Cardio1- Electrophysiology

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  1. What is normal resting membrane potential?
    -80 to -90 mV
  2. Changes in trans-membrane polarity are mostly due to... (2)
    opening of ion channels, movement of ions across the cell membrane
  3. Depolarization means the trans-membrane potential is...
    less negative/closer to zero.
  4. What are the phases of cell membrane potentials?
    • phase 0- depolarization
    • phase 1- brief repolarization (ignore)
    • phase 2- plateau
    • phase 3- repolarization
    • phase 4- resting membrane potential
  5. What is conductance (g)?
    permeability of the membrane to a certain molecule/ion
  6. Conductance is altered by... (4)
    trans-membrane voltage (voltage-gated channels), time after opening (time-dependent channels), extracellular ion concentrations, ligands (ligand-gated channels: Ach and NE)
  7. Inside of cell has very high ____, which is very low outside the cell; therefore, this ion moves out of the cell, along its concentration gradient, until...
    K+; it is eventually held in the cell by electrical force of negatively-charges proteins (which themselves are trapped inside because of their large size).
  8. Resting membrane potential in cardiomyocytes is mainly related to the _____________ and _____________.
    K+ conc and conductance of this ion
  9. During phase 4, resting membrane potential is ___________, and ion distribution is replaced to normal by the ____________.
    relatively constant; Na+K+ATPase pump (removes 3Na+ and replaces 2K+)
  10. Sodium channels are _______-voltage operated channels, which means...
    fast; they are activated at a threshold membrane potential and rapidly close after opening (time-dependency).
  11. How are Na+ channels regulated?
    voltage-gated and time-dependent
  12. What is the purpose of fast Na+ channels?
    depolarization (Phase 0) of muscle cells and Purkinje cells
  13. What is the Vaughan Williams anti-arrhythmic drug Class I? What drugs are in this class?
    Sodium channel blockers; IA- procainamide, quinidine; IB- lidocaine, mexiletine; IC- flecainide, propafenone
  14. What are some clinical issues that are related to ion channels of the heart? (3)
    • inherited channelopathies: cause of SCD- altered repolarization
    • heart disease: can affect channel function and lead to heart rhythm disturbances
    • Ionophores: coccidiostat feed additives- preferentially transport ions across cell membranes- cause myocardial injury if given in too high dose or if accidentally ingested by horses or camelids.
  15. What forces keep K+ in the cell? (2)
    negatively-charged proteins that are too large to leave the cell, high Na+ conc outside the cell
  16. What forces keep Na+ out of the cell? (1)
    membrane is relatively impermeable to Na+
  17. How does hyperkalemia cause bradycardia?
    when you have high extracellular K+ compared to intracellular, transmembrane voltage becomes less negative, effectively bypassing the membrane potential at which Na+ channel open--> Na+ don't open--> atrial mm. are inexcitable--> brady
  18. What are the purposes of the Ca2+ channels of the heart?
    contraction of cardiac and smooth mm. myocytes, depolarization of pacemaker cells in SA and AV nodes
  19. What are the 2 types of Ca2+ channels in the heart?
    T-type (transient) channels that are activated at more negative potentials, L-type (long-lasting) channels that are ligand-operated (catecholamines)
  20. What is the Vaughan Williams anti-arrhythmic drug Class IV? What drugs are in this class?
    Calcium channel blockers- directly block L-type channels; Diltiazem, Amlodipine
  21. What is the Vaughan Williams anti-arrhythmic drug Class II? What drugs are in this class?
    beta-blockers that indirectly decrease Ca2+ influx by modulating opening/closing of L-type channels; "lol" drugs (end in "-lol")
  22. What is the purpose of K+ channels of the heart?
    repolarization by allowing K+ to move out of the cell, along its conc gradient
  23. How are K+ channels regulated?
    voltage and ligand-operated
  24. Describe the ligand-dependent operation of K+ channels.
    Vagal (parasympathetic) Ach opens a specific K+ channel, slowing depolarization and enhancing repolarization in pacemaker cells (in supraventricular tissues- atria, SA node, AV node)
  25. K+ channels are the rate of repolarization contribute significantly to the ____________ of the cell, which is...
    refractory period; time period when the cell cannot be re-stimulated after depolarization.
  26. Why is inhomogeneity of RPs dangerous?
    facilitates development of fragmented spread of current across the ventricles, leading to myocardial fibrillation
  27. What is the Vaughan Williams anti-arrhythmic drug Class III? What drugs are in this class?
    block ion movement across K+ channels, prolonging repolarization; sotalol, amiodarone
  28. Cell repolarization correlates to the __________ on EKG; _______ is lengenthed by drugs that prolong this.
    ST interval; RP
  29. What causes depolarization of slow current Ca2+ channels in the pacemaker cells?
    slow inward current of Ca2+--> drifting upward toward action potential--> spontaneous depolarization
  30. Why isn't there really a Phase 2 plateau with slow current Ca2+ channels?
    cells in the SA and AV nodes are not contracting muscles, their only purpose to si RAPIDLY conduct current
  31. What are the EKG effects of hyperkalemia? (4)
    bradycardia from depression of SA node activity, inexcitability of atrial cardiomyocytes leading to absence of P waves, depressed cell-to-cell depolarization of ventricles leading to depression of phase 0, large T waves due to opening of K+ channels and more rapid repolarization
  32. What part of the EKG lead corresponds to repolarization?
    T wave (ie. more rapid repolarization with hyperK+--> taller/more tented T wave)
  33. What is occurring during the plateau phase 2?
    Ca2+ is entering the myocytes to stimulate muscle contraction
  34. What are the insulators of the atria and ventricles, and what are the chambers connected by?
    cardiac valves and fibrous connective tissues are insulators; chambers are connected electrically by microscopic conduction pathway, AV node and Bundle of His
  35. What part of the EKG lead corresponds to atrial depolarization?
  36. What part of the EKG corresponds with current spread across the AV node?
    PQ interval
  37. What part of the EKG lead corresponds with sequential depolarization of the ventricular myocytes?
    QRS complex
  38. What is the distribution of Ca2+ across the cell membrane?
    intracellular Ca2+ is low compared to extracellular; Ca2+ does not contribute to the transmembrane potential b/c most of the intracellular C2+ is sequestered in the sarcoplasmic reticulum
  39. What is the distribution of Na+ across the cell membrane?
    intracellular Na+ is low compared to extracellular
  40. Define an activated membrane ion channel.
    once a specific ion channel is open or activated, ions can flow through the channel by their concentration gradient
  41. Describe how the process of Na+ channels opening and depolarization occurs.
    spontaneous depolarization of pacemaker cells in the SA node--> current flow across gap junctions--> depolarization of atrial and ventricular muscle cells and specialized conduction cells of the His-Purkinje system
  42. _____________ have a prominent affect on L-type Ca2+ channels, increasing the probability of opening and Ca2+ influx; this facilitates __________ and generation of a ___________.
    Catecholamines (sympathetic NS); depolarization; faster HR
  43. High vagal tone __________ the refractory period of atrial muscle cells .
  44. What is the purpose of the Na+K+ATPase pump?
    maintain the negative intracellular potential (during phase 4) while also re-establishing the normal partitioning of ions of each side of the membrane.
  45. Normally, the ________ is the pacemaker of the heart; the __(2)__ serve as back-up or escape pacemakers should the primary fail.
    SA node; AV node and His-Purkinje cells [subsidiary pacemaker cells]
  46. Both NE and Ach enhance ____________ and _____________ the SA nodal membrane; however, NE, the activation of the ___________ causes fuller opening of the ____________, promoting more rapid ___________; the opposite occurs with vagal Ach.
    repolarization; hyperpolarize; funny pacemaker current; long-lasting Ca2+ channels; depolarization
  47. What is ventricular escape?
    Ventricular escape beat is a self-generated electrical discharge initiated by, and causing contraction of, the ventricles of the heart; normally the heart rhythm is begun in the atria of the heart and is subsequently transmitted to the ventricles.
Card Set:
Cardio1- Electrophysiology
2016-03-02 01:06:47
vetmed cardio1

vetmed cardio1
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