Dual AV Nodal Pathways & ECG

• AV nodal duality means,
• that there are 2 pathways from the atrium to the compact AV node:
• Fast pathway
• Slow pathway
• Fast pathway is always present.
• 10-35% of the population has both fast and slow pathways.
• So the patient has AV nodal duality (because they have both fast and slow pathways)
• In AV nodal duality, the impulse from the atrium is conducted only through the fast pathway.
• under certain circumstances, however, it may conduct through the slow pathway
• which we see on ECG as a sudden prolongation of the PQ interval (>50ms)
• One small square on the ECG represents 40ms.
• In the presence of AV nodal duality, AVNRT occurs in practice
• but this is not a rule.
• AV nodal duality on ECG and ECG Holter:
• Atrial extrasystole and PQ jump
• Adenosine and PQ jump
• Parasympathicotonia and PQ jump
• Atrial fibrillation and Dual RR interval
• Slow-Fast AVNRT
• Fast-Slow AVNRT
• Ventricular extrasystole and PQ interval change
• Pseudo-interpolated ventricular extrasystole
• Double fire

Koch's Triangle

• It is a virtual triangle on the endocardium of the septum in the right atrium.
• It serves to localize the compact (continuous) AV node.
• The compact AV node is located at the apex of the triangle.
• Its boundaries are formed by:
• Anteriorly - septal leaflet of the tricuspid valve (TrCh).
• Posteriorly - Tendon of Todaro (ToT).
• ToT is a collagenous band that goes from the Eustachian ridge,
• to the central fibrous body (CFB).
• The AV node ends in CFB and continues as His into the ventricles.
• Apex - where the septal leaflet of TrCh and ToT meet.
• It is in the area of the central fibrous body.
• The compact AV node is located here.
• Base - is at the level of the lower part of the coronary sinus ostium.

AV Node

• The AV node is located in the apex of Koch's triangle.
• The compact (continuous) AV node
• It is 5-7mm long and 3-4mm wide.
• Macroscopically, it cannot be distinguished from the surrounding tissue.
• It has different electrophysiological properties than surrounding tissue.
• It is responsible for decremental (slowing) properties,
• Decrementality means that conduction lengthens with increasing frequency.
• As the frequency of impulses arriving at the AV node increases,
• the conduction time of impulses through the AV node lengthens.
• The compact AV node thus ensures that:
• The ventricles can "wait" in diastole for the completion of atrial systole,
• and protects the ventricles from high frequency during atrial fibrillation.
• The AV node has 3 "extensions" through which an impulse can enter
• from the atria to the compact AV node.

• The AV node has 3 extensions.
• If an impulse can
• enter the compact AV node through an extension from the atria,
• then the extension is referred to as an AV nodal pathway.
• AV nodal pathways are non-decremental.
• This means that conduction through the pathways does not lengthen with increasing frequency.
• Every AV node has at least 1 AV nodal pathway.
• The 3 extensions of the AV node are located at specific sites:
• The 1st extension is located in the apex of Koch's triangle.
• If it conducts an impulse from the atria, it is called the fast pathway,
• because it conducts the impulse most rapidly compared to other AV nodal pathways.
• Every heart has an active fast pathway.
• The other 2 pathways may not be active in the heart.
• The 2nd extension is located inferiorly to the right (towards the right atrium).
• If it conducts an impulse from the atria, it is called the slow pathway.
• This pathway is active in 10-35% of the population.
• The 3rd extension is located inferiorly to the left (towards the left atrium).
• If it conducts an impulse from the atria, it is also called the slow pathway.
• This pathway is very rarely active (1-5% of the population).
• The term slow pathway always refers to the right-sided pathway.
• The left-sided pathway must be specified in the text as the left-sided pathway.
• The pathways are histologically and electrophysiologically different from surrounding tissue,
• they are not visible macroscopically, neither are the AV node.
• The distance between the fast and slow pathways is approximately 15mm.
• Each pathway can conduct an impulse:
• Anterogradely - from the atria to the ventricles
• Retrogradely - from the ventricles to the atria
• Bidirectionally - in both directions

• Every individual has an anterogradely conducting fast pathway.
• AV nodal duality means that there is an additional
• second anterograde conducting slow pathway,
• almost always it is a right-sided inferior slow pathway.
• A patient has 2 anterograde pathways (fast and slow pathways)
• These pathways may or may not conduct impulses retrogradely.
• Usually, however, at least one conducts impulses retrogradely,
• one pathway is therefore bidirectional.
• AV nodal duality is present in 10-35% of the population.
• In order for AVNRT to occur in AV nodal duality
• one pathway must be bidirectional,
• to allow re-entry (impulse cycling).
• AV nodal duality is almost always associated with AVNRT.
• However, this is not a rule,
• for example, AVNRT does not occur if both pathways are only anterograde.
• However, if we have a patient with paroxysmal palpitations,
• which are often not captured on ECG or Holter monitoring,
• and we can identify AV nodal duality on the ECG,
• then the patient almost certainly has AVNRT.

• Fast Pathway
• It is always present.
• Located at the apex of Koch's triangle (superiorly)
• Has high conduction velocity,
• It conducts the impulse in approximately 100 ms, where 100 ms represents:
• from the impulse entering the fast pathway - to the activation of the His bundle,
• this includes conduction through the compact AV node.
• Has long effective refractory period (ERP) approximately 380 ms
• 380 ms is the time required for the pathway to recover after the previous depolarization.
• Thus, it needs at least 380 ms to recover to conduct the next impulse.
• Slow Pathway
• Present in 10-35% of the population
• The term slow pathway always refers to right-sided slow pathway.
• Located at the base of Koch's triangle (inferiorly)
• Has low conduction velocity,
• It conducts the impulse in approximately 200 ms
• Has short ERP approximately 280 ms
• recovers quickly (280 ms) after the previous depolarization/impulse.
• If AV nodal duality is present,
• Then the difference in conduction velocity is >50 ms.
• We observe this on the PQ interval in EKG, for example:
• With fast pathway, PQ is 130ms
• With slow pathway, PQ is 220ms (>50ms)
• PQ interval begins when the impulse leaves the SA node
• and then progresses through the atria and enters the fast pathway after approximately 30-50 ms
• so the length of PQ is 30-50 ms + conduction time through fast pathway (approximately 100 ms)
• or 30-50 ms + conduction time through slow pathway (approximately 200ms)

Short PQ Interval (Fast Pathway)

• Let's assume that the patient has AV nodal duality and these parameters:
• Fast pathway (ERP: 380ms)
• Slow pathway (ERP: 280ms)
• Every sinus beat with a conduction interval >380ms proceeds as follows:
• The impulse enters both fast and slow pathways
• It rapidly (100ms) passes through the fast pathway to the ventricles.
• In the slow pathway, the impulse is blocked because it encounters the active fast pathway.
• Thus, the PQ interval will be short: 160ms (4 EKG squares)

Long PQ Interval (Slow Pathway)

• The same patient with AV nodal duality:
• Fast pathway (ERP: 380ms)
• Slow pathway (ERP: 280ms)
• A atrial extrasystole with a conduction interval of 340ms proceeds as follows:
• The impulse from the extrasystole encounters the ERP of the fast pathway where it is blocked,
• because it arrived in the fast pathway before it had recovered from the previous impulse.
• The impulse is then conducted slowly to the ventricles through the slow pathway (200ms).
• This results in a sudden prolongation of the PQ interval (>50ms) on the EKG,
• the PQ interval will be 240ms (6 EKG squares).
• On the EKG, we see a PQ jump from 160 to 240 ms
• If the fast pathway recovers in time and is able to conduct retrogradely,
• the impulse enters it retrogradely and activates the atrium,
• then enters antegradely into the slow pathway and creates reentry: AVNRT
• An atrial extrasystole with a conduction interval of < 280ms is not conducted at all,
• because it encounters the ERP of both the fast and slow pathways.

Autonomic Nervous System

• The autonomic nervous system can affect:
• Conduction velocity and ERP of AV nodal pathways.
• Sympathetic Nervous System:
• Accelerates pathway conduction.
• Shortens ERP.
• Parasympathetic Nervous System:
• Slows pathway conduction.
• Prolongs ERP.
• Increases the chance of an extrasystole "hitting" the ERP of the fast pathway.
• During stress (sympathicotonia):
• Heart rate increases (PP interval shortens).
• Conduction through the AV node speeds up and ERP shortens.
• Dekrementality manifests minimally.
• PQ interval shortens on an EKG.
• At rest (without sympathicotonia):
• During atrial stimulation (during electrophysiological examination).
• Dekrementality of the AV node is more pronounced.
• PQ interval prolongs on an EKG.

ECG and AV Nodal Duality

• AV nodal duality provides the terrain for the occurrence of AVNRT.
• It's not a rule,
• because AVNRT does not occur if both pathways are only anterograde
• and the pathways' ERPs must create a "gap" to prevent the impulse from hitting the ERP during reentry.
• However, if the patient reports paroxysmal palpitations that are often difficult to capture,
• and we observe AV nodal duality on the ECG,
• the patient almost certainly has AVNRT.
• AV nodal duality on ECG and Holter ECG:
• Atrial extrasystole and PQ jump
• Adenosine and PQ jump
• Parasympathicotonia and PQ jump
• Atrial fibrillation and Dual RR intervals
• Slow-Fast AVNRT
• Fast-Slow AVNRT
• Ventricular extrasystole and PQ interval change
• Pseudo-interpolated ventricular extrasystole
• Double fire

• If a patient has AV nodal duality, then
• The coupling interval of the atrial extrasystole,
• which is shorter than the ERP of the fast pathway (but longer than the ERP of the slow pathway)
• is observed on the ECG as a PQ jump (>50ms)
• which is a sudden prolongation of the PQ interval
• because the atrial extrasystole conducts to the ventricles through the slow pathway.
• These extrasystoles are best captured on a Holter ECG
• The chance of capturing such an extrasystole with a 12-lead ECG is lower.

• A low dose of adenosine (3mg i.v.) blocks the fast pathway,
• a higher dose (>6mg i.v.) blocks both the fast and slow pathways.
• If a patient has AV nodal duality and we are continuously monitoring the patient's ECG,
• after administration of adenosine (3mg i.v.),
• a PQ jump (>50ms) appears within 20 seconds,
• if it does not appear, we can increase adenosine by 1mg every 3 minutes:
• Up to a dose of 6mg.

• Increased parasympathetic tone prolongs the ERP of the fast pathway more than the slow pathway.
• If a patient has AV nodal duality,
• we may see a longer PQ interval on ECG Holter monitoring during the night.
• or a PQ jump.
• A PQ jump is observed during a stable sinus rhythm or after a atrial premature beat.
• Parasympathetic tone prolongs the ERP of the fast pathway and increases the likelihood
• that the coupling interval (impulse) of an atrial premature beat or sinus beat
• "collides" with the ERP of the fast pathway, leading to its blockage
• and impulse conduction to the ventricles through the slow pathway, resulting in a PQ jump.
• Carotid sinus massage induces more intense parasympathetic tone
• blocking the entire AV node (both slow and fast pathways).
• It is used to terminate AV node-dependent tachycardias (AVNRT, AVRT).
• Prior to massage, carotid plaque should be ruled out by ultrasound examination.
• During the massage, an atherosclerotic plaque may be dislodged, causing a stroke.

Atrial Fibrillation and RR Interval Duality

• During atrial fibrillation (AF), impulses are conducted to the AV node irregularly.
• Every coupling interval is represented because the impulses are irregular.
• Let's assume that AV nodal duality has the following characteristics:
• ERP of the fast pathway: 400 ms
• ERP of the slow pathway: 300 ms
• Impulses arrive at the AV node irregularly
• The fast pathway conducts all impulses
• which are delayed from the previous impulse by more than 400 ms.
• The slow pathway conducts all impulses
• which are delayed from the previous impulse by 300-400 ms.
• All impulses arriving at the AV node with a delay of <300 ms from the previous impulse
• are blocked because they encounter the ERP of both the fast and slow pathways.
• The difference in conduction speed between the fast and slow pathways is >50 ms
• Therefore, during AF, 2 groups of RR intervals will dominate in the presence of AV nodal duality.
• Longer RR intervals (conducted through the fast pathway, as it has a longer ERP)
• Shorter RR intervals (conducted through the slow pathway, as it has a shorter ERP)
• If there are 2 groups of RR intervals on the RR histogram during AF
• then the patient has AV nodal duality.

• Slow-Fast AVNRT is the most common type of AVNRT.
• It constitutes 90% of all AVNRT cases.
• It is termed as Slow-Fast because the impulse during AVNRT circulates as follows:
• Anterogradely through the slow pathway
• After atrial (P) activation, the impulse travels slowly (via the slow pathway) to the ventricles (QRS).
• Retrogradely through the fast pathway
• After ventricular (QRS) activation, the impulse travels rapidly (via the fast pathway) to the atria (P wave). This results in a short RP interval.
• Therefore, Slow-Fast AVNRT is referred to as short RP tachycardia
• as the RP interval is < than 1/2 of the RR interval.

• Fast-Slow AVNRT is the second most common type of AVNRT.
• It constitutes 5-10% of all AVNRT cases.
• There is also Slow-Slow AVNRT which is very rare.
• It is termed as Fast-Slow because the impulse during AVNRT circulates as follows:
• Anterogradely through the fast pathway.
• After atrial (P) activation, the impulse travels rapidly (via the fast pathway) to the ventricles (QRS).
• Retrogradely through the slow pathway.
• After ventricular (QRS) activation, the impulse travels slowly (via the slow pathway) to the atria (P). This results in a long RP interval.
• Therefore, Fast-Slow AVNRT is termed as long RP tachycardia,
• as the RP interval is > than 1/2 of the RR interval.

• Linking is a rare phenomenon where
• two impulses traveling towards each other "merge".
• When these impulses "merge," they cancel each other out,
• because two depolarization waves collide.
• Linking can unmask AV nodal duality.
• During sinus rhythm, the impulse travels to the ventricles via the fast pathways,
• PQ interval is 0.16s.
• If a specifically timed ventricular extrasystole or extrasystoles occur,
• where the impulse from the extrasystole enters retrogradely into the fast pathway which
• partially penetrates it, blocks it, and alters its electrical properties,
• so that the next impulse conducts slower.
• The ventricles are subsequently activated from the SA node via the slow pathway,
• which is observed as a PQ jump from 0.16s to 0.4s.
• This prolonged PQ interval persists because
• further during sinus rhythm, two impulses repeatedly meet in the fast pathway (linking phenomenon):
• 1. wave from the SA node,
• 2. wave from the AV nodal slow-fast echo:
• "echo" means something is reflected and returns back.
• The impulse from the SA node via the slow pathway activates the ventricles (long PQ interval)
• and simultaneously reflects or turns back,
• and retrogradely enters the fast pathway, where it collides with the passing impulse from the SA node.
• This recurring phenomenon is called linking.

• During sinus rhythm, a ventricular premature contraction occurs,
• which retrogradely conducts through the fast pathway to the atria,
• resulting in a retrograde P wave.
• However, the impulse then reverses direction and passes through the slow pathway,
• from the atria (retrograde P) to the ventricles (QRS),
• resulting in a prolonged PQ interval followed by a QRS complex.
• This phenomenon resembles interpolated ventricular premature contractions,
• but it is actually a retrograde AV nodal echo.

• It is a rare phenomenon.
• It is also referred to as:
• Dual ventricular response
• Ventricular double firing
• Dual AV nodal nonreentry tachycardia (DAVNNT)
• This tachycardia occurs when double fire continuously persists.
• It is often mistaken for atrial fibrillation.
• It causes tachycardia-induced cardiomyopathy.
• The definitive treatment is ablation of the slow pathway.
• Double fire occurs when the patient has:
• AV nodal duality and
• A very slow slow pathway.
• During sinus rhythm, the impulse enters both the fast and slow pathways simultaneously from the SA node:
• The “fast” impulse travels quickly through the fast pathway and depolarizes the ventricles (1st QRS)
• The “slow” impulse simultaneously progresses slowly through the slow pathway, which is so slow,
• that the His-Purkinje system has time to recover after the preceding activation from the fast pathway
• and the “slow” impulse again depolarizes the ventricles (2nd QRS)
• On the ECG, we see
• A sinus P wave followed by 2 QRS complexes (P-QRS-QRS) (P-QRS-QRS)...
• this cycle can be intermittent, paroxysmal, or even permanent
• if this phenomenon persist for a longer time (paroxysmal or permanent),
• it indicates Dual AV nodal nonreentry tachycardia
• If the fast pathway also conducts retrogradely, it can lead to slow-fast AVNRT.
• Double fire thus creates terrain for 2 tachycardias:
• Dual AV nodal nonreentry tachycardia (DAVNNT)
• AVNRT (Slow-Fast)
• which can alternate intermittently
• thus it is often mistakenly taken for atrial fibrillation