Pharmacology Heart

  1. What systemic parameter constitutes Heart Failure?
    <45% Ejection Fraction
  2. What is Heart Failure in terms of Systole?
    Failure of the pump function of the heart due to destruction of myocytes (EF <45%)
  3. What is Heart Failure in terms of Diastole?
    Diminished Ventricular capatance (stiffening) due to ventricular hypertrophy or chronic hypertension
  4. What is Systolic Dysfunction?
    Enlarged Ventricles that only pump out 40-50% of blood
  5. What is Diastolic Dysfunction?
    Stiff ventricles fill with less blood than normal, about 60% is pumped out, but less blood than normal is in them
  6. What type of drugs would you use to treate Diastolic Failure?
    ACEI, ARBs, Thiazide or Loop Diuretics, Spirolactone and BBs
  7. What type of drugs would you use to treat Systolic failure?
    ACEIs, ARBs, Diuretics, Digitalis, Spirolactone or BBs
  8. What drug options are different between Systole and Diastole failure treatment options?
    • Diastole: Thiazide of Loop Diuretics
    • Systole: Digitalis, Diuretics not specified
  9. What characteristics does Ventricular remodeling have alter?
    Alters shape, size and function, genes, molecules, cells and interstitium
  10. During ventricular modeling, Dilation can occur, what is this?
    Myocyte lengthening and cell slippage
  11. Can cell loss occur in Ventricular remodeling?
  12. Would you expect Hypertrophy and interstitial fibrosis with Ventricular remodeling?
  13. What is Concentric Hypertrophy of the ventricle?
    Congestion of the ventricle, wall thickening
  14. What is Eccentric Hypertrophy of the ventricle?
    Thinning of the wall
  15. In heart failure there is a decrease in CO, compensation mechanism cause what changes?
    Sympathetic discharge, Renin/Angiotensin/Aldosterone activation, fluid retention, ↑ preload/afterload, ↑ deleterious structural remodeling
  16. Compensation mechanisms for reduced Cardiac output due to heart failure have what effect on the overall well-being of the system?
  17. What are the goals of Treatment for Heart Failure?
    1.) Treat the precipitating Factors 2.) Prevent Deterioration of Cardiac Function 3.) Control CHF state
  18. What drugs can help control CHF state?
    Diuretics and digoxin
  19. What drugs prevent deterioration of Cardiac Function in Heart Failure?
    ACEIs, ARBs, BB, Spirolactone and Vasodilators
  20. What reaction does Renin catalyze?
    Conversion of angiotensinogen to angiotensin
  21. What reaction does Angiotensin converting enzyme catalyze?
    Angiotensin I to Angiotensin II
  22. What are physiological ramifications of Angiotensin II?
    Peripheral vasoconstriction, ↑BP, ↑ Extracellular volume, ↑ Aldosterone secretion, cardiovascular remodeling
  23. Less Angiotensin leads to what physiological changes?
    Les vasoconstriction, aldosterone and cell proliferation/remodeling
  24. ACE inhibitors are the major drugs for the treatment of heart failure?
  25. What is the MOA of ACEIs?
    Inhibit angiotensin II formation
  26. Enalapril is an active or prodrug?
  27. How do you identify an ACE inhibitor by name?
    ending –pril
  28. Who should receive ACE inhibitors for heart failure?
    Pregnant, hypotensive, kidney function <1/3, hyperkalemia or not tolerated
  29. What would be common signals that ACEI is not being tolerated by the patient?
    Angioedema or cough
  30. What patient should receive ACE inhibitors for Heart Failure?
    LV systolic failure or LV dysfunction w/o heart failure
  31. How can you identify the Angiotensin receptor blockers by name?
    ending –sartan
  32. How do ARBs compare to ACEIs?
    Similar effects, but ARBs: have lower bradykinin side effects, directly block receptors and less clinical information
  33. Would you give and ARB or ACEI to a pregnant patient?
  34. What can you replace ACEIs with if they are not tolerated?
  35. How can you identify a BB by name?
    ending –olol or –lol
  36. How do BB treat heart failure?
    Prevent down regulation of B adrenergic receptors in the heart as a result of sympathetic stimulation
  37. Do BBs prevent against arrhythmias?
  38. Do BBs inhibit the sympathetic responsiveness of the heart?
    No, maintains the sympathetic responsiveness
  39. Do BBs enhance Renin Secretion?
    No, reduce
  40. Do BBs reduce myocardial oxygen consumption?
  41. Do BBs limit heart muscle remodeling and aptoptosis?
  42. (True/False) Beta blockers can be administered to clinically unstable patients.
    False, should only be administered to clinically stable patients
  43. What are the adverse effects of BBs?
    Bradycardia, Withdrawal, Hypoglycemia in diabetes, Bronchospasm in asthma, CNS effects
  44. Patients with symptomatic CHF and low LVEF are good candidate for BBs, unless they have what compounding issues?
    Bronchospastic disease, Symptomatic bradycardia or Heart Block
  45. B-blockers are used in patients with ____________systolic dysfunction caused by myocardial infarction to reduce mortality.
    left ventricular
  46. Locally produced _____________ leads to cardiac fibrosis.
  47. What beneficial effects do Spirolactone and Eplerenone have on the heart?
    ↓ Myocardial fibrosis, ↓ Mortality due to heart failure
  48. What are the adverse effect of Spirolactone and Eplerenone?
    Hyperkalemia, Spirolacton: gynecomastia, hirsutism, menstrual irregularities
  49. Does Eplerenone cause gynecomastia?
    Very little compared to Spirolactone
  50. What are the clinical uses for Spirolactone and Eplerenone?
    Symptomatic Heart Failure with reduced Systole function
  51. What general positive effects would you expect Spirolactone and Eplerenone to have?
    Cardioprotective and antiarrhythmatic, reduce morbidity and mortality
  52. Spirolactone and Eplerenone are well used for Heart Failure (True/False)
    False, underused
  53. What vasodilators are used to treat Heart Failure?
    Isosorbide dinitrate/hydralazine
  54. What is the trade name for Isosorbide dinitrate/hydralazine?
  55. What is the physiological effect of Isosorbide Dinitrate?
    Dilate veins and decrease preload
  56. What is the physiological effect of Hydralazine?
    Dilates arteries, decreases afterload
  57. Why are isosrbide dinitrate and hydralazine beneficial together?
    Isosorbide dinitrate decreases preload, while Hydralazine decreases afterload
  58. Can Diuretics be used in combination with eachother?
  59. How does Matolazone compare to Hydrochlorothiazide?
    Longer half-life and more potent
  60. Which type of diuretics are most used in Heart Filure?
    Loop diuretics
  61. What are the adverse effect of Loop diuretics when used for Heart Failure?
    Hypokalemia, Hypomagnesemia, Hypotension
  62. Would you expect a rapid or slow improvement in symptoms with Loop diuretics?
  63. (True/False)Loop diuretics have been shown to reduce admission for worsening heart failure.
  64. Spirolactone and Eplerenone cause a small or large decrease in Na and water retention?
  65. What effect do loop diuretics have in ventricular remodeling?
  66. Which Heart Failure treatment is a Cardiac Glycoside?
  67. Digitalis has profound effects on what properties of the heart?
    Mechanical and electrical properties
  68. What effect does Digitalis have on Myocardial contractility of the heart?
    Increases (positive inotropic effects)
  69. What is the major adverse effect of Digitalis?
    Severe arrhythmias
  70. Is Digoxin a first line drug for Heart failure?
  71. What is the MOA for Digoxin?
    Inhibitions of Na/K ATPase, leading to increased intracellular Ca and contractility
  72. Digoxin directly interacts with Ca receptors to increases Ca in the cell?
    False, interacts with Na/K ATPase to increase gradient for Ca exchange into the cell
  73. What is the major therapeutic outcome of Digoxin use?
    Increases the force of ventricular contractions
  74. When Digoxin binds the Na/K ATPase on the heart, it binds in place of which ion?
  75. What effect does too little K present have on Digoxin, Increased blockage, leading to toxicity
  76. What are the Hemodynamic effects of Digoxin?
    • ↑ CO due to: ↓ sympathetic tone, ↓ Renin release ↑
    • Urine production
  77. What electrical effects does Digoxin have?
    ↑ firing rate of vagal fibers, ↑ SA responsiveness to ACH, slows HR, effects impulse conduction in AV and perkinje fibers
  78. What ECG effect would you expect during Digoxin toxicity?
    P wave without QRST
  79. At therapeutic levels of Digoxin, what ECG changes would you expect?
    Depression of ST segment and longer PR interval
  80. What are the Cardiac adverse effects of Digoxin?
    Bradycardia and abnormal impule conduction
  81. What are the Non-Cardiac adverse effects of Digoxin?
    Anorexia, N and V, Salivation, excessive urination, Fatigue, Visual disturbances (blurred vision, halos, yellow/green tint to things)
  82. Does Digoxin have a wide or narrow therapeutic window?
  83. Why is absorption inconsistent for Digoxin?
    Variable dissolution rate of oral formulation, effected by disease states
  84. What effect do drugs that cause Hypokalemia have on Digoxin?
    Increase binding and toxicity
  85. ACE inhibitors have what effect on Digoxin?
    Decrease binding due to hyperkalemia
  86. How is Digoxin eliminated?
    Mainly renaly
  87. Which drug classes used in the treatment of Heart Failure Reduce preload and afterload?
    Loop Diuretics and Vasodilators
  88. Which drug classes used in the treatment of Heart Failure Reduce fluid volume?
    Loop Diuretics
  89. Which drug classes used in the treatment of Heart Failure Reduce synthesis of angiotensin II?
    ACE inhibitors
  90. Which drug classes used in the treatment of Heart Failure Prevent Remodeling?
    ACE inhibitors, Angiotensin II receptor Blockers and B-Blockers
  91. Which drug classes used in the treatment of Heart Failure Prevent Arrhythmias?
  92. Which drug classes used in the treatment of Heart Failure have Cardiotonic properties?
  93. Which drug classes used in the treatment of Heart Failure Have a sympathetic effect?
  94. Which drug classes used in the treatment of Heart Failure Reduce synthesis of Angiotensin II?
    ACE inhibitors
  95. Inotropic agents other than Digitalis are used for what situation in Heart Failure?
    Short term-Rescue
  96. What are the Sympathomimetic Inotropic agents?
    Dobutamine and Dopamine
  97. What is the MOA for Dobutamine?
    Selectively activates B1 receptors
  98. Which drug is usually preferred and why, dopamine or dobutamine?
    Dobutamine, because it is B1 selective
  99. Describe the makeup of Dobutamine?
    Synthetic catecholamine
  100. What is the MOA of dopamine?
    Activates B1 receptors, increasing rate and contractility (Can also activate a1, causing NOR release and ↑ BP)
  101. What are the inotropic phosphodiesterase inhibitors used for the treatment of Heart Failure?
    Inamrinone and Milrinone
  102. What is the MOA of Phosphodiesterase inhibitors?
    Block degradation of cAMP, increasing cardiac contractility and vasodilation
  103. What route of administration are phosphodiesterase inhibitors given?
  104. Are Phosphodiesterase inhiitors a safe and well tolerated treatment for Heart Failure?
    No, numerous significant adverse effects, shown to decrease survival
  105. What vasodilators can you use for short term rescue therapy of Heart Failure?
    Nesiritide, Nitroglycerin, Sodium Nitroprusside
  106. What is the makeup of Nesiritide?
    Synthetic B-natriuretic peptide
  107. By what route is Nesititide given?
  108. What situations would prompt you to give Nesiritide for Heart Failure?
    Decompensated Heart Failure and Dyspnea due to HF
  109. What is the MOA for Nesiritide?
    Stimulates guanyl cyclase receptor, increasing cGMP formation, suppresses Renin-Angiotensin system
  110. What effect does Nesiritide have on preload and afterload?
    Decreases both
  111. What is the physiological effect of giving Nesiritide?
  112. What are the major adverse effects of Nitroglycerin?
    Hypotension and Reflex Tachycardia
  113. What is the MOA of Nitroglycerin?
    Converted into NO
  114. What is the MOA of Sodium nitroprusside?
    Converted into NO
  115. What are the major adverse effects of Sodium Nitroprusside?
    Profound Hypotension and reflex tachycardia
  116. Sodium Nitroprusside is what class of drug?
  117. Nitroglycerin is what class of drug?
  118. Which acute treatment drugs used for Heart failure reduce preload and afterload?
    Phosphodiesterase inhibitors, Nesiritide, Nitroglycerin and Sodium nitroprusside
  119. What drugs used for Acute Heart Failure have direct Cardiotonic effects?
    Dobutamine, Dopamine and Phosphodiesterase inhibitos
  120. Describe Heart Failure Stage A:
    High risk for HF without structural change sor symptoms
  121. Describe Heart Failure Stage B:
    Structural heart disease w/o symptoms or signs
  122. Describe Heart Failure Stage C:
    Structural heart disease with prior or current symptoms
  123. Describe Heart Failure Stage D:
    Refractory HF requiring specialized interventions
  124. What drugs might be used in a person with Stage A Heart Failure?
    ACEI or ARB
  125. What drugs might be used in a person with Stage B Heart Failure?
    ACEI, ARBs, B-blockers
  126. What drugs might be used in a person with Stage C Heart Failure?
    ACEI, Diuretics, ARBs, Digitalis, Hydralazine/Nitrates
  127. What drugs might be used in a person with Stage D Heart Failure?
    Usually more extreme measures are used for Stage D, like heart transplant
Card Set
Pharmacology Heart
Pharmacology Heart