4.3 Atrioventricular Blocks & Intraventricular Conduction Delays

First-Degree & Second-Degree Mobitz Type I AV Blocks

Atrioventricular (AV) Blocks represent impaired electrical impulse propagation from the atria to the ventricles. They are classified into three degrees based on severity and electrophysiological location (AV node vs. His-Purkinje system).

First-Degree AV Block

• Electrocardiographic Criteria: Constant, prolonged PR interval > 0.20 seconds (200 ms or > 5 small boxes) with a 1:1 P-to-QRS conduction ratio (every P wave is followed by a QRS complex).
• Anatomical Site: Conduction delay occurs predominantly within the AV Node.
• Etiologies & Clinical Significance: Often benign and asymptomatic. Caused by heightened vagal tone, aging conduction system fibrosis, or AV nodal blocking medications (beta-blockers, non-dihydropyridine CCBs, digoxin). No treatment is required; monitor for progression.

Second-Degree AV Block Type I (Mobitz I / Wenckebach)

• Electrocardiographic Criteria: Progressive PR interval lengthening on consecutive beats until a P wave fails to conduct to the ventricles (a 'dropped QRS complex').
  • Grouped Beating: Features characteristic grouped QRS complexes.
  • PR Pattern: The PR interval following the dropped beat is the shortest, and the PR interval immediately preceding the dropped beat is the longest.
  • RR Interval Pattern: The RR intervals progressively shorten prior to the dropped beat.
• Anatomical Site: Almost always localized within the AV Node.
• Etiologies: High vagal tone (athletes, sleep), inferior wall myocardial infarction (occlusion of the Right Coronary Artery / RCA supplying the AV nodal artery), or drug toxicity.
• Clinical Prognosis & Management: Usually transient and benign. Rarely progresses to complete heart block. If symptomatic (hypotension, dizziness), the first-line intervention is Atropine 1 mg IV (repeat q3-5 min up to max 3 mg).

Second-Degree Mobitz Type II & Third-Degree (Complete) AV Blocks

Second-Degree AV Block Type II (Mobitz II)

• Electrocardiographic Criteria: Fixed, constant PR intervals on conducted beats, interspersed with unpredictable, non-conducted P waves (e.g., 2:1, 3:1, or 4:1 block).
  • Unlike Mobitz I, there is no progressive PR lengthening prior to the dropped beat.
  • Conducted QRS complexes are frequently wide (> 120 ms) due to underlying bundle branch disease.
• Anatomical Site: Localized infranodally within the His-Purkinje system (below the AV node).
• Etiologies: Acute anterior wall myocardial infarction (occlusion of the Left Anterior Descending / LAD artery supplying the septal branch and bundle branches) or extensive degenerative conduction system disease (Lev-Lenègre disease).
• Prognosis & Management: High risk of sudden, unpredictable progression to complete heart block or asystole. Atropine is ineffective or contraindicated (see below). Immediate Transcutaneous Pacing (TCP) or Transvenous Pacing (TVP) is required as a bridge to permanent pacemaker implantation.

Third-Degree (Complete) AV Block

• Electrocardiographic Criteria: Complete absence of AV conduction leading to total AV Dissociation.
  • Atrial Rate: Regular P-P intervals (atrial rate typically 60-100 bpm).
  • Ventricular Rate: Regular R-R intervals (ventricular rate 20-60 bpm).
  • No Relationship: P waves and QRS complexes operate completely independently; P waves may appear buried within, on top of, or after QRS complexes.
• Site of Escape Rhythm Determines Clinical Stability:
  • Junctional Escape Rhythm: Originates in the AV junction / Bundle of His. Ventricular rate 40 to 60 bpm with a narrow QRS complex (< 120 ms). Patients may be hemodynamically stable at rest.
  • Ventricular Escape Rhythm: Originates in the Purkinje network. Ventricular rate 20 to 40 bpm with a wide, aberrant QRS complex (≥ 120 ms). Hemodynamically unstable, prone to Stokes-Adams syncope, severe hypotension, and cardiac arrest.

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Pharmacological Responsiveness & Emergency Pacing Protocols

Why Atropine Fails in Infranodal AV Block

Atropine is a competitive anticholinergic agent that blocks muscarinic acetylcholine receptors, thereby vagolytically enhancing conduction velocity through the AV Node.

• Nodal Block Response (1st Degree & Mobitz I): Atropine successfully increases AV nodal conduction and improves ventricular rate.
• Infranodal Block Response (Mobitz II & 3rd Degree with Wide QRS): Atropine increases the sinus node rate (increasing P wave frequency) but has no effect on diseased His-Purkinje tissue. By increasing the number of atrial impulses reaching an infranodal block, Atropine increases the block ratio, worsens ventricular rate, and can precipitate hemodynamic collapse!

Emergency Pacing Protocol

1. Transcutaneous Pacing (TCP): Apply pacing pads (anterior-posterior orientation preferred). Set mode to Demand, rate to 60-80 bpm, and increase current output (mA) from zero until electrical capture (a wide QRS and broad T wave following every pacing spike) is achieved.
2. Confirm Mechanical Capture: Always verify mechanical capture by palpating a right femoral pulse or inspecting an arterial line waveform. Palpating carotid or radial pulses can lead to false readings due to skeletal muscle twitching caused by TCP.
3. Analgesia & Sedation: TCP causes painful skeletal muscle contractions. Administer IV opioids (fentanyl) and sedatives (midazolam/propofol) as soon as possible.
4. Transvenous Pacing (TVP): Insert a bipolar pacing catheter via the internal jugular or subclavian vein into the right ventricular apex as a stable bridge to permanent pacemaker implantation.

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Bundle Branch Blocks & Sgarbossa Criteria

Intraventricular conduction delays occur when propagation down the right or left bundle branch is blocked, prolonging total ventricular depolarization time (QRS ≥ 120 ms).

Right Bundle Branch Block (RBBB)

• ECG Criteria: QRS duration ≥ 120 ms.
  • Lead V1-V3: rsR' ('rabbit ears') or QR pattern.
  • Lead I, aVL, V5-V6: Wide, slurred S wave.
• Pathophysiology: Delayed right ventricular depolarization occurring after left ventricular depolarization.

Left Bundle Branch Block (LBBB)

• ECG Criteria: QRS duration ≥ 120 ms.
  • Lead I, aVL, V5-V6: Broad, notched, or slurred R waves; absent Q waves in lead I and V6.
  • Lead V1-V3: Deep, wide S waves.
• Pathophysiology: Normal septal depolarization (left-to-right) is lost. Delayed LV depolarization alters repolarization, causing baseline ST segments and T waves to be directed opposite (discordant) to the main QRS deflection.

Sgarbossa Criteria: Diagnosing Acute MI in Pre-Existing LBBB

Baseline LBBB distorts ST segments, making standard STEMI criteria unreliable. The Sgarbossa Criteria identify acute myocardial infarction in the presence of LBBB or ventricular pacing:

• Interpretation: A score ≥ 3 points has a 90% specificity for acute evolving myocardial infarction, requiring immediate emergent coronary angiography and reperfusion therapy.

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Fascicular Blocks & Multibundle Conduction Disease

The Left Bundle Branch divides into two main fascicles: a thin Left Anterior Fascicle and a thick, dual-supplied Left Posterior Fascicle.

• Left Anterior Fascicular Block (LAFB):
  • Axis: Extreme Left Axis Deviation (-45° to -90°).
  • ECG Features: qR pattern in leads I and aVL; rS pattern in leads II, III, and aVF. QRS duration is normal or slightly prolonged (80-110 ms).
• Left Posterior Fascicular Block (LPFB):
  • Axis: Right Axis Deviation (+90° to +180°).
  • ECG Features: rS pattern in leads I and aVL; qR pattern in leads II, III, and aVF. Diagnostic only after excluding right ventricular hypertrophy (RVH) and lateral MI.
• Bifascicular Block: RBBB + LAFB OR RBBB + LPFB. Indicates extensive disease in two of the three main conduction pathways.
• Trifascicular Block: Bifascicular block PLUS a prolonged PR interval (1st-degree AV block) or intermittent 2nd/3rd-degree block. High risk of complete heart block.