Pharmacology Antiarrhythmics 1

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kyleannkelsey
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249661
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Pharmacology Antiarrhythmics 1
Updated:
2013-11-29 17:21:04
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Pharmacology Antiarrhythmics
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Pharmacology Antiarrhythmics 1
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  1. K is higher in or out of the cell?
    In
  2. Na is higher in or out of the cell?
    Out
  3. Ca is higher in or out of the cell?
  4. Out
  5. Define the equilibrium potential:
    membrane potential that will exactly balance the diffusion gradient
  6. What is the Nernst equation?
    • EX = 61/Z log[Xo]/[Xi]
    • EX= equil. Pot. for ion in mV, Xo = conc. outside cell, Xi = conc. inside the cell, Z = valence of ion
  7. Ex in the Nernst equation has what meaning?
    Membrane potential of Ex inside the cell is required to balance the ion gradient
  8. What is the relevance of the membrane potential equaling the Nernst potential for an ion?
    No net flux of the ion
  9. How do Em and Ek relate during hyperkalemia?
    Em is more negative than Ek, causing K influx into the cell, leading to depolarization
  10. How do Em and Ek relate during hypokalemia?
    Em is more positive than Ek, causing K outflow from the cell, leading to hyperpolarization
  11. When the equilibrium potential for an ion differs from the membrane potential, that ion will tend to____________________________ for the purpose of __________________.
    • Flow across membrane
    • for the purpose of correcting the difference.
  12. ___________ dependent conformational changes determine current flow through Na+ channels.
    Voltage
  13. What do waves moving through the SA node look like?
  14. What do waves moving through the Heart’s Atrium look like?
  15. What do waves moving through the AV node look like?
  16. What do waves moving through the Heart’s Ventricle look like?
  17. What is the effective refractory period?
    • Period of time that a new action potential cannot be initiated
  18. What is the Relative Refractory Period?
    • Period shortly after the firing of a nerve fiber when partial repolarization has occurred and a GREATER THAN NORMAL STIMULUS can cause a second response
  19. What is the Relative Refractory Period?
    • Decreased phase 4 slope, causing delayed action potential and reducing spontaneous automaticity
  20. Describe the effects of Na and Ca Channel blockers on the action potential:
    • Increased Threshold, causing delayed action potential and reducing spontaneous automaticity
  21. Describe the effects of Adenosine and Aceylcholine on the action potential:
    • Increased Maximum diastolic potential, causing delayed action potential and reducing spontaneous automaticity
  22. Describe the effects of K channel blockers on the action potential:
    • Increased duration of action potential, causing delayed action potential and reducing spontaneous automaticity
  23. What does DAD stand for?
    Delayed afterdepolarizations
  24. What does EAD stand for?
    Early afterdepolarizations
  25. What can cause EADs?
    Hypokalemia, Congenital long QT syndrome, Drug induced increases in action potential
  26. What can causes DADs?
    Ca overload caused by: MI, Adrenergic stress, Digoxin, HF
  27. What are the three major mechanisms of Cardiac arrhythmias?
    Enhanced automaticity, Afterpolarizations, Reentry
  28. What is Reentry?
    Wave of excitation transverses the heart muscle in a circuitous pathway and returns to the point of origin
  29. What cardiac physiology must be present for Reentry to occur?
    Shortened Refractory Period and reduced Conduction velocity
  30. What ways do drugs suppress reentry?
    • Depress the conduction to produce a bidirectional block
    • Lengthen the refractory period
  31. What is the Vaughn-Williams Classification?
    Antiarrhythmatic drug classification used to classified based on ability to block ionic currents and beta adrenergic receptors
  32. What are the advantages of the Vaughn-Williams Classification?
    Physiologically based and Highlights benefits and deleterious effects of specific drugs
  33. What is a Vaughn-Williams Class I drug?
    Na channel blocker
  34. What is a Vaughn-Williams Class II drug?
    Sympatholytic agent
  35. What is a Vaughn-Williams Class III drug?
    Prolongs repolarization
  36. What is a Vaughn-Williams Class IV drug?
    Ca Channel blocker
  37. Vaughn-Williams Class I – Subgroup IA has what characteristics?
    • Moderate reduction in Phase 0 slope, ↑ ERP and AP duration, Medium duration of blockade
  38. What drugs are classified as Vaughn-Williams Class I – Subgroup IA?
    Quinidine, Procainamide and Disopyramide
  39. What basic characteristics does Disopyramide have?
    Only treating ventricular arrhythmias, extended DOA
  40. What basic characteristics does Procainamide have?
    ↑ RP but has substantial side effects
  41. What basic characteristics does Quinidine have?
    • 1st Antiarrhythmic drug
    • Used for atrial and ventricular arrhythmias
    • ↑ RP
  42. Vaughn-Williams Class I – Subgroup IB has what characteristics?
    • Small ↓ in Phase 0 slope
    • may ↓ ERP and AP duration
    • Brief duration of blockade
    • preferential interaction with inactivated Na channels
    • negligible interaction with Na channels
  43. What drugs are classified as Vaughn-Williams Class I – Subgroup IB?
    Lidocaine and Mexiletine
  44. What are the basic characteristics of Lidocaine?
    Blocks Na channels mostly in ventricular myocytes
  45. What are the basic characteristics of Mexiletine?
    Oral lidocaine derivative, Blocks Na channels mostly in ventricular myocytes
  46. Vaughn-Williams Class I – Subgroup IC has what characteristics?
    • Pronounced ↓ in Phase 0 slope
    • ↓ conduction
    • little effect on AP duration and ERP
    • LONG duration of blockade
  47. What drugs are classified as Vaughn-Williams Class I – Subgroup IC?
    Flecainide and Propafenone
  48. What are the basic characteristics of Flecainide?
    Slows conduction all of heart, inhibits abnormal automaticity, local anesthetic
  49. What are the basic characteristics of Propafenone?
    ↓ Conduction, Ca channel blockade, Weak B-blocker
  50. Describe the changes in action potential, ERP and Na channel blockade expected with a Class IA drug:
    • Moderate Na channel blockade, Increased ERP
  51. Describe the changes in action potential, ERP and Na channel blockade expected with a Class IB drug:
    • Weak Na channel blockade, Decreased ERP
  52. Describe the changes in action potential, ERP and Na channel blockade expected with a Class IC drug:
    • Strong Na channel blockade, no effect on ERP

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