost always infra-nodal (His bundle [20%], bundle branches or fascicles). Usually the morphology of the QRS complex is wide, except when the site of block is the His bundle. In this variant of second degree heart block the PR interval is constant with occasional dropped beats as compared to the gradually prolonging PR interval in Mobitz type I. Bifascicular or trifascicular disease is seen in two thirds of the patients with Mobitz type II.[2][3]
Causes
The potential etiologies of Mobitz type II second degree AV block include reversible (both pathologic and iatrogenic) and idiopathic causes that are similar to other degrees of AV block (table 1). Common potentially reversible causes include:
●Pathologic – Myocardial ischemia (acute or chronic) involving the conduction system, cardiomyopathy (eg, amyloidosis, sarcoidosis), myocarditis (eg, Lyme disease), endocarditis with abscess formation, hyperkalemia, and hypervagotonia.
●Iatrogenic – Medication-related (AV nodal blocking medications), post-cardiac surgery, post-catheter ablation, post-transcatheter aortic valve implantation.
Mobitz type II second degree AV block is rarely seen in patients without underlying heart disease. When identifiable, the reversible causes most commonly associated with Mobitz type II second degree AV block are myocardial infarction with ischemia of the AV node and medications that alter conduction through the AV node (eg, digoxin, beta blockers, calcium channel blockers). When no specific reversible cause is identified, the block is often felt to be related to idiopathic progressive cardiac conduction disease with myocardial fibrosis and/or sclerosis that affects the conduction system.
| Physiologic and pathophysiologic | |
|---|---|
| Increased vagal tone | |
| Ischemic heart disease, including acute myocardial infarction | |
| Progressive cardiac conduction system disease | With fibrosis and/or sclerosis (Lenegre disease) |
| With calcification (Lev disease) | |
| Infections (eg, viral myocarditis, Lyme carditis) | |
| Cardiomyopathy | Infiltrative processes (eg, sarcoidosis, amyloidosis, hemochromatosis, malignancy, etc) |
| Other non-ischemic cardiomyopathies (eg, idiopathic, infectious, etc) | |
| Congenital AV block | Related to structural congenital heart disease |
| As part of neonatal lupus syndrome | |
| Other | Hyperkalemia |
| severe hypo- or hyperthyroidism | |
| trauma | |
| degenerative neuromuscular diseases | |
| Iatrogenic | |
| Drugs | Beta blockers |
| calcium channel blockers | |
| digoxin | |
| antiarrhythmic drugs | |
| adenosine | |
| Transcatheter aortic valve implantation | |
| Cardiac surgery | Post valvular surgery |
| post surgical correction of congenital heart disease | |
| Catheter ablation of arrhythmias | |
| Alcohol septal ablation for hypertrophic cardiomyopathy | |
| Transcatheter closure of ventricular septal defect | |
Life Threatening Causes
Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated[4].
- Acute myocardial infarction[5][6]
- Acute rheumatic fever
- Bacterial endocarditis
- Myocarditis
- Severe hypothermia
Common Causes
- Acute rheumatic fever
- Bacterial endocarditis[7]
- Calcific aortic stenosis
- Digoxin
- Dilated cardiomyopathy
- Diltiazem
- Enhanced vagal tone
- HCM
- Hypertension
- Iatrogenic after surgical correction of VSD, tetralogy of Fallot, and endocardial cushion defect
- Inferior ST elevation MI
- Massive calcification of the mitral annulus
- Myocarditis
- Normal variants[3]
- Penetrating and non-penetrating trauma of the chest
- Sclerodegenerative disease of the electrical conduction system
- Verapamil
- β blockers
Causes by Organ System
Causes in Alphabetical Order
Differentiating ((Page name)) from other Diseases
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Epidemiology and Demographics
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In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.
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Patients of all age groups may develop [disease name].
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The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.
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[Acute disease name] commonly affects [age group].
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[Disease name] affects men and women equally.
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Risk Factors
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Screening
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According to the [guideline name], screening for [disease name] is not recommended.
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According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].
Natural History, Complications, and Prognosis
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Diagnosis
Diagnostic Study of Choice
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History and Symptoms
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Physical Examination
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The presence of [finding(s)] on physical examination is diagnostic of [disease name].
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The presence of [finding(s)] on physical examination is highly suggestive of [disease name].
Laboratory Findings
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Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
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[Test] is usually normal among patients with [disease name].
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Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
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There are no diagnostic laboratory findings associated with [disease name].
Electrocardiogram
There are no ECG findings associated with [disease name].
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An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
References
- ↑ Upshaw CB, Silverman ME (2000). "John Hay: discoverer of type II atrioventricular block". Clin Cardiol. 23 (11): 869–71. doi:10.1002/clc.4960231118. PMC 6655013 Check
|pmc=value (help). PMID 11097138. - ↑ Puech P, Wainwright RJ (1983). "Clinical electrophysiology of atrioventricular block". Cardiol Clin. 1 (2): 209–24. PMID 6544636.
- ↑ 3.0 3.1 Wogan JM, Lowenstein SR, Gordon GS (1993). "Second-degree atrioventricular block: Mobitz type II". J Emerg Med. 11 (1): 47–54. doi:10.1016/0736-4679(93)90009-v. PMID 8445186.
- ↑ Mangi MA, Jones WM, Napier L. PMID 29493981. Missing or empty
|title=(help) - ↑ Misumida N, Ogunbayo GO, Kim SM, Abdel-Latif A, Ziada KM, Elayi CS (November 2018). "Frequency and Significance of High-Degree Atrioventricular Block and Sinoatrial Node Dysfunction in Patients With Non-ST-Elevation Myocardial Infarction". Am. J. Cardiol. 122 (10): 1598–1603. doi:10.1016/j.amjcard.2018.08.001. PMID 30227965.
- ↑ Barold SS, Herweg B (December 2012). "Second-degree atrioventricular block revisited". Herzschrittmacherther Elektrophysiol. 23 (4): 296–304. doi:10.1007/s00399-012-0240-8. PMID 23224264.
- ↑ Kamatani T, Akizuki A, Kondo S, Shirota T (Fall 2016). "Second-Degree Atrioventricular Block Occurring After Tooth Extraction". Anesth Prog. 63 (3): 156–9. doi:10.2344/15-00042.1. PMC 5011958. PMID 27585419.
- ↑ Menicagli F, Lanza A, Sbrocca F, Baldi A, Spugnini EP (2016). "A case of advanced second-degree atrioventricular block in a ferret secondary to lymphoma". Open Vet J. 6 (1): 68–70. doi:10.4314/ovj.v6i1.10. PMC 4833871. PMID 27200273.