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Nursing Semester 2 > Monica - Final Exam: Anti-anginal, Anti-arrhythmic > Flashcards

Monica - Final Exam: Anti-anginal, Anti-arrhythmic Flashcards

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1
Q

angina

A

coronary atherosclerosis leads to angina (chest pain):

- plaque impairs elasticity and dilation leading to myocardial ischemia, which deprives cells of needed O2 and nutrients

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2
Q

Angina is precipitated by ______ or _______.

A

exertion or stress

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3
Q

Angina can be relieved with _____ and ______.

A

rest (decreased cardiac demand) and nitrates

- pain relief with decreased cardiac workload and increased O2 supply

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4
Q

sxs of angina in men

A

pressure, squeezing, “crushing” pain, radiating pain felt on left side
dyspnea, diaphoresis, tachycardia

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5
Q

sxs of angina in women

A

sxs are not as clear with women:

flu-like symptoms, nausea, fatigue, back pain, jaw pain

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6
Q

Goal of tx of angina:

A
  • inc. blood flow
  • dec. myocardial O2 demand
  • dec. duration + intensity of anginal pain
  • minimize freq of attacks
  • prevent MI
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7
Q

forms of rapid-acting nitroglycerin:

A

sublingual, spray

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8
Q

rapid-acting nitroglycerin forms are indicated for:

A

acute/emergency anginal episodes b/c SL and sprays bypass first pass.

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9
Q

forms of nitroglycerin for long-term management of angina:

A

PO, transdermal patch, isosorbide

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10
Q

nitroglycerin: action

A
  • vasodilation
  • dec. amount of blood returning to heart decreases workload and O2 demand
  • inc. blood flow to coronary arteries
  • inc. O2 supply
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11
Q

nitroglycerin: AEs

A

dizziness, *HA, tachycardia, hypotension

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12
Q

If a patient has a headache after taking nitroglycerin that means:

A

it’s working!

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13
Q

nitroglycerin: D-D interactions

A

concurrent use w/ sildenafil (Viagra), tadalafil (Cialis) increases risk of life-threatening hypotension

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14
Q

Nitrates should not be taken within ___ hours before or after using _____

A

24 hours of sildenafil or tadalafil

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15
Q

If an ER nurse needs to administer nitro to a patient, he should first ask:

A

if the patient has taken any medication for erectile dysfunction.

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16
Q

nitroglycerin: outcome

A
  • decreased frequency and severity of anginal attacks

- increased activity tolerance

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17
Q

How should SL nitro tabs be stored?

A

in a dark container

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18
Q

When should SL nitro tabs be taken?

A

first sign of chest pain

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19
Q

SL nitro tabs may be repeated q__min for __ doses.

A

q5min x 3 doses

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20
Q

If anginal pain is not relieved by SL nitro tabs:

A

call 911

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21
Q

Nitroglycerin ointment is administered using

A

dosing paper. Based on the order, an amount in inches is spread onto the paper and applied to the chest wall.

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22
Q

When applying nitroglycerin ointment the RN should:

A
  • wear gloves to prevent contact
  • rotate sites
  • removal all residual dose
  • write dose, date, and initial
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23
Q

A transdermal nitro patch should be left on for __-__ hours and then:

A

left on for 12-14 hours and removed for 10-12 hours at night.
*NOC RN may need to look at original order to know what time to remove patch

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24
Q

alpha-1 receptors: location - action

A

vascular smooth muscle - vasocontriction

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25
Q

beta-1 receptors: location - action

A

heart - inc. conractility, HR, and conduction

kidney - inc. renin secretion

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26
Q

beta-2 receptors: location - action

A

vascular/non-vascular smooth muscle - bronchodilation

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27
Q

Why are non-selective beta blockers contraindicated for patient s with COPD?

A

block beta-2 receptors causing bronchoconstriciton

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28
Q

Adrenergic receptors include ____, _____, and _____ and are activated by _______.

A

alpha-1, beta-1, and beta-2 are activated by catecholamines (epinephrine, norepinephrine)

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29
Q

Beta-adrenergic antagonists are called “___ _______”

A

beta-blockers

30
Q

Which beta blockers are cardioselective/cardioprotective? Why?

A

selective beta-1 blockers b/c they protect the heart from catecholemines (epi/NE) by blocking beta-1 adrenergic receptors:

  • decreasing HR
  • reducing the force of contraction (dec. CO and O2 demand)
  • prevents renin release (dec. BP)
31
Q

Selective beta-1 blockers may slow conduction of the heart.

A

True - decreased electrical impulses may lead to cardiac dysrhythmias

32
Q

beta blocker drug names end in:

A

-lol

33
Q

beta-1 blocker: atenolol

indications

A
  • HTN
  • angina
    • prevention of MI
34
Q

beta-1 blocker: metoprolol

indications

A
  • HTN
  • angina
  • prevention of MI
    • dec. mortality if recent MI
    • manage stable HF
35
Q

beta-1 blockers (atenolol, metoprolol): AEs

A

dizziness, bradycardia, hypotension, erectile dysfunction, hypo/hyperglycemia, bronchospasm, wheezing

36
Q

beta-1 blockers (atenolol, metoprolol): D-D interactions

A

anti-HTN, nitrates - hypotension
digoxin, CCB - bradycardia
hypoglycemics - fluctuations in glucose levels

37
Q

beta-1 blockers (atenolol, metoprolol): implementation

A
  • assess apical pulse (1 min)
  • hold if < 50 bpm or arrhythmia
  • abrupt d/c can cause rebound HTN, angina, life-threatening arrhythmia
38
Q

beta-1 blockers (atenolol, metoprolol): outcome

A
  • dec BP and HR
  • dec frequency of angina
  • prevention of MI
  • *only metoprolol - maintain stable HF
39
Q

Beta-blockers are classified as _______ and _______.

A

antianginals, antihypertensives

40
Q

non-selective beta-blocker: prototypical drug

A

carvedilol (Coreg)

41
Q

non-selective beta-blockers block ______, ______, and ______ receptors.

A

beta-1
beta-2
alpha-1

42
Q

carvedilol: indications

A
  • HTN
  • management of HF (when unstable)
  • left ventricular function after MI (low EF, heart is not able to pump enough blood to meet the needs of the body)
43
Q

Which drug would be more appropriate for a patient with unstable HF, metoprolol or carvedilol?

A

carvedilol

44
Q

Non-selctive beta-blockers have the same side effects as selective beta-blockers, in addition to _____ ______.

A

orthostatic hypotension

45
Q

Why do non-selective beta-blockers (carvedilol) cause orthostatic hypotension?

A

They block alpha-1 receptors leading to vasodilation.

46
Q

Non-selective beta-blockers (carvedilol) have the same drug-drug interactions as selective.

A

True - anti-HTN/nitrates increased hypotension; digoxin/CCB leads to bradycardia; hypoglycemics leads alterations in glucose levels

47
Q

carvedilol: contraindications

A

asthma and other bronchospastic disorders

- b/c carvedilol blocks beta-2 receptors causing bronchoconstriction

48
Q

carvedilol: outcome

A
  • decreased HR and BP
  • improved CO
  • slowing severity of HF
49
Q

calcium channel blocker (CCB): prototypical drug

A

diltiazem (Cardizem)

50
Q

prototypical selective beta-1 blockers

A

atenolol, metoprolol

51
Q

prototypical nonselective beta-blocker

A

carvedilol

52
Q

diltiazem: indications

A
  • HTN
  • angina
  • supraventricular tachyarrhythmia (SVT)
  • rapid ventricular rates (RVR) in Afib
    • SVT w/ RVR means heart is erratic and ineffective
53
Q

diltiazem: action

A
  • inhibits transport of Ca+ into myocardial and vascular smooth muscle cells, resulting in inhibition of excitation-contraction coupling and contractions
    • slows cardiac conduction
  • vessel vasodilation
  • coronary artery vasodilation: inc O2 supply and dec O2 demand
54
Q

diltiazem: outcomes

A
  • dec BP
  • dec frequency and severity of anginal attacks
    • prevention of tacharrythmia
55
Q

diltiazem: AEs

A

dizziness, arrhythmias, peripheral edema, sexual dysfunction

56
Q

diltiazem: D-D interactions

A
  • ant-HTN, nitrates - inc. hypotension

- beta-blockers, digoxin - risk of bradycardia

57
Q

diltiazem: implementations

A
  • assess BP and HR
    HOLD if:
  • SBP < 90
  • HR < 50 bpm
58
Q

prototypical cardiac (digitalis) glycoside

A

digoxin

59
Q

digoxin: indication

A
  • HF

- atrial fibrillation

60
Q

digoxin: action and outcome

A
  • increased force of myocardial contraction
  • increased CO, increased EF
  • slows contraction
61
Q

digoxin: outcome

A
  • increase CO
  • decrease severity of HF
  • decrease ventricular response
62
Q

digoxin: AEs

A

fatigue, bradycardia, anorexia, n/v

63
Q

digoxin: D-D interactions

A

concurrent use w/ beta-blockers and other anti-arrhythmics - bradycardia and inc. digoxin levels

64
Q

What labs need to be monitored with digoxin?

A

electrolytes: hypoK+ and hypoMg+ can increase the risk of digoxin toxicity

65
Q

digoxin: implementation

A
  • assess apical pulse
  • HOLD if <60 bpm
  • drug monitoring
66
Q

digoxin: therapeutic levels

A

very narrow! 0.5 - 2 ng/ml

67
Q

sxs of digoxin toxicity

A

abd pain, anorexia, n/v, bradycardia, visual disturbances (ex. yellow/green halos)

68
Q

How is digoxin toxicity treated?

A

It depends of the severity of sxs.

May only require d/c-ing the drug OR, if life-threatening, may require the antidote.

69
Q

What is the antidote for digoxin?

A

digoxin immune Fab

70
Q

digoxin: drug-food interaction

A

high-fiber meal may decrease absorption

71
Q

Digoxin immune Fab

A

Digibind, DigiFab
IV - complex formed with digoxin that prevents the drug from reaching tissues
- excreted by kidneys
* serum dig levels not valid 5-7 days after administration - assess for dig toxicity

72
Q

Digoxin immune Fab: AE

A

hypokalemia

Nursing Semester 2 (7 decks)

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