L7.3 Cardiac hypertrophy and arrhythmia. A cellular view

Question 1

What is arrhythmia?

Answer 1

• Arrhythmia = abnormalities of electrical rhythm
  
  • Can be benign or malignant

Question 2

Symptom and cause of arrhythmia?

Answer 2

• Symptoms: Palpitations to critical decrease in CO
• Cause: Altered AP generation and/or conduction processes

Question 3

What causes arrhythmia?

Answer 3

• Altered AP generation
• Altered AP conduction

Question 4

Altered AP generation

Answer 4

• Normal nodal automaticity altered
  
  • Produce unstable rhythms
  • Alternative pacemaker emerges
• Triggered activity in ventricles
  
  • Altered Ca homeostatsis and unstable RMP
  • EAD/DAD

Question 5

Normal nodal automaticity

Answer 5

• 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

Question 6

Triggered impules: EAD (Early afterdepolarisation)

Answer 6

• 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

Question 7

What is the long QT syndrome?

Answer 7

• 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

Question 8

Triggered impulse: DAD (delayed afterdpolarisation)

Answer 8

• 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

Question 9

Altered AP conduction

Answer 9

• 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

Question 10

3 abnormalities associated with altered AP conduction

Answer 10

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)

Question 11

Conditions needed to produced re-entry arrhythmia

Answer 11

1. Branch point
2. And partial blockage in one of the branches involving a slowed unidirectional conduction

Question 12

Overview of hypertrophy + arrhythmia

Answer 12