L7.3 Cardiac hypertrophy and arrhythmia Flashcards Preview

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Flashcards in L7.3 Cardiac hypertrophy and arrhythmia Deck (10)
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Definition, symptom, and cause of arrhythmia?

  • Arrhythmia = abnormalities of electrical rhythm
    • Can be benign or malignant
  • Symptoms: Palpitations to critical decrease in CO
  • Cause: Altered AP generation and/or conduction processes


Arrthymia arises from?

  • Altered AP generation 
    • Normal nodal automaticity altered
    • Triggered activity in ventricles
  • Altered AP conduction


Normal nordal automaticity altered

  • Normal nodal automaticity
  • Normally SA node takes lead
  • Abnormal influenced by:
    • SNS: Latent pacemakers may take over
    • PNS: latent pacemakers may emerge
  • Ischemia to node area:
    • cells may develop pacemaker function
    • Loss of RMP leading to oscillations


Triggered impulse: EAD (early afterdepolarisation)

  • Not fully repol → Depol signal → may continue glitch or restore to norm
  • Occurs when AP is long (i.e. with long QT syndrome)
  • VG Ca current reactivates during long AP
    • Self perpetuating tachyarrhythmia


What is the long QT syndrome?

  • ECG (With the PQRST graph) → elongated Q to T portion
  • Na channel mutations: 
    • SCN5A
    • Channel fails to stay inactive, inward current occurs late in plateau to extend duration
  • K channel mutation
    • KCNQ1 or HERG
    • repol K efflux → plateau and termination delayed


Triggered impulse: DAD (Delayed afterdepolarisation)

  • Just after AP repol (Before next AP normally occurs)
  • Great reliance on Na/Ca ex for relaxation and/or RMP is depolarised (Lowered)
  • Inward depol current reaches threshold → self perpetuating tachyarrhythmia
  • More Ca cycling (elevated [Ca] → release SR Ca → exit via Na/Ca ex → depol)
  • Relationship to digitalis toxicity (Foxglove plant) → plant inhibits Na/K ATPase & reverses Na/Ca ex 
  • increase intracellular [Ca] → may result in tachyarrhythmia


How does an altered AP conduction arise?

  • Conduction block (decrease rhythm/dysrhythm)
    • Inexcitable area (from ischemia/fibrosis)
      • May be temporary/permanent
      • Latent pacemakers 'escape'
    • Re-entry circuit (increase rhythm)
      • Unidirectional conduction block
      • Tachyarrhythmia


Three methods of altering AP conduction?

  1. Branches: Branch via a & b routes (OKAY)→ signals cancel out each other
  2. Fwd point at branch blocked (OKAY)
    • B route blocked
    • a cannot traverse b route from retrograde
  3. Velocity
    • If b orthograde is blocked but retrograde is not blocked → may have complications
      • If fast → no problem as a route still in refractory (OKAY)
      • If slow → presents problem as a route becomes is set-up again → allows re-entry circuit (NOT OKAY)


What are the conditions to produce arrhythmia?

  • Branch point
  • And partial blockage in one of the branches involving a slowed unidirectional conduction


Overview of how hypertrophy links with arrhythmia