Cardiovascular Drugs Flashcards
Hydralazine
MOA:increases cGMP –> smooth muscle relaxation, preferentially in arterioles. Decreases Afterload.
USE: Severe HTN - Pregnancy HTN admin w/ methlydopa - Always give with B-Blocker
ADR’s: Compensatory tachcardia - Lupus like Syndrome
Nifedipine > Diltiazem > Verapamil
Preference for Vascular
MOA: Block voltage-dependent L-type ca+ channels of smooth muscle, thus decreasing muscle contractility
Use: HTN, angina, Prinzmetal angina, Raynaud’s
ADR’s: cardiac depression, AV block, peripheral edema, constipation
Verapamil > Diltiazem
Preference for Cardiac Tissue
MOA: Block voltage-dependent L-type ca+ channels of smooth muscle, thus decreasing muscle contractility
Use: HTN, angina, Prinzmetal angina, Raynaud’s
ADR’s: cardiac depression, AV block, peripheral edema, constipation cannot use Nifedipine –> arrythmias)
1) Nitroprusside
2) Fenoldopam
3) Diazoxide
1) Vasodilating veins>arterioles - Short acting - increases cGMP via direct release of NO - sequesters Ca+ in SR - ADR: cyanide toxity
2) Dopamine D1 receptor agnoist - relaxes renal vacular smooth muscle
3) K+ channel opener - Hyperpolarizes and relaxes vascular smooth muscle - ADR: can cause hyperglycemia
Nitroglycerin, Isosorbide, Dinitrate
MOA: Vasodilator by releasing NO in smooth muscle - increases cGMP and relaxes smooth muscle - Veins»_space; arteries, decreases preload
USE: Angina, pulmonary edema, erection enhancer
ADR’s: reflex tachycardia, hypotension, tolerance develops
Goals of Antianginal Therapy
Reduction of myocardial O2 consumption via a decrease in:
- end-diastolic volume, BP, HR, Contractility, Ejection time
Nitrates: Decreases EDV, BP, Ejection time, MVO2 - Increase: Contractility and HR (both reflex responses
B-Blockers: Decrease: BP, Contractillity, HR, MVO2 - Increases: EDV, Ejection time
Nitrates + B-Blocker: Decrease: BP, HR, MVO2 - Little effect: EDV, Contractility, Ejection time
Lipid Lowering Agents (Subsets)
- HMG-CoA reductase inhibitors (HMG-CoA Synthase –> Lipid and K.A. Synthesis
- Niacin
- Bile Acid Resins
- Cholesterol Absorption blockers
- Fibrates
Lovastatin, prevastatin, simvastatin, atorvastatin, rosuvastatin
MOA: HMG-CoA Reductase, inhibits mevalonate, a cholesterol precursor
Main: lowers LDL
Other: increases HDL and decreases Tryglycerides
ADR’s: Hepatoxicity (increased LFT’s), Rhabdomyolysis - Teratogen
Niacin
MOA: inhibits lipolysis in adipose tissue (HSL) - reduces hepatic VLDL secretion into circulation
Main: Increases HDL
Other: decreases LDL and triglyerides
ADR’s: Hyperglycemia, Hyperuricemia (Gout), red flushed face decreased w/ aspirin
Cholestyramine, Colestipol, colesevelam
Bile Acid Resins
MOA: Prevent intestinal reabsorption of bile acids - Liver must use cholesterol to make more –> from Cholesterol
Main: decreases LDL
Other: slight increases in HDL and Triglyerides
ADR’s: Bad taste - GI discomfort - decreases absorption of fat (A,D,E,K fit deficiency) - Cholesterol Gallstones
Ezetimibe
Cholesterol absorption Blockers
MOA: Prevent Cholesterol reabsorption in the small intestine
Main: Decrease in LDL
ADR: rare increases in LFT’s
Gemfibrozil, clofibrate, bezafibrate, fenofibrate
Fibrates
MOA: Up-regulate LPL –> increase triglyceride clearance
Main: Decrease in triglycerides
Other: small decrease in LDL and HDL
ADR;s: myositis, hepatoxicity (LFT’s), Cholesterol gallstones
Digoxin
Cardiac Glycoside
MOA: Direct inhibition of Na+/K+ ATPase; indirect inhibition of Na+/Ca+ exchanger/antiport ==> Increases [Ca], thus positive Inotropy - Stimulates CN XII
Use: CHF (Increases Contractility) A-Fib (decreases conduction at AV node and depression of SA node)
ADR’s:
- Cholinergic (N/V, diarrhea, blurry yellow vision
- ECG: increase PR, decrease QT, T-wave inversion, hyperkalemia
Clearance: Kidney
Nesiritide
Recombiant B-type natriuetic peptide - Causes increase in cGMP & vasodilation
USE: Acute decompensated Heart Failure
ADR: Hypotension
Quinidine, Procainamide, Disopyramide
MOA:Class Ia antiarrhythmics (Na+ channel blocker)
- Increase action potential duration, effective refractory period, and QT interval
USE: atrial and ventricular arrhythmias (supraventicular and ventricular tachycardia)
ADR’s
Quinidine: Cinchonism –> headache, tinnitus - Thrombocytopenia- Torsades depointes - decreases Digoxin clearence
Procainamide: reversible SLE-like (antinucleur AB)
Lidocaine, Mexiletine, Tocainide
MOA: Class Ib antiarhymic - decreases action potential (preferentially ischemic or depolarized purkinje and ventricle tissues)
USE: Acute ventricular arrhythmias (esp. post MI and in digitalis induced arrhythmias
ADR’s: local anesthetic - CNS depression/stimulation - Cardio depression
Flecainide, Propafenone
MOA: Class Ic antiarrhytmic - no effect on Action potential
USE: V-Tachs that progress to ventricular fibs - last resort for refractory tachyarrhythmias
ADR’s: proarrhythmic (esp. post MI) - prolongs refractory period in AV node
(olol)
Propraolol, esmolol, metoprolol, atenolol, timolol
MOA: Beta-Blockers Class II antiarrythmics - Decreased cAMP and [Ca] current - decreases phase four slope (Esp at AV node) - Increases PR interval
USE: V-Tach, SVT, slowing ventricular rate during AFib and Aflutter - Post MI
Esmolol: very short acting used IV for emergency to decrease ventricular rate
ADR’s: Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation), masks signs of hypoglycemia
Metoprolol: dyslipidemia
Ibutilide, Sotalol, Breylium, amiodarone, dofetilide
MOA: [K+] channel blockers class III antiarrhymics - increase action potential duration, effective refractory period, increases QT interval
USE: Used when other antiarrhymics fail
ADR;s
Sotaolol: torsades de pointes, excessive B-block
Ibutilide: Torsades
Bretylium: New arrhythmias, hypotension
Amiodarone: Pulmonary fibrosis, hepatoxicity, hypo/hyperthyroidism
Verapamil, Diltiazem
MOA: [Ca+] channel blocker class IV antiarrhythmic - decreases conduction velocity - increases effective refractory period and PR interval
USE: prevention of nodal arrhythmias
ADR’s: Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression
Adenosine
Antiarrhythmic
MOA: increases [K+] out of cells –> hyperpolarization & decreased Iontrope effects
USE: DOC for Dx/Tx supraventricular tachycardia - Very short acting
ADR’s: Flushing, hypotension, chest pain - effects blocked by theophylline
Mg++
Antiarrhythmic
USE: effective in Torsades de pointes and digoxin toxicity
