EXAM2/CH14- Acute Coronary Syndromes Flashcards
1
Q
cardiovascular disease (CVD) includes what 4 things
A
-CHD (aka CAD)
-heart failure
-hypertension
-stroke
2
Q
what is coronary heart disease (CHD) also called
A
coronary artery disease (CAD)
3
Q
what is the leading cause of death in the US
A
cardiovascular disease (CVD)
4
Q
what % of all CVD deaths are from CHD
A
50%
5
Q
how frequently does someone in the US suffer from a heart attack
A
every 42 seconds
6
Q
average age of first MI in men
A
65
7
Q
average age of first MI in women
A
72
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
9
Q
ACS stands for
A
acute coronary syndromes
10
Q
what 3 things do acute coronary syndromes (ACS) include
A
- unstable angina pectoris (chest pain)
- acute MI
- potential sudden cardiac death
11
Q
unstable angina pectoris in ACS is a result of what
A
ischemia (decreased blood flow/oxygen)
12
Q
ischemia
A
decreased blood flow/oxygen to the heart
13
Q
acute myocardial infarction
A
death of cardiac muscle cells due to prolonged ischemia
14
Q
acute MI occurs due to what
A
PROLONGED ischemia
15
Q
difference between angina and MI
A
MI is a more CHRONIC level of ischemia while angina is more acute
16
Q
sudden cardiac death
A
-abrupt loss of heart function caused by electrical disturbance
-electrical disturbance may be triggered by MI
17
Q
artery anatomy
endothelium
A
innermost layer
18
Q
artery anatomy
what does the endothelium do
A
protects against atherothrombosis
19
Q
artery anatomy
intima
A
thin layer of connective tissue on top of endothelium
20
Q
artery anatomy
what occurs at the intima
A
formation site of atherosclerotic lesions (aka plaque)
21
Q
artery anatomy
media
A
-located on top of intima
-contains mainly smooth muscle cells along with some connective tissue
22
Q
artery anatomy
adventitia
A
-outermost layer
-contains connective tissue, fibroblasts, + a few smooth muscle cells
23
Q
artery anatomy
lumen
A
opening where blood comes through
24
Q
artery anatomy
**what is the official site for plaque/atherosclerotic lesion formation
A
intima
25
# artery anatomy
what layers are responsible for vasodilation/vasoconstriction
-media
-adventitia
26
atherogenesis
disease process that may result in blood flow-limiting lesions in the
-epicardial coronary
-carotid
-iliac
-femoral arteries
-aorta
27
atherogenesis vs artherosclerosis
same thing
28
overview of pathophysiology of artherogenesis
1. endothelial injury
2. inflammatory response
3. endothelial dysfunction
4. plaque formation
29
# pathophysiology of atherogenesis
who experiences endothelial injury
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
30
# pathophysiology of atherogenesis
1. endothelial injury
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)
31
shear stress
the amount of pressure put on the vessel wall because you have a liquid that is flowing through it
32
what causes shear stresses
high BP
-as blood flows under high pressure, this applies excess stress to the vessels
33
glycated substances
molecule that has a sugar attached to it
34
can uncurable STI contribute to endothelial injury
yes
-it is in your system for the rest of your life + is therefore chronic + can contribute to endothelial injury
35
# pathophysiology of atherogenesis
what is endothelial injury caused by
-tobacco smoke + irritants
-LDL cholesterol (aka bad cholesterol)
-hypertension
-glycated substances (from hyperglycemia + diabetes)
-infectious agents (like chlamydia, herpes)
36
# pathophysiology of atherogenesis
2.. inflammatory (immune) response
-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)
37
# pathophysiology of atherogenesis
3.. endothelial dysfunction
-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)
38
# pathophysiology of atherogenesis
4.. plaque formation
-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
39
progression of atherogenesis
progression varies by
-size + volume of lesions
-stability of plaque
40
embolus
a blood clot or a piece of atherosclerotic plaque that acts like a clot
41
risk for embolus is due to what
due to plaque rupture or fissuring of the fibrous cap
42
when is plaque most dangerous
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
43
how are ACS diagnosed
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)
44
dyspnea
labored breathing
45
silent MI (painless MI) accounts for what % of ACS cases
25%
46
will chest pain always be present in a heart attack
no
-called a silent MI
-pretty common
47
shoulder pain symptom of ACS
radiating through shoulder down the arm
48
fatigue symptom of ACS
makes sense because heart is what provides adequate nutrients to the body
49
dyspnea symptom of ACS
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
50
clinical considerations for ACS- physical examination
-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
tachycardia
rapid HR, >100 bpm at rest
-if the heart is not getting adequate blood flow, it will try to compensate by. beating more
52
tachypnea
rapid ventilation
-if the heart is not getting adequate oxygen, the brain will tell the lungs to pick up the slack
53
pulmonary rales
-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
clinical testing for ACS
-electrocardiogram (EKG)
-echocardiogram
-chest x-ray
-laboratory results
55
# clinical testing for ACS
EKG
-in the case of a suspected heart attack, immediately hook them up to EKG
-EKG can help confirm diagnosis
56
# clinical testing for ACS
what do we look for on EKG
-ST elevation (STEMI)
-nonspecific T-wave abnormalities
57
# clinical testing for ACS
echocardiogram
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
# clinical testing for ACS
chest x-ray
tests for
-heart size
-pulmonary edema
59
# clinical testing for ACS
laboratory results
tests cardiac troponin (cTn)
60
what does cardiac troponin measure
cardiac cell necrosis
-the only test we can do to DIRECTLY measure cardiac cell necrosis (aka what happens during a heart attack)
61
after a MI, we see elevated levels of ____
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
how many direct ways to measure byproduct of MI
only 1- cardiac troponin
-every other way is INDIRECT
63
how does T wave indicate a MI
T wave can look a variety of different ways + still indicate a MI
64
how to diagnose an acute MI
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
66
after we get the diagnosis of a MI, we do we do
classify it
67
classification of MI (2)
-ST-segment elevation (STEMI)
-non-ST-segment elevation (NSTEMI)
68
# clinical testing for ACS
ST-segment elevation (STEMI)
-occluded coronary artery
-extensive damage + worse prognosis
69
# clinical testing for ACS
non-ST-segment elevation (NSTEMI)
-less damage (typically due to clot dissolution)
-better prognosis
70
# clinical testing for ACS
STEMI or NSTEMI is worse
STEMI is worse
-generally more necrosis with STEMI, therefore worse prognosis
71
medications for treatment + management of ACS
(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
# medications for treatment + management of ACS
antiplatelet- primary effects
-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
# medications for treatment + management of ACS
antiplatelet- exercise effects
none
74
# medications for treatment + management of ACS
antiplatelet- side effects
increases bleeding
75
# medications for treatment + management of ACS
beta blocker- primary effects
-reduces HR + BP
-improves survival
-antiarrhythmic
76
# medications for treatment + management of ACS
beta blocker- exercise effects
decreases HR + BP
(we willl not see a typical BP or HR response during exercise for patients taking these meds)
77
# medications for treatment + management of ACS
beta blocker- side effects
-fatigue
-hypotension
-bradycardia
78
# medications for treatment + management of ACS
ACE inhibitor- primary effects
-reduces BP
-improves survival
79
# medications for treatment + management of ACS
ACE inhibitor- exercise effects
reduces BP
(we will not see a typical BP response during exercise for patients taking these meds)
80
# medications for treatment + management of ACS
ACE inhibitor- side effects
-cough
-hypotension
81
# medications for treatment + management of ACS
ARB- primary effects
-reduces BP
-improves survival
82
# medications for treatment + management of ACS
ARB- exercise effects
reduces BP
(we will not see a typical BP response during exercise for patients taking these meds)
83
# medications for treatment + management of ACS
ARB- side effects
hypotension
84
# medications for treatment + management of ACS
aldosterone antagonist- primary effects
-decreases BP
-diuresis
85
# medications for treatment + management of ACS
aldosterone antagonist- exercise effects
decreases BP
(we will not see a typical BP response during exercise for patients taking these meds)
86
# medications for treatment + management of ACS
aldosterone antagonist
hypotension
87
what 4 medications will we not see a typical BP or HR response during exercise
-beta blocker
-ACE inhibitor
-ARB
-aldosterone antagonist
88
# medications for treatment + management of ACS
statin- primary effects
-decreases blood cholesterol
-improves survival
-targets LDL (bad cholesterol)
-directly interferes with what is contributing to plaque buildup
89
# medications for treatment + management of ACS
statin- exercise effects
none
90
# medications for treatment + management of ACS
statin- side effects
-muscle pain
-weakness
91
# medications for treatment + management of ACS
nitrate (nitroglycerin)- primary effects
coronary vasodilation
92
# medications for treatment + management of ACS
nitrate (nitroglycerin)- exercise effects
raises ischemic threshold
93
# medications for treatment + management of ACS
nitrate (nitroglycerin)- side effects
-headache
-hypotension
94
# medications for treatment + management of ACS
what medications do you take everyday
ALL but nitrate/nitroglycerin
95
# medications for treatment + management of ACS
what medications are only taken AS NEEDED
nitrate/nitroglycerin
-ONLY take when suspected MI
96
# medications for treatment + management of ACS
how is nitrate/nitroglycerin taken
sublingual, under the tongue to get into bloodstream
97
# medications for treatment + management of ACS
how does nitrate/nitroglycerin work
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
# medications for treatment + management of ACS
ACE inhibitor stands for
angiotensin-converting enzyme inhibitor
99
# medications for treatment + management of ACS
ARB stands for
angiotensin receptor blocker
100
reperfusion therapy
surgically going in to repair the vessel to reperfuse the heart
101
2 types of reperfusion therapy
-percutaneous coronary intervention (PCI)
-coronary artery bypass graft surgery (CABG)
102
reperfusion therapy- percutaneous coronary intervention (PCI)
through coronary catheterization
103
reperfusion therapy- coronary artery bypass graft surgery (CABG)
open heart surgery
104
reperfusion therapy- PCI or CABG is more invasive
CABG
105
factors associated with poor prognosis for ACS
-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
biggest indicator of prognosis post-MI
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
poor prognosis- LVEF
less than or equal to 35%
108
poor prognosis- exercise capacity
less than 5 METs
109
benefits of exercise testing after MI
-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
exercise testing after MI- assessment of future risk + prognosis is based on what
-inability to exercise
-capacity less than 5 METs
-exercise-induced ischemia
-failure of SBP to increase greater or equal to 10 mmHg
111
does every MI need surgical intervention
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
stress testing after acute MI- absolute contraindications
-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
old vs new standard of care for MI
old: bedrest
-study was done that shows bedrest was detrimental after MI
new: get up + moving (mobilization) as soon as possible after MI
113
exercise prescription after MI
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
exercise prescription after MI- inpatient rehab
-quick turnaround (usually 2-3 days) to discharge
-mobilization ASAP
115
secondary coronary prevention done during inpatient rehab after MI
-medication adherence
-diet
-exercise
-tobacco cessation
116
exercise prescription after MI- how do we start program
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
at the absolute minimum, a program after an MI should include
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
ExRx special considerations after MI (4)
-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
# ExRx special considerations after MI
intensity BELOW ischemic/anginal threshold
-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
# ExRx special considerations after MI
stretching
-chest stretches for open heart patients
-after open heart surgery, chest muscles become extremely sore + tight so chest stretches are essential
121
# ExRx special considerations after MI
take medications on schedule for performance of exercise training sessions
-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
# ExRx special considerations after MI
educate patient on importance of lifestyle physical activity
-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
