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DPT 528 > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

what are the ischemic heart diseases?

A

atherosclerosis, coronary artery disease (CAD), acute MI, hypertension (HTN), cerebral vascular disease (CVD), peripheral artery disease (PAD), renal artery disease, and aneurysms

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2
Q

who is at the greatest risk for CV disease?

A

minority groups

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3
Q

t/f: COVID leads to an increased risk for CV disease

A

true :(

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4
Q

what is the PT’s role in treatment of CV disease?

A

educate pts on risk factor modification

manage cardiometabolic diseases and risk factors

fitness and exercise programs

vitals on EVERY pt

SHOULD be part of preventative medicine programs

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5
Q

what are some modifiable risk factors for CV disease?

A

smoking

body weight

physical activity

diet

BP

cholesterol

stress

blood glucose

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6
Q

what are non-modifiable risks for CV disease?

A

heredity

male sex

increased age

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7
Q

how does cigarette smoking contribute to the development of CVD?

A

leukocytosis (increased WBCs) leads to the development of ATHEROSCLEROSIS, PLAQUES, and lowered HDL

increased fibrinogen, BP, and inflammation

constriction of the arteries increases the pressure in the arteries leading to high BP

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8
Q

smoking ____ times a day leads to an increased risk of CVD above a non-smoker

A

4

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9
Q

what percentage of adults don’t engage in the minimum amount of physical activity?

A

60%

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10
Q

sedentary lifestyle is increased in _____ and _____

A

women, diabetics

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11
Q

physical activity has a beneficial effect on…

A

lipid profile

BP

insulin sensitivity

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12
Q

what are the long term benefits of physical activity?

A

increased fibrinolysis and RBC deformability

decreased platelet aggregability

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13
Q

exercise can be ____, _____, or both

A

resistive, aerobic

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14
Q

what is the goal for exercise?

A

150 minutes per week of moderate intensity OR 75 minutes per week of vigorous intensity

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15
Q

what is considered the MAIN risk for CVD?

A

body weight

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16
Q

what percentage of the population is obese/overweight?

A

68%

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17
Q

what BMI is associated with increased risk for CVD?

A

greater than or equal to 30 kg/m^2

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18
Q

adipose tissue where in the body is especially associated with increased significance of CVD risk?

A

abdomen

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19
Q

adequate nutrition can decrease the risk of what?

A

HTN

hyperlipidemia

obesity

glucose levels

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20
Q

what are the nutritional goals to decrease CVD risk?

A

4 1/2 cups fruits and veg

2 servings fish/week

3 servings whole grains daily

limit sugary drinks to 36 oz/week or less

limits sodium intake to less than 150 mg/day

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21
Q

t/f: BP is considered an independent risk factor for the development of CVD

A

true!

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22
Q

t/f: decreased BP lowers the risk of stroke more than MI

A

true

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23
Q

increase BP can cause…

A

increased pressure on arteries, injuring the vascular endothelium

increased permeability of vessel wall to LDL

increased foam cell and smooth muscle production leads to increased LDL in the intima layer causing plaques to form

increased systemic inflammation stimulates oxidative stress and cytokine production

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24
Q

t/f: there is a direct link b/w increased cholesterol and the development of CAD

A

true!

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25
Q

how does high cholesterol contribute to development of atherosclerosis?

A

high cholesterol leads to abnormal circulating lipid levels, especially LDL

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26
Q

can increased saturated fat in the diet contribute to increased cholesterol levels?

A

yes

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27
Q

how does increased HDL levels protect against development of atherosclerosis?

A

it transports cholesterol away from peripheral tissues

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28
Q

poorly controlled diabetes can ____ HDL levels

A

lower

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29
Q

what is HDL?

A

carries good cholesterol in blood to the liver where it is broken down and removed from your body

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30
Q

what is LDL?

A

carries cholesterol to your cells and arteries causing buildup

hardens and narrows vessels so less blood can flow through

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31
Q

what makes up total cholesterol?

A

HDL, LDL, and triglycerides

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32
Q

what is the best predictor for the development of CVD?

A

cholesterol levels

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33
Q

what ratio of total cholesterol to HDL leads increased risk of atherosclerosis?

A

greater than 4.5

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34
Q

triglyceride level of ____ can contribute to atherosclerosis

A

greater than 150 mg/dL

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35
Q

HDL level of ____ can contribute to atherosclerosis

A

less than 35 mg/dL

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36
Q

_____ _____ influences development of atherosclerosis 20x more than cholesterol content of food

A

saturated fat

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37
Q

what are ideal LDL levels?

A

less than 70 mg/dL

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38
Q

what is the suggested blood glucose levels to reduce risk of diabetics getting CAD?

A

less then 100 mg/dL

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39
Q

why does blood glucose levels increase risk for CAD?

A

the binding of glucose to proteins or fibrinogen w/o enzymes leads to increased risk for thrombus formation

diabetes can cause impaired endothelial function which allows for accumulation of cholesterol in arterial walls

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40
Q

t/f: family history is considered a major risk for CAD

A

false, it’s a “minor” risk bc there’s not much good evidence yet

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41
Q

is there a genetic link established for CAD?

A

no

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42
Q

what doubles risk for CAD?

A

premature/early CAD in your family

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43
Q

what is recommended in pt’s with a strong family history of CAD?

A

aspirin use

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44
Q

what is the average age of MI in men?

A

64.7 y/o

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45
Q

what is the average age of MI in women?

A

72.2 y/o

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46
Q

who is at a larger risk for acute MI before 55 y/o, men or women?

A

men

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47
Q

what is the leading cause of death in both men and women?

A

CAD

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48
Q

who has a higher mortality rate after a 1st MI, men or women?

A

women

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49
Q

what women are at an increased risk for CAD?

A

post-menopausal and diabetic women (estrogen may play protective role)

women who had pre-eclampsia w/pregnancy

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50
Q

t/f: increased hostility/anger leads to increased risk for CVD?

A

true

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51
Q

what are other factors that affect CVD?

A

homocysteine

lipoprotein

c-reactive protein

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52
Q

homocysteine

A

may contribute to oxidative stress, vascular inflammation, and platelet adhesiveness

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53
Q

lipoprotein

A

a varient of LDL that encourages inflammation and thrombosis

can’t be effected by diet and exercise

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54
Q

what has the greatest effect against lipoprotein

A

niacin

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55
Q

c-reactive protein

A

marker of systemic inflammation

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56
Q

t/f: c-reactive protein can be an independent predictor of MI, stroke, PAD, and sudden cardiac death

A

true

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57
Q

what is arterial pressure regulated by?

A

baroreceptor reflex

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58
Q

where are the baroreceptor reflex receptors?

A

the aortic arch and carotid sinuses

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59
Q

what do baroreceptors monitor?

A

stretch and deformation of arteries

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60
Q

can the baroreceptor response regulate BP long term?

A

no

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61
Q

how does the baroreceptor response work?

A

the baroreceptors are stimulated by increased arterial pressure and signal the CNS to send negative feedback to circulation via the ANS to bring the BP back to baseline

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62
Q

how does the ANS lower BP?

A

by lowering peripheral vascular resistance and cardiac output due to vasodilation, and decreased HR and contractility

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63
Q

what is HTN?

A

diastolic BP over 90 mmHg OR systolic BP consisttently over 140 mmHg

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64
Q

when does the heart relax?

A

during diastole

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65
Q

what is the role of diastole?

A

allows blood to fill coronary arteries to supply the heart w/blood supply

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66
Q

why is high DBP bad?

A

is leads bad blood supply to heart tissues

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67
Q

what is SBP?

A

the heart contracting to supply the body with blood or blood to the lungs

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68
Q

what are the types of HTN?

A

labile, primary/essential, secondary, and malignant

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69
Q

what is labile HTN?

A

BP that fluctuates b/w normal and hypertensive values

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70
Q

what type of HTN is the most common?

A

labile HTN

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71
Q

labile HTN is most common in what group?

A

advanced age groups

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72
Q

labile HTN is most likely due to…

A

multiple defects in BP regulation along with environmental stressors, possible insulin resistance, obesity, and diabetes

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73
Q

what is primary/essential HTN?

A

HTN with no discernable cause

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74
Q

what are some suspected causes of primary/essential HTN?

A

genetics, environment, high sodium intake, stress, obesity, alcohol, or smoking

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75
Q

what is secondary HTN?

A

there is an identifiable medical condition/cause of the HTN

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76
Q

what a percentage of HTN cases are secondary HTN?

A

5-10%

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77
Q

what is secondary HTN associated with?

A

renovascular health conditions and endocrine disorders

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78
Q

what is malignant HTN?

A

a hypertensive crisis where there is marked elevated BP w/target organ damage

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79
Q

what are some effects of malignant HTN?

A

retinal hemorrhages, heart failure, encephalopathy, renal insufficiency, stroke

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80
Q

in malignant HTN, DBP is…

A

over 125 mmHg

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81
Q

what is normal BP?

A

SBP: <120
and
DBP: <80

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82
Q

what is high-normal, elevated, pre-hypertensive BP?

A

SBP: 120-129
and
DBP: <80

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83
Q

what is stage 1 HTN?

A

SBP: 130-139
or
DBP: 80-89

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84
Q

what is stage 2 HTN?

A

SBP: >140
or
DBP: >90

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85
Q

what is hypertensive crisis?

A

SBP: >180
and/or
DBP: >120

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86
Q

what are symptoms?

A

what the patient tells us

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87
Q

what are signs?

A

changes in body structure and function

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88
Q

what are the symptoms of HTN?

A

headache

spontaneous epitaxis (bloody nose)

dizziness

flushing

sweating

blurred vision

nocturnal urinary frequency

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89
Q

what are the signs of HTN?

A

L ventricular hypertrophy (thickened myocardium)

retinopathy (vision changes)

arterial bruits in carotid and femoral arteries

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90
Q

why does a thickened myocardium affect BP?

A

the tissue becomes stiff and can’t pump properly

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91
Q

what are bruits?

A

swooshing artery sounds

turbulence due to atherosclerosis

S2 heart sounds due to L atrium contractions in a stiff LV

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92
Q

what happens as BP continues to increase?

A
  1. destruction of arterial bed and narrowing of arterioles
  2. elasticity of arteries decreases (can’t return to og shape)
  3. viscocity of blood increases (doesn’t move through as well)
  4. decrease in tissue perfusion (target organs-heart, kidneys, brain)
  5. increase in wall tension of LV
  6. acceleration of atherosclerosis
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93
Q

with HTN, there is a _____ in TPR and _____ in CO (cardiac output)

A

increase, decrease

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94
Q

what happens to the renal system with increased BP?

A

activation of the renin-angiotensin system

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95
Q

what is the renin-angiotensin system?

A

a decrease in blood flow to kidneys causes the secretion of renin and formation of angiotensin which causes the secretion of aldosterone, promoting sodium and water retention by the kidneys

the retention causes increased intravascular volume and continues the cycle that increases BP

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96
Q

what would continued abnormal BP cause?

A

abnormal calcium metabolism leading to loss of calcium

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97
Q

when is there secondary activation of the parathyroid gland?

A

when there is a loss of blood calcium

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98
Q

what does the parathyroid do to raise blood calcium levels?

A

increases movement of calcium from the bone

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99
Q

what is the downside of parathyroid increasing calcium from the bone to the blood?

A

risk for urinary tract stones and osteoporosis

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100
Q

t/f: pts with mild-moderate HTN are usually asymptomatic

A

true

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101
Q

why should we ALWAYS take BP?

A

mild to moderate HTN is usually asymptomatic

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102
Q

what is hypertensive heart disease?

A

changes in body structure and function related to the heart as a result of persistently elevated BP

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103
Q

what happens to the LV in hypertensive heart disease?

A

it hypertrophies (stiffens) so it can’t relax and fill as well

LV filling pressures increase

104
Q

what other structure is enlarged due to LV hypertrophy?

A

the L atrium

105
Q

what are the effects of LV hypertrophy in hypertensive heart disease?

A

decreased ability to fill and perfuse the coronaries

LA enlargement

myocardium ischemia or necrosis

106
Q

what are the changes in structure and function of the LV with HTN?

A

increased pressure causes the muscles to hypertrophy

hypertrophy impairs filling ability

decreased compliance of the LV also impairs its filling ability

decreased filling decreases coronary perfusion

107
Q

HTN leads to ____ O2 demand and ____ blood supply

A

increased, decreased

108
Q

what does persistent HTN lead to?

A

decreased coronary perfusion

cardiac arrythmias

decreased compliance

decreased blood volume in the LV

stroke

end result is that HTN causes LV failure if left untreated

usually ends in CHF

109
Q

what does decreased coronary perfusion lead to?

A

myocardial injury, ischemia, death

110
Q

HTN is a major contributor to the development of ____ and ____

A

MI and CAD

111
Q

what causes cardiac arrythmias?

A

electrolyte imbalance

112
Q

what does decreased compliance lead to?

A

decreased blood filling the LV

113
Q

what does decreased blood volume lead to?

A

decreased CO and SV

114
Q

what does persistent HTN usually end up as?

A

CHF (congestive heart failure)

115
Q

if HTN leads to to heart failure and decreased CO, what CV s/s would you expect to see?

A

fatigue, angina, edema in LE, pulmonary edema, SOB, dizziness, or palpitations

116
Q

what is the most common way to manage HTN?

A

pharmacological methods

117
Q

other than meds what lifestyle modifications can be done to manage HTN?

A

decrease weight

decrease sodium

decrease alcohol consumption

smoking cessation

regular aerobic exercise

118
Q

what are common meds used to manage HTN?

A

diuretics

beta-blockers

alpha adrenergic blockers

vasodilators

centrally acting adrenergic antagonists

calcium channel blockers

angiotensin 2 receptor blockers

ACE inhibitors

119
Q

how do diuretics work to manage HTN?

A

they increase fluid output to lower BP and stop pulmonary and LE edema

120
Q

how do beta-blockers work to manage HTN?

A

they keep the HR down

121
Q

are HTN meds more effective at rest or with exercise?

A

at rest

122
Q

what happens to BP measurements in pts on anti-hypertensive meds?

A

they are exaggerated with exercise

123
Q

what are the benefits of exercise for pts with HTN?

A

exercise controls BP better w/o or w/less meds

help the pt from going into hypertensive crisis

124
Q

medical clearance is necessary and on prescribed meds if the SBP is _____ and DBP is ____

A

greater or equal to 180 mmHg, greater or equal to 110 mmHg

125
Q

if retinopathy, renal disease, or LVH (LV hypertrophy) are present…

A

BP MUST be controlled at rest and w/activity b4 PT

126
Q

exercise should be terminated if BP increases above SBP of _____ or DBP of ____

A

greater than 250 mmHg , greater than 115 mmHg

127
Q

patients with HTN have an increased risk of what?

A

myocardial ischemia

128
Q

what are the 3 ischemic heart diseases?

A
  1. atherosclerosis
  2. coronary artery disease (CAD)
  3. acute myocardial infarction (MI)
129
Q

myocardial ischemia results from atherosclerosis which causes what 3 things?

A
  1. endothelial cells dysfunction
  2. arterial vessel narrowing
  3. abnormal vascular tone
130
Q

when does the myocardium receive blood supply?

A

during diastole (relaxation)

131
Q

the myocardium receives its own blood supply via…

A

coronary arteries

132
Q

when are the coronary arteries perfused?

A

during diastole

133
Q

what artery is extremely important in supplying the LV?

A

left anterior descending artery

134
Q

what arteries are often diseased in CAD?

A

left main

left anterior descending

left circumflex

obtuse marginal

right coronary artery

posterior descending artery

135
Q

what 4 things determine myocardial blood flow?

A
  1. DBP
  2. vasomotor tone
  3. resistance to flow
  4. left ventricular end diastolic pressure (LVEDP)
136
Q

what is diastolic blood pressure (DBP)?

A

the force that drives blood into the myocardium during diastole

137
Q

what is vasomotor tone?

A

force that regulates the caliber of artery and volume of blood delivered to the tissue

138
Q

does vasomotor tone differ throughout the coronary tree?

A

no, it is uniform throughout the coronary tree

139
Q

what maintains optimal resting level of contraction of smooth muscle fibers?

A

the vasomotor tone

140
Q

does atherosclerosis increase or decrease resistance to flow?

A

increase

141
Q

do collaterals increase or decrease resistance to flow?

A

decrease

142
Q

how do collaterals decrease resistance to flow?

A

they provide a route for blood to flow around obstructions

143
Q

what are collateral arteries?

A

small arteries that develop over time if there is a blockage in myocardial blood flow to try and provide a different route around the obstruction

144
Q

what is left ventricular end diastolic pressure?

A

pressure in the LV at the end of diastole

145
Q

what is the normal LVEDP?

A

3-5 mmHg

146
Q

when LVEDP is elevated, it leads to _____ blood flow and ______ myocardial oxygen demand.

A

decreased, increased

147
Q

if LVEDP remains elevated, what can it lead to?

A

MI bc the myocardium will become ischemic and maybe even necrotic

148
Q

what is the difference b/w coronary and peripheral vasculature?

A

coronary arteries have anastomotic connections that lack capillary beds called collateral vessels

149
Q

do collaterals vessels have a role under normal circumstances?

A

no, they are only present with issues

150
Q

what is a possible downside of collateral vasculature in coronaries?

A

they can prolong the onset of symptoms related to coronary atherosclerosis and ischemia so the patient won’t know they have an obstruction

151
Q

what are the 3 determinants for myocardial oxygen demand?

A
  1. ventricular wall stress
  2. heart rate
  3. contractility
152
Q

what is ventricular wall stress?

A

measure of the force acting on the myocardial fibers that pulls them apart

153
Q

when ventricular wall stress increases, does myocardial oxygen demand increase or decrease?

A

increase

154
Q

what changes in heart structure and function would causes increased ventricular wall stress?

A

HTN, valve stenosis, valve regurgitation, and atherosclerosis

155
Q

when HR increases, does the myocardial oxygen demand increase or decrease?

A

increase

156
Q

why does myocardial oxygen demand increase when HR increases?

A

bc there is an increased ATP consumption that demands more blood flow from the coronary arteries

157
Q

what is considered the most important factor in determining myocardial oxygen demand?

A

HR

158
Q

what is contractility?

A

a measure of the force of contraction

159
Q

contractility increases with the use of what?

A

catecholamines or meds that increase oxygen consumption

160
Q

contractility decreases with what?

A

meds that decrease oxygen consumption

161
Q

t/f: a small amount of oxygen is consumed for cardiac basal metabolism and electrical depolarization

A

true

162
Q

decreased coronary blood flow caused by ______ leads to decreased blood flow to the myocardium

A

atherosclerosis

163
Q

when oxygen demand increases but coronary blood flow is inadequate, oxygen ______ exceeds oxygen _____

A

demand, supply

164
Q

myocardial ischemia occurs at what percentage occlusion of the artery?

A

70%

165
Q

at what percent occlusion of the artery lumen are basal oxygen requirements not met and ischemia can develop AT REST?

A

90%

166
Q

when will ischemia occur at rest?

A

when the basal oxygen requirements are not met

90% occlusion of the artery

167
Q

t/f: decreased oxygen to tissues is accompanied by electrolyte disturbances

A

true

168
Q

with myocardial ischemia, there is cellular loss of what 3 minerals?

A
  1. potassium
  2. calcium
  3. magnesium
169
Q

cellular loss of potassium, calcium, and magnesium can lead to what?

A

further loss of cardiac contractility and pumping ability

170
Q

with myocardial ischemia, what is released that can cause serious imbalance in sympathetic and parasympathetic function, arrhythmias, and heart failure

A

catecholamines (E and NE)

171
Q

can ischemia be reversed?

A

yes! as long as it is reversed b4 tissue death starts to occur

172
Q

what is atherosclerosis?

A

pathologic process that causes progressive buildup of plaque and hardening and narrowing of systemic arteries

173
Q

what vessels can be affected by atherosclerosis?

A

any blood vessels

174
Q

t/f: ischemia can cause stroke

A

true

175
Q

atherosclerosis results in dysfunction of what cells?

A

endothelial

176
Q

what can cause the dysfunction of endothelial cells that’s seen in atherosclerosis?

A

toxic substances, abnormal circulating lipid levels, diabetes, and increased pressure from HTN

177
Q

damage to endothelial cells can lead to increase in what 2 things?

A
  1. inflammation and release of cytokines
  2. permeability to LDL
178
Q

LDL accumulates in what layer?

A

intima layer

179
Q

what are plaques composed of?

A

lipids (cholesterol) and thrombus (platelets)

180
Q

plaques develop in what layers?

A

endothelium and intima layers

181
Q

what is the first visible sign of endothelial damage?

A

fatty streak

182
Q

what does the fatty streak consist of?

A

lipid laden macrophages and smooth muscle cells

183
Q

where does the fatty streak build up?

A

in the endothelial and intima layers

184
Q

the fatty streak causes the endothelium to stretch and separate, which exposes ____ and _____ to circulation

A

intima, CT

185
Q

how does a rupture in the tan fibrous cap cause a thrombus to form?

A

when it ruptures, plaque content is released into the blood stream which stimulates a response to injury cascade and platelet activation and aggregation

186
Q

what is the difference b/w an obstruction and a rupture?

A

an obstruction is when plaque completely blocks the artery

a rupture is when the plaque causes a blood clot to form and block the artery or the clot becomes an embolus and travels to occlude a vessel

187
Q

what is the presentation of coronary artery disease?

A

sudden cardiac death

chronic unstable angina

acute coronary syndrome (ACS)/myocardial ischemia

cardiac muscle dysfunction

188
Q

what is sudden cardiac death?

A

occurs w/in an hour of the onset of symptoms and v fib leads to no cardiac output and death

189
Q

does sudden cardiac death have any symptoms?

A

it may or may not

190
Q

what is coronary muscle dysfunction?

A

heart failure

191
Q

what is angina?

A

substernal pressure

192
Q

where can angina be located?

A

from the epigastric region to the jaw

193
Q

what are some common symptoms of angina?

A

squeezing, tightness, crushing, feeling like an elephant/rock on the chest

194
Q

what is angina a result of?

A

temporary lack of blood flow to the myocardium due to an imbalance in supply and demand of blood

195
Q

what causes symptoms in angina?

A

ischemia of the myocardium

196
Q

what are typical male symptoms of angina?

A

central crushing chest pain, left arm pain, sweating

197
Q

what are typical female symptoms of angina?

A

jaw pain, shoulder blade pain, right arm pain sometimes, nausea, indigestion-like symptoms, SOB, fatigue

198
Q

what is usually the #1 symptom of angina in people with diabetes?

A

SOB

199
Q

what is chronic stable angina?

A

angina with a predictable onset of symptoms that develop w/exertion and diminish w/rest

associated with a set level of myocardial oxygen demand

200
Q

how is chronic stable angina controlled?

A

decreased intensity of activity or use of sublingual nitroglycerine

201
Q

what is unstable angina?

A

angina where the symptoms get worse in frequency or severity and may even occur AT REST

symptoms occur w/o and increased in myocardial O2 demand

202
Q

which type of angina has increased mortality and morbidity rates

A

unstable angina

203
Q

what is acute coronary syndrome?

A

MI

defined as unstable angina that lasts>20 minutes

204
Q

what 3 things cause an acute MI?

A
  1. lack of blood flow
  2. myocardial ischemia
  3. myocardial necrosis
205
Q

what 3 things define an acute MI? (VERY IMPORTANT)

A
  1. increased troponin I blood serum levels
  2. ECG changes
  3. echocardiogram imaging abnormalities
206
Q

what are ECG changes seen with acute MI?

A

pathologic Q wave

ST segment changes (elevated/depressed)

new left bundle branch block (LBBB) which supplies the LV

207
Q

what are echocardiogram imaging abnormalities seen with acute MI?

A

cardiac muscle damage

ventricular wall motion abnormalities

208
Q

what are the 3 ways to diagnose an acute MI?

A
  1. specific blood serum enzyme levels
  2. troponin I
  3. CPK-MB isoenzymes
209
Q

what are specific blood serum enzyme levels?

A

cardiac enzymes released into circulation when myocardial damage occurs

released at variable rates

210
Q

t/f: absence of specific blood serum enzymes means there was no injury

A

false, the absence of enzymes doesn’t mean no injury!!!

211
Q

what is the gold stand for diagnosing an acute MI

A

troponin I

212
Q

what is normal troponin I levels?

A

<0.1 ug/mL

213
Q

why is troponin I the gold standard?

A

bc it occurs earlier and lasts longer in the blood (up to 10 days post-MI)

214
Q

t/f: troponin I had a high sensitivity and specificity

A

true

215
Q

troponin I can also be elevated in what 2 conditions?

A

CHF and acute pulmonary embolism

216
Q

what is CPK-MB isoenzyme?

A

creatine phosphate myocardial band

217
Q

why is CPK-MB not always the best diagnostic test?

A

it rises quickly, but also disappears quickly

218
Q

when else can CPK-MB levels be elevated?

A

post bypass surgery, sepsis, or renal failure

219
Q

if a patient is still symptomatic, should you continue with PT?

A

NO! don’t continue with PT until the patient is medically stable

220
Q

what determines if a patient is medically stable for PT following an acute MI?

A

decreasing trend in serial troponin I levels

221
Q

what is a STEMI?

A

ST elevation MI

transmural infarct (full thickness or near full thickness)

abnormal Q wave with 24-48 hours

ST segment elevation

injury distal to TOTALLY occluded coronary

due to thrombus and plaque OR ruptured plaque

extent of injury determined by collateral blood flow and vasospasm

more significant

increased short-term mortality

222
Q

what is a NSTEMI?

A

non-ST elevation MI

subendocardial infarct (circumferential)

no Q wave abnormality

increased troponin I levels

ST segment DEPRESSION or inverted t-wave

due to INCOMPLETE occlusion

risk for death and another heart attack is higher when troponin I is higher

223
Q

is a STEMI or NSTEMI transmural?

A

STEMI

224
Q

is a STEMI or NSTEMI due to INCOMPLETE occlusion?

A

NSTEMI

225
Q

does a STEMI or NSTEMI have greater risk for death and another heart attack?

A

NSTEMI

226
Q

does a STEMI or NSTEMI have an abnormal Q wave?

A

STEMI

227
Q

does a STEMI or NSTEMI had an inverted T-wave?

A

NSTEMI

228
Q

does a STEMI or NSTEMI have ST segment elevation?

A

STEMI

229
Q

is a STEMI or NSTEMI due to thrombus and plaque or ruptured plaque?

A

STEMI

230
Q

is a STEMI or NSTEMI more significant?

A

STEMI

231
Q

does a STEMI or NSTEMI have increase troponin I levels?

A

NSTEMI

232
Q

is a STEMI or NSTEMI due to COMPLETE occlusion?

A

STEMI

233
Q

t/f: a STEMI has increased short term mortality?

A

true

234
Q

is a STEMI or NSTEMI subendocardial?

A

NSTEMI

235
Q

what is embolization?

A

rare

emboli in the LA from a clot in the LV from aneurysms/failure, prosthetic heart valve, infected heart valve

236
Q

what is arteritis-?

A

inflammation of the arteries that can affect the coronaries

237
Q

what is amyloidosis?

A

a metabolic disease that causes thickened arteries

238
Q

what is coronary artery vasospasm?

A

Prinzmetal angina

chest pain from a coronary artery vasospasm where the heart thinks it’s not getting enough blood

239
Q

what are medical/surgical management methods for acute coronary syndrome?

A

early reperfusion through thrombolytic agents, coronary angioplasty or CABG

meds

supplemental oxygen

angioplasty/stenting

treatment of arrythmias

treatment of complications

240
Q

what are common meds used to manage acute coronary syndrome?

A

aspirin, plavix, brilinta, anti-coagulants, nitrates (for chest pain), and beta blockers

241
Q

what are some complications of acute MI?

A

ventricular wall motion abnormalities (abnormal contraction patterns)

damage to myocardium of LV

persistent arrythmias post STEMI

pulmonary, endocrine, circulation, and renal problems

RAS system activation

242
Q

what are some ventricular wall motion abnormalities?

A

dyssynchrony

hypokinesis

akinesis

dyskinesis

243
Q

what is dyssynchrony?

A

uncoordinated contraction

244
Q

what is hypokinesis?

A

reduced strength of contraction

245
Q

what is akinesis?

A

no contraction

246
Q

what is dyskinesis?

A

abnormal movement during contraction

247
Q

15% damage to the myocardium of the LV leads to what?

A

decreased SV and coronary perfusion

increased EDP

248
Q

25% damage of the LV leads to what?

A

s/s of CHF and poor long term prognosis

249
Q

40% damage of the LV leads to what?

A

can lead to patient death

250
Q

a left infarct results in…

A

LBBB

251
Q

a right infarct results in…

A

SA node dysfunction or atrial arrythmias

252
Q

what are pulmonary problems that result from acute MI?

A

problems with gas exchange

pulmonary edema from CHF

253
Q

what are endocrine problems that result from acute MI?

A

impaired glucose tolerance

hyperglycermial insulin resistance

increased secretion of catecholamines

254
Q

what are circulation problems that result from acute MI?

A

increased platelet aggregation

decreased affinity of Hgb for O2

255
Q

what are renal problems that result from acute MI?

A

acute renal failure due to decreased CO (cardiac output)

256
Q

what does increased RAS system activation result in?

A

vasocontriction

sodium retention

257
Q

what does the prognosis of acute MI depend on?

A

complications

infarct size

presence of disease on other coronary arteries

improvements in ventricular function

DPT 528 (9 decks)

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