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Flashcards in vasodilators/antiarrhythmics Deck (30):

Sodium Nitroprusside class

direct acting nonselective peripheral arterial and vasodilator



prodrug that combines with oxyhemoglobin and forms methemoglobin; during this process cyanide and nitric oxide are released! Nitric oxide activates guanylate cyclase to produce cGMP- stimulating an increase of Ca2+ into the sER and inhibits Ca in vascular smooth muscle= vasodilation


snp PK

onset immediate e1/2 5min; DOA transient. metabolism- transfer of an electron from iron to SNP yields methemoglobin and SNP radical- 5 cyanide ions released; 1 reacts with methemoglobin to from cyanomethemoglobin (nontoxic) and the rest are metabolized in the liver and kidney and converted to thiocyanate which is cleared by the kidney (slowly takes 2-7days)


snp SE

methemoglobinemia- higher risk with gtt>2mcg/kg/min, cyanide toxicity, thiocyanate toxicity (causing seizures and mental status changes), hypotension, HA, increased ICP, tachyphylaxis, anoxia, muscle spasms, lactic acidosis


snp CI

renal failure, hypotenstion, increased ICP, dilated chf, aortic stenosis, don't use with PDIs, decrease SVR


snp dose

0.5-10mcg/kg/min or 1-2 mcg/kg/min for HTN crisis


Nitroglycerine class

organic nitrate


Nitroglycerine MOA

generates NO through gluthathione stimulating the production of cGMP causing peripheral and SM vasodilation (venous>arterial).


Nitroglycerine PK

60% PB, large Vd, onset- immediate; DOA 3-5min; e1/2 1.5min; metabolized rapidly with nitrate metabolite that is capable of producing methemoglobin by oxidation of ferrous to ferric ion with Hgb with very <1% excreted unchanged in the urine


Nitroglycerine SE

dizziness, facial flushing, ha, syncope, N/V, MI, tachycardia, CA vasodilation, relaxes SM and decreases SOO spasm, increased ICP, can cause tachyphylaxis (need nitrate free time), increase bleeding time, decrease venous return


Nitroglycerine CI

severe AS, hypertophic cardiomyopathy, hypotension, increased ICP, glaucoma, anemia, cardiac tamponade, cation in liver failure from methemoglobin, do not use with PDIs


Nitroglycerine dose

initially 5-10mcg/min and titrate 5-200mcg/min


hydralazine class

phthalazine derivative vasodilator; arterial >venous.


hydralazine MOA

unclear- activates guanylate cyclase and is thought to work on the membrane by causing K+ channel activation-hyper polarizing and inhibition of IP3 and Ca2+ release from SR in vascular SM thereby decreasing MAP


hydralazine PK

onset 5-20min, peak 15-20min; DOA 6hours; E1/2 4hrs; metabolized by the liver and excreted 14% unchanged by the kidneys


hydralazine Se

tachycardia , palpitations, increase ICP, HA, SLE syndrome, paradoxical HTN, peripheral edema, flushing, DBP>SBP, decrease SVR


hydralazine CI

hypersensitivity, use with caution in CAD and pulmonary hypertension, wait appropriate amount of time before redoes or will get hypotensive NO MAOis, can increase BB effects


hydralazine dose

2.5-10mg IV q4hr


Adenosine class

endogenous nucleotide


Adenosine MOA

binds to A1 purine nucleotide receptors and activate adenosine receptors via a g coupled protein receptor to open K+ channels and increase K= currents = hyper polarizing cardiac tissue; slowing SA node and delaying AV node conduction


Adenosine PK

very rapid onset and termination of action; E1/2t 30sec, e1/2L <10sec; eliminated by plasma and vascular endothelial cells


Adenosine SE

chest pain, dyspnea, facial flushing, hypotension, asystole, nausea, bronchospasm, excessive SA or AV node inhibition


Adenosine CI

hypersensitivity, AV HB, SSS; caution asthma/COPD


Adenosine dose

6mg rapid IVP, then can repeat in 1min 6-12mg if needed


Digoxin class

cardiac glycoside


Digoxin MOA

inhibits NA+/K= ATP pum causing increase intracellular Na+ and Ca2+ = increase contractility and decreasing HR by increasing vagal tone and prolonging SA to AV node conduction;


Digoxin PK

low PB- 25%; large Vd 9L/kg; onset 5-30min, Peak 1-5 hours; e1/2 30-48hrs; excreted in the kidneys 90%unchanged


Digoxin SE

prolong PRI, St depression, T waave changes, dysrhythmias/HB, N/V/D/A, HA, can cause hypokalemia


Digoxin CI

decrease dose in elderly; VF/VT, HB, hypertrophic cardiomyopathy, digoxin toxicity potentiated by decreased K/Mg and increased Ca2+; don't use in renal disease; potentiated by decrease K and Mg; , AV block, abx decrease absorption; verapamil, amiodarone and quinidine increases levels


Digoxin dose

loading dose- 0.5-1mg Iv over 12-24hours; maintenance 0.25mg, therapeutic window 0.5-1.2ng/ml