Third degree AV block pathophysiology: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
| (5 intermediate revisions by 2 users not shown) | |||
| Line 3: | Line 3: | ||
{{CMG}}; {{AE}} {{Soroush}} {{CZ}}; {{RT}} [[User:Qasim Khurshid|Qasim Khurshid, M.B.B.S[5]]] | {{CMG}}; {{AE}} {{Soroush}} {{CZ}}; {{RT}} [[User:Qasim Khurshid|Qasim Khurshid, M.B.B.S[5]]] | ||
==Overview== | ==Overview== | ||
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. | |||
==Pathophysiology== | ==Pathophysiology== | ||
===Physiology=== | ===Physiology=== | ||
The normal physiology of the | The normal physiology of the electrical activity of the heart can be understood as follows: | ||
* Normal impulse | * Normal impulse is generated in the [[sinoatrial node]] (SAN). | ||
* Electrical pulse then travels through the [[Atrium (heart)|atrium]]. | * Electrical pulse then travels through the [[Atrium (heart)|atrium]]. | ||
* | * P wave is recorded in the [[ECG]] | ||
* Wave reaches the [[atrioventricular node]] (AVN). | * Wave reaches the [[atrioventricular node]] (AVN). | ||
* Atrioventricular node later conducts the impulse to the [[Bundle of His|His bundle]]. | * 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. | * 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. | *[[Complete heart block]] occurs when complete block of this conduction occurs. | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
* Morphology of the [[QRS complex]] helps in determining the location at which the escape rhythms are occurring. | ** 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 [[Sinoatrial node|SA node]]. [[EKG]] will show two rhythms independent of each other | |||
* 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]]. | *** One independent pacemaker will activate the atria and create the [[P waves]] with typically with a regular [[PP interval|P to P interval]]. | ||
* If the site of block is the [[Bundle of His|His bundle]], typically a narrow [[QRS complex]] is seen. | *** The second independent pacemaker in ventricles will activate the ventricles and produce the [[QRS complex]] with typically regular [[RR interval|R to R interval]]. | ||
* Patients with [[trifascicular block]] have a [[wide QRS]] complex (seen in 80% of the cases). | *** 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]]. | ||
*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. | ** Morphology of the [[QRS complex]] helps in determining the location at which the escape rhythms are occurring. | ||
*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. | ** 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]]. | ||
*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]]. | ** If the site of block is the [[Bundle of His|His bundle]], typically a narrow [[QRS complex]] is seen. | ||
*These patients are hemodynamically unstable and their heart rate is unresponsive to exercise and | ** 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== | ||
*[[Third degree AV block]] is the result of ischemia in majority of the patients. | *[[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. | * In certain disease like lyme disease also we might observe [[Atrioventricular block|AV block]]. | ||
* Nevertheless, there are some rare cases of idiopathic AV block | * Nevertheless, there are some rare cases of idiopathic [[AV block]] | ||
* In those cases, third degree AV block is transmitted in [[Autosomal dominant|autosomal dominan]]<nowiki/>t pattern most of the time. | * In those cases, third degree AV block is transmitted in [[Autosomal dominant|autosomal dominan]]<nowiki/>t pattern most of the time. | ||
Latest revision as of 13:31, 15 July 2020
|
Third degree AV block Microchapters | |
|
Diagnosis | |
|---|---|
|
Treatment | |
|
Case Studies | |
|
Third degree AV block pathophysiology On the Web | |
|
American Roentgen Ray Society Images of Third degree AV block pathophysiology | |
|
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 |
|
| AV CONDUCTION DISEASE, VENTRICULAR HYPERTROPHY, AND WOLFF-PARKINSON-WHITE SYNDROME |
|
| AV CONDUCTION DISEASE : A CHANNELOPATHY |
|
Associated Conditions
Conditions associated with third degree AV block include:
- Ischemic heart disease (Major)
- Congenital cardiac malformations
- Ventricular hypertrophy
- WPW syndrome
- Chenlopatioes such as Andersen-Tawil syndrome
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
- ↑ 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.