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NUR 326 Exam 3 > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

1
Q

goals of pharm with stable angina

A

–relieve CP
–reduce HLD
–improve morbidity and mortality

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2
Q

what pharm is used to relieve CP in stable angina?

A

–nitrates
–beta blockers
–calcium channel blockers
–ranolazine

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3
Q

what pharm is used to reduce HLD in stable angina?

A

–lipid lowering drugs (statins)
–aspirin or clopidogrel (antiplatelets)

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4
Q

what pharm is used to improve morbidity and mortality in stable angina?

A

ACE inhibitor or ARB

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5
Q

nitrate mechanism of pain relief for stable angina

A

dilates veins –> decreases preload

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6
Q

beta blocker mechanism of pain relief for stable angina

A

decreases HR and contractility

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7
Q

CCB mechanism of pain relief for stable angina

A

–dilates arterioles, which decreases afterload
–decrease HR and contractility

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8
Q

ranolazine mechanism of pain relief for stable angina

A

helps the myocardium generate energy more efficiently

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9
Q

first line meds for stable angina

A

BB or CCB + nitrates

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10
Q

secondary prevention for stable angina

A

–ACEi
–statin
–aspirin

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11
Q

organic nitrate example

A

nitroglycerin

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12
Q

MOA of nitro

A

–dilates veins
–decreases preload

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13
Q

adverse effects of nitro

A

–related to vasodilation: HA, hypotension, reflex tachycardia
–tolerance

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14
Q

route of nitrostat

A

sublingual

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15
Q

usage of nitrostat

A

–put underneath tongue
–repeat q 5 min x 3 as needed

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16
Q

when should nitrostat be used?

A

for active angina

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17
Q

route of transderm-nitro

A

skin patch

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18
Q

directions for transderm-nitro

A

–apply to chest or thigh area
–daily
–no hair
–change site with each use

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19
Q

route of Nitro-Bid

A

ointment

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20
Q

directions for Nitro-Bid

A

apply 1-2 inches to chest or thigh area

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21
Q

route for isosorbide

A

sublingual or oral

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22
Q

use of isosorbide

A

–long acting
–prevention of anginal attacks
–tolerance builds up over time

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23
Q

nursing implications with nitrates

A

–monitor for HA (most subside in 20 minutes)
–apply nitro patches in morning and remove in evening
–only take as many SL as needed
–don’t swallow
–risk for dizziness/hypotension
–no relief in 5 min = call 911

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24
Q

IV nitrate nursing considerations

A

–glass bottle with special tubing
–monitor for severe HA, HA, and tachycardia

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25
Q

long acting nitrate considerations

A

taper when d/c to prevent increased CP from vasospasm

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26
Q

interactions of nitrates

A

severe hypotension when taken with:
–sindenafil/Viagra
–antihypertensives
–ETOH

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27
Q

MOA of ranolazine

A

–unknown
–possible helps the myocardium use energy more efficiently

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28
Q

warnings with ranolazine

A

–prolongs QT interval
–acute renal failure
–liver cirrhosis

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29
Q

adverse reactions with ranolazine

A

–HA
–dizziness
–nausea
–constipation

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30
Q

nursing considerations for ranolazine

A

CYP340 inhibitor–avoid grapefruit juice and other meds that are CYP inhibitors

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31
Q

pharm treatment of HF

A

–ACEi or ARBs, ARNIs
–BB
–mineralocorticoid receptor antagonist (potassium-sparing diuretics)
–SLGT2 inhibitors
–diuretics
–digitalis
–nitrates

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32
Q

example of ARNI (angiotensin receptor-neprilysin inhibitor)

A

sacubitril/valsartan

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33
Q

survival benefit of RAAS inhibitors in HF

A

decrease mortality with decreased EF

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34
Q

RAAS inhibitors

A

ACEi
ARBs
ARNIs

35
Q

MOA of RAAS inhibitors

A

–decreases preload and afterload
–suppresses aldosterone
–favorably impact cardiac remodeling

36
Q

dose of RAAS with HF

A

highest dose possible

37
Q

which RAAS inhibitor is favored in HF treatment?

A

–ARBs might be tolerated better
–ARNI is currently thought to be best–but newer and more expensive

38
Q

adverse effects of RAAS inhibitors

A

–hypotension
–hyperkalemia
–cough (ACEi)

39
Q

preferred BB in HF

A

carvedilol (beta and alpha blockade)

40
Q

MOA of carvedilol

A

–protects against SNS activation and dysrhythmias
–reverses cardiac remodeling

41
Q

adverse effects of carvedilol

A

–fluid retention or worsening HF
–fatigue
–hypotension
–bradycardia

42
Q

use of spironolactone in HF

A

–used for suppression of sodium/water retention to help with offloading the LV
–decreased hospitalizations and cardiac death
–watch for hyperkalemia and worsening renal failure

43
Q

SLG2 inhibitor example

A

dapaglifozin

44
Q

role of dapaglifozin in HF

A

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

45
Q

adverse effects of diuretics in HF

A

–hypokalemia
–hypotension
–Digoxin toxicity

46
Q

examples of inotropic drugs

A

–cardiac glycosides (digitalis)
–sympathomimetics (dopamine and dobutamine)

47
Q

cardiac glycoside example

A

digitalis

48
Q

important info about digitalis

A

considered second line drug because of risk of dysrhythmias

49
Q

role of sympathomimetics

A

helps the heart pump squeeze harder

50
Q

what does positive inotropic effect mean?

A

if we can increase the contractility of the heart muscle, then we increase the force of contraction –> increasing the CO

51
Q

what is digitalis made from?

A

foxglove plant

52
Q

MOA of digitalis

A

–inhibits sodium-potassium ATP pump causing calcium to collect within the cells of the heart, helping to increase myocardial contractility
–increases blood flow to kidneys to help with excretion of sodium and water
–decreases sympathetic action and increases parasympathetic action = decreased HR

53
Q

adverse effects of digitalis/digoxin

A

–cardiac dysrhythmias
–digitalis toxicity

54
Q

who is at highest risk for digitalis toxicity?

A

–increased age
–women
–combination drugs (digoxin and diuretic therapy)

55
Q

preventing digoxin toxicity

A

–reduced dose
–periodic monitoring of serum digitalis levels
–supplemental potassium

56
Q

nursing implications when giving digoxin

A

–monitor serum potassium levels (hypokalemia)
–take apical pulse for full minute prior to admin
–hold if pulse < 60
–monitor cardiac rhythm
–digibind = antidote
–pt education = taking own pulse

57
Q

s/s of digitalis toxicity

A

–bradycardia
–headache
–dizziness
–confusion
–nausea
–visual disturbances

58
Q

meds used for rhythm and rate control

A

–BB
–CCB
–amiodarone
–adenosine
–atropine
–dofetilide

59
Q

MOA of amiodarone

A

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

60
Q

route for amiodarone

A

IV or PO

61
Q

uses for amiodarone

A

–one of the most effective antidysrhythmics for PSVT and ventricular dysrhythmias
–afib with RVR

62
Q

adverse effects of amiodarone

A

–thyroid alterations
–corneal microdeposits
–pulmonary toxicity

63
Q

black box warning for amiodarone

A

–pulmonary toxicity
–hepatotoxicity
–proarrythmic effects

64
Q

drug interactions with amiodarone

A

–digoxin (increase levels by 50%)
–warfarin (increase INR by 50-100%)

65
Q

half life of amiodarone and effects

A

–extremely long half-life
–adverse effects may take 2-3 months to fully go away

66
Q

contraindications of amiodarone

A

–severe bradycardia
–heart blocks

67
Q

class for atropine

A

anticholinergic/antimuscarinic

68
Q

MOA for atropine

A

–poisons the vagus nerve
–inhibits postganglionic acetylcholine receptors and direct vagolytic action

69
Q

route for atropine

A

IV push only for bradycardia

70
Q

dose of atropine

A

1mg every 3-5 minutes, 3mg MAX

71
Q

adverse effects of atropine

A

–xerostomia (dry mouth)
–blurry vision
–photophobia
–tachycardia
–flushing
–hot skin

72
Q

nursing implications for atropine

A

–need to be on cardiac monitoring
–give second dose if doesn’t work quickly

73
Q

MOA for adenosine

A

slows the conduction time through the AV node

74
Q

half life for adenosine

A

very short; may need multiple doses

75
Q

how does adenosine work?

A

causes a short burst of asystole until sinus rhythm returns

76
Q

route for adenosine

A

only IV

77
Q

dosing for adenosine

A

(1) 6mg
(2) 12 mg if not converted
(3) 12 mg
always follow with rapid NS flush or 2 saline flushes

78
Q

class for dofetilide

A

antidysrhythmic

79
Q

indications for dofetilide

A

conversion from afib/aflutter to NSR

80
Q

MOA for dofetilide

A

selectively blocking the rapid cardiac ion channel carrying potassium currents

81
Q

side effects of dofetilide

A

–TORSADES
–SVT
–HA
–dizziness
–chest pain

82
Q

nursing implications of dofetilide

A

–start in hospital with ECG monitoring d/t risk of Torsades
–don’t give to patients with long QT intervals or other drugs that may prolong QT intervals

83
Q

what should you do if your patient falls into Torsades?

A

immediately start CPR

84
Q

what other medication should be monitored with dofetilide?

A

warfarin

NUR 326 Exam 3 (11 decks)

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