6.3 His Bundle Electrogram Recording, Split His Potentials & Infranodal Conduction

6.3 His Bundle Electrogram Recording, Split His Potentials & Infranodal Conduction

The bundle of His is a compact cylindrical fascicle of specialized conduction tissue approximately 15 to 20 mm in length. Originating at the anterior-superior apex of the triangle of Koch, it penetrates the central fibrous body (where it is termed the penetrating bundle), courses along the crest of the muscular interventricular septum beneath the membranous septum, and bifurcates into the left and right bundle branches (branching bundle).

Recording and interpreting potentials from this specialized conduit is essential for evaluating complex conduction disturbances. Dissecting whether an atrioventricular block is suprahisian (AV nodal), intra-Hisian (within the His trunk), or infra-Hisian (within the distal bundle branches) determines whether the patient requires urgent permanent pacing or can be managed conservatively.

---

Technical Challenges in His Bundle Recording

Navigating a diagnostic catheter to record a reproducible His bundle electrogram requires fine mechanical manipulation and continuous real-time electrogram analysis:

1. Catheter Manipulation Technique: Via femoral venous access, a steerable or pre-curved quadripolar catheter is advanced across the tricuspid valve into the right ventricle under fluoroscopy. The catheter is curled slightly toward the interventricular septum with gentle clockwise torque. As the catheter is slowly withdrawn across the septal leaflet of the tricuspid valve into the right atrium, the operator observes the electrograms transition from a pure ventricular deflection ($V$) to an electrogram exhibiting an atrial deflection ($A$), a His potential ($H$), and a ventricular deflection ($V$).
2. Proximal vs. Distal His Bundle Recordings:
   • Proximal His Recording: Positioned at the non-branching penetrating bundle adjacent to the compact AV node. Displays a prominent atrial electrogram ($A:V \ge 1:1$), a sharp His spike, and a longer, true HV interval. In pacing maneuvers, pacing the proximal His often requires higher outputs and may capture adjacent low atrial tissue.
   • Distal His Recording: Positioned along the branching segment near the bundle bifurcation. Displays a diminutive atrial electrogram ($A:V < 0.5:1$) and a large ventricular electrogram. The His potential lies closer to the $V$ wave, which increases the risk of the His spike blending into the ventricular electrogram, obscuring the true onset of infranodal conduction.
3. Catheter Instability & Micro-Dislodgement: Because the tricuspid annulus moves dynamically with cardiac contraction and respiration, the catheter tip can shift by millimeters. A minor backward displacement causes complete loss of the His spike (recording only low RA); minor forward displacement into the RV causes the His spike to merge into the ventricular complex or captures an isolated right bundle branch potential.

---

Validating True His Deflection vs. Right Bundle Branch (RBB) Potential

A critical diagnostic pitfall in the EP laboratory is mistaking a right bundle branch (RBB) potential for a true His bundle deflection. Because the RBB courses subendocardially along the right ventricular septum toward the base of the anterior papillary muscle, a catheter advanced slightly too far into the RV apex can record an RBB spike that mimics a His deflection with an abnormally short HV interval.

True His Bundle Recording:           (A) -------- (H) ------------------------ (V)
                                                  |                            |
                                                  +-------- HV: 35 - 55 ms ----+

Right Bundle Branch Recording:       [Tiny A]            (RB) --------------- (V)
                                                           |                   |
                                                           +--- RB-V: 10-25 ms +

Diagnostic Criteria for Differentiation

| Electrographic Feature | True His Bundle Potential ($H$) | Right Bundle Branch Potential ($RB$) | | :--- | :--- | :--- | :--- | | Conduction Interval | HV interval = 35 - 55 ms | RB-V interval = 10 - 25 ms (strictly <30 ms) | | Atrial Electrogram ($A$) | Prominent ($A:V \approx 1:2\text{ to }1:1$) | Absent or tiny far-field atrial signal ($A:V < 0.2:1$) | | Anatomical Position | Superior-anterior triangle of Koch at tricuspid annulus | More apical, distal, and inferior along the right ventricular septum | | Precordial V6 Relation | $H$ potential precedes surface QRS by $\ge 35\text{ ms}$ | $RB$ potential precedes local RV activation but may align with surface QRS onset | | Pacing Response | Selective His capture yields narrow QRS matching intrinsic conduction | Pacing yields complete LBBB morphology with wide, delayed left ventricular activation |

Pacing Validation: Selective vs. Non-Selective His Capture

Pacing through the recording bipole provides definitive physical validation of the His potential:

• Selective His Bundle Pacing: Low-output stimulation captures only the His bundle. The resulting surface QRS complex is completely normal, identical in duration and morphology to intrinsic conduction, preceded by an isoelectric interval matching the intrinsic HV interval.
• Non-Selective His Bundle Pacing: Stimulation captures both the His bundle and adjacent septal myocardium. The QRS displays a pseudo-delta wave (local myocardial capture) but retains a narrow terminal portion due to rapid activation via the specialized Purkinje network.
• RBB Pacing: Stimulation captures the right bundle branch, producing an artificial left bundle branch block (LBBB) pattern with broad QRS (>120 ms) and delayed left ventricular activation.

---

Intra-Hisian Conduction Disease & Split His Potentials ($H-H'$)

Under pathological conditions, the common bundle of His can develop localized, intramural conduction slowing or functional block. This phenomenon gives rise to split His potentials, designated as $H$ and $H'$.

Pathophysiological Mechanisms

1. Longitudinal Dissociation: Anatomical and electrophysiological studies (originally described by Damato, Narula, and Scherlag) demonstrate that fibers within the His bundle trunk are organized into distinct, longitudinally insulated channels destined for the right and left bundles. Fine connective tissue septa isolate these fascicular tracts. Focal fibrocalcific degeneration, ischemia, or mechanical trauma can selectively slow conduction along one tract while sparing another.
2. Transverse Lesions / Focal Conduction Block: A micro-lesion across the trunk divides the His bundle into a proximal His segment ($H$) proximal to the diseased zone and a distal His segment ($H'$) distal to the diseased zone.

Electrographic Manifestations

• Morphology: Two separate, distinct, high-frequency spikes ($H$ and $H'$) recorded within a single cardiac cycle between the atrial deflection ($A$) and the ventricular deflection ($V$).
• Diagnostic Threshold: A split His potential is diagnosed when the $H-H'$ interval exceeds 30 to 40 ms.
• Segmental Timing:
  • The $A-H$ interval reflects conduction from the low RA to the proximal His segment.
  • The $H-H'$ interval reflects conduction delay across the diseased intra-Hisian segment.
  • The $H'-V$ interval reflects conduction from the distal His segment to the ventricular myocardium (typically normal, 30 to 40 ms).

Normal His Tracing:             (A) ---------- (H) ------------------------ (V)
                                                |
                                                +------- HV = 45 ms --------+

Split His Tracing:              (A) ----- (H) ========= (H') --------------- (V)
                                           |             |
                                           +-- H-H' >35 -+
                                           |             |
                                           +------- Total HV = 85 ms -------+

Clinical Instability of Intra-Hisian Disease

Intra-Hisian block is notoriously unstable. Unlike AV nodal conduction delays (which are physiologically stable and responsive to autonomic modulation), intra-Hisian conduction disease is immune to autonomic rescue and exhibits unpredictable, sudden progression to complete, irreversible AV block. Pacemaker cells within the His bundle below the site of block are sparse and slow (producing unreliable escape rhythms of 30 to 40 bpm); therefore, identification of intra-Hisian block warrants urgent permanent pacemaker implantation.

---

Electrophysiological Localization of Atrioventricular Block

Intracardiac electrogram analysis definitively differentiates between suprahisian (AV nodal), intra-Hisian, and infra-Hisian AV conduction blocks:

                               [Atrium (A)]
                                    |
                 ===== LEVEL 1: AV NODAL BLOCK (Suprahisian) =====
                 Blocked beat shows: (A) without (H)
                                    |
                              [Proximal His (H)]
                                    |
                 ===== LEVEL 2: INTRA-HISIAN BLOCK =====
                 Blocked beat shows: (A)-(H) without (H')
                                    |
                              [Distal His (H')]
                                    |
                 ===== LEVEL 3: INFRA-HISIAN BLOCK =====
                 Blocked beat shows: (A)-(H)-(H') without (V)
                                    |
                              [Ventricle (V)]

1. First-Degree AV Block

• Nodal (Suprahisian): PR prolongation on the surface ECG is caused entirely by an elongated AH interval (>120 ms). The HV interval is completely normal (35 to 55 ms). Prognosis is excellent; no pacing required in asymptomatic patients.
• Infranodal: PR prolongation on the surface ECG occurs in the setting of a normal AH interval, driven entirely by an abnormally prolonged HV interval (>55 ms). Signifies widespread, latent His-Purkinje conduction disease.

2. Second-Degree AV Block

• AV Nodal Mobitz Type I (Wenckebach):
  • Occurs in 75% to 80% of Mobitz I cases.
  • Conducted beats show progressive, beat-to-beat prolongation of the AH interval until conduction fails. The HV interval remains strictly constant on all conducted beats.
  • The Blocked Beat: Displays a normal low atrial deflection ($A$) that fails to generate a His potential—recorded as an $A$ without an $H$ deflection ($A \text{ blocked proximal to } H$).
• Infranodal Mobitz Type I (His-Purkinje Wenckebach):
  • Rare (<5% of cases). The AH interval remains constant, while the HV interval progressively prolongs before an $H$ deflection fails to conduct to the ventricles ($A-H$ without $V$).
• Infranodal Mobitz Type II:
  • Represents structural disease of the His-Purkinje system.
  • Conducted beats display a fixed AH interval and a normal or prolonged (fixed) HV interval.
  • The Blocked Beat: Normal low atrial depolarization conducts through the AV node into the His bundle, producing a normal His spike, but fails to reach the ventricles—recorded as an $A-H$ deflection with NO subsequent $V$ deflection ($H \text{ blocked proximal to } V$).
• Intra-Hisian Second-Degree Block:
  • Conducted beats display split His potentials ($H$ and $H'$).
  • The Blocked Beat: Displays an $A$ wave followed by the proximal His spike ($H$), but conduction blocks within the His trunk—recorded as $A-H$ with absence of $H'$ and $V$.

3. Third-Degree (Complete) AV Block

• Suprahisian (AV Nodal):
  • Complete dissociation between atrial deflections ($A$) and ventricular deflections ($V$).
  • Every ventricular escape complex is preceded by an identical His potential with a normal, constant HV interval (35 to 55 ms). This proves that the escape pacemaker originates from the junction/His bundle below the level of block.
  • Characteristics: Narrow QRS (<100 ms), rate 40 to 60 bpm, stable hemodynamics, accelerates with atropine or exercise.
• Intra-Hisian Complete Block:
  • Atrial deflections conduct to proximal His ($A-H$). Ventricular escape complexes originate from the distal His segment, preceded by the distal His spike ($H'-V$).
• Infra-Hisian (His-Purkinje):
  • Atrial deflections conduct through the AV node into the common His bundle; therefore, every $A$ wave is followed by a non-conducting His spike ($A-H$).
  • The ventricular escape complexes are broad, bizarre, and completely dissociated from the His potentials ($V$ deflections without preceding $H$ spikes).
  • Characteristics: Wide QRS (>120 ms), rate 20 to 40 bpm, highly unstable, unheralded ventricular standstill/syncope (Stokes-Adams attacks), fails to respond to atropine.

---

Master Diagnostic Table: Electrophysiological Localization of AV Block