Infra-Hisian Block: Difference between revisions

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*[[Myocardial infarction]]
*[[Myocardial infarction]]
*[[Torsades de pointes]] is a form of polymorphic VT that is often associated with a prolonged [[QT interval]]
*[[Torsades de pointes]] is a form of polymorphic VT that is often associated with a prolonged [[QT interval]]
|}
The table below provides information on the [[differential diagnosis]] of ventricular tachycardia in terms of [[ECG]] appearance:
{| border="3"
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! style="background: #4479BA; width: 100px;" | {{fontcolor|#FFF| Disease Name}}
! style="background: #4479BA; width: 100px;" | {{fontcolor|#FFF| Causes}}
! style="background: #4479BA; width: 100px;" | {{fontcolor|#FFF| ECG Characteristics}}
! style="background: #4479BA; width: 100px;" | {{fontcolor|#FFF| ECG view}}
|-
! style="padding: 5px 5px; background: #DCDCDC; " align="left"| '''[[Ventricular tachycardia]]''' <ref name="AjijolaTung2014">{{cite journal|last1=Ajijola|first1=Olujimi A.|last2=Tung|first2=Roderick|last3=Shivkumar|first3=Kalyanam|title=Ventricular tachycardia in ischemic heart disease substrates|journal=Indian Heart Journal|volume=66|year=2014|pages=S24–S34|issn=00194832|doi=10.1016/j.ihj.2013.12.039}}</ref><ref name="Meja LopezMalhotra2019">{{cite journal|last1=Meja Lopez|first1=Eliany|last2=Malhotra|first2=Rohit|title=Ventricular Tachycardia in Structural Heart Disease|journal=Journal of Innovations in Cardiac Rhythm Management|volume=10|issue=8|year=2019|pages=3762–3773|issn=21563977|doi=10.19102/icrm.2019.100801}}</ref><ref name="CoughtrieBehr2017">{{cite journal|last1=Coughtrie|first1=Abigail L|last2=Behr|first2=Elijah R|last3=Layton|first3=Deborah|last4=Marshall|first4=Vanessa|last5=Camm|first5=A John|last6=Shakir|first6=Saad A W|title=Drugs and life-threatening ventricular arrhythmia risk: results from the DARE study cohort|journal=BMJ Open|volume=7|issue=10|year=2017|pages=e016627|issn=2044-6055|doi=10.1136/bmjopen-2017-016627}}</ref><ref name="El-Sherif2001">{{cite journal|last1=El-Sherif|first1=Nabil|title=Mechanism of Ventricular Arrhythmias in the Long QT Syndrome: On Hermeneutics|journal=Journal of Cardiovascular Electrophysiology|volume=12|issue=8|year=2001|pages=973–976|issn=1045-3873|doi=10.1046/j.1540-8167.2001.00973.x}}</ref><ref name="de RivaWatanabe2015">{{cite journal|last1=de Riva|first1=Marta|last2=Watanabe|first2=Masaya|last3=Zeppenfeld|first3=Katja|title=Twelve-Lead ECG of Ventricular Tachycardia in Structural Heart Disease|journal=Circulation: Arrhythmia and Electrophysiology|volume=8|issue=4|year=2015|pages=951–962|issn=1941-3149|doi=10.1161/CIRCEP.115.002847}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Ischemic heart disease]]
*Illicit drug use such as [[cocaine]] and [[methamphetamine]]
*[[Structural heart diseases]]
*[[Electrolyte disturbances]]
*[[Congestive heart failure]]
*[[Myocarditis]]
*[[Obstructive sleep apnea]]
*[[Pulmonary artery catheter]]
*[[Long QT syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Ventricular tachycardia originates from a [[ventricular]] focus.
* Lasts more than 30 seconds.
* [[Broad QRS complex]]es: rate of >90 BPM.
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
[[File:Capture V tach.PNG|center|300px]]<ref> ECG found in of https://en.ecgpedia.org/index.php?title=Main_Page </ref>
|-
! style="padding: 5px 5px; background: #DCDCDC; " align="left"| '''[[Ventricular fibrillation]]''' <ref name="pmid19252119">{{cite journal |vauthors=Koplan BA, Stevenson WG |title=Ventricular tachycardia and sudden cardiac death |journal=Mayo Clin. Proc. |volume=84 |issue=3 |pages=289–97 |date=March 2009 |pmid=19252119 |pmc=2664600 |doi=10.1016/S0025-6196(11)61149-X |url=}}</ref><ref name="pmid28222965">{{cite journal |vauthors=Maury P, Sacher F, Rollin A, Mondoly P, Duparc A, Zeppenfeld K, Hascoet S |title=Ventricular arrhythmias and sudden death in tetralogy of Fallot |journal=Arch Cardiovasc Dis |volume=110 |issue=5 |pages=354–362 |date=May 2017 |pmid=28222965 |doi=10.1016/j.acvd.2016.12.006 |url=}}</ref><ref name="pmid1638716">{{cite journal |vauthors=Saumarez RC, Camm AJ, Panagos A, Gill JS, Stewart JT, de Belder MA, Simpson IA, McKenna WJ |title=Ventricular fibrillation in hypertrophic cardiomyopathy is associated with increased fractionation of paced right ventricular electrograms |journal=Circulation |volume=86 |issue=2 |pages=467–74 |date=August 1992 |pmid=1638716 |doi=10.1161/01.cir.86.2.467 |url=}}</ref><ref name="BektasSoyuncu2012">{{cite journal|last1=Bektas|first1=Firat|last2=Soyuncu|first2=Secgin|title=Hypokalemia-induced Ventricular Fibrillation|journal=The Journal of Emergency Medicine|volume=42|issue=2|year=2012|pages=184–185|issn=07364679|doi=10.1016/j.jemermed.2010.05.079}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Coronary ischemia|Acute coronary ischemia]]
*[[cardiomyopathy|Cardiomyopathies]]
*[[Congenital heart disease]]
*[[Myocardial infarction]]
*[[Heart surgery]]
*[[Electrolyte abnormalities]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Poorly identifiable [[QRS complexes]] and absent [[P waves]]
* The [[heart rate]] is >300 BPM
*[[Rhythm]] is irregular
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
[[File:Capture VF.PNG|center|300px]]<ref> ECG found in https://en.ecgpedia.org/index.php?title=Main_Page </ref>
|-
! style="padding: 5px 5px; background: #DCDCDC; " align="left"| '''[[Ventricular flutter]]''' <ref name="ThiesBoos2000">{{cite journal|last1=Thies|first1=Karl-Christian|last2=Boos|first2=Karin|last3=Müller-Deile|first3=Kai|last4=Ohrdorf|first4=Wolfgang|last5=Beushausen|first5=Thomas|last6=Townsend|first6=Peter|title=Ventricular flutter in a neonate—severe electrolyte imbalance caused by urinary tract infection in the presence of urinary tract malformation|journal=The Journal of Emergency Medicine|volume=18|issue=1|year=2000|pages=47–50|issn=07364679|doi=10.1016/S0736-4679(99)00161-4}}</ref><ref name="KosterWellens1976">{{cite journal|last1=Koster|first1=Rudolph W.|last2=Wellens|first2=Hein J.J.|title=Quinidine-induced ventricular flutter and fibrillation without digitalis therapy|journal=The American Journal of Cardiology|volume=38|issue=4|year=1976|pages=519–523|issn=00029149|doi=10.1016/0002-9149(76)90471-9}}</ref><ref name="pmid250503">{{cite journal |vauthors=Dhurandhar RW, Nademanee K, Goldman AM |title=Ventricular tachycardia-flutter associated with disopyramide therapy: a report of three cases |journal=Heart Lung |volume=7 |issue=5 |pages=783–7 |date=1978 |pmid=250503 |doi= |url=}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Electrolyte disturbances]]
*[[Medications]] such as:
**[[Disopyramide]]
**[[Quinidine]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*The [[ECG]] shows:
**A typical [[sinusoidal]] pattern
**Frequency of 300 bpm
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
[[File:Capture Ven Flu.PNG|center|300px]]<ref> ECG found in https://en.ecgpedia.org/index.php?title=Main_Page </ref>
|-
! style="padding: 5px 5px; background: #DCDCDC;" align="left" | '''[[Asystole]]''' <ref name="ACLS_2003_H_T">''ACLS: Principles and Practice''. p. 71-87. Dallas: American Heart Association, 2003. ISBN 0-87493-341-2.</ref><ref name="ACLS_2003_EP_HT">''ACLS for Experienced Providers''. p. 3-5. Dallas: American Heart Association, 2003. ISBN 0-87493-424-9.</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Hypovolemia]]
*[[Hypoxia (medical)|Hypoxia]]
*[[Acidosis]]
*[[Hypothermia|Hypothermia]]
*[[Hyperkalemia|Hyperkalemia]] or [[Hypokalemia|Hypokalemia]]
*[[Hypoglycemia|Hypoglycemia]]
*[[Cardiac tamponade|Cardiac Tamponade]]
*[[Tension pneumothorax|Tension pneumothorax]]
*[[Thrombosis|Thrombosis]]
*[[Myocardial infarction]]
*[[Thrombosis|Thrombosis]]
*[[Pulmonary embolism]]
*[[Cardiogenic shock]]
*Degeneration of the [[sinoatrial]] or [[atrioventricular]] nodes
*[[Ischemic stroke]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* There is no electrical activity in the asystole
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
[[Image:Lead II rhythm generated asystole.JPG|center|300px]]<ref> ECG found in https://en.ecgpedia.org/index.php?title=Main_Page </ref>
|-
! style="padding: 5px 5px; background: #DCDCDC;" align="left" | '''[[Pulseless electrical activity]]''' <ref name="ECC_2005_7.2">"2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 7.2: Management of Cardiac Arrest." ''Circulation'' 2005; '''112''': IV-58 - IV-66.</ref><ref>Foster B, Twelve Lead Electrocardiography, 2nd edition, 2007</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[Hypovolemia]]
*[[Hypoxia]]
*Hydrogen ions ([[Acidosis]])
*[[Hypothermia]]
*[[Electrolyte disturbances]]
*[[Hypoglycemia]]
*Tablets or [[Toxins]] (Drug overdose) such as [[beta blockers]], [[tricyclic antidepressants]], or [[calcium channel blockers]]
*[[Tamponade]]
*[[Tension pneumothorax]]
*[[Thrombosis]] ([[Myocardial infarction]])
*[[Thrombosis]] ([[Pulmonary embolism]])
*[[Trauma]] ([[Hypovolemia]] from [[blood loss]])
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*Several pattern are possible including:
**[[Normal sinus rhythm]]
**[[Sinus tachycardia]], with discernible [[P waves]] and [[QRS complexes]]
**[[Bradycardia]], with or without [[P waves]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
[[File:Capture PEA.PNG|center|300px]]<ref> ECG found in wikimedia Commons </ref>
|-
! style="padding: 5px 5px; background: #DCDCDC;" align="left" |'''[[Torsade de Pointes]]''' <ref name="pmid28674475">{{cite journal |vauthors=Li M, Ramos LG |title=Drug-Induced QT Prolongation And Torsades de Pointes |journal=P T |volume=42 |issue=7 |pages=473–477 |date=July 2017 |pmid=28674475 |pmc=5481298 |doi= |url=}}</ref><ref name="SharainMay2015">{{cite journal|last1=Sharain|first1=Korosh|last2=May|first2=Adam M.|last3=Gersh|first3=Bernard J.|title=Chronic Alcoholism and the Danger of Profound Hypomagnesemia|journal=The American Journal of Medicine|volume=128|issue=12|year=2015|pages=e17–e18|issn=00029343|doi=10.1016/j.amjmed.2015.06.051}}</ref><ref name="pmid11330748">{{cite journal |vauthors=Khan IA |title=Twelve-lead electrocardiogram of torsades de pointes |journal=Tex Heart Inst J |volume=28 |issue=1 |pages=69 |date=2001 |pmid=11330748 |pmc=101137 |doi= |url=}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* *[[Electrolyte disturbances]]
*[[Medications]] such as:
**[[Amiodarone]]
** [[Azithromycin ]]
** [[Clozapine ]]
**[[Famotidine]]
** [[Flecainide ]]
** [[Foscarnet ]]
** [[Levofloxacin ]]
** [[Lithium ]]
** [[Mirtazipine]]
** [[Quetiapine ]]
** [[Risperidone ]]
** [[Tacrolimus ]]
** [[Tamoxifen ]]
** [[Ziprasidone]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
# Paroxysms of [[VT]] with irregular RR intervals.
# A [[ventricular]] rate between 200 and 250 beats per minute.
# Two or more cycles of [[QRS complex]]es with alternating polarity.
# Changing amplitude of the [[QRS complexes]] in each cycle in a [[sinusoidal]] fashion.
# Prolongation of the [[QT interval]].
# Is often initiated by a [[PVC]] with a long coupling interval, R on T phenomenon.
# There are usually 5 to 20 complexes in each cycle.
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
[[File:Capture Tors De P.PNG|center|300px]]<ref> ECG found in https://en.ecgpedia.org/index.php?title=Main_Page </ref>
|}
|}


Revision as of 23:26, 21 April 2020

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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.

Type 2 Mobitz 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]

  • Type 2 second degree AV block, also known as Mobitz II is almost always a disease of the distal conduction system (His-Purkinje System).
  • Although the terms infranodal block or infrahisian block are often applied to this disorder, 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[4].

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.

Major causes of atrioventricular (AV) block
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[7].

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[11]
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 the United States, the prevalence of second-degree AV block is believed to be 3 in 100,000 individual.[12]
  • Nearly 3% of 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:[13][14][15][16]
    • 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 block inferior to the AV node (infra-Hisian structures) and it progresses to complete heart block.[17]

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.[13]

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

  • Patients with Mobitz II can appear asymptomatic as well. However, in more cases they may be in distress or progress to the more severe third degree AV block.
  • Patients may appear pale in cases of bradycardia with decreased cardiac output.[23]
  • Bradycardia with an irregular pulse[24]
  • Lightheadedness
  • Hypotension[25]
  • Syncope or presyncope
  • Jugular venous distension
  • Bibasilar crackles in patients with exacerbated heart failure
  • Peripheral edema

Laboratory Findings

Patients with second degree AV block should be checked for the following laboratory tests:[26]

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, in approximately 27 to 35% of patients however, 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

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[28] First degree [29][30]
  • 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.
Second degree[12][31]
  • 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[32][33]
  • 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)[34][35]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 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
Atrial Flutter[36]
  • 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
Atrioventricular nodal reentry tachycardia (AVNRT)[37][38][39][40]
  • Regular
  • 140-280 bpm
  • Slow-Fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R' in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • 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
Multifocal Atrial Tachycardia[41][42]
  • 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
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)[43][44]
  • 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:
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[45][46]
  • Regular
  • Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm
  • 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.
Ventricular Fibrillation (VF)[47][48][49]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[50][51]
  • 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
  • 5-10% of patients presenting with AMI

References

  1. ↑ 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.
  2. ↑ Puech P, Wainwright RJ (1983). "Clinical electrophysiology of atrioventricular block". Cardiol Clin. 1 (2): 209–24. PMID 6544636.
  3. ↑ 3.0 3.1 3.2 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.
  4. ↑ 4.0 4.1 Li X, Xue Y, Wu H (2018). "A Case of Atrioventricular Block Potentially Associated with Right Coronary Artery Lesion and Ticagrelor Therapy Mediated by the Increasing Adenosine Plasma Concentration". Case Rep Vasc Med. 2018: 9385017. doi:10.1155/2018/9385017. PMC 5933017. PMID 29850368.
  5. ↑ 5.0 5.1 Fu Md J, Bhatta L (2018). "Lyme carditis: Early occurrence and prolonged recovery". J Electrocardiol. 51 (3): 516–518. doi:10.1016/j.jelectrocard.2017.12.035. PMID 29275956.
  6. ↑ 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.
  7. ↑ 7.0 7.1 7.2 7.3 Mangi MA, Jones WM, Napier L. PMID 29493981. Missing or empty |title= (help)
  8. ↑ 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.
  9. ↑ 9.0 9.1 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 12.0 12.1 Zehender M, Meinertz T, Keul J, Just H (1990). "ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance". Am Heart J. 119 (6): 1378–91. doi:10.1016/s0002-8703(05)80189-9. PMID 2191578.
  13. ↑ 13.0 13.1 13.2 Meimoun P, Zeghdi R, D'Attelis N, Berrebi A, Braunberger E, Deloche A; et al. (2002). "Frequency, predictors, and consequences of atrioventricular block after mitral valve repair". Am J Cardiol. 89 (9): 1062–6. doi:10.1016/s0002-9149(02)02276-2. PMID 11988196.
  14. ↑ Meimoun P, Zeghdi R, D'Attelis N, Berrebi A, Braunberger E, Deloche A; et al. (2002). "Frequency, predictors, and consequences of atrioventricular block after mitral valve repair". Am J Cardiol. 89 (9): 1062–6. doi:10.1016/s0002-9149(02)02276-2. PMID 11988196.
  15. ↑ Kerola T, Eranti A, Aro AL, Haukilahti MA, Holkeri A, Junttila MJ, Kenttä TV, Rissanen H, Vittinghoff E, Knekt P, Heliövaara M, Huikuri HV, Marcus GM (May 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.
  16. ↑ Schoeller R, Andresen D, Büttner P, Oezcelik K, Vey G, Schröder R (March 1993). "First- or second-degree atrioventricular block as a risk factor in idiopathic dilated cardiomyopathy". Am. J. Cardiol. 71 (8): 720–6. doi:10.1016/0002-9149(93)91017-c. PMID 8447272.
  17. ↑ Rodstein M, Wolloch L, Iuster Z (1979). "The natural history intraventricular conduction disturbances in the aged: an analysis of the developing second and third degree heart block with clinical pathological correlations". Am. J. Med. Sci. 277 (2): 179–88. doi:10.1097/00000441-197903000-00006. PMID 463945.
  18. ↑ 18.0 18.1 Bexton RS, Camm AJ (March 1984). "Second degree atrioventricular block". Eur. Heart J. 5 Suppl A: 111–4. doi:10.1093/eurheartj/5.suppl_a.111. PMID 6373268.
  19. ↑ Thiruganasambandamoorthy V, Hess EP, Turko E, Tran ML, Wells GA, Stiell IG (July 2012). "Defining abnormal electrocardiography in adult emergency department syncope patients: the Ottawa Electrocardiographic Criteria". CJEM. 14 (4): 248–58. PMID 22813399.
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  21. ↑ 21.0 21.1 Kashou AH, Goyal A, Nguyen T, Chhabra L. PMID 29083636. Missing or empty |title= (help)
  22. ↑ Zeppilli P, Fenici R, Sassara M, Pirrami MM, Caselli G (September 1980). "Wenckebach second-degree A-V block in top-ranking athletes: an old problem revisited". Am. Heart J. 100 (3): 281–94. doi:10.1016/0002-8703(80)90140-4. PMID 7405798.
  23. ↑ Rosen KM, Dhingra RC, Loeb HS, Rahimtoola SH (1973). "Chronic heart block in adults. Clinical and electrophysiological observations". Arch Intern Med. 131 (5): 663–72. PMID 4701376.
  24. ↑ Schneider MD, Roller DH, Morganroth J, Josephson ME (July 1978). "The syndromes of familial atrioventricular block with sinus bradycardia: prognostic indices, electrophysiologic and histopathologic correlates". Eur J Cardiol. 7 (5–6): 337–51. PMID 699934.
  25. ↑ Trappe HJ (September 2016). "[Consciousness disorders from cardiological view]". Dtsch. Med. Wochenschr. (in German). 141 (19): 1361–9. doi:10.1055/s-0042-103177. PMID 27642736.
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  29. ↑ 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.
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  37. ↑ 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.
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  39. ↑ "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
  40. ↑ 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.
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