Coronary Artery Disease:
Coronary Artery Disease:
Atherosclerosis—Fat deposits, intima of vessel walls.
Arteriosclerosis—elasticity and hardening
I. CAD—development of CAD
A) Stages
1. fatty streak—lipids in intima of vessel walls
Starts at age 15.
2. Raised fibrous plaque
--Appears by age 30
--Initiated by endothelial injury
✓ Increased BP—shearing of endothelium lining called denuding injury.
✓ Increased Cholesterol
✓ Cigarettes
? inflammation?
3. complicated lesion
✓ plaque has lipid core surrounded by dead tissue.
4. collateral circulation
✓ over months or years develop collateral circulation around hallowing.
✓ A young person having a MI is worse than an older person because haven’t developed collateral circulation.
Is inherited and the presence of chronic ischemia.
5. B) Risk factors:
unmodifiable—age, gender, heredity, and family hx
Modifiable:
a) Elevated serum level—lipids
Cholesterol—diet and liver
~ Normal 140-200
HDL normal Male >45 Females >50
~ carries lipids AWAY from vessel
LDL Should be < 130
~ Have more cholesterol and attach to arterial walls.
VLDL—contains triglycerides should be < 200.
~ ETOH and simple sugars Inc. Triglycerides
Homocysteniene levels
Amino acid contains sulfur
~ alters endothelial lining
~ Inc. chances of clotting
~ to decrease levels take Vit B12, B6 and folic acid
SMOKING: increases BP and Decreases O2 Inc. Workload of heart and Inc. HR.
II. Prevention and Treatment
health promotion
lifestyle changes
~ Diet—step 1 decrease sat. fat—decrease cholesterol by 10-15%
Step 2 go to if no change after 6 months.
~ decrease tryglycerides—sugar and ETOH
Rx—drug therapy
1. enhances lipid protein removal
Resins lower LDL and increase HDL
Welchol and Questran
SE: Belching
2. Restricts lipoprotien production
Niacin (B Vit.)
3. Statins--
Locar
SE: Rash and gas
III. Manifestations of CAD
Angina
MI
Sudden Death
1. Angina Pectoris
transient (comes and goes) chest pain
lasts 3-5 minutes
Coronary arteries are chronically dilated
Factors that affect O2 demand:
Low BP
Vasoconstriction—HTN
Aortic stenosis
Precipitating factors:
Exertion—Increase HR and Increase O2 demand, Heart can’t meet.
Strong emotions
Consumption of heavy meal—blood transported to GI to digest food.
Change of temp. Heat—vasodilation, Cold—vasoconstriction
Cigarettes
Sex
Stimulates—drugs—cocaine
Circadian rhythms—happens in AM stimulation of SNS.
2. Unstable Angina
Preinfarct
Progressing
Unpredictable—occurs at rest or minimal exertion
BIGGEST RISK—complete occlusion
3. Manifestations Signs and Symptoms
Most common—pain—describe pain (squeezy, ache and heaviness)
Feelings of doom
SOB
Cold sweat—diaphoretic
4. Complications
Arrhythmias
PVA’s ventricular fibrillation
5. Diagnostics
H and P
EKG 12 lead
Nuclear techniteum scan—identifies areas of inadequate circulation in heart “hot spots.”
6. Medications
1st line of treatment
a) Platelet aggregate inhibitors
ASA
Plavix
Ticlid
b) Nitroglycerin
Decreases preload and after load
~ Coronary vasodilators==increase flow in coronary arteries
decreases workload of heart
~ Routes—SL, PO IV (titrate for effect) Transdermal (remove x 8 hr)
~ SE—headache and hypotension.
c) Beta Blockers
~ decreases HR, BP and O2 consumption
Lopressor
Zobeta
Inderal
Corgard
~ Can cause bronchoconstriction
~ Obtain a baseline HR and BP, hold if pulse < 60 and Systolic ................
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