Dobutamine – Positive inotropic agent = Increased contractility and cardiac output, but not heart rate
(decreased chance of irregular heartbeat; no change in peripheral resistance. ONLY for ACUTE HF;
Chronic HF = Increased doses = Increased HR = Increased workload of heart = Greater HF
Furosemide – Loop diuretic = Induce fluid loss = Decrease blood volume
Digitalis – Positive inotropic agent = Increased contractility
Brain Natriuretic Peptide – Increased and released by the ventricles in response to pressure and volume
overload – Biomarker for heart failure; Drugs that increase BNP = promotion of diuresis, natriuresis, and
vasodilation of systemic and pulmonary vascular, and reduce circulating levels of endothelin and
aldosterone
Atrial Natriuretic Peptide – Increased excretion of Na+ and water (decreased blood volume), promotes
vasodilation, inhibit renin secretion (Inhibit angiotensinogen to angiotensin I conversion = reduced
formation of angiotensin II = vasodilation; NORMAL: Angiotensinogen -> *Renin* -> Angiotensin I ->
*ACE* -> Angiotensin II: Cardiac and vascular hypertrophy, Systemic Vasoconstriction, Increased thirst =
increased blood volume, Stimulate Adrenal Cortex release of Aldosterone = Renal sodium and fluid
retention, Simulate Pituitary release of ADH = Renal sodium and fluid retention), Antagonizes the effects
of angiotensin II and ADH
Sulfa Drugs = Antibiotics
Primaquine = Antimalarials
Aspirin = Antipyretics
Statins – Inhibition of cholesterol synthesis by competitively binding to HMG CoA Synthase (Ratelimiting)
PCSK9 Inhibitors = Increased LDLR (inhibits degradation of LDLR); Monoc. Ab against PCSK9 = inactivate
Bile Acid Binding Drugs (Cholestyramine) – Reduces reuptake of bile acids in terminal ileum and the liver
uses free cholesterol to synthesize bile acids = increased hepatic LDLR synthesis because cytosolic free
cholesterol levels are lower than normal
Ezetimibe – Inhibits intestinal cholesterol transporter
Verapamil – Calcium Channel Blocker = Negative Inotrope
Propranolol – Beta Receptor Blocker = Negative Inotrope; decreases HR (chronotrope) and decreased
conduction velocity
Warfarin – Blocks Vitamin K Epoxide Reductase = Decreased regeneration of active Vitamin K –
Prothrombin (F2), F7, F9, F10 and Protein C+S required Vitamin K as a cofactor/coenzyme
Heparin – Activates antithrombin 3 (inhibits F10 of common pathway) and inactivates thrombin
Streptokinase/Urokinase – Thrombolytic agent, plasminogen activator – Converts plasminogen to
plasmin enabling dissolution of clots
Tissue Plasminogen Activator – Dissolves thrombus
Digoxin – Treat HF, controls ventricular rate in atrial fibrillation; class of glycosides; Positive inotropic
and negative chronotropic activity -> Digoxin inhibits Na-K ATPase – Increased Calcium = Increased
contraction
Prazosin