CAD 34 Flashcards
1
Q
Major cause of death in US
A
cardiovascular dz
2
Q
most common type of cardiovascular dz
A
CAD
3
Q
CAD is included in what general category?
A
atherosclerosis
4
Q
Word Break down: “athere” is Greek for
A
“fatty mush”
5
Q
Word Break down: “skleros” is Greek for
A
“hard”
6
Q
CAD is
A
focal deposit of cholesterol and lipid, primarily within the intimal wall of the artery
7
Q
Two things that play a central role in the development of atherosclerosis
A
inflammation and endothelial injury
8
Q
C-reactive protein is
A
a protein produced by the liver, nonspecific marker of inflammation
9
Q
CRP rises in?
A
systemic inflammation, many patient with CAD have a increase CRP
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
11
Q
When CAD because symptomatic the dz is_______.
A
advanced
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
13
Q
What is are Fatty Streaks?
A
the earliest leasion of atherosclerosis. Characterized by lipid filled smooth muscle cells
14
Q
When does a yellow tinge appear on smooth muscle cells?
A
when streaks of fat develop
15
Q
What is it called when collagen covers the fatty streak?
A
Fibrous Plaque
16
Q
What are complicated lesions?
A
final stage in atherosclerosis. Fibrous plaque grows, and inflammation can result in plaque instability, ulceration and rupture
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
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
19
Q
what are the nonmodifiable risk factors for CAD?
A
age, gender, ethnicity, family hx, genetic inheritance
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
21
Q
who has the highest incidence of CAD and MI? (gender/race/age)
A
white, male middle aged
22
Q
compare heart disease to breast cancer (risk)
A
heart dz kills 10 times more women than breast cancer
23
Q
Serum cholesterol level associated with a risk for CAD?
A
more than 200mg/dL
24
Q
fasting triglyceride level associated with a risk for CAD?
A
more than 150mg/dL
25
what are lipoproteins?
lipids that combine with proteins. Vehicles for fat mobilization and transport
26
The three classifications of lipoproteins
high density lipoproteins, low density lipoproteins, and very low density lipoproteins
27
what do HDLs do?
carry lipids away from arteries and to the liver for metabolism
28
What are the two types of HDLs?
HDL2 and HDL3
29
who have higher levels of HDL?
children and women
30
HDL levels decrease with
CAD and with age
31
things that increase HDLs
physical activity, moderate alcohol consumption and estrogen administration
32
describe LDLs
contain more cholesterol than any of the other lipoproteins and have affinity for arterial walls
33
desribe VLDLs
contain both cholesterol and triglycerides and may deposit cholesterol directly on the walls of the arteries
34
Diseases/drugs and genetic disorders associated with elevated triglycerides
type 2 diabetes, chronic renal failure, corticosteroids, HRT, and some genetic disorders
35
lifestyle factors that contribute to elevated triglycerides
high alcohol, high intake of refined carbohydrates and simple sugars, and physical inactivity
36
what are the 7 factors that generate a risk score for having a nonfatal MI or dying from a coronary event
age, gender, use of tobacco, Systolic BP, use of BP medication, total cholesterol, HDL levels
37
Low risk for development of CAD
one of the risk score factors and an LDL <160mg/dL
38
HTN increase the risk of death from CAD by
10 fold in all persons
39
Normal BP
<120/80
40
prehypertension
120-139/80-89
41
Stage 1 HTN
140-159/90-99
42
Stage 2 HTN
> or equal to 160/100 mmHg
43
third major risk for CAD
tobacco use
44
tobacco use increase risk of development of CAD by
two to six fold
45
benefits from smoking cessation
are dramatic and almost immediate, CAD mortality rates drop to those of nonsmokers within 12 months
46
examples of smoking cessation strategies
group counseling sessions, nicotine replacement therapy, smoking cessation medications and hypnosis
47
describe physical inactivity
lack of physical exercise on a regular basis
48
healthpromoting regular physical activty example
brisk walking for at least 30 minutes five or more times a week
49
define obesity
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
50
obese persons may increase
levels of LDLs and triglyercerides
51
likelyhood of an obese person developing HTN
three times more likely than a person of normal weight
52
management of diabetes
lifestyle changes and drug therapy to achieve a hemoglobin A1C level <7%
53
personality type that may be more prone to MI
type A person: suppress anger and hostility, sense or time urgency, is impatient and often creates stress and tension
54
psych factors that increase risk of CAD
depression, acute and chronic stress, anxiety, hostility, anger, lack of social support
55
homocysteine is
produced by the breakdown of the essential amino acid methionine
56
high homocysteine levels possibly contribute to atherosclerosis by
damaging the inner lining of blood vessels, promoting plaque buildup, altering the clotting mechanisms to make clots more likely to occur
57
use of cocaine and mathamphetamine can (heart related SE)
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.
58
health history screening topics
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
59
FITT formula
Frequency, Intensity, Type, Time of exercise
60
American College of Cardiology/ AHA recommended exercise program
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
61
diet teaching: food types that are major sources of saturated fat and cholesterol
red meats, eggs, whole milk
62
diet teaching: fat intake
30% of calories, most coming from monounsaturated fats
63
fatty acids that reduce the risks associated with CAD when consumed regularly
Omega 3
64
dietary teaching: for individuals without CAD - AHA recommends eating (omega 3 topic)
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
65
dietary teaching: supplement teaching for CAD patients
recommend taking EPA and DHA supplements
66
how often is a complete lipid profile recommended
every 5 years beginning at age 20
67
elevated cholesterol treatment (nonmed)
dietary caloric intake, restriction (if overweight), decreased dietary fat and cholesterol intake, and increased physical activity
68
most widely used lipid lowering drug
statins- drug inhibit the synthesis of cholesterol in the liver by blocking hydromethylglutaryl coenzyme A reductase
69
another drug common prescribed for people at risk for CAD (unless contraindicated)
low dose aspirin (81 mg)
70
chronic stable angina
chest pain that occurs intermittently over a long period with the same pattern of onset, duration and intensity of symptoms
71
silent ischemia
ischemia that occurs in the absence of any subjective symptoms
72
patients with diabetes have an increased prevalence of silent ischemia because
diabetic neuropathy affecting the nerves that innervate the cardiovascular system
73
nocturnal angina
occurs only at night, but not necessary when the person is sleeping or in a recumbent posiion
74
angina decubitus
occurs only when a person is lying down and usualy relieved by standing or sitting
75
prinzmetal's angina
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
76
prinzmetal angina spasm may occur ( health hx)
in the absense of CAD or with documented dz
77
prinzmetal's angina: spasm cause
strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium
78
diagnostic studies for angina
cardiac catheterization and coronary angiography provided images of the coronary circulation and ID the location and severity of any lesions
79
Acute Coronary syndrome
develops and encompassess the spectrum of unstable angina, non ST segment elevation myocardial infarction and ST segment elevation myocardial infarction
80
relationship between atherosclerotic plaque and ACS
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
unstable angina
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
most common prominent symptom of unstable angina
fatigue
83
Myocardial infarction
occurs because of a sustained ischemia, causing irreversible myocardial cell death (necrosis)
84
80 to 90% of all acute Mis are secondary to
thrombus formation
85
clinical manifestations of MI
pain, N/V, fever, complications of MI dysrhthmias, heart faiulre, cardiogenic shock, papillary muscle dysfunction, ventricular aneurysm, pericarditis dressler syndrome
86
dx of ACS (acute coronary syndrome)
ECG, serum cardiac markers, coronary angiography,
87
ECG primary tool to rule out UA or MI because
changes in the QRS complex, ST segment, and T wave caused by ischemia and infarction can develop quickly with UA and MI
88
Initial management of chest pain
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
tx for patients with UA or NSTEMI with negative cardiac markers and ongoing angina
combination of aspirin, heparin (UH or LMWH) and glycoprotein Iib/Iia (eptifibatide, intergrilin)
90
once the patient is stabilized and angia is controlled, or if angina returns or increases in severity
coronary angiography with possible PCI
91
tx for patients with STEM or NSTEMI with positive cardiac markers
reperfusion therapy (which may include emergent PCI or fibrinolytic therapy)
92
if the PCI fails, patient may be considered for
coronary surgical revascularization
93
goal of tx of MI
salvage as much myocardial muscle as possible
94
Emergent PCI
first like of treatment for patients with confirmed MI
95
PCI timeline
goal is to open affected artery within 90 minutes of arrival to facility with an interventional cardiac catherization lab
96
complications of PCI
dissection of the newly dilated coronary artery, cardiac tamponade, infarction, coronary spasm, abrupt closure (first 24 hours)
97
treatments for confirmed MI
placement of drug eluting stents, some may need additional IABP therapy, may need CABG therapy
98
advantages of PCI
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
Normal convalescence after CABG
6-8 weeks
100
nomal hospitalization with CABG
4-6 days
101
advantages of fibrinolytic therapy
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
Purpose of fibrinolytic therapy
stop the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium
103
When is fibrinolytic therapy given?
ideally within the first hour of onset of symptoms (and perferably within the first 6 hours after the onset of symptoms)
104
mortality is reduced by what percentage if reperfusion occurs within 6 hours
25%
105
route of fibinolytics
IV
106
what guides the choice of thrombolytic agents
cost, efficacy and ease of adminstration
107
thrombolytics may differ by
mechanism of action and pharmacokinetic
108
All thrombolytics
produce an open artery by lysis of the thrombus in the coronary artery
109
goal of administration of a fibrinolytic
within 30 minutes of the patient's arrival to a facility without an interventional cardiac catheterization laboratory
110
inclusion criteria for fibrinolytic therapy
chest pain typical of acute MI < or = to 6 hours during duration, 12 lead ECG findings consistent with acute MI, No absolute contraindications
111
Tx: patient with chest pain >6 hours induration and ECG changes indicative of MI
maybe considered for fibrinolytic therapy, but research on the benefit on this therapy in inconclusive
112
procedure for thrombolytic therapy
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
most reliable marker when reperfusion occurs
return of ST segment to baseline on ECG
114
other markers of reperfusion
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
when do necrotic myocardial cells release CK-MB enzymes into circulation
after perfusion is restored to the heart
116
tx for reperfusion dysrrhythmias
they are ususally self limiting and do not require aggressive tx)
117
major concern of fibrinolytic therapy
reocclusion of the artery- the site of thrombus is unstable, and other clot may form or spasm of the artery may occur
118
to prevent reocclusion of the artery, which treatment is usually initiated
IV herparin therapy
119
Signs and symtoms of secondary clot after fibrinolytic therapy
similar complaints of chest pain, ECG changes return
120
tx of second clot formation after fibrinolytic therapy
another dose of fibrinolytic or transferred to facility with cardiac catheterization lab for PCI or coronary surgical revascularization
121
major complication of fibrinolytic therapy
bleeding
122
how do you control minor bleeding as a result of fibrinolytic therapy
apply pressure dressing or ice packs. Minor bleeding is expected
123
S/S of major bleeding
drop in BP, increase in HR, sudden change in the patient's level of consciousness, blood in urine or stool
124
what do you do if patient has major bleeding after giving fibrinolytic therapy
STOP therapy and notify physicians
125
Coronary Surgical Revascularization is recommended for patients who
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
procedure for CABG
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
Vessels that can be used in CABG
internal mammory, saphenous vein, radial artery, gastroepiploic artery and/or inferior epigastric artery
128
most common vessel used in CABG
internal mammary artery (IMA)
129
sternotomy
opening the chest cavity
130
CABG requires (2 medical procedures)
sternotomy and cardiopulmonary bypass
131
CABG is what kind of treatment for CAD
palliative
132
minimally invasive direct coronary artery bypass
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
Robot assisted cardiothoracic surgery
use of a robot in performing CABG or mitral valve replacement
134
Transmyocardial Laser revascularization
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
initial drug tx choices for ACS
IV NTG, aspirin, and systemic anticoagulation with either LMWH given subcu or IV UH
136
drugs given if PCI is anticipated
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
contrainidications for beta adrenergic blockers
HF, heart block, hypotension
138
another possible drug given for select patients following MI
ACE inhibitors
139
IV NTG (Tridil)
initial tx for patients with ACS
140
goal of IV NTG tx
reduce angina pain and improve coronary blood flow
141
what does IV NTG do?
decreases preload and afterload while increasing the myocardial oxygen supply
142
onset of IV NTG
immediate
143
NTG therapy may need to be
titrated to control and stop chest pain
144
common side effects of IV NTG
hypotension
145
tx for patients who become hypotensive as result from NTG therapy
as the hypotension is often do to volume depletion, they may receive IV fluid bolus
146
effective strategy for tolerance of IV nitrate therapy
titrate dose down at night during sleep and titrate dose up during the day
147
drug of choice for chest pain that is unrelieved by NTG
Morphine sulfate
148
how does morphine sulfate work
vasodilator, it decreases cardiac workload by lowering myocardial oxygen consumption, reducing contractility and decreasing BP and HR
149
in addition to reduction of pain, morphine may
reduce anxiety and fear
150
SE of Morphine sulfate
depress respirations
151
Nursing considerations regarding morphine sulfate
monitor for signs of bradypnea or hypoxia
152
B adrenergic blockers work by
decreasing myocardial oxygen demand by reducing HR, BP, and contractility
153
when are B adrenergic blockers are used in patients who are not at risk for complications. How long are they used?
in the first 24 hours of MI. reduces risk of reinfarction and ventricular fibrillation.s should be continued indefinitely
154
What should be started and continued indefinitely in patients recovering from STEMI with an EF of less than or equal to 40%
ACE inhibitors
155
How do ACE inhibitors help
prevent ventricular remodeling and prevent or slow the progression of HF
156
blood test done all patients admitted with ACS
fasting lipid panel
157
Cholesterol lowering drugs should be given to
patients with elevated triglycerides and LDL cholesterol
158
why should stool softeners be given?
after an MI, patients may be predisposed to constipation because of bed rest and opioid adminstration. Prevent straining and resultant vagal stimulation
159
vagal stimulation produces
bradycardia and prevoke dysrhythmias
160
Nutritional therapy teaching
NPO except sips of water until stable. Advance the diet as tolerated to a low salt, low saturated-fat and low cholesterol diet
161
Overall goals for a patient with ACS
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
Acute intervention of Chronic stable angina
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
list some nonverbal cues of pain
restlessness, elevated HR, RR, or BP, clutching bedclothes, facial expressions
164
important to remember when documenting pain
use scale of 1 to 10, and always use the patients own words
165
teaching topics necessary for angina prevention
precipitationg factors for angina, risk factor reduction, and medication as well as general information about CAD and angina
166
precipitating factor teaching
avoid exposure to extremes of weather, and avoid consumption of large, heavy meals
167
Why is body weight important in controlling angina?
excess weight increases myocardial workload
168
Teaching for NTG
NTG tablets, sprays or ointments may be used prophylactically before an emotionally stressful situation, sexual intercourse, or physical exertion
169
Priority nursing interventions in initial phase of ACS
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
Nursing implementation: pain
provide NGT, morphine sulfate, and ox as needed to eliminate or reduce chest pain. Ongoing eval and documentation
171
patient may interpret absense of pain as
absense of cardiac dz and this requires further teaching
172
Nursing implementation: monitoring
continous ECG in ED and ICU and after transfer to step down or general unit. I and O. physical assessment. SpO2
173
Nursing Implementation: anxiety
assess and identify source of anxiety and assist patient with reducing it
174
Research shows anxiety (in cardiac patient)
have a greater risk for adverse outcomes such as recurrent ischemic events and dysrhythmias
175
Nursing implementation: emotional and behavioral reactions
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
major nursin responsibilities for the care following PCI
monitoring for signs of recurrent angina, frequent vitals, evaluation of puncture site for bleeding and maintenance of bed rest per institution policy
177
CABG: location ofr first 24 to 36 hours post surgery
ICU
178
critical assessment post CABG
hemodynamic status
179
Most patients will be excubated within
6 hours
180
for the first 3 days post CABG watch for
artial dysrhythmias
181
post operative complications from CABG
dysrhythmias, stroke, infection
182
initial cardiac event for men is
more often MI than angina
183
initial cardiac event for women is
more often angia than MI
184
leading cause of death for women, regardless of race or ethnicity
CAD
185
Healthy People goals
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
recommended intake as percentage of total daily calories: total fat
25%-35%
187
recommended intake as percentage of total daily calories: saturated fat
<7%
188
recommended intake as percentage of total daily calories: polyunsaturated fat
up to 10%
189
recommended intake as percentage of total daily calories: monounsaturated fat
up to 20%
190
recommended intake as percentage of total daily calories: carbohydrate
50%-60%
191
recommended intake as percentage of total daily calories: protein
approx 15%
192
recommended intake as percentage of total daily calories: cholesterol
<200mg
193
recommended intake as percentage of total daily calories: sodium
less than or equal to 2400mg
194
recommended intake as percentage of total daily calories: dietary fibers
20-30g
195
recommended intake as percentage of total daily calories: total calories
balance energy intake and expenditure to achieve or maintain desirable body wt and prevent wt gain
