Cardiovascular Drugs

Question 1

Hydralazine

Answer 1

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

Question 2

Nifedipine > Diltiazem > Verapamil

Answer 2

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

Question 3

Verapamil > Diltiazem

Answer 3

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)

Question 4

1) Nitroprusside
2) Fenoldopam
3) Diazoxide

Answer 4

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

Question 5

Nitroglycerin, Isosorbide, Dinitrate

Answer 5

MOA: Vasodilator by releasing NO in smooth muscle - increases cGMP and relaxes smooth muscle - Veins&raquo_space; arteries, decreases preload
USE: Angina, pulmonary edema, erection enhancer
ADR’s: reflex tachycardia, hypotension, tolerance develops

Question 6

Goals of Antianginal Therapy

Answer 6

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

Question 7

Lipid Lowering Agents (Subsets)

Answer 7

• HMG-CoA reductase inhibitors (HMG-CoA Synthase –> Lipid and K.A. Synthesis
• Niacin
• Bile Acid Resins
• Cholesterol Absorption blockers
• Fibrates

Question 8

Lovastatin, prevastatin, simvastatin, atorvastatin, rosuvastatin

Answer 8

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

Question 9

Niacin

Answer 9

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

Question 10

Cholestyramine, Colestipol, colesevelam

Answer 10

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

Question 11

Ezetimibe

Answer 11

Cholesterol absorption Blockers
MOA: Prevent Cholesterol reabsorption in the small intestine
Main: Decrease in LDL
ADR: rare increases in LFT’s

Question 12

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

Answer 12

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

Question 13

Digoxin

Answer 13

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

Question 14

Nesiritide

Answer 14

Recombiant B-type natriuetic peptide - Causes increase in cGMP & vasodilation
USE: Acute decompensated Heart Failure
ADR: Hypotension

Question 15

Quinidine, Procainamide, Disopyramide

Answer 15

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)

Question 16

Lidocaine, Mexiletine, Tocainide

Answer 16

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

Question 17

Flecainide, Propafenone

Answer 17

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

Question 18

(olol)

Propraolol, esmolol, metoprolol, atenolol, timolol

Answer 18

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

Question 19

Ibutilide, Sotalol, Breylium, amiodarone, dofetilide

Answer 19

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

Question 20

Verapamil, Diltiazem

Answer 20

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

Question 21

Adenosine

Answer 21

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

Question 22

Mg++

Answer 22

Antiarrhythmic

USE: effective in Torsades de pointes and digoxin toxicity