Download
acute myocardial infarctions n.
Skip this Video
Loading SlideShow in 5 Seconds..
Acute Myocardial Infarctions PowerPoint Presentation
Download Presentation
Acute Myocardial Infarctions

Acute Myocardial Infarctions

228 Vues Download Presentation
Télécharger la présentation

Acute Myocardial Infarctions

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Acute Myocardial Infarctions Howard L. Sacher, D.O. Chief, Division of Cardiology Adjunct Clinical Associate Professor of Medicine New York College of Osteopathic Medicine

  2. To understand current concepts of the pathophysiology of acute myocardial infarction (AMI). To understand and apply current strategies in the evaluation of patients with AMI. To understand and apply current strategies in the management of patients with uncomplicated AMI. To understand and apply current strategies in the evaluation and management of patients with complications of AMI. Learning Objectives

  3. Acute Myocardial Infarction • Acute Myocardial infarction • A. usually caused by sudden thrombotic occulusion of a coronary artery at the site of an atherosclerotic plaque that has become unstable due to a combination of ulceration, fissuring and rupture. • B. CHF if 25% of the left ventricle is infarcted • C. Cardiogenic shock if 40% of left ventricle is infarcted • D. Right ventricular ischemia or infarction occurs in up to ½ of inferior wall infarctions.

  4. E. EKG • 1.inferior wall myocardial infarction changes leads II, III and aVF. • 2. Anterior septal MI-V1, V2, V3 • 3. Anterior wall MI- V2, V3, V4 • 4. Lateral wall MI-V5,V6, I, aVL ST segment elevation and T wave changes occur first, then Q waves form

  5. Coronary syndromes have exploded since the early 1920’s

  6. Excess LDL-C leads to Accumulation in Intima Trapped LDL particles undergo oxidation Oxidized LDL are not recognized - Activate macrophage which produces, and stimulates endothelial cells to produce IL-6, IL-1, TNF-a, neopterin. This in turn causes endothelial cells to produce adhesion molecules. The Progress of Atherosclerosis IL-6 IL-1 TNF-  Liver Bone marrow LDL particle Monocyte T-cell Activated macrophage Adhesion molecules Endothelial cell IL-6 IL-1 TNF-  ‘Oxidised’ LDL Monocytes attach and drop from circulation, mature to macrophages and engulf LDL = Foam Cell Foam cells – beginning of fatty streak Smooth muscle cells

  7. There is a direct correlation between the amount of fatty streaks in the intralumenal surface and coronary events in young individuals

  8. Pathophysiology • Atherosclerotic plaques rich in foam cells that are susceptible to sudden plaque rupture and hemorrhage into the vessel wall, which may result in the sudden partial or total occlusion of the coronary artery. • After total occlusion myocardial necrosis is complete in 4-6 hours. Flow to ischemic area must remain above 40% of pre-occlusion levels for that area to survive.

  9. The infarctions can be divided into Q-wave and non Q-wave, with the former being transmural and associated with totally obstructed infarct-related artery and the latter being non-transmural and associated with patent • Total occlusion of the left main coronary artery which usually supplies 70% of the LV mass is catastrophic and results in death in minutes.

  10. Common Signs/Symptoms Pain - arm, back, jaw, epigastrium, neck, chest Anxiety Lightheadedness, pallor, weakness, syncope Nausea, vomiting, diaphoresis Chest heaviness, tightness Cough, diaphoresis, dyspnea, rales, wheezing

  11. Hypercholesterolemia (increased LDL; decreased HDL) Premature (<55) familial onset of coronary disease Smoking Diabetes mellitus Hypertension Sedentary life style Aging Hostile, frustrated personality Hypertriglyceridemia Obesity Pertinent Risk Factors

  12. Estimating future CHD,developed by Framingham Heart Study Group, stratifies Pt’s by their age number and severity of their risk factors. Separate one for men and women

  13. S4/S3 heart sound Arrhythmias Hypertension, hypotension Levine’s sign Jugular venous distention Diaphoresis Pallor Bradycardia, tachycardia, or irregular pulses Fourth heart sound Physical Exam

  14. Serum Cardiac Markers • A. cTnI/Troponin I • 1.Becomes positive in 3-12 hours • 2. Peaks at 24 hours • 3. Remains elevated for 4-10 days • 4. Highly sensitive for early detection of myocardial injury • 5. Can be used to help decide whether it is safe to discharge patients who present to the emergency room with acute chest pain

  15. Cont’d • 6. Patients without ST segment elevations during pain and 2 negative troponin I determinations (one at least 6 hours after the onset of symptoms) have a low risk of death or fatal acute MI (.3%) during the next 30 days.

  16. Cont’d • B.CKMB subforms, • 1. CKMB1 (plasma) and CKMB2 (tissue)-myocardial necrosis can be detected earlier with subform analysis then with traditional CKMB measurement. • 2.Within 6 hours CKMB2 greater than 1.0 U/L with a ratio of CKMB2/CKMB1 greater than 1.5 is more sensitive and specific than CKMB for diagnosis of MI

  17. Cont’d • 3. If a patient presents more than 24 hours after a presumed MI, and the CK isoenzymes are inconclusive, troponin I is now preferred over LDH.

  18. Early Assessment of Infarct Size • A. Currently two dimensional echocardiography is the technique used most frequently in the hospital course to evaluate acute MI infarction size. • B. Echo reveals • 1. Extent and location of ventricular wall abnormalities • 2. Provides an assessment of overall ventricular function • 3. Demonstrates left ventricular thrombus • 4. Color flow doppler provides information about the extent of valvular disease and mechanical complications of acute MI.

  19. Approach to the patient with Acute MI • A. History I. Aspirin • B. Physical J. O2 • C. EKG K. Thrombolytic Therapy • D. Enzymes L. Heparin • E. Chest X-Ray M. Angiography • F. Nitrates N. PTCA with stenting • G. Beta-Blockers O. CABG • H. Morphine P. GPIIB/IIIA antagonists

  20. Acute Reperfusion Therapy • A. Rapid reperfusion of the infarct related artery with IV thrombolytic therapy or primary PTCA is the main treatment strategy for acute MI. The main goal is to improve survival and outcome(decrease incidence of CHF). The benefit of reperfusion therapy are time dependent, the sooner the blood flow is restored to the ischemic zone, the greater the advantage in terms of survival and functional recovery.

  21. Cont’d • B. Risk of hemorrhage • 1. Age greater than 65 • 2. Weight less than 70 kg. • 3. Female • 4. Hypertension Although patients greater than 75 years have a greater risk of hemorrhage and stroke with thrombolytic therapy, they have a net benefit in overall outcome because of a significant mortality reduction with thrombolytic therapy.

  22. Thrombolytic therapy with in the 1st 6hr of a coronary event

  23. After the 1st 10hrs the benefits mortality benefits decrease

  24. Pt presents to ED s/p chest heaviness X-3hrs

  25. 30min post arrival terminal inverted T waves are noted septally

  26. 1hr post arrival the patient develops ST segment elevation in the anteroseptal walls

  27. The lack of ST segment elevation decrease the mortality of a coronary event

  28. Those with a new onset LBBB has the worst Px

  29. Management Protocol

  30. No one thrombolytic has been shown to be superior, they differ really only by the Bolus and infusion rates…as well as price

  31. The most important factor in tx with thrombolytics is time

  32. GUSTO shows that higher the TIMI grade for flow rate, the lower the mortality

  33. Those patients Tx with frontloaded t-Pa as compared to streptokinase had achieved TIMI grade 3 54% of the time as compared to 33%

  34. Heparin – yes or no?

  35. Gusto I

  36. Pharmacokinetics • ASA • GP IIb IIIa • Ticlopidine • Anti-Thrombins • Dipyridomol • Epoprostenol