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 atherosclerosisshearing 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 BPincreased 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