class + prototype/EPA

ACE inhibitors - captopril, lisinopril

block enzyme that converts angiotensin 1 to 2, decreasing vasoconstriction and aldosterone —> vasodilation and k+ retention

ARBS - losartan

blocks vasoconstriction and aldosterone effects of angiotensin II. increases renal blood flow. —> vasodilation and k+ retention.

Aldosterone antagonists - eplerenone

blocks aldosterone receptors —> blocking effects of aldosterone —> secretion of Na+, water, and retention of k+

Direct renin inhibitors - aliksiren 

binds with renin, inhibiting activation of angiotensin I → vasodilation and urinary secretion of sodium and water

Calcium channel blockers - nifedipine

block calcium channels in vascular smooth muscle cells of peripheral arteries → vasodilation and decreased BP

Alpha 1 Blockers - doxazosin

block alpha 1 receptors → venous and arteriolar dilation

Beta blockers - atenolol

block beta 1 receptors → dec in HR and contractility → cardiac output and supresses reflex tachy, block beta 1 in kidney → blocks renin release, cardioselective 

Direct acting vasodilators - hydrazaline

acts directly on arterioles to relax smooth muscle → vasodilation, stimulates SNS, affecting heart rate

HMG-CoA reductase inhibitors - atorvastatin

increase HDL, decrease LDL and cholesterol, inhibits HMG CoA reductase, an enzyme that synthesizes cholesterol in the liver

Fibrates - Gemfibrozil

increases oxidation of fatty acids in the liver and tissues → decreases production of triglycerides 

Nitrates - nitroglycerin

converts to nitric oxide, potent vasodilator, relaxes smooth muscle in blood vessel walls. relieve angina pain by venous dilation, coronary artery dilation, arteriole dilation 

Class IB/Sodium channel blockers - lidocaine

blocks na+ channels → shortens repolarization phase of the cardiac cycle → decreases rate of contraction

Class IC/Sodium channel blockers - flecainide

black na+ channels → slows conduction velocity/refractory period

Class III/Potassium channel blockers - amiodarone

blocks k+ channels → slows repolarization and prolongs refractory period → slow down HR

Class IV/calcium channel blockers - diltiazem

blocks ca+ channels → slower conduction through SA/AV nodes → slow down HR

Unclassified antidysrhythmic drugs

adenosine - treats SVT, given fast, IV

magnesium - treats torsades de pointe 

Inotropic agent: cardiac glycoside - digoxin

positive inotropic effect - improves the contractility/pumping ability of the heart. Increases myocardial contractility force by inhibiting the enzyme NA, K, ATPase (increased ca → increased contraction)

Inotropic agents: sympathomimetics - dobutamine

beta-1 adrenergic agonist → increased inotropy → increased cardiac output 

Inotropic agent: phosphodiesterase inhibitor - milrinone

blocks PDE3 (Breaks down cyclic AMP) → positive inotropic event

thrombin/Xa inhibitor - heparin

inhibits factor Xa and thrombin → block clotting process

Low molecular weight heparins - lovenox

take at home

Vitamin K antagonists - Warfarin

acts on liver, prevents synthesis of vitamin k dependent clotting factors

Direct thrombin inhibitors - dabigatran

reversibly binds to catalytic thrombin active site → inhibit activation of factors V, VIII, XIII (coagulant factors), prevents fibrin formation and platelet aggregation

Direct factor Xa inhibitors - rivaroxaban 

antidote: andexxa

adenosine diphosphate receptor (ADP) inhibitor - clopidogrel

inhibits platelet aggregation by blocking ADP receptors on PLTs

thrombolytics - alteplase

converts plasminogen into plasmin → breaks down fibrin in clot

Erythropoietic growth factor - epoetin alfa 

mimics erthropoeitn in bone marrow → production of RBCs