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Myocardial Infarction Chapter 18

Myocardial Infarction Chapter 18. Acute Myocardial Infarction (AMI). AKA ST segment elevation myocardial infarction (STEMI) Occlusion of coronary artery causes myocardium to be ischemic and tissue death occurs. AMI continued. Until the ‘80’s, AMI was treated symptomatically

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Myocardial Infarction Chapter 18

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  1. Myocardial Infarction Chapter 18

  2. Acute Myocardial Infarction (AMI) • AKA ST segment elevation myocardial infarction (STEMI) • Occlusion of coronary artery causes myocardium to be ischemic and tissue death occurs

  3. AMI continued • Until the ‘80’s, AMI was treated symptomatically • pain control, arrhythmias resolved, bed rest, nitrates, B-blockers to minimize oxygen requirement of heart

  4. AMI continued • Angiographic studies showed that 87% had occluded coronary arteries that led to development of thrombolytics and PTCA (percutaneous transluminal coronary angioplasty ) which are now first line therapies.

  5. AMI continued • 1/2 million have AMI every year • 30% dead before hospital (v.fib) • if make it to hospital, 1 year death rate is greater than or equal to 15% • usually located in specific region (anterior, lateral, inferior,posterior) see Fig. 18-3. (anterior worse than inferior or lateral)

  6. AMI Continued • Can develop permanent ECG changes after MI (Q waves) • Q wave MI-STEMI • Now Q wave MI - Non-ST segment elevation (NSTEMI) or acute coronary syndrome (ACS)

  7. Clinical Presentation • Substernal chest pain or pressure, short of breath, diaphoresis, nausea and vomiting. • Can look like indigestion or other diseases may present like STEMI (table 18-1) • 20% of AMI are “silent” - elderly and diabetics, may present with hypotension or cerebrovascular symptoms rather than chest pain.

  8. Clinical Presentation continued • Physical exam - may have increased or decreased BP, tachycardia (>120 BPM) suggest large area of damage. Fourth heart sound (S 4 ) may be heard

  9. Diagnosis • In addition to H+P, ECG and enzymes help to diagnose • usually 2 of the 3 are needed to assign diagnosis of MI • ECG- St segment elevation, 12-lead helps to determine location of infarct • New Q wave, new bundle branch block, ST elevation are all consistent with/MI

  10. Diagnosis Continued • IF have chest pain without ST elevation or enzyme changes, then called Unstable Angina. • IF have chest pain without ST elevation but have enzyme changes then called AMI, NSTEMI • These pts have some limited blood flow with partial occlusion due to platelets and fibrinogen-Thrombolytics don’t help these pts.

  11. Cardiac Enzymes • Released when cardiac cell is injured • CK-MB - most specific of creatinine kinase (CK) enzymes for cardiac tissue • appears 3-6 hrs. after damage, PK 12-24 hrs • “false” elevations Table 18-2 • LDH - lactate dehydrogenase -24-48 hours after MI & pk in 3-6 days • false elevations-liver disease, hemolysis, leukemia, PE, etc. • Troponin - most sensitive, has replaced LDH

  12. Compilcations • Pump failure, arrhythmias, recurrent ischemia and reinfarction • H.F. common if MI affects 20-25% of left ventricle • cardiogenic shock and death - >40% of left ventricle

  13. Complications continued • Ventricular remodeling- results from decreased contractility and compensatory increase in left ventricle volume and pressure. • Arrhythmias - post infarction, heart is irritable and subject to ventricular arrhythmias.

  14. Drug Therapy (table 18-5) • Thrombolytics- opens occluded artery, Timi grade 3- (complete repurfusion), the earlier the better. Reduced mortality by 1/3, • binds to plasminogen -> plasmin -> fibrinolytic (acts on fibrin clot) • Table 18-3 • problems- doesn’t open 100% of occlusions, may not remain open, bleeding (need to select properly) • Table 18-4

  15. Drug Therapy continued • When fibrin clot disintegrates, paradoxical increase in local thrombin generation and increase platelet aggregability. • So need heparin, LMWH and ASA / GPIIBIIIA • B-blockers decrease morbidity and mortality • decrease myocardial oxygen requirements • limits damage and decreases complications • should be used in AMI unless CI

  16. Drug Therapy continued • Vasodilators - decrease myocardial oxygen demand by decreasing afterload and decreasing preload and can limit remodeling. • Also increase myocardium blood supply by coronary vasodilation

  17. Acute Myocardial Infarction (AMI) • AKA ST segment elevation myocardial infarction (STEMI)

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