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FA17 Cardio 2 > Coronary Artery Disease > Flashcards

Coronary Artery Disease Flashcards

1
Q

collection of diseases of the heart and arterial vascular system

A

arteriosclerotic cardiovascular disease

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2
Q

ASCVD diseases (6)

A

coronary heart/artery disease

congestive heart failure/cardiomyopathy

peripheral artery disease (Carotid/peripheral)

aortic atherosclerosis

CVA/stroke

valvular heart disease

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3
Q

etiologies of CVD

A

atherosclerosis and hypertension

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4
Q

diseases of coronary arteries result in:

A

stable angina

acute coronary syndromes (unstable angina, STEMI, NSTEMI)

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5
Q

Arteriosclerosis pathophysiology

A

begins in early life (visible disease in arteries)

  1. lipoproteins penetrate endothelial layer and aggregate
  2. Expression of adhesion molecules attract and bind monocytes
  3. monocytes move into intima and ingest lipoproteins = foam cells
  4. endothelial cell death decreases prostacyclin and NO production (vasoconstriction, pro clotting)
  5. Foam cell releases inflammatory cytokines
  6. fibrous cap formation
  7. calcium deposition (decreased flexibility)
  8. foam cell necrosis and lipid pool formation
  9. enzymatic break down and inflammation cause degradation of fibrous cap (rupture risk and thrombogenic particles)
  10. plaque ages and becomes more stable
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6
Q

in what regions to atheroma typically occur?

A
  1. branching and curvature of vessels
  2. areas where vessel is irregular shape
  3. where blood has sudden change in velocity

*all sites of turbulent flow

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7
Q

accumulation of lipoproteins in the intimidating is accelerated by

A

systemic HTN
hypercholesterolemia
cigarette smoking
inflammation/oxidative stress

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8
Q

loss of prostacyclin in due to endothelial cells causes

A

inability to relax and vasodilate vessels

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9
Q

which plaques are more vulnerable to rupture

A

small new ones

they are not blocking artery but they are weaker and have pro-thrombogenic abilities

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10
Q

which plaques are more likely to cause ACS/stroke/Cva?

A

young, easily ruptured plaques

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11
Q

which plaques are more likely to cause stable angina, claudication, unstable angina

A

long known, established plaques

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12
Q

two ways atherogenesis can end:

A
  1. plaque slowly grows to block vessels

2. plaque ruptures and causes occlusion

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13
Q

40-70% occlusion clinical presentation

A

asymptomatic

may or may not cause a change on stress test

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14
Q

70% occlusion clinical presentation

A

exertion symptoms

extertional angina and claudication

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15
Q

90% occlusion

A

symptoms at rest

unstable angina

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16
Q

plaque remodel the coronary artery in two ways

A
  1. positive remodeling (bulging of wall)

2. negative remodeling (narrowing

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17
Q

positive remodeling

A

most common, less likely to cause angina

arterial wall BULDGES out at plaque

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18
Q

negative remodeling

A

plaque narrows the vessel lumen as it grows

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19
Q

etiologies of cardiac tissue ischemia

A

vasospasm (prinzmetal angina)
emboli
congenital lesions
arteriosclerosis

when oxygen demand increases, supply must also increase or ischemia occurs

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20
Q

what causes increased myocardial oxygen demand

A

increased heart rate
increased wall stress/tension (LVH)
increased contractility

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21
Q

regulation of myocardial oxygen supply

A

endothelial lining of coronary arteries

22
Q

exertion and coronary supply

A

systole = no blood flow to heart due to SQUEEZE

diastole supplies heart - arteriolar dilation

23
Q

pathophys of cardiac ischemia

A

regional myocardial hypoxia causes anaerobic respiration, lactic acid release

myocardial relaxation is altered by acidosis causing less compliance and contractility

(visible on echo and EKG)

transient ischemia is reversible

prolonged ischemia can cause stunning or hibernation

24
Q

modifiable arteriosclerosis risk factors

A 
hypertension 
dyslipidemia 
diabetes 
smoking 
heavy alcohol use 
obesity 
sedentary lifestyle
25
non-modifiable arteriosclerosis risk factors
male sex advanced age family history of premature CAD
26
what impact does modification make?
the top risk factors are responsible for 50% of CVD risks smoking is the worse thing you can do modest exercise lowers CVD risk substantially
27
who is screened for CAD?
symptomatic persons determine if they meet risk factors
28
exercise stress testing
treadmill pt gets to >85% of max HR or symptomatic EKG records changes in ST to predict CAD excellent if patient is able to exercise
29
pharmacological stress testing
drugs (adenosine, Lexiscan, Persantine) to cause vasodilation of coronary artery vasodilation causes increased blood flow to non diseased arteries and decreased flow to diseased armies used if patients can't exercise or baseline EKG issues that obscure ST elevation during exercise
30
contraindications of stress testing
acute MI/cardiac ischemia vasodilators shouldn't be used in those with hypotension, high degree AV block, SSS, and active wheezing, COPD/asthma
31
when is MPI used?
if patient has EKG abnormalities (LBBB) used to enhance stress testing can be used in pharm and exercise testing
32
MPI Stress test procedure
NPO exervises to bruce protocol or given vasodilation agent at rest EKG is monitored, and if changes occur, test is ended after administration of radiotracer and tracked with gamma camera patient then rests and the radio tracer to see if there are areas of reversible ischemia
33
reversible ischemia
areas of darkness in EXERCISE but not during resting areas with no charge are dead areas
34
MPI c.i. and indications
Pregnancy positive result means that more testing (cardiac cath)
35
stress echo
resting echo first then stress induced with exercise or medications evaluates wall motion abnormalities caused by ischemia can evaluate viability of myocardium
36
who gets cardiac stress testing? 5
1. symptoms of angina, intermediate or high risk CHD 2. Recent ACS 3. history of CHD 4. newly diagnosed HF or cardiomyopathy 5. pre-op eval of elective surgery in cardio history patients
37
who DOES NOT get cardiac stress testing?
1. active chest pain or other symptoms 2. patients with prior coronary revascularization or no new symptoms 3. patients without symptoms of coronary artery disease
38
cardiac Cath
Femoral or radial a. ran up to heart with fluoroscope cannulation of coronary a. and contrast dye film clip is produced
39
what can a cardiac cath tell us>
determines degree of stenosis if left ventricuolgram also can tell us EF can be therapeutic with stent placement (PCI or PCTA)
40
framingham
used to evaluate risk of CHD event within 10 yrs Low (< 10%), intermediate (10-20%), high (+20%) takes into account all CVD risk, divided by sex, overestimates risk fails to account family history, double risk if present
41
ACC/AHA risk calculator
looks at age, sex, race, total cholesterol, BP more valid in ethnic minorities > 7.5% risk should talk about risk reduction
42
CAD in asymptomatic patients
use Framingham and ACC/AHA predictor of risk us age
43
CHD risk equivalents
increase risk of corona event to same degree as having known cvd DM CKD
44
approach to risk modification (9)
1. lipid panel 2. CV risk evaluation 3. other risk factors 4. determine presence of OTHER risk factors 5. stepwise approach to asses 10 yr risk and est. LDL goal 6. therapeutic lifestyle change 7. addition of medicaments 8. metabolic syndrome evaluation 9. treat TG and HDL issues
45
desirable LDL levels in lipid panel
< 100 high is 160+
46
events that confer a high risk of clinical atherosclerotic disease other
clinical CHD symptomatic carotid disease AAA PAD other: smoking, HTN, family history, sex and age
47
LDL goals
high risk of event: <100 low risk= <160 moderate risk = <130
48
metabolic syndrome HABIT-3
``` HDL low (<40) Abdominal obesity Blood pressure >130/85 Imaired fasting glucose Triglycerides >150 ``` must have 3
49
treatment for elevated TGs and HDL
vibrates and omega 3s exercise
50
HTN goal
<140/90 (all others) <150/90 (80+) <130/90 (DM, CKD)
51
DM goal
A1c <6.5% early dz or long life <7% significant comorbidities or long dz <8% limited life expectancy

FA17 Cardio 2 (10 decks)

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