Acute Coronary Syndromes

Transcription

1 Acute Coronary Syndromes Kelly Kreimer, MSN Acute Coronary Syndromes Coronary Anatomy Coronary Anatomy MediaPlayer.aspx?ClientID=66&TopicID =719 Electrophysiology of the Heart SA Node (in right atrium) is the major pacemaker of the heart. (Intrinsic rate ) AV Node receives impulse from the atria and slows it down before sending it to the ventricles. (Intrinsic rate 40-60) 1

2 Bundle of His Bundle of His is point where impulse divides into the right and left bundle branches and further proceeds on to the Purkinje fibers Depolarization Repolarization Cycle Movement of electrical charges inside and outside the cell involves positive ions - sodium, potassium, calcium, and magnesium and negative ions (chloride and phosphate.) Pacemaker battery-powered device that sends electrical signals to your heart to beat at a proper rate or pace. used to treat bradycardia and atrial fibrillation associated with bradycardia Implantable Cardiac Defibrillator (ICD) is a battery-powered device placed under your skin It is connected to your heart by one or more wires (leads) and keeps track of your heartbeat sends electrical signals that shock your heart out of the dangerous rhythms Structures and Functions Coronary Artery System Heart Chambers-atria, ventricles Heart Muscle Walls -epicardium (outer layer) -myocardium (muscle mass) -endocardium (inner layer) AV valves/ Semilunar valves Valves 2

3 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 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 Circulatory System Heart-Pump Arteries-regulate blood supply Capillaries-exchange of cell nutrients and wastes Veins-reservoir blood volume, return blood to heart 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 3

4 Preload Is the volume of blood in the ventricle at the end of diastole The most important component of SV Is affected by many things: absolute blood volume, how well the blood volume is distributed throughout the body, the atrial contribution, ventricular function, and ventricular compliance. 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.) Oxygenation Perfusion Components necessary for oxygen delivery: Adequate pump = cardiac output Adequate volume = stroke volume Adequate oxygen Oxygen Utilization Components necessary for oxygen utilization Adequate functional vascular bed SVO2 = represents Oxygen utilization 4

5 Mixed Venous Oxygen Saturation (SVO2) Is the percent of Hgb saturated with oxygen after being drained from the tissues and now is returning to the right atrium to be re-oxygenated in the lungs 4 Factors effect SVO2 Balance Cardiac Output-(oxygen delivery) Hemoglobin-(oxygen delivery) SAO2(oxygen supply) VO2-(oxygen utilization) Normal Range is 60-80% = adequate tissue perfusion 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 5

6 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 Angina * pain, discomfort, or pressure often localized in the chest that is caused by an insufficient supply of blood to the heart muscle. Differential Diagnosis A. esophageal spasm B. esophagitis C. gall bladder D. Pulmonary embolism E. musculoskelatal F. pericarditis Causes of Angina *Causes may include but are not limited to: Acute Coronary Syndromes -atherosclerosis, hypertension Hypovolemia, Shock Anemia/CHF Infection Dysrhythmias Coronary spasms Case Study Only 20% of patients present with classic symptoms Mr. Smith presents to his family physician with intermittent chest pain. 6

7 History History of the pain Previous episodes? Medical history-comorbidities (DM/HTN, hyperlipidemia) Medications Risk Factors A. age > 45 years B. sex male C. family history of MI-parent/sibling D. hypertension 156/96 E. low HDL 40 F. high LDL 160 G. current cigarette smoking no 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 7

8 Remitting Factors Rest/ exercise Position Food/antacid NTG Normal EKG Stress Tests Treadmill Thallium ECHO Dobutamine/Adenosine Stress Test Thallium Stress Test 8

9 Echocardiogram Velocity of blood flow Measure size of heart /chambers Cardiac wall movement abnormalities Valve function Ejection Fraction CT Image Mr. Smith is scheduled for an Angiogram and stress test. At home, he develops chest pain unrelieved by 3 NTG. His wife calls 911, and he is taken to the ER. An EKG is done Pathophysiology of Acute Coronary Syndromes Simoons ML, et al. Lancet 1999; 353: II-26. Coronary Occlusion Plaque Rupture 9

10 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 EKG T wave inversion Ischemia ST segment elevation Injury Q wave infarction *Acute coronary syndrome Assess Initial 12 Lead ECG Findings Coronary Anatomy 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. AMI Localization The Inferior Leads II, III, and avf I lateral avr V 1 septal V 4 anterior II inferior avl lateral V 2 septal V 5 lateral III inferior avf inferior V 3 anterior V 6 lateral 10

11 Inferior MI Acute 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 EKG changes leads 2, 3, AVF 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 EKG Changes With Pericarditis 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) 11

12 Mr. Smith had a BP of 140/90, and a HR of 100. He was given NTG sl, an IV was started, blood drawn, he was put on O2 and an IV NTG GTT was started. Labs CK MB, MM, BB Troponin Protein specific to cardiac muscle Done on admission and after 12 hrs Negative troponin > ng/ml. Treatment VS IV 12 lead History MONA Enzymes, coags, electrolytes Pain Relief NTG Dilates epicardial arteries Increases collateral flow Decreases preload some afterload Decrease spasm Inhibits platelet aggregation Tolerance after 24hr Pain Relief Morphine Decrease anxiety Decrease pain perception Decrease respiration Increase GI upset Oxygen- 4 liters nasal canula/check O2 sat Aspirin 12

13 The Role of Platelets in Atherothrombosis The role of the thrombus mechanism of action in ST segment elevation ACS 1 Adhesion 3 Aggregation Generally caused by a completely occlusive thrombus in a coronary artery Results from stabilization of a platelet aggregate at site of plaque rupture by fibrin mesh platelet RBC fibrin mesh GP IIb-IIIa 2 Activation Reproduced with permission from Cannon CP. Atherothrombosis slide compendium. Available at: The Thrombus Fibrin Mesh Trapped RBCs % Cumulative mortality at 6 months 6-month Mortality for Acute Coronary Syndromes ST ACS 8.9% ST MI with fibrinolytics 6.8% T-wave inversion ACS 3.4% National Geographic Society, 1986 Used by permission. Granger CB et al. J Am Coll Cardiol. 1998; 31:79A. Further history was done to determine if Mr. Smith was a candidate for fibrinolytic therapy. EKG changes in at least 2 consistent leads Unrelieved chest pain >20min but <12 hours Time to treatment Age? <75, oriented x 3 -cooperative No contraindications 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 13

14 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 Mr. Smith received Retavase and was sent to the CCU. His pain was relieved, and he had partial resolution of his EKG changes. He had a 5 beat run of VT toward the end of his lytic run. Nursing Considerations Vital Signs Neuro checks Temp increase>104 =internal bleeding Continue to monitor for bleeding 24 hours post administration 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 Mr. Smith was put on a 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) 14

15 Mr. Smith Was Scheduled for a Coronary Angiogram With Possible Angioplasty Summary of ACS wyw - which leads look where jr2c shorter version- might be better 15