Thursday, April 23, 2015

Diagnosis: Acute Anterior STEMI

The patient's ECG revealed grossly elevated ST segments in anterior leads including "tombstone T-waves" consistent with diagnosis of acute anterior ST-segment elevation myocardial infarction. The Cath Lab was immediately activated by the ED and the patient started on a heparin drip after negative FOBT. 

In the Cath Lab the patient was found to have 100% stenosis of the proximal left anterior descending (LAD) artery, 80% stenosis of the mid LAD artery, and 70% stenosis of the proximal right coronary artery (RCA). A stent was placed in the LAD reducing the occlusion to 0% stenosis. The patent's left ventricular ejection fracture post-procedure was 35-40%. 

The patient expired 2 days later in the Cardiac Intensive Care Unit secondary to respiratory complications.

In the ECG below, note that there are ST-segment elevations in leads V1 through V6 and slight elevation in lead I suggesting septal (V1-V2), anterior (V3-V4) and lateral (V5-V6, I) wall involvement, as well as reciprocal changes in the inferior wall leads (II, III, aVF) 




ED Management of Acute STEMI

Why we care? 
  • Acute coronary syndromes are a leading cause of death in adults in many developed countries 
Quick Pathophys Review
  • Coronary blood flow fails to meet myocardial O2 demand --> ischemia/infarction
  • Most coronary stenosis preceding an acute MI is <50% - the problem is acute plaque rupture
  • Acute plaque rupture --> platelet activation --> thrombus formation --> acute total occlusion --> exacerbated by subsequent vasospasm
  • Further damage due to reperfusion injury secondary to oxygen free radicals, calcium, and neutrophils
ED Management
  • Primary goal = early coronary patency and revascularization 
    • primary angioplasty vs fibrinolysis 
    • treatment within first 1-2 hours of event confers substantial benefit 
  • Management goals for ED provider: IV, O2, Monitor
    • early recognition (history, physical, ECG) 
    • early activation of hospital "STEMI system" and cardiology consult
    • early pharmacological therapy
  • Nitroglycerin (0.4 mg or 400 ug sublingual) 
    • reduce preload --> reduce myocardial O2 demand --> pain relief 
    • reduces afterload to lesser extent
    • thought to increase myocardial perfusion by increasing collateral coronary flow
    • mostly provides pain relief, no significant mortality benefit identified
    • CAUTION in preload-dependent states:
      • inferior wall MI
      • right ventricular infarction
      • sudden drop in preload may cause profound hypotension
  • Morphine (2-5 mg IV q5-30 min)
    • additional pain relief agent when symptoms refractory to nitroglycerin 
    • pain relief and anxiolysis reduce O2 consumption and myocardial work
    • some preload reduction as well
    • CAUTION in hypotensive patients as can further reduce BP
  • Aspirin (160-325 mg po)
    • large RCTs have demonstrated as much as a 25-50% reduction in mortality
    • irreversibly inhibits platelet cyclooxygenase --> block thromboxane A2 enzyme production (platelet aggregator) --> reduced thrombus formation
  • Heparin (80 units/kg bolus, 18 units/kg drip)
    • strong synergistic effect with aspirin in preventing death from acute MI 
    • activates antithrombin III --> inactivates Factors II and X --> prevent conversion of fibrinogen to fibrin --> inhibits clot propagation (no clot lysis) 
    • CAUTION in patients with any signs, symptoms or history of bleeding
      • always perform FOBT before administering 
  • Fibrinolytic therapy - tPA, Streptokinase 
    • activates intrinsic tissue plasminogen enzyme --> dissolves thrombus
    • ACC/AHA Level I Recommendation in acute MI
    • The Good
      • well-studied
      • improves coronary flow
      • limits infarct size
      • improves survival in acute MI
    • The Bad
      • numerous relative and absolute contraindications limit its use
      • high risk for bleeding complications including intracranial hemorrhage
  • Percutaneous coronary intervention (PCI)
    • mechanical clot disruption by endovascular instrumentation under fluoroscopy
    • increased number of eligible patients
    • lower risk for intracranial bleeding
    • significantly higher reperfusion rate 
    • earlier characterization of coronary anatomy to guide surgical intervention
    • risk stratification allowing early and safe hospital discharge 
Disposition = Cath Lab
  • studies suggest <90 minute door-to-ballon time necessary for optimal myocardial salvage
  • Time = Myocardium!


References: 

Kurz MC, Mattu A, Brady WJ, Rosen's Emergency Medicine Concepts and Clinical Practice, 8th Ed, 2014, Chapter 78: Acute Coronary Syndrome


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