Lecture 9: Drugs for Heart Failure Flashcards
Catopril
What is its MOA, what 3 things is it used for (H/HF/DN), and what are its 3 major toxicities?
What are Enalapril, Benazepril, and Lisonopril?
MOA: competitive inhibitor of ACE blocking angiotensin II production = lower BP; used for hypertension, HFrEF, diabetic neuropathy
Toxicities: cough (number 1 reason for stopping), angioedema, FETAL TOXICITY
E: prodrug, active enalaprilat available for IV
B: widely used, longer 1/2 life (once daily dose)
L: widely used, longer 1/2 life (once daily dose)
Losartan
What is its MOA, what 3 things is it used for (H/HF/DN), and what its 3 major adverse effects?
What are Valsartan and Candesartan?
MOA: competitive NONpeptide Angiotensin II receptor antagonist for AT1 receptors, blocking vasoconstriction and aldosterone secretion; used for hypertension, HF if ACEi intolerant, and diabetic neuropathy
Toxicities: adverse effects more common in diabetics, cough (less than ACEi), and FETAL TOXICITY
V: not prodrug, excreted in FECES (pts. w/Liver failure)
C: ARB w/irreversible binding
What are 5 reasons NOT to administer ACE inhibitors/ARBS to patients with LV dysfunction? (T/P/H/SC/H)
- not tolerated (cough, angioedema –> use ARB)
- pregnant = FETAL TOXICITY
- hypotensive
- serum creatinine > 3 mg/dL
- hyperkalemia (OK up to 5.5 mEq/L)
Valsartan + Sacubitril
What is their MOA, what are they used, and are 4 common toxicities? (H/H/SC/A)
MOA: sacubitril blocks neutral endopeptidase (NEP) and prevents degradation of ANP; Valsartan is an ARB that is co-crystalized with sacubitril
- used for HEART FAILURE (inc. ANP/BNP lvls)
Toxicities: hypotension, hyperkalemia, inc. serum creatinine, angioedema
Carvedilol
What is its MOA, what is it used for, and what is a major contraindication of use?
MOA: nonselective alpha/beta blocker (more beta) that is used in CLINICALLY STABLE pts. with HFrEF to prevent symptomatic HF
CI: do not abruptly withdraw Beta Blocker due to possible massive inc. in HR and BP
inverse agonist that helps keep the heart responsive to sympathetic drive (dysrhythmia protection)
Ivabradine
What is its MOA, what is it used for, and who should it be used with?
MOA: inhibits If (Funny) channels within the SA node and prolongs diastole/slow HR; used to treat resting HR > 70 bpm in pts with stable symptomatic chronic HF
- give to pts. on max tolerated beta blockers
- give also if beta blockers are contraindicated
Spironolactone (eplerenone)
What is its MOA, what is it used for, and what are 3 common toxicities of use? (H/A/G)
MOA: competitive aldosterone receptor antagonist (K-sparing diuretic) that blocks aldosterone fibrosis effects and counteracts K loss induced by other diuretics
- slow on and slow off effect
Toxicities: hyperkalemia, amenorrhea, gynecomastia
Furosemide (Loop Diuretic)
What is its MOA, what is it used for, and what are two major toxicities of use?
What is ethacrynic acid?
MOA: directly inhibits Na/K/2Cl cotransporter in thick ascending loop of Henle used to manage edema in HF pts. and hypertension (works in pts. with low GFR unlike Thiazides) with rapid IV onset
Toxicities: ototoxicity (vertigo, nystagmus) and sulfa hypersensitivity
ethacrynic acid can be used in pts. w/sulfa allergy
What two molecules are inc. in the urine of pts. taking Furosemide?
How should diuretics be used?
Calcium and Magnesium
- disruption of the NA/K/2Cl cotransporter in the Thick Ascending Limb blocks their passive movement across the cell
- use Loop Diuretics FIRST, then add K-sparing diuretics if needed, and thiazide diuretics if STILL needing more diuresis
Nitroglycerin (isosorbide dinitrate)
What is its MOA, what is it used for, and what vasculature does it commonly affect?
MOA: forms free radical NO that inc. cGMP that dephosphorylates myosin light chain and causes SM relaxation
- affects VEINS more prominently
- used for angina pectoris and acute decompensated HF
- isosorbide dinitrate used for angina and HFrEF
Hydralazine
What is its MOA, what is it used for, and what vasculature does it commonly affect?
What are some of its common toxicities? (A/P/DIL)
MOA: direct vasodilator of arterioles that decreases systemic resistance (hyperpolarizes, endo dependent) and is used for HTN, HFrEF in ACEi/ARB intolerance, and HTN emergency in pregnancy
- especially useful for African American pts.
Toxicities: angina pectoris, pruritis, drug-induced lupus-like syndrome
Digoxin (Digitalis)
What is its MOA, what are its two major uses, and how does it affect pregnant patients?
MOA: inhibits NA/K ATPase pump in myocardial cells, causing inc. sodium/calcium exchange = inc. contractility
- direct AV node conduction suppression
- positive inotrophic effect
Use: control ventricles in pts with A Fib and HF
Pregnancy: crosses placenta; safe for use with supraventricular tachycardia
How does Digoxin cause Cardiac Toxicity?
- competes with K for binding to the Na/K ATPase pump, so if there is too little potassium in the pt, there will be TOO MUCH block
- myocytes become overloaded with Calcium, coupled with SR release, cause delayed after-polarizations and aftercontractions = arrhythmias
uncouples the atria from the ventricles, making cardiomyocytes MORE prone to arrhythmias
What does Digoxin toxicity look like on ECG?
What must a patient have before receiving Digoxin?
What visual disturbance do pts. taking Digoxin experience?
- starts with A-V conduction problems, with lack of P and QRS relationship (dropped QRS waves)
- can worsen to have ectopic ventricular beats (deep Q wave during ventricular depolarization) = BIGEMINY
pts must have NORMAL HR before digoxin administration
Visual: blurred, yellowish/greenish halos and tinge to objects
How are these ADHF patients treated:
- Hypertensive
- Normotensive
- Hypotensive
- treat with Loop Diuretic and Vasodilator
- VD = nitroglycerin or nitroprusside
- treat with Loop Diuretic +/- Vasodilator
- VD = nitroglycerin
- Hypotensive = treat with Loop Diuretic
