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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