Week 6: Cardiovascular Pharmacology Flashcards

(57 cards)

1
Q

Which classes of drugs are to relieve stable angina?

A

nitrates, beta blockers, calcium channel blockers, and ranolazine

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2
Q

What class of drugs is to reduce stable angina?

A

lipid lowering drug, Aspirin, or clopidogrel

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3
Q

What class of drugs is used to improve morbidity and mortality with stable angina?

A

ACE and ARBs

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4
Q

What are the first line meds for stable angina?

A

beta blocker OR CCB
AND
Nitrates

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5
Q

MOA of nitroglycerin

A

dilates veins and decreases preload

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6
Q

S/E of nitroglycerin

A

vasodilation, headache, hypotension, reflex tachycardia

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7
Q

What routes are offered with nitroglycerin?

A

sublingual, translingual, intravenous, patch, ointment, and oral

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8
Q

What routes are considered rapid acting nitro?

A

sublingual, translingual and IV

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9
Q

what routes are considered short acting nitro?

A

skin patch and ointment

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10
Q

What routes are considered long acting nitro?

A

sublingual or oral isosorbide

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11
Q

What is important pt education when taking nitroglyceirn?

A

If pain is not relieved in 5 minutes call 911

and dont take more than 3 doses

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12
Q

What drugs interact with nitoglycerin?

A

sindenafil/Viagra, antihypertensive, and ETOH

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13
Q

MOA of ranolazine

A

unknown? possibly helps the cardiac muscles use energy more efficiently

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14
Q

S/E of ranolazine

A

prolonged QT interval acute renal failure, and liver cirrhosis

headache, dizziness, nausea and constipation

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15
Q

Is ranolazine a CYP340 inhibitor or inducer?

A

inhibitor

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16
Q

what should be avoided when taking ranolazine?

A

grapefruit juice and other CYP340 inhibitor

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17
Q

MOA for RASS inhibitors : ACE ARB and ARNI (in regards to heart failure)

A

decrease preload and afterload, suppresses aldosterone and favorably impact cardiac remodeling

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18
Q

Which RAAS inhibitor is seen as the best?

A

ARNI, Sacubitril/valsartan

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19
Q

S/E of RAAS inhibitors

A

hypotension, hyperkalemia, and cough

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20
Q

What beta blocker is used for heart failure?

A

carvedilol

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21
Q

MOA for carvedilol

A

protect against SNS activation and dysrhythmias, reverses cardiac remodeling

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22
Q

S/E of carvedilol

A

fluid retention, fatigue, hypotension, bradycardia

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23
Q

Why do we use spironolactone in heart failure?

A

the suppression of sodium and water retention to help with offloading the left ventricle

24
Q

What SLG2 inhibitor is used in heart failure?

A

dapagliflozin

25
MOA for dapagliflozin
not well understood in HF thought to help with ventricular unloading through osmotic diuresis without depleting volume
26
What diuretic is used with heart failure?
loop, furosemide
27
S/E of furosemide
hypokalemia, hypotension, and digoxin toxicity
28
What class is digitalis (digoxin)?
cardiac glycosides
29
What does positive inotropic effect mean?
if we can increase the contractility of the heart muscle then we can increase the force of contraction, and thus increasing the cardiac output
30
MOA of digitalis
inhibits sodium-potassium ATP pump channel causing calcium to collect within the cells of the heart helping to increase myocardial contractility
31
What does increasing myocardial contractility do?
increase blood flow to the kidneys decrease sympathetic action increase parasympathetic action decreases heart rate
32
S/E of digitalis
cardiac dysrhythmias and digitalis toxicity
33
who is at highest risk for digitalis toxicity?
age, women and combination drugs (diuretic therapy)
34
How to prevent digitalis toxicity?
reduced dose, periodic monitoring of levels, and supplemental potassium
35
S/S of digitalis toxicity
bradycardia, headache, dizziness, confusion, nausea and blurry/yellow vision
36
What does the nurse need to do before giving digoxin?
take apical pulse for one minute don't give if pulse is less than 60 and monitor cardiac rhythm
37
What is the antidote for digitalis toxicity?
digoxin immune dab (given IV)
38
MOA of amiodarone
prolongs the action potential duration and the effective refractory period in all cardiac tissue blocks alpha and beta adrenergic receptors in the SNS
39
What is amiodarone usually used for?
PSVT, ventricular dysrhythmias, afib with RVR
40
S/E of amiodarone
pulmonary toxicity, thyroid alterations, corneal microdeposits, black box warning: pulmonary toxicity, hepatoxicity, and pro-arrhythmic effects
41
What 2 drugs interact with amiodarone?
digoxin and warfarin
42
Does amiodarone have short or long half life?
EXTREMELY long (many days)
43
When is amiodarone contraindicated?
severe bradycardia or heart blocks
44
What class is atropine?
anticholinergic/antimuscarinic
45
MOA for atropine
poisons the vagus nerve, inhibits postganglionic acetylcholine receptors and diret vagolytic action
46
Indications for atropine
bradycardia (IV push only)
47
S/E of atropine
xerostomia, blurry vision, photophobia, tachycardia, flushing, hot skin
48
What is adenosine used for?
PSVT
49
MOA for adenosine
slows the conduction time through the AV node
50
Does adenosine have a short or long half life?
VERY short
51
S/E of adenosine
causes a short burst of asystole until sinus rhythm returns
52
Dosing of adenosine
6mg IVPB, if that doesnt work give 12mg IVPB, and can give a third 12mg IVPB
53
What should always follow administering adenosine?
rapid normal saline flush (or 2)
54
Indication for dofetilide
conversion from afib/aflutter to normal sinus
55
MOA for adenosine
selectively blocking the rapid cardiac ion channel carrying potassium currents
56
S/E of adenosine
torsade, SVT, headache, dizziness, chest pain
57
Nursing implications when giving dofetilide
start on EKG monitoring do NOT give to pts with long QY intervals OR with other drugs that may prolong QT intervals