CAD Flashcards
CAD
coronary artery disease: specific to what’s goin on in the arteries in the heart
most common form of CV disease
type of atherosclerosis
chronic and progressive
fat deposits in intima of the coronary artery, endothelial injury, inflammation, plaque formation, clot formation
What is cholesterol?
naturally occurring waxy substance made of proteins and lipids; needed to form cell walls, hormones, Vitamin D, bile
made in the liver; broken down in the liver
needed in right amounts and proportions
LDL
Low density lipids
transport cholesterol to artery wall
contain more cholesterol than any other lipoprotein
want low amounts of these
HDL
High density lipids
remove cholesterol from blood and take to liver where it is broken down
want high amounts of these
VLDL
Very low density lipids
contain more triglycerides and can deposit directly on the wall of the arteries
Triglycerides
most common type of fat in the blood
store excess energy for diet, best way to get rid of these is through diet and exercise
Guidelines for Cholesterol Levels
used to assess risk for developing CAD/CHD (through fasting blood work)
Total cholesterol: <200 mg/dL
HDL: >40 mg/dL
Triglycerides: <150 mg/dL
LDL (treat to specific target goals):
- no risk factors: low <130mg/dL
- 2 or less risk factors: <100 mg/dL
- high risk: < 70 mg/dL
Cholesterol Meds
Bile Acid Sequestrants: increase cholesterol conversion to bile acid which is excreted in feces; lowers LDL (ex. cholestryamin, colestipol, colesevelam)
Cholesterol Absorption Inhibitor: inhibits absorption along intestinal wall from bringing it into the body (ex. ezetimibe)
Niacin: lowers cholesterol and triglyceride levels by inhibiting synthesis; also increase the HDL levels; controversial drug w/ terrible SE - N/V (ex. niaspan)
Fibric Acid Derivatives: decrease the making and secretion of VLDL which will reduce triglycerides; also increase HDL (ex. fenofibrate, gemfibrozil)
HMG Coa Reductase Inhibitors - Statins: reduce synthesis of cholesterol in liver by blocking the key enzyme in its synthesis of cholesterol (HMG Coa); also increases LDL receptor activity in liver cells
- statins are most common type of cholesterol med prescribed
- pt’s need to report muscle pain as CoA plays role in muscle cell energy production (can take CoQ10 supplement from store to help)
Natural Products that Manage Cholesterol
Red yeast
Rice
Soy
Omega 3 fatty acids
Overall Goal of Cholesterol Meds
decrease LDL
decrease triglycerides
increase HDL’s
CAD: Men vs. Women
Highest incidence in middle age men
but higher mortality in women (especially african american females)
CAD: Risk Factors
HTN Hyperlipidemia PMHx and FHx of CV disease Smoking Sedentary Lifestyle Obesity (central/apple shaped) DM Metabolic Syndrome Substance Abuse
CAD: Gerontologic Considerations
Leading cause of death of older folks
More likely to make lifestyle changes if they’ve been hospitalized or have had sx associated with CAD
PMHx and FHx
Hx of: MI unstable angina CAD PVD AAA Carotid stenosis TIA CVA HTN FHx: Premature heart disease -male: first degree relative <55 -female: first degree relative <65
Diet for CAD
low fat
low cholesterol
increased fiber
If they smoke cigarettes:
ask about:
# of pack years (pk/day x # years smoking)
attitude towards smoking
attempts to stop
Risk factor: Sedentary Lifestyle
Definition: less than 20 min/day of demanding physical activity or when activity is less than 3x per week
recommendation: 30 min exercise, 5x week or 150 min weekly
FITT: frequency, intensity, type and time
Benefits of exercise: decrease LDL and increase HDL
Target HR: 220-age x .7 or .8
Ask if pt develops symptoms with exercise.
Risk factor: Obesity
Target BMI <25
Waist circumference:
-female: less than or equal to 35in
-male: less than or equal to 40in
Risk factor: Diabetes
FBG: less than 126
Random: less than or equal to 200
2 Hour OGG: less than or equal to 200
Preload
volume of blood in ventricles at end of diastole (end diastolic pressure)
increased in:
hypervolemia
regurgitation of cardiac valves
HF
Afterload
Resistance left ventricle must overcome to circulate blood
increased in:
HTN
vasoconstriction
Increased afterload = increased CO
Chronic Stable Angina
Myocardial demand of O2 exceed the supply of O2
angina = chest pain = muscle ischemia
precipitating factors: exercise stress sexual activity cocaine circadian rhythms (often experienced first thing in the morning)
only lasts a few minutes and subsides when precipitating factor is resolved
described as: pain, pressure heavy, squeezing. NOT sharp or stabbing
Tx of Chronic Stable Angina
decrease O2 demand and/or increase O2 supply
meds to optimize myocardial perfusion:
- Antiplatelet
- Lipid lowering agents
- nitrates (short acting nitrates are first line therapy - dilate peripheral blood vessels and coronary arteries)
- ACEI
- beta blockers
- CCB
Acute Coronary Syndrome (ACS) - Unstable Angina
- stable angina can become unstable angina
- new onset
- occurs at rest
- occurs with increased frequency, duration
- may be the first clinical sign of CAD
- prompt tx is needed (could be MI)
MI
an ACS
-abrupt stoppage of blood flow through a coronary artery from a thrombus cause by platelet aggregation
- irreversible myocardial cell death
- CAD
- pain not relieved by rest, position change or NTG
- N/V
- fever
Non-Invasive Diagnostic Studies of CV System
chest x-ray
ECG (ambulatory, stress test)
Echocardiogram (structure and motion of valves, chambers, ventricular muscle)
Nuclear test:
-cardiolite: IV injection of radioisotope, hot spots seen if area of MI (evaluated at rest and w/ exercise at specific intervals)
-dipyridamole: injected to stress the heart to mimic exercise
-PET scan: 1st scan - radioisotope shows perfusion of heart muscle, 2nd scan - shows metabolic function (normal = scans match; abnormal = scans differ)
MRI: info about tissue integrity and will indicate area of MI
Blood tests
MRA: evaluates arterial disease, uses IV contrast which can be very hard on kidneys as kidneys have to excrete this from body.
Invasive Diagnostic Studies of CV System
cardiac catheterization
coronary angiography
EPS: study electrical activity
hemodynamic monitoring
Blood Tests for CV System:
injured cells leak their contents into circulation which are detected with specific test of SX:
- CRP: identifies specific CV inflammation, used to predict CAD risk and monitor effectiveness of meds
- CK-MB
- Myoglobin: cardiac and skeletal muscle (elevated 1-2 hours after MI)
- Troponin: proteins released after MI, peaks at 12 hours, highly specific 4-6 hours after onset; biomarker of choice for ACS (Q6Hx3)
