CHF

Question 1

Candesartan / Valsartan

Answer 1

Potent competitive ARBs
Use: HF in pt’s who can’t tolerate ACE inhibitors (severe cough or angioedema)
SE: similar to ACE inhibitors (no cough bc do NOT affect bradykinin levels)
TERATOGENIC

Question 2

Hydralazine

Answer 2

Direct arteriolar vasodilators
Mechanism: 👆🏽vasodilation (arteriole) + nitrate = 👆🏽venous dilation
Action: 👇🏽preload, 👇🏽PVR, 👇🏽afterload
SE: HA, dizziness
Contra: Sildenafil

Question 3

Carvedilol / Metoprolol

Answer 3

β-blockers
Action: 👇🏽ΗR and contractility, inhibition of renin release (β1)
Use: reverse/decrease cardiac remodeling and hypertrophy in CHF pt’s
SE: initial exacerbation of sx’s (so start at low dose and gradually increase over several wks)

Question 4

Spironolactone

Answer 4

Aldosterone antagonist
Mechanism: prevents Na+ retention, myocardial hypertrophy and hypokalemia
Use: adjunct w/ ACEIs = decrease in morbidity/mortality in pt’s w/ severe CHF
SE: hyperkalemia (esp in pt taking ACEIs/ ARBs, K+ supplements or who have renal failure), gastritis/PUD, CNS effects, endocrine stuff (gynecomastia, 👇🏽libido, menstrual irregularities)

Question 5

Digoxin

Answer 5

Cardiac glycoside
Mechanism: positively inotropic (👆🏽 force of heart contraction), negative chronotropic (👇🏽HR)
*masks sx’s but does not increase survival

Question 6

Inamrinone / Milrinone

Answer 6

PDE3 Inhibitors
Mechanism: inhibit myocardial cAMP PDE activity
Action: increased cAMP levels (+ve inotropic effect w/ 👆🏽CO), increase AV conduction, systemic and pulmonary vasodilator effects
Use: short-term therapy in pt’s w/ intractable HF

Question 7

Dopamine

Answer 7

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Question 8

Dobutamine

Answer 8

Use: increase CO in acute management of HF (s/p MI)

Question 9

Glucagon

Answer 9

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Question 10

Hydralazine + Isosorbide Dinitrate

Answer 10

Use: pt’s who cannot tolerate ACEIs or ARBs OR black pt’s w/ advanced HF as adjunct