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Purkinje fibre network

Fascicles, Purkinje, muscle · 20–40/min 2–4 m/s

Terminal ramifications of both bundle branches: large-diameter, glycogen-rich, myofibril-poor cells forming a subendocardial lattice that penetrates only the inner third of the wall. They deliver the impulse almost simultaneously to the whole endocardial surface so both ventricles contract as a unit from apex to base.

Traced from the start

  1. Sinoatrial node
  2. Internodal pathways (anterior, middle, posterior)Right atrial myocardium
  3. Atrioventricular node
  4. Bundle of His (atrioventricular bundle)
  5. Right bundle branchLeft bundle branch
  6. Purkinje fibre network

Detail

Conduction velocity
2–4 m/s, the fastest tissue in the heart (large fibres, abundant gap junctions)
Intrinsic rate
20–40/min (ventricular escape), the last line of pacemaker back-up
Action potential
The longest of any cardiac cell, so the network is still refractory when the muscle behind it is excitable again — a natural barrier to retrograde re-entry
Distribution
Subendocardial, apex first, sparse at the base and outflow tracts (activated last); conduction slows to muscle speed at the Purkinje–muscle junction

When it goes wrong

Complete heart block below the His bundle

Ventricular escape rhythm at 20–40/min with a broad QRS — unreliable and liable to stop (ventricular standstill), which is why infranodal block needs pacing

Enhanced Purkinje automaticity after reperfusion of an infarct

Accelerated idioventricular rhythm 50–110/min with broad complexes — a benign marker of reperfusion, not to be suppressed

Early after-depolarisations in Purkinje cells when the action potential is prolonged (QT-prolonging drugs, hypokalaemia, hypomagnesaemia, congenital long QT)

Torsades de pointes — polymorphic VT twisting around the baseline; IV magnesium, correct potassium, isoprenaline or overdrive pacing, stop the offending drug

Delayed after-depolarisations from Ca2+ overload (digoxin toxicity, catecholamine excess)

Ventricular ectopics and, classically, bidirectional VT in digoxin toxicity — digoxin-specific antibody fragments

Short-coupled ectopics arising from Purkinje tissue in a structurally normal heart

Idiopathic VF triggered from the Purkinje network, treatable by ablating the culprit focus

Practise this structure

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