Pharmacology Ch 5 Dr Brown: Cardiovascular

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  1. Pacemaker of the heart
    SA node
  2. Delays the electrical impulses coming from the atria into the ventricles and allows the ventricles to fill with blood
    AV node
  3. Ion that passes into the cardiac cell on depolarization
  4. Specific receptor that is found in the heart and increases the heart rate
  5. Receptor that helps regulate the release of norepinephrine
  6. Specific receptor that causes peripheral vasoconstriction
  7. Specific receptor that is located in smooth muscle surrounding the heart and causes bronchodilation
  8. Part of the ECG representing movement of depolarization wave through the AV node
    PR interval
  9. Two types of cholinergic receptor
    Muscarinic and nicotinic
  10. Neurotransmitter associated with the sympathetic nervous system
    Norepinephrine and epinephrine
  11. Site from which electrical activity of an arrhythmia originates
    Ectopic focus
  12. DOC for controlling ventricular arrhythmias (ectopic focus); cannot be given orally because of GI upset and first pass effect; cats are more sensitive to this drug
  13. Decreases arrhythmias by decreasing the stimulatory effect of the sympathetic nervous system on the heart
    B-blocker antiarrhythmias like atenolol and propranolol
  14. Most commonly used positive inotropic agent; has a narrow therapeutic index and toxicosis is common
  15. Sodium-blocking antiarrhythmic used to control lidocaine-responsive arrhythmias
  16. Positive inotropic drug; can only be used effectively for short periods before the heart muscle downregulates
  17. Diuretic of choice, called a loop diuretic because of its site of action in the kindey
  18. Potassium-sparing diuretic, not as effective as furosemide
  19. Vasodilator of choice, ACE inhibitor
  20. Decreases spontaneous clot formation
  21. Topically applied vasodilator
  22. Reveres first or second degree heart block
  23. TRUE OR FALSE. QRS complex on the ECG represents atrial depolarization
  24. TRUE OR FALSE. Upregulation is the increased number of receptors produced by a cell that increases the sensitivity of the cell to a stimulus or a drug
  25. TRUE OR FALSE. During absolute refractory periods no amount of stimulus can cause the cell to depolarize again
  26. TRUE OR FALSE. Hypokalemia (low blood potassium) increases the risk for digoxin toxicosis
  27. TRUE OR FALSE. Early signs of digoxin toxicosis that the owner needs to be aware of are related to the GI tract
  28. TRUE OR FALSE. A positive inotropic drug is one that decreases the heart rate
  29. TRUE OR FALSE. Blood is pumped to the lungs from the left ventricle
  30. TRUE OR FALSE. Advantage of B-blocker drugs over the antiarrhythmics is that if problems arise after several weeks of therapy, the drug can be safely stopped immediately
  31. TRUE OR FALSE. When switching from liquid form of digoxin to tablet form the dose has to be decreased to provide an equivalent amount
  32. TRUE OR FALSE. Rapid heart rate causes by a problem in the atria would be classified as a supraventricular tachycardia
  33. TRUE OR FALSE. In severe digoixin toxicosis a slow heart rate would be expected
  34. TRUE OR FALSE. Sympathetic nervous system stimulation of the heart causes an increase in rate and force of the heart contraction
  35. TRUE OR FALSE. Acetlycholine in the neurotransmitter associated with parasympathetic nervous system effects
  36. TRUE OR FALSE. Angiotensin II is a potent vasodilator
  37. TRUE OR FALSE. Peripheral vasoconstriction causes an increased resistance to blood flow
  38. TRUE OR FALSE. Aldosterone is a hormone that causes sodium to be reabsorbed from the renal tubule
  39. TRUE OR FALSE. First degree AV block with digoxin toxicosis is seen on the ECG as an increase in the PR interval
  40. TRUE OR FALSE. Nonspecific B receptor blockers can cause bronchodilation as a side effect
  41. What kind of noncardiac drugs do we use to help an animal that has aerophagia associated with CHF?
    Sedatives or tranquilizers
  42. What drug slows the ventricular contraction rate in animals with atrial filbrillation without eliminating the atrial fibrillation itself?
  43. What organ of the body eliminiates digoxin?
  44. Lidocaine  
    Use, how it works, contraindications, side effects
    • Use: Antiarrhythmic, local & topical anesthetic 
    • How it works: Blocks sodium ions and prevents messages from cell to cell 
    • Cons: Hypersensitivity to local anesthetic  
    • Side effects: CNS, nausea, vomiting
  45. Propranolol  
    Use, how it works, contraindications, side effects
    • Use: Antiarrhythmic, B blocker
    • How it works: Blocks the B1 and B2 receptors of epinephrine and norepinephrine
    • Cons: CHF
    • Side effects: Bradycardia, lethargy, depression
  46. Atenolol 
    Use, how it works, contraindications, side effects
    • Use: Antiarrhythmic, B blocker 
    • How it works: Blocks B1 receptor of epinephrine 
    • Cons: Anesthesia, Furosemide, insulin 
    • Side effects: Lethargy, vomiting, diarrhea
  47. Diltiazem 
    Use, how it works, contraindications, side effects
    • Use: Antiarrhythmic 
    • How it works: Calcium channel blocker
    • Cons: Hypotension, CHF 
    • Side effects: Vomiting, bradycardia
  48. Epinephrine / norepinephrine  
    Use, how it works, contraindications, side effects
    • Use: Positive inotrope, anaphylaxis
    • How it works: Opens airways, narrows blood vessels 
    • Cons: Glaucoma, hypovolemia, prefibrillatory cardiac rhythm  
    • Side effects: Anxiety, tremors, vomiting
  49. Dobutamine
    Use, how it works, side effects
    • Use: Positive inotrope, shock
    • How it works: Stimulation of the β receptors of the heart
    • Side effects: Increased HR and BP
  50. Digoxin  
    Use, how it works, contraindications, side effects
    • Use: Positive inotrope, treat CHF
    • How it works: Increase calcium avaliable to the heart
    • Cons: V-fib, digitalis intoxication
    • Side effects: High or toxic blood levels, GI upset
  51. Enacard  
    Use, how it works, contraindications, side effects
    • Use: Ace inhibitor, vasodialator 
    • How it works: Blocking conversion of angiotensin in the renin angiotensin system
    • Cons: Hypersensitivity to ace inhibitors  
    • Side effects: GI distress, hypotension
  52. Benazepril  
    Use, how it works, contraindications, side effects
    • Use: Vasodialator, ACE inhibitor 
    • How it works: Decrease fluid retetnion by dilating veins 
    • Cons: Hypersensitivity to ace inhibitors
    • Side effects: GI distress, renal disfunction
  53. Furosemide  
    Use, how it works, contraindications, side effects
    • Use: Loop diuretic, CHF
    • How it works: Inhibits Na reabsoprtion 
    • Contraindications: Amuria, hypersensitivity to the drug
    • Side effects: Fluid and electrolyte abnormalities
  54. Nitroglycerin topical  
    Use, how it works, contraindications, side effects
    • Use: Vasodilator, CHF 
    • How it works: Dilates blood vessels 
    • Cons: Anemia
    • Side effects: Hypotension
  55. Spironolactone
    Use, how it works, contraindications, side effects
    • Use: Diuretic, CHF
    • How it works: Retains potassium and excretes sodium and chloride 
    • Cons: Diabetes, liver/kidney failure 
    • Side effects: Sedation, constipation
  56. Each heart muscle cell has the potential to depolarize spontaneously and independently
  57. Atrial depolarization as shown on an ECG
    P wave
  58. Specialized conduction pathway in the heart
    Bundle branches
  59. Located at the apex of the heart
    Purkinje fibers
  60. Depolarization of the ventricles as shown on a ECG
    QRS complex
  61. Ventricular muscle cells relax and reset in preparation for the next depolarization wave
  62. Phase 0 of depolarization where there is a rapid influx of Na+ ions
    Absolute refractory period
  63. Phase 2, cells begin to repolarize, Ca2 and Na continue to move through slow channels
    Relatively refractory period
  64. Receptors typically found in neurons associated with parasympathethic nervous system
    Muscarinic receptors
  65. Receptors found both in the parasympathetic and sympathetic nervous system
    Nicotinic receptors
  66. Abnormal pattern of electrical activity in the heart
  67. Depolarization of the ventricles out of the normal sequence, causing ventricles to contract prematurely
    Premature ventricular contraction
  68. Short series of PVC
  69. Longer series of PVC
    Ventricular flutter
  70. If the ventricular contraction becomes so uncoordinated that the heart simply quivers
    Ventricular fibrillation
  71. Source of the arrhythmia is above the ventricles and thus originates in the SA node, atria, or AV node
    Supraventricular arrhythmia
  72. Rapid heart rate caused by a problem in the atria
    Atrial fibrillation
  73. Drugs that block B receptors
    B antagonists or B blockers
  74. Prolongation of the PR interval
    First degree AV block
  75. Cardiac muscle begins to produce more B1 receptors on the surface of the cell to counteract B blockers
  76. Decrease the strength of contraction
    Negative inotropic drugs
  77. Increased stimulation of B1 receptors by catecholamines causes the myocardial cells to decrease the number of catecholamine receptors
  78. Bodys most potent vasoconstrictor
    Angiotensin II
  79. Hormone released from the adrenal cortex and increases Na reabsorption from the kidney
Card Set
Pharmacology Ch 5 Dr Brown: Cardiovascular
Ch5 Cardiovascular
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