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NRSG 213 > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

Review anatomy of heart

A

vena cava –> right atria –> tricuspid –> Right ventricle –> Pulmonary valve –> pulmonary artery –> lungs/gets oxygen –> pulmonary veins –> left atria –> mitral valve - left ventricle –> aortic valve –> aorta –> coronary arteries

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2
Q

Electrical activity originates from… (3)

A

SA node (natural pacemaker)
AV node
Purkinjie fibers

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3
Q

Inside a cardiac cell there is a ___ charge because….

A

there exists a negative charge because of the high K+ and low Na+ and Ca2+ on the inside of the cell as compared to the outside.

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4
Q

The ____ automatically builds up an electrical charge about _____ times per minute

A

SA node & 60 - 100

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5
Q

Electrical phases & cardiac muscle contraction

–> Phase 0

A

electrical charge starts to build

fast channels for sodium open

Na+ comes into the cell quickly

The faster the influx, the faster the electrical impulse

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6
Q

Phase 1

A

When the fast channels close

The electrical changes start to occur

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7
Q

Phase 2

A
  • When the slow channels for Ca2+ are open
  • This is a slow process that causes the electrical impulse to plateau
  • Ca2+ is necessary for any muscle contraction
  • After the peak of the electrical impulse, K+ ions leave the cell. They are “pushed out”.
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8
Q

Phase 3

A
  • Ca2+ channels close
  • The Na+/K+ pump brings the K+ back in and pushes the Na+ out
  • Sodium stabilizes the cell to its resting membrane potential
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9
Q

Phase 4

A
  • Polarized state is reestablished or repolarized to the baseline state
  • Ready to start over
  • Entire process took about 400 milliseconds
  • Any abnormality in any of this will cause a dysrhythmia
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10
Q

Congestive heart failure…What is it?

A

A condition where the heart is unable to pump the blood that arrives at the heart

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11
Q

What is CHF caused by?

A
  1. Myocardial infarction
  2. Age
  3. valve problems
  4. coronary artery disease
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12
Q

Does CHF hurt like an MI?

A

No. Painful, but different.

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13
Q

If the heart can’t pump enough blood…Kidneys:

A

Build up of waste in blood

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14
Q

If the heart can’t pump enough blood…brain

A

disorientation/lack of concentrating

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15
Q

If the heart can’t pump enough blood…Lungs

A

SOB, gasping on exertion, drowning in own fluid

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16
Q

If the heart can’t pump enough blood…cells

A

slowing of cellular processes

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17
Q

If the heart can’t pump enough blood…heart muscle

A

poorer and poorer pumping

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18
Q

hearts reaction to lack of blood in vital organs is to _________ to try to pump faster and “keep up”

A

increase HR

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19
Q

As the cardiac muscles get less rest between beats, the ___ & ___ are lost from the cells, then…

A

Na+ & Ca2+

then eventually there are no effective beats as this issue compounds on itself to get worse

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20
Q

Cardiac Glycosides act by:

A

Inhibiting the Na+/K+ pump and increasing the sodium and calcium in the myocardial cells. Which slows and strengthens the heart’s pumping ability.
(affects phase 3)

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21
Q

Positive inotropic effect

A

Increased force of the contraction

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22
Q

Negative Chronotropic effect

A

decreases heart rate

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23
Q

Negative Dromotropic effect

A

Delays impulse from SA node to AV node

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24
Q

Once cardiac glycosides are taken…

A
  • Decrease in waste buildup
  • Increased mental alertness
  • Better breathing
  • Better oxygen to cells
  • More blood to heart muscle itself
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25
Q

Side effects of cardiac glycosides

A
  • very narrow therapeutic level
  • easy to become toxic
  • requires constant monitoring of blood levels
  • women complain of SEVERE vaginal dryness (K jelly)
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26
Q

S/S of toxicity cardiac glycosides

A
  1. arrhythmia
  2. GI upset/diarrhea
  3. change in vision (yellow halo around lights); very late sign
  4. headache
  5. high K+ level (monitor!!)
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27
Q

medication to counter cardiac glycoside toxicity

A

Digibind

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28
Q

cardiac glycosides are the main treatment for…

A

CHF

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29
Q

Digoxin (Lanoxin)

A

cardiac glycoside

  • very strong action
  • very narrow therapeutic window
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30
Q

nursing considerations for cardiac glycosides

A
  1. take apical pulse for full 60 s
  2. ensure good perfusion – do not give Digoxin if HR < 60; not mentating; low BP; not urinating
  3. do not switch brands, miss or double a dose
  4. don’t give with antacids or milk (decreases action)
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31
Q

IRL consideration vs NCLEX consideration of grapefruit juice and Digoxin (cardiac glycosides)

A

IRL: do not give with grapefruit juice

on NCLEX: it’s fine to give with grapefruit juice

(research is conflicting; IRL, err on the side of caution)

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32
Q

Antidysrhythmic agents are given to patients with…

A

slow, fast, or otherwise irregular rhythms

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33
Q

class 1 antidysrhythmics

A

“membrane stabilizing agents”

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34
Q

effect of Class 1 Membrane Stabilizing Agents (phase it affects and how)

A
  • slows electrical conduction of the heart by blocking fast Na+ channels
  • prolongs Phase 0
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35
Q

when to use membrane stabilizing agents

A
  • fast heart conduction problems

- when AV node is not communicating with SA node

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36
Q

what do membrane stabilizing agents treat

A

tachycardia, fibrillation, premature ventricular contractions

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37
Q

membrane stabilizing agents S/E (side effects)

A
  • stomach upset
  • headache
  • dizziness
  • blurred vision
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38
Q

S/S of membrane stabilizing agent toxicity

A

exaggerated action of the desired effect (bradycardia, hypotension, cardiac arrest)

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39
Q

interactions of membrane stabilizing agents

A

grapefruit juice and Quinidine (DO NOT MIX) and Warfarin (thrombolitic – monitor levels)

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40
Q

specific membrane stabilizing agents to remember

A

Quinidine (PO) and Lidocaine (IV)

both decrease cells’ sensitivity to impulses

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41
Q

class 2 of antidysrhythmic agents

A

beta-blockers

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42
Q

beta-blocker effects

A
  • blocks sympathetic nervous system stimulation of the heart (blocks beta1 and beta2 receptor sites in heart and lungs)
  • prevents catecholamine stimulation of the heart
  • makes heart harder to stimulate out of phase 4 (resting phase)
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43
Q

catecholamine

A

epinephrine and norepinephrine

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44
Q

effects of beta-blockers

A
  • negative chronotropic effect

- negative dromotropic effect

45
Q

beta-blockers also treat…

A
  • HTN

- chest pain

46
Q

Propranolol (Inderal)

A

beta-blocker medication (note “olol” ending)

47
Q

class 3 of antidysrhythmic medications

A

no specific name

48
Q

class 3 effects

A

decrease excitability of the heart – blocks the reeptors of the sympathetic nervous system

49
Q

class 3 uses

A

very effective with ventricular tachycardia and some atrial tachycardia

50
Q

class 3 cautions (side effects)

A

have many side effects…

  • can harm the thyroid gland, vision, and alveoli
  • long half-life; side effects take a long time to go away
51
Q

Amiodarone

A 
class 3 cardiac glycoside medication
(PO and IV)
52
Q

corvert (ibutilide)

A

class 3 cardiac glycoside

  • chemical cardioverter
  • immediate change in HR
  • MD should be present before administering
  • can’t be given within 4 hrs of Class 1 or Class 3 meds
53
Q

class 4 medications

A

calcium channel blockers

54
Q

calcium channel blocker effects (phase and what part of the heart it affects)

A
  • slow the inward flow of Ca2+ ions into atria and AV node
  • no effect on ventricles
  • works primarily on phase 2
55
Q

calcium channel blockers uses

A
  • treat atrial flutter and fibrillation

- also used to treat HTN and chest pain

56
Q

calcium channel blockers side effect

A

decreased blood psi

57
Q

calcium channel blocker medications to remember

A

Verapamil (Calan)

Diltiazem (Cardizem)

58
Q

Important info for all antidysrhythmic meds

A
  • do not miss or double dose
  • check pulse; do not admin if <60
  • watch for signs of v. low BP
  • monitor INR levels
59
Q

Chest pain/angina is caused by…

A

ischemia to the heart muscle

60
Q

physiology behind angina

A

1) atherosclerotic plaques in coronary arteries (usually no pain until 70-90% clogged)
2) spasm of coronary arteries (irritated walls “pinch” together)

buildup of plaques or recurrent spasm leads to lack of O2 and nutrients for the heart to pump adequately

61
Q

3 classifications of medications used to treat chest pain

A
  1. nitrates (anti-anginal)
  2. beta blockers
  3. calcium channel blockers
62
Q

Nitrates effects

A
  • dilates all blood vessels, but primarily coronary arteries

- pools blood in venous system (takes work off heart, increases blood flow to myocardium

63
Q

S/E of nitrates

A
  • increased HR
  • decreased B/P
  • HA (common)
  • flushing
  • dizziness
64
Q

contraindication of nitrates

A

do not take with ED meds (both drop BP)

65
Q

Nitroglycerin

A

nitrate

  • cannot be taken PO (destroyed by liver)
  • sublingually for angina attacks
  • IV and spray options
  • long term – patch or paste on skin changed q24h
  • monitor BP
66
Q

beta blockers (chest pain version) effects

A
  • slows HR, decreases contractility
  • decreases oxygen demand and helps conserve energy of heart muscle
  • blocks beta receptors of the heart so catecholamines cannot stimulate the heart
67
Q

s/e of beta blockers (chest pain)

A
  • fatigue and lethargy
  • constipation
  • depression
    (mostly in elderly; admin at bedtime to avoid these)
68
Q

why should you monitor diabetics taking beta blockers?

A

may mask tachycardia associated w low blood sugar

69
Q

contraindications for beta blockers

A
  • asthma (narrows bronchioles)
  • CHF (exceptions - carvedidol and metoprolol XL)
  • avoid abrupt discontinuation of beta blockers
70
Q

what else are beta blockers used to treat?

A

HTN, chest pain, and helping the heart rest after MI

71
Q

beta blocker meds for angina

A

Metoprolol (lopressor)

Atenolol (tenormin)

72
Q

calcium channel blockers effects for angina

A
  • reduces cardiac contractility
  • dilates peripheral arteries (Relaxing smooth muscle)
  • esp effective on coronary artery soasms
73
Q

calcium channel blockers are also used for the treatment of…

A

HTN and migraine HAs

74
Q

calcium channel med for angina

A

Nifedipine (v. rapid fx on BP)! often given sublingually

75
Q

HTN

A

BP of over 140/90 for a prolonged period of time

76
Q

pre-hypertension

A

120-140/80-90 (start getting treatment before heart damage)

77
Q

formula for bp

A

cardiac output x systemic vascular resistance = blood pressure

78
Q

types of hypertension

A
  1. essential/primary HTN (no known cause)

2. secondary HTN (cause known; e.g. renal, pregnancy)

79
Q

6 categories of antihypertensives

A
  1. beta-blockers
  2. calcium channel blockers
  3. centrally acting adrenergic agents
  4. angiotensin-converting enzyme inhibitors (ACE inhibitors)
  5. angiotensin II receptor blockers (ARBs)
  6. diuretics
80
Q

centrally acting adrenergic agent actions

A
  • decrease stimulation by the sympathetic nervous system
  • work by stimulating alpha2 receptros which…
    a) negative chronotropic
    b) negative inotropic
    c) dilating blood vessels
    d) stopping secretion of renin
81
Q

renin

A

potent vasoconstrictor made by kidneys; increases vascular resistance

82
Q

S/E of centrally acting adrenergic agents

A

bradycardia

orthostatic hypotension

83
Q

clonidine (catapress)

A

centrally acting adrenergic agent

PO, patch

84
Q

ACE inhibitors effects

A
  • inhibits angiotensin converting enzyme of kidneys
  • this blocks production of angiotension II (vasoconstrictor) and aldosterone (retains H2O and Na+)
  • decreases afterload (decreasing vascular resistance)
  • decreases preload (decreasing blood volume)
85
Q

ACE inhibitors S/E

A
  • dry cough (most common; irritating but not lethal)
  • hypotension
  • dizziness
  • avoid high levels of potassium – monitor
86
Q

ACE inhibitors examples

A

Captopril (capoten)

Enalapril (vasotec)

87
Q

ARBs effect

A
  • blocks action of angiotensin (can still be formed even if ACE inhibitors are used)
  • affects smooth muscle and adrenal glands
  • block vasoconstriction and aldosterone secretion
88
Q

ARBs S/E

A

URI (upper respiratory infection) and HAs (headaches)
hypotension
monitor potassium levels

89
Q

ARB medication

A

Losartan (Cozaar)

- does not cause dry irritating cough

90
Q

diuretics

A

accelerate urine formating by stimulating the nephron

91
Q

types of diuretics

A

a) loop diuretics
b) osmotic diuretics
c) potassium sparing diuretics
d) thiazides

92
Q

loop diuretic actions

A
  • block Na+ and Cl- absorption at loop of Henle
  • this decreases the vascular volume
  • works rapidly and strongly or about 2 hrs
  • wastes potassium and can cause dehydration;
  • can also cause permanent deafness; give <10mg/min if giving IV push (ICU)
93
Q

loop diuretic uses

A
  • decreases edema
  • help with CHF
  • control HTN
94
Q

loop diuretic example

A

Furosemide (Lasix)

95
Q

osmotic diuretic actions

A
  • inhibit reabsorption of water and solutes; causes reapid diuresis
  • wastes electrolytes and can cause dehydration
96
Q

osmotic diuretic uses

A
  • increase excretion of toxic substances (OD)

- reduce intracranial psi and cerebral edema

97
Q

osmotic diuretic example

A

Osmitrol (Mannitol)

98
Q

Potassium sparing diuretic actions

A
  • excrete Na+ and H2O, but retains K+

- weak overall diuretic, but can be used when there is concern about K+ availability to the heart

99
Q

potassium sparing diuretic example

A

Spironolactone (Aldactone)

100
Q

thiazides action

A
  • loss of H2O, Cl-, Na+, K+
  • not good to take if renal blood flow poor
  • can cause electrolyte deficiencies
  • very inexpensive, often used in combo w other diuretics
  • PO only
101
Q

thiazide example

A

hydrochlorothiazide (HCTZ)

102
Q

antiocaogulants action

A

inhibits the clotting of blood by blocking coagulation pathway, binding with substance or blocing an action

103
Q

anticoagulant uses

A

prevents clot formation

104
Q

S/E of anticoagulants

A
  • uncontrolled bleeding; no clotting when needed (hemorrhage)
105
Q

3 anticoagulant meds

A
  1. heparin (SQ or IV; antidote = protamine sulfate)
  2. lovenox (low mol. weight heparin; lasts longer, easier to absorb)
  3. warfarin sodium (coumadin) (PO, IM; antidote is Vit K)
106
Q

antilipidemics

A

HMG-CoA-Reductase inhibitors = statins

107
Q

statin action

A
  • decreases blood chol. by decreasing rate of chol prod by the liver (blocks an enzyme)
  • fewer LDLs, more HDLs
108
Q

statin side effects

A

few other than body aches

109
Q

statin example

A

atorvastatin (lipitor)

NRSG 213 (9 decks)

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