Lecture 16

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Author:
jknell
ID:
114712
Filename:
Lecture 16
Updated:
2011-11-05 19:15:15
Tags:
Cardiac Electrophysiology
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Description:
Cardiac action potentials
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  1. Fast Fibers Location
    • Atrial myocytes
    • Ventricular myocytes
    • Purkinje Fibers
  2. Slow Fibers Location
    • SA node
    • AV node
  3. Fast v Slow Fibers
  4. Fast Fiber: phase 0
    • Fast inward Na+ current (INa+)
    • slight outward IKir
  5. Fast Fiber: Phase 1
    • termination of INa+
    • Transient activation of outward K+ channels ITO
    • -small repolarization
  6. Fast Fiber: Phase 2
    • -Slow inward Ca Channels via L type Ca channels (activated in phase 0 and are slowly inactivated) ICa-L
    • -balanced by ourtward K+ currents
    • -IKir (small)
    • -IKv (delayed rectifier channels)
  7. Slow inward Ca current
    • -Ca bind TnC
    • -triggers CICR from SR

    • Can be regulated by ANS:
    • 1. ACh: M2 negative inotropic effect
    • 2. NE: b1 positive inotropic effect
  8. Fast Fiber: Phase 3
    • -Termination of ICa-L (inactivation)
    • -Outward K+ currents:
    • -IKv and IKir (now larger)

    determines APD
  9. Slow Fiber: Phase 0
    • -decreased slope and amplitude compared to Fast Fiber
    • -no INa
    • -instead ICa-L responsible for depolarization
  10. Slow Fiber: Phase 2
    ionic events similar to fast AP
  11. Slow Fiber: Phase 3
    ionic events similar to fast AP
  12. Major Determinants of Conduction Velocity
    • 1. Fiber diameter (increase D causes increased CV)
    • 2. Phase 0 slope and amplitude
  13. Interventions with Positive Dromotropic Effects in slow fibers
    -increase ICa-L

    • 1. NE/E (beta 1)
    • 2. b1 agonists
    • 3. mAChR antagonists (block M2)
  14. Interventions with Negative Dromotropic Effects in slow fibers
    -decrease ICa-L

    • 1. ACh (M2)
    • 2. b1 antagonists
    • 3. Ca channel blockers
  15. Interventions with Negative Dromotropic Effects in Fast fibers
    -decrease INa

    • 1. Class I antiarrhythmics (block Fast Na+ channels)
    • 2. Hyperkalemia (make RMP less negative)
    • 3. myocardial injury (make RMP less negative)
    • 4. gradual depolarization (channels inactivate before)
  16. Determinants of Firing Rate
    • 1. Automaticity
    • 2. Threshold potential
    • 3. APD
    • 4. Maximum Diastolic Potential (Vm at start of phase 4)
  17. Automaticity
    • -pacemaker potential
    • -steady depolarization during phase 4
    • -occurs in: SA, AV and Purkinje
  18. Overdrive Suppression
    • when a pacemaker cell is driven at a faster rate than it's intrinsic rate it's automaticity is suppressed
    • (w/o Purkinje cells would be slow, and gradual depol would inactivate Na channels)
  19. Automaticity Mechanism
    • 1. Membrane clock
    • -membrane ion channels that cause repolarization of pacemaker cells activating HCN channels

    • 2. HCN channels (funny channels)
    • -non-specific cation channels activated by hyperpolarization

    If
  20. Interventions to Change Firing Rate
    • 1. ACh (M2 increases IK-Ach, decreases ICa-L and decreases If ) decreases phase 4 slope
    • 2. NE/EPI (b1 increases ICa-L, increases If) increases phase 4 slope
  21. Phase 4 slope
    =automaticity

    -determines firing rate
  22. Phase 0 Slope
    -determines conduction velocity

    • -Slow fibers: slow inward Ca
    • -Fast fibers: fast inward Na
  23. Phase 3 slope
    -determines APD

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