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36 Cards in this Set

  • Front
  • Back
Sodium Channel Blockers
Indications: ventricular dysrhythmias
Potassium Channel Blockers
Used for dysrhythmias that are difficult to treat
Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia
Calcium Channel Blockers
Similar effect as ß blockers
Useful in breaking reentrant circuit

First-line drugs for treatment of angina, hypertension, & supraventricular tachycardia
Slows conduction through the AV node
Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
Very short half-life—less than 10 seconds
Only administered as fast IV push
May cause asystole for a few seconds
Other adverse effects minimal
Management of severe HF when used with cardiac glycosides & diuretics
Drugs of choice in hypertensive patients with HF

Drugs of choice for diabetic patients
Remember dry cough & 1st dose hypotension
do not cause dry cough
blocks H+ ions in proximal tubules

Used when other diuretics not effective
Metabolic acidosis reduces diuresis in 2-4 days
Loop Diuretics
Rapid onset of action so particularly useful when rapid diuresis is needed
Distinct advantage over thiazide diuretics as they work when creatinine clearance decreases

To increase renal excretion of calcium in patients with hypercalcemia
In cases of HF resulting from diastolic dysfunction
Directly relax arteriolar &/or venous smooth muscle
Osmotic Diuretics
To reduce intracranial pressure
NOT indicated for peripheral edema
IV only & danger of crystalization/need filter
Potassium-Sparing Diuretics
Work in collecting ducts & distal convoluted tubules

Relatively weak when compared with thiazide & loop diuretics
May be used as adjuncts to thiazide diuretics (synergistic)

Certain cases of HF: especially hyperactive R-A-R
Cardioprotective/prevents remodeling
Thiazide Diuretics
Action primarily in the distal convoluted tubule

Should not be used if creatinine clearance > 30-50
Metolazone is used with creatinine clearance =10
Inhibit the action or formation of clotting factors
Prevent clot formation
Do not lyse existing clots
Antiplatelet drugs
Inhibit platelet aggregation
Prevent platelet plugs
Hemorheologic drugs
Alter platelet function
Thrombolytic drugs
Lyse (break down) existing clots
Hemostatic or antifibrinolytic drugs
Promote blood coagulation
Monitored by activated partial thromboplastin times (aPTTs)
MI, PE, DVT, ischemic CVA
Antidote for heparin OD: protamine sulfate.
First-line drug therapy for hypercholesterolemia
Bile Acid Sequestrants
Prevent resorption of bile acids from small intestine; excreted in bowel movement

May be used along with statins
Vitamin B3

Lipid-lowering properties require much higher doses than when used as a vitamin

Effective, inexpensive, often used in combination with other lipid-lowering drugs
Fibric Acid Derivatives
Believed to work by activating lipase
Suppress release of free fatty acid from adipose tissue, inhibit synthesis of triglycerides in liver, & increase secretion of cholesterol in the bile

Increase HDL by as much as 25%
Inhibits absorption of cholesterol & related sterols from the small intestine

Currently recommended only when patients have not responded to other therapy
Fluids given IV that supply water and electrolytes

Help to maintain osmotic gradient between extravascular and intravascular compartments

Plasma-volume expanders caused by sodium concentrations
Protein substances
Increase COP

For colloids to be effective total protein level must be in the range of 7.4 g/dL. If it drops below 5.3 g/dL fluid shifts out of the blood vessels and into the tissues.
Centrally acting alpha2-receptor agonists
Stimulate alpha2-adrenergic receptors in the brain
Decrease sympathetic outflow from the CNS
Decrease norepinephrine production
Stimulate alpha2-adrenergic receptors, thus reducing renin activity in the kidneys
Results in decreased blood pressure

Usually used after other drugs have failed because of adverse effects

clonidine (Catapres)
methyldopa (Aldomet)
Peripheral alpha1-blockers/antagonists
Block alpha1-adrenergic receptors
So, circulating norepinephrine is blocked from stimulating the receptors
And, blood pressure is decreased

doxazosin (Cardura)
terazosin (Hytrin)
Dual-action alpha1- & beta-receptor blockers
Block alpha1-adrenergic receptors
Reduction of heart rate (beta1-receptor blockade)
Vasodilation (alpha1-receptor blockade)

carvedilol (Coreg) & labetalol
Calcium Channel Blockers: Mechanism of Action
Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction
Results in
Decreased peripheral smooth muscle tone
Decreased systemic vascular resistance
Decreased blood pressure
Statin adverse effect
B-type Natiuretic Peptides: Mechanism of Action
Vasodilating effects on arteries and veins
Indirectly increases cardiac output
Suppresses renin-angiotensin system
Phosphodiesterase Inhibitors
Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response

Given when patient does not respond to treatment with digoxin, diuretics, and/or vasodilators
most commonly prescrbed
least expensive
thiazide diuretic...
used with renal dysfunction