Third degree AV block pathophysiology
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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]
Overview
Physiologically AV node receives an impulse from the SA node. That impulse gets delayed in the AV node, assuring the contraction cycle in the atria is complete before a contraction begins in the ventricles. From the AV node, the electrical impulse passes through the His-Purkinje system to activate ventricular contraction. When there is a pathological delay in the AV node, it 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 rhythm, 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 typically be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable. This rhythm is unresponsive to atropine and exercise.
Pathophysiology
Physiology
The normal physiology of the heart electrical activity can be understood as follows:
- Normal impulse initiation begins 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).
- The AVN then conducts the impulse to the His bundle.
- The His bundle divides into the right and left bundles, which distribute 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.
- 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 P to P interval.
- The second will activate the ventricles and produce the QRS complex, typically with a regular R to R interval.
- The PR interval will be variable, as the hallmark of complete heart block is 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 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.
- 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.
Complete Heart Block in Myocardial Infarction
- 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.
- 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 pacemaker to be placed.
- The escape rhythm typically originates in the ventricles, producing a wide complex escape rhythm.
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 | |
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| AV CONDUCTION DISEASE AND CONGENITAL CARDIAC MALFORMATIONS |
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| AV CONDUCTION DISEASE, VENTRICULAR HYPERTROPHY, AND WOLFF-PARKINSON-WHITE SYNDROME |
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| AV CONDUCTION DISEASE : A CHANNELOPATHY |
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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
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).
Please note that sometimes the atrial and ventricular rates are so close that the tracing would suggest normal AV conduction; In this case, careful examination of the long rhythm strip is warranted to reveal a variation in the PR interval.
- 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.