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Angina Pectoris and Acute Coronary Syndrome (ACS) Jenny Huri 2015 PATHOPHYSIOLOGY CAD refers to the development and progression of plaque accumulation in the coronary arteries. It is a continuum that starts with: stable angina-> unstable angina-> MI Smeltzer and Bare (2004) Management of Patients with Coronary Vascular Disorders – pg723-730 Angina Pectoris Angina Pectoris is the result of myocardial ischaemia caused by an imbalance between myocardial blood supply and oxygen demand. Angina or chest pain is the common symptom of this imbalance. What is happening? Coronary blood flow becomes inadequate to meet myocardial oxygen demands Myocardial ischaemia develops Contractility decreased , CO decreased Myocardial cells switch from aerobic to anaerobic metabolism due to cellular hypoxia (10 seconds) Lactic acid produced – irritates sensory afferent nerve fibres in coronary arteries, myocardium and upper thoracic posterior nerve roots. Types of Angina Stable –chest pain precipitated by exertion or stress. Myocardial oxygen demands increased. Unstable (preinfarction) chest pain occurring at rest. Intractable - severe Silent ischaemia diabetics Prinzmetal Angina (varient) - vasospasm http://www.nlm.nih.gov/medlineplus/ency/images/ency/fullsize/18054.jpg Angina http://www.bing.com/videos/search?q=stable+angina&qs=n&form=QBVR &pq=stable+angina&sc=6-13&sp=1&sk=#view=detail&mid=B777293AD5EAE34D41EDB777293AD5EAE34D 41ED Clinical manifestations Pain – varying in severity Pain often felt deep in chest (retrosternal) may radiate to neck,jaw, shoulders and inner aspects of upper arms (left) numbness with pain SOB, diaphoresis, nausea and vomiting, dizziness light-headedness,syncope subsides with rest or GTN (glyceryl trinitrate Common sites of Anginal pain Diagnosis and Management Management Diagnosis clinical picture 12 lead ECG bloods stress exercise echocardiogram nuclear scan angiography objectives are to decrease oxygen demand & increase supply & prevent MI oxygen pharmacological revascularisation reduce anxiety self care and lifestyle changes SDL – Teaching Plan Acute Coronary Syndrome Unstable angina and acute MI Same disease process on different points along a continuum Pathophysiology of chest pain Lewis Pg 868 narrowing of coronary arteries insufficient blood flow myocardial oxygen demands exceed supply anaerobic metabolism with lactic acid accumulation Myocardial nerve fibres irritated pain message transmitted to cardiac nerves and upper posterior nerve roots Myocardial Infarction (MI) Exterior views of the heart Anterior view Posterior view http://heart.healthcentersonline.com/angiogram/coronaryangiogram.cfm acquired 24-04-06 Myocardial Infarction Occlusion of coronary artery for >4-6hrs Cell death -irreversible necrosis of myocardium Cause of over 40% of all deaths in NZ “Time is muscle” What happens in a MI ? http://www.youtube.com/watch?v=H_VsHmoRQKk&feat ure=related Myocardial Infarction What has happened ? myocardial cells are permanently destroyed reduced blood flow in coronary artery cell injury and necrosis Pain usually longer than 30mins characteristic ECG changes Phases of an MI Phases of an MI MI Locations Right coronary artery supplies R atrium, R ventricle, and part of posterior and inferior surface of L ventricle as well as part of AV & SA node and bundle of His Circumflex mainly supplies parts of the left atrium and left ventricle Left anterior descending (LAD) coronary artery supplies portions of the R & L ventricular myocardium and most of the interventricular septum Circumflex and LAD branches of left main CLINICAL MANIFESTATIONS Severe chest pain not relieved by rest and/or GTN Pain may radiate to arms, neck , back and jaw Hypertension/hypotension brady/ tachycardia Anxiety, fear , feeling of doom Lightheadedness and syncope Neuro changes – disorientation, restlessness Dyspnea, rales, cough (could be productive ) Diaphoresis with clammy skin and facial pallor Nausea and vomiting and /or hiccups ECG: ST elevation/ depression, Q waves, T wave abnormal May present with fever Smeltzer and Bare (2004) Management of Patients with Coronary Vascular Disorders – pg723-729 Class assignment Discuss the clinical manifestations of an acute Myocardial infarction with reference to pathophysiology, under the following headings. cardiovascular respiratory genitourinary skin GI neurological psychological Divide into 4 groups and pick a spokesperson DIAGNOSTIC TESTS Blood tests (Troponin T&I, CPK-MB ) Electrocardiograph (ECG): ST elevation/depression Q waves and new LBBB Imaging tests Echocardiography – evaluates ventricular function WHO markers = History of severe prolonged chest pain , abnormal persistent Q waves and changes in serial enzymes that indicate injury and infarction Lewis page 706-710 (821 -824) Smeltzer and Bare (2004) Management of Patients with Coronary Vascular Disorders – pg723-729 NSTEMI (non ST elevation MI) No ST elevation …. If Troponin is Pos. the diagnosis is Acute MI. Neg. Troponin the DX is Unstable Angina. S T Elevation M. I. Evolution of an acute MI http://www.frca.co.uk/images_main/resources/ECG/ECGresource44.jpg Effects on ECG Farrell, M. (2005).Textbook of Medical Surgical Nursing, Philadelphia: Lippincott. p.730 STEMI - InvasiveTreatment http://www.youtube.com/watch?v=36_qHWLFzI0 Differential diagnosis -MI Anxiety Aortic stenosis Asthma Billary colic Indigestion CORD Chest infection Aortic dissection Myocarditis Pericarditis Emergency Care for MI FIRST: MONA Morphine,Oxygen,Nitrate,Aspiri n PROCEDURES: IV access ECG Cardiac Monitoring SpO2 CXR Bloods -Troponin I & T & CK-MB Invasive therapy MEDICATIONS: ß-blockade ACE inhibitor Thrombolysis Heparin - IV LMWH (low molecular weight heparin)- Sub cut Platelet aggregation inhibitors (IIb/IIIa) Anxiolytic (anti-anxiety drugs) Management of MI Goal is to minimize damage, preserve function and prevent complications Reduce and eliminate Chest pain Morphine IV Oxygen ( Myocardial oxygen demands exceed supply ) Nitroglycerin spray Aspirin Monitor for decreased systemic and Myocardial tissue perfusion. Monitor abnormal heart rate,rhythm,BP, Resp,cyanosis, decreased urinary output and confusion Prepare for Reperfusion Therapy –Thrombolysis if candidate Pharmacological management Reduce anxiety Nursing Management Plan Chest discomfort related to imbalance between myocardial oxygen demands and supply Goals detection reduce or eliminate prevention Decreased myocardial tissue perfusion related to imbalance between myocardial O2 supply and demand Decreased systemic perfusion related to decrease in cardiac output Fear or anxiety from patient and family related to Dx , Tx and prognosis Knowledge deficit about disease, plan, risk factors, normal ADL’s PROGNOSIS for MI Better Early reperfusion Inferior wall intact Preserved LV function Short and long term - ß-blockade, ACE + Aspirin Poor Delay in reperfusion LV dysfunction Chest Pain group activity Chest Pain flow chart and documentation COMPLICATIONS of CAD/MI Tachyarrhythmia Brady arrhythmia Cardiogenic shock Valvular insufficiency CHF Ventricular aneurysms Peri, endo and myocarditis Pericardial effusion CardiacTamponade Ventricular Aneurysm