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*CLINICAL EXERCISE PHYSIOLOGY > EXAM2/CH14- Acute Coronary Syndromes > Flashcards

EXAM2/CH14- Acute Coronary Syndromes Flashcards

1
Q

cardiovascular disease (CVD) includes what 4 things

A

-CHD (aka CAD)
-heart failure
-hypertension
-stroke

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2
Q

what is coronary heart disease (CHD) also called

A

coronary artery disease (CAD)

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3
Q

what is the leading cause of death in the US

A

cardiovascular disease (CVD)

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4
Q

what % of all CVD deaths are from CHD

A

50%

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5
Q

how frequently does someone in the US suffer from a heart attack

A

every 42 seconds

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6
Q

average age of first MI in men

A

65

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7
Q

average age of first MI in women

A

72

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8
Q

what is age discripancy for first MI in men/women due to

A

testosterone/estrogen
-estrogen is CARDIOPROTECTIVE; protects the heart up until a woman hits menopause

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9
Q

ACS stands for

A

acute coronary syndromes

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10
Q

what 3 things do acute coronary syndromes (ACS) include

A
  1. unstable angina pectoris (chest pain)
  2. acute MI
  3. potential sudden cardiac death
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11
Q

unstable angina pectoris in ACS is a result of what

A

ischemia (decreased blood flow/oxygen)

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12
Q

ischemia

A

decreased blood flow/oxygen to the heart

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13
Q

acute myocardial infarction

A

death of cardiac muscle cells due to prolonged ischemia

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14
Q

acute MI occurs due to what

A

PROLONGED ischemia

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15
Q

difference between angina and MI

A

MI is a more CHRONIC level of ischemia while angina is more acute

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16
Q

sudden cardiac death

A

-abrupt loss of heart function caused by electrical disturbance
-electrical disturbance may be triggered by MI

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17
Q

artery anatomy

endothelium

A

innermost layer

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18
Q

artery anatomy

what does the endothelium do

A

protects against atherothrombosis

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19
Q

artery anatomy

intima

A

thin layer of connective tissue on top of endothelium

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20
Q

artery anatomy

what occurs at the intima

A

formation site of atherosclerotic lesions (aka plaque)

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21
Q

artery anatomy

media

A

-located on top of intima
-contains mainly smooth muscle cells along with some connective tissue

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22
Q

artery anatomy

adventitia

A

-outermost layer
-contains connective tissue, fibroblasts, + a few smooth muscle cells

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23
Q

artery anatomy

lumen

A

opening where blood comes through

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24
Q

artery anatomy

**what is the official site for plaque/atherosclerotic lesion formation

A

intima

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25
Q

artery anatomy

what layers are responsible for vasodilation/vasoconstriction

A

-media
-adventitia

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26
Q

atherogenesis

A

disease process that may result in blood flow-limiting lesions in the
-epicardial coronary
-carotid
-iliac
-femoral arteries
-aorta

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27
Q

atherogenesis vs artherosclerosis

A

same thing

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28
Q

overview of pathophysiology of artherogenesis

A
  1. endothelial injury
  2. inflammatory response
  3. endothelial dysfunction
  4. plaque formation
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29
Q

pathophysiology of atherogenesis

who experiences endothelial injury

A

everyone does, but very minimal compared to what we are talking about in this course
-people with disease have chronic or excessive amounts of this

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30
Q

pathophysiology of atherogenesis

  1. endothelial injury
A

chronic or excessive injury
-endothelium is incredibly thin, so it doesn’t take much to wipe out the endothelium completely, exposing the intima, where plaque will now form (this is why the intima is the formation site of plaque not the endothelium)

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31
Q

shear stress

A

the amount of pressure put on the vessel wall because you have a liquid that is flowing through it

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32
Q

what causes shear stresses

A

high BP
-as blood flows under high pressure, this applies excess stress to the vessels

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33
Q

glycated substances

A

molecule that has a sugar attached to it

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34
Q

can uncurable STI contribute to endothelial injury

A

yes
-it is in your system for the rest of your life + is therefore chronic + can contribute to endothelial injury

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35
Q

pathophysiology of atherogenesis

what is endothelial injury caused by

A

-tobacco smoke + irritants
-LDL cholesterol (aka bad cholesterol)
-hypertension
-glycated substances (from hyperglycemia + diabetes)
-infectious agents (like chlamydia, herpes)

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36
Q

pathophysiology of atherogenesis

2.. inflammatory (immune) response

A

-product of chronic/excessive injury
-platelet aggregation
-monocyte accumulation
-foam cell/LDL-C accumulation

(this is normally a good thing, but since it is CHRONIC in this case, it becomes a bad thing)

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37
Q

pathophysiology of atherogenesis

3.. endothelial dysfunction

A

-product of chronic injury
-increased adhesiveness of platelets + monocytes to artery wall
-increased permeability to lipoproteins in the blood
-impaired vasodilation/increased vasospasm

(muscle loses ability to properly constrict/dilate + it is hard for blood to flow through vessels)

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38
Q

pathophysiology of atherogenesis

4.. plaque formation

A

-growth factors from platelets exacerbate growth + proliferation of plaque
-lesion progresses from intima to other layers + leads to eventual narrowing of lumen
-firm, pale gray plaque with a fibrous cap

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39
Q

progression of atherogenesis

A

progression varies by
-size + volume of lesions
-stability of plaque

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40
Q

embolus

A

a blood clot or a piece of atherosclerotic plaque that acts like a clot

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41
Q

risk for embolus is due to what

A

due to plaque rupture or fissuring of the fibrous cap

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42
Q

when is plaque most dangerous

A

in BEGINNING stages
-because when plaque is in initial stages, it is far less stable
-when plaque has progressed, it has established its “home” + is very stable + harder to disrupt
-THEREFORE, YOU ARE AT GREATER RISK OF STROKE AT INITIAL STAGES OF DISEASE; this is why routine check ups are so necessary

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43
Q

how are ACS diagnosed

A

clinical assessment
-history of symptoms (chest pain or other anginal sensations)
-silent myocardiac infarction (painless MI)
-dyspnea (labored breathing)
-atypical symptoms (flu symptoms, shoulder pain, fatigue)

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44
Q

dyspnea

A

labored breathing

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45
Q

silent MI (painless MI) accounts for what % of ACS cases

A

25%

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46
Q

will chest pain always be present in a heart attack

A

no
-called a silent MI
-pretty common

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47
Q

shoulder pain symptom of ACS

A

radiating through shoulder down the arm

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48
Q

fatigue symptom of ACS

A

makes sense because heart is what provides adequate nutrients to the body

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49
Q

dyspnea symptom of ACS

A

points us back to how closely the heart is linked to the pulmonary system
-if the heart is having problems, it will eventually present through the lungs as well

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50
Q

clinical considerations for ACS- physical examination

A

-BP may be high, low, or normal
-diaphoresis (excessive sweating)
-sinus tachycardia (rapid HR; >100 bpm at rest)
-tachypnea (rapid ventilation)
-new murmur of mitral regurgitation
-pulmonary rales (crackling)

51
Q

tachycardia

A

rapid HR, >100 bpm at rest
-if the heart is not getting adequate blood flow, it will try to compensate by. beating more

52
Q

tachypnea

A

rapid ventilation
-if the heart is not getting adequate oxygen, the brain will tell the lungs to pick up the slack

53
Q

pulmonary rales

A

-when you have a heart attack, it is caused by build up of plaque, which prevents enough blood getting through to myocardium
-as the pressure increases, it puts pressure on the vessels, which starts to go BACK into the lungs causing a build up of pressure in the lungs which forces fluid out of the vessels + into the lungs

54
Q

clinical testing for ACS

A

-electrocardiogram (EKG)
-echocardiogram
-chest x-ray
-laboratory results

55
Q

clinical testing for ACS

EKG

A

-in the case of a suspected heart attack, immediately hook them up to EKG
-EKG can help confirm diagnosis

56
Q

clinical testing for ACS

what do we look for on EKG

A

-ST elevation (STEMI)
-nonspecific T-wave abnormalities

57
Q

clinical testing for ACS

echocardiogram

A

identify area of heart damage
-takes picture of vessels to see where build up is occurring
-more of a CONFIRMATORY test, not typically done during initial stages; most likely will come after we have intervened
-will show us parts of the heart that have died/becomes necrotic as a result

58
Q

clinical testing for ACS

chest x-ray

A

tests for
-heart size
-pulmonary edema

59
Q

clinical testing for ACS

laboratory results

A

tests cardiac troponin (cTn)

60
Q

what does cardiac troponin measure

A

cardiac cell necrosis
-the only test we can do to DIRECTLY measure cardiac cell necrosis (aka what happens during a heart attack)

61
Q

after a MI, we see elevated levels of ____

A

cardiac troponin
-typically 3-6 hours later, another blood draw would be done + we would see that cardiac troponin is even further elevated from the initial draw

62
Q

how many direct ways to measure byproduct of MI

A

only 1- cardiac troponin
-every other way is INDIRECT

63
Q

how does T wave indicate a MI

A

T wave can look a variety of different ways + still indicate a MI

64
Q

how to diagnose an acute MI

A

AT LEAST 2 OF THE FOLLOWING 3 VARIABLES to confirm diagnosis of a MI:
-chest pain persisting for >30 min
-ECG showing ST-segment elevation or T-wave changes (abnormalities)
-presence of biomarkers of myocyte necrosis (elevated cardiac troponin levels, cTn)

65
Q
A
66
Q

after we get the diagnosis of a MI, we do we do

A

classify it

67
Q

classification of MI (2)

A

-ST-segment elevation (STEMI)
-non-ST-segment elevation (NSTEMI)

68
Q

clinical testing for ACS

ST-segment elevation (STEMI)

A

-occluded coronary artery
-extensive damage + worse prognosis

69
Q

clinical testing for ACS

non-ST-segment elevation (NSTEMI)

A

-less damage (typically due to clot dissolution)
-better prognosis

70
Q

clinical testing for ACS

STEMI or NSTEMI is worse

A

STEMI is worse
-generally more necrosis with STEMI, therefore worse prognosis

71
Q

medications for treatment + management of ACS

A

(won’t just be prescribed to people that had a MI, but also people at significant risk for one)

-antiplatelet
-beta blocker
-ACE inhibitor
-ARB
-aidosterone antagonist
-statin
-nitrate (aka nitroglycerin)

72
Q

medications for treatment + management of ACS

antiplatelet- primary effects

A

-blocks platelet aggregation
-improves survival

-directly affects atherosclerotic process because platelets are what rushes to the site + is part of the plaque that builds up
-antiplatelet medication INHIBITS platelet aggregation + therefore inhibits plaque build up

73
Q

medications for treatment + management of ACS

antiplatelet- exercise effects

A

none

74
Q

medications for treatment + management of ACS

antiplatelet- side effects

A

increases bleeding

75
Q

medications for treatment + management of ACS

beta blocker- primary effects

A

-reduces HR + BP
-improves survival
-antiarrhythmic

76
Q

medications for treatment + management of ACS

beta blocker- exercise effects

A

decreases HR + BP

(we willl not see a typical BP or HR response during exercise for patients taking these meds)

77
Q

medications for treatment + management of ACS

beta blocker- side effects

A

-fatigue
-hypotension
-bradycardia

78
Q

medications for treatment + management of ACS

ACE inhibitor- primary effects

A

-reduces BP
-improves survival

79
Q

medications for treatment + management of ACS

ACE inhibitor- exercise effects

A

reduces BP

(we will not see a typical BP response during exercise for patients taking these meds)

80
Q

medications for treatment + management of ACS

ACE inhibitor- side effects

A

-cough
-hypotension

81
Q

medications for treatment + management of ACS

ARB- primary effects

A

-reduces BP
-improves survival

82
Q

medications for treatment + management of ACS

ARB- exercise effects

A

reduces BP

(we will not see a typical BP response during exercise for patients taking these meds)

83
Q

medications for treatment + management of ACS

ARB- side effects

A

hypotension

84
Q

medications for treatment + management of ACS

aldosterone antagonist- primary effects

A

-decreases BP
-diuresis

85
Q

medications for treatment + management of ACS

aldosterone antagonist- exercise effects

A

decreases BP

(we will not see a typical BP response during exercise for patients taking these meds)

86
Q

medications for treatment + management of ACS

aldosterone antagonist

A

hypotension

87
Q

what 4 medications will we not see a typical BP or HR response during exercise

A

-beta blocker
-ACE inhibitor
-ARB
-aldosterone antagonist

88
Q

medications for treatment + management of ACS

statin- primary effects

A

-decreases blood cholesterol
-improves survival

-targets LDL (bad cholesterol)
-directly interferes with what is contributing to plaque buildup

89
Q

medications for treatment + management of ACS

statin- exercise effects

A

none

90
Q

medications for treatment + management of ACS

statin- side effects

A

-muscle pain
-weakness

91
Q

medications for treatment + management of ACS

nitrate (nitroglycerin)- primary effects

A

coronary vasodilation

92
Q

medications for treatment + management of ACS

nitrate (nitroglycerin)- exercise effects

A

raises ischemic threshold

93
Q

medications for treatment + management of ACS

nitrate (nitroglycerin)- side effects

A

-headache
-hypotension

94
Q

medications for treatment + management of ACS

what medications do you take everyday

A

ALL but nitrate/nitroglycerin

95
Q

medications for treatment + management of ACS

what medications are only taken AS NEEDED

A

nitrate/nitroglycerin
-ONLY take when suspected MI

96
Q

medications for treatment + management of ACS

how is nitrate/nitroglycerin taken

A

sublingual, under the tongue to get into bloodstream

97
Q

medications for treatment + management of ACS

how does nitrate/nitroglycerin work

A

systemic vasodilation- takes all the vessels in the body + causes them to expand
-this helps in a MI as a last ditch effort to vasodilate as much as possible
-not a treatment for MI, but rather BUYS YOU TIME in the case of an MI

98
Q

medications for treatment + management of ACS

ACE inhibitor stands for

A

angiotensin-converting enzyme inhibitor

99
Q

medications for treatment + management of ACS

ARB stands for

A

angiotensin receptor blocker

100
Q

reperfusion therapy

A

surgically going in to repair the vessel to reperfuse the heart

101
Q

2 types of reperfusion therapy

A

-percutaneous coronary intervention (PCI)
-coronary artery bypass graft surgery (CABG)

102
Q

reperfusion therapy- percutaneous coronary intervention (PCI)

A

through coronary catheterization

103
Q

reperfusion therapy- coronary artery bypass graft surgery (CABG)

A

open heart surgery

104
Q

reperfusion therapy- PCI or CABG is more invasive

A

CABG

105
Q

factors associated with poor prognosis for ACS

A

-LVEF (left ventricle ejection fraction) equal or less than 35% or congestive heart failure (CHF)
-poor exercise capacity, less than 5 METs
-evidence of extensive myocardial ischemia during exercise or pharmacologic stress testing
-complications such as renal failure, stroke

106
Q

biggest indicator of prognosis post-MI

A

LVEF (left ventricle ejection fraction)
-tells us how much blood is being ejected from left ventricle with each heartbeat

-lower ejection, the worse off you’ll be

107
Q

poor prognosis- LVEF

A

less than or equal to 35%

108
Q

poor prognosis- exercise capacity

A

less than 5 METs

109
Q

benefits of exercise testing after MI

A

-evaluate symptoms + possible ischemia
-determine need for angiography (if initially treated with noninvasive procedure)
-determine effectiveness of medication therapy
-assess future risk + prognosis
-determine exercise capacity

110
Q

exercise testing after MI- assessment of future risk + prognosis is based on what

A

-inability to exercise
-capacity less than 5 METs
-exercise-induced ischemia
-failure of SBP to increase greater or equal to 10 mmHg

111
Q

does every MI need surgical intervention

A

no
-if we catch the heart attack soon enough, we can give medications that will dissolve the plaque
-if caught soon enough, we can do a GXT to see if functional capacity is low, to know if we need an angiography

112
Q

stress testing after acute MI- absolute contraindications

A

-MI within prior 2 days or other acute cardiac event
-change in ECG suggesting MI or other acute cardiac event
-unstable angina
-symptomatic severe aortic stenosis
-uncontrolled symptomatic heart failure
-acute pulmonary embolism or infarction
-acute myocarditis or pericarditis
-acute infection
-suspected or known ventricular or dissecting aortic aneurysm

112
Q

old vs new standard of care for MI

A

old: bedrest
-study was done that shows bedrest was detrimental after MI

new: get up + moving (mobilization) as soon as possible after MI

113
Q

exercise prescription after MI

A

inpatient rehab (usually 2-3 days)->
while they are still at the hospital, we want to address all secondary coronary prevention factors ->
initial home prescription (super basic, for safety) ->
outpatient cardiac rehab (initial 1-2 weeks after going home, they will start cardiac rehab for 2-3 days/week which will last around 2-3 months)

114
Q

exercise prescription after MI- inpatient rehab

A

-quick turnaround (usually 2-3 days) to discharge
-mobilization ASAP

115
Q

secondary coronary prevention done during inpatient rehab after MI

A

-medication adherence
-diet
-exercise
-tobacco cessation

116
Q

exercise prescription after MI- how do we start program

A

start with a program that is DOABLE for patient then progress
-we start with everything the patient can give us, even if it starts with only 3 minutes
-they will progress from there

117
Q

at the absolute minimum, a program after an MI should include

A

CARDIORESPIRATORY
-10 min per bout of exercise
-2-3 days per week

RESISTANCE TRAINING
-2-3 days per week

FLEXIBILITY + BALANCE
-as often as possible

118
Q

ExRx special considerations after MI (4)

A

-intensity BELOW ischemia/anginal threshold
-stretching
-take medications on schedule for performance of exercise training sessions
-educate patient on importance of lifestyle physical activity

119
Q

ExRx special considerations after MI

intensity BELOW ischemic/anginal threshold

A

-stay below the point where chest pain kicks in
-this is an instance where baseline GXTs are helpful; if we can identify the RPE or HRR that chest pain kicks in, we can use that to stay under these levels

120
Q

ExRx special considerations after MI

stretching

A

-chest stretches for open heart patients
-after open heart surgery, chest muscles become extremely sore + tight so chest stretches are essential

121
Q

ExRx special considerations after MI

take medications on schedule for performance of exercise training sessions

A

-make sure patient has been taking medications regularly, as well as the SIDE EFFECTS of these medications
-while they should be reporting these to their physician, they will be seeing you at cardiac rehab much more frequently than the physician

122
Q

ExRx special considerations after MI

educate patient on importance of lifestyle physical activity

A

-give patient the tools that will facilitate them having healthier behaviors BESIDES the immediate need
-don’t ever underestimate the impact this education can have on the patient

*CLINICAL EXERCISE PHYSIOLOGY (15 decks)

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