Infra-Hisian Block: Difference between revisions

	Infra-Hisian Block Microchapters
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
Treatment
Prevention
Differentiating Infra-Hisian Block from other Diseases

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Revision as of 00:00, 15 May 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Mohsin, M.D.[2]

Overview

Infra-Hisian block is defined as an impaired conduction in the electrical system of the heart that occurs below the atrioventricular node.

Historical Perspective

In 1899, Dr. Wenckebach described the 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]
While Dr. Hay was examining a patient who complained of a slow pulse and had dyspnea on exertion for more than 2 years, he 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 the pulsation 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

Infra-hisian block describes the block of distal conduction system.
Types of infra-hisian block are shown in the following table:

Classification of Infra-Hisian Block
Types of Infra-Hisian Block	Sub-type
Type 2 second degree heart block (Mobitz II)	_
Left bundle branch block	Left anterior fascicular block
Left bundle branch block	Left posterior fascicular block
Right bundle branch block	_

Out of all these types of infra-hisian block, Mobitz II heart block is considered as the most important because of the possible progression to a complete heart block.

Pathophysiology

Normal Cardiac Conduction

The normal cardiac conduction proceeds in a way so as to allow time for the atrium to relax during atrial diastole.
The electrical impulse generated in the SA node travels through the internodal pathways towards the AV node.
The conduction through the AV node is slowed down as it travels through it. This decrease in velocity of conduction allows time for the atrium to contract ahead of the ventricle so that the blood from the atria can fill up the ventricles through the atrioventricular valves.
As the impulse flows through the compact AV node, it rapidly conducts through the ventricular myocardial cells. Once the depolarization is complete, the ventricle relaxes during diastole in preparation for the next impulse.

Anatomy

The conduction system of heart consists of specialized cells designed to conduct electrical impulse faster than the surrounding myocardial cells.
Anatomically, the AV node is divided into three regions as follows:
- Transitional cell zone: This is the region where the internodal atrial pathways merge with the compact AV node.
- Compact AV node: This region is located at the apex of the triangle of Koch, which is formed by the ostium of coronary sinus, tricuspid annulus and the tendon of Todaro.
- Penetrating portion of the AV bundle: This region enters the tendon of Todaro and runs within the fibrous body of the membranous interventricular septum and eventually divides at the crest of the muscular interventricular septum into right and left branches.
The left bundle branch penetrates the membranous portion of the interventricular septum and divides into several smaller branches. Parts of the left bundle branch include a pre-divisional segment, anterior fascicle/hemibundle and posterior fascicle/hemibundle. Rarely a median fascicle is present in some hearts.
- The anterior fascicle supplies the anterior papillary muscle and the Purkinje network of the antero-lateral surface of the left ventricle.
- The posterior fascicle supplies the posterior papillary muscle and the Purkinje network of the postero-inferior surface of the left ventricle.
- Left bundle branch receives its blood supply from left anterior descending artery.

Structure of the heart's conduction system

Pathophysiology of LBBB

Unlike right bundle branch block (RBBB), left bundle branch block completely modifies the way of depolarization of the conduction system of the heart. In LBBB the activation of interventricular septum is from right to left due to uninterrupted conduction in the RBB.
Then the electrical impulse propagates inferiorly to the left resulting in delayed depolarization and activation of the left ventricle especially the left lateral wall.^[2]
In LBBB the right to left activation of the septum causes a small negative deflection (Q wave) in lead V₁ and a positive deflection (R wave) in lead V₆. Right ventricle depolarizes earlier than the left ventricle giving an R wave in lead V₁ and an S wave in lead V₆. Subsequent delayed depolarization of the left ventricle results in an S wave in lead V₁ and another R wave in lead V₆.

Pathophysiology of Mobitz type II second degree AV block

Mobitz type II second degree AV block is characterized by a PR interval that remains unchanged with occasional dropped beats prior to a P wave that fails to conduct to the ventricles as compared to the gradually prolonging PR interval in Mobitz type I.
ECG findings include intermittently non-conducted P waves not preceded by PR prolongation and not followed by PR shortening.
It almost always results from a disease of the conduction system below the level of AV node, occurring in the bundle of His in approximately 20% of the cases and in the bundle branches in the remainder.
Depending upon the location of the block, patients having bundle branch involvement also have axis shifts and QRS widening.
At least two-thirds of the patients with Mobitz type II second degree AV block have bifascicular or even trifascicular disease.^[3]^[4]
In the presence of 2:1 AV block, Mobitz type I and Mobitz type II second degree AV block cannot be differentiated on the basis of electrocardiographic findings. In such cases, every other P wave is non-conducted without a chance to observe the constant PR interval that is characteristic of Mobitz type II second degree AV block.
The conduction delay seen in Mobitz type II second degree block is almost always at the infra-nodal level involving the distal conduction system (His bundle (20%), bundle branches or/and fascicles).

Although often both the terms, infranodal block or infrahisian block are applied to Mobitz type II second degree AV block, they are not synonymous with it.

Infranodal block and infra-Hisian block are terms which refer to the anatomic location of the block, whereas
Mobitz II refers to an electrocardiographic pattern associated with block at these levels.^[5]

Causes

Mobitz type II second degree AV block 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

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.

Major reversible causes of atrioventricular (AV) block
Physiologic and pathophysiologic
Increased vagal tone	Also known as hypervagotonia
Ischemic heart disease	Acute or chronic myocardial infarction/ischemia involving the conduction system.
Progressive cardiac conduction system disease	Associated with: Calcification in Lev's disease Fibrosis and/or sclerosis in Lenegre's disease
Infections	Viral myocarditis Lyme carditis Endocarditis with abscess formation
Cardiomyopathy	Infiltrative processes such as: Sarcoidosis Hemochromatosis Amyloidosis Malignancy Other non-ischemic cardiomyopathies include: Idiopathic Infectious
Congenital AV block	It is related to structural congenital heart disease It occurs as a part of neonatal lupus syndrome
Other reversible causes	Hyperkalemia Severe hypo- or hyperthyroidism Degenerative neuromuscular diseases Trauma
Iatrogenic
Drugs (altering conduction through AV node)	Beta-blockers Digoxin Calcium channel blockers Adenosine Antiarrhythmic drugs
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
Post-transcatheter aortic valve implantation

Life Threatening Causes

Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated.^[6]

Common Causes

Causes by Organ System

Cardiovascular	Acute myocardial infarction, acute rheumatic fever, ASD, dilated cardiomyopathy, Ebstein's anomaly, hypersensitive carotid sinus syndrome, hypertension, hypertrophic cardiomyopathy, Lev's disease, myocardial bridging, myocarditis, normal variants, post aortic valve replacement, post catheter ablation for arrhythmias, post closure of a ventricular septal defect, post mitral valve replacement, tetralogy of Fallot, endocardial cushion defect, transposition of the great vessels, valvular heart disease, VSD
Chemical / poisoning	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Amiodarone, beta-blockers, digitalis, calcium channel blockers, cholinesterase inhibitors, disopyramide, dofetilide, dolasetron, donepezil, eslicarbazepine acetate, fesoterodine, fingolimod, flecainide, ibutilide, lacosamide, magnesium, paliperidone, pramipexole, procainamide, propafenone, propoxyphene, quinidine, sotalol, terodiline
Ear Nose Throat	No underlying causes
Endocrine	Hyperthyroidism, myxedema, thyrotoxic periodic paralysis
Environmental	Hypothermia
Gastroenterologic	Hemochromatosis
Genetic	Emery-Dreifuss muscular dystrophy, Fabry disease, glycogenosis type 2b, hereditary neuromuscular disease, Kearns-Sayre syndrome
Hematologic	Multiple myeloma Lymphoma^[10]
Iatrogenic	Post aortic valve replacement, post catheter ablation for arrhythmias, post closure of a ventricular septal defect, post mitral valve replacement
Infectious Disease	Acute rheumatic fever, Chagas disease, diphtheria, Lyme disease, myocarditis, neonatal lupus erythematosus, protozoal infection, sarcoidosis, SLE, tuberculosis
Musculoskeletal / Ortho	Ankylosing spondylitis, hereditary neuromuscular disease, Kearns-Sayre syndrome, mitochondrial genome inherited conditions, muscular dystrophy
Neurologic	Enhanced vagal tone
Nutritional / Metabolic	Fabry disease, glycogenosis type 2b
Obstetric/Gynecologic	No underlying causes
Oncologic	Multiple myeloma
Opthalmologic	No underlying causes
Overdose / Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	Sarcoidosis
Renal / Electrolyte	Hyperkalemia, hypokalemia
Rheum / Immune / Allergy	Ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, SLE
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	Amyloidosis, degenerative diseases

Causes in Alphabetical Order

Epidemiology and Demographics

Prevalence

In United States, the prevalence of second-degree AV block is believed to be 3 in 100,000 individuals.^[11]
Nearly 3% of the patients with underlying structural heart disease develop some form of second-degree AV block.
The male-to-female ratio of second-degree AV block is 1:1.

Gender

Men and women are affected equally by second degree AV block.

Risk Factors

Common risk factors associated with second degree AV block include the following:^[12]^[13]^[14]^[15]
- Intrinsic atrioventricular node disease
- Myocarditis
- Acute myocardial infarction
- Prior cardiac surgery
- Older age
- Heart attack or coronary artery disease
- Cardiomyopathy
- Sarcoidosis
- Lyme disease
- High potassium levels
- Severe hypothyroidism
- Certain inherited neuromuscular diseases
- Medicines that slow the heart rate
- After open heart surgery

Natural History, Complications and Prognosis

Natural History

Mobitz II second degree AV block is due to the block inferior to the AV node (infra-Hisian structures) and it rapidly progresses to a complete heart block in which no escape rhythm may emerge.^[16]

Complications

Prognosis

Mobitz II, as it involves the infra-nodal structures, carries the risk of progression to complete heart block and carries an unfavorable prognosis.^[12]

Diagnosis

Electrocardiogram

There are intermittent blocked P waves.
In the conducted beats, the PR intervals remain constant.
The PR is fairly constant except that slight shortening may occur in the first beat after the blocked cycle. This is the result of improved conduction following the block.
Most patients with type II second-degree AV block have associated bundle branch block.
In these instances, the block is usually located distal to the His bundle. However, in approximately 27% to 35% of the patients, the lesion is located in the His bundle itself, and a narrow complex may be inscribed.
2:1 AV Block:

Impossible to determine whether the second-degree AV block is type I or type II.
A long rhythm strip is helpful to document any change in the behavior of the conduction ratio.
When the atrial rate is increased by exercise or by atropine, the AV block in type I tends to decrease and that in type II tends to increase.

Shown below is an electrocardiogram of a 12 lead EKG with a 2:1 AV block.

Copyleft image obtained, courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page

Shown below is an electrocardiogram of a type II second degree AV block (Mobitz type II).

Copyleft image obtained, courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page

Treatment

Medical therapy for Mobitz II

Correction of reversible causes of the block such as ischemia, medications, and vagotonic conditions should be considered.^[5]
Treatment may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce the risk factors associated with heart attack and stroke.^[28]
Treatment in emergency situations are atropine and an external pacer.^[8]^[4]

Contraindicated medications

Second degree AV block(except in patients with a functioning artificial pacemaker)^[29]^[30] is considered an absolute contraindication to the use of the following medications:

Adenosine
Atenolol
Betaxolol
Bisoprolol
Brimonidine tartrate and Timolol maleate
Carteolol
Diltiazem
Disopyramide
Dronedarone
Flecainide
Metoprolol
Mexiletine
Nadolol
Nebivolol
Penbutolol
Pindolol
Propranolol
Sotalol
Timolol
Labetalol^[31]

Surgery for Mobitz II

Definitive treatment-Pacemaker insertion

Type II Mobitz (symptomatic or asymptomatic) is by itself an indication for insertion of a pacemaker (definitive treatment). Other indications include:^[20]^[32]^[33]^[34]:
- Myotonic dystrophy
- Kearns-Sayre syndrome
- Erb's dystrophy
- Peroneal muscular atrophy. These neuromuscular disorders have a high potential for unpredictable rapid progression to complete heart block.
Implantation of permanent pacemakers in both asymptomatic and symptomatic patients is usually done. Asymptomatic Mobitz II are prone to be converted to symptomatic or third degree heart block. Thus, they should be considered for a pacemaker even if asymptomatic.
A dual chamber DDD pacemaker is preferred over a single chambered VVI pacemakers as it maintains physiologic AV synchrony.
A dual-chamber artificial pacemaker is a type of device that typically listens for a pulse from the SA node and sends a pulse to the AV node at an appropriate interval, essentially completing the connection between the two nodes. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation.

Prevention

Primary Prevention

Effective treatment of hypertension and maintenance of normal blood glucose levels may be useful strategies in preventing the AV block.

Differentiating Infra-Hisian Block from other Diseases


Arrhythmia		Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrioventricular block^[35]	First degree ^[36]^[37]	Regular		Normal	Prolonged PR interval (>200 msec)	Less than 0.12 seconds, consistent, and normal in morphology.	No treatment required	Prevalence: 650 to 1600 per 100,000 individuals in the United States.	Heart failure Coronary heart disease Cardiomyopathy Sarcoidosis Lyme disease Degenerative muscle disorders as Lev's disease and Lenegre's disease. Overly active vagus nerve.
	Second degree^[11]^[38]	Regular irregular		Normal	Mobtiz I: Progressive PR prolongation Mobitz II: Normal PR interval	QRS is normal but dropped as the following: Mobitz I: QRS complex is dropped after a progressive lengthening of PR Mobitz II: QRS complex is dropped after a normal PR	Can be reversed by using a pacemaker.	Prevalence: 3 per 100,000 individuals in the United States.
	Third degree^[39]^[40]	Regular		Normal but no relationship between P wave and the QRS. More P waves than the QRS complexes.	Varies	Normal QRS	Can be reversed by using a pacemaker.	The prevalence: 20 per 100,000 individuals worldwide.
Atrial Fibrillation (AFib)^[41]^[42]		Irregularly irregular	On a 10-second 12-lead EKG strip, multiply number of QRS complexes by 6	Absent Fibrillatory waves	Absent	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Does not break with adenosine or vagal maneuvers	2.7–6.1 million people in the United States have AFib 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement
Atrial Flutter^[43]		Regular or Irregular	75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common	Sawtooth pattern of P waves at 250 to 350 bpm Biphasic deflection in V1	Varies depending upon the magnitude of the block, but is short	Less than 0.12 seconds, consistent, and normal in morphology	Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm	Incidence: 88 per 100,000 individuals	Elderly Alcohol
Atrioventricular nodal reentry tachycardia (AVNRT)^[44]^[45]^[46]^[47]		Regular	140-280 bpm	Slow-Fast AVNRT: Pseudo-S wave in leads II, III, and AVF Pseudo-R' in lead V1. Fast-Slow AVNRT P waves between the QRS and T waves (QRS-P-T complexes) Slow-Slow AVNRT Late P waves after a QRS Often appears as atrial tachycardia. Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)	Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction QRS alternans may be present	May break with adenosine or vagal maneuvers	60%-70% of all supraventricular tachycardias	Structural heart disease Atrial tachyarrhythmias
Multifocal Atrial Tachycardia^[48]^[49]		Irregular	Atrial rate is > 100 beats per minute	Varying morphology from at least three different foci Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude	Variable PR intervals, RR intervals, and PP intervals	Less than 0.12 seconds, consistent, and normal in morphology	Does not terminate with adenosine or vagal maneuvers	0.05% to 0.32% of electrocardiograms in general hospital admissions	Elderly Chronic obstructive pulmonary disease (COPD)
Paroxysmal Supraventricular Tachycardia		Regular	150 and 240 bpm	Absent Hidden in QRS	Absent	Narrow complexes (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex	Prevalence: 0.023 per 100,000	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome
Premature Atrial Contractrions (PAC)^[50]^[51]		Regular except when disturbed by premature beat(s)	80-120 bpm	Upright	> 0.12 second May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node Ashman’s phenomenon: PAC displaying a right bundle branch block pattern	Usually narrow (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex		Infants Cardiomyopathy Myocarditis Elderly Coronary artery disease Stroke Increased atrial natriuretic peptide (ANP) Hypercholesterolemia
Wolff-Parkinson-White Syndrome^[52]^[53]		Regular	Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm	With orthodromic conduction due to a bypass tract, the P wave generally follows the QRS complex, whereas in AVNRT, the P wave is generally buried in the QRS complex.	Less than 0.12 seconds	A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.	May break in response to procainamide, adenosine, vagal maneuvers	Worldwide prevalence of WPW syndrome is 100 - 300 per 100,000	Ebstein's anomaly Mitral valve prolapse: This cardiac disorder, if present, is associated with left-sided accessory pathways. Hypertrophic cardiomyopathy: This disorder is associated with familial/inherited form of WPW syndrome. Hypokalemic periodic paralysis Pompe disease Tuberous sclerosis
Ventricular Fibrillation (VF)^[54]^[55]^[56]		Irregular	150 to 500 bpm	Absent	Absent	Absent (R on T phenomenon in the setting of ischemia)	Does not break in response to procainamide, adenosine, vagal maneuvers	3-12% cases of acute myocardial infarction (AMI) Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm	Myocardial ischemia / infarction Cardiomyopathy Channelopathies e.g. Long QT (acquired / congenital) Electrolyte abnormalities (hypokalemia/hyperkalemia, hypomagnesemia) Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis) Sepsis Hypothermia Pneumothorax Seizures Stroke
Ventricular Tachycardia^[57]^[58]		Regular	> 100 bpm (150-200 bpm common)	Absent	Absent Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation	Wide complex, QRS duration > 120 milliseconds	Does not break in response to procainamide, adenosine, vagal maneuvers	5-10% of patients presenting with AMI	Coronary artery disease Aortic stenosis Cardiomyopathy Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) Inherited channelopathies (e.g., long-QT syndrome) Catecholaminergic polymorphic ventricular tachycardia Arrhythmogenic right ventricular dysplasia Myocardial infarction Torsades de pointes is a form of polymorphic VT that is often associated with a prolonged QT interval

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↑ Gupta PK, Lichstein E, Chadda KD (1976). "Chronic His bundle block. Clinical, electrocardiographic, electrophysiological, and follow-up studies on 16 patients". Br Heart J. 38 (12): 1343–9. doi:10.1136/hrt.38.12.1343. PMC 483178. PMID 1008977.
↑ Steere AC, McHugh G, Damle N, Sikand VK (2008). "Prospective study of serologic tests for lyme disease". Clin Infect Dis. 47 (2): 188–95. doi:10.1086/589242. PMC 5538270. PMID 18532885.
↑ Schernthaner C, Kraus J, Danmayr F, Hammerer M, Schneider J, Hoppe UC, Strohmer B (March 2016). "Short-term pacemaker dependency after transcatheter aortic valve implantation". Wien. Klin. Wochenschr. 128 (5–6): 198–203. doi:10.1007/s00508-015-0906-4. PMID 26745972.
↑ Brignole M, Deharo JC, Guieu R (August 2015). "Syncope and Idiopathic (Paroxysmal) AV Block". Cardiol Clin. 33 (3): 441–7. doi:10.1016/j.ccl.2015.04.012. PMID 26115830.
↑ Kelkar PN (August 1998). "Atenolol induced high grade AV block". J Assoc Physicians India. 46 (8): 748, 751. PMID 11229299.
↑ Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, Viskin S (July 2004). "Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug". J. Am. Coll. Cardiol. 44 (1): 105–8. doi:10.1016/j.jacc.2004.03.057. PMID 15234417.
↑ Tuohy S, Saliba W, Pai M, Tchou P (January 2018). "Catheter ablation as a treatment of atrioventricular block". Heart Rhythm. 15 (1): 90–96. doi:10.1016/j.hrthm.2017.08.015. PMID 28823599.
↑ Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD (August 2019). "2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society". J. Am. Coll. Cardiol. 74 (7): e51–e156. doi:10.1016/j.jacc.2018.10.044. PMID 30412709.
↑ Strasberg B, Amat-Y-Leon F, Dhingra RC, Palileo E, Swiryn S, Bauernfeind R, Wyndham C, Rosen KM (May 1981). "Natural history of chronic second-degree atrioventricular nodal block". Circulation. 63 (5): 1043–9. doi:10.1161/01.cir.63.5.1043. PMID 7471363.
↑ Kerola T, Eranti A, Aro AL, Haukilahti MA, Holkeri A, Junttila MJ; et al. (2019). "Risk Factors Associated With Atrioventricular Block". JAMA Netw Open. 2 (5): e194176. doi:10.1001/jamanetworkopen.2019.4176. PMC 6632153 Check |pmc= value (help). PMID 31125096.
↑ Barold SS (1996). "Indications for permanent cardiac pacing in first-degree AV block: class I, II, or III?". Pacing Clin Electrophysiol. 19 (5): 747–51. doi:10.1111/j.1540-8159.1996.tb03355.x. PMID 8734740.
↑ Upshaw CB (2004). "Comparison of the prevalence of first-degree atrioventricular block in African-American and in Caucasian patients: an electrocardiographic study III". J Natl Med Assoc. 96 (6): 756–60. PMC 2568382. PMID 15233485.
↑ Friedman HS, Gomes JA, Haft JI (1975). "An analysis of Wenckebach periodicity". J Electrocardiol. 8 (4): 307–15. doi:10.1016/s0022-0736(75)80003-3. PMID 1176840.
↑ OSTRANDER LD, BRANDT RL, KJELSBERG MO, EPSTEIN FH (June 1965). "ELECTROCARDIOGRAPHIC FINDINGS AMONG THE ADULT POPULATION OF A TOTAL NATURAL COMMUNITY, TECUMSEH, MICHIGAN". Circulation. 31: 888–98. doi:10.1161/01.cir.31.6.888. PMID 14297523.
↑ Movahed MR, Hashemzadeh M, Jamal MM (October 2005). "Increased prevalence of third-degree atrioventricular block in patients with type II diabetes mellitus". Chest. 128 (4): 2611–4. doi:10.1378/chest.128.4.2611. PMID 16236932.
↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
↑ Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
↑ Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
↑ Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
↑ "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
↑ Schernthaner C, Danmayr F, Strohmer B (2014). "Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias". Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
↑ Scher DL, Arsura EL (September 1989). "Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment". Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
↑ Goodacre S, Irons R (March 2002). "ABC of clinical electrocardiography: Atrial arrhythmias". BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
↑ Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). "Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome". J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
↑ Strasburger JF, Cheulkar B, Wichman HJ (December 2007). "Perinatal arrhythmias: diagnosis and management". Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). "Evaluation and management of wolff-Parkinson-white in athletes". Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
↑ Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
↑ Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). "Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction". J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
↑ Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
↑ Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). "Sudden cardiac death: epidemiology and risk factors". Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
↑ Koplan BA, Stevenson WG (March 2009). "Ventricular tachycardia and sudden cardiac death". Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
↑ Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

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[pmid26745972-28] Schernthaner C, Kraus J, Danmayr F, Hammerer M, Schneider J, Hoppe UC, Strohmer B (March 2016). "Short-term pacemaker dependency after transcatheter aortic valve implantation". Wien. Klin. Wochenschr. 128 (5–6): 198–203. doi:10.1007/s00508-015-0906-4. PMID 26745972.

[pmid26115830-29] Brignole M, Deharo JC, Guieu R (August 2015). "Syncope and Idiopathic (Paroxysmal) AV Block". Cardiol Clin. 33 (3): 441–7. doi:10.1016/j.ccl.2015.04.012. PMID 26115830.

[pmid11229299-30] Kelkar PN (August 1998). "Atenolol induced high grade AV block". J Assoc Physicians India. 46 (8): 748, 751. PMID 11229299.

[pmid15234417-31] Zeltser D, Justo D, Halkin A, Rosso R, Ish-Shalom M, Hochenberg M, Viskin S (July 2004). "Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug". J. Am. Coll. Cardiol. 44 (1): 105–8. doi:10.1016/j.jacc.2004.03.057. PMID 15234417.

[pmid28823599-32] Tuohy S, Saliba W, Pai M, Tchou P (January 2018). "Catheter ablation as a treatment of atrioventricular block". Heart Rhythm. 15 (1): 90–96. doi:10.1016/j.hrthm.2017.08.015. PMID 28823599.

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[pmid7471363-34] Strasberg B, Amat-Y-Leon F, Dhingra RC, Palileo E, Swiryn S, Bauernfeind R, Wyndham C, Rosen KM (May 1981). "Natural history of chronic second-degree atrioventricular nodal block". Circulation. 63 (5): 1043–9. doi:10.1161/01.cir.63.5.1043. PMID 7471363.

[pmid311250962-35] Kerola T, Eranti A, Aro AL, Haukilahti MA, Holkeri A, Junttila MJ; et al. (2019). "Risk Factors Associated With Atrioventricular Block". JAMA Netw Open. 2 (5): e194176. doi:10.1001/jamanetworkopen.2019.4176. PMC 6632153 Check |pmc= value (help). PMID 31125096.

[pmid8734740-36] Barold SS (1996). "Indications for permanent cardiac pacing in first-degree AV block: class I, II, or III?". Pacing Clin Electrophysiol. 19 (5): 747–51. doi:10.1111/j.1540-8159.1996.tb03355.x. PMID 8734740.

[pmid15233485-37] Upshaw CB (2004). "Comparison of the prevalence of first-degree atrioventricular block in African-American and in Caucasian patients: an electrocardiographic study III". J Natl Med Assoc. 96 (6): 756–60. PMC 2568382. PMID 15233485.

[pmid1176840-38] Friedman HS, Gomes JA, Haft JI (1975). "An analysis of Wenckebach periodicity". J Electrocardiol. 8 (4): 307–15. doi:10.1016/s0022-0736(75)80003-3. PMID 1176840.

[pmid14297523-39] OSTRANDER LD, BRANDT RL, KJELSBERG MO, EPSTEIN FH (June 1965). "ELECTROCARDIOGRAPHIC FINDINGS AMONG THE ADULT POPULATION OF A TOTAL NATURAL COMMUNITY, TECUMSEH, MICHIGAN". Circulation. 31: 888–98. doi:10.1161/01.cir.31.6.888. PMID 14297523.

[pmid16236932-40] Movahed MR, Hashemzadeh M, Jamal MM (October 2005). "Increased prevalence of third-degree atrioventricular block in patients with type II diabetes mellitus". Chest. 128 (4): 2611–4. doi:10.1378/chest.128.4.2611. PMID 16236932.

[pmid24837984-41] Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.

[pmid22518390-42] Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.

[pmid28835836-43] Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.

[pmid27617092-44] Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.

[pmid20458824-45] Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.

[urlAtrioventricular_Nodal_Reentry_Tachycardia_(AVNRT)_-_StatPearls_-_NCBI_Bookshelf-46] "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".

[pmid25196716-47] Schernthaner C, Danmayr F, Strohmer B (2014). "Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias". Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.

[pmid2570520-48] Scher DL, Arsura EL (September 1989). "Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment". Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.

[pmid11884328-49] Goodacre S, Irons R (March 2002). "ABC of clinical electrocardiography: Atrial arrhythmias". BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.

[pmid26316525-50] Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). "Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome". J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.

[pmid18063110-51] Strasburger JF, Cheulkar B, Wichman HJ (December 2007). "Perinatal arrhythmias: diagnosis and management". Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.

[pmid24982705-52] Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). "Evaluation and management of wolff-Parkinson-white in athletes". Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.

[pmid10597097-53] Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.

[pmid27899944-54] Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). "Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction". J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.

[pmid11334828-55] Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.

[pmid20142817-56] Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). "Sudden cardiac death: epidemiology and risk factors". Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.

[pmid19252119-57] Koplan BA, Stevenson WG (March 2009). "Ventricular tachycardia and sudden cardiac death". Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.

[pmid21505622-58] Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

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@@ Line 65: / Line 65: @@
 ===Pathophysiology of LBBB===
-* Unlike [[right bundle branch block]] ([[RBBB]]), left bundle branch block completely modifies the way of depolarization of the conduction system of the heart.  In LBBB the activation of the [[interventricular septum]] is from right to left due to uninterrupted conduction in the RBB.
+* Unlike [[right bundle branch block]] ([[RBBB]]), [[left bundle branch block]] completely modifies the way of [[depolarization]] of the [[Electrical conduction system of the heart|conduction system of the heart]].  In [[Left bundle branch block|LBBB]] the [[Activation energy|activation]] of [[interventricular septum]] is from right to left due to uninterrupted [[Conductance|conduction]] in the [[Right bundle branch block|RBB]].
 * Then the electrical impulse propagates inferiorly to the left resulting in delayed depolarization and activation of the [[left ventricle]] especially the left lateral wall.<ref name="pmid17385703">{{cite journal |author=Francia P, Balla C, Paneni F, Volpe M |title=Left bundle-branch block--pathophysiology, prognosis, and clinical management |journal=Clinical Cardiology |volume=30 |issue=3 |pages=110–5 |year=2007 |month=March |pmid=17385703 |doi=10.1002/clc.20034 |url=}}</ref>
 * In LBBB the right to left  activation of the septum causes a small negative deflection ([[Q wave]]) in lead V<sub>1</sub> and a positive deflection ([[R wave]]) in lead V<sub>6</sub>. Right ventricle depolarizes earlier than the left ventricle giving an R wave in lead V<sub>1</sub> and an S wave in lead V<sub>6</sub>.  Subsequent delayed depolarization of the left ventricle results in an [[S wave]] in lead V<sub>1</sub> and another R wave in lead V<sub>6</sub>.