Drugs Used in Heart Failure Flashcards
Reduces excessive sympathetic stimulation
Beta blockers
Reduces preload and afterload
Vasodilators
Augments depressed cardiac contractility
Positive inotropes
DOC for acute heart failure
Loop diuretics
If very severe: positive inotropes (beta-agonists or PDE inhibitors) and vasodilators
DOC for chronic heart failure
ACEI (slows down cardiac remodeling)
Loop + spironolactone + ACEI
If tolerated, + BB
MOA of digoxin
Inhibits Na/K/ATPase–> increased intracellular sodium–> Sodium-Calcium exchanger is altered–> reduced calcium expulsion –> increased Ca stored in sarcoplasmic reticulum–> increased cardiac contractility
SE of digoxin
Arrhythmia
Visual changes
Drugs with narrow therapeutic index
WALA na Cyang PaPa! vasTeD na! Warfarin Aminoglycoside Lithium Amphotericin B Carbamazepine Phenobarbital Phenytoin Vancomycin Theophylline Digoxin
Digitalis toxicity is increased by?
Hypokalemia
Hypomagnesemia
Hypercalcemia
DOC for digoxin-induced arrhythmia
Lidocaine
2nd line: phenytoin
Beta blockers which reduce progression of chronic heart failure; no value in acute failure
Carvedilol
Labetalol
Metoprolol
No value in acute heart failure
Beta blockers
No value in chronic heart failure
PDEIs (inamrinone and milrinone)
CCB
Effective in CHF due to increased afterload (HTN + infarct)
Nitroprusside
Nitroglycerine
Improve survival in heart failure
ABA! Buhay ka pa!
ACEIs
BB
Aldosterone antagonists
Used to remove retained salt and water
Diuretics
Positive inotropic drugs used in heart failure
Cardiac glycosides (digoxin) Beta agonists (dobutamine) PDE inhibitors (inamrinone)
Vasodilators used in the management of heart failure
PDEI (Inamrinone)
Nitroprusside
Nitrates
Hydralazine
MOA of furosemide
Decreases NaCl and KCl reabsorption in thick ascending loop of Henle –> reduces peripheral edema, preload, and afterload
Vasodilates pulmonary vessels –> reduces pulmonary edema
Toxicities of furosemide
Ototoxicity
Hypovolemia
Hypokalemia
MOA of hydrochlorothiazide
Decreases NaCl reabsorption in the DCT–> Reduces edema and preload
Toxicites of thiazides
HyperGlycemia HyperLipidemia HyperUricemia HyperCalcemia HypoKalemia
MOA of spironolactone
Blocks cytoplasmic aldosterone receptors in collecting tubules of nephron –> increases salt and water excretion; reduces remodelling; reduces mortality
Toxicities of spironolactone
Hyperkalemia
Gynecomastia
Reduces afterload and salt and water retention
ACEIs
Cardiac effect of ACEIs and ARBs
Arteriolar and venous dilation;
Reduces aldosterone secretion;
Increases cardiac output;
Reduces cardiac remodelling
MOA of Carvedilol
Competitively blocks B1 receptors –> slows heart rate; reduces BP; reduces heart failure mortality; used in CHRONIC heart failure
MOA of isosorbide dinitrate
Releases nitric oxide; activates guanylyl cyclase –> venodilation –> reduces preload and ventricular stretch; used for acute and chronic heart failure as well as angina
MOA of hydralazine
Probably increases NO synthesis in endothelium –> reduces BP and afterload –> increases CO
MOA of nitroprusside
Releases NO spontaneously; activates guanylyl cyclase –> marked vasodialtion –> reduces preload and afterload
MOA of dobutamine
Beta 1-selective agonist; increases cAMP synthesis–> increases cardiac contractility and CO
MOA of dopamine
Dose-dependent; Increases renal blood flow; higher doses increase cardiac force and BP
MOA of Bypiridines (inamrinone and milrinone)
Phosphodiesterase type 3 inhibitors; decrease cAMP breakdown –> vasodilation –> reduces peripheral vascular resistance; Also increases cardiac contractility
MOA of nesiritide (natriuretic peptide)
Activates BNP receptors; increases cGMP –> vasodilation; diuresis
Used for acute decompensated heart failure
Nitroprusside Dobutamine Dopamine Inamrinone, milrinone Nesiritide
