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10 Cards in this Set

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Inotropic Agents

common
CHF DRUG

most common: digoxin/lanoxin

Antidote – digibind
Inotropic Agents

MOA
increase cardiac contractility. Inhibits enzyme – sodium-potassium ATPase ->

promotes Ca accumulation, incr contractility -> incr CO. HR decrease, ventricular filling increases.

Slows down heart, increases contractility--- greater CO
Inotropic Agents

IND
CHF, dysrhythmias
Inotropic Agents

AE
predisposing factor for toxicity:

Hypokalemia; low K increases digoxin toxicity. Digoxin & K bind at same sites

Signs of digoxin toxicity:

early S&S:

visual changes (changes in color, halos, yellowish or green caste), anorexia, n/v, fatigue.

late S&S:

ventr dysrhythmias b/c digoxin slows HR-can lead to AV block
Inotropic Agents

DI
diuretics b/c of risk of low K—so must be on K supplement

Quinidine (antidysrhythmic drug)

Verapamil- increases digoxin levels
Inotropic Agents

NC
Monitor/assess apical HR for one minute before giving.

Hold if HR<60
monitor serum K level, digoxin level
Diuretics

common
CHF DRUGS

Loop (lasix most common), thiazide diuretics

Patients frequently on lasix, digoxin and K
Diuretics

MOA
Increase renal excretion of water, Na, other e-lytes.

Increase urine output, decrease fluid overload – decr pulmonary & peripheral edema.
Ace Inhibitors

MOA
block enzyme that converts angiotensin I to angiotensin II -reduces aldosterone

Causes:

vasodilation – dec BP
decrease blood volume since it reduces retention of Na and H2O

reverses pathological changes in heart and blood vessels
Ace Inhibitors

AE
some patients w/kidney issues cannot take