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Cardiology- Coronary Artery Diseases
 
Coronary Artery Disease
 
Type of blood vessel disorder affecting the coronary artery resulting to atherosclerosis or hardening of the arteries due to fatty deposits. Narrow coronary artery
 limited blood O2 to myocardium
 ischemia
 
Atherosclerosis is the major cause- lipid deposits within the intima of the artery. Endotherlial injury and inflammation  play a central roll in the development of atherosclerosis
 
Heart Attack
 – 
 leading cause of Cardiovascular disease death and death in general
 
1.1 Million estimated Americans will have MI in 2003
 
460,000 will die, half of them before reaching a hospital
 
Theories of Atherogenesis
 
Endothelial Injury- Hyperlipidemia and some other irritants in blood can damage endothelium (inner most layer)
 
Lipid Infiltration-
lipid doesn’t only damage smooth layer, lipids infiltrate tunica media and swelling creates rough surfaces for
lipids to accumulate upon
 
Aging- relax and constriction of vessels diminish as aging progresses
 
Thrombogenic- More pressure = more injury. As more accumulation happens in the vessel, it becomes narrower
 higher  pressure
 
Vascular Dynamics-
 
Inflammation- intima layer damaged r/t infection=plaque
 
Developmental Stages of CAD
 
Fatty Streak
 
Earliest lesion of atherosclerosis
 
Lipids accumulate and migrate into smooth muscle cells
 
Raised Fibrous Plaque
 
Beginning of progressive changes of arterial wall- rounded shape of inner vessel is altered as early as 30yo
 
Collagen covers the fatty streak and forms a fibrous plaque with a grayish or whitish appearance= narrowing of lumen and reduction in the blood flow to the distal tissues
 
Complicated lesion
 
Final stage in he development of atherosclerotic lesion
 
As the fibrous plaque grows, continued inflammation can result in plaque instability, ulceration, and rupture. Once the integrity of the artery wall is compromised, platelets accumulate in large numbers
 thrombus
 
Thrombus can adhere to wall leading to narrowing or occlusion
 
Ischemia - death of tissue
 
CAD Risk Factor Categories
 
Unmodifiable Risk Factors-
 
Modifiable Major Risk Factors
 
Modifiable Contributing Factors
 
Unmodifiable Risk Factors
 
Age and Gender- highest risk among middle aged men. Kills more women than breast cancer- leading cause of death
 
Family History and Hereditary- genetic contribution is as high as 40-60%
 
Modifiable Major Risk Factors (research shows definite significant increase of CAD)
 
Elevated serum lipids
 
Serum cholesterol
 – 
 above 200mg/dl
 
HDL (High Density Lipoprotien)
 
Lower than 35mg/dl - major risk factor
 
Carry lipids away from arteries and to the liver for metabolism.
 
Prevent lipid accumulation within arterial walls
 
Desirable- lower the risk of CAD
 
LDL (Low Density Lipoprotein)
 
Above 160mg/dl high risk for CAD
 
Contain more cholesterol then any of the lipoproteins and have an attraction for arterial walls.
 
Elevated levels correlate closely with an increased incidence of atherosclerosis and CAD
 
Low serum levels are desireable
 
Hypertension
 
BP greater than or equal to 140/90 mm Hg
 
Increases the risk of death from CAD 10-fold in all people
 
Stress of an elevated BP increases the rate of atherosclerosis
shearing stress that causes endothelial injury
 
Stress from atherosclerosis + elevated BP
 left ventricular hypertrophy and decreased stroke volume with each contraction.
 
Smoking
 
2-6 x higher risk to develop CAD
 
 Nicotine causes catecholamine release
 increased HR, peripheral vasoconstriction, increased BP
increased heart workload
 
 
Tobacco smoke is related to an increase in LDL evel, decrease in HDL, and release of toxic O2 radicals
 vessel inflammation and thrombosis
 
Physical Inactivity
 
30 minutes of brisk exercise 5 or more times a week
 
Obesity
 
Weight 30% more than the standard weight
 
Often linked to hypertension and insulin resistance
 
Apple shaped figure has higher incidence of CAD than pear figure shape
 
Modifiable Contributing Risk Factors
 
Diabetes Mellitus
 
2-4x greater incidence among diabetics, even those with controlled glucose levels
 
Undiagnosed DM is often discovered when a patient has an MI
 
Stress and Behavior Patterns
 
Type A personality- perfectionist, hard working and driven
 
Depression, acute and chronic stress, anxiety, hostility and anger, lack of social support
 
SNS stimulation and effect on heart
 increased release of catecholamines
 increased HR, and the force of myocardial contraction
 increased myocardial O2 demand.
 
Cause elevated lipid and glucose levels and changes in blood coagulation
 increased atherosclerosis
 
Homocysteine
 
Increase level linked to increase risk for CAD
 
Produced in the breakdown of sulfur containing amino acid methionine, which is found in dietary protein
 
Damage inner lining of vessels, promote plaque buildup, alter clotting mechanism to make clots more likely to occur
 
B complex vitamins to lower blood levels of homocysteine.
 
Major Clinical Manifestations of CAD
 
Angina Pectoris- caused by anaerobic respiration and lactic acid accumulation. Clinical manifestation of myocardial ischemia
 
Acute Coronary Syndrome (MI)
 
Sudden Cardiac Death
 
Types of Angina
 
ANGINA
 – 
 pain in the chest
 
Stable Angina Pectoris
o
 
Controlled with medication
o
 
Provoked by an increased demand of O2 or decreased supply- physical activity- predictable
o
 
 Narrowing of one or more coronary artery by atherosclerosis
 
Silent Ischemia (asymptomatic)
o
 
Patients with DM have an increased prevalence
 diabetic neuropathy=loss of feeling
o
 
Same prognosis as regular angina
 
Prinzmetal’s Angina (variant angina)
 
o
 
Occurs at rest, due to spam of the coronary artery
o
 
Usually due to spasm of major coronary artery
o
 
Strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium
o
 
 Not r/t plaque deposit, can happen during rest. Not predictable
 
 Nocturnal Angina and Angina Decubitus
o
 
Occurs at night, chest pain while lying relieved by standing
o
 
Usually lasts 10 minutes or more
 
Unstable Angina
o
 
 New onset, unpredictable, worsening pattern
o
 
May be first sign of CAD
 
Clinical Manifestations of CAD
 
Angina
 
Appears substernally, in the neck, radiate to jaw, shoulder and down to the arm
 
Myocardial Infarction
 
Pain is severe, immobilizing, not relieved by rest or nitrate administration.
 
Skin ashen, clammy, cool to the touch
 
Describe as heaviness, pressure (elephant on chest), tightness, burning, crushing
 
 Nausea and vomiting, fever- tissue injury (ischemia)
 
Cardiovascular manifestations
 
Elevated HR
 
Decrease BP and urine output- decreased CO
 
Crackles-LV dysfunction
 
Hepatic engorgement
 
JVD- right ventricular dysfunction
 
Peripheral edema- right ventricular dysfunction
 
 
Complications of MI
 
Arrhythmias
 
Most common complication of MI (80%)
 
Specifically Ventricular fibrillation
 
Incomplete emptying, decreased CO= death- lack of O2 can cause sudden death post MI
 
CHF- when pumping action is reduced.
 
Left sided- mild dyspnea, restlessness, agitation, slight tachycardia, pulmonary congestion, S3 or S4 heart sounds, crackles, orthopnea
 
Right sided- jugular vein distention, hepatic congestion, lower extremity edema
 
Cardiogenic Shock- decreased pumping r/t ischemia- lack of O2- high death rate
 
Diagnostic Studies- Angina
 
Chest X-ray- non invasive, visualize the size of heart, see enlargement, calcification, pulmonary congestion
 
ECG
 
Primary tool to dx Unstable angina or STEMI (ST elevation Myocardial Infarction), or NSTEMI (non-ST elevation myocardial infarction
 
Serial 12 lead ECG
 
STEMI- usually have a complete coronary occlusion- ST elevation, t wave inversion and pathologic Q waves later.
 
 NSTEMI or UA usually have transient thrombosis or incomplete coronary occlusion- often develop ST depression or T wave inversion.
 
Laboratory Test
 
Serum lipids
 
Cardiac markers- serial draw over 24 hours to differentiate between UA and NSTEMI
 
C-reactive protein
 
Treadmill Exercise Testing- stress test- mimic increase in O2 demand in a controlled environ with 12 lead ECG
 
 Nuclear Imaging (IV injection of radioisotope)- Dye- check for iodine allergies, kidney function. Check output, increase fluid intake. IV access before injection (0.9% NSS)
 
PET scan-
 
Coronary Angiography-within 90 minutes of presentation or receive thrombolytic therapy within 30 min in agencies without PCI capability
 
Opens the occluded arteryand limit the infarction size
 
Echocardiogram- uses ultrasound to create a visual image of your heart.
 
Diagnostic Studies Myocardial Infarction
 
Pt. History
 
ECG
 
Changes in ST segment- STEMI
 
Serum Cardiac Marker
 
CK (creatine kinase) (MB band is cardiac specific)- begin to rise about 6 hours after an MI, peak at 18 hours, and return to normal within 24-36 hours
 
Troponin (myocardial protein) - increase 4-6 hours after the onset of MI, peak at 10-24 hours, and return to baseline over 10-14 days
 
Collaborative Care- Angina
 
Treatment aimed at decreasing oxygen demand and /or increasing oxygen supply.
 
Drug Therapy
 
Use of nitrate initial therapeutic intervention a.
 
Antiplatelet Aggregation Therapy (first line of treatment) Ex. Aspirin, Ticlid, Plavix  b.
 
 Nitrates
o
 
Administration of Nitrates
-
Sublingual- break through pain. Used along side other mode
-
 Nitroglycerin ointment
-
Transdermal controlled
-
Long acting nitrates-MDOR- angina maintenence
-
Intravenous nitroglycerin- only ICU- immediate MI c.
 
B- Adrenergic Blockers- inhibit SNS, decrease HR, decrease afterload, vasodilation d.
 
Calcium Channel Blocker- Create systemic vasoresistance, improve afterload
 
Percutaneous Coronary Intervention (PCI)
 
Insertion of catheter equipped with an inflatable tip to the coronary artery resulting to vessel dilation.
 
Locate and assess the severity of the blockage, determine the presence of collateral circulation, and evaluate LV function.
 
Stent Placement
 
Expandable mesh like structures designed to maintain vessel patency by compressing the arterial walls and resisting vasoconstriction.
 
Bare metal stent (BMS) or Drug eluting stent (DES) is inserted into the blocked coronary artery
 
Atherectomy- removal of plaque by scraping with blade and plaque is sucked out

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