Physiology, AV Junction

Issues of Concern

The AV junction plays a significant role in the propagation of a signal from the sinoatrial (SA) node to the ventricles. Understanding the structure-function relationship will allow further advances in treatment regarding arrhythmias and AV blockage.

Cellular Level

The AV junction consists of the AV node and the bundle of his. AV node divides into a compact node (CN) and a lower nodal bundle. The lower nodal bundle extends to the rightward inferior nodal extension (INE) which spreads along with the tricuspid valve toward the coronary sinus, and the leftward nodal extension spreads from the CN along the tendon of Todaro.[1]

The AV junction is found to have two conduction pathways a slow pathway (SP) and a fast pathway(FP). The slow pathways are located in the inferior nodal extension while the fast pathway is less defined. AV node consists of numerous types of cells including rounded cells, transitional cells, Purkinje cells, and myocardial cells. The pacemaker cells are oval containing sparse and randomly organized myofibrils with numerous sarcoplasmic reticulum. Cell size dictates conduction velocity with the larger cells promoting faster conduction and smaller cells conducting at a slower velocity. Heterogeneity within the AV node could account for dual pathways. The SP contains small cells while the longer FP contains cells with a larger diameter. Myofibrils adjacent to the SP exhibit decreased density versus closer to the CN. Decreased striation density also occur near the CN in comparison to the surrounding cells.  Comparatively the Bundle of His is composed of elongated cells. Due to the connection of the left nodal extension and the  CN, a substrate is formed allowing slow conduction and potential re-entrant arrhythmias within the AV node. Additionally, in dilated cardiomyopathy, it was found that the left nodal extension is longer.[1] The bundle of His consist of connection between the AV node and the left and right bundle branch located in the deep, dense connective tissue. Bundle of His is a group of organized collagen that separates it from the AV node on histology. Signals are sent through gap junctions, using connexions. The composition of connexions is heterogeneous within the AV node which leads to several functional consequences including AV delay.[1]

Development

AV junction forms from the fusion of the atrioventricular sulcus and cushions. The disruption of the continuity between the atria and the ventricles lies at the ventricle margin of the atrioventricular junctional myocardium. The process of separation between the atria and ventricle begins at 7 weeks at the anteromedial portion of the right atrioventricular junction. At 12 weeks the fusions of the atrioventricular sulcus and cushions have been completed. During development, the atrioventricular insulation matures first while the left-sided fibrous annulus is shown to better developed in an adult heart.[2] The heart develops from the mesoderm, and as the newly formed heart starts to develop cardiomyocytes begin to depolarize, creating a slow electrical impulse. The specialized conductor cells become insulated by fibroblasts that originate from multipotent neural stem cells. The annulus fibrous which is fibrous tissue that develops from the epicardial mesenchyme and separated the developing atria and ventricles.[3]

Function

The AV node and the bundle of His comprise the AV junction. The AV node plays a gatekeeper role delaying the signal between the atria and the ventricles; this prevents premature contractions of the ventricle that has not filled. It also can function in a protective role in becoming the dominant pacemaker of the heart in times of SA node failure. The bundle of His conducts the signal from the AV node to the left and right bundles to the Purkinje cells of the ventricles.[1]

Mechanism

Similar to the SA node, the AV node has the potential to be a pacemaker. The difference in nodes is the rate with the SA node 60 to 100 bpm and AV node 20 to 60 bpm. Pacemakers cells in the nodes depolarized during diastole through Funny current Na+ and K+ channels that increase, which triggers an action potential. The action potential upstroke involves Ca2+ rushing in contrast to Na+, which is prominent in the myocyte action potential. The cell them repolarizes to its resting membrane potential due to the efflux of K+.[1]

Pathophysiology

Due to the structure and function of the AV junction, it is susceptible to re-entry. Atrioventricular nodal re-entry tachycardia is the most common. AV block is also a common pathology due to AV nodal dysfunction.

Atrioventricular nodal re-entry tachycardia:

The reentrant circuit directly involves the AV node. The AV node has two pathways, the fast which has a longer refractory period and the slow, which has a shorter refractory period. It forms from the re-entry circuits between the AVN, fast pathway, slow pathway, and the atrial myocardium. Most common being slow-fast AVNRT with slow AV nodal pathway for anterograde conduction and Fast av nodal conduction for retrograde conduction. If there is a premature atrial beat, then the slow pathway can travel up the fast pathway and restimulate itself, creating a loop, which increases the heart rate much higher than a normal with supraventricular tachycardia found on electrocardiogram (ECG).

Atrioventricular block:

Mobitz type 1 is the prolongation of the PR interval until finally complete block of the atrial impulse and a drop of the QRS. While Mobtiz type 2 is a constant PR interval until one atrial impulse is blocked, resulting in no QRS following. It is most likely from damage to the infranodal conduction system so a widened QRS may present on EKG. Mutations in sodium channels are highly suggested to result in AVN block; this may be congenital or due to exogenous factors including ischemia and Lyme disease, which cause damage to the AV conduction pathway.

Atrioventricular reentrant tachycardia:

This condition is due to an accessory pathway outside the AV node that allows for re-entry stimulation of the AV node, which can lead to a tachyarrhythmia. It classifies as supraventricular tachycardia. It can get triggered by a premature atrial or ventricular contraction, which can stimulate a reentrant impulse[4]Wolff-Parkinson White: 

Wolff-Parkinson White is an electrical cardiac disorder resulting from an accessory pathway that communicates between the atria and the ventricles. The accessory pathway has the name of the bundle of Kent. It does not have rate slowing properties and conducts electrical activity at a higher rate, leading to stunning of the heart resulting in cardiogenic shock.[4]

Clinical Significance

Patients with AVNRT will present with an increased heart rate (over150 bpm) and supraventricular tachycardia on ECG. Treatment modalities include performing the Valsalva maneuver and pharmacologic intervention with non-dihydropyridine calcium channel blockers and adenosine. For individuals with arrhythmias that are recurrent, minimally invasive procedures are available, including catheter ablation of the middle or inferior portion of the triangle of Koch.[1] AV blocks are treated differently depending on the circumstance. Mobitz Type 1 treatment is not necessary, but if hypotension and bradycardia occur, then atropine is recommended to increase the rate. In Mobitz Type 2 implies damage to the AV conduction system, causing the rhythm to progress to complete heart block, which is why transvenous pacing is necessary until placement of a permanent pacemaker. Mobitz type 2 patients do not respond to atropine.[5] Wolff-Parkinson White presents with palpations, dizziness, and shortness of breath. ECG presents with a shortened PR, widened QRS and delta waves. Fainting may be present in episodes of supraventricular tachycardia. Recommended treatment includes procainamide or amiodarone and catheter ablation of the accessory pathway.[6]