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Nursing: 201 > CAD 34 > Flashcards

CAD 34 Flashcards

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1
Q

Major cause of death in US

A

cardiovascular dz

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2
Q

most common type of cardiovascular dz

A

CAD

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3
Q

CAD is included in what general category?

A

atherosclerosis

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4
Q

Word Break down: “athere” is Greek for

A

“fatty mush”

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5
Q

Word Break down: “skleros” is Greek for

A

“hard”

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6
Q

CAD is

A

focal deposit of cholesterol and lipid, primarily within the intimal wall of the artery

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7
Q

Two things that play a central role in the development of atherosclerosis

A

inflammation and endothelial injury

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8
Q

C-reactive protein is

A

a protein produced by the liver, nonspecific marker of inflammation

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9
Q

CRP rises in?

A

systemic inflammation, many patient with CAD have a increase CRP

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10
Q

Chronic elevations of CRP are associated with

A

unstable plaques and oxidation of LDL, leading to increasing uptake by macrophages in the endothelial lining

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11
Q

When CAD because symptomatic the dz is_______.

A

advanced

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12
Q

What are the developmental stages in atherosclerosis?

A

1) Fatty streak, 2) fibrous plaque resulting from smooth muscle cell proliferation, 3) Complicated lesion

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13
Q

What is are Fatty Streaks?

A

the earliest leasion of atherosclerosis. Characterized by lipid filled smooth muscle cells

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14
Q

When does a yellow tinge appear on smooth muscle cells?

A

when streaks of fat develop

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15
Q

What is it called when collagen covers the fatty streak?

A

Fibrous Plaque

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16
Q

What are complicated lesions?

A

final stage in atherosclerosis. Fibrous plaque grows, and inflammation can result in plaque instability, ulceration and rupture

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17
Q

What happens when the inner wall of the artery is compromised?

A

platelets accumulate in large numbers which may lead to a thrombus

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18
Q

what are the two factors that contribute to the growth of collateral circulation

A

1) the inherited predisposition to develop new blood vessels, 2) the presence of chronic ischemia

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19
Q

what are the nonmodifiable risk factors for CAD?

A

age, gender, ethnicity, family hx, genetic inheritance

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20
Q

what are the modifiable risk factors for CAD?

A

elevated serum kipds, elevated blood pressure, tobacco use, physical inactivity, obesity, diabetes, metabolic syndrome, psychological states and elevated homocysteine level

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21
Q

who has the highest incidence of CAD and MI? (gender/race/age)

A

white, male middle aged

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22
Q

compare heart disease to breast cancer (risk)

A

heart dz kills 10 times more women than breast cancer

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23
Q

Serum cholesterol level associated with a risk for CAD?

A

more than 200mg/dL

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24
Q

fasting triglyceride level associated with a risk for CAD?

A

more than 150mg/dL

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25
Q

what are lipoproteins?

A

lipids that combine with proteins. Vehicles for fat mobilization and transport

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26
Q

The three classifications of lipoproteins

A

high density lipoproteins, low density lipoproteins, and very low density lipoproteins

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27
Q

what do HDLs do?

A

carry lipids away from arteries and to the liver for metabolism

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28
Q

What are the two types of HDLs?

A

HDL2 and HDL3

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29
Q

who have higher levels of HDL?

A

children and women

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30
Q

HDL levels decrease with

A

CAD and with age

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31
Q

things that increase HDLs

A

physical activity, moderate alcohol consumption and estrogen administration

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32
Q

describe LDLs

A

contain more cholesterol than any of the other lipoproteins and have affinity for arterial walls

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33
Q

desribe VLDLs

A

contain both cholesterol and triglycerides and may deposit cholesterol directly on the walls of the arteries

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34
Q

Diseases/drugs and genetic disorders associated with elevated triglycerides

A

type 2 diabetes, chronic renal failure, corticosteroids, HRT, and some genetic disorders

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35
Q

lifestyle factors that contribute to elevated triglycerides

A

high alcohol, high intake of refined carbohydrates and simple sugars, and physical inactivity

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36
Q

what are the 7 factors that generate a risk score for having a nonfatal MI or dying from a coronary event

A

age, gender, use of tobacco, Systolic BP, use of BP medication, total cholesterol, HDL levels

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37
Q

Low risk for development of CAD

A

one of the risk score factors and an LDL <160mg/dL

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38
Q

HTN increase the risk of death from CAD by

A

10 fold in all persons

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39
Q

Normal BP

A

<120/80

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40
Q

prehypertension

A

120-139/80-89

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41
Q

Stage 1 HTN

A

140-159/90-99

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42
Q

Stage 2 HTN

A

> or equal to 160/100 mmHg

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43
Q

third major risk for CAD

A

tobacco use

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44
Q

tobacco use increase risk of development of CAD by

A

two to six fold

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45
Q

benefits from smoking cessation

A

are dramatic and almost immediate, CAD mortality rates drop to those of nonsmokers within 12 months

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46
Q

examples of smoking cessation strategies

A

group counseling sessions, nicotine replacement therapy, smoking cessation medications and hypnosis

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47
Q

describe physical inactivity

A

lack of physical exercise on a regular basis

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48
Q

healthpromoting regular physical activty example

A

brisk walking for at least 30 minutes five or more times a week

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49
Q

define obesity

A

body mass index greater than or equl to 30kg/m2 and a waist circumference greater than or equal to 40 inches for men and 35 inches for women

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50
Q

obese persons may increase

A

levels of LDLs and triglyercerides

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51
Q

likelyhood of an obese person developing HTN

A

three times more likely than a person of normal weight

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52
Q

management of diabetes

A

lifestyle changes and drug therapy to achieve a hemoglobin A1C level <7%

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53
Q

personality type that may be more prone to MI

A

type A person: suppress anger and hostility, sense or time urgency, is impatient and often creates stress and tension

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54
Q

psych factors that increase risk of CAD

A

depression, acute and chronic stress, anxiety, hostility, anger, lack of social support

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55
Q

homocysteine is

A

produced by the breakdown of the essential amino acid methionine

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56
Q

high homocysteine levels possibly contribute to atherosclerosis by

A

damaging the inner lining of blood vessels, promoting plaque buildup, altering the clotting mechanisms to make clots more likely to occur

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57
Q

use of cocaine and mathamphetamine can (heart related SE)

A

produce coronary spasm resulting in MI and chest pain. Sinus tachycardia, high BP, angina, anxiety Likely to be seen in ED for chest pain are initially indistinguishable from a patient with CAD.

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58
Q

health history screening topics

A

family hx, cardiovascular symptoms, environmental factor including eating habits, diet, level of exercise, psychosocial hx (tobacco use, ETOH, stress) negative psych states, work environment, and stress associated with work

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59
Q

FITT formula

A

Frequency, Intensity, Type, Time of exercise

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60
Q

American College of Cardiology/ AHA recommended exercise program

A

at least 30 minutes of moderate physical activity on most days of the week, resistance weight training added two days a week can help treat metabolic syndrome and improve muscle strength

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61
Q

diet teaching: food types that are major sources of saturated fat and cholesterol

A

red meats, eggs, whole milk

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62
Q

diet teaching: fat intake

A

30% of calories, most coming from monounsaturated fats

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63
Q

fatty acids that reduce the risks associated with CAD when consumed regularly

A

Omega 3

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64
Q

dietary teaching: for individuals without CAD - AHA recommends eating (omega 3 topic)

A

fatty fish twice a week because fatty fish such as salmon and tuna contain two types of omega 3 fatty acids, recommends eating tofu, and other forms of soybean, canola walnut, flaxseed because these products contain alpha linolenic acid which becomes an omega 3 in the body

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65
Q

dietary teaching: supplement teaching for CAD patients

A

recommend taking EPA and DHA supplements

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66
Q

how often is a complete lipid profile recommended

A

every 5 years beginning at age 20

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67
Q

elevated cholesterol treatment (nonmed)

A

dietary caloric intake, restriction (if overweight), decreased dietary fat and cholesterol intake, and increased physical activity

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68
Q

most widely used lipid lowering drug

A

statins- drug inhibit the synthesis of cholesterol in the liver by blocking hydromethylglutaryl coenzyme A reductase

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69
Q

another drug common prescribed for people at risk for CAD (unless contraindicated)

A

low dose aspirin (81 mg)

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70
Q

chronic stable angina

A

chest pain that occurs intermittently over a long period with the same pattern of onset, duration and intensity of symptoms

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71
Q

silent ischemia

A

ischemia that occurs in the absence of any subjective symptoms

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72
Q

patients with diabetes have an increased prevalence of silent ischemia because

A

diabetic neuropathy affecting the nerves that innervate the cardiovascular system

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73
Q

nocturnal angina

A

occurs only at night, but not necessary when the person is sleeping or in a recumbent posiion

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74
Q

angina decubitus

A

occurs only when a person is lying down and usualy relieved by standing or sitting

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75
Q

prinzmetal’s angina

A

often occurs at rest, in response to a spasm of the major coronary artery. Rare. Frequently seen in patients with hx of migraine headache or Raynaud’s phenomenon. Is not usually precipitated by increased physical demand

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76
Q

prinzmetal angina spasm may occur ( health hx)

A

in the absense of CAD or with documented dz

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77
Q

prinzmetal’s angina: spasm cause

A

strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium

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78
Q

diagnostic studies for angina

A

cardiac catheterization and coronary angiography provided images of the coronary circulation and ID the location and severity of any lesions

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79
Q

Acute Coronary syndrome

A

develops and encompassess the spectrum of unstable angina, non ST segment elevation myocardial infarction and ST segment elevation myocardial infarction

80
Q

relationship between atherosclerotic plaque and ACS

A

a once stable atherosclerotic plaque deteriorates. The plaque reptures, exposing the intima to blood and stimulating platelet aggregation and local vasoconstriction with thrombus formation

81
Q

unstable angina

A

chest pain that is new in onset, occurs at rest, or has a worsening pattern. UA may be first clinical manifestation of CAD, unpredictable and represents an emergency

82
Q

most common prominent symptom of unstable angina

A

fatigue

83
Q

Myocardial infarction

A

occurs because of a sustained ischemia, causing irreversible myocardial cell death (necrosis)

84
Q

80 to 90% of all acute Mis are secondary to

A

thrombus formation

85
Q

clinical manifestations of MI

A

pain, N/V, fever, complications of MI dysrhthmias, heart faiulre, cardiogenic shock, papillary muscle dysfunction, ventricular aneurysm, pericarditis dressler syndrome

86
Q

dx of ACS (acute coronary syndrome)

A

ECG, serum cardiac markers, coronary angiography,

87
Q

ECG primary tool to rule out UA or MI because

A

changes in the QRS complex, ST segment, and T wave caused by ischemia and infarction can develop quickly with UA and MI

88
Q

Initial management of chest pain

A

establish an IV route to provide access for emergency drug therapy, O2 by NC 2-4L/min, ECG monitoring, Sublingual NTG and aspirin, Morphine sulfate for unrelieved pain, monitor vitals, pulse ox frequently, maintain bed rest and limit activity for 12-24 hours, with a gradual increase in activity unless contraindicated

89
Q

tx for patients with UA or NSTEMI with negative cardiac markers and ongoing angina

A

combination of aspirin, heparin (UH or LMWH) and glycoprotein Iib/Iia (eptifibatide, intergrilin)

90
Q

once the patient is stabilized and angia is controlled, or if angina returns or increases in severity

A

coronary angiography with possible PCI

91
Q

tx for patients with STEM or NSTEMI with positive cardiac markers

A

reperfusion therapy (which may include emergent PCI or fibrinolytic therapy)

92
Q

if the PCI fails, patient may be considered for

A

coronary surgical revascularization

93
Q

goal of tx of MI

A

salvage as much myocardial muscle as possible

94
Q

Emergent PCI

A

first like of treatment for patients with confirmed MI

95
Q

PCI timeline

A

goal is to open affected artery within 90 minutes of arrival to facility with an interventional cardiac catherization lab

96
Q

complications of PCI

A

dissection of the newly dilated coronary artery, cardiac tamponade, infarction, coronary spasm, abrupt closure (first 24 hours)

97
Q

treatments for confirmed MI

A

placement of drug eluting stents, some may need additional IABP therapy, may need CABG therapy

98
Q

advantages of PCI

A

provides an alternative to surgical interventions, it is performed with local anesthesia, patient is able to ambulate 24 hours after the procedure, hospital length of stay is 1-3 days, patient can return to work approximately 5-7 days after PCI

99
Q

Normal convalescence after CABG

A

6-8 weeks

100
Q

nomal hospitalization with CABG

A

4-6 days

101
Q

advantages of fibrinolytic therapy

A

available and rapid adminstration in facilities thatt do not have interventional cardiac catherterization laboratory or oee that is is unsafe to transfer the patient to

102
Q

Purpose of fibrinolytic therapy

A

stop the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium

103
Q

When is fibrinolytic therapy given?

A

ideally within the first hour of onset of symptoms (and perferably within the first 6 hours after the onset of symptoms)

104
Q

mortality is reduced by what percentage if reperfusion occurs within 6 hours

A

25%

105
Q

route of fibinolytics

A

IV

106
Q

what guides the choice of thrombolytic agents

A

cost, efficacy and ease of adminstration

107
Q

thrombolytics may differ by

A

mechanism of action and pharmacokinetic

108
Q

All thrombolytics

A

produce an open artery by lysis of the thrombus in the coronary artery

109
Q

goal of administration of a fibrinolytic

A

within 30 minutes of the patient’s arrival to a facility without an interventional cardiac catheterization laboratory

110
Q

inclusion criteria for fibrinolytic therapy

A

chest pain typical of acute MI < or = to 6 hours during duration, 12 lead ECG findings consistent with acute MI, No absolute contraindications

111
Q

Tx: patient with chest pain >6 hours induration and ECG changes indicative of MI

A

maybe considered for fibrinolytic therapy, but research on the benefit on this therapy in inconclusive

112
Q

procedure for thrombolytic therapy

A

obtain baseline vital; initiate two or three lines for IV therapy; depending on drug selected, therapy is administered in one IV bolus or over a period of time (30 to 90 min); note time that therapy begins and monitor patient the patient during and after therapy; evaulate heart rhythm, vitals and pulse ox; assess the heart and lungs to assess patients response

113
Q

most reliable marker when reperfusion occurs

A

return of ST segment to baseline on ECG

114
Q

other markers of reperfusion

A

resolution of chest pain, an early, rapid rise of the CK-MB enzymes within 3 hours of therapy and peaking within 12 hours, reperfusion dysrhythmias

115
Q

when do necrotic myocardial cells release CK-MB enzymes into circulation

A

after perfusion is restored to the heart

116
Q

tx for reperfusion dysrrhythmias

A

they are ususally self limiting and do not require aggressive tx)

117
Q

major concern of fibrinolytic therapy

A

reocclusion of the artery- the site of thrombus is unstable, and other clot may form or spasm of the artery may occur

118
Q

to prevent reocclusion of the artery, which treatment is usually initiated

A

IV herparin therapy

119
Q

Signs and symtoms of secondary clot after fibrinolytic therapy

A

similar complaints of chest pain, ECG changes return

120
Q

tx of second clot formation after fibrinolytic therapy

A

another dose of fibrinolytic or transferred to facility with cardiac catheterization lab for PCI or coronary surgical revascularization

121
Q

major complication of fibrinolytic therapy

A

bleeding

122
Q

how do you control minor bleeding as a result of fibrinolytic therapy

A

apply pressure dressing or ice packs. Minor bleeding is expected

123
Q

S/S of major bleeding

A

drop in BP, increase in HR, sudden change in the patient’s level of consciousness, blood in urine or stool

124
Q

what do you do if patient has major bleeding after giving fibrinolytic therapy

A

STOP therapy and notify physicians

125
Q

Coronary Surgical Revascularization is recommended for patients who

A

fail medical management; have left main coronary artery or three vessel dz; are not candidates for PCI, failed PCI with ongoing chest pain; have DM

126
Q

procedure for CABG

A

placement of one or more vessel grafts to transport blood between the aorta, or other major arteries and the myocardium distal to the obstructioned coronary artery

127
Q

Vessels that can be used in CABG

A

internal mammory, saphenous vein, radial artery, gastroepiploic artery and/or inferior epigastric artery

128
Q

most common vessel used in CABG

A

internal mammary artery (IMA)

129
Q

sternotomy

A

opening the chest cavity

130
Q

CABG requires (2 medical procedures)

A

sternotomy and cardiopulmonary bypass

131
Q

CABG is what kind of treatment for CAD

A

palliative

132
Q

minimally invasive direct coronary artery bypass

A

technique that offers patients requiring only one or two bypasses in one ore two coronary arteries located on the anterior surface of the heart an approach to surgical tx that does not involve sternotomy or CBP

133
Q

Robot assisted cardiothoracic surgery

A

use of a robot in performing CABG or mitral valve replacement

134
Q

Transmyocardial Laser revascularization

A

indirect revascularizaton procedure used for patients with advanced CAD who are not candidates for traditional CABG sx who have persistent angina after maximum medical therapy

135
Q

initial drug tx choices for ACS

A

IV NTG, aspirin, and systemic anticoagulation with either LMWH given subcu or IV UH

136
Q

drugs given if PCI is anticipated

A

IV antiplatelet agents (e.g glycoprotein Iib or IIIa inhibitor), beta adrenergic blocker (IV or orally within 24 hrs if there are no contraindications)

137
Q

contrainidications for beta adrenergic blockers

A

HF, heart block, hypotension

138
Q

another possible drug given for select patients following MI

A

ACE inhibitors

139
Q

IV NTG (Tridil)

A

initial tx for patients with ACS

140
Q

goal of IV NTG tx

A

reduce angina pain and improve coronary blood flow

141
Q

what does IV NTG do?

A

decreases preload and afterload while increasing the myocardial oxygen supply

142
Q

onset of IV NTG

A

immediate

143
Q

NTG therapy may need to be

A

titrated to control and stop chest pain

144
Q

common side effects of IV NTG

A

hypotension

145
Q

tx for patients who become hypotensive as result from NTG therapy

A

as the hypotension is often do to volume depletion, they may receive IV fluid bolus

146
Q

effective strategy for tolerance of IV nitrate therapy

A

titrate dose down at night during sleep and titrate dose up during the day

147
Q

drug of choice for chest pain that is unrelieved by NTG

A

Morphine sulfate

148
Q

how does morphine sulfate work

A

vasodilator, it decreases cardiac workload by lowering myocardial oxygen consumption, reducing contractility and decreasing BP and HR

149
Q

in addition to reduction of pain, morphine may

A

reduce anxiety and fear

150
Q

SE of Morphine sulfate

A

depress respirations

151
Q

Nursing considerations regarding morphine sulfate

A

monitor for signs of bradypnea or hypoxia

152
Q

B adrenergic blockers work by

A

decreasing myocardial oxygen demand by reducing HR, BP, and contractility

153
Q

when are B adrenergic blockers are used in patients who are not at risk for complications. How long are they used?

A

in the first 24 hours of MI. reduces risk of reinfarction and ventricular fibrillation.s should be continued indefinitely

154
Q

What should be started and continued indefinitely in patients recovering from STEMI with an EF of less than or equal to 40%

A

ACE inhibitors

155
Q

How do ACE inhibitors help

A

prevent ventricular remodeling and prevent or slow the progression of HF

156
Q

blood test done all patients admitted with ACS

A

fasting lipid panel

157
Q

Cholesterol lowering drugs should be given to

A

patients with elevated triglycerides and LDL cholesterol

158
Q

why should stool softeners be given?

A

after an MI, patients may be predisposed to constipation because of bed rest and opioid adminstration. Prevent straining and resultant vagal stimulation

159
Q

vagal stimulation produces

A

bradycardia and prevoke dysrhythmias

160
Q

Nutritional therapy teaching

A

NPO except sips of water until stable. Advance the diet as tolerated to a low salt, low saturated-fat and low cholesterol diet

161
Q

Overall goals for a patient with ACS

A

relief of pain; preservation of myocardium; immediate and appropriate tx; effective coping with illness-associated anxiety; participation in a rehabilitation plan; reduction of risk factors

162
Q

Acute intervention of Chronic stable angina

A

administer oxygen and position patient in upright position unless contraindicated; vitals; 12 lead ECG; provide prompt pain relief first with nitrate by an opioid analgesic if needed; ascultate heart sounds

163
Q

list some nonverbal cues of pain

A

restlessness, elevated HR, RR, or BP, clutching bedclothes, facial expressions

164
Q

important to remember when documenting pain

A

use scale of 1 to 10, and always use the patients own words

165
Q

teaching topics necessary for angina prevention

A

precipitationg factors for angina, risk factor reduction, and medication as well as general information about CAD and angina

166
Q

precipitating factor teaching

A

avoid exposure to extremes of weather, and avoid consumption of large, heavy meals

167
Q

Why is body weight important in controlling angina?

A

excess weight increases myocardial workload

168
Q

Teaching for NTG

A

NTG tablets, sprays or ointments may be used prophylactically before an emotionally stressful situation, sexual intercourse, or physical exertion

169
Q

Priority nursing interventions in initial phase of ACS

A

1) pain assessment and relief, 2) physiologic monitoring, 3)promotion of rest and comfort, 4) alleviation of stress and anxiety, 5) understanding of the patient’s emotional and behavioral reactions

170
Q

Nursing implementation: pain

A

provide NGT, morphine sulfate, and ox as needed to eliminate or reduce chest pain. Ongoing eval and documentation

171
Q

patient may interpret absense of pain as

A

absense of cardiac dz and this requires further teaching

172
Q

Nursing implementation: monitoring

A

continous ECG in ED and ICU and after transfer to step down or general unit. I and O. physical assessment. SpO2

173
Q

Nursing Implementation: anxiety

A

assess and identify source of anxiety and assist patient with reducing it

174
Q

Research shows anxiety (in cardiac patient)

A

have a greater risk for adverse outcomes such as recurrent ischemic events and dysrhythmias

175
Q

Nursing implementation: emotional and behavioral reactions

A

understand what the patient is currently experiencing, assist pt in testing reality and support use on constructive coping styles. Denial may be a positive coping style in early recovery from ACS

176
Q

major nursin responsibilities for the care following PCI

A

monitoring for signs of recurrent angina, frequent vitals, evaluation of puncture site for bleeding and maintenance of bed rest per institution policy

177
Q

CABG: location ofr first 24 to 36 hours post surgery

A

ICU

178
Q

critical assessment post CABG

A

hemodynamic status

179
Q

Most patients will be excubated within

A

6 hours

180
Q

for the first 3 days post CABG watch for

A

artial dysrhythmias

181
Q

post operative complications from CABG

A

dysrhythmias, stroke, infection

182
Q

initial cardiac event for men is

A

more often MI than angina

183
Q

initial cardiac event for women is

A

more often angia than MI

184
Q

leading cause of death for women, regardless of race or ethnicity

A

CAD

185
Q

Healthy People goals

A

achieve and maintain a healthy weight, reduce sodium intake, increase level of physical activity, avoid use of and exposure to all tobacco products, limit daily ETOH intake to small or moderate amounts, choose a deit that is low in dietary cholesterol and total and saturated fat. high in fruits and vegs

186
Q

recommended intake as percentage of total daily calories: total fat

A

25%-35%

187
Q

recommended intake as percentage of total daily calories: saturated fat

A

<7%

188
Q

recommended intake as percentage of total daily calories: polyunsaturated fat

A

up to 10%

189
Q

recommended intake as percentage of total daily calories: monounsaturated fat

A

up to 20%

190
Q

recommended intake as percentage of total daily calories: carbohydrate

A

50%-60%

191
Q

recommended intake as percentage of total daily calories: protein

A

approx 15%

192
Q

recommended intake as percentage of total daily calories: cholesterol

A

<200mg

193
Q

recommended intake as percentage of total daily calories: sodium

A

less than or equal to 2400mg

194
Q

recommended intake as percentage of total daily calories: dietary fibers

A

20-30g

195
Q

recommended intake as percentage of total daily calories: total calories

A

balance energy intake and expenditure to achieve or maintain desirable body wt and prevent wt gain

Nursing: 201 (6 decks)

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