N301- Drugs for treating Heart Failure

  1. Cardiac Output (CO)
    • - CO= SVxHR
    • -if the SV decreases, the HR must increase to sustain CO
    • -if the HR decreases, SV musct increase to sustain Co
  2. Preload
    amount of blood that has filled the ventricles by the end of diastole
  3. Contractility
    force of squeezing achieved by ventricles
  4. Afterload
    Amount of pressure ventricles must overcome to eject blood
  5. CHF
    • systemic and pulmonayr congestion aren't always present in chronic CHF
    • progressive changes that result in declining pumping ability
  6. Cardiac Remodeling
    • ventricles get bigger and walls get thicker b/c its working harder, pump out more volume, increased HR
    • fibrosis
    • the heart gets round instead of cone shape
    • makes it harder to contract causing increased preload
  7. Increased Sympathetic Tone
    • everything is constricted/tense increasing afterload
    • affects rate, contractility, venous and arterial tone
  8. Naturetic Peptides
    • two peptides in blood get released trying to get rid of sodium, but they are not effective
    • ANP and BNP- check serum levels to measure degree of failure
  9. Thiazide Diuretics
    • Moderate Diuresis
    • not effective if CO or GFR is low
  10. Loop Diuretics
    • profound diuresis
    • effective even when CO is low
  11. Potassium Sparing Diuretics
    • very mild diuresis
    • risk for hyperkalemia
  12. ACE Inhibitors
    • Angiotensin Converting Enzyme inhibitor
    • Block production of angiotensin II
    • dilate arterioles and veins
    • Decrease release of aldosterone reducing sodium and water retention effecting preload and afterload
    • prevents cardiac remodeling because they affect SV
  13. ARBs
    • Angiotensin Receptor Blockers
    • reserved fir yse when patients cannot tolerate ACE inhibitors
    • Should NOT be used together with ACE because of hyperkalemia potential
    • prevents cardiac remodeling b/c affects SV
  14. Aldosterone Receptor Blockers
    • Aldosterone contributes to volume overload, myocardial and vascular fibrosis
    • Spironlactone blocks receptors in heart and blood vessels, helps to decrease remodeling, adverse effects->hyperkalemia and gynecomastia
  15. Beta Adrenergic Blocking Agents
    • possible negative effects because of beta 1 blocking
    • dose is started small and gradually increased
    • increased vasodialtion and decreased peripheral resistance
    • beneficial effects may take up to 3 months
  16. Carvedilol
    • beta blocker used as an adjunct in treating mild to moderate CHF
    • non selective- decreases force of contraction and CO (Can make HF worse initially)
    • alpha 1 blocking activity- increases casodilation and decreases peripheral resistance
  17. Metoprolol XL
    • SELECTIVE bata 1 blocking agains
    • is also approved for HF
  18. Inamrinone
    • drug for HF
    • for short term, inpatient use
  19. Milrinone
    • outpatient use for HF in patietns who are not responding to other drug therapy for acute HF
    • Can't stop taking it or actions get reversed
    • produces inotropic action (increaced contractility)
    • vasodilation by relaxing vascular smooth muscle
    • IV adminsitration only
  20. Phoshpoidestrase Inhibitors
    • produce ionotropic action
    • (increase contractility)
  21. Nesitritide
    • IV vasodilatore for HF
    • Human B-type natriuretic pepetide- it tries to get rid of sodium
    • direct dilation of cascular smooth muscle
    • supression of sympathetic outflow (supressing vasoconstriction)
    • Supresses renin secretion
  22. Nitroglycerin
    • ACUTE SITUATIONS- IV vasodilator for HF
    • Venous Dilation- decreases venous return decreasing preload and O2 demand
    • Arteriolar Dilation- reduces systemic vascular resistance and arterial pressure, reduces afterload
    • decreases overall myocardial oxygen consumption
    • reduces pulmonary edema (frothy pink sputum)
    • AE: hypotension and reflex tachycardia (have to be given with beta blockers)
  23. Dopamine
    • Sympathomimetic druc
    • used short term for SEVERE failure, so heart doesn't stop
    • catecholamine and a precursosr to NE
    • stimulation of alpha 1 and beta 1 and dopamine receptors
    • the higher the dose, the more vasoconstriction
  24. Dobutamine
    • Sympathomymetic Drugs
    • short term in SEVERE failure
    • Stimulation of beta 1 receptors ONLY
  25. Digoxin
    • Manage symptoms of HF
    • therapeutic range: 0.5-0.8 mg/ml
    • treat atrial fibrillation (irregular, no p-wave)
    • treat atrial flutter (regular, but not effective, over 300 bpm)
    • slows heart rate and regulates rhythym
    • strengthems contraction (positive inotropic)
    • slows conduction (negative dromotropic)
    • slows HR (negative chronotropic)
    • need anticoagulate to prevent clotting in Afib**
  26. Digoxin Toxicity
    • caused by hypokalemia- b/c K+ and digozin compete for the same receptors, so if there is not enough K+, too much digoxin binds
    • keep K+ within normal range
    • watch out for with loop and thiazide diuretics
    • also alcohol has effect
    • 0.5-0.8 mg/ml
  27. Antidote fore Digoxin overdose
    • Digoxin immune FAB (DigiBind)
    • activated cahrcoal (not supposed to mix it with anything, usually given with lexative)
Card Set
N301- Drugs for treating Heart Failure
heart failure drugs