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Cardiopulmonary > Unit 2 Week 5 CAD > Flashcards

Unit 2 Week 5 CAD Flashcards

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
Q

what are the negative effects of smoking?

A

enhances atherosclerosis
increases LDL production
increase work of the heart (partially by increasing BP)

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26
Q

every increase of __ systolic/___ diastolic doubles the risk of cardiovascular events.

A

20mmHg systolic/ 10mmHg diastolic

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27
Q

what is HTN associated with?

A

CVA, MI, aneurysm, chronic renal failure

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28
Q

how does diabetes increase the risk of CVD?

A

high blood glucose –> nonenzymatic glycosylation = attachment of glucose proteins without enzymes –> accelerates atherosclerosis

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29
Q

what BMI is considered obesity and therefore a risk factor of CVD?

A

> or equal to 30 kg/m2

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30
Q

before age __, men are 6 times more likely than women to have an MI.

A

55

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31
Q

what is the second leading cause of death in all women <45 years?

A

CHD

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32
Q

lack of exercise increase the risk of CVD by about ___%.

A

20%
sedentary lifestyles are related to increases in BW and diabetes and insulin resistance

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33
Q

how do stress and depression increase risk of CVD?

A

almost triple the risk
can cause changes in BP, cortisol, and inflammatory response

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34
Q

what dietary changes should be considers to reduce risk of CVD?

A

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

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35
Q

how does regular exercise effect LDL and HDL?

A

results in small reductions in LDLs and elevated levels of HDLs

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36
Q

how does a person develop type 2 diabetes?

A

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

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37
Q

HTN is __ more prevalent in those who are obese.

A

5x

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38
Q

Ischemic vessel disease causes __ and __ in the heart.

A

angina and myocardial infarction

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39
Q

Ischemic vessel disease causes __ and __ in the brain.

A

TIA (transient ischemic attack) and CVA (cerebrovascular accident)

40
Q

Ischemic vessel disease causes __ or __ in the LE.

A

intermittent claudication or PAD

41
Q

what factors lead to ACS (acute coronary syndrome)?

A

-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
Q

True/false: MI can occur at any time, even at rest and during sleep.

A

true

43
Q

what causes vessel narrowing and decreased perfusion? explain.

A

atherosclerosis: plaques composed of lipid and thrombus
thrombus: occludes vessel or piece breaks off (embolus)
vasospasm: hyperplasia of smooth muscle cells

44
Q

what is prinzmetal angina?

A

variant angina associated with ST-segment elevation, at rest, and not associated with any preceding increase in myocardial oxygen demand

45
Q

what signs and symptoms of MI occur more commonly in women?

A

unusual fatigue, SOB, and indigestion (more subtle)

46
Q

what signs and symptoms of MI occur in men?

A

referred pain patterns
substernal pressure type of pain, radiating down the left UE, through to the back and up to the jaw

47
Q

what are the differences in presentation of MI among men and women?

A

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
Q

what is angina?

A

the classic symptoms of ischemic heart conditions
distress/pain of the chest

49
Q

Angina is secondary to ___.

A

imbalance of coronary oxyegn delivery

50
Q

what are the 3 types of angina?

A

stable
unstable
prinzmetal’s

51
Q

what is stable (typical) angina?

A

caused by fixed atherosclerotic lesion
reduced reserve for coronary blood flow
not present at rest
occurs when oxygen demand is increased

52
Q

stable angina is reproducible in terms of exertion:

A

intensity of effort
length of time of exertion
and relieved at rest and with administration of nitrates

53
Q

what is unstable angina?

A

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
Q

what type of angina is considered an emergency?

A

unstable angina
requires intervention before MI occurs

55
Q

what is prinzmetal’s angina?

A

variant
caused by coronary vasospasm due to endothelial dysfunction

56
Q

which type of angina is more difficult to diagnose and why?

A

prinzemetal’s angina due to its unpredictable onset, occurring even at rest

57
Q

what is ergonovine stimulation?

A

used to diagnose suspected prinzmetal angina
elicits coronary spasm and makes it occur predictably

58
Q

when perfusion of the myocardium does not meet oxygen demands __ will result.

A

ischemia

59
Q

what are the 3 clinical courses of ischemia?

A

sudden cardiac death
acute coronary syndrome (ACS)
chronic stable angina

60
Q

what indicates acute coronary syndrome?

A

unstable angina
ST-segment elevation myocardial infarction
non-stemi
progression to cardiac muscle dysfunction

61
Q

how does a non-stemi appear on an EKG?

A

ischemia shown with ST segment depression and t-wave inversion

62
Q

how does a stemi appear on an EKG?

A

ST segment elevation followed by a significant q wave. indicates a full thicken or transmural infarct

63
Q

how can an acute MI (non-stemi) be identified?

A

with a rise in serum troponin levels or ckmb plus either EKG changes or cardiac wall motion damage

64
Q

what does the speed of myocardial necrosis progression depend on?

A

amount of ischemia and how long the ischemia lasts

65
Q

what is a non-stemi?

A

rupture of coronary plaques –> partial occlusion of coronary artery –> subendocardial wall infarction

66
Q

what is a ST-elevation MI?

A

rupture of coronary plaques –> thrombus/clot –> total occlusion of a coronary artery –> transmural infarction

67
Q

what EKG lead are you looking at to find right coronary artery?

A

II, III, aVF

68
Q

what EKG lead are you looking at to find left anterior descending artery?

A

V1-V4

69
Q

what are the potential complications of ACS?

A

arrhythmias, contractile issues (can lead to CHF, mural thrombi), and wall weakening (can lead to rupture of CHF

70
Q

what do serum enzymes represent? and what two are used with ACS?

A

injury to cardiac cells
CK-MB seen first, troponin rises later and stays longer

71
Q

how is ACS medically managed?

A

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
Q

what is used to control cardiac pain?

A

nitrates, morphine, beta-blockers

73
Q

what is pharmacological treatment of ACS based on?

A

correcting the imbalance of oxygen supply and demand and lowering the workload of the heart

74
Q

how do beta blocking drugs work for ACS?

A

they reduce the work of the heart by blocking epinephrine or adrenaline effect decreasing HR causing blood vessel dilation

75
Q

how do organic nitrates work for ACS?

A

reduce preload, thereby work, potential for excessive preload reduction (by venous dilation)

76
Q

what are the clinical implications of cardiac drugs?

A

cause decreased cardiac response to exercise
but increase exercise tolerance in pts with angina
may lead to peripheral vasodilation and orthostatic intolerance

77
Q

what are the clinical implications of anti-thrombotic drugss?

A

risk of bleeding and bruising, internal hemorrhage risk, avoid bumping (avoid heavy lifting and plyometric type activities)

78
Q

what are the surgical options for ACS?

A

PTCA (PCI) w/ or w/o stents
CABG

79
Q

what are the indications for PTCA or PCI surgery?

A

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
Q

what are the indications for CABG surgery?

A

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
Q

what are the potential complications of an MI?

A

arrhythmias, contractile issues, wall weakening
(all can lead to decreased cardiac output)

82
Q

what is cardiogenic shock?

A

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
Q

what is the most common lethal complication of persistent angina and arrhythmias (STEMI)? why?

A

esp V-fib
necrotic tissue releases ion, enzymes and other chemicals that interfere with the normal depolarization of the heart

84
Q

what are other complications of persistent angina and arrhythmias (STEMI)?

A

A-fib, heart block, particularly when affects R side of heart

85
Q

what are the results/complications of ventricular remodeling?

A

contractile issues and wall weakening
with STEMI, changes in shape, size, and thickness of myocardium
areas of ventricular dilation and ventricular hypertrophy

86
Q

what factors affect remodeling?

A

size of infarct, ventricular load, patency of the artery that was infarcted

87
Q

with both atrial and ventricular fibrillation there is an increased risk of ___ with right side involvement?

A

pulmonary embolism

88
Q

with both atrial and ventricular fibrillation there is an increased risk of ___ with left side involvement.

A

CVA

89
Q

what is a ventricular aneurysm?

A

ballooning out of a weakened LV

90
Q

what is dyskinesia?

A

uncoordinated contraction

91
Q

what is hypokinesia?

A

decreased or no wall movement

92
Q

what is a mural thrombus?

A

a clump of atherosclerotic plaque buildup

93
Q

what is the severity of function impairment related to?

A

left ventricular hypertrophy
conduction defects
smoking
DM
HTN
VO2max

94
Q

what is the best predictor of function post-ACS?

A

VO2max
less than 21 mL/kg/min indicated inability to perform ADLs independently and is a poor prognosis for survival

95
Q

what does the prognosis for ACS depend on?

A

number of vessels involved
degree of injury to the heart

96
Q

what are the signs and symptoms of MI

A

history of chest pain
SOB
diaphoresis

Cardiopulmonary (23 decks)

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