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
  Laser Angioplasty- laser to target and break plaque
 Myocardial Revascularization (CABG)- If catheter can’t pass through plaque, CABG.
 2 surgical sites- donor vessel and thoracic cavity- may be single, double, triple, quadruple graft
 After surgery, patient will have a chest tube
 Straight to cardiac ICU
 Blood transfusions
 Collaborative Care- Myocardial Infarction
 Initial management is best accomplished in ICU
 Fibrinolytic Therapy
 Produce an open artery by lysis of thrombus to reperfuse the myocardium.
 Only for patients with a STEMI
 Aims to limit infarction sized by dissolving the thrombus in the coronary artery and reperfusing the heart muscle.
 Goal is to give the therapy within 30 minutes of the patients arrival to the ED
 For hospitals with no PCI capabilities
 Very expensive medication
 Contraindicated for any pt with bleeding issues- makes bleed more
 Cardiac Catherization- Balloon, stent, etc.  cath. lab
 Drug Therapy
a. IV nitroglycerine- Monitor- will be in OR or ICU if they are getting this
b. Antiarrhythmic dugs- Arrhythmia is most common side effect of MI
c. Morphine Sulfate- Acute chest pain, angiolytic-anti- anxiety=decreased HR and breathing decreased O2
need and consumption
d. B-Adrenergic blockers- decrease preload
e. Angiotensin-Converting Enzyme Inhibitors- decrease systemic resistance to myocardium. Prevents
ventricular remodeling and prevents or slows the progression of HF.
f. Stool Softeners- Colace- want to give softener that does not stimulate peristalsis but keeps in water
increased peristalsis= increased O2 consumption. Prevent straining and the resultant vagal stimulation
from valsalva maneuver. Vagal stimulation produces bradycardia and can provoke dysrhythmias
 Nutritional Therapy- Low sodium, clear liquid and slowly progress to solid- decrease GI motility (and O2 needs)
Nursing Therapies/ Plans of Care- Angina
 Health Promotion
 Aimed to decrease risk factors- modifiable
 Acute Interventions
 Administration of Oxygen
 Monitor vital signs, ECG, heart sounds
 Give nitrate followed by narcotic analgesic
 Position for comfort- HOB elevated
 Ambulatory/ Home Care
 Pt. assurance- they can still live normal productive life- they need to be an active part of their own care
 Health Teaching- reduce risk factors, teach about new meds, follow up appointments, exercise program
 Counseling- any psychological, emotional problems. Grieving process is likely. Help through stages in a safe way-
facilitate expression
Nursing Therapeutics- Myocardial Infarction
 Acute Interventions (Prioritize Action)
 Pain- follow up, evaluate
 Monitoring- EKG, arrhythmia(A-fib), edema, JVD
 Rest and Comfort-
 Control Anxiety- facilitate safe expression
 Emotional and Behavioral reactions
 Ambulatory/ Home Care
 Patient Teaching
o Anticipatory guidance- make sure they are ready to learn- when they start asking questions
 Physical Exercise
 Resumption of Sexual Activity
o Use matter of fact approach
o Determine comfort and readiness to learn
o Give info without judgment
o Remind them they can take prophylactic nitro prior to sexual activity
o Can’t take Viagra
o No sex after heavy meal (peristalsis decreases O2) or alcohol
o Avoid anal stimulation vagal response
o Resume sexual activity 7-10 days post uncomplicated MI or when patient can climb 2 flights of
stairs without dyspnea or pain