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NURS 2500 > Class 20: Intro to CAD > Flashcards

Class 20: Intro to CAD Flashcards

1
Q

what should be asked during the health interview for CVS assessment

A
  • Hx of heart problems, surgeries, meds, etc.
  • family Hx
  • personal habits
  • comorbid disease?
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2
Q

what is another word for chest pain

A
  • angina
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3
Q

what is angina a sign of

A
  • cardiac tissue ischemia –> decreased blood flow
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4
Q

what can angina be described as

A
  • tightness
  • squeezing
  • pressure
  • clenched fist
  • crushing
  • elephant on chest
  • sense of impending doom
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5
Q

how can we distinguish from pleuritic pain, muscular chest wall pain, gastric upset, and angin?

A
  • pleuritic pain: follows breathing pattern
  • gastric upset/gallbladder: go away with antacid
  • angina: does not change w breathing, can be brought on by exertion and relieved w rest
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6
Q

what are some questions to ask regarding angina?

A
  • OPQRSTU
  • brought on by activity? relieved w rest?
  • associated symptoms?
  • referred or radiating pain?
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7
Q

what are some associated symptoms w angina?

A
  • sweating/diaphoresis
  • pale/ashen grey
  • heart skipping a beat
  • heart fast or slow
  • SOB
  • N&V
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8
Q

how come SOB is associated w angina

A
  • compensation for decreased blood flow & O2 to tissues
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9
Q

what causes the associated symptoms of angina

A
  • visceral pain in ischemic heart

- SNS/PSNS stimulation

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10
Q

where might you feel radiated pain w angina?

A
  • lower jaw (NOT upper)
  • midsternal
  • left should
  • down both arma
  • neck
  • epigastric
  • intrascapular
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11
Q

how come radiated pain occurs with angina?

A
  • nerve impulses from the heart and other places get mixed up in the spine
  • this causes the pain to misinterpret where the pain is
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12
Q

how is angina graded

A

4 classes

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13
Q

describe class 1 of angina

A
  • angina not caused by ordinary physical activity
    ex. walking, climbing stairs
  • angina occurs with strenuous, rapid, and prolonged exertion
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14
Q

describe class 2 of angina

A
  • slight limitation of normal activity
  • occurs when walking or climbing stairs rapidly
  • walking uphill
  • walking or climbing stairs after meals
  • in cold, wind, or under emotional stress
  • during few hours after awakening
  • walking 2 blocks on level
  • climbing more than 1 flight of ordinary stairs at normal pace
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15
Q

describe class 3 of angina

A
  • marked limitations of physical activity
  • walking 1 or 2 blocks on level
  • climbing 1 flight of stairs under normal conditions & at normal pace
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16
Q

describe class 4 of angina

A
  • inability to carry on any physical activity without discomfort
  • may be present at rest
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17
Q

describe dyspnea r/t CVS assessment

A
  • SOB
  • SOBOE or at rest
  • what type of activity brings it on
  • how does it affect ADLs
  • paroxysmal nocturnal dyspnea = awaken at night, occurs w heart failure
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18
Q

what is orthopnea? what are indicators of it

A
  • SOB when lying down
  • causes inability to sleep flat
  • ask if the number of pillows they sleep w at night has changed
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19
Q

describe cough r/t CVS assessment

A
  • productive?
  • dry?
  • hacking?
  • hemopytsis? (pulmonary disorder)
  • what meds? ACE inhibitor can have side effect of cough
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20
Q

describe fatigue r/t CVS assessment

A
  • recent change?
  • affect ADLs?
  • walk stairs?
  • 6 min walk test
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21
Q

what causes cyanosis or pallor?

A
  • cyanosis = lack of oxygenation
  • pallor = anemia or vasoconstriction of blood vessles
  • both occur with MI & low CO
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22
Q

describe edema r/t CVS assessment

A
  • dependent when caused by heart failure
  • bilaterial if cardiac
  • gets better w elevation
  • can be peripheral, pulmonary, or abdominal
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23
Q

describe nocturia r/t CVS assessment

A
  • if have to awaken at night with urgency to void

- occurs w HF

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24
Q

describe auscultation of the carotid arteries

A
  • assess for bruit (swooshing sound)

- press lightly

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25
Q

describe palpation of the carotid artery

A
  • avoid carotid sinus –> can cause vagul stimulation = slowed down HR
  • do not do simultaneousloy
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26
Q

why is the carotid artery important

A
  • yields important info about cardiac function
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27
Q

what does jugular venous pressure tell us

A
  • fluid gage

- can tell us about central venous pressure

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28
Q

what should the jugular vein look like normally

A
  • should be flat

- distended = build up of fluid

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29
Q

what is hepatojugularr eflux test

A
  • do if venous pressure is elevated or suspect HF
  • push in the right upper quadrant on abdomen
  • if heart functioning normal, will pump out this additional volume = jugular vein rises for few seconds then recedes
  • if HF is present, jugular vein will stay elevated entire time
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30
Q

what is a heave or lift

A
  • sustained forceful thrusting of ventricle during systole

= visible at the sternal border or apex

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31
Q

what is the PMI

A
  • point of maximal impulse

- AKA the apical impulse (if normal)

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32
Q

what is a thrill

A
  • palpable vibration
  • feels like purring cat
  • signifies turbulent flow & often accompanies murmurs
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33
Q

what are the S1 and S2 heart sounds

A
  • S1 = mitral & tricupsid valve closing = beginning of systole = beginning of systole
  • S2 = aortic & pulmonic valve closing = beginning of diastole
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34
Q

what is the splitting of S2

A
  • normal
  • occurs toward end of inspiration
  • occurs when aortic & pulmonic valve do not close together
    = T-DUB sound
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35
Q

what is a murmur

A
  • blowing, swishing sound

- occurs with turbulent blood flow

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36
Q

what is the S3 heart sound

A
  • ventricular gallop
  • heard after S2
  • LUB DUB-T
  • sound of blood hitting the ventricles
  • can be due to volume overload or HF
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37
Q

what is the S4 heart sound

A
  • atrial gallop
  • before S1
  • T-LUB DUB
  • due to atria trying to push blood into resistant ventricles
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38
Q

what is hyperlididemia

A
  • condition of having too many lipids in the blood
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39
Q

why is hyperlipidemia problematic

A
  • high amounts of specific lipids can cause atherosclerosis
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40
Q

what is astherosclerosis

A
  • hardening, occlusion, or damage to the arteries
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41
Q

what can atherosclerosis lead to

A
  • CAD
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42
Q

what are the 3 types of serum lipids

A
  1. cholestrol
  2. triglycerides
  3. phospholipids
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43
Q

what is cholestrol

A
  • steroid used in plasma membranes to build vit D, bile acids, cortisol, estrogen, and testosterone
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44
Q

what are lipoproteins? why are they important?

A
  • lipid carrying proteins

- imp bc water insoluble fats (such as cholestrol) must be bound to apolipoproteins

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45
Q

what are the different types of lipoproteins? which are good vs bad>

A
  1. high density lipoproteins = good
  2. very low density lipoproteins = bad
  3. low density lipoproteins = bad
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46
Q

what do LDLs do`

A
  • carry cholestrol from liver to other tissues

- major carrier of cholestrol

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47
Q

what do HDLs do

A
  • returns excess cholestrol to the liver
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48
Q

what do high levels of LDL cause

A
  • associated w cholestrol plaque build up & cardio diseases
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49
Q

what are triglycerides

A
  • lipid stored in the body as a source of energy
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50
Q

how do triglycerides contribute to the development of CAD

A
  • when body is in fasting state, they are bound to VLDL
  • inceased triglyceride level = increased risk of CAD
  • increased levels cause LDL particles to become more atherogenic
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51
Q

how do HDL contribute to CAD

A
  • low levels = increased risk
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52
Q

what can cause increased triglyceride & LDL levels

A
  • obesity
  • inactivity
  • diabetes
  • increased alcohol intake
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53
Q

what are phospholipids

A
  • lipids used for plasma membranes

- not used as a clinical indicator for hyperlipidemia in the context of atherscleritis disease

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54
Q

what is the primary risk factor for atherosclerotic disease

A
  • elevated LDL
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55
Q

why are LDLs the primary risk factor for atherosclerotic disease

A
  • deposit cholestrol in vessel walls for storage

- strongly associated w plague formation & PAD/heart disease

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56
Q

what do low HDL levels cause

A
  • less removal of cholestrol from the vessels
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57
Q

what is the goal for lipid levels

A
  • maximize HDL

- minimize LDL <2.5 mmol/L

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58
Q

what is total cholestrol? what is the target range

A
  • ratio of total cholestrol in blood

- want to be less than 4.0

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59
Q

what are optimal triglyceride levels

A
  • 1.7 mmol/L
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60
Q

describe the transpot of lipids

A
  • lipids are hydrophobic = problem because they need to get into the blood
  • to be transported, they are put into lipoproteins
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61
Q

describe the structure of lipoproteins

A
  • fat surrounded by proteins
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62
Q

what do VLDLs do?

A
  • transport lipids from liver to body cells

- contain high levels of triglycerides

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63
Q

what do high VLDLs indicate

A
  • high levels of TG = increased risk of CAD
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64
Q

what is ischemic pain in the heart called

A
  • angina
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65
Q

how do supply & demand affect angina

A
  • narrowing of blood vessels = decreased supply of O2 and blood
  • activity = increased demand for O2 and blood
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66
Q

how does rest affect demand

A
  • rest reduces demand = pain goes away
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67
Q

what is a primary mechanism for narrowing of arteries

A
  • development of atherosclerosis in the arteries
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68
Q

what is atherosclerosis

A
  • changes in the vessel wall that lead to thickening & plague formation in the vessel wall
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69
Q

what can narrowing of the vessel wall lead to

A
  • can trap small arterial emboli, that cause further/fast blocking of blood flow & greater ischemia to distal (down stream) tissue
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70
Q

how does hypertension r/t atherogenesis

A
  • causes increased pressure = injure vessel wall & start inflammatory process
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71
Q

how does high cholestrol r/t atherogenosis

A
  • provides material needed to develop the plagues
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72
Q

what are the developmental stages of atherosclerosis

A
  1. fatty streak
  2. fibrous plague
  3. complicated lesion
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73
Q

describe the stage of fatty streak

A
  • damaged endothelium = increased permeability of wall = lipids accumulate and migrate into sm. m cells
  • yellow tinge
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74
Q

what may cause endothelial damage

A
  • hypertension
  • high cholestrol
  • hyperlipidemia
  • smoking
  • obesity
  • diabetes
  • infections
  • toxins
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75
Q

what forms a fibrous plague

A
  • collagen covers the fatty streak
    = vessel lumen narrowed = blood flow reduced
  • may form a fissure
  • fibrous plague = grey or white
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76
Q

describe a complicated lesion

A
  • plague ruptures = thrombus formation = further narrowing or total occlusion of vessel
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77
Q

what is collateral circulation

A
  • when the body creates new circulation in the heart around a blockage
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78
Q

what can cause collateral circulation

A
  • atherosclerosis
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79
Q

what 2 factors contribute to the growth & extent of collateral circulation

A
  • inherited predisposition to develop new blood vessels (angiogenesis)
  • presence of chronic ischemia
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80
Q

how does chronic ischemia lead to collateral circulation

A
  • when an occlusion of a coronary artery occurs slowly over time, there is greater chance of developing collateral circulation = allows myocardium to recieve an adequate intake of O2
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81
Q

what causes where atherosclerotic plaques form

A
  • forms wherever they are the most stressed

- typically bending & branching points

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82
Q

what is the current theory for the development of atherosclerosis

A
  • plaque formation involves an inflammatory event stimulated by vessel wall injury
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83
Q

what are 2 ways the intima of an artery can become injured

A
  1. mechanical stress

2. oxidative stress

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84
Q

what is mechanical stress

A
  • high bp

- high viscosity

85
Q

what is oxidative stress

A
  • high levels of reactive oxygen species which damage cell structures
86
Q

what are ROS

A
  • reactive chemicals containing O2
87
Q

what is associated with increased production of ROS

A
  • hyperlipidemia

- hyperglycemia

88
Q

how do ROS damage the artery wall

A
  • oxidize LDL
89
Q

what is superoxide

A
  • type of ROS

- O2-

90
Q

what does superoxide do

A
  • destroys nitric oxide which has protective mechanisms on arteries bc it causes vasodilation
91
Q

how do phagocytes affect the artery wall

A
  • produce superoxide during inflammation

- when the vessel wall is damaged the inflammatory response brings WBCs to the area

92
Q

describe macrophages r/t to oxidized LDL

what happens when they die?

A
  • consume the oxidized LDL

- macrophages die & become lipid filled foam cells that form a bulge in the side of the artery wall = plaque

93
Q

describe how inflammation forms plaque r/t oxidative stress

A
  • vessel wall damaged = inflammation
  • inflammation brings WBCs to the area
  • phagocytes produce superoxide when oxidize LDL
  • oxidized LDLs are consumed by macrophages
  • macrophages die & become lipid filled foam cells & form a bulge = plaque
94
Q

what is coronary artery disease

A
  • condition where blood vessels that supply the heart muscle w blood (coronary arteries) become narrowed due to plaque in the artery wall
    = prevent blood flow
95
Q

what is a myocardial infarction

A
  • heart attack
96
Q

what causes a myocardial infarction

A
  • when the blood supply to an area of the heart is interrupted due to blocked coronary arteries
  • causes myocardial tissue to die or become necrosis
  • caused by CAD
97
Q

describe the damage to heart muscle: is it temp? permanent? what does this mean

A
  • will be permanently damaged
  • heart muscle does not have the ability to regenerate
    = heart will not able to function properly
98
Q

what is cardiac arresr

A
  • when the heart stops pumping completely
  • medical emergency
  • after recovery may develop heart failure
99
Q

what is heart failure

A
  • heart cannot pump blood properly
100
Q

symptoms of heart failure

A
  • sob
  • edema
  • fatigue
101
Q

what is the end result of CAD

A
  • myocardial infarction

- cardiac arrest

102
Q

define atherosclerosis

A
  • formation of plaque that causes narrowing or blockage of the blood vessels
103
Q

what is the difference between CAD and atherosclerosis

A
  • CAD = specifically refers to athero in the coronary arteries
  • atherosclerosis = general term that describes a condition that can affect anywhere in the body
104
Q

how can atherosclerosis cause an MI

A
  • plaque that forms can rupture forming a blood clot

- this can get lodged in the coronary arteries

105
Q

what does a blood clot in the brain cause

A
  • stroke
106
Q

is CAD progressive or sudden

A
  • progressive
107
Q

what are the 2 types of risk factors for CAD

A
  1. nonmodifiable

2. modifiable

108
Q

what are nonmoodifiable risk factors for CAD

A
  • increasing age
  • sex (men > women until 65 y.o)
  • ethnicity (white> black)
  • genetic predisposition
  • family history of heart disease
109
Q

what are the major modifiable risk factors of CAd

A
  • serum lipid alteration: high LDL, triglyc & low HDL
  • high bp: >140/90
  • DM
  • tobacco use
  • physical inactivitiy
  • obesity
110
Q

what is defined as obesity

A
  • waist circumference >102 in men

- >88cm women

111
Q

what are contributing modifiable risk factors for CAD

A
  • fasting blood glucose >10 mmol/L
  • psychosocial factors
  • elevated homocysteine levels
112
Q

what psychosocial factors contribute to CAD

A
  • depression
  • hostility
  • anger
  • stress
113
Q

compare risk factors for atherosclerosis in the heart & PVS

A
  • the same
114
Q

what is the Framingham Risk tool

A
  • tool that provides an estimation of 10 year risk of CAD
115
Q

describe supply & demand of the heart in normal conditions

A
  • normally, the amount of blood delivered to the heart via coronary artiers matches the myocardial o2 demand
116
Q

what determines the heart’s demand

A
  • heart rate
  • contractility
  • preload
  • afterload
117
Q

what does it mean if the lumen size is reduced to 75%

A
  • ischemia can occur during times of elevated myocardial o2 demand
    ex. physical activity, emotional stress, hot or cold exposure, large meal
118
Q

what occurs if the lumen size is reduced to 90%

A
  • ischemia can occur at rest
119
Q

describe supply & demands role in ischemia

A
  • ischemia can be caused by icnreased demand or decreased supply or both
120
Q

how long does it take for the myocardium to become hypoxic on a cellular level?

A
  • within the first 10 sec
121
Q

contractility stop after ____ min with total occlusion

A

several

122
Q

what occurs when the myocardium becomes hypoxic? what does this cause?

A
  • anerobic metabolism
    = lactic acid accumulates
    = pain fibers stimulated
    = cross over = referred pain, specifically to left shoulder & arm
123
Q

how long does it take for cardiac cells to die

A
  • 20 min
124
Q

what happens to cardiac cells if blood flow returns in time

A
  • process reverses & contracility is restored

- repair begins

125
Q

what might cardiac ischmemia result in (5 things)

A
  1. diastolic dysfunction
  2. systolic dysfunction
  3. electrical disturbance in heart rhythmn
  4. angina pectoris
  5. cardiac muscle death = MI
126
Q

what is diastolic dysfunction

A
  • muscle becomes stiff = reduced muscle relaxation & filling
    = reduced preload = reduced SV, CO, and BP
127
Q

what is systolic dysfunction

A
  • failure of heart to properly contract = decreased contracility
    = reduced SV, CO, BP
128
Q

how do electrical disturbances occur as a result of cardiac ischemia

A
  • conduction moves around ischemic tissue
  • or heart muscle is irritable
    = ECG changes, irregular pumping, ineffective pumpin
  • brady and tachy = altered CO
129
Q

what causes angina pectoris

A
  • visceral pain from cardiac muscle ischemia
130
Q

what can cause high blood viscosity

A
  • polycythemia

- hyperglycemia

131
Q

how does tobacco use cause endothelial injury

A
  • effect platelet agg
132
Q

what is hyperhomocysyteinemia? what can it cause?

A
  • high homocysyteine
  • linked to inflammation
    = endothelial injury
133
Q

how does diabetes cause endothelial injury

A
  • creates thicke blood = mechanical stress
134
Q

how do infections & toxins cause endothelial injury

A
  • trigger inflammation
135
Q

when will we open a blockage

A
  • only if 75% or greater
136
Q

what do free radicals of o2 cause

A
  • steal protons or electrons from healthy cells = destabilize the cells = cell death
    ex. superoxide can do this
  • also elicit the inflammatory resposne
137
Q

what can cause increased ROS

A
  • hyperlipidemia

- hyperglycermia

138
Q

what does increased triglyceride cause

A
  • causes LDLs to become more atherogenic
139
Q

why do low HDL cause risk of athersclerosis

A
  • provides less removal of cholestrol from the vessels
140
Q

what is the total cholestrol ratio

A

total cholestrol: HDL cholestrol

- want to be <4.0

141
Q

what age groups should be screened for CAD

A
  • men > 40

- women > 50 or postmenopausal

142
Q

people with which conditions should be screened for CAd

A
  • smoking
  • diabetes
  • HTN
  • family history of hyperlipid or premature CVD
  • erectile dysfunction
  • chronic kidney disease
  • inflammatory disease
  • HIV infection
  • obesity (BMI > 27)
  • manifestations of hyperlipid
  • clinical evidence of atherosclerosis
143
Q

what does a framingham risk score of <5% mean? > 5%

A
  • <5 = repeat every 3-5 years

- >5% = repeat every year

144
Q

what tests should be run for screening for CAD

A
  • history
  • examination
  • LDL, HDL, TG levels
  • glucose
  • GFR
145
Q

what does an increased in BUN or Cr mean

A
  • decreased kidney function
146
Q

what are antilipemic drugs? what are they used as an adjunct with?

A
  • drugs used to lower lipid levels

- used as an adjunct to diet therapy

147
Q

what influences drug choice for antilipemic

A
  • based on the specific lipid profile of the pt
148
Q

what are the classes of antilipemic

A
  • HMG-CoA reductase inhibitors (HMGs or statins)
  • bile acid resins
  • nicotinic acid
  • fibric acid derivatives (fibrates)
  • misc.
149
Q

what drugs are the most potent LDL reducers

A
  • statins (HMG-CoA Reductase inhibitors)
150
Q

what is the MOA of statins

A
  • inhibit HMG-CoA reductase (enzyme)
  • this enzyme is used by the liver to produce cholestrol = reduced cholestrol production
  • causes liver to produce more LDL receptors on surface of liver = collect more LDL = less circulating in blood
151
Q

what do statins result in

A
  • decreased LDL and TG

- increased HDL

152
Q

what are statins the first line drug therapy for

A
  • hypercholesterolemia
153
Q

what are 2 types of statins

A
  • atorvastatin (lipitor)

- simvastatin (zocor)

154
Q

what types of hyperlipidemias do statins work on

A
  • type 2a
  • type 2b
    = familial or genetic
155
Q

how do statins effect LDL

A
  • decreases by 30-40%
156
Q

how statins effect HDL

A
  • increased by 2-15%
157
Q

how statins effect TG

A
  • reduced by 10-30%
158
Q

how long must statins be taken for

A
  • take for lifetime

- or until diet/lifestyle changes permanently lower cholestrol levels

159
Q

when is most cholestrol produced? how does this effect med administration?

A
  • most produced at night

= short acting lovastatin must be taken hs

160
Q

what is a drug interaction w statins

A
  • grapefruit
161
Q

what are adverse effects of statins

A
  • myopathy (muscle pain) & muscle breakdown lead to
  • rhabdomyolysis
  • rash
  • mild GI symptoms
  • elevated liver enzymes or liver disease= avoid with liver dysfunction
  • insomnia
  • lens opacities
162
Q

what is rhabdomyolysis? what can it lead to?

A
  • breakdown of skeletal muscle

- may lead to renal failure due to blockage of kidneys by myoglobin

163
Q

why should serum CK levels by monitored when taking statins?

A
  • monitor for rhabdomyolysis

- product of muscle damage

164
Q

what liver enzymes are increased with statins

A
  • LDH

- lactate dehydrogenase

165
Q

describe nursing considerations with statins

A
  • monitor w eye exams
  • monitor liver function tests
  • monitor serum CK levels
166
Q

what is the MOA of bile acid resins

A
  • in small bowel, binds to bile acids containing dietary cholestrol to form insoluble complex
  • prevent absorption
    = increased bowel excretion of cholesterol
167
Q

what is a type of bile acid resins

A
  • cholestyramine (questran)
168
Q

why are bile acid resins not first line

A
  • adverse effects
169
Q

what are bile acid resins used for

A
  • relief of pruritus associated w partial biliary obstruction
  • may be used along w statins
170
Q

what are side effects of bile acid resins

A
  • unpleasant gritty taste
  • GI disturbances (nausea, dyspepsia, constipation, belching)
  • may cause increase in TG levels
171
Q

what are nursing considerations regarding bile acid resins

A
  • avoid other meds/vit 1h before and 4 hr after (bc will bind & excrete them)
  • adverse effects diminish with time
  • take with lots of water to help w GI upset
172
Q

what meds do bile acid resins interact w

A
  • digoxin
  • thiazides
  • B blockers
  • fat soluble vitamins
  • folic acid
  • vanocmyosin
173
Q

what is a type of nicotinic acid

A
  • nicotinic acid = niacin, vit B3
174
Q

what is the MOA of nicotinic acid

A
  • inhibit synthess & secretion of VLDL and LDL

- enhances HDL

175
Q

how does nicotinic acid effect lipid level

A
  • reduced VLDL = reduced LDL
  • reduced TG levels
  • increases HDL
176
Q

describe the dose required for niacin

A
  • lipid-lowering properties require much higher doses than when used as a vitamin
177
Q

describe the use of niacin

A
  • effective
  • inexpensive
  • often used in combo w other lipid-lowering drugs
178
Q

what are the adverse effects of niacin

A
  • histamine release = hot flashes, flushing, pruritis in upper torso & face
  • GI upset
  • hepatotoxicity
  • gout
  • hyperglycemia in diabetes
179
Q

what are nursing considerations regarding niacin

A
  • most adverse effects subside w time
  • decreased liver function & arrthymias may occur w high doses
  • aspirin 30 min to 1 hr before niacin may reduce flushing
  • taken w food
180
Q

what is a type of fibric acid derivitative (fibrate)

A
  • gemofibrozil (lopid)

- fenofibrate (lipidil)

181
Q

what is the MOA of fibrates

A
  • decrease TG by decreasing VLDL
  • suppress release of free FA from adipose tissue
  • may elevate HDL levels
182
Q

what are adverse effects of fibrates

A
  • GI upset & cramping
  • increased risk of gallstones
  • increase effect of warfarin & anticoagulants & hypoglycemics
  • liver studies may show increased function
183
Q

what are nursing considerations for fibrates

A
  • monitor PT/INR (bc of effect on warfarin & anticoagulants)
184
Q

what are misc agents from antilipemics

A
  • cholestrol absorption inhibitor
  • omega-3 FA
  • orlistat
185
Q

what are cholestrol absorption inhibitors

A
  • inhibit abs of cholesterol & related sterols from the SI
    = reduced total cholesterol, LDL, and TG
  • increased HDL
  • often combined w statins
186
Q

what is a type of cholesterol absorption nhibitors

A
  • ezetimibe (Zetia)
187
Q

what do omega-3 FA do

A
  • decrease CAD
188
Q

what are types of omega-3 FA

A
  • tuna
  • salmon
  • halibut
  • flaxseed
  • soybeans
  • walnuts
  • pumpkin seeds
189
Q

what is the MOA of orlistat

A
  • prevents ab of TG

- may promote weight loss & lower LDL

190
Q

what are side effects of orlistat

A
  • oily fecal spotting
  • oily stools
  • flatulence
  • urgency
  • pain
191
Q

describe the decision tree used to determine how to manage cholestrol

A
  1. assess LDL-C and total CV risk
    - indication for drug treatment?
    - if yes = define LDL-C target & give statin
  2. LDL-C target reached?
    - yes = stay
    - no = consider adding ezetimibe
  3. LDL-C target reached?
    - no = consider PCSK9 inhibitor
    - or consider bile acid sequestrant
192
Q

what are 3 basic cardiac diagnostic studies

A
  1. 6 min walk test
  2. stress-exercise test
  3. angiogram
193
Q

describe a 6 minute walk test

A
  • sees how far the pt can walk in 6 min

- also see if they have any chest pain, SOB

194
Q

describe the stress-exercise test

A
  • pt on treadmill or bike
  • put ECG leads, gradually increase resistance & look at ECG for signs of ischemia
  • if cant get on treadmill or bike = stress heart with drugs that increase HR
195
Q

what is an angiogram

A
  • use catheter to put dyes in arteries of heart to see heart in xray
  • aka cardiac cathetrization
  • uses fluroscopy
196
Q

what is the myocardium

A
  • muscular tissue of the heart
197
Q

how does the myocardium receive blood

A
  • from the 2 coronary arteries coming from base of aorta

- left & right coronary arteries

198
Q

what does the left main (coronary artery) split into

A
  1. circumflex

2. left anterior descending

199
Q

what does the left anterior descending (LAD) supply?

A
  • the anterior left ventricle & septum
200
Q

what does the circumflex supply

A
  • the lateral & posterior LV
201
Q

which coronary artery is more dangerous to obstruct

A
  • left
202
Q

what does blockage of the right coronary artery cause

A
  • can affect SA node if up high

= arrythmia

203
Q

what does the right coronary artery & branches supply

A
  • the anterior & posterior right ventricle

- SA/AV nodes

204
Q

what is the posterior descending artery? what does supply

A
  • branch of the right coronary artery

- supplied the inferior & apex of the myocardium

205
Q

describe the progression of CAD

A
  • unpredictable

- manifests as a broad range of unpredictable clinical symptoms

206
Q

how might CAD manifest

A
  • chronic stable angine
  • acute coronary syndrome
  • MI
  • cardiac arrythmias
  • HF
  • sudden cardiac death
207
Q

what can acute coronary syndrome be split into

A
  • unstable angina/nonSTEMI

- STEMI

208
Q

what is the difference between a STEMI and non-STEMI

A
  • stemi = full thickness effected = more dangerous

- nonstemi = partial thickeness

NURS 2500 (5 decks)

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