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 ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download