Week 2 Coronary Artery Disease, Angina, ACS, MI Notes PDF

ORONARY RTEY P R E PA R E D BY : EARL JOHN S. AMADO, RN, ISEASE MSN CORONARY ARTERY DISEASE Coronary artery disease develops when the major blood vessels that supply your heart become damaged or diseased. Cholesterol-containing deposits (pl...

ORONARY RTEY P R E PA R E D BY : EARL JOHN S. AMADO, RN, ISEASE MSN CORONARY ARTERY DISEASE Coronary artery disease develops when the major blood vessels that supply your heart become damaged or diseased. Cholesterol-containing deposits (plaques) in your coronary arteries and inflammation are usually to blame for coronary artery disease. ARTERY A buildup of plaque can narrow these arteries, decreasing blood flow to your heart. Eventually, the complete blockage can cause a heart attack. CORONARY ATHEROSCLEROSIS The most common cause of cardiovascular disease in the United States and is characterized by an abnormal accumulation of lipid or fatty substances and fibrous tissue in the vessel wall.  Atherosclerosis Arteriosclerosis A type of arteriosclerosis Thickening or hardening caused by formation of PLAQUE (chiefly of the arterial wall composed of cholesterol)  RISK FACTOR Non Modifiable Modifiable Age(>45/M & 55/F) Hyperlipidemia/ Gender(M can develop at Hypercholesterolemia early age than F) Cigarette smoking, Race(higher incidence in tobacco use African Americans than in Elevated BP Caucasians) Hyperglycemia(DM) Heredity(history of CAD in Obesity 1st-degree relative at 55/M Physical inactivity/ & 65/F or younger) Sedimentary living  RISK FACTOR Non Modifiable Modifiable Stress Diet Alcohol Behavioral Factor Contraceptive Pills PHATOPHYSIOLOGY  RISK FACTOR Non Modifiable Modifiable A. Non specific Injury to Arterial wall(Endothelial Lining)  Desquamation of Endothelium Increased Permeability/ Adhesion Molecules B. Lipids (LDL, VLDL) and Platelets Assimilation into the Area C. Oxidized LDL attracts Monocytes and Macrophages to the Site D. Plaque Begin to Form from Cells which Imbed into the Endothelium E. Lipids are Engulfed by Cells(foam cells) and smooth Muscle Cells Develop Coronary Atherosclerotic Heart Disease Decrease Coronary Tissue Perfusion Decrease Myocardial Oxygenation Angina Pectoris Myocardial Infarction CLINICAL MANIFESTATIONS Symptoms and complications develop according to the location and degree of narrowing of the arterial lumen thrombus formation, and obstruction of blood flow to the myocardium.  Clinical Manifestations Ischemia Myocardial Infarction Chest pain: angina Dysrhythmias pectoris Sudden death Atypical symptoms of myocardial ischemia (shortness of breath, nausea, and weakness)  ASSESSMENT Identification of risk Elevated homocysteine factors ( risk if level > 15mmol/L)  taking a thorough history  making cell wall less elastic blocks the production of (family history) nitric oxide on the physical examination endothelium & permitting  BP plaque to build up.  Weight  Diet: B-complex vitamin Elevated FBS rich diet ,folic acid - homocysteine  LABORATORY FBS, LIPID PROFILE cholesterol levels [low-density lipoprotein (LDL) to high-density lipoprotein (HDL)], glucose). INTERVENTION Cholesterol screening Diet (Low Salt, Low Fat) Smoking cessation Exercise Drug therapy  HMG-CoA reductase inhibitors “Statins” (As Ordered)  PREVENTION The major management goal is prevention of CHD modifiable risk factors Cholesterol abnormalities Cigarette/tobacco use Hypertension diabetes mellitus(DM) ANGINA PECTORIS(Myocardial Ischemia) Angina pectoris is a clinical syndrome characterized by paroxysms of pain or a feeling of pressure in the anterior chest. The cause is insufficient coronary blood flow, resulting in an inadequate supply of oxygen to meet the myocardial demand. FACTORS AFFECTING ANGINAL PAIN Physical exertion Precipitating Factors (4 E’s) Exposure to cold Eating a heavy meal 1. Exertion stress or any emotion- 2. Emotion provoking situation that 3. Eating increases: 4. Environment/Exposure  BP  HR  Myocardial Workload  TYPES OF ANGINA PECTORIS STABLE ANGINA  Chest pain last less than 15min.  Recurrence is less frequent. UNSTALE ANGINA(Pre-infarction Angina, Crescendo Angina, Intermittent Coronary Syndrome)  Chest pain last for more than 15min. but less than 30min.  Recurrence is more frequent, may occur at night.  Intensity of pain increases.  TYPES OF ANGINA PECTORIS VARIANT ANGINA (Prinzmetal’s Angina).  Chest pain is of longer duration and may occur at rest.  The attacks tend to occur in the early hours of the day.  May result from coronary artery spasm. NOCTURNAL ANGINA  Occur only during night and is possibly associated with rapid eye movement(REM) sleep. ANGINA DECUBITUS  Paroxysmal chest pain that occurs when the client sits or stands up.  TYPES OF ANGINA PECTORIS INTRACTABLE ANGINA  Chronic, incapacitating angina unresponsive to intervention. POSTINFARCTION ANGINA  Occurs after MI, when residual ischemia may cause episodes of angina. PHATOPHYSIOLOGY  CAUSES Atherosclerosis, Hypertension, Diabetes Mellitus, Thromboangitis Obliterans, Polycythemia Vera, Aortic regurgitation Reduced Coronary Tissue Perfusion Diminished Myocardial Oxygenation Anaerobic Metabolism Increased Lactic Acid Production(Lactic Acidosis) CHEST PAIN  CLINICAL MANIFESTATION PAIN  Transient, paroxysmal substernal or precordial pain.  Describe as heaviness or tightness of the chest, “indigestion”, crushing.  Radiates down one or both arms, left shoulder, jaw, neck and back.  Precipitated by activity or exertion.  CLINICAL MANIFESTATION PAIN  Relieved by rest and nitroglycerine(NTG). CLINICAL MANIFESTATION SAVERS S-ubsternal A-anterior chest V-ague(Radiates) E-xertion-related R-elieved by rest and NTG S-hort duration(Circumflex coronary artery(Cx) – LA, lateral & posterior surfaces of LV, portion of interventricular septum RIGHT CORONARY ARTERY RA, RV, a portion of the septum, inferior portion of LV, SA node and AV node MYOCARDIAL INFARCTION(MI) An area of the myocardium is permanently destroyed, typically because plaque rupture and subsequent thrombus formation result in complete occlusion of the artery. MYOCARDIAL INFARCTION(MI) Prolonged ischemia lasting more than 20 minutes produces irreversible cellular damage and necrosis of the myocardium. If ischemia persists, it takes approximately 4-6 hours for entire thickness of the heart muscle to become necrosed.  MYOCARDIAL INFARCTION(MI) Non-ST-segment-elevation myocardial Infarction (NSTEMI) ST-segment elevation myocardial Infarction (STEMI)  OTHER CAUSES OF MI Vasospasm (sudden constriction or narrowing) of a coronary artery. Decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure). Increased demand for oxygen (eg, from a rapid heart rate, Thyrotoxicosis, or ingestion of cocaine) PHATOPHYSIOLOGY  CAUSES Coronary Atherosclerotic Heart Disease Coronary Thrombosis/ Embolism Decrease Blood Flow with Shock and/ or Hemorrhage Direct Trauma Myocardial Myocardial Ischemia Oxygen Supply  Altered Cell Cellular Hypoxia Membrane Integrity Myocardial Contractility Arterial Pressure Cardiac Output Stimulation of Stimulation of Sympathetic Baroreceptors Receptors  Peripheral Afterload Vasoconstriction Myocardial Oxygen Demand  Myocardial Heart Rate Contractility Coronary Diastolic Filling Tissue Perfusion  CLINICAL MANIFESTATION PAIN  Crushing, severe, prolonged, unrelieved by rest or nitroglycerine; often radiating to one or both arms, the neck and the back.  Characterized by "Levine's sign" (chest hand- clutching). This is the universal sign of distress in angina pectoris and MI.  CLINICAL MANIFESTATION ANXIETY AND APPREHENSION  Feeling of "doom," restlessness. SHOCK  This is manifested by systolic pressure below 80mmHg, gray, facial color, lethargy, cold diaphoresis, peripheral cyanosis, tachycardia / bradycardia, weak pulse,  CLINICAL MANIFESTATION OLIGURIA  Urine flow of less than 30ml/ hour.(Renal Hypoxia) FEVER  Slight elevation of temperature occurs within 24 hours and extends 3 to 7 days accompanied by leukocytosis and elevated ESR. INDIGESTION:  "Gas pains around the heart," nausea and vomiting.  CLINICAL MANIFESTATION ACUTE PULMONARY EDEMA  Sense of suffocation, dyspnea, orthopnea, gurgling/ bubbling respiration.(Pulmonary Congestion)  CLINICAL MANIFESTATION ECG CHANGES  MI causes elevation on ST segment, inversion of T wave, and enlargement of Q wave.  Elevated ST Segment = Area of damage.  Inverted T wave = Zone of ischemia. ELEVATED CK-MB, LDH(Lactic dehydrogenase), AST(aspartate aminotransferase)  Cellular damage and death ELEVATED TROPONIN LEVEL  Troponin I 1.5ng/ml  Troponin T: above 01 ng/ml  ASSESSMENT Assess level of Measure blood pressure to consciousness. determine response to pain Evaluate chest pain (most and treatment; note pulse important clinical finding). pressure, which may be Assess heart rate and narrowed after an MI, rhythm; dysrhythmias may suggesting ineffective indicate not enough oxygen to the myocardium. ventricular contraction. Assess heart sounds; S3 Assess peripheral pulses: can be an early sign of rate, rhythm, and volume. impending left ventricular Evaluate skin color and failure. temperature.  ASSESSMENT Auscultate lung fields at Observe urinary output frequent intervals for and check for edema; an signs of ventricular failure early sign of cardiogenic (crackles in lung bases). shock is hypotension with Assess bowel motility; oliguria. mesenteric artery Examine IV lines and thrombosis is a sites frequently. potentially fatal complication.  DIAGNOSTICS Cardiac enzymes and Electrocardiography biomarkers (ECG) within 10 minutes (CK-MB)Creatinine kinase of pain onset or arrival at – Myocardial band(creatine the emergency kinase isoenzymes) department; Myoglobin test echocardiography to troponin I, Troponin T evaluate ventricular function.  INTERVENTIONS Goal  Prevention of further tissue injury and limitation of infarct size.  Maximizing myocardial tissue perfusion and reduce myocardial tissue demands.  INTERVENTIONS PROMOTING OXYGENATION AND TISSUE PERFUSION  Supplemental Oxygen by Nasal Cannula 24-48hrs or longer if pain, hypotension, dyspnea or dysrhythmias.  Position: Semi – Fowler’s.  INTERVENTIONS PROMOTING ADEQUATE CARDIAC OUTPUT MONITOR  Vital Signs(Pulse rate and rhythm)  Cardiac Monitoring(Dysrhythmias)  Effect of cardiac activities on cardiac output. Bed rest and minimize unnecessary disturbances.  INTERVENTIONS PROMOTING CONFORT  Administer MORPHINE(as ordered) re relieve pain. PROVIDING REST  Bed rest 24-48hrs with commode privileges.  Administer DIAZEPAN(as ordered).  CCU/CCC/ICU(monitoring and safety)  Provide psychological support to the client and family.  INTERVENTIONS PROMOTING NUTRITION AND ELIMINATION  Small frequent feeding.  Low calories, Low cholesterol, Low sodium Diet.  Avoid stimulants.  Use bedside commode(DO NOT USE BEDPAN).  Administer stool softener(as ordered).  INTERVENTIONS PROMOTING RELIEF OF ANXIETY AND FEELING OF WELL-BEING.  Provide opportunity for the client and family to explore their concerns and identify methods of coping. FACILITATE LEARNING (Teaching starts when client id free of pain and anxiety)  Promote positive attitude and active participation of the client and family.  MEDICAL MANAGEMENT MEDICATIONS ANALGESIC  MORPHINE SULFATE(Drug of choice)  LIDOCAINE or NITROGLYCERINE THROMBOLYTIC THERAPHY  Disintegrate blood clot.  Streptokinase, urokinase and tissue plasminogen activator(tPA).  Administration is crucial between 3-6hrs after initial infarction.  MEDICAL MANAGEMENT  FOBT (During and after therapy).  Anticoagulant and Antiplatelet after (Maintain arterial patency). OTHER MEDICATION Beta – adrenergic blocking agents; DIAZEPAM(Valium)  COMPLICATION OF MI  Dysrhythmias  Cardiogenic shock  Thromboembolism  Pericarditis(Dressler’s Syndrome)  Rupture of myocardium.  Ventricular aneurysm.  Congestive Heart Failure(CHF) SURGICAL PROCEDURES: CORONARY Reperfusion procedures may be used to restore the blood supply to the myocardium. Percutaneous Coronary Intervention(PCI) procedures percutaneous transluminal coronary angioplasty [PTCA] Intracoronary stents Atherectomy coronary artery bypass graft (CABG). SURGICAL PROCEDURES: CORONARY PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY [PTCA] INTRACORONARY STENTS SURGICAL PROCEDURES: CORONARY ATHERECTOMY SURGICAL PROCEDURES: CORONARY CORONARY ARTERY BYPASS GRAFT (CABG) THANK YOU FOR LISTENING