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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Gnawing Discomfort

An 82 year-old male with history of hypertension presents to the emergency department in the early morning for insomnia. He reports being awoken approximately 6 hours prior to arrival by a 2/10 "squeezing" pressure in his right chest that came on insidiously. The pressure has been constant since onset, is non-radiating, and associated with shortness of breath. The patient denies having any pain and describes his symptoms as rather a "gnawing discomfort." He reports feeling well the night before and denies having symptoms like this in the past. He denies any personal or family history of heart or lung disease. On review of systems he denies having nausea, vomiting, cough, fever, or chills. 

Vital signs T 37.5 | P 102| 146/73 | 20 | 100% on RA
On exam the patient is an elderly male in minimal distress sitting upright in bed. 
Heart sounds are rapid and regular with no murmurs or gallops.
Breath sounds are clear bilaterally.

An electrocardiogram is obtained and shown below:

What is the diagnosis?

How would you manage this patient? 

Please leave a comment below and share your thoughts. 

The diagnosis for this case will be posted in approximately 1 week.