aldosterone antagonist

decrease mortality by 30%

potassium sparing

ACE Inhibitor

block AT1 to AT2

hyperkalemia when +ARB

cough b/c failure to inactivate bradykinin.

ARB

block Ag2 at AT-1 receptor

pan beta, alpha 1 blocker

decrease contractility via beta 1

decrease O2 demand via alpha 1

65% drop mortality

conra: when pt. has decrease contractility.

vasodilator

to venous pool

beta 1 blocker, ionotropic + chronotropic.

increase CO at expense of MI + arrhythmia

for acute LVF with pulmonary edema

prolonged adm. gives desensitization tachyphylaxis

D1B1A1 blocker, ionotropic, chronotropic + pressor

prevent Acute Tubular necrosis via D1 receptor

increase CO

risk arrhythmia + MI

cardiac glycoside

no net survival improvement.

ionotrophic agent: increase Ca.

digitalization: long half life, give loading dose early.

toxicity: due to increased vagal tone: throwing up, visual, polymorphic v. arrhythmia, gynecomastia.

Ca blockers

inhibit Coronary artery vasospasm

pryzmetal angina

contra: CHF, bradycardia, blocks, WPW.

mortality: decrease preload + afterload

decrease preload: Diuretics + vasodilator + ACE I+ natuiuretic peptide

decrease afterload: dopamine (cardiogenic shock)

doputamine (pulmonary edema)

digitalis:

dopamine

dobutamine.

decrease CO

remodeling of CO via RAS

reduce symptom

diuretics + ACEI/ARB

Beta blockers: carvedilol

Digitalis

need negative ionotrops to decrease cocntractility via decrease O2 demand

vasodilators

Beta blockers: propanolol, metoprolol, atenolol

Ca blocker: Diltiazem, Nifedipine.

combined vasodilator and natriuretic effect

bind to cGMP increase NO.

result in vasodilation and increase GFR, Diuresis, depress RAAS

ANP

BNP: surrogate for ventricular dilation and heart failure