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NUR 326 > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

1
Q

stable angina goals of pharm

A

relieve chest pain
reduce HLP
improve morbidity and mortality

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2
Q

what drugs are used for stable angina to address relieving chest pain

A

nitrates
beta blockers
CCB
ranolazine

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3
Q

what drugs are used for stable angina to address reducing lipids

A

lipid lowering drugs
aspirin or clopidogrel

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4
Q

what drugs are used for stable angina to address improve morbidity and mortality

A

ACE inhibitors or ARBs

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5
Q

what is the mechanism of nitrates to treat angina

A

dilates veins which dec preload

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6
Q

what is the mechanism of beta blockers to treat angina

A

dec heart rate and contractility

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7
Q

what is the mechanism of CCB to treat angina

A

dilates arterioles, which dec afterload
dec HR and contractility

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8
Q

what is the mechanism of ranolazine to treat angina

A

helps the myocardium generate energy more efficiently

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9
Q

what is the moa of nitrates

A

dilates veins
dec preload

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10
Q

what are adverse effects of nitrates

A

related to vasodilation: h/a (blood more likely to stay in venous system to not as good of blood), hypotension, reflex tachycardia (response to low BP)
tolerance (teaching point)

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11
Q

what are the forms of rapid acting nitrates

A

nitrostat: put underneath tonuge and repeat q 5 mins and do 3x as needed

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12
Q

what are the forms of short acting nitrates

A

transderm-nitro: apply to chest or thigh area daily
nitrobid: apply 1-2 inches to chest or thigh area

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13
Q

what are the forms of long acting nitrates

A

isosorbide: for prevention of anginal attacks
- tolerance builds up over time

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14
Q

what are the nursing implications for nitrates

A

monitor for headaches
- should subside in about 20 mins
apply nitro patches in the morning and remove in the evening
- hairless sites, rotate sites
pt education of treatment and acute chest pain
- monitor for tolerance, SL so dont swallow, fall precautions, no relief in 5 mins then call 911
IV form
- glass bottle with special tubing, monitor for h/a and tachycardia
long acting forms
- taper when d/c to prevent inc chest pain from vasospasms

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15
Q

what class is ranolazine

A

anti anginals

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16
Q

what is the moa of ranolazine

A

unknown

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17
Q

what are warning associated with ranolazine

A
  • prolonged QT interval
  • acute renal failure
  • liver cirrhosis
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18
Q

what are adverse effects of ranolazine

A

headache, dizzy
N, C

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19
Q

what interactions does ranolazine cause

A

CYP450 inhibitor
- NO grapefruit or other CYP450 inhibitor meds

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20
Q

what types of meds are used to treat HF

A

ACEi, ARBs, ARNI *
beta blockers *
mineralocorticoid receptor antagonist *
SLG2 inhibitors *
diuretics
digitalis
nitrates

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21
Q

what is sacubitril

A

HF medications that help dec mortality in pts with dec EF

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22
Q

what is the moa of sacubitril

A

dec preload and afterload
suppresses aldosterone
favorably impact cardiac remodeling

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23
Q

what are the adverse effects of sacubitril

A

hypotension
hyperkalemia
cough (ACEi)

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24
Q

what are nursing considerations for RAAS inhibitors in HF

A

use highest dose possible
ARNIs are thought to be best bc they have the neprilysin inhibitor which helps w the cardiac remodeling
ARBs tolerated best

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25
Q

what are the beta blockers used in HF

A

carvedilol

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26
Q

why is carvedilol typically used for HF

A

they block both beta and alpha receptors

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27
Q

what is carvedilol moa

A

protects against SNS activation and dysrhythmias
reverses cardiac remodeling

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28
Q

what are the adverse effects of carvedilol

A

fluid retention or worsening HF
fatigue
hypotension !!!
bradycardia

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29
Q

what is a mineralocorticoid receptor antagonist

A

sprinolactone

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30
Q

what is the moa of sprinolactone

A

for HF, suppresses Na and water retention which helps offload the LV
- associated w dec hospitalizations and cardiac death

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31
Q

what are nursing considerations for sprinolactone

A

monitor K levels because it can cause HYPERkalemia
- watch for dysrhythmias
monitor for worsening renal failure

32
Q

what class is dapaglifozin

A

SLG2 inhibitor

33
Q

what is the moa of dapaglifozin

A

for HF it is not well understood
- helps w ventricular offloading through naturiesis/osmotic diuresis w/out actually depleting volume like tradition diuretics
- may affect cardiac metabolism/bioenergetics

34
Q

what are the benefits of dapaglifozin

A

dec readmission, mortality and morbidity

35
Q

what diuretic are HF pts typically on

A

loop diuretics

36
Q

what are diuretics used to treat

A

volume overload
- symptom relief, no survival benefit

37
Q

how are diuretics given

A

PO, IV

38
Q

what are the adverse effects of diuretics

A

hypokalemia
hypotension
digoxin toxicity

39
Q

what are inotropic drugs

A

cardiac glycosides –> digitalis
sympathomimetics –> dopamine, dobutamine

40
Q

when is digitalis used

A

typically second line therapy because inc risk of dysrhythmias

41
Q

how are sympathomimetics given

A

IV drips

42
Q

what do sympathomimetics do?

A

get the heart to squeeze harder

43
Q

what does a positive inotrophic effect mean

A

if we can inc contractility of the heart muscle then we can inc the force of contraction
ultimately inc cardiac output

44
Q

what is digitalis class

A

cardiac glycoside

45
Q

what is the moa for digitalis

A

inhibits Na/K pump causing Ca to collect w/in cells of the heart to inc myocardial contractility
- inc blood flow to the kidneys helping with excretion of Na and water
- dec sympathetic action and increase parasympathetic action to dec HR

46
Q

what are the adverse effects of digitalis

A

cardiac dysrhythmias
digitalis toxicity

47
Q

who is at risk for digitalis toxicity

A

older
womens
combination drugs (digitalis and diuretic therapy)

48
Q

how do we prevent digitalis toxicity

A

reduce dose
serum digitalis levels
supplemental K (as long as good kidneys)

49
Q

what are the nursing implications for digitalis

A

monitor serum K levels: if on digitalis, we dont want their K levels to be low bc can cause
- toxicity, cardiac dysfunction, serious dysrhythmias

50
Q

what are the s/s of digitalis toxicity

A

bradycardia –> hallmark sign
headache
dizzy
confusion
N
visual disturbances–> blurry, yellow vision

51
Q

what do we teach pts about taking digitalis

A

take your apical pulse for a full min before taking the medication and hold if below 60
- teach about also being on diuretics and the need to monitor K levels

52
Q

what is the antidote for digitalis

A

digoxin immune Fab given IV

53
Q

what drugs are used for rate and rhythm control

A

beta bockers
CCB
amiodarone
adenosine
atropine
dofetilide

54
Q

what is the ideal of HR and rhythm

A

less than 100 and normal rhythm

55
Q

what is the moa of amiodarone

A

prolongs the AP duration and the effective refractory period in all cardiac tissues
- blocks alpha and beta adrenergic receptors in the SNS

56
Q

how is amiodarone given

A

IV, PO

57
Q

what class is amiodarone

A

anti dysrhythmic

58
Q

what are nursing considerations for amiodarone

A

one of the most effective anti dysrhythmics
used for PVST, ventricular dysrhythmias, afib and RVR
75 % of pt will experience adverse affects
contraindicated for ppl w severe bradycardia or heart blocks

59
Q

what are the adverse effects of amiodarone

A

it is lipophyllic –> fat loving so it will accumulate in ppls fat
- thyroid alterations: iodine is in its make up
- corneal microdeposits –> light sensitivity, visual halos
- can accumulate in pulm causing pulmonary toxicity which is fatal in 10% of cases
*black box warning –> pulm and hepatoxicity, pro arhythmic effect

60
Q

what are the interactions of amiodarone

A

digitialis and warfarin
- inc digitoxin
- inc INR
extremely long half life: can take 2-3 months for symptoms to go away

61
Q

what is atropine used for

A

sinus brady cardia
- experiencing symptoms

62
Q

what class is atropine

A

anticholinergic
antimuscarinic

63
Q

what is the moa for atropine

A

poisons the vagus nerve
inhibits protaglanlionic acetylcholine receptors and direct vagolytic action
* only works if bradycardia is vagal induced*

64
Q

how is atropine given

A

IV push
1 mg q 3-5 mins
3 mg MAX

65
Q

what are the adverse effects of atropine

A

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

66
Q

what are the nursing implications for atropine

A

must be on cardiac monitoring
if doesnt work quickly then give second dose

67
Q

what is adenosine used for

A

PSVT (SVT) and sinus tachycardia

68
Q

what is the moa for adenosine

A

slows the conduction time through the AV node

69
Q

what are the nursing implications for adenosine

A

very short half life so may need to give multiple doses
only given IV
must use a 3 way stop cock

70
Q

how is adenosine given

A

IVP
6 mg then 12 mg max
can give a 3rd 12 mg
always follow w rapid normal saline flush or 2 saline flushes

71
Q

what is dofetilide class

A

antidysrhythmic

72
Q

what are the indications for dofetilide

A

conversions from afib/atrial flutter to NSR and stay in NSR

73
Q

what is the moa of dofetilide

A

selectively blocks the rapid cardiac ion channels carrying potassium currents

74
Q

what are the adverse affects fo dofetilide

A

torsades –> funky rhythm, deadly rhythm that requires CPR black box warning
SVT
headache
dizzy
chest pain

75
Q

what are the nursing implications of dofetlide

A

must be started in hospital while pt is on ECG to monitor for torsades
dont give to pts with long QT intervals or other drugs that may prolong QT intervals
must also be on warfarin bc of risk of stroke w afib

NUR 326 (20 decks)

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