Heartbeats on Backup: Junctional vs. Ventricular Escape Rhythms

A complete heart block is a form of AV dissociation (see Drs. Davila’s and Robinson’s post on AV Dissociation and Complete AV Block: What’s the Difference?) where there is complete interruption of electrical conduction between the atria and the ventricles, leading to an atrial rhythm that occurs independently of the ventricular rhythm. The P waves will "march out" through the ECG unrelated to the QRS complexes and produce regular P-P intervals that are unrelated to the regular R-R intervals.[1]

Figure 1: 3rd degree AV Block

In a normally functioning conduction system, electrical activity in the heart is orchestrated by the SA node, leading to a stepwise depolarization of the myocardium as the impulse goes from the SA node to the internodal pathways, AV node, Bundle of His, bundle branches, fascicles (in the case of the left side of the heart), and finally the purkinje system.[2]

Figure 2: Electrical Conduction System of the Heart

Although the SA node sets the pace, as it has the fastest intrinsic rate, other pacemaker cells act as backup if the SA node fails to pace at a sufficient rate.[2]

Figure 3: Intrinsic Pacemaker Cells of the Conduction System

Junctional and Ventricular escape rhythms arise as compensatory mechanisms when the primary pacemaker, the SA node, fails to pace fast enough. Failure of adequate SA node pacing can be due to a myriad of causes, such as primary SA node dysfunction, AV dissociation, increased parasympathetic tone, digoxin toxicity, beta-blocker toxicity, calcium channel blocker toxicity, myocardial ischemia, sick sinus syndrome, age-related degeneration of the conduction system such as Lev's and Lenegre's disease, and infectious and inflammatory conditions like myocarditis or Lyme carditis.[3]

In a junctional rhythm, the electrical activity is initiated by the tissues between the atria and the ventricles. This is typically initiated from the AV node or the Bundle of His.[3][4]

In a ventricular escape rhythm, the electrical activity is initiated below the level of the Bundle of His in the bundle branches, fascicles, or Purkinje system.[5]

Junctional escape rhythms originate in the AV node or the Bundle of His and have an intrinsic rate of 40-60 beats/min. Since the electrical impulse is initiated at the level of the Bundle of His or above, the impulse is conducted down through the bundle branches, fascicles, and purkinje fibers, leading to organized ventricular contractions and thus narrow QRS complexes (assuming no instrinsic bundle branch block). Additionally, the electrical impulse travels retrograde to the atria. Therefore, you will usually not see a P-wave on ECG as they are “buried” in the QRS complex (as in AV nodal reentrant tachycardia). Without simultaneous activation of the atria and ventricles, you may see retrograde p-waves before or after the QRS complex in Leads II, III, and aVF. But don’t be fooled! There is no association between QRS complexes and preceding atrial activity (e.g., P-waves, flutter waves).[4] 

Ventricular escape rhythms originate in the ventricle below the level of the Bundle of His with an intrinsic rate of 20-40 beats/min. These impulses must spread via cell-to-cell transmission to achieve ventricular myocardial contraction, leading to slower depolarization, which is seen as widened QRS complexes with morphologies similar to RBBB/LBBB.[5] 

Ventricular escape rhythms are the most common escape rhythms that arise in the setting of complete heart block, as seen in the presented case.

Table 1: Comparison of Junctional vs Ventricular Escape

1) High-grade second-degree heart block

2) Third-degree heart block

3) SA node dysfunction

4) Increased vagal tone

5) Myocardial ischemia

6) Digoxin, beta blockers, calcium channel blockers, adenosine

7) Age-related degeneration of the conduction system

8) Hyperkalemia

9) Infectious and inflammatory conditions (myocarditis or Lyme carditis)

First, you want to evaluate the patient's hemodynamics and stabilize ("ABCs", pacer pads, ACLS). Then you want to get a thorough H&P. It is important to figure out the underlying cause of the dysrhythmia and potentially reverse it. In general, if there is a high-grade or complete AV block that is not quickly reversible, consult cardiology, as there may be an indication for permanent pacemaker placement.

The patient’s medication list was significant for daily labetalol and amlodipine use. She had no LE edema or JVD and clear breath sounds. The creatinine was 2.2 mg/dL (baseline was 1.13 mg/dL), potassium 5.5 mmol/L, and troponin 0.046 ng/mL. Given this, the patient’s presentation was concerning for possible BRASH syndrome. 

BRASH syndrome is a clinical condition that stands for Bradycardia, Renal Failure, AV nodal blockade, Shock, and Hyperkalemia. The key concept in BRASH is the synergistic interaction between mild hyperkalemia and AV nodal blockade medications, which leads to a vicious cycle of worsening bradycardia, renal failure, and shock.[6][7][8] See Drs. Davila’s and Galeano-Londono’s blog post on BRASH for a deeper dive into the pathophysiology and treatment of BRASH (BRASH Part 1 and BRASH Part 2).

The hyperkalemia was treated with calcium gluconate 2 g, insulin 5 units, and 50% dextrose 25 g. Cardiology recommended urgent transfer for electrophysiology study and permanent pacemaker placement. On follow-up visits, the pacemaker has been normally functioning with atrial sensing and ventricular pacing suggesting persistent, complete AV block.