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Cardiopulmonary > Unit 2 Week 5 CAD > Flashcards

Unit 2 Week 5 CAD Flashcards

(96 cards)

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1
Q

what is the #1 leading cause for death in the US?

A

CAD

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2
Q

what are the basic rules of fluid dynamics?

A

fluids flow from an area of high pressure to low pressure
fluids follow the path of least resistance

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3
Q

how do coronary arteries provide nutrients to the heart muscle tissue?

A

through perfusion

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4
Q

what is the primary driving force moving blood into the myocardial tissue?

A

DPB

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5
Q

___ plays a role in determining volume of blood passed along to tissue.

A

vasomotor tone

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6
Q

what is a common cause of resistance to flow?

A

atherosclerosis

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7
Q

when does perfusion occur? explain this.

A

when the muscle relaxes
-in systole when the heart contracts the aortic valve is open and blood rushes through the valve. when the heart contracts the muscles and arteries are compressed and blood cannot flow through.
-in diastole as the muscle relaxes the pressure drops in the ventricle and the blood in the aorta pushes the aortic valve shut. the blood then moves from the aorta to the coronary arteries perfusing the myocardium

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8
Q

what is atherosclerosis? and how does it affect blood flow?

A

build up of plaque inside the arteries
increase the back pressure/resistance to flow

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9
Q

what does elevation in diastolic pressure indicate?

A

there is more resistance to flow and therefore the heart is working harder to pump

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10
Q

what happens when oxygen demand exceeds oxygen supply?

A

ischemia/tissue death

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11
Q

what are the three layers of the arterial wall? explain each.

A

-intima: endothelial layer; designed to be selectively permeable to low-density lipoproteins
-media: made up of multiple layers of smooth muscle; function is to make adjustments to luminal diameter
-adventitia: basic supports; structure/basement membrane

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12
Q

what is most likely to accumulate in the intima?

A

lipoproteins and fibrinogen

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13
Q

what does atherosclerosis develop in response to?

A

endothelial injury

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14
Q

what are the two development phases of atherosclerosis? describe each.

A

-atherosis: fatty streak of lipid-laden macrophages and smooth muscle cells; cholesterol permeates the endothelium and deposits between the layers, monocytes are attracted to the area and engulf the lipid after becomes macrophages. once engulfed they become foam cells.
-sclerosis: reduces blood vessel compliance; organization of fibrous cap of thrombi over advanced plaques that develop on the endothelial lining surface. causes turbulent flow and the increased BF through the narrowed area caused more damage. injury to the area causes platelets to aggregate and form a clot.

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15
Q

when there is irritation to the blood vessels, endothelial wall, or intima it causes ___.

A

an inflammatory response

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16
Q

describe the progression of atherosclerosis.

A

plaque deposits remain external to the lumen initially. as the amount of plaque increase it begins to intrude into the lumen, decreasing the diameter of the coronary artery and causing obstruction. the resulting plaque fissure or erosion leads to angina

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17
Q

why are the coronary vessels so susceptible to atherosclerosis?

A

they have short branches under high pressure so flow is more likely to become turbulent

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18
Q

what are the risk factors for atherosclerosis?

A

smoking, poorly controlled DM, high velocity/turbulent flow, HTN, hyperlipidemia, systemic inflammation (Hs-CRP, homocysteine)

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19
Q

what are the risk factors for CVD?

A

smoking, physical inactivity, obesity, suboptimal diet, hypertension, elevated serum total cholesterol (elevated LDL, decreased HDL), diabetes, family history, age, gender (male higher until female menopause, then equal), stress

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20
Q

what are the nonmodifiable risk factors for CVD?

A

heredity and increased age

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21
Q

what are the modifiable risk factors of CVD?

A

cigarette/tobacco smoking, physical inactivity, high BP (over 140/90), high blood cholesterol levels

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22
Q

what is considered normal, borderline, and high total cholesterol?

A

normal < 200 mg/dL
borderline = 200-239 mg/dL
high > or equal to 240 mg/dL

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23
Q

what is considered normal, borderline, and high LDL?

A

normal < 130 mg/dL
borderline = 130-159 mg/dL
high > 160 mg/dL

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24
Q

what is considered low and cardioprotective HDL?

A

low < 40 mg/dL
cardioprotective > 60 mg/dL

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25
what are the negative effects of smoking?
enhances atherosclerosis increases LDL production increase work of the heart (partially by increasing BP)
26
every increase of __ systolic/___ diastolic doubles the risk of cardiovascular events.
20mmHg systolic/ 10mmHg diastolic
27
what is HTN associated with?
CVA, MI, aneurysm, chronic renal failure
28
how does diabetes increase the risk of CVD?
high blood glucose --> nonenzymatic glycosylation = attachment of glucose proteins without enzymes --> accelerates atherosclerosis
29
what BMI is considered obesity and therefore a risk factor of CVD?
> or equal to 30 kg/m2
30
before age __, men are 6 times more likely than women to have an MI.
55
31
what is the second leading cause of death in all women <45 years?
CHD
32
lack of exercise increase the risk of CVD by about ___%.
20% sedentary lifestyles are related to increases in BW and diabetes and insulin resistance
33
how do stress and depression increase risk of CVD?
almost triple the risk can cause changes in BP, cortisol, and inflammatory response
34
what dietary changes should be considers to reduce risk of CVD?
limit fats, salts and sugars consume 2 servings of fish per week, 3 servings of whole grains and 4-5 servings of fruits and veggies per day
35
how does regular exercise effect LDL and HDL?
results in small reductions in LDLs and elevated levels of HDLs
36
how does a person develop type 2 diabetes?
elevated glucose levels over time = high insulin levels = decrease in insulin sensitivity = development of type 2 diabetes this leads to accelerated atherosclerosis and an inflammatory response
37
HTN is __ more prevalent in those who are obese.
5x
38
Ischemic vessel disease causes __ and __ in the heart.
angina and myocardial infarction
39
Ischemic vessel disease causes __ and __ in the brain.
TIA (transient ischemic attack) and CVA (cerebrovascular accident)
40
Ischemic vessel disease causes __ or __ in the LE.
intermittent claudication or PAD
41
what factors lead to ACS (acute coronary syndrome)?
-fixed atherosclerotic lesions that progress over years w/o symptoms until a critical degrees of occlusion is attained -thrombosis superimposed acutely over a plaque (usual cause) -associated with strenuous activity
42
True/false: MI can occur at any time, even at rest and during sleep.
true
43
what causes vessel narrowing and decreased perfusion? explain.
atherosclerosis: plaques composed of lipid and thrombus thrombus: occludes vessel or piece breaks off (embolus) vasospasm: hyperplasia of smooth muscle cells
44
what is prinzmetal angina?
variant angina associated with ST-segment elevation, at rest, and not associated with any preceding increase in myocardial oxygen demand
45
what signs and symptoms of MI occur more commonly in women?
unusual fatigue, SOB, and indigestion (more subtle)
46
what signs and symptoms of MI occur in men?
referred pain patterns substernal pressure type of pain, radiating down the left UE, through to the back and up to the jaw
47
what are the differences in presentation of MI among men and women?
men <55 are 6x more likely than women CAD is 2nd leading cause of death in women <55 y/o women are still likely to have an event < 55, its just less likely than men women have more silent MIs first sign is women is typically angina (men first sign is MI) younger women < 55 have higher mortaility rates
48
what is angina?
the classic symptoms of ischemic heart conditions distress/pain of the chest
49
Angina is secondary to ___.
imbalance of coronary oxyegn delivery
50
what are the 3 types of angina?
stable unstable prinzmetal's
51
what is stable (typical) angina?
caused by fixed atherosclerotic lesion reduced reserve for coronary blood flow not present at rest occurs when oxygen demand is increased
52
stable angina is reproducible in terms of exertion:
intensity of effort length of time of exertion and relieved at rest and with administration of nitrates
53
what is unstable angina?
implies worsening athersc. process progressive in terms of severity of pain, less exertion required to elicit it typically caused by thrombosis of coronary plaque
54
what type of angina is considered an emergency?
unstable angina requires intervention before MI occurs
55
what is prinzmetal's angina?
variant caused by coronary vasospasm due to endothelial dysfunction
56
which type of angina is more difficult to diagnose and why?
prinzemetal's angina due to its unpredictable onset, occurring even at rest
57
what is ergonovine stimulation?
used to diagnose suspected prinzmetal angina elicits coronary spasm and makes it occur predictably
58
when perfusion of the myocardium does not meet oxygen demands __ will result.
ischemia
59
what are the 3 clinical courses of ischemia?
sudden cardiac death acute coronary syndrome (ACS) chronic stable angina
60
what indicates acute coronary syndrome?
unstable angina ST-segment elevation myocardial infarction non-stemi progression to cardiac muscle dysfunction
61
how does a non-stemi appear on an EKG?
ischemia shown with ST segment depression and t-wave inversion
62
how does a stemi appear on an EKG?
ST segment elevation followed by a significant q wave. indicates a full thicken or transmural infarct
63
how can an acute MI (non-stemi) be identified?
with a rise in serum troponin levels or ckmb plus either EKG changes or cardiac wall motion damage
64
what does the speed of myocardial necrosis progression depend on?
amount of ischemia and how long the ischemia lasts
65
what is a non-stemi?
rupture of coronary plaques --> partial occlusion of coronary artery --> subendocardial wall infarction
66
what is a ST-elevation MI?
rupture of coronary plaques --> thrombus/clot --> total occlusion of a coronary artery --> transmural infarction
67
what EKG lead are you looking at to find right coronary artery?
II, III, aVF
68
what EKG lead are you looking at to find left anterior descending artery?
V1-V4
69
what are the potential complications of ACS?
arrhythmias, contractile issues (can lead to CHF, mural thrombi), and wall weakening (can lead to rupture of CHF
70
what do serum enzymes represent? and what two are used with ACS?
injury to cardiac cells CK-MB seen first, troponin rises later and stays longer
71
how is ACS medically managed?
primary goal is to limit or prevent lasting damage of the heart which is done by decreasing the demand and increasing the supply of oxygen by restoring BF to the heart and decreasing the workload
72
what is used to control cardiac pain?
nitrates, morphine, beta-blockers
73
what is pharmacological treatment of ACS based on?
correcting the imbalance of oxygen supply and demand and lowering the workload of the heart
74
how do beta blocking drugs work for ACS?
they reduce the work of the heart by blocking epinephrine or adrenaline effect decreasing HR causing blood vessel dilation
75
how do organic nitrates work for ACS?
reduce preload, thereby work, potential for excessive preload reduction (by venous dilation)
76
what are the clinical implications of cardiac drugs?
cause decreased cardiac response to exercise but increase exercise tolerance in pts with angina may lead to peripheral vasodilation and orthostatic intolerance
77
what are the clinical implications of anti-thrombotic drugss?
risk of bleeding and bruising, internal hemorrhage risk, avoid bumping (avoid heavy lifting and plyometric type activities)
78
what are the surgical options for ACS?
PTCA (PCI) w/ or w/o stents CABG
79
what are the indications for PTCA or PCI surgery?
persistent chest pain or angina, blockage of only one or two arteries with severe symptoms, a change in symptom severity, failed medical therapy, and worsening of left ventricular dysfunction
80
what are the indications for CABG surgery?
presence of triple vessel disease, severe left main artery stenosis, left coronary artery has combined 70% or greater stenosis of the left anterior descending and proximal left circumflex artery, left ventricular function is impaired
81
what are the potential complications of an MI?
arrhythmias, contractile issues, wall weakening (all can lead to decreased cardiac output)
82
what is cardiogenic shock?
death of greater than 40% of LV the heart is damages so much that it is unable to supply enough blood to the organs of the body
83
what is the most common lethal complication of persistent angina and arrhythmias (STEMI)? why?
esp V-fib necrotic tissue releases ion, enzymes and other chemicals that interfere with the normal depolarization of the heart
84
what are other complications of persistent angina and arrhythmias (STEMI)?
A-fib, heart block, particularly when affects R side of heart
85
what are the results/complications of ventricular remodeling?
contractile issues and wall weakening with STEMI, changes in shape, size, and thickness of myocardium areas of ventricular dilation and ventricular hypertrophy
86
what factors affect remodeling?
size of infarct, ventricular load, patency of the artery that was infarcted
87
with both atrial and ventricular fibrillation there is an increased risk of ___ with right side involvement?
pulmonary embolism
88
with both atrial and ventricular fibrillation there is an increased risk of ___ with left side involvement.
CVA
89
what is a ventricular aneurysm?
ballooning out of a weakened LV
90
what is dyskinesia?
uncoordinated contraction
91
what is hypokinesia?
decreased or no wall movement
92
what is a mural thrombus?
a clump of atherosclerotic plaque buildup
93
what is the severity of function impairment related to?
left ventricular hypertrophy conduction defects smoking DM HTN VO2max
94
what is the best predictor of function post-ACS?
VO2max less than 21 mL/kg/min indicated inability to perform ADLs independently and is a poor prognosis for survival
95
what does the prognosis for ACS depend on?
number of vessels involved degree of injury to the heart
96
what are the signs and symptoms of MI
history of chest pain SOB diaphoresis

Cardiopulmonary (23 decks)

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