Third degree AV block pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
 
(23 intermediate revisions by 4 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Third degree AV block}}
{{Third degree AV block}}
{{CMG}}; {{AE}} {{Soroush}} {{CZ}}; {{RT}}
{{CMG}}; {{AE}} {{Soroush}} {{CZ}}; {{RT}} [[User:Qasim Khurshid|Qasim Khurshid, M.B.B.S[5]]]
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
Normally [[Sinoatrial node|SA node]] generates impulses that travel to the [[Atrioventricular node|AV node]] and gets delayed there to assure that the [[contraction]] cycle in [[atria]] is complete before a contraction begins in the [[ventricles]]. From the [[AV node]], the impulses pass through the [[Bundle of His|His-Purkinje]] system to cause ventricular contraction. Pathological delay in the [[AV node]] is visualized on an [[electrocardiogram]] as a change in the [[PR interval|P-R interva]]<nowiki/>l. These delays are known as an [[AV block]]. No impulses from the [[SA node]] get conducted to the ventricles, and this leads to a complete [[atrioventricular dissociation]]. The SA node continues to activate at a set rate, but the ventricles will activate through an escape rhythm that can be mediated by either the AV node, one of the fascicles, or by ventricular myocytes themselves. The heart rate will mostly be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable.
 
OR
 
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==
===Physiology===
===Physiology===
The normal physiology of [name of process] can be understood as follows:
The normal physiology of the  electrical activity of the heart can be understood as follows:
 
* Normal impulse is generated  in the [[sinoatrial node]] (SAN).
* Electrical pulse then travels through the [[Atrium (heart)|atrium]].
* P wave is recorded in the [[ECG]]
* Wave reaches the [[atrioventricular node]] (AVN).
* Atrioventricular node later conducts the impulse to the [[Bundle of His|His bundle]].
* The bundle of his again gets divided into the right and left bundles, ultimately conducting this impulse to the ventricles.
* PR segment is recorded (atrial, AVN, and His-Purkinje conduction)
*[[Complete heart block]] occurs when complete block of this conduction occurs.


===Pathogenesis===
===Pathogenesis===
*The exact pathogenesis of [disease name] is not completely understood.
 
OR
** In [[complete heart block]], because the impulse is blocked, an accessory [[pacemaker]] below the level of the block will typically activate the ventricles; this is known as an escape rhythm.
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
** When there is no electrical connection between atria and ventricles, two independent pacemakers will generate impulse independent of [[Sinoatrial node|SA node]]. [[EKG]] will show two rhythms independent of each other
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*** One independent pacemaker will activate the atria and create the [[P waves]] with typically with a regular [[PP interval|P to P interval]].
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*** The second independent pacemaker in ventricles will activate the ventricles and produce the [[QRS complex]] with typically regular [[RR interval|R to R interval]].
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*** The [[PR interval|PR interva]]<nowiki/>l will be a variable that is a hallmark feature of complete heart block and with no apparent relationship between [[P wave|P waves]] and [[QRS complex|QRS complexes]].
*The progression to [disease name] usually involves the [molecular pathway].
** Morphology of the [[QRS complex]] helps in determining the location at which the escape rhythms are occurring.
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
** If the site of [[complete heart block]] is at the level of [[AV node|the AV node]], two-thirds of the escape rhythms have a narrow [[QRS complex]].
** If the site of block is the [[Bundle of His|His bundle]], typically a narrow [[QRS complex]] is seen.
** Patients with [[trifascicular block]] have a [[wide QRS]] complex (seen in 80% of the cases).
** In short, if escape rhythm has a narrow QRS complex, the level of the block can be either AV node or [[His bundle]], and if the QRS duration is prolonged, the level of block is in the fascicles or bundle branches.
** Block at the level of the AV node gives rise to an escape rhythm that generally arises from a junctional pacemaker with a heart rate of 45-60 beats per minute. Such patients are hemodynamically stable.
** Escape rhythms arise from the [[Bundle of His|His bundle]] or bundle branch Purkinje system at rates slower than 45 beats per minute when the block is below the [[AV node]].
** These patients are hemodynamically unstable, and their heart rate is unresponsive to exercise and [[atropine]].


==Genetics==
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.


OR
*[[Third degree AV block]] is the result of ischemia in majority of the patients.
* In certain disease like lyme disease also we might observe [[Atrioventricular block|AV block]].
* Nevertheless, there are some rare cases of idiopathic [[AV block]]


Genes involved in the pathogenesis of [disease name] include:
* In those cases, third degree AV block is transmitted in [[Autosomal dominant|autosomal dominan]]<nowiki/>t pattern most of the time.
*[Gene1]
*[Gene2]
*[Gene3]
 
OR
 
The development of [disease name] is the result of multiple genetic mutations such as:
 
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]


{| class="wikitable"
|+
! colspan="2" |Genes involved in the pathogenesis of third degree AV block
|-
|AV CONDUCTION DISEASE AND CONGENITAL CARDIAC MALFORMATIONS
|
* '''NKX2.5'''
|-
|AV CONDUCTION DISEASE, VENTRICULAR HYPERTROPHY, AND WOLFF-PARKINSON-WHITE SYNDROME
|
* '''PRKAG2'''
|-
|AV CONDUCTION DISEASE : A CHANNELOPATHY
|
*'''SCN5A'''
*'''KCNJ2 (type 1 Andersen-Tawil syndrome) <ref name="pmid15372490">{{cite journal| author=Benson DW| title=Genetics of atrioventricular conduction disease in humans. | journal=Anat Rec A Discov Mol Cell Evol Biol | year= 2004 | volume= 280 | issue= 2 | pages= 934-9 | pmid=15372490 | doi=10.1002/ar.a.20099 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15372490  }} </ref>'''
|}
<br />
==Associated Conditions==
==Associated Conditions==
Conditions associated with [disease name] include:
Conditions associated with third degree AV block include:


*[Condition 1]
*[[Ischemic heart disease]] (Major)
*[Condition 2]
* Congenital cardiac malformations
*[Condition 3]
*[[Ventricular hypertrophy]]
 
*[[WPW syndrome]]
==Gross Pathology==
* Chenlopatioes such as Andersen-Tawil syndrome
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
==Pathophysiology==
*In complete heart block because the impulse is blocked, an accessory pacemaker below the level of the block will typically activate the ventricles.  This is known as an escape rhythm. Since this accessory pacemaker activates independently of the impulse generated at the [[SA node]], two independent rhythms can be noted on the [[electrocardiogram]] (EKG). 
** One will activate the atria and create the P waves, typically with a regular [[PP interval|P to P interval]].
** The second will activate the ventricles and produce the QRS complex, typically with a regular [[RR interval|R to R interval]]. The PR interval will be variable, as the hallmark of complete heart block is no apparent relationship between [[P wave]]s and [[QRS complex]]es.


Morphology of the [[QRS complex]] helps in determining the location at which the escape rhythms are occurring. 
*[[AV dissociation]]
* If the site of complete heart block is at the level of [[AV node]], two-thirds of the escape rhythms have a narrow QRS complex.
* If the site of block is the His bundle, typically a narrow QRS complex is seen.
* Patients with [[trifascicular block]] have a [[wide QRS]] complex (seen in 80% of the cases).


In short, if escape rhythm has a narrow QRS complex the level of block can be either AV node or [[His bundle]] and if the QRS duration is prolonged the level of block is in the fascicles or bundle branches.
=== AV dissociation ===
AV dissociation is defined as:


Block at the level of AV node gives rise to an escape rhythm that generally arises from a junctional pacemaker with a heart rate of 45-60 beats per minute. Such patients are hemodynamically stable.  Escape rhythms arise from the His bundle or bundle branch Purkinje system at rates slower than 45 beats per minute when the block is below the AV node.  These patients are hemodynamically unstable and their heart rate is unresponsive to exercise and atropine.
* Independent atrial and ventricular activation  either due to complete heart block or as a result of physiologic refractoriness of conduction tissue.
* It also may develop when the atrial/sinus rate is slower than the ventricular rate (accelerated junctional [[tachycardia]] or VT).


===Complete Heart Block in Myocardial Infarction===
* This is called isorhythmic AV dissociation.
* An inferior wall [[myocardial infarction]] may cause damage to the [[AV node]], causing third degree heart block.  In this case, the damage is usually transitory, and the AV node may recover.  Studies have shown that third degree heart block in the setting of an inferior wall myocardial infarction typically resolves within 2 weeks. The escape rhythm typically originates in the AV junction, producing a narrow complex escape rhythm.
* Acceleration of the atrial/sinus rate with either maneuvers or medications will result in restoration of normal conduction.
* An anterior wall myocardial infarction may damage the distal conduction system of the heart, causing third degree heart block.  This is typically extensive, permanent damage to the conduction system, necessitating a permanent [[artificial pacemaker |pacemaker]] to be placed. The escape rhythm typically originates in the ventricles, producing a wide complex escape rhythm.


==References==
==References==

Latest revision as of 13:31, 15 July 2020

Third degree AV block Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Third degree AV block from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Third degree AV block pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

slides

Images

American Roentgen Ray Society Images of Third degree AV block pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Third degree AV block pathophysiology

CDC on Third degree AV block pathophysiology

Third degree AV block pathophysiology in the news

Blogs on Third degree AV block pathophysiology

Directions to Hospitals Treating Third degree AV block

Risk calculators and risk factors for Third degree AV block pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]; Raviteja Guddeti, M.B.B.S. [4] Qasim Khurshid, M.B.B.S[5]

Overview

Normally SA node generates impulses that travel to the AV node and gets delayed there to assure that the contraction cycle in atria is complete before a contraction begins in the ventricles. From the AV node, the impulses pass through the His-Purkinje system to cause ventricular contraction. Pathological delay in the AV node is visualized on an electrocardiogram as a change in the P-R interval. These delays are known as an AV block. No impulses from the SA node get conducted to the ventricles, and this leads to a complete atrioventricular dissociation. The SA node continues to activate at a set rate, but the ventricles will activate through an escape rhythm that can be mediated by either the AV node, one of the fascicles, or by ventricular myocytes themselves. The heart rate will mostly be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable.

Pathophysiology

Physiology

The normal physiology of the electrical activity of the heart can be understood as follows:

  • Normal impulse is generated in the sinoatrial node (SAN).
  • Electrical pulse then travels through the atrium.
  • P wave is recorded in the ECG
  • Wave reaches the atrioventricular node (AVN).
  • Atrioventricular node later conducts the impulse to the His bundle.
  • The bundle of his again gets divided into the right and left bundles, ultimately conducting this impulse to the ventricles.
  • PR segment is recorded (atrial, AVN, and His-Purkinje conduction)
  • Complete heart block occurs when complete block of this conduction occurs.

Pathogenesis

    • In complete heart block, because the impulse is blocked, an accessory pacemaker below the level of the block will typically activate the ventricles; this is known as an escape rhythm.
    • When there is no electrical connection between atria and ventricles, two independent pacemakers will generate impulse independent of SA node. EKG will show two rhythms independent of each other
      • One independent pacemaker will activate the atria and create the P waves with typically with a regular P to P interval.
      • The second independent pacemaker in ventricles will activate the ventricles and produce the QRS complex with typically regular R to R interval.
      • The PR interval will be a variable that is a hallmark feature of complete heart block and with no apparent relationship between P waves and QRS complexes.
    • Morphology of the QRS complex helps in determining the location at which the escape rhythms are occurring.
    • If the site of complete heart block is at the level of the AV node, two-thirds of the escape rhythms have a narrow QRS complex.
    • If the site of block is the His bundle, typically a narrow QRS complex is seen.
    • Patients with trifascicular block have a wide QRS complex (seen in 80% of the cases).
    • In short, if escape rhythm has a narrow QRS complex, the level of the block can be either AV node or His bundle, and if the QRS duration is prolonged, the level of block is in the fascicles or bundle branches.
    • Block at the level of the AV node gives rise to an escape rhythm that generally arises from a junctional pacemaker with a heart rate of 45-60 beats per minute. Such patients are hemodynamically stable.
    • Escape rhythms arise from the His bundle or bundle branch Purkinje system at rates slower than 45 beats per minute when the block is below the AV node.
    • These patients are hemodynamically unstable, and their heart rate is unresponsive to exercise and atropine.

Genetics

  • Third degree AV block is the result of ischemia in majority of the patients.
  • In certain disease like lyme disease also we might observe AV block.
  • Nevertheless, there are some rare cases of idiopathic AV block
  • In those cases, third degree AV block is transmitted in autosomal dominant pattern most of the time.
Genes involved in the pathogenesis of third degree AV block
AV CONDUCTION DISEASE AND CONGENITAL CARDIAC MALFORMATIONS
  • NKX2.5
AV CONDUCTION DISEASE, VENTRICULAR HYPERTROPHY, AND WOLFF-PARKINSON-WHITE SYNDROME
  • PRKAG2
AV CONDUCTION DISEASE : A CHANNELOPATHY
  • SCN5A
  • KCNJ2 (type 1 Andersen-Tawil syndrome) [1]


Associated Conditions

Conditions associated with third degree AV block include:

AV dissociation

AV dissociation is defined as:

  • Independent atrial and ventricular activation either due to complete heart block or as a result of physiologic refractoriness of conduction tissue.
  • It also may develop when the atrial/sinus rate is slower than the ventricular rate (accelerated junctional tachycardia or VT).
  • This is called isorhythmic AV dissociation.
  • Acceleration of the atrial/sinus rate with either maneuvers or medications will result in restoration of normal conduction.

References

  1. ↑ Benson DW (2004). "Genetics of atrioventricular conduction disease in humans". Anat Rec A Discov Mol Cell Evol Biol. 280 (2): 934–9. doi:10.1002/ar.a.20099. PMID 15372490.


Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Third_degree_AV_block_pathophysiology&oldid=1627168"