Quiz 6 Flashcards

1
Q

Contraindication of captopril

A

Pregnancy: teratogonic
Salt substitues containing potassium
Potassium-sparing diuretics

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2
Q

Lorsatan side effects

A

dizziness, hypotension, electrolyte imbalance: Hyperkalemia
Fluid loss

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3
Q

Nursing interventions of losartan

A

Monitor electrolytes
Taper
Fall precautions
education on orthostatic hypotension

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4
Q

Which receptors does anti-adrenergics/sympatholytics include

A

Alpha 1 and beta 1 adrenergic blockers
Alpha 2 agonists

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5
Q

Side effects of beta adrenergic blockers

A

Hypotension, dizziness, fatigue, depression, sexual dysfunction, bradycardia

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6
Q

Side effects of Alpha 1 and beta 1 adrenergic blockers

A

Hypotension, bradycardia, dizziness,
Insomnia, sexual dysfunction
Nasal Congestion

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7
Q

Nursing interventions of beta-adrenergic blockers

A

VS
Tapering = rebound hypertension
Avoid OTC drugs without first checking with a health care provider

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8
Q

Nursing interventions for clonidine

A

Hypoactive bowel sounds
Take off old patch and rotate
Caution when standing up

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9
Q

Hydralazine, minoxidil
MOA

A

Direct-acting arteriolar vasodilatiors
Vasodilation of smooth muscles of blood vessels

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10
Q

Hydralazine side effects

A

Tachycardia (HR increases to compensate), palpitations, headache, dizziness, nasal congestion, edema, lupus-like symptoms
AKA Minoxidil

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11
Q

How can antihypertensives lower BP

A
  1. Decrease HR
  2. Dilate blood vessels
  3. Decrease fluid volume
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12
Q

Function of aldosterone

A

responsible for renal absorption of sodium & excretion of potassium

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13
Q

Adverse effects of captopril

A

Persistent cough: do not stop taking
Angioedema: life threatening, stop taking
Electrolyte imbalance
Hypotension
Hyperkalemia

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14
Q

MOA of captopril
What is it?

A

Vasodilation and fluid loss
ACE inhibitor

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15
Q

ACE vs ARBS

A

ACE inhibitors block the PRODUCTION of angio II, ARBs block the ACTIONS of angio II

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16
Q

MOA of losartan
What is it?

A

Vasodilation and fluid loss
ARBs (angiotensin receptor blockers)

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17
Q

Amlodipine MOA
What is it

A

Slow calcium channels in vascular smooth muscle
Causes vasodilation
Calcium channel blocker

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18
Q

Adverse effects of amlodipine

A

Flushing, headache, hypotension, peripheral edema

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19
Q

Nursing interventions of amlodipine

A

monitor VS
telemetry

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20
Q

What are anti-adrenergics/sympatholytics

A

Drugs that block the activation of adrenergic receptors

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21
Q

Types of beta-adrenergic blockers

A

Nonselective: inhibit beta 1 and beta 2 receptors
Cardioselective beta blockers: selective to beta 1

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22
Q

MOA of beta adrenergic blockers

A

Decreases heart rate by inhibiting beta 1 and beta 2 receptors

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23
Q

Nursing interventions for beta-adrenergic blockers

A

Hold for low BP
Hold if HR is lower than 60

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24
Q

Clonidine
Action
Administration type

A

Alpha 2 agonist
Stimulate alpha 2 receptors- cause vasodilation
PO and transdermal

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25
Q

Adverse reactions to clonidine

A

Decreased peristalsis
Decreased acid production

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26
Q

Nursing interventions for minoxidil

A

Seizure precautions, monitor weight, telemetry
AKA hydralazine

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27
Q

What is variant (prinzmetal, vasospatic) angina?

A

occurs during rest

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28
Q

MOA nitroglycerin

A

Causes vasodilation & < O2 demand. > oxygen supply
Decrease preload and afterload

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29
Q

Action of atenelol

A

Decreases HR=Decrease in O2 demand
Block the action of epinephrine and norepinephrine

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30
Q

Function of coronary artery

A

Perfuse the heart (supply oxygen to the heart)

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31
Q

What is coronary artery disease

A

plaque buildup

32
Q

Why can coronary artery disease lead to myocardial infarction (acute coronary syndrome)

A

Chest pain due to lack of O2 to the heart

33
Q

What is classic angina (stable)

A

Occurs with predictable stress or exertion
Ex walking up stairs

34
Q

What is unstable angina (preinfarction)

A

Coronary atherosclerotic disease unpredictable regarding stress/exertion and intensity

35
Q

Side effects of nitroglycerin

A

Headache, hypotension, and flushing

36
Q

Routes of administration nitroglycerin

A

sublingual, IV, oral, topical

37
Q

Routes of administration Nitro-Bid

A

Sublingual, IV

38
Q

3x5 rule

A

take 3 tabs 5 min apart. Take 1 tab, let it absorb and wait 5 min if pain goes away you can stop, but if pain remains repeat after 3 tabs they might be having a heart attack

39
Q

Long-acting nitrates

A

Isosorbide (Imdur)- BID
Transderm-Nitro (nitroglycerin) 12 on, 12 off (put it on when going out and take it off when at home)

40
Q

Long-acting nitrates caution

A

do no abruptly discontinue
Taper-chest pain can come back = heart attack/spasms

41
Q

Discontinuing of beta-blockers

A

tapering
take daily

42
Q

Nifedipine action

A

Relax coronary and peripheral arteries
Take every day for prevention

43
Q

Nifedipine adverse effects

A

relax tachycardia

44
Q

Classic angina pectoris suggested steps for treatment

A

Step 1: Nitrates
Step 2: + beta blockers
Step 3: + calcium blockers
Step 4: coronary artery bypass graft

45
Q

Variant angina pectoris suggested steps for treatment

A

Step 1: nitrates/calcium blockers
Step 2 + clacium blockers
Step 3: coronary artery bypass graft

46
Q

Causes of heart failure

A

Heart muscle weakens and enlarges
Compensatory mechanisms fail
Loses ability to pump blood adequately
Lungs and periphery become congested

47
Q

Nonpharmacologic treatment of heart failure

A

Limit salt and saturated fat intake.
Limit or avoid alcohol intake; stop smoking.
Perform mild exercise.

48
Q

Positive inotropic

A

Increases myocardial contractility = strength

49
Q

Side effects of digoxin

A

Bradycardia, cardiac dysrhythmias, anorexia, N/V/D, headache, blurred or yellow vision

50
Q

Phosphodiesterase inhbitors
MOA

A

Positive inotropic effects
Vasodilation: decrease stress of the heart

51
Q

Administration considerations of phosphodiesterase inhibitors

A

Only given IV for acute exacerbations
decrease HR and BP

52
Q

Pathophysiology of heart failure

A

High preload (volume) = > stretching of heart
High afterload (pressure) = > pressure on heart

53
Q

Laboratory tests-Diagnosis
Heart failure

A

Atrial natriuretic peptide (ANP): natural diuretic
Brain natriuretic peptide (BNP): natural diuretic

54
Q

MOA digitalis/digoxin

A

Positive inotropic
Negative chronotropic
Negative dromotropic
Increases stroke volume = > cardiac ouptut

55
Q

Negative chronotropic

A

Slowing/decreasing heart rate (how many times it contracts in a minute)

56
Q

Negative dromotropic

A

Decreases conduction. How fast nerve signals gets to the heart

57
Q

Therapeutic range of digoxin

A

Heart failure: 0.5-0.8ng/ml (narrow range)

58
Q

Digitalis toxicity side effects

A

slow -irregular pulse
confusion
headache
delirium
Green vision
halos around dark objects
NVD
>2 ng/mL

59
Q

Antidote of digoxin

A

digoxin immune FAB

60
Q

How does hypokalemia affect the heart

A

Causes increases sensitivity to digoxin = digoxin toxicity

61
Q

drug interactions of digoxin: antacids

A

Decrease digitalis absorption, causing increased excretion

62
Q

Drug interactions of digoxin: glucocorticoids

A

Cause hypokalemia

63
Q

Other agents used to treat heart failure

A

Beta blockers: decrease heart rate
Diuretics
ACE inhibitors

64
Q

A patient is ordered to receive digoxin to treat congestive heart failure. The nurse is most concerned about which assessment finding?
A. Heart rate 56 beats/min
B. BP 138/90 mm Hg
C. RR 21 breaths/min
D. 1+ pitting edema of the lower extremities

A

A.Heart rate 56 beats/min

65
Q

A nurse is preparing to administer digoxin to a patient. Which laboratory result is the nurse most concerned about?
A. Sodium 140 mEq/L
B. Potassium 3.0 mEq/L
C. Digitalis level 1.8 ng/mL
D. BNP 200 pg/mL

A

B. Potassium 3.0 mEq/L

66
Q

A nurse is administering digoxin, 0.125 mg, to a patient. Which nursing interventions will the nurse implement? (Select all that apply.)
A. Checking the apical pulse rate before administration.
B. Monitoring the patient’s serum digoxin level.
C. Instructing patient to report pulse rate less than 60.
D. Advising patient to avoid foods high in potassium.
E. Always giving an antacid with digoxin to reduce GI distress.

A

Checking the apical pulse rate before admin
Monitoring the pt’s serum digoxin level
Instructing pt to report pulse rate < than 60

67
Q

MOA of medication of dysrhythmias

A

Blocks adrenergic sitmulation of the heart
< myocardial excitability and strength
< conduction velocity in cardiac tissue
> recovery time of myocardium
Suppresses automaticity

68
Q

Adverse effects of antidysrhythmics

A

Cardiac dysrhthmias, chest pain, bradycardia, hypotension: dizziness, lightheadedness, CNS changes (weakness, dizziness)

69
Q

Nursing interventions for dysrhythmias

A

VS
ECG abnormal patterns
Education: side effects and what to warn to provider
Avoid alcohol, caffeine, and tobacco

70
Q

MOA of sodium channel blocker

A

Decrease automaticity
Slow conduction velocity
Prolong refractory period (reduces influx of sodium into cells = slower, regular heart rhythm)

71
Q

MOA beta-adrenergic blockers

A

< HR & BP and < fluid
< blood glucose, < peristalsis and acid, and < RR
(blocks impulse that may cause irregular heart rhythm, slows speed of impulses, increase recovery, prevent spontaneous action potentials)

72
Q

MOA of potassium channel blockers

A

Prolong action potential duration
Prolong repolarization (prolong relaxation stage of action potential)

73
Q

MOA of calcium channel blockers

A

Slow conduction velocity (slows down the speed of an electrical impulse)
Prolong refractory period (prolong recovery phase, phase after a neuron has fired action potential)

74
Q

What is hemodynamic shock

A

Severe hypotension that leads to a decreased perfusion

75
Q

Drugs that can be used to treat shock

A

Dopamine, epinephrine
Increases contractility and heart rate thus increasing blood pressure