Q2 antiarrhythmic drugs

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Q2 antiarrhythmic drugs
2010-12-11 14:56:46
Q2 antiarrhythmic drugs

Q2 antiarrhythmic drugs
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  1. Most common arrhythmia
    Atrial fibrillation
  2. How many fascicles do the LBB and RBB have?
    • LBB: 2 (anterior, posterior)
    • RBB: 1
  3. Is RBBB clinically significantly?
  4. Is LBBB clinically significant?
    • Yes - indicates that both fascicles knocked out --> extensive myocardial damage
    • Often seen in advanced HF, coronary disease, MIs
  5. What phases of the AP are repolarizing phases?
    • 1 (K+ out)
    • 3 (K+ out rapidly)
  6. What phase of the AP is the depolarizing phase?
    Phase 0
  7. What phase of the AP is the plateau phase?
    Phase 2
  8. What is response for maintenance of phase 4?
    • Na+/K+ ATPase pump
    • Na+ out
    • K+ in
  9. What phases of the AP are associated with Ca2+ coming into the cell?
  10. What ion enters the cell rapidly in phase 0 of AP?
  11. Cause of early afterdepolarizations
    QT prolonging drugs
  12. Cause of late afterdepolarization
    Digitalis toxicity
  13. 3 mechanisms of cardiac arrythmias
    • Enhanced automaticity
    • Afterdepolarizations
    • Re-entry
  14. Atrial re-entry arrhythmia associated with multiple reentry circuits and the one with one large big reentry circuit in atrium
    • Multiple reentry circuits: atrial fibrillation
    • One big circuit: atrial flutter
  15. Early afterdepolarization affects what phase?
    Phase 3
  16. Late afterdepolarization affects what phase?
    Phase 4
  17. QT intervals begins where and ends where?
    • Beginning of QRS complex
    • End of T wave
  18. 3 mechanisms of anti-arrhythmic drugs
    • Slowing or abolition of automatic rhythms
    • Blocking of impulse propogation in re-entry
    • Prevention or blocking of EADs and DADs
  19. Vaughan Williams Classification of Antiarrhythmic Drugs
    • I: Na+ channel blockade
    • II: β blockade
    • III: K+ channel blockade
    • IV: Ca2+ channel blockade
  20. Action of class I (Na+ channel blockade) on phase 0
    Reduces phase 0 slope and peak of action potential
  21. Action of class II (β blockade)
    Block sympathetic activity --> reduction of rate and conduction
  22. Action of class III (K+ channel blockade)
    Delay phase 3 --> increase of action potential and increases refractory period (QT prolongation)
  23. Action of class IV (Ca2+ channel blockade)
    • Blocks L-type channels
    • Reduces rate and conduction