Coronary Artery Disease

Front 1

When does the heart receive its blood supply?

Back 1

during diastole

Front 2

Law of supply and demand

Back 2

the amount of arterial blood flow the heart muscle is demanding has to be equal to the amount of arterial blood flow supplied by the coronary arteries

Front 3

How much O2 needed formula

Back 3

RPP = HR x SYSTOLIC BP

if HR and systolic BP go up the heart will need more O2 and therefore will have to increase coronary blood flow

when the heart demands more blood flow than the coronary arteries can deliver = ischemia

Front 4

Risk Factors for CAD (10)

Back 4

- HTN
- hypercholesterolemia
- smoking
- diabetes
- age
- gender
- hemochromotosis
- obesity/sedentary
- homocysteine
- family history

Front 5

Pathophysiology of CAD

Back 5

- damage in the inner lining of the arterial wall
- WBC (macrophages) begins to migrate to the damaged area and eat the cellular debris
- because cell membranes are mostly fat = macrophage become engorged with lipid and become foam cells (scrubbing bubbles)
- foam cells adhere to damaged area and attract chemo attractants = causes muscular lining of the artery to grow into the lumen of the artery
- overtime LDL adhere to the foam cells
- over many years LDL accumulates closing off more and more of the arterial lumen
- fibrous capsule forms over the accumulation
- fibrous capsule rips off = forms clots = formation of coronary thrombosis = myocardial ischemia = cell injury = if blood flow is not re-established = myocardial infarction

Front 6

CAD Clinical Manifestations (6)

Back 6

- chest pain or pressure
- SOB
- sweating (diaphoresis)
- dizziness/lightheadedness
- nausea
- death

Front 7

Women CAD Clinical Manifestations (5)

Back 7

- fatigue
- depression
- difficulty sleeping
- SOB with exertion
- epigastric pain

Front 8

Diagnosis of CAD

Back 8

- history
- EKG changes
- lab tests

Front 9

EKG ST- segments

Back 9

- ST depression = ischemia
- ST elevation = full obstruction = coronary artery occlusion

Front 10

CAD lab tests

Back 10

Heart cells have unique chemicals inside them (enzymes and proteins)
- Troponin T and I
- CPK-MB
- LDH
- myoglobin

if these are elevated in the blood= ischemic heart disease (myocardial infarct)

Front 11

CAD EKG tests

Back 11

- 12-lead EKG
- during exercise= myocardium is demanding more coronary blood flow and if there is a blockage in 1 or more coronary arteries supply cannot meet demand
- because HR is higher= the period of ventricular relaxation (diastole) is lessened = less time to fee oxygenated blood to the myocardium

Front 12

CAD- Thallium stress test

Back 12

- Thallium 201 is a radioactive material that is injected into the vein at peak exercise
- Thallium is then taken up by healthy heart cells by the Na/K pump
- heart cells that are ischemic or dead will not take up the Thallium
- images are taken after exercise and 4 hours later

Front 13

CAD stress echocardiogram

Back 13

- can detect coronary artery disease by detecting abnormal heart wall motion
- resting ECG is taken
- the another after peak exercise

Front 14

CAD pharmacological stress tests

Back 14

- dobutamine= medication that increase HR and BP
- persantine= potent vasodilator= takes advantage of coronary steal effect

Front 15

Treatment for CAD (4)

Back 15

- Beta blockers
- nitrates (nitroglycerin)
- HMG-COA-REDUCTASE (prevents the liver from forming and dumping cholesterol into the blood)

- anticoagulants
- aspirin
- Coumadin
- plavix

Front 16

HMG-COA-REDUCTASE

Back 16

statins
- lipitor
- zocor
- crestor

Front 17

Aspirin and plavix

Back 17

inhibits platelet aggregation

Front 18

Coumadin

Back 18

- Vitamin K is required for blood clot
- Coumadin interfere with vitamin K= preventing clotting
- prothrombin time must be assessed routinely

Front 19

Nitrate

Back 19

dilates arterial vessels and systemic veins