Heart failure drugs and their mechanisms Flashcards
Nitroglycerin
Increase NO in smooth muscle –> increase cGMP and smooth muscle relaxation –> vasodilation –> decrease preload and afterload
Furosemide (lasix)
Inhibits cotransport system NKCC transporter in thick ascending loop of Henle, stopping reabsorption. Also stimulates PGE release leading to vasodilation
Captopril, enalapril, lisinopril, ramipril (ACE inhibitors)
Inhibits conversion of angiotensin I –> Angiotensin II, decreasing aldosterone and decreasing reuptake of Na and water
Losartan, candesartan, valsartan (Angiotensin II receptor blockers)
selectively blocks angiotensin II receptors (similar effect as ACE)
Metoprolol, propanolol (Beta blockers)
Block Beta 1 receptors and their sympathetic activity on heart rate (decreases SA and AV nodal activity)
Spironolactone (K sparing diuretics)
Competitive aldosterone receptor antagonists on collecting tubule
Chlorothalidone, hydrochlorothiazide (thiazides)
Inhibits NaCl reabsorption in early distal convoluted tubule
Hydralazine
Increase cGMP –> smooth muscle relaxation
Ethacrynic acid
Phenoxyacetic acid derivative, essentially same action as furosemide
Aspirin (antiplatelet)
Irreversible inhibits COX-1 and COX-2 to inhibit formation of TXA2
Morphine (analgesic)
Binds mu opioid receptor to block calcium channels, decreases substance P and glutamate release from 1st order neuron
Statins
Inhibits HMG-CoA reductase to inhibit mevalonate (cholesterol precursor)
Terazosin (alpha-blocker)
blocks adrenergic receptors (alpha 1 is for SM contraction, Alpha 2 usually releases NE)
Verapamil (calcium channel blocker)
Block L-type voltage gated calcium channels to prevent calcium from entering cell (decrease SM contraction). Calcium channel blockers also shift fast-reacting cells that are dependent on Calcium for contraction to sodium for depolarization. This can cause negative inotropic and chronotropic effects.
Minodoxil (potassium channel OPENER)
hyperpolarizes cells by allowing potassium to exit cell