Atherosclerosis/Vascular Disease Flashcards
(230 cards)
1
Q
Triphasic wave form
A
- strong forward component of blood flow during systole
- short reversal of blood flow during early diastole
- low amplitude foward blood flow during remaining diastole (loses vacuum, going back)
INACTIVE - when exercise - both systolic and diastolic flow increase
2
Q
Bernoulli’s
A
as speed of a moving fluid increass, pressure within fluid decreases (and speed increases)
75% - flow begins to decreases and pressure downstream decreases to form a pressure gradient
3
Q
aneurysm vs diffuse ectasia
A
smaller increase generaly in diameter = de
aneurysm - widen, dilate (at least 50% increase over normal arterial diameter)
4
Q
AAA
A
cystic medial degeneration - of elastic fibers
acuumulation of collagenous and mucoid material in the medial layer
mostly with aging and hypertension (marfan, ehlers danlos)
5
Q
Type A Aortic Dissection
A
involves part of ascendinga aorta
surgical!
emergency and high mortality
lower BP in all
6
Q
Type B Aortic Dissection
A
does not involve ascending aorta
complicated - surgical
uncomplicated - medical
7
Q
AAA risk factors
A
increasing age
smoking
male
genetic
8
Q
aortic wall tension
A
variation in wall tension in aneurysm
proportional to the product of pressure and radius
bigger radius = more tension = bigger chance of ruptiur
P is the same
9
Q
AAA therapy
A
medican (smoking HTN)
endovascular/open therapy
10
Q
PAD mechanism
A
if stenosis - high resistance
turbulent flow - pressure drops across stenosis and impaired endothelial function
inapility to increase flow with execise
mismatched O2 supply and demand (IC)
inefficient oxidation
can’t dilate because endothelial dysfunction - angina and claudation
11
Q
claudication
A
cramping tightness aching fatigue
bluttock, hip, thigh, calf, foot
exercise induced
not with stating (relief)
less than 5 min
12
Q
ABI
A
Under .90 is PAD!
measure P in both arms and legs
put highest angle P over highest arm P on eich side
add 2 numbers together
13
Q
Toe Brachial Pressure
A
divide te pressure by higher of the two brachial ressures
when ABI not possible because calcified
14
Q
PAD therapy
A
exercise
smoking cessation
STATINS
HTN
antiplatelets
symtomatic relief
revascularization (if gangrene, non healing ulcers, ischemic rest paid, bad claudication)
15
Q
Raynauds Disease
A
rare disease that causes vasospasm of the arteries and reduces blood flow to fingers and toes
idiopathic or secondary (lupus, sjogrens)
vascular constriction - white/blue/numb extremities
16
Q
Treatment for Raynauds Disease
A
CCBs
Alpha block
ARBs (vasodilate)
surgery (rare)
17
Q
varicose veins
A
dilated tortuous veins
reflux bc valvular insufficiency
obesity, prenancy, familial
usually cosmetic - can be stasis dermatitis
18
Q
Carotid artery disease therapy
A
can lead to stroke!
antiplatelet/anticoagulation
statins
risk factor modification (smoking, HTN, diabetes)
revascularization (stenting)
19
Q
arteriovenous malformation
A
embryonic/fetal development
direct connections between arteries and veins! more common in brain or SC
20
Q
risk factors for CAD
A
herediatry
lipids (high LDL)
smoking
diabetes
HTN
obesity
21
Q
CRP
A
inflammation marker
predictor of first MI/ischemic stroke (also high if another stressor)
22
Q
Atherosclerosis Pathway
A
- endothelial injury
- LDLs enter, smoooth muscle cells migrate
- macrophages roll and enter epithelial cell and eat LDL and turn into foam cell
- secrete cytokines to recruit more
- more macrophages enter - fatty streak
- TGF beta increases collagen
macrophages make MMP-9 which breaks down fatty cap
23
Q
Thinning of fibrous cap
A
degraded by foam cells secreting MMP
rupture!!
24
Q
synthesis of fibrous cap
A
smooth muscle cless promote collagen and elastin
25
NO mechanism
ACH/sheer stress - cleave cNOS to NO
moves across wall and increases cGMP to stim smooth muscle cell relaxation
26
CT scan
regular scan or use for coronary calcium studies
27
characteristics of angina
intermittent, recurrent
strangling, pain, pressure, tightness
location - retrosternal, shoulders - arms
dyspnea
30 s - 10 min
28
plaque and ischemic impact
stenotic - few, fibrotic, thick cap, less compensatory enlargement (ischemia - angina, postive stress test)
non-stenotic - many, lipid rich, thin cap, compensatory enlargement (infarction)
29
therapeutic targets
lower LDL (source of inflammation and building blocks of plaques) - stop progression and decrease chance of rupture
dampen inflammation and restore homeostasis
restore fibrous cap
30
intima
where everything happens
31
pathophysiology of atherosclerosis
1. endothelial dysfunction (increased permeability, WBC adhesion)
2. smooth muscleemigration from media to intima, macrophage activation
3. liids from blood enter intima and phagocytosesd by macrophages in intima
4. smooth muscle proliferation, collagen and other ecm deposition, extracellular lipid
1-2 don't see anything, 3-4 do see
32
complications from atherosclerosis
thrombosis
embolism
aneurysm and rupture
dissection
33
true aneurysm
dilation of segment of vessel
34
false aneurysm
dissection
extravasation of blood
looks like true aneurysm
35
fusiform aneurysm
true aneurysm
in the brain
36
saccular aneurysm
brain
true aneurysm
37
etiologies of aneurysms
atherosclerotic\*\*
infectious
inflammatiory
autoimmune
degenerative
traumatic
38
Giant Cell Arteritis
large vessels - head
headches
visual problems
steroids!
usually older people, inflammation of arteries around forehead
39
Polyarteritis Nodosa
middle vessels
transmural inflammation
necrossis and thickening
fever, weight loss, abdominal pain
corticosteroids
40
Wegener Granulomatosis
respirator involvement
acute necrotizing granulomas and vasculitis
fever, mucosal alterations
80% death if unreaed
41
thromboangiitis obliterans (Buerger's disease)
smokers,
segmntal thrombising infammation of distal limb arteries
ulcerations of toes, feet, fingers, gangrene
smoking cessation is only thing that helps!
42
DVT etiology
OCP
dehydration
inactivity
surgery
trauma
MI
strok
43
DVT therapy
Heparin
44
chylomicron
absorbed cholesterl from brush border into lymph to liver
45
primordial prevention
prevent the development of risk factors for CVD
46
primary prevention
prevent the first CVD event
47
secondary prevention
prevent subsequent CVD events (decrease LDL)
48
Bile Acids Mechanism
breakdown product of cholesterol - most is reabsorbed in the small bowel
act as a detergent - make cholesterol soluble
49
Bile Acid Resins
i.e. WelChol
No outcomes data!!
Used as add on for additional LDL lowering
inhibits cholesterol absorption
They disrupt the enterohepatic circulation of bile acids by combining with bile constituents and preventing their reabsorption from the gut
Liver makes more bile acids since it is not reabsorbled, which uses a lot of LDL cholesterol (liver compensates so not as effective)
50
Bile acid resin Side Effects
bloating
interfere with absorption of vitamins or meds
can raise TG
51
Ezetimibe
selective cholesterol absorption inhibitor
acts on brush border to inhibit reabsorption of cholesterol itself
Liver has to absorb more cholesterol from blood
\*\* mainly add on to statins
52
Ezitimide - decreases events?
yes!
with a statin
53
Niacin
decreases VLDL production, LDL formation, increases hepatic clearance of LDL precursors
raises HDL
NO decrease in events
54
Niacin side effects
gout!! elevated uric acid levls
hepatic toxicity
flushing and pruritis
55
Fibrates Indications
lowers TG by a lot! no real effect on LDL, raises HDL a little
used for severe hypertriglyceridemia
hgih TH or low LDL
56
Fibrates Mechanism
activate PPAR alpha - activates lipoprotein lipase and increases lipoysis in the plasma
57
Fibrates side effects
avoid in patients wiht hepatic/renal function issues
increased risk with statins of rhabdomyolysis
58
HMG-CoA Reductase Inhibitor Mechanism
Statin!!
if inhibit - increase HMG-CoA to make more cholesterol but also increase transcription of LDL R so take more out of blood and decrease LDL by a lot
59
Statin - decrease events?
yes!!
60
Statin side effects
increase in transaminasess
muscle pain or weakness
61
Statin studies
primary prevention!
educe morbidity and mortality
cost effective
lifestyle also needed
62
PCSK9 mechanism
antibody to LDL -R that allows it to be destroyed - dysfunctional!
more LDL-R because it is recycled
decrease LDL by a olot - decrease events!
63
PCSK9 Side Effects
injection site swelling
64
how to lower TGs?
fibrates
niacin
fish oil
(not as important as LDL)
65
how to lower LDL?
statins
ezetimibe
pcsk9 abs
bile acid resins
niacin
66
what happens from vessel injury?
vasoconstriction (reduced blood flow)
platelet adhesion/activation/aggregation
blood coagulation cascade
67
local control of vasoconstriction
thromboxane and other local controls released
68
systemic control of vasoconstriction
epinephrine
69
extrinsic pathway
damage to tissue outside the vessel activates factor X
first pathway to start but turns off when a little factor Xa is made
vessel injury
triggered by tissue factor
70
intrinsic pathway
after extrinsic pathway makes a little Xa and is turned off
most fibrin is made from intrinsic pathway
71
initation of the clotting cascade
interaction of plasma bound TF exposed by vascular injury
interacts with factor 7 (extrinsic)
activates factor 10
10a acivates a small amount of thrombin and TFPI which rapidly inactivates the pathway!
72
Extrinsic Xase
TF + VIIa
activates factor XI and facor X
73
thrombin generation
primed by extrinsic pathway but becomes reliant on intrinsic pathway to make Xa
74
Intrinsic Xase
IXa + VIIIa
greatly amplifies Xa
75
Prothrombinase Complex
Xa + Va
explosive generation of thrombin
76
Factor v Leiden
mutated form of factor V cannot be inactivated by protein C
tons of V --\> clots
77
What does thrombin activate?
XI, V, 13
78
formation and stabilization of fibrin
thrombin hydrolyzes fibrinogen to fibrin
calcium - acts like glue to hold fibrin monomers together (loose insoluble fibrin polymer - clot)
factor XII also activated by thrombin and stabilizes the fibrin polymers
79
what does thrombin do?
1. activate protein C (anti inflammatory - helps dissolve clot)
2. activate platelests
3. form fibrin
80
Vitamin K dependent factors
thrombin, Vii, IX, X
protein C and S
81
TFPI
synthesized in endothelial cells
present in plasma and platelets
inhibits Xa, VIIa and TF
82
Antithrombin
circulating plasma protease inhibotr
neutralizes many enzymes in the clotting cascade (esp thrombin and factor Xa)
83
Protein C/Protein S
inhibit coagulation cofactors V and VIII (inactivate prothrombinase and Intrinsic Xase
84
fibrinolysis
normal hemostatic response to vascular injury (body doesn't need clot anymore
plasminogen --\> plasmin (intrinsic and extrinsic factors
release of tPA from endothelial cells!
plasmin digest many of the proteins cleave peptide bonds
85
intrinsic activation of plamsin
XIIa
86
extrinsic activation of plasmin
tPA and urokinase
activate plasmin
activate fibrin
87
d dimer
major fibrin degredation factors
sign that high clot burden
88
tissue factor
initates coagulation
89
prostacyclin
vasodilation/inhibition of platelet aggregation
90
NO
vasodilation/inhibition of platelet aggregation
91
vWF
platelet collagen adhesion - complex with factor VIII
92
AT
inhibition of blood coagulation
93
tPA
fibrinolysis
94
factors of plaque vulnerability
size of atheromatous core
thickness of fibrous cap
inflammation and repair of fibrous cap
95
subendocardial vs transmural MI
96
Diagnostic criteria of abnormal Q waves
width \> .04 s
depth \> 25% of R wave
97
EKG of AMI - acutely
ST elevation
98
EKG hours after AMI
ST elevation
decreased R wave
Q wave begins
99
ekg after ami 1-2 days later
t wave inversion
deep q wave
100
ekg days after acute mi
st normalizes
t wave inverted
101
ekg weeks after ami
st and t are normal
q wave persists
102
cardiac markers
CK (start late peak early)
troponin (start early peak late)
103
left ventricle dysfynction - complications
heart failure (rales)
pulmonary edema
cardiogenic shock
104
myocardial healing complications
VSD
ventricular free wall rupture
aneurysm formation
105
process of thrombolysis
plasminogen --\> plasmin
plasmin breaks down fibrin (in thrombus and circulating)
106
streptokinase
binds with plasminogen
sk-plasminogen complex cleaves plasminogen to plasmin
plasmin breaks down fibrin
107
tPA
binds with fibrin
cleaves plasminogen to plasmin
breaks down fibrinogen to fibrin
108
kringle dowmains
on tpa
allow tpa to recognize and bind to fibrin
create higher affinity
109
TNKase
tPA mutant form to increase half life and specificity
also retaplase
110
indications for thrombolysis or stent
1. chest pain consistent with AMI
2. EKG changes (ST segment elevation, new BBB)
3. time from onset less than 12h
111
determinants of survival (MI)
1. rapidity of reperfusion
2. magnitude of restortation of flow
3. persistence of flow
4. major complications (bleeding, reinfarction)
112
drugs with SURVIVAL BENEFIT post-mi
BB
ACEI
aspirin
statins
113
stable angina
no change in frequency, severity, duration, or precipitating factors in the previous 60 days
generally occurs with xexertion and relieved by rest
good prognosis
114
pathophysiology of stable angina
one or more severe narrowings in large epicardial coronary artery
generlly atherosclerosis (no superimposed thrombus)
115
treatment goals of stable angina
relieve discomfort (supply ad demand)
revascularization of medical therapy fails
prevent progression
116
medications for stable angina
BB
CCBs
nitrates
asirin
statins
(ranolazine if resistant)
117
vasospastic angina
at rest or exertion
may be associated w atherosclerosis
118
treatment of vasospastic angina
nitrates
CCBs
statins + aspirin
119
unstable angina
angina increasing in frequency, intesnity, or duration
at rest!
transient ECG changes
high risk of MI and death
120
pathophysiology of unstblae angina
ruptured atherosclerotic plaque
partially occluding thrombus in lumen of large coronary artery
high mechanical stress points
cap may thin due to monocyte production of proteases - chemically digest plaque cap
121
coronary thrombosis
underlying tissue is exposed, clotting mechanisms are activated
thrombus forms
thrombus may be non occlusive and eventually incorporated into atherosclerotic plaque (subclinical)
partially occlusive --\> unstable angina, STEMI
122
AMI
thrombus is totally occlusive and leds to AMI
severe chest pain
st segment elevation
123
treatment goals for unstable angina
relieve discomfort (supply demand)
prevent MI
aggressive revascularization
124
medications for unstable angina
BB
CCBs
nitrates
aspirin
heparin (unfractionated and LMW)
newer anti platelets (GB2b/3a)
statins
125
First line antianginal
nitrates
CCBs
BBs
126
second line antianginal
ranolazine
127
nitrates mechanism
venodilation!
reduce preload - decrease size of heart
decrease BP - decrease afterload
stop vasospasm!
128
nitrate effect in angina
decreased myocardial oxygen requirement (decrease wall stress)
129
cellular affect of nitrates
enzymatic degredation to NO --\> activate guanylyl cyclase in smooth muscle
inactivate A-M and vasodilate
only affects smooth muscle
viagra is the same!! can't mix
130
nitrates - adverse effects
hypotension, reflex tachy, headache due to hypotension
tolerance!
rebound due to withdrawl (don't give 24/7) = decrease blood flow to kidneys so retain water and salt
131
CCB mechanism
arterial vasodilation
lowers BP
```
coronary vasodilation (choice for coro vasospasm!)
negative inotropy
```
negative chronotropy
132
CCB cellular mechanism
block voltage dep L type ca channels
decrease transmembrane calcium flux
skeletal muscle not depressed (uses intracellular pools)
133
CCB effects in angina
increase oxygen (relieves vasospasm)
decrease demand (neg inotrope, vasodilation decreases wall pressure, some slow HR)
134
Verapamil
CCB
useful as antiarrhythmic for SVT
135
Diltiazem
CCB
136
Amlodipine
safest CCB for CHF
well tolerated
137
CCB side effects
lower extremity edema
sinus brady/av block
138
BB mechanism
neg chrono, neg ino
lower BP
increase duration of diastole
anti arrhythmic (suppress)
survival benefit - post MI and comp CHF
139
BB adverse effects
bronchospasm
exacerbation of CHF
impotensce/depression
excessive sinus brady and AV block
140
Ranolazine
indicated for patients with angina on meds or can't tolerate
block late I(na) channels (some are open during plateau phase so Na enters during systole - if block, less cytosolic Ca)
low HR, low BP, CHF, DM
prevents intracellular calcium overload!
141
treatment of stable angina
1. BB (first line) + aspirin + statin
2. give bottle of sublingual nitroglycerin
3. CCBs if BB are not tolerated (added if angina persists or to treat HTN)
4 ranolazine for persistant angina
5. risk stratification
142
strategies for treatment of unstable angina
1. hospitalization
2. treatment with nitrates and BB
3. treatment of ruptured plaque with throbus (aspirin, plavix, statin, antithrombin like heparin)
4. cardiac cath to determine risk
143
significant coronary stenosis
greater than 75% (with exercise)
greater than 90 - symptoms at rest, no compensatory dilation
144
AMI path - 1 day
wavy fibers
interstital edema
after sarcolemma has been disrupted but before inflammation
145
AMI Path - 3-4 days
coagulative necrosis of myocytes
loss of nuclei and cross striations
dense interstital neutrophilic infiltrates
pm breaks - exposes
increase neutrophils to clean up dead myocytes
146
AMI path: 7-10days
nearly complete phagocytosis of necrotic myocytes by macrophages
keep BP down! don't want to pressure wall
147
AMI path 10-14 days
granualtion tissue with new vessels and collagen
148
AMI path after 2 months
necrotic myocardium is replaced by dense collagenous scar
149
stunned myocardium
reperfusion injury!
biochemically altered myocytes after reperfusion
prolonged cardiac failure induced by short term ischemia that recovers after a fw days
short period of cardiac failure you wouldn't predict
150
coronary artery spasm
with or without atherosclerosis
smokers, alcohol withdrawl
stimulants - cocaine, meth
presents with angina - key is removing stimulating factors
151
coronary artery dissection
presenting symptom - angina
pre meno women
hypertension
surgery
stents
thrombolytics
152
ADP
recruit circulating platlnts
after platelets are activated they release ADP to create a plug
153
initation of platelet activation
collagen! via vWF
shape change (to increase SA) and degranulation (platelet is circulating drug delivery system)
154
glycoprotein IIB/IIIa
receptor on platelets
when stimmulated - platelets cloumb together
final common pathway in platelet aggregation
155
anti-platelet drugs
salicylates (aspirin)
ADP receptor antagonists
cAMP agonists
thrombin receptor (PAR-1)
g IIb/IIIa antagonists
156
salicylates indications
aspirin
weak platelet antagonists - impairs plately function
MI, secondary prevention of MI, stroke prevention with low CHADS score
157
salicylates mechanism
irreversible acetylation and inactivation of COX
blocks TxA2 production
158
salicylates side effects
GI bleeding
159
ADP antagonists mechanism
anti-platelet
block P2Y12 receptor, prevent recruitment of circulating platelets
clinical effects irreversible for days
(clopidogrel)
more potent than ASA!
160
ADP receptor indications
strok prevention (secondary)
1 year after ACS
2/4 weeks after bare metal stent
prolonged course after drug eluding stents
161
ADP recptor agonist side effects
irreversible for days
drug drug (CYP450)
162
cAMP antagonist mechanism
inhibits uptake of adenosine by platelets, endothelial cells, RBCs
increases local adenosine levels
inhibit platelets and vasodilate
antiplatelet!
163
indications for cAMP antagonists
stroke prevention (if NSR)
vasodilater in vascular disease
164
PPAR-1 antagonist
aka Thrombin receptor antagonist
another receptor to antagonize on PLATELETS
165
indication for PPAR-1 antagonist
secondary prevention post MI
166
Side effects of PPAR1 antagonists
increased risk of ICH in patients with prior stroke
167
glycoprotein IIb/IIIa mechanism
antiplatelet
most potent platelet antagonizer
IV ONLY!!!
abs
only anti=platelet that is IV!!!!
168
indication for 2b3a
treatment of ACS
only anti=platelet that is IV!!!!
169
side effect of 2b/3a
excessive bleeding
170
anticoagulants
warfarin
unfractionatedheparin
low MW heparin
Xa inhibitor
direct thrombin inhibitors
171
warfarin mechanism
inhibits synthesis of vitamin K dependent clotting factors
II, VIII IX, X
inhibits protein c and s
oral - chronic use
172
indications for warfarin
mechanical heart valve
a fib
PE/DVT
recent anterior wall MI
173
warfarin side effects
bleeding!
hemorrhagic skin necrossis
teratogenic
(slow onset, requires INR, interacts with everything)
174
warfarin reversal
vitamin K
IV = temporary low dose
PO = prolonged
intravenous fresh froxen plasma - replace clotting factors
175
NOAC mechanism
direct thrombin inhibitor
| (now reversal agent for one of them)
176
NOAC indications
stroke prevention (a fib)
DVT
no monitoring, no interactions, safer
177
NOAC side effects
no reversal agents (until now)
$$
bleeding
178
unfractionated heparin mechanism
from pig and cow
binds to and activates ATIII - inhibits thrombin, Xa, enhances TFPI
reversable (protamin)
length of heparin sugars indicate if it binds to thrombin or XA
179
heparin indications
anti coagulation bridge to warfarin
ACS
cardiac cath/surg
SQ = prophylaxis of venous thrombo embolic disease
180
side effects of heparin
bleeding
hypercoagulble period
heparin induced thrombocytopenia (abs bind to platelets - clotting but platelet count decreases!!
non specific - need testing
181
low molecular weight heparin indications
same mechanism of action as heparin - binds ATIII
less potein binding (more reliable)
SQ administration
fewer side effects
182
Xa inhibitors mechanism
ATIII mediated inhibition of Xa
SQ
183
Xa inhibitor indications
prevention of DVT
ACS
stroke (a fib)
184
direct thrombin inhibitors indication
i.e. bivalrudin
ACS
185
IV anticoagulants
direct thrombin inhibitors, unfractionated heparin
186
SC anti-coagulants
heparin (unfractionated, low MW)
Xa inhibitors
187
PO anticoagulants
Warfarin, NOACs
188
Anti-coag for Afib
Warfarin
NOACs
Unfractionated heparin (inpatinet - IV)
189
anti-coag for ACS
heparin (Both)
Xa inhibitors
thrombin inhibotrs
190
fibrinolytics mechanism
convert plasminogen to plasmin - beaks down fibrin clot
191
indications for fibronolytic (thrombolytic) therapy
acute MI only (not effective in unstable angina
chestpain under 6 hours in duration
ecg changes (ST elevation in 2 limb leads or big elevation in 2 precordal leads or LBBB)
192
absolute contraindications to thrombolytic therapy
A: aortic dissection
P: pregnancy
E: expected bleeding
S: surgery (2 weeks)
H: hypertension (chronic \> 200/100)
I: internal bleeding (known)
T: trauma (recent 2 weeks, hemorrhagic, head)
193
streptokinase
thrombolytic
can use once!
194
obstructive CAD
more than 70% cross sectional arrowing in a major coronary artery
195
small vessel CAD
abnormal flow in coronary arteries not typically visualized by angiogram
often due to endothelial disfunction
196
stable angina
stable (un-ruptured) plaque with ischemic symptoms that do not occur at rest and are predictably provoked
innapropriate vasoconstriction
197
unstable angina
ruptured plaque that causes ischemic symptoms to occur at rest or with progressively less exertion
no myocardial injury!! no biomarkers!
thrombus formation
198
MI
myocardial injury from ruptured coronary plaue or severe supply demand mismatch
199
Carotid IMT
no radiation
no contrast
visual of carotid thickening in I-M layer before palaque
surrogate - if it's there it's likely to be anywhere
TEST: to asses presence of atherosclerosis (not ischemia)
200
Coronary calcium scan
minimal radiation
no contrast
Ca on coro arteries - likely older because have to have hard plaque
201
tests to assess presence of atherosclerosis (not ischemia)
Carotid IMT
Coronary Ca Scan
202
people with atypical angin
women
elderly
diabetes
203
features of unstable angina
rest symptoms
increasing frequency
increasing duration
lower threshold for symptoms
biomarker negative!
NO stress test if unstable angina, stemi, nstemi
204
supply and demand balance
if you give a man a FiSH he will eat What He Can
Flow
saturation
hgb
wall stress
HR
contractility
205
myocardial energy supply
usually fatty acids (if have a lot of oxygen available --\> more ATP)
in ischemia - switches to glucose
206
coronary effect of vasoconstriction
hypoxic vasoconstriction
icchemic regions - dilate inhpoxic regions (opp of lungs)
(opp of lungs)
207
vasodilation in ischemia - mechanism
during ischemia, can't make ATP - ADP,AMP are converted to adenosine
adenosine is a vasodilator and prime mediator of vascular tone (decreased Ca into the cells --\> relaxation/vasodilation)
NO - vasodilation via cGMP
increased sheer stress - Ach, thrombin, plateless = NO released to compensate lead to vasodilation
208
Ach and coronary arteries
Ach - vasoconstrction of smooth muscles (without endothelial lining)
vasodilation (with endothelial lining)
Ach --\> No in endothelial cells --\> vasodilation
209
Endothelial dependent vasodialtors
Ach, thrombin, serotonin, sheer stress
210
endolthelial independent factors
nitroglycerine (makes NO in the smooth muscle cell)
211
healthy endothelium vs endothelial dysfunction
dysfunction - don't make NO, no relaxation signals to smooth muscle, contraction WINS
212
decrease in coronary pressure affects what part of the heart
higher flow at epicardial level (where bv come from) then endocardial level
213
threholds of stenossi
less than 70% - little change in blood flow at rest, artery can dilate in exercise
70-90 - autodilation of the resistance vessels at rest and normal flow, exercise - can't dilate further and ischemia
90 - max dilation at rest, may be suboptimal
214
stunning myocardium
acute ischemia!!
related to time of ischemia
perfusion is normal following ischemia
function returns to normal in 1 week
oart of heart is stunnd, doesn't just start moving normally
215
hibernating mycoardium
frequent or prolonged ischemia
perfusion is usually reduced!
downregulation of ATP uptake and oxygen consumption
216
preconditioning
upregulation of factors (NO synthase) to condition - less infarction
217
ischemic cascade
1. metabolic alteration
2. perfusion abnormalities
3. diastolic dysfunction
4. regional wall motion changes
5. ECG changes
6. Angina
218
C/I stress test
AMI
unstable angina
decompensated HF
arrhytmias
AV block
myocardiits
aortic stenosis
HOCM
uncontroleld HTN
acute systemic illness
219
mechanisms of stress (Stress Test)
treadmill/bike
adenosine
domutamine (beta agonist)
220
PET - when?
earliest (metabolism changes)
221
Cardiac MRI - when?
Early (perfusion changes)
222
Nuclear imaging - when?
early (perfusion changes)
223
ECG - when?
late - systolic dysfunction
224
ECG - when?
latest
225
Max stress test
85% of predicted HR
Max Predicted HR = 220-age
226
Nuclear Evidence of ischemia
after exercise - less uptake of isotope - not normal
227
PET and ischemia
abnormal metabolism - if using glucose it is abnormal
228
adenosine stress test
if stenosis - max dilated
give adenosine - more update and more flow
onl arterioles distal to normal epicardial artery can dilate!!
at rest - normal flow to both
in stress - relatively increased to one area (others are already max dilated)
229
sensitivity
unlikely to miss a Negative
good screening test!
SNOut
Sensitive test when negative rules out
230
specificity
Unlikely to wrongly label a Positive (good conformation test )
SpIN specific test when Positive rules IN
