Overview

Conduction velocity≈1.5–4 m/s (fastest in the heart)

Intrinsic rate≈15–40/min

Ventricular activation time≈0.06–0.10 s (QRS)

Histology. Purkinje cells are larger than ordinary ventricular myocytes. Their cytoplasm is pale and rich in glycogen, their few myofibrils lie at the cell edges and they have no T-tubules. They are joined by abundant gap junctions (connexins 40 and 43), which makes them the fastest-conducting tissue in the heart, at about 1.5–4 m/s.

Sequence of activation. The network reaches the apex and the papillary muscles first and the base last. From the Purkinje fibres the impulse spreads through ordinary myocardium (about 0.3–0.5 m/s) from the endocardium out to the epicardium. The ventricles therefore contract from the apex upward, squeezing blood toward the outflow valves. Activation of the whole ventricular mass takes only about 0.06–0.10 s, which is the width of the QRS complex.

Escape rhythm. Purkinje cells are pacemakers of last resort. If they take over, they fire at about 15–40/min and produce a broad-complex ventricular escape rhythm.

Location: Beneath the endocardium of both ventricles, including the papillary muscles and the trabeculae.

Anatomy

Histology: Large, pale, glycogen-rich cells with few, peripherally placed myofibrils, no T-tubules and abundant gap junctions. They lie in the subendocardial connective tissue.

Function

Distribute the impulse rapidly and nearly simultaneously to the ventricular myocardium.
Ensure that the ventricles contract from the apex toward the base.
Act as the last back-up pacemaker (ventricular escape, 15–40/min).

Clinical significance

Ventricular escape rhythm

In complete heart block with disease below the bundle of His, the ventricles may be driven only by a slow, broad-complex Purkinje escape rhythm. This can cause syncope (Stokes–Adams attacks).

Arrhythmogenesis

Purkinje fibres are prone to early and delayed afterdepolarisations. Early afterdepolarisations trigger torsades de pointes in long QT syndrome. Delayed afterdepolarisations underlie digoxin toxicity. Purkinje triggers can start ventricular fibrillation, and these can be targeted by ablation.

Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.