Myocardial Infarction NUR 409 Fall 52016-2017 JUST/ School of Nursing
Anatomy Review Three Layers for the Heart • Epicardium: • outer layer • Myocardium: • middle layer • Endocardium: • inner layer
Anatomy Review Myocardium • Muscular wall of the heart • Atrial myocardium wraps around great vessels • 2 divisions of ventricular myocardium: • Superficial ventricular muscles: surround ventricles • Deep ventricular muscles:spiral around and between ventricles
Coronary Arteries • Coronary arteries and cardiac veins Supplies blood to muscle tissue of heart • Left and right • Originate at aortic sinuses • High blood pressure, elastic rebound force blood through coronary arteries between contractions
Coronary Arteries Right Coronary Artery • Supplies blood to: • right atrium • portions of both ventricles • cells of sinoatrial(SA) and atrioventricular nodes • marginal arteries (surface of right ventricle) • posterior interventricular artery
Coronary Arteries Left Coronary Artery • Supplies blood to: • left ventricle • left atrium • interventricular septum. • 2 main branches: • circumflex artery • anterior interventricular artery
Question Which of the following infarctions is a result of the occlusion of the left anterior descending coronary artery? A. Anterior left ventricle B. Lateral and posterior left ventricle C. Inferior left ventricle D. Right ventricle
Answer • A. Anterior left ventricle • Rationale: Infarctions of the anterior wall of the left ventricle and the interventricular septum result from occlusion of the left anterior descending (LAD) coronary artery. The LAD coronary artery supplies oxygenated blood to the anterior wall of the left ventricle, the interventricular septum, and the ventricular conducting tissue.
Coronary Arteries Ischemia, injury or death involving the right coronary artery (RCA) most often result in changes in the inferior surface of the heart: Leads II, III, AVF Obstruction of blood flow in the circumflex artery is associated with lateral changes from ischemia or infarction: LeadsI, AVL, V5, V6 Left anterior descending branch (LAD) of the left coronary artery (LCA) flow obstructions are associated with anterior wall and/or septal changes: Leads V1 and V2 (septal)…Leads 2,3,4 (anterior wall)
MI Definition • A result of occlusion of arterial flow to the myocardium. • Occlusion occurs via spasm, blood clot or stenosis • Irreversible damage to the myocardium
MI Definition • Either one of the following criteria; -Typical rise and gradual fall (Tn) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following • Ischemic symptoms • Development of pathological Q wave • ECG changes suggesting ischemia • Pathological findings of an acute myocardial infarction
MI Definition WHO Criteria 2 out of 3 Characteristics • Typical Symptoms • Enzyme Rise and Fall • ECG Pattern Involving Development of Q-waves
Myocardial Infarction • Prolonged ischemia • Plaque rupture triggers thrombus formation at the site of an atherosclerotic lesion. • Occlusion of blood flow results in MI. • Irreversible damage occurs after 20 to 40 minutes. • Tissue can be salvaged if flow is restored within 6 hours. • Cellular changes depend on extension and expansion of infarct and ventricular remodeling.
Atherosclerosis—Pathophysiology • Triglycerides, hypertension, and cigarette smoking cause damage to the endothelium. • Fatty substances, cholesterol, cellular waste products, calcium, and fibrin pass are deposited forming lipid plaque (atheroma). • White blood cells, smooth muscle cells, and platelets to aggregate at the site forming a fibrous plaque • Blood flow is reduced, decreasing oxygen supply to tissues. • Symptoms occur with 75% or more occlusion.
Pathophysiology • When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time
Size of the Infarction • Extent, severity, and duration of ischemia • Size of the vessel • Collateral circulation • Status of intrinsic fibrinolytic system, vascular tone, and metabolic demands • Transmural—necrosis of tissue in all layers of the myocardium • Normal motion is affected.
Type of Infarction • Q-wave • Infarcted the full muscle wall • Formation of pathological Q waves in area of infarct • Greater than one small box in duration • Deeper then 1/3 of the R wave • Non–Q-wave • Infarcted only partial amount of muscle wall
Type of Infarction • Significant Q-wave where none previously existed • Why? • Impulse traveling away from the positive lead • Necrotic tissue is electrically dead • No Q-wave in Subendocardial infarcts • Why? • Not full thickness dead tissue • But will see a ST depression • Often a precursor to full thickness MI • Criteria • Depth of Q wave should be 25% the height of the R wave • Width of Q wave is 0.04 secs • Diminished height of the R wave
Type of Infarction There are two distinct patterns of ECG change depending if the infarction is: • ST Elevation((Transmural orQ-wave), or • Non-ST Elevation (Subendocardialor non-Q-wave)
Location of the Infarction • Anterior left ventricle • Occlusion of left anterior descending (LAD) • Lateral and posterior left ventricle • Left circumflex artery • Inferior left ventricle • Occlusion of right coronary artery • Right ventricle • Occlusion of right coronary artery
V1, V2, V3, V4 Anterior infarctwith ST elevation Left Anterior Descending Artery (LAD) V1 and V2 may also indicate septal involvement which extends from front to the back of the heart along the septum Left bundle branch block Right bundle branch block 2nd Degree Type2 Complete Heart Block Anterior MI
Lateral MI • I, AVL, V5, V6 • Lateral Infarction with ST elevations • Left Circumflex Artery • Rarely by itself • Usually in combo
Posterior MI • leads V1, V2 • Posterior Infarct with ST Depressions and/ tall R wave • RCA and/or LCX Artery • Understand Reciprocal changes • The posterior aspect of the heart is viewed as a mirror image and therefore depressions versus elevations indicate MI • Rarely by itself usually in combo
Inferior MI • leads II, III, AVF • Inferior Infarct with ST elevations • Right Coronary Artery (RCA) • 1st degree Heart Block • 2nd degree Type 1, 2 • 3rd degree Block • N/V common, Brady
RVI • Hypotension • Jugular vein distention • Dry lung sounds
A 59-year-old man has been admitted. He has a 90-minute history of severe crushing chest pain. His ECG shows 3mm ST segment elevation in leads V1 to V4consistent with an acute anterior myocardial infarction. He is given loading doses of aspirin and clopidogrel. Forty-five minutes after admission, he undergoes successful primary percutaneous coronary intervention (PCI) with the insertion of a drug eluting stent into his critically narrowed left anterior descending coronary artery. By the time he is returned to the coronary care unit 30 minutes after the procedure, he is pain free and there is partial resolution of his ECG changes.
His U + Es, full blood count, blood glucose, renal, hepatic and thyroid function are all normal. Fasting lipid profile: cholesterol = 6.8mmol/litre; HDL cholesterol = 1.2mmol/litre; LDL cholesterol = 4mmol/litre; triglycerides = 3.5mmol/litre Although he has a history of asthma, it is well controlled and he has never been hospitalized for it. He uses his salbutamol inhaler rarely. He also has a history of gastro-oesophageal reflux with endoscopically confirmed oesophagitis two years ago. He smokes 20 cigarettes per day and consumes approximately 35 units of alcohol per week. His body mass index = 26kg/m2
Assessment • History • Physical exam • Diagnostic studies • Electrocardiogram • Laboratory test
Assessment History Heaviness, squeezing, choking, or smothering sensation Substernal pain can radiate to the neck, left arm, back, or jaw Prolonged and unrelieved by rest or nitroglycerin Nausea/vomiting Diaphoresis, dyspnea, weakness, fatigue, anxiety, restlessness, confusion, shortness of breath, or a sense of impending death
Risk Factors Associated with Acute Coronary Syndrome: Modifiable • Tobacco smoke • Hypertension • Physical activity • Obesity • Dyslipidemia • Diabetes mellitus
Risk Factors Associated with Acute Coronary Syndrome: Nonmodifiable • Age: Death generally occurs over age 65 • Gender: Men are at greater risk than women. After menopause mortality increase in women • Heredity: Children of parents with heart disease are at greater risk
Risk Factors Associated with Acute Coronary Syndrome: Other • Stress • Alcohol consumption • Hormone Replacement Therapy (HRT)
Physical Examination • May appear restless, agitated, in distress • Skin cool and moist • VS, low-grade fever, hypertension, and tachycardia or hypotension and bradycardia • Irregular, faint pulse • Lack of point of maximal impulse • Diminished S1, S3 ,, and S4, pericardial friction rub • JVD, heart failure, pulmonary edema • Labored breathing, crackles, rhonchi
Diagnostic Tests • The electrocardiogram (ECG) • Detects patterns of ischemia, injury, and infarction • Depolarization and repolarization of cardiac cells are altered causing ECG changes • Ischemia—T-wave inversion, ST-segment depression • Injury—ST-segment elevation • Infarction—T-wave, ST-segment, and Q-wave changes • Reveals the anatomical region involved
Question Which biomarker is preferred for diagnosing a coronary event? A. Creatine kinase B. Creatine kinase isoforms C. Myoglobin D. Troponin
Answer • D. Troponin • Rationale: Troponin is a contractile protein with two subforms (troponin T and troponin I) that are highly specific for cardiac muscle. Troponin levels are not detected in the healthy person, and skeletal muscle injury does not affect the level. Troponin has been found to be a sensitive marker during the early hours after an MI. Because the cardiac troponins are highly sensitive and specific for MI, they are the preferred biomarker for diagnosing this coronary event.
Laboratory Tests • Creatine kinase • CK-MB specific to myocardial cell damage • Rises in 3 to 12 hours, peaks in 24 hours, returns to normal in 48 to 72 hours • Creatine kinase isoforms • CK-MB2/CK-MB1 ratio greater than 1—diagnostic for MI • Myoglobin • Rises in 1 to 4 hours, peaks in 6 to 7 hours, not specific for the diagnosis of MI
Laboratory Tests (cont.) • Troponin • Preferred biomarker • Troponin I rises in 3 to 12 hours, peaks at 24 hours, and remains elevated for 5 to 10 days. • Troponin T rises in 3 to 12 hours, peaks in 12 hours-2 days, and remains elevated for 5 to 14 days. • Other diagnostic tests • CXR, echocardiogram, radionuclide angiography, MRI,
ST elevation & depression T-waves peaked flattened inverted Appearance of pathologic Q-waves ECG Changes
Evolving MI and Hallmarks of AMI Q wave ST Elevation T wave inversion 1 year