Acute Coronary Syndromes

Transcription

1 Acute Coronary Syndromes Kelly Kreimer, MSN and Shane Johnson, RN, BSN, CCRN Cardiovascular Circulatory System Heart-Pump Arteries-regulate blood supply Capillaries-exchange of cell nutrients and wastes Veins-reservoir blood volume, return blood to heart Structures and Functions Coronary Anatomy Heart Chambers-atria, ventricles Heart Muscle Walls -epicardium (outer layer) -myocardium (muscle mass) -endocardium (inner layer) AV valves/ Semilunar valves Valves Blood Supply and Systemic Circulation - Right Coronary Artery - Left Coronary Artery Right Coronary Artery RCA Supplies right atrium and ventricle The conduction system Posterior and inferior sections of left ventricle *Occlusion can cause bradycardia type dysrhythmias 1

2 Left Coronary Artery LCA Divides into left anterior descending and circumflex artery It is the main supply of the left ventricle, septum, and anterior wall *Occlusion to LAD can result in pump failure Cardiovascular Hemodynamics Cardiac Output Cardiac Output: the volume of blood ejected from the heart over a one-minute period. -Normal range is 4-8 L/min -heart rate X stroke volume - normal SV is cc/heart beat Cardiac Index: cardiac output in relation to body surface area Stroke Volume The amount of blood (ml) pumped by the ventricle with each contraction/heart beat Normal range is ml/beat Exercise-SV increases by filling with more blood volume and increasing contraction 2

3 Afterload Is the resistance of the arterial system that the ventricle must overcome in order to eject the blood into the systemic circulation. Normal Systemic Vascular Resistance is Contractility The amount of squeeze your heart muscle has for ventricular ejection Increased contraction with fight or flight response, hypovolemia, pain, anxiety, stress, and exercise. Starling s Law Describes the relationship between contractility and overall cardiac function The longer the stretch on the myocardium (the more you stretch a rubber band, for example,) the stronger the contraction (the harder it snaps.) Acute Coronary Syndromes 3 Types of Acute Coronary Syndromes Unstable Angina Non ST-elevated Myocardial Infarction (NSTEMI) ST-elevated Myocardial Infarction (STEMI) 3

4 Atherosclerosis Pathophysiology of Acute Coronary Syndromes Simoons ML, et al. Lancet 1999; 353: II-26. Angina pain, discomfort, or pressure often localized in the chest that is caused by an insufficient supply of blood to the heart muscle. Myocardium demand > Oxygen supplied = Pain Causes of Angina *Causes may include but are not limited to: Acute Coronary Syndromes -atherosclerosis, hypertension Hypovolemia, Shock Anemia/CHF Infection Dysrhythmias Coronary spasms Chronic Stable Angina Coronary artery unable to dilate due to atherosclerosis and plaque formation Pain triggered by exertion or stress Usually relieved by rest or Nitroglycerin SL DEMAND ISCHEMIA, NO INFARCT Coronary Occlusion 4

5 Plaque ruptures and thrombus forms around the ruptured plaque causing partial occlusion of the vessel Pain occurs at rest Pain is more intense and lasts longer than stable angina EKG = Normal, Inverted T-waves, or ST depression SUPPLY ISCHEMIA, NO INFARCT Unstable Angina Plaque Rupture Non ST Elevated Myocardial Infarction (NSTEMI) Plaque ruptures and thrombus formation causes partial occlusion to the vessel resulting in injury and infarct the to the subendocardial myocardium. Severe pain at rest, lasts longer then 20 minutes EKG = Normal, inverted T-Waves, or ST depression CK-MB and Troponin Elevated Subendocardial Injury ST Elevated Myocardial Infarction (STEMI) Complete Occlusion Ruptured plaque causes complete occlusion of the blood vessel lumen, resulting in transmural injury and infarct to the myocardium EKG = ST segment elevation and/or hyperacute T- waves CK-MB and Troponin Elevated 5

6 Transmural Infarct Normal EKG EKG T wave inversion Ischemia ST segment elevation Injury Q wave infarction *Acute coronary syndrome Normal 12 Lead EKG Anterior MI Locations Septal Lateral Inferior 6

7 Anterior MI Left Coronary and Left Anterior Descending Artery (LAD) Anterior wall of LV and ventricular septum 2 nd degree heart block BBB Ventricular irritability Left-sided heart failure EKG changes leads V3 to V4 Acute Anterior MI Septal MI Left Anterior Descending Artery (LAD) and septal branches off LAD Ventricular Septum High risk for ventricular septal defect Commonly accompanies an anterior wall MI EKG Changes leads V1 and V2 Acute Septal MI Lateral MI Left Circumflex Artery Supplies left atrium, posterior and lateral walls of LV, and part of anterior papillary muscle PVC s and varying degrees of heart block Commonly accompanies an anterior or inferior wall MI EKG changes in leads I, avl, V5, and V6 7

8 Acute Lateral MI Inferior MI Right Coronary Artery RV, inferior wall, posterior wall, sinus node, atria, AV node GI upset Hypotension 1 st and 2 nd degree heart block Papillary muscle rupture EKG changes leads II, III, AVF Acute Inferior MI Right Ventricular Infarct Right heart failure JVD Hypotension Hepatomegaly Tachycardia Peripheral edema Weight gain and fatigue Inferior MI Complications Pericarditis Cause: MI/leukemia (Injury/inflammation) Diagnosis Symptoms Rub EKG Treatment Anti-inflammatory agents What do we have here?? 8

9 General Risk Factor Reduction Risk Factors for ACS Smoking Cessation Blood Pressure <140/90 <130/85 if CRI or CHF <130/80 if diabetic Diet <10% saturated fat <300mg/ day cholesterol Alcohol <2/ day men <1/ day women Salt <3gm/ day Low Dose Aspirin (high risk pts) AHA 2002 NIH, NCEP guidelines LDL level Individuals with Initiate therapy LDL goal Antioxidants can help prevent plaque build up No CHD and < 2 risk factors No CHD but 2 or more risk factors >190 mg/dl After > 6mo of diet >160mg/dl After > 6mo diet <160mg/dl <130mg/dl Vitamin E Betacarotine Vitamin C CHD or other atherosclerotic disease >130mg/dl After 6-12 wks diet <100mg/dl Nurses study HOPE study Alcohol Moderation Low to moderate intake may reduce CV risk Intake of greater than1 2 oz may increase BP Stimulates catecholamines Intake should not exceed 2 oz whiskey 10 oz wine 24 oz beer Thin individuals and women ½ Differential Diagnosis A. esophageal spasm B. esophagitis C. gall bladder D. Pulmonary embolism E. musculoskelatal F. pericarditis 9

10 Symptoms Only 20% of patients present with classic symptoms Location Substernal Levine s Sign Radiation L and or R shoulder Epigastric Neck Jaw / teeth Back Exacerbating Factors Exercise Eating Inspiration Position Palpation Cocaine Duration Long term-chronic pain is not angina Acute angina needs intervention Quality Burning Pressure Dull ache Sharp Remitting Factors Rest/ exercise Position Food/antacid NTG 10

11 Treatment VS IV 12 lead History MONA Enzymes, coags, electrolytes Assess Initial 12 Lead ECG Findings ST elevation or new or presumably new LBBB: strongly suspicious for injury ST-elevation AMI ST depression or dynamic T-wave inversion: strongly suspicious for ischemia High-risk unstable angina/ non ST-elevation AMI Nondiagnostic ECG: absence of changes in ST segment or T waves Intermediate/low-risk unstable angina Classify patients with acute ischemic chest pain into 1 of the 3 groups above within 10 minutes of arrival. History History of the pain Previous episodes? Medical history-comorbidities (DM/HTN, hyperlipidemia) Medications Immediate General Treatment for Suspected Acute MI Oxygen at 4 L/min if SaO2<94% Aspirin 160 to 325 mg-chew Nitroglycerin SL or spray Morphine IV (if pain not relieved with nitroglycerin) Aspirin Pain Relief NTG Dilates epicardial arteries Increases collateral flow Decreases preload some afterload Decrease spasm Inhibits platelet aggregation Tolerance after 24hr 11

12 Pain Relief Morphine Decrease anxiety Decrease pain perception Decrease respiration Increase GI upset Oxygen- 4 liters nasal canula/check O2 sat Labs CK MB, MM, BB Troponin Protein specific to cardiac muscle Done on admission and after 12 hrs Negative troponin > ng/ml. Problem Cath lab interventions tend to focus on vessels that are 70+% blocked BUT 2/3 of ruptured plaque had previous 50% or less stenosis and 97% had a less than 70% stenosis Fibrinolytics Streptokinase, Eminase Allergic reaction risk up to 3 weeks after given Can cause hypotension Slower acting Stays active longer -less specific TPA-alteplase(rTPA) Retaplase(retavase) Produced by the body Acts quickly Less systemic effect Contraindications for Lytic Therapy Active internal bleeding History of CVA Recent intracranial or intraspinal surgery or trauma Intracranial neoplasm, AV malformation, or aneurysm Severe uncontrolled hypertension 180/110 Any condition where bleeding constitutes a significant hazard Nursing Considerations Vital Signs Neuro checks Temp increase>104 =internal bleeding Continue to monitor for bleeding 24 hours post administration 12

13 Heparin gtt Weight adjusted dosing Event adjusted dosing Unstable angina Lytics Without lytics Prevents thrombus formation and extension of existing thrombi Prevent re-occlusion after lytics Low Molecular Weight Heparin Given sq Measurement of PTT not required Indicated for non-q-wave MI and unstable angina Enoxaparin (Lovenox) Noninvasive Markers of Reperfusion Pain resolution Should be rapid Resolving of EKG changes Stunned heart may prevent resolution of changes Re-perfusion dysrhythmias VT, Accelerated Idioventricular Rhythm, Bradycardia Stress Tests Treadmill Thallium ECHO Dobutamine/Adenosine Stress Test Thallium Stress Test 13

14 Echocardiogram Velocity of blood flow Measure size of heart /chambers Cardiac wall movement abnormalities Valve function Ejection Fraction References Cardiology secrets ( , ), Fifth edition. / Levine, Glenn N.. Elsevier, Current diagnosis & treatment cardiology / [edited by] Michael H. Crawford, MD, Professor of Medicine, University of California, San Francisco, Lucie Stern Chair in Cardiology, Director, Cardiology Fellowship Program, Chief of Clnical Cardiology, UCSF Medi ( , ), Fifth Edition. / Crawford, Michael H.. McGraw-Hill Education, Essential Cardiology Principles and Practice ( , ), 3rd ed / Rosendorff, Clive. Springer New York, Critical cardiology : evaluation and treatment of common cardiovascular disorders ( X, ), 2nd ed. / Eagle, Kim A. Wolters Kluwer Health/Lippincott Williams & Wilkins, Jain, S. K. A., Larsen, T. R., Darda, S., Saba, S., & David, S. (2013). A forgotten devil; Rupture of mitral valve papillary muscle. The American Journal of Case Reports, 14,