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26 Cards in this Set
- Front
- Back
cardiac glycosides
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digoxin (Lanoxin, Lanoxicaps, Digitek)
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cardiac glycosides MOA
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positive inotropic effect- increased force of myocardial contraction
increased force and effeciency of myocardial contraction improves the heart's effectiveness as a pump; improving stroke volume and cardiac output negative chronotropic effect= decreased heart rate at therapeutic levels, digoxin slows the rate of SA node depolarization and the rate of impulses through the conduction system of the heart decreased heart rate gives the ventricles more time to fill with blood coming from the atria which leads to increased SV and increased CO |
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cardiac glycosides use
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treatment of heart failure
dysrhythmias (atrial fibrillation) |
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cardiac glycosides adverse
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dysrhythmias- digoxin-induced dysrhythmias include hypokalemia, increased serum digoxin levels, and HD. Older adult clients are particularly at risk
cardiotoxicity leading to bradycardia GI effects CNS effects |
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cardiac glycosides contraindications
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pregnancy category risk C
disturbances in ventricular rhythm, including ventricular fibrillation, ventricular tachycardia, and second and third degree heart block hypokalemia, partial AV block, advanced heart failure, and renal insufficiency |
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cardiac glycosides interactions
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thiazide diuretics, such as HCTZ, and loop diuretics suchas furosemide (Lasix), may lead to hypokalemia, which increases the risk of developing dysrhythmias
ACE inhibitors and ARBs increase risk of hyperkalemia, which can lead to decreased therapeutic effects of digoxin sympathomimetic medication such as dopamine (Intropin) compelemnt the inotropic actio nof digoxin and increase the rate and force of heart muscle contraction increase risk of tachydysrhymias quinidine increases risk of digoxin toxicity when used concurrently verapamil (Calan) increases plasma levels of digoxin antacids decrease absorption of digoxin and can decrease its effectiveness |
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cardiac glycosides admin
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notify provider if pulse rate is less than 60/BPM
less than 70 BPM in child monitor digoxin levels periodically during treatment and maintain therapeutic levels between 0.5 to 2.0 ng/mL to prevent digoxin toxicity If administering IV digoxin infuse over 5 min, and monitor for dysrhythmias |
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management of digoxin toxicty
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digoxin and potassium sparing meds should be stopped immediately
Monitor K+ levels treat dysrhythmias with phenytoin (Dilantin) or lidocaine treat bradycardia with atropine for excessive overdose, activated charcoal, cholestyramine, or Digibind can be used to bind digoxin and prevent absorption |
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cardiac glycosides effectiveness
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control of heart failure
absence of cardiac dysrhythmias |
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adrenergic agonist
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proto: catecholamines
epinepherine (Adrenaline) dopamine (Intropin) dobutamine others: isoproterenol: cataecholamine terbutaline: noncatechlamine |
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alpha 1 (adrenergic agonists) MOA
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activation of receptors in the arterioles of the skin, viscera and mucous membranes, and veins leads to vasoconstriction
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beta 1 (adrenergic agonist) MOA
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heart stimulation leads to increased heart rate, increased myocardial contractility, and increased rate of conduction through the AV node
Activation of receptors in the kidney lead to the release of renin |
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beta 2 (adrenergic agonist) MOA
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activation of receptors in the arterioles of the heart, lungs, and skeletal muscles leads to vasodilation
bronchial stimulation leads to bronchodilation activation of receptors in uterine smooth muscle causes relaxation activation of receptors in the liver cause glycogenolysis skeletal muscle receptor activation leads to muscle contraction |
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dopamine (adrenergic agonist) MOA
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activation of receptors in the kidney cause the renal blood vessels to dilate
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alpha 1 (adrenergic agonist) use (epinepherine)
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vasoconstriction
slows absorption of local anesthetics manages superficial bleeding decreased congestion of nasal mucosa increased BP |
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beta 1 (adrenergic agonist) use (epinepherine)
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increased heart rate, increased myocardial contractility, increased rate of conduction through the AV node
treatment of AV block and cardiac arrest |
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beta 2 (adrenergic agonist) use (epinepherine)
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bronchodilation
treats asthma |
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dopamine (adrenergic agonist) use
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renal blood vessel dilation (low dose)
renal blood vessel dilation, increased heart rate, increased myocardial contractility, increased rate of conduction through the AV node (moderate dose dopamine, beta 2) renal blood vessel constriction increased heart rate increased myocardial contractility increased rate of conduction through AV node vasoconstriction (High dose: dopamine, beta1, alpha 1) treats shock, heart failure |
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dobutamine (adrenergic agonist) use (beta 1)
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increased heart rate
increased myocardial contractility increased rate of conduction through AV node treats heart failure |
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epinepherine adverse
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vasoconstriction from activation of alpha 1 receptors in the heart can lead to hypertensive crisis
beta 1 receptor activation in the heart can case dysrhythmias beta 1 receptor activation also increases the workload of the heart and increases oxygen demand, leading to development of angina |
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dopamine adverse
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beta 1 receptor activation in the heart can cause dysrhythmias
beta 1 receptor activation also increases the workload of the heart and increases oxygen demand, leading to the development of angina necrosis can occur from extravasation of high doses of dopamine |
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dobutamine adverse
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increased HR
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adrenergic agonist contraindications
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epinepherine and dopamine are pregnancy category C
dobutamine is category b tachydysrhythmias and ventricular fibrillation hyperthyroidism, angina, history of MI, hypertension and diabetes |
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adrenergic agonist interactions
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MAOIs
TCAs anesthteics can cause heart to become hepersenstive to the effects of epinepherine, leading to dysrhythmias alpha-adrenergic blocking agents such as phentolamine, block action at alpha receptors beta-adrenergic blocking agents such as propranolol diuretic promote beneficial effects of dopamine |
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adrenergic agonist admin
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IV pump to control infusion
dosage is titrated based on BP response stop infusion of dopamine at first evidence of infiltration extravasation can be treated with local injection of an alpha-adrenergic blocking agent, such as phentolamine assess for chest pain monitor urine output frequently for signs of decreased renal perfusion |
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adrenergic agonist effectiveness
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improved perfusion as evidenced by urine output of greater than or equal to 30 mL per hour with normal renal function, improved mental status, and systolic BP maintained at greater than or equal to 90 mmHG
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