8.1 Narrow-Complex Tachycardias: Differential Diagnosis of AVNRT, AVRT & AT

8.1 Narrow-Complex Tachycardias: Differential Diagnosis of AVNRT, AVRT & AT

Narrow-complex tachycardias, defined by a surface QRS duration $< 120\text{ ms}$, represent arrhythmias that originate at or above the atrioventricular (AV) junction and utilize the physiological His-Purkinje specialized conduction system for ventricular depolarization. In the clinical electrophysiology (EP) laboratory, distinguishing between the three primary mechanisms—Atrioventricular Nodal Reentrant Tachycardia (AVNRT), Orthodromic Atrioventricular Reentrant Tachycardia (O-AVRT), and Atrial Tachycardia (AT)—is paramount for guiding targeted catheter ablation. This differentiation relies on systematic evaluation of the relationship between ventricular and atrial activation on the 12-lead surface electrocardiogram (ECG) and multielectrode intracardiac electrograms (EGMs).

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The Fundamental Classification: Short-RP vs. Long-RP Tachycardias

The initial diagnostic framework categorizes narrow-complex tachycardias according to the temporal relationship between ventricular depolarization ($R$ wave) and retrograde atrial depolarization ($P$ wave). On the surface ECG, this is measured as the RP interval (from the onset of the QRS complex to the onset of the subsequent P wave) relative to the PR interval (from the onset of the P wave to the subsequent QRS complex).

Short-RP SVT (RP < PR):             Long-RP SVT (RP > PR):

  QRS   P                             QRS         P       QRS
   |    |                              |          |        |
   +----+-----------+                  +----------+---+----+
     RP      PR                             RP         PR   
  (RP < 50% of RR)                     (RP > 50% of RR)     

1. Short-RP Tachycardias ($RP < PR$)

A tachycardia is classified as Short-RP when the $RP$ interval is shorter than the subsequent $PR$ interval ($RP < 50%$ of the total tachycardia cycle length). In the EP laboratory, this corresponds to an intracardiac septal ventriculoatrial (VA) interval $\le 70\text{ to }90\text{ ms}$, measured from the earliest surface QRS or ventricular electrogram to the earliest high-frequency atrial deflection recorded on the His bundle catheter or proximal coronary sinus.

Typical Slow-Fast AVNRT

• Mechanism: Functional microreentry confined to the triangle of Koch in the right atrium. The reentrant circuit utilizes a slowly conducting slow pathway (located inferiorly and posteriorly near the coronary sinus ostium) for antegrade conduction and a rapidly conducting fast pathway (located superiorly and anteriorly along the tendon of Todaro near the apex of the triangle of Koch) for retrograde conduction.
• Surface ECG Features: Because antegrade conduction down the slow pathway and retrograde conduction up the fast pathway occur nearly simultaneously, atrial depolarization coincides with, or is buried within, the terminal portion of the QRS complex:
  • Pseudo-$r'$ in Lead $V_1$: A narrow, positive terminal deflection in lead $V_1$ mimicking a right bundle branch block pattern, which disappears during sinus rhythm.
  • Pseudo-$S$ Waves in Inferior Leads (II, III, aVF): Negative terminal notches in the inferior leads representing superiorly directed retrograde atrial activation, absent during normal sinus rhythm.
  • RP Interval: Typically $< 70\text{ ms}$ on the surface ECG, and frequently undetectable ($0\text{ ms}$) when entirely submerged within the QRS.
• Intracardiac Electrogram Characteristics:
  • Septal VA Interval: Extremely short, standardly $\le 70\text{ ms}$ (frequently $0\text{ to }40\text{ ms}$ or even negative relative to the surface QRS offset).
  • Atrial Activation Sequence: Concentric. Retrograde atrial excitation proceeds superiorly up the fast pathway, yielding the earliest retrograde atrial electrogram at the His bundle catheter ($His_A$) or proximal Coronary Sinus ($CS_{9-10}$), spreading symmetrically and centrifugally outward to the lateral right atrium (HRA) and distal coronary sinus ($CS_{1-2}$).

Orthodromic AVRT (O-AVRT)

• Mechanism: Macroreentry utilizing the normal AV conduction axis (AV node $\to$ His bundle $\to$ bundle branches $\to$ Purkinje network $\to$ ventricular myocardium) in the antegrade direction, and an extranodal accessory pathway (Kent bundle) in the retrograde direction.
• Surface ECG Features: Because the electrical wavefront must completely depolarize the ventricles and traverse working ventricular myocardium before reaching the ventricular insertion of the accessory pathway and conducting to the atrium, retrograde P waves are clearly separated from the QRS complex. They are typically inscribed within the ST segment or early T wave ($RP > 70\text{ to }80\text{ ms}$ on surface ECG).
• Intracardiac Electrogram Characteristics:
  • Septal VA Interval: Standardly $> 100\text{ ms}$ (rarely between $70\text{ and }90\text{ ms}$ for rapid-conducting septal pathways, but never $\le 70\text{ ms}$).
  • Atrial Activation Sequence:
    • Eccentric Activation: If the accessory pathway is located along the left free wall (mitral annulus) or right free wall (tricuspid annulus), the earliest retrograde atrial activation is recorded at a site remote from the AV node. In a left lateral pathway, the earliest A is recorded on the distal coronary sinus pair ($CS_{1-2}$), preceding the atrial electrogram at the His bundle.
    • Concentric Activation: If the accessory pathway is located along the septum (e.g., anteroseptal, midseptal, or posteroseptal), retrograde activation is earliest near the septum (His bundle or CS ostium). However, the septal VA interval remains significantly longer ($> 100\text{ ms}$) than in typical AVNRT.

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2. Long-RP Tachycardias ($RP > PR$)

A tachycardia is classified as Long-RP when the $RP$ interval exceeds the subsequent $PR$ interval ($RP > 50%$ of the tachycardia cycle length). In these arrhythmias, the P wave is positioned in the second half of the cycle, closer to the following QRS complex.

Atypical AVNRT

• Fast-Slow AVNRT: Antegrade conduction proceeds down the superior fast pathway, while retrograde conduction ascends the inferior slow pathway. Because retrograde slow pathway conduction is sluggish and decremental, the retrograde atrial deflection is markedly delayed, producing a prolonged septal VA interval ($> 100\text{ ms}$, typically $150\text{ to }300\text{ ms}$). Retrograde P waves are negative in leads II, III, and aVF (superior axis). Earliest retrograde atrial activation is concentric but recorded at the coronary sinus ostium ($CS_{os}$) rather than the His bundle.
• Slow-Slow AVNRT: Antegrade conduction utilizes one slow pathway, and retrograde conduction ascends a second distinct slow pathway (e.g., left-sided slow pathway extensions along the coronary sinus roof), producing a long RP interval with earliest retrograde activation at the CS os or proximal CS.

Permanent Junctional Reciprocating Tachycardia (PJRT)

• Mechanism: A persistent, often incessant form of orthodromic AVRT mediated by a concealed, slowly conducting, decremental accessory pathway. The pathway is almost universally located in the posteroseptal region, situated within or adjacent to the coronary sinus ostium or middle cardiac vein.
• Surface ECG Features: Incessant narrow-complex tachycardia with deeply inverted, negative retrograde P waves in the inferior leads (II, III, aVF) and leads $V_4\text{-}V_6$. The RP interval is characteristically very long ($RP > PR$).
• Intracardiac Findings: Earliest retrograde atrial activation is located at the coronary sinus ostium or posteroseptal tricuspid annulus. The accessory pathway demonstrates classic decremental conduction: pacing the right ventricle at accelerating rates results in progressive prolongation of the local ventriculoatrial ($V-A$) conduction interval.

Atrial Tachycardia (AT)

• Mechanism: Focal ectopic automaticity, microreentry, or triggered activity originating within either the right atrium (crista terminalis, tricuspid annulus, coronary sinus os) or left atrium (pulmonary vein ostia, mitral annulus, left atrial appendage).
• Surface ECG Features: P wave morphology differs distinctly from the normal sinus P wave. The axis depends on the site of origin (e.g., negative in II, III, aVF for low atrial or CS os foci; positive in $V_1$ with negative limb leads for left atrial foci). The PR interval depends entirely on passive, rate-dependent antegrade AV nodal decremental conduction.
• Intracardiac Findings: Ventricular activation is purely passive. The atrial activation sequence begins at the ectopic atrial focus and spreads centrifugally across the atria. Crucially, AV nodal block (Wenckebach or 2:1 block) can occur spontaneously or during diagnostic maneuvers without terminating or perturbing the atrial cycle length.

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Comprehensive Differentiation Matrix

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Diagnostic Clues from Spontaneous Onset and Termination

Careful inspection of telemetry strips and continuous EP recording channels during transition events provides pivotal diagnostic insight.

Onset Dynamics: The AH / PR Jump

• AVNRT Initiation: Typically initiated by an atrial premature depolarization ($A_2$) that blocks in the fast pathway (due to its longer effective refractory period at long cycle lengths) and conducts antegradely over the slow pathway (which has a shorter effective refractory period). This produces an abrupt jump in the $AH$ interval (defined as $\Delta AH \ge 50\text{ ms}$ for a $10\text{ ms}$ decrement in atrial coupling interval) or a sudden, marked prolongation of the surface $PR$ interval.
• AVRT Initiation: Does not require dual pathway conduction. May be initiated by an atrial or ventricular premature beat that encounters unidirectional block in one limb of the circuit (e.g., antegrade block in a manifest bypass tract with conduction down the AV node, or antegrade conduction down the AV node while the accessory pathway recovers retrograde excitability).
• AT Initiation: Often begins with a warm-up phenomenon (progressive acceleration of cycle length over the first several beats) if automatic, or abruptly following a single trigger beat without requiring an antecedent AH jump.

Termination Dynamics: A-Block vs. V-Block

Termination with an A Wave (AV Block):     Termination with a V Wave (VA Block):

   A       A       A       A                  A       A       A       -
   |       |       |       |                  |       |       |       
   V       V       V       - (Block)          V       V       V       V (Block)
   [Excludes Atrial Tachycardia]             [Block in AV Node or Bypass Tract]

1. Termination with an A Wave (A-Block):
   • The last recorded intracardiac deflection of the tachycardia is an atrial electrogram that fails to conduct to the ventricles (AV block).
   • Definitive Rule: Termination with an A wave unequivocally EXCLUDES Atrial Tachycardia! In AT, the tachycardia generator resides within the atrial myocardium; block in the AV node prevents conduction to the ventricle but cannot extinguish the autonomous atrial driver. Termination with an A wave isolates the site of block to the AV node (in AVNRT or AVRT) or an antegrade accessory pathway.
2. Termination with a V Wave (V-Block):
   • The last recorded deflection is a ventricular electrogram that fails to conduct retrogradely to the atrium (VA block).
   • This confirms block in the retrograde limb of the circuit: either block in the retrograde fast/slow pathway in AVNRT, or block in the retrograde accessory pathway in AVRT.

Pharmacological & Autonomic Interventions: Adenosine and Atropine

When baseline electrograms yield equivocal findings, autonomic maneuvers (carotid sinus massage, Valsalva maneuver) or pharmacological probes provide definitive differentiation.

Adenosine Protocol and Responses

Adenosine is an endogenous purine nucleoside that acts on cardiac $A_1$ adenosine receptors, activating the inward-rectifier potassium current ($I_{K,Ado}$) and inhibiting cyclic AMP ($cAMP$)-mediated L-type calcium currents ($I_{Ca,L}$). This causes marked, transient suppression of sinus node automaticity and pronounced prolongation of AV nodal refractoriness and conduction time.

• Response 1: Abrupt Tachycardia Termination via AV Block:
  • Occurs with termination following a P wave (A wave) that fails to conduct to the ventricle.
  • Clinical Meaning: Proves that the AV node is an indispensable, obligate limb of the reentrant circuit. This finding is diagnostic of AVNRT or AVRT.
• Response 2: Transient AV Block with Ongoing Atrial Tachycardia:
  • The ventricular response abruptly slows (e.g., development of transient 2:1, 3:1, or high-grade AV block), exposing unperturbed, continuous atrial deflections marching through at the exact baseline cycle length.
  • Clinical Meaning: Conclusively establishes Atrial Tachycardia or Atrial Flutter! The arrhythmia does not depend on the AV node for perpetuation.
• Response 3: Tachycardia Acceleration or Degeneration:
  • In patients with pre-excited tachycardias (antidromic AVRT or atrial fibrillation with bystander bypass tracts), adenosine can shorten bypass tract refractoriness via reflex sympathetic activation, potentially precipitating rapid ventricular rates or ventricular fibrillation. Hence, a defibrillator must always be immediately operational during administration.

Atropine and Isoproterenol

• Atropine (muscarinic cholinergic antagonist) and Isoproterenol (pure beta-adrenergic agonist) enhance AV nodal conduction, shorten refractory periods, and facilitate tachycardia induction during electrophysiological testing when baseline programmed stimulation fails.
• If a patient presents in suspected PJRT or atypical AVNRT with intermittent 1:1 or 2:1 AV conduction, isoproterenol enhances antegrade AV nodal conduction and facilitates 1:1 driving of the clinical tachycardia.