Week 6: Cardiovascular Pharmacology Flashcards

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
Q

MOA for dapagliflozin

A

not well understood in HF

thought to help with ventricular unloading through osmotic diuresis without depleting volume

26
Q

What diuretic is used with heart failure?

A

loop, furosemide

27
Q

S/E of furosemide

A

hypokalemia, hypotension, and digoxin toxicity

28
Q

What class is digitalis (digoxin)?

A

cardiac glycosides

29
Q

What does positive inotropic effect mean?

A

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
Q

MOA of digitalis

A

inhibits sodium-potassium ATP pump channel causing calcium to collect within the cells of the heart helping to increase myocardial contractility

31
Q

What does increasing myocardial contractility do?

A

increase blood flow to the kidneys
decrease sympathetic action
increase parasympathetic action
decreases heart rate

32
Q

S/E of digitalis

A

cardiac dysrhythmias and digitalis toxicity

33
Q

who is at highest risk for digitalis toxicity?

A

age, women and combination drugs (diuretic therapy)

34
Q

How to prevent digitalis toxicity?

A

reduced dose, periodic monitoring of levels, and supplemental potassium

35
Q

S/S of digitalis toxicity

A

bradycardia, headache, dizziness, confusion, nausea and blurry/yellow vision

36
Q

What does the nurse need to do before giving digoxin?

A

take apical pulse for one minute

don’t give if pulse is less than 60 and monitor cardiac rhythm

37
Q

What is the antidote for digitalis toxicity?

A

digoxin immune dab (given IV)

38
Q

MOA of amiodarone

A

prolongs the action potential duration and the effective refractory period in all cardiac tissue
blocks alpha and beta adrenergic receptors in the SNS

39
Q

What is amiodarone usually used for?

A

PSVT, ventricular dysrhythmias, afib with RVR

40
Q

S/E of amiodarone

A

pulmonary toxicity, thyroid alterations, corneal microdeposits, black box warning: pulmonary toxicity, hepatoxicity, and pro-arrhythmic effects

41
Q

What 2 drugs interact with amiodarone?

A

digoxin and warfarin

42
Q

Does amiodarone have short or long half life?

A

EXTREMELY long (many days)

43
Q

When is amiodarone contraindicated?

A

severe bradycardia or heart blocks

44
Q

What class is atropine?

A

anticholinergic/antimuscarinic

45
Q

MOA for atropine

A

poisons the vagus nerve, inhibits postganglionic acetylcholine receptors and diret vagolytic action

46
Q

Indications for atropine

A

bradycardia (IV push only)

47
Q

S/E of atropine

A

xerostomia, blurry vision, photophobia, tachycardia, flushing, hot skin

48
Q

What is adenosine used for?

A

PSVT

49
Q

MOA for adenosine

A

slows the conduction time through the AV node

50
Q

Does adenosine have a short or long half life?

A

VERY short

51
Q

S/E of adenosine

A

causes a short burst of asystole until sinus rhythm returns

52
Q

Dosing of adenosine

A

6mg IVPB, if that doesnt work give 12mg IVPB, and can give a third 12mg IVPB

53
Q

What should always follow administering adenosine?

A

rapid normal saline flush (or 2)

54
Q

Indication for dofetilide

A

conversion from afib/aflutter to normal sinus

55
Q

MOA for adenosine

A

selectively blocking the rapid cardiac ion channel carrying potassium currents

56
Q

S/E of adenosine

A

torsade, SVT, headache, dizziness, chest pain

57
Q

Nursing implications when giving dofetilide

A

start on EKG monitoring
do NOT give to pts with long QY intervals OR with other drugs that may prolong QT intervals