vasodilators/antiarrhythmics

Question 1

Sodium Nitroprusside class

Answer 1

direct acting nonselective peripheral arterial and vasodilator

Question 2

SNP MOA

Answer 2

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

Question 3

snp PK

Answer 3

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)

Question 4

snp SE

Answer 4

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

Question 5

snp CI

Answer 5

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

Question 6

snp dose

Answer 6

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

Question 7

Nitroglycerine class

Answer 7

organic nitrate

Question 8

Nitroglycerine MOA

Answer 8

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

Question 9

Nitroglycerine PK

Answer 9

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

Question 10

Nitroglycerine SE

Answer 10

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

Question 11

Nitroglycerine CI

Answer 11

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

Question 12

Nitroglycerine dose

Answer 12

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

Question 13

hydralazine class

Answer 13

phthalazine derivative vasodilator; arterial >venous.

Question 14

hydralazine MOA

Answer 14

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

Question 15

hydralazine PK

Answer 15

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

Question 16

hydralazine Se

Answer 16

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

Question 17

hydralazine CI

Answer 17

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

Question 18

hydralazine dose

Answer 18

2.5-10mg IV q4hr

Question 19

Adenosine class

Answer 19

endogenous nucleotide

Question 20

Adenosine MOA

Answer 20

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

Question 21

Adenosine PK

Answer 21

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

Question 22

Adenosine SE

Answer 22

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

Question 23

Adenosine CI

Answer 23

hypersensitivity, AV HB, SSS; caution asthma/COPD

Question 24

Adenosine dose

Answer 24

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

Question 25

Digoxin class

Answer 25

cardiac glycoside

Question 26

Digoxin MOA

Answer 26

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;

Question 27

Digoxin PK

Answer 27

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

Question 28

Digoxin SE

Answer 28

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

Question 29

Digoxin CI

Answer 29

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

Question 30

Digoxin dose

Answer 30

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