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Imbalance Between Myocardial Supply and Demand Irma B.Ancheta,PhD,RN.

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Learning Guide: Pathophysiology of atherosclerosis, arteriosclerosis, Acute Coronary Syndrome Modifiable and non-modifiable risk factors for CAD (Coronary Artery Disease) Anti-platelet medications: aspirin Plavix (clopidogrel) Medications for dyslipidemia: HMG Co-reductase inhibitors Niacin Fibric acid derivatives Anti-anginal medications: Nitroglycerin preparations Beta blockers Calcium channel blocke

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Learning Guide: Assessment of men and women presenting with s/s of angina, or ACS (Acute Coronary Syndrome) Definitions and defining characteristics of: Decreased cardiac output r/t ventricular damage, dysrhythmias Acute pain r/t myocardial tissue damage from inadequate blood supply Risk for bleeding r/t thrombolytic therapy Risk for peripheral neurovascular dysfunction Definition and Indicators of these NOCs: Cardiac pump effectiveness Tissue perfusion, peripheral Review these NICs: Cardiac Care Cardiac care, acute Circulatory precautions

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Learning Objectives: Describe assessment strategies (and related nursing care) for patients with ACS: Stress tests, echocardiography, cardiac catheterization, ECG monitoring Plan, implement and evaluate care for patients experiencing Unstable angina, NSTEMI, MI Plan, implement and evaluate care for patients post interventional cardiology procedures Describe interventional (cath lab)/surgical interventions for myocardial revascularization Describe health promotion strategies (and teaching plans) for patients at risk of CAD/ACS.

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Cardiac Review

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A&P Review Layers of the Heart Pericardium Epicardium Myocardium Endocardium

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A&P Review Cardiac Chambers Atria Ventricles

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Cardiac Valves Atrioventricular Valves Tricuspid and mitral Semilunar Valves Pulmonic and aortic

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A&P Review Conduction System Atria Sinoatrial node Internodal pathways Intraatrial bundle AV Node to Bundle of HIS Ventricles Right and left bundle branches Purkinjie fibers

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Electrical Conduction System

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A&P Review Coronary Blood Supply Coronary Arteries Left coronary artery divides into left anterior descending and left circumflex Right coronary artery perfuses the right side of the heart and in most people the SA and AV nodes In 70% of the population the RCA perfuses the posterior coronary artery

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Right coronary artery Coronary Arteries

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A&P Review Venous Return from the Heart Coronary sinus Thebesian vessels drain directly into the chambers of the heart and produce physiologic shunt

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A&P Review Systemic Circulation Arterial system of resistance vessels Capillary bed: tissue perfusion Venous system of capacitance vessels

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A&P Review Physiology Properties of cardiac tissue Excitability Conductivity Automaticity Rhythmnicity Contractility Refractoriness

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A&P Review Electrical Activity Action potential

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A&P Review Cardiac Cycle Ventricular systole Ventricular diastole Cardiac Output

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A&P Review Regulation of Heartbeat Nervous control Intrinsic regulation

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A&P Review Control of Peripheral Circulation Intrinsic Control Extrinsic control

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Ejection Fraction

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Normal = 50% or higher Low = < 40%

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Ejection Fraction [1] MUGA (multiple-gated acquisition) Scan [2] echocardiogram [3] Cardiac Catheterization [4] Nuclear tests

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Risk Factors associated with Coronary Artery Disease

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Objectives: Definition of CAD Identifying risk factors (a) effects (b) treatments (c) management Latest developments

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CAD Statistics Affects nearly 13 million people in the USA Causes 500,000 deaths each year

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Framingham Heart Study (FHS)

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Definition of Coronary Artery Disease A narrowing of the inside diameter of arteries that supply the heart with blood. The condition arises from the accumulation of plaque and greatly increases the risk of having a heart attack or myocardial infarction (Cooley, 1996).

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Modifiable Risk factors Pathophysiologic factors: Hypertension Diabetes Hyperlipidemia Life style factors Smoking Obesity Physical Inactivity Stress

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Nonmodifiable risk factors AGE GENDER RACE/ETHNIC BACKGROUND HEREDITY

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Emerging Risk Factors Homocysteine= blocks NO production < elastic Blood vessels permit plaque formation TTT= B complex Folic acid, Niacin LDL-C = mechanical injury Prothrombotic state (e.g., high fibrinogen or plasminogen activator inhibitor1 in the blood) Proinflammatory state (e.g., elevated C-reactive protein in the blood causes inhibition of NO) Low Adiponectin levels increase CRP production

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Five Major Risk Factors 1.Smoking 2.Hypertension 3.High cholesterol 4.Diabetes 5.Family History

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Smoking Effects of Smoking Roughening effect of inside diameter of the arterial wall>formation of plaque,constriction of arteries>HPN Increases heart rate and produces irregular heartbeats>clots>stroke Decrease HDL levels and increase LDL > increase risk CAD

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Management of Smoking Quit Smoking Avoid secondary smoke

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Hypertension: Or high blood pressure.. SBP >120 mm Hg..DBP>80 mm Hg Indicates a problem in the mechanism that regulates blood pressure in the circulatory system hyper too much tension pressure

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Hypertension Effects of HPN [Mechanical Injury] Causes thickening or hardening of the walls off the arteries>causes narrowing >decrease blood flow to coronary arteries>MI. Thickening of left ventricle >decrease Cardiac output > causes CHF > kidney damage>Renal dialysis In the diabetic population, HPN>retinal damage(retinopathy)>BLINDNESS

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For persons over age 50, SBP is a more important than DBP as CVD risk factor. Starting at 115/75 mmHg, CVD risk doubles with each increment of 20/10 mmHg throughout the BP range. Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN. Those with SBP 120139 mmHg or DBP 8089 mmHg should be considered prehypertensive who require health-promoting lifestyle modifications to prevent CVD. (JNC 7, 2003) New Features and Key Messages

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New Features and Key Messages (Continued) Thiazide-type diuretics should be initial drug therapy for most, either alone or combined with other drug classes. Certain high-risk conditions are compelling indications for other drug classes. Most patients will require two or more antihypertensive drugs to achieve goal BP. If BP is >20/10 mmHg above goal, initiate therapy with two agents, one usually should be a thiazide-type diuretic. (JNC 7, 2003)

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Blood Pressure Classification Normal100 (JNC 7, 2003) BP ClassificationSBPDBP

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Benefits of Lowering BP Average Percent Reduction Stroke incidence 3540% Myocardial infarction 2025% Heart failure 50% (JNC 7, 2003)

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BP Control Rates Trends in awareness, treatment, and control of high blood pressure in adults ages 1874 National Health and Nutrition Examination Survey, Percent II 197680 II (Phase 1) 198891 II (Phase 2) 19919419992000 Awareness51736870 Treatment31555459 Control10292734 Sources: Unpublished data for 19992000 computed by M. Wolz, National Heart, Lung, and Blood Institute; JNC 6.

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Summary:

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Treatment Overview Goals of therapy Lifestyle modification Pharmacologic treatment Algorithm for treatment of hypertension Classification and management of BP for adults Follow-up and monitoring (JNC 7, 2003)

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Management of hypertension Exercise Proper stress management Quit Smoking Healthy diet Decrease sodium intake. Anti- HPN Medication

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Lifestyle Change: What Difference Does it Make ? Weight loss. (decreases SBP*1.6 mm Hg for each kg lost) Dietary Approaches to Stop Hypertension: DASH diet: (decreases systolic BP 8-14 mmHg) Reducing salt in the diet.(decreases SBP 2-8 mmHg) 30-45 minutes daily aerobic exercise (decreases systolic BP 4-9 mmHg) Limit alcohol. (decreases SBP* 2-4 mm Hg) Avoidance of tobacco products. (*SBP = systolic blood pressure)

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Medications for HPN Diuretics Beta-Blockers Calcium channel Blockers ACEI Vasodilators

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Diabetes Causes vasoconstriction of coronary arteries >decrease blood flow > decrease oxygen supply >increase risk of heart attack or MI

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Management of Diabetes Healthy diet. Exercise Stress Management Medications Check Blood sugar regularly

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CHOLESTEROL Effects of Increased Cholesterol levels Causes plaguing of the coronary walls, narrows coronary arteries, creates blockage of coronary arteries less blood flow to heart cells >MI

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Cholesterol LDL cholesterol HDL cholesterol Total cholesterol Triglycerides

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Serum cholesterol levels LDL Cholesterol Primary Target of therapy Very High Total cholesterol < 200 Desirable 200 - 239 Borderline 240 > High HDL 60 High (NCEP/ATP III Guidelines, 2004)

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Management of Cholesterol Levels DIET MEDICATION NON-SMOKING EXERCISE

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Family History Parent or sibling that died of CAD less than 60 years of age...

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Medications for CAD [1] Anti-platelet medications [2] Medications for dyslipidemia [3] Anti- anginal medications

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Anti-platelet medications [1] Aspirin [2]Clopidogrel (Plavix)

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Medications for dyslipidemia HMG CoA-reductase inhibitors Nursing Interventions (statins) [1] Rosuvastatin No grapefruit [2] Simvastatin Monitor liver enzymes [3] Atorvastatin Instruct pts. mm tenderness [4] Pravastatin Take at night Niacin [1] Niaspan,Niacin With meals/Flushing/?med Fibric Acid Derivatives [1] Lopid 30 minutes before or with meals [2] Zetia

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Anti- anginal medications [1] NTG preparations [2]Beta-blockers [3] Calcium channel blockers

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Summary of risk factors for CAD [1] ? [2] ? [3] ? [4] ? [5] ?

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How many risk factors for CAD do you have?

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Coronary Artery Disease

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Coronary Artery Disease (CAD) CAD is a broad term that includes stable angina pectoris and acute coronary syndromes. When blood flow through the coronary arteries is blocked, ischemia or infarction of the myocardium may result.

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Ischemia and Infarction Ischemia occurs when insufficient oxygen is supplied to meet the requirements of the myocardium Infarction (necrosis of the cells, cell death) occurs when sever ischemia is prolonged and irreversible damage to tissue results.

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Acute Coronary Syndromes Angina- coronary ischemia- a temporary imbalance between the coronary arteries ability to supply oxygen and the cardiac muscles demand for oxygen (no permanent damage to myocardial tissue). Stable Angina- predictable; fixed lesions Unstable Angina- more intense, may occur at rest or with exertion and causes marked limitations of activity. Attacks increase in intensity and pain. Includes new-onset angina, variant (Prinzmentals) angina, pre-infarction angina and crescendo angina

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Angina Location Duration Quality Radiation Precipitating Factors Medication Relief

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Myocardial Infarction Irreversible necrosis due to an abrupt decrease or total cessation of coronary blood flow. Plaque rupture New thrombus in coronary artery

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Process of Infarction Tissue Ischemia Hypoxemia Autonomic Nervous System Influences Metabolic Derangement Acid-base imbalances Hemodynamic disturbances Electrolyte disturbances Fiber stretch

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Zone of Infarction Dependent on Three Factors: Collateral circulation Anaerobic metabolism Workload demands

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Types of Infarction Subendocardial Infarction (non-Q wave) (multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall. These do not show the same evolution of changes seen in a transmural MI. ) Transmural Infarction (Q wave) (involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%). Physiologic response = ventricular remodeling (change in shape and size of L ventricle causing decrease L V F leading to HF)

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Zones of Infarction Zone of Ischemia = T-wave inversion Zone of Injury = ST elevation Zone of Necrosis = Abnormal Q wave

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Classification of MI by Location Inferior: Abnormalities that appear in leads II, III, and F (called the inferior leads) indicate pathology on the inferior or diaphragmatic surface of the heart. Lateral: Leads I, F, and V5-V6 are called lateral leads. Abnormality in these leads indicates pathology on the lateral, upper surface of the heart. Anterior: Anterior pathology is seen in leads V1-V4, and often in lead I. Posterior: Problems on the posterior surface of the heart are difficult to diagnose using the standard 12 ECG leads. The pathology may be seen as reflected through V1 and V2. Combination: Abnormalities may not be limited to one of the four areas above. Inferolateral damage will show up in a combination of the inferior and lateral leads. Anterolateral damage will be seen in both the anterior and the lateral leads.

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Normal 12 lead EKG

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? MI????

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Identify which coronary artery is affected? [1] severe crushing chest pressure/pain/radiating to neck [2] chest pressure/pain with radiation to L arm [3] chest pressure radiating to the back/scapula.

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Cultural Considerations Black and Hispanic women have a higher incidence of CAD risk than white women with comparable socioeconomic status Native Americans/American Indians/Alaskan Natives >18 years of age have greater incidence of HTN, smoking, high cholesterol, excess weight, and/or diabetes mellitus Leading cause of death in men and women in the most prevalent ethnic groups is cardiac disease even though there are genetic predispositions to develop risk factors (AHA, 2003)

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Cultural Considerations Higher incidence of HTN in Black community and in whites in the South Black individuals experience longer delays in seeking treatment Symptom may be dyspnea and not chest pain Symptoms in older adults may not be associated with acute chest pain

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Women and Heart Disease More women than men have angina but many women experience atypical angina. What does atypical mean? Women have MI at older ages than men Lack of education in women that CAD is the leading cause of death in women Pathophysiology in women is different than men i.e. smaller vessels, less collateral circulation than men Impaired glucose tolerance seriously increase risk

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Heart Disease: The Leading Cause of Death for American Women American Heart Association

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Cardiovascular Disease Mortality Trends United States: 1979-2001 Source:CDC/NCHS.

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Why The Gender Gap? Women present to emergency rooms or chest pain centers 1- 2 hours later than men. Do the multiple roles a woman takes on delay care because of her responsibilities to others? Do women delay care because they perceive that heart disease is something that happens to ones father, brother, or spouse?

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Differences in Heart Attack Symptoms Men Sub-sternal chest pain or pressure Rest pain Pain down left arm and shoulder Weakness Women Pain in chest, upper back, jaw or neck Shortness of breath Flu-like symptoms: nausea or vomiting, cold sweats Fatigue or weakness Feelings of anxiety, loss of appetite, malaise

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Postmenopausal Hormone Therapy (HT) Postmenopausal HT is no longer recommended as a strategy to prevent heart disease. Hormone therapy, generally short term, may still be used to treat symptoms of menopause - this is a decision between a woman and her healthcare provider.

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The Red Dress Campaign

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Cardiac Management

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Collaborative Management History Pain Assessment Cardiovascular Assessment Psychosocial Assessment Laboratory Assessment Radiographic Assessment Other Diagnostic Assessments

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History/ Pain Assessment Historical data If chest pain present, describe and find out for how long (time is muscle) Attempt to differentiate between angina pain and infarction pain Associated symptoms patient describes i.e. N/V, diaphoresis

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Cardiovascular and Physical Assessment Vital signs Monitor for dysrhythmias Distal peripheral pulses Heart and Lung sounds

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Cardiac Auscultation

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Psychosocial Assessment Denial Fear Anxiety Anger

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Laboratory Assessment Troponin T and I- myocardial muscle protein released into the bloodstream with injury to the myocardial muscle (not found in healthy clients) Creatine kinase- MB (CK-MB) is an enzyme specific to cells of the brain, myocardium and skeletal muscle. Indicates tissue necrosis or injury, Cardiac specificity is determined by measuring the isoenzyme activity CK- MB is found in myocardial muscle CK-MM (skeletal) CK-BB (brain) Myoglobin early marker of MI is a low-molecular-weight heme protein found in cardiac and skeletal muscle, appears as early as 2 hours after an MI with rapid decline after 7 hours C-Reactive Protein is a marker of inflammation. Any inflammatory process can increase CRP in the blood

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Additional Laboratory Tests Homocysteine Serum Lipids PT, PTT, INR Arterial Blood Gases Serum Electrolytes CBC

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Radiographic and Other Diagnostic Tests Chest X-ray ECG- what are we looking for? Stress Tests- exercise tolerance testing with or without pharmacologic agents Myocardial Perfusion Imaging- Thallium scans Cardiac Catherization

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This procedure is performed to determine the extent and exact location of obstruction of the coronary arteries. Helps to identify course of therapy for patients i.e. PTCA/stent or CABG

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Nursing Diagnosis & collaborative problems. Acute pain related to biologic injury agents Ineffective tissue perfusion related to interruption of arterial blood flow Activity intolerance related to fatigue Ineffective coping related to effects of acute illness and major changes in lifestyle Potential for dysrhythmias Potential for heart failure Potential for recurrent symptoms and extension of injury

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NICs/NOCs NIC Pain Management Drug Therapy NOC Ineffective Tissue Perfusion- expect to have adequate blood flow to maintain heart function Ejection fraction Pulmonary wedge pressure Apical heart rate Systolic and diastolic blood pressure

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Collaborative Management MONA- M=morphine O= oxygen N= nitroglycerine A= aspirin Thrombolytic Therapy Beta Blockers or Calcium Channel Blocker) ACE Inhibitors Antiplatelet Agents- ASA, Plavix, Ticlid

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Potential Complications and Interventions Dysrhythmias- ventricular in origin Ventricular Failure- Class I- IV Cardiogenic Shock- Intra-Aortic Balloon Pump (IABP) Thrombolytic Therapy- Fibrinolytics and/ or Glycoprotein IIb/IIIa inhibitors PTCA