G2ii: Abnormal conduction & arrhythmias

Arrhythmia = abnormality in rate, generation & propagation of an AP

2 major causes of arrhythmias are:

  1. Abnormal Automaticity
  2. Abnormal Conduction

Abnormal Automaticity

  • Fast AP cells do not normally undergo spont. Depolarisation
  • Can become “Fast → Slow Response” cells by blockage of Fast Na+ channel
  • If fast Na+ channel blocked (drugs, hypoxia) the AP relies on Ca2+ channels to depolarise
  • The AP looks more like a ‘slow AP’
  • ∴producing arrhythmias as cell which is not a PM cell starts pacing

Triggered Automaticity → always caused by after-depolarisations

Fast AP cells can undergo spontaneous depolarisation in Ph 3-4 (relative refractory period)

  • 2 types:

1. Early afterdepols

  • More likely with low HR
  • Long Ph 2 → Ca2+ channels activated at beginning of Ph 2 have inactivated & can be reactivated to carry new AP
  • Occurs in Ph 3
Early afterdepols

2. Delayed afterdepolarisations

  • Associated with rapid HR
  • Due to ↑Ca2+ intracellularly
    • Hypercalcaemia
    • Digoxin toxicity
    • Excess catecholamine stimulation

Abnormal Conduction

  1. Conduction block
  2. Reflection
  3. Re-entry

1) Conduction block

  • An ectopic focus ‘escapes’ the SA Node to become the dominant PM
  • There is a block between the ectopic focus & the SA Node, so the SA cannot control it

2) Reflection

  • An adjacent cell that has already repolarised becomes stimulated by a cell that has not repolarised yet
  • e. ventricular arrhythmias associated with long QT syndrome

3) Re-Entry

  • When a cardiac impulse can re-excite some regions through which it has previously passed
  • Responsible for most SVTs