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  1. What is the term for the inability of the body to maintain adequeate cardiac output to meet the metabolic demands of the body?
    heart failure
  2. What are the clinical findings with Right heart failure?
    with Left heart failure?
    Right - vascular engorgement and peripheral edema

    Left - CHF
  3. What type of heart failure is most common?
    low out put (decreased CO due to functional problem)
  4. What are some hypertrophic growth factors that lead to cardiac remodeling?
    • cathecolamines
    • angiotensin II
    • and/or aldosterone
  5. Describe the viscious cycle of heart failure.
    • starts with decreased CO; this causes reflex response of SNS and RAS
    • Essentially, the heart has an impaired abilitiy to contract and empty so residual volume is left in the left ventricle; causes increased preload because the heart can;t contract sufficiently; heart dilates til it can't any further and preload starts backing into pulmonary capillaries; pt has rails, congestion, and chief complain of SOB
  6. What are the 3 key goals of treatment for heart failure?
    1) decrease cardiac work; espcially preload in the left ventricle to decreased O2 demand of heart

    2) Increase CO via + ionotrophic drugs (digitalis) or decrease afterload (TPR)

    3) control Na and H2O: CHF causes trouble with breathing
  7. What is the DOC for heart failure?
    • Beta receptor antagonists
    • (mechaism unknown but does increase longevity)
  8. T/F

    Diurectics ONLY improve symptoms but do not increase longevity so they are not used so much in asymptomatic patients.
  9. What is the goal of diuretics?
    • excrete Na and H2O:
    • decrease vascular volume
    • decrease edema
    • decrease preload
    • decrease pulmonary congestion (major complaint in pts)
  10. What diuretic is used in the decompensated patient (in ER with pulmonary edema and SOB)?
    • loop diuretics; "the mides"
    • DOC for getting rid of volume
  11. If loop diuretics fail in treatment of heart failure, what next?
    thiazide or thiazide + loop
  12. When are thiazides used in CHF?
    • in resistance/tolerance to loops or combined with loop (synergistic natriuresis)
    • in patients with HTN
  13. What diuretic blocks the effects of aldosterone on the heart - atteenuating remodeling (can reverse remodeling)?
    spironolactone (K+ sparing diuretic)
  14. T/F
    Spironolactone alone and incombination with ACE(-) can increase survival.
  15. What is the #1 way to decrease preload and afterload?
    target the RAS
  16. What effect does activation of AT1 receptors have?
    • vasoconstriction
    • sympathethic stimulation
    • cellular hypertrophy
    • renovascular effects
  17. What is the goal of ACE(-) "the prils"?
    • decrease peripheral resistance which decreases afterload and preload which increases CO
    • Na+ and H2O absorption
    • decreased aldosterone release (blocked)
    • decreased cardiac hypertrophy and remodeling
    • decreased SNS and sensitivity to NE
  18. What are the side effects of ACE(-)?
    • cough (due to increased bradykinin, a potent vasodilator)
    • can increase serum K+
    • hypotension
  19. T/F
    ACE(-) increase survival (longevity) and decrease hopital admissions in CHF and post MI patients. And it's cheap!
  20. What are the contraindications associated with ACE(-)?
    • pregnancy
    • renal stenosis
    • markedly hypotensive people
    • African Americans
  21. What are the advantages of an AT1 antagonist? "the sartans"
    • decreased side effects compared to ACE(-) because no effect on bradykinin
    • AT2 receptors are not blocked
    • acoid angiotension "escape"
    • is as effective as ACE(-)
  22. When are the AT1 antagonists contraindicated?
  23. What is the ONLY way to administer sodium nitroprusside?
  24. To what is Sodium Nitroprusside converted?
    NO (vasodilator)
  25. T/F
    Sodium Nitroprusside is for emergency tx for acute heart failure when you need a FAST decrease in pressure.
  26. Sodium Nitroprusside decreases preload and afterload quickly. This can lead to...?
    • hypotension (ischemia)
    • reflex tachycardia
  27. What is a potential bad side effect of Sodium Nitroprusside?
    • thiocynate toxicity (pts with kidney failure)
    • it is metabolized to thiocynate in the liver and normally excreted by the kidneys
  28. What effects does nitroglycerin have?
    decreased preload and some effects on afterload
  29. What are the side effects of nitroglycerin?
    • hypotension
    • refelx tachycardia
    • ischemia
    • tolerance
  30. What is used at night in lieu of nitroglycerin to decrease chances of developing tolerance?
  31. What meds are given to pregnant women and African Americans to treat for heart failure?
    • Hydralazine (oral)
    • Isosorbide dinitrate (oral)

    • given in combo (Bidil) for patients who cannot take
    • ACE(-)
  32. What effect does Hydralazine have?
    decrease afterload (a hypertensive drug)
  33. What effect does Isosorbide dinitrate have?
    • decrease preload
    • increase renal blood flow

    *it is converted to NO
  34. What are the drawbacks of Bidil (Hydralazine + Isososorbide dinitrate)?
    • pateint compliance due to frequent dosing
    • headache and GI side effects
  35. What is released when the ventricle is stressed or damaged?
    brain natriuretic peptide (BNP)
  36. What drug is a recombinant ofrm of BNP?
    Nesiritide (IV infusion)
Card Set:
2012-02-25 17:09:18

Lecture B1
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