Myocardial Infarction

See also Ischemic Chest Pain Algorithm (ACLS)
See also Post-Acute Care Management (ACLS)
See also Treatment by Group or Facility (ACLS)

Acute Treatment

Background

1. Myocardial necrosis from O2 supply/ demand mismatch
2. Epidemiology
   • > 1million MI cases in US/yr; 8million CP ED visits/yr
   • 75% of pts have severe 1 vessel Dz; up to 66% w/3 vessel Dz
3. Morbidity/ mortality
   • 30% fatality rate; 50% of deaths occur in first hr secondary to arrhythmias
     • 5-10% mortality in first yr
   • Survivors: 6% reinfarct w/in 1yr, 10x risk HF, 4 x risk sudden death
   • Higher mortality w/elderly (>65 yo), younger women

Pathophysiology

1. Etiology
   • Rupture/ fissure of atherosclerotic plaques in coronary arteries most common cause
     • Exposed subendothelium leads to plt activation, thrombin formation & release of growth factors
     • Thrombus occludes blood flow
     • Majority of occlusions occur in vessels with <50% stenosis
   • Reduced blood flow decreases contractile funct; necrosis if prolonged
     • Necrosis depends on extent of collateral flow, degree of stenosis, myocyte metabolism
     • LV funct/CO decr, LVESV incr
       • Wall thins, infarct expands, & ventricle dilates increasing wall stress & isch
     • RAAS activation, fibrosis, & remodeling as compensatory mechanism
     • Incr catecholamines cause Sx, arrhythmias, & incr O2 demand
   • ECG changes with full thickness (transmural) or subendocardial necrosis
     • Q waves (75%), ST elev (25% w/o Q waves)
     • More prolonged, severe plaque rupture & less extensive necrosis: NSTEMI
       • Positive cardiac markers for necrosis vs USA
       • May have Q waves
   • See also Acute Coronary Syndrome
2. Etiologies other than plaque rupture (6% of MI pts)
   • Coronary artery spasm w/fixed stenosis
   • Arteritis, trauma, amyloidosis, intimal hyperplasia, viral illness
   • Homocystinuria, aortic dissection, embolic, in situ thrombosis
   • Congenital coronary anomalies, CO poisoning, hypoxemia
   • Cocaine, prolonged hypotension, thyrotoxicosis
3. Risk factors
   • CAD, USA, AS, NTG w/d, trauma
   • Heavy exertion, drugs
4. High risk features in ACS pts (add IIb/IIIa, PCI)
   • Elev TnT/CKMB
   • Elev CRP
   • Age >65yo
   • ST-T changes
   • TIMI >4
   • Refractory Sx & ECG changes despite Tx, DM

Diagnosis

1. Symptoms
   • Classic: SSCP w/radiation to neck, jaw, & left arm
     • Pain variable in intensity, usually lasts >30 min
     • Described as crushing, squeezing, stabbing, or burning
     • Pain represents ischemia, not infarct
       • Insufficient predictive value
     • Levine's sign:
       • Clenching of fist over chest to describe pain of MI
   • Diaphoresis, N/V, palpitations, dyspnea, syncope, impending sense of doom
   • Atypical (women, elderly): Vague discomfort, abd pain
2. Physical exam
   • Cold, clammy skin; fever w/severe infarct
   • Variable HR, BP; elevated RR
   • Signs of CHF if LV failure
   • New SEM (papillary muscle rupture)
   • R/O other causes of CP
3. Diagnostic testing
   • ECG
     • ST elev, T wave inversion, ST dep w/abnl R waves (only 50% w/ST elev or Q waves on presentation)
     • Any new LBBB
     • Q waves >0.04 s other than aVR/V1
     • W/LBBB: Concordant deviation of ST w/maj QRS vector >1mm
     • Discordant deviation >5 mm
     • Useful for Localization of infarct
     • Fairly accurate test in Dx of MI
   • General Labs
     • CBC: r/o anemia, low plts, normally see leukocytosis
     • Lytes, BUN/Cr, Ca, Mg, phos: r/o abnormal renal funct
     • Coags: decr with large infarct; guide Tx
     • BNP: elev levels correlate w/worse prog
     • CRP >3 mg/L: High risk group
   • Cardiac Biomarkers: monitor trends q 8-12hr
     • Troponin (TOC); diagnostic & predictive value
       • Rise: 3-12 hr; peak: 12 hr-2d; nl: 5-14 d
       • May be elev in renal Dz, end stage HF, PE, sepsis
       • Useful in late Dx of MI; 72hr TnT may correlate w/infarct size
     • CKMB
       • Rise: 3-12 hr; peak: 24 hr; nl: 48-72 hr
       • MB/CK >2.5 indicates myocardial source
       • Helps w/timing if troponins elev
     • Myoglobin
       • Rise: 1-4 hr; peak: 6-7 hr; nl: 24 hr
       • Sens test in first 6 hr (50-75%); lacks cardiac spec
   • Diagnostic imaging
     • CXR: r/o causes of CP, aortic dissection (no anticoagulants)
     • MRI: localization, estimate of severity, early recognition
       • Currently limited practical application
     • Cardiac ECHO: aids Dx if other tests nondiagnostic
       • Assesses: wall motion abnl, EF, valvular d/o, septal rupture
     • Cath: Dx & Tx
       • Immediate use in: recurrent CP, sig isch, shock, intractable angina, severe CHF

Differential Diagnosis

1. See DDx of CP
   • Aortic dissection, aortic aneurysm, tamponade
   • PE, pericarditis, pneumothorax
   • Angina, USA, mediastinitis, myocarditis

Acute Treatment

Evidence-Based Inquiry

1. How accurate is the use of ECGs in the diagnosis of myocardial infarct?
2. What elements of a patient's chest pain history are the best predictors for ruling in or out acute myocardial infarction?