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Myocardial Infarction Chapter 18

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Myocardial Infarction Chapter 18 Acute Myocardial Infarction (AMI) AKA ST segment elevation myocardial infarction (STEMI) Occlusion of coronary artery causes ... – PowerPoint PPT presentation

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Title: Myocardial Infarction Chapter 18


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 80s, 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 (gt120 BPM) suggest large area of
    damage. Fourth heart sound (S 4 ) may be heard

9
Diagnosis
  • In addition to HP, 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 dont 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 - gt40 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 -gt plasmin -gt fibrinolytic
    (acts on fibrin clot)
  • Table 18-3
  • problems- doesnt 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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