1. What are the goals of therapy for heart failure?
    • Decrease signs and symptoms of congestion.
    • Maintain normal lifestyle.
    • Prolong life.
  2. What causes heart failure?
    • Systolic dysfunction (most commom); results in reduced contractility
    • Diastolic dysfunction; results in reduced ventricular filling
  3. Systolic dysfunction
    • reduced contractility
    • decreased ejection fraction
    • increased left vent end diastolic volume
    • ventricular hypertrophy r/t pressure or volume overload
  4. Diastolic dysfunction
    • reduced vent filling
    • normal ejection fraction
    • decreased left vent end diastolic volume
  5. How is the renal system involved in heart failure?
    • heart failure leads to decreased cardiac output
    • decreased CO leads to release of renin, angiotensin II, and aldosterone and stimulation of symp NS
    • release of aldosterone increases reabsoption of water and sodium
    • increased reabsoprtion increases plasma volume, preload, and edema
    • stim of symp NS increases HR, contractility and vasoconstriction resulting in increased afterload and decreased CO
  6. Frank-Starling mechanism
    • compensatory mechanism activating the renin/angiotensin/aldosterone system, increasing stroke volume
    • may result in volume overload, increased myocardial oxygen demand
  7. Compensatory mechamisms in heart failure:
    • Frank-Starling mechanism
    • increased heart rate: r/t SNS activation; increases oxygen demand, ischemia, arrhythmias, and decreases filling time
    • vasoconstriction: decreases stroke volume
    • ventricular hypertrophy and remodeling: increases myocardial cell death, ischemia, arrhythmias
  8. How does reducing preload affect heart failure?
    reducing preload decreases the amount of blood returning to heart, therefore helping to alleviate symptoms of pumonary congestion
  9. How does reducing afterload affect heart failure?
    reducing afterload reduces the force that the heart must contract against, therefore allowing an increase in CO
  10. What types of drugs decrease preload?
    diuretics, NSAIDS, nitrates, ACEI, nitroprusside, nesiritide
  11. What types of drugs decrease afterload?
    nitrates, ACEI, nitroprusside, nesiritide, hydralazine
  12. What types of drugs reverse remodeling of the heart?
    beta blockers (metoprolol, carvedilol, bosoprolol), ACEI, ARBs, aldosterone antagonists (spironolactone)
  13. What do you monitor for when givine heart failure medications?
    • Left-sided heart failure
    • Right-sided heart failure
    • Excessive fluid loss
    • Drug toxicities
  14. How do you respond to a person with high CO and low PCWP (end diastolic pressure)?
    Do nothing, this is normal.
  15. How do you respond to a patient with low CO and low PCWP (end diastolic pressure)?
    Give fluids, patient is experiencing hypoperfusion.
  16. How do you respond to a patient experiencing high CO and high PCWP (end diastolic pressure)?
    Administer loop diuretics and vasodilators, pt is experiencing pumonary congestion.
  17. How do you resond to a pt experiencing low CO and high PCWP (end diastolic pressure)?
    Administer diuretics, vasodilators, pt is experiencing pulmonary congestion and hypoperfusion.
  18. Action of diuretics (general)
    decrease preload, do no effect CO (decreases symptoms)
  19. Meds that are vasodilators
    nitroglycerin, nitroprusside, nesiritide
  20. Nitroglycerine
    • a vasodilator
    • induces smooth muscle relaxation in veins and arteries (mainly venodilator)
    • AE: HA, hypotension, tachycardia
    • tolerance can develope w/i 12hrs (tachyphylaxis)
  21. nitroprusside
    • vasodilaor
    • potent, dilates veins and arteries
    • decreases preload and afterload
    • can become toxic quickly, usually short term med
  22. Neriritide
    • a vasodilator
    • antagonizes renin/agiotensin/aldosterone system and SNS
    • toxicity: excessive hypotension
  23. Drugs that are inotropic agents (increase force of contraction).
    milrinone, dobutamine, dopamine
  24. Milrinone
    • positive inotropic effect and vasodilation
    • decreases preload and afterload
    • used short term (long term increases mortality rate)
  25. Dobutamine
    • inotropic effects
    • beta 1 agonist leading to increased HR and contractility
    • beta 2 agonist results in vasodilation
  26. Dopamine
    • inotropic effects
    • increases MAP by stimulating alpha 1 receptors
  27. chronic treatment of diastolic HF
    • goal: relax heart so that it fills better, increase diastole
    • low sodium diet (2g/day)
    • diuretics
    • ACEI
    • beta blockers or nondihydropyridine CCBs (not nifedipine)
  28. chronic treatment of systolic HF
    • lifestyle modifications
    • diuretic plus ACEI and beta blocker
    • hydralazine plus nitrates and/or digoxin in AA
  29. Diuretics
    • control symptoms of pumonary congestion and fluid overload
    • do not increase survival (exceptions: spironolactone and inspra)
  30. ACEI and ARBs
    • mild to severe HF
    • reduce mortality rate, esp in pts with CHF
    • ACEI cough generall improves after several weeks
    • correct dose is important
  31. Hydralazine plus nitrates
    • often used for AA or pts who cannot tolerate ACEI or ARBs
    • when used with diuretics and digoxin, reduces mortality (not as much asn ACEI)
  32. beta blockers (in HF)
    • used in all stable HF pts
    • protects heart from chronic toxicity of high norepinephrine levels (ischemia, remodeling)
    • used in combo with ACEI
    • contraindicated in symptomatic bradycardia, hypotension, 2/3 degree heart block
  33. aldosterone antagonist in HF
    • ex: spironolactone
    • major risk is hyperkalemia
    • monitor serum creatinin and potassium before and after therapy initiation
  34. digoxin in HF
    • cardiac glycoside
    • positive inotropic effect (direct) - inhibits Na-K pump increasing intracellular Na and Ca resulting in increased force of contraction
    • vagotonic effect (take apical pulse and EKG before admin)
    • high renal elimination
    • dose based on IBW
    • toxicities: bradycardia, arrhythmias, AV block, fatigue, vision probs, weakness, anorexia, nausea, hallucinations/confusion/insomnia
    • not been shown to increase survival
    • reduces risk of hospitalization when used with diuretic and ACEI
  35. Factors that alter digoxin effects:
    • increase effect w/o increasing levels: hypokalemia, hypomagnesemia (prob w/alcoholics), vagal stim, hyperstimulation
    • increase levels: renal failure, amiodarone, verapamil, basing dose on actual wt instead of IBW, erythromycin (in some pts)
    • decrease levels: antacids (binds w/dig in stomach) and rifampin (stims metabolism)
  36. Drugs to avoid in HF
    • NSAIDS (increases Na and H2O retention)
    • drugs that cause adrenergic stimulation (decongestants, some beta blockers)
    • TZDs (used to treat DM, can cause fluid retention)
    • antiarrhythmics with negative inotropic activity (quinidine, procainamid) - good for diastolic HF, bad for systolic HF
    • antiarrhythmics that prolong QTc interval (increases r/o arrhythmias)
    • CCBs (may increase r/o death in systolic HF; nondihydropyridines like verapamil and diltiazam may be helpful in treating diastolic HF however)
Card Set
Pharm exam 2