Rosen & Barkin's 5-Minute Emergency Medicine Consult (33 page)

• Patients with an AMI require hospital admission.
  
• If the diagnosis is unclear, admission to the hospital or an ED observation unit may be useful for serial cardiac enzymes, ECGs, and exercise stress testing and/or cardiac catheterization if needed.
  

No patient with an AMI should be discharged from the ED.

• If PCI is unavailable at the treating institution, particularly if the patient is in cardiogenic shock, he should be transported to another hospital if PCI can be initiated within 120 min of 1st medical contact.
  
• Patients with failed reperfusion should be transported urgently to a PCI-capable facility
  
• Patients undergoing reperfusion therapy may benefit from transfer to a PCI-capable facility within 3--24 hr as part of an invasive strategy
  

• Goal of thrombolytic therapy is a 30 min door to needle time if PCI not possible.
  
• New or presumably new LBBB at presentation occurs infrequently, and should not be considered diagnostic of AMI in isolation
  

• Filippo C, Giovanna L. Pathogenesis of acute coronary syndromes.
  J Am Coll Cardiol.
  2013;61:1–11.
  
• Hartman SM, Barros AJ, Brady WJ. The use of a 4-step algorithm in the electrocardiographic diagnosis of ST-segment elevation myocardial infarction by novice interpreters.
  Am J Emerg Med
  . 2012;30:1282–1295.
  
• Mehta N, Huang HD, Bandeali S, et al. Prevalence of acute myocardial infarction in patients with presumably new left bundle-branch block.
  J Electrocardiol
  . 2012;45:361–367.
  
• O’Gara PT,Kushner FG, AscheimDD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction AReport of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.
  Circulation
  .2013;127:e362–e425.
  
• Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule.
  Ann Emerg Med
  . 2012;60:766–776.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Cardiac Testing
  
• Reperfusion Therapy
  
• Unstable Angina
  

CODES

• 410.90 Acute myocardial infarction, unspecified site, episode of care unspecified
  
• 410.91 Acute myocardial infarction of unspecified site, initial episode of care
  
• 410.92 Acute myocardial infarction of unspecified site, subsequent episode of care
  

BASICS

• Non–ST-elevation myocardial infarction (NSTEMI) is a part of a clinical syndrome that also includes unstable angina and ST-elevation MI (STEMI).
  
• Caused by subtotal occlusion of coronary blood flow:
  
  • Often indicates an incomplete ischemic event
    
• Coronary plaque disruption:
  
  • Endothelial disruption exposes subendothelial collagen and other platelet-adhering ligands, von Willebrand factor (vWF), and fibronectin.
    
  • Release of tissue factors activates factor VII and extrinsic pathway.
    
• Thrombus generation:
  
  • Platelet adhesion via glycoprotein (GP) Ia/IIa to collagen; GP Ib to vWF:
    
    • Platelet activation: Release of ADP, thromboxane A
      ₂
      , and serotonin alters the platelet GP IIb/IIIa receptor; also causes local vasoconstriction
      
    • Platelet aggregation: GP IIb/IIIa receptor binds fibrinogen, cross-links platelets, forming local platelet plug
      
  • Platelet stabilization: Thrombin converts fibrinogen to fibrin, provides fibrin mesh, stabilizes platelet aggregate
    
• Microembolization to downstream coronary arterioles may occur
  

• Coronary thrombosis
  
• Coronary vasospasm, idiopathic or cocaine induced
  
• In situ thrombosis/hypercoagulable states
  
• Embolic event (e.g., endocarditis, paradoxical emboli through PFO)
  
• Arteritis
  

DIAGNOSIS

• Pain:
  
  • Pressure or tightness or heaviness
    
  • Substernal, epigastric
    
  • +/– radiation to arm, jaw, back
    
  • More likely nonpositional, nonpleuritic, nonreproducible on palpation
    
• Nausea, vomiting
  
• Diaphoresis
  
• Cough
  
• Dyspnea
  
• Anxiety
  
• Light-headedness
  
• Syncope
  
• Recent cocaine or amphetamine use
  
• Family history of coronary disease
  
• Atypical presentations common, especially in women, diabetics, and the elderly
  

Geriatric patients may present with atypical symptoms or silent ischemia.

• Pallor or diaphoresis
  
• Hypertension or hypotension
  
• Arrhythmias
  
• S4 gallop
  
• Physical exam is often normal
  

ECG, cardiac biomarkers, CXR

• Cardiac markers:
  
  • Troponins: Specific indicators of myocardial infarction, rises within 3–6 hr after MI, peaks at 9–10 days
    
  • Creatine kinase (CK): Rises within 4–8 hr, peaks at 18–24 hr, subsiding at 3–4 days; isoenzyme CK-MB more specific for cardiac origin
    
  • Myoglobin: Rises within 2–6 hr, returns to baseline within 24 hr, highly sensitive but very nonspecific
    
  • LDH: Rises within 24 hr, peaks at 3–6 days, returns to baseline at 8–12 days
    
• CBC
  
• Serum electrolytes including magnesium
  
• PT/PTT/INR for patients on warfarin
  
• NT-proBNP: Higher levels correlate with increased mortality in NSTEMI patients.
  

• ECG:
  
  • ST-segment depression or transient elevation indicates increased risk.
    
  • T-wave inversion in regional patterns does not increase risk but helps differentiate cardiac pain from noncardiac pain.
    
  • Deep (>2 mm) precordial T-wave inversion suggests cardiac ischemia.
    
• CXR:
  
  • To assess heart size, pulmonary edema/congestion or identify other causes of chest pain
    
• ECHO (generally not part of ED evaluation):
  
  • To identify wall motion abnormalities and assess ventricular function
    
• Radionuclide studies (if conservative management; generally not part of ED evaluation):
  
  • Sestamibi scan: Identify viable myocardium
    
  • Technetium 99: Identify recently infarcted myocardium
    

Coronary angiography (+/− PCI), typically as an inpatient, depending on patient’s risk profile and comorbidities

• STEMI
  
• Pulmonary embolus
  
• Aortic dissection
  
• Acute pericarditis/myocarditis
  
• Pneumothorax
  
• Pancreatitis
  
• Pneumonia
  
• Esophageal spasm/gastroesophageal reflux
  
• Esophageal rupture
  
• Musculoskeletal pain/costochondritis
  

TREATMENT

• IV access
  
• Oxygen administration
  
• 12-lead EKG, cardiac monitoring, and treatment of arrhythmias
  
• Aspirin, analgesia, anxiolytics
  

• Oxygen administration
  
• IV access
  
• 12-lead EKG, cardiac monitoring, and treatment of arrhythmias
  

• Anti-ischemic therapy to reduce demand and increase supply of oxygen to myocardium:
  
  • β-blockers: IV only if hypertensive with ongoing pain, else use orally within 24 hr; contraindicated in heart failure
    
  • Nitrates: Contraindicated with critical AS, suspicion of RV infarct or recent use of phosphodiesterase inhibitors (e.g., sildenafil)
    
  • Oxygen
    
  • Morphine sulfate
    
  • Calcium-channel blockers (nondihydropyridines—e.g., diltiazem, verapamil) may be used in patients with ongoing ischemia and contraindications to β
    -
    blockade. Contraindicated in heart failure
    
• Dual antiplatelet therapy to decrease platelet aggregation:
  
  • Aspirin: Only withhold if prior anaphylaxis
    
  • ADP Inhibitor: Clopidogrel (substitute for ASA if hypersensitivity), ticagrelor or prasugrel (if low bleeding risk, CABG unlikely, no history of CVA, age <75 yr)
    
• GP IIb/IIIa inhibitors (eptifibatide, tirofiban):
  
  • Only if ongoing ischemia, positive cardiac markers and PCI planned; can defer to inpatient administration
    
  • May omit if loading dose of clopidgrel administered at least 6 hr prior to PCI or bivalirudin used for anticoagulation
    
• Anticoagulation therapy to prevent thrombus propagation:
  
  • Unfractionated heparin or enoxaparin are 1st-line therapies.
    
  • Fondaparinux (factor Xa inhibitor) is a reasonable alternative, especially for medically managed patients; may have reduced bleeding risk.
    
  • Reserve bivalirudin (direct thrombin inhibitor) for patients with known heparin-induced thrombocytopenia
    
• Anxiolytics to suppress sympathomimetic release