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<aside> 🫀 Atypical features (i.e., no or minimal chest pain, nausea) of MI are more common in older people, individuals with diabetes, and women. Reinfarction can happen at any time following MI but the risk increases over time.

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Clinical Features

Classic presentation

• Acute retrosternal chest pain
• Typical: dull, squeezing pressure and/or tightness
• Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or epigastrium
• Precipitated by exertion or stress
• Symptom relief after administration of nitrates is not a diagnostic criterion for cardiac ischemia.
• The peak time of occurrence is usually in the morning.
• Dyspnea (especially with exertion)
• Pallor
• Nausea, vomiting
• Diaphoresis, anxiety
• Dizziness, lightheadedness, syncope
• Other findings
  • Tachycardia, arrhythmias
  • Symptoms of CHF (e.g., orthopnea, pulmonary edema) or cardiogenic shock (e.g., hypotension, tachycardia, cold extremities)
  • New heart murmur on auscultation (e.g., new S4)

Atypical presentations: more likely in elderly, diabetic individuals, and women

• Stabbing, sharp chest pain
• No or minimal chest pain
• ”Silent MI” without chest pain is more common in patients with diabetes, as a result of polyneuropathy.
• Autonomic symptoms (e.g., nausea, diaphoresis)
• More common in inferior wall infarction
• Epigastric pain
• Bradycardia
• Clinical triad in right ventricular infarction: hypotension, elevated jugular venous pressure, clear lung fields

• An atrial gallop (S4) results from atrial contraction against a stiff ventricle. It is frequently heard in the acute phase of an MI because of impaired relaxation of the ischemic left ventricle.
  • An S4 may also be heard in conditions that cause ventricular hypertrophy, such as hypertrophic cardiomyopathy, aortic stenosis, or hypertension.
  • Older patients can have an S4 as a normal finding because ventricular compliance decreases with age.
• A ventricular gallop (S3), on the other hand, is caused by a sudden deceleration of blood flow from the left atrium into the left ventricle during early diastole.
  • This finding can be normal in young adults (< 40 years) or pregnant women, but it is abnormal in older adults.
  • An S3 may be heard in dilated cardiomyopathy, congestive heart failure, or valvular diseases such as chronic mitral or aortic regurgitation. It is not a common finding in acute MI.

Blood Supply & Infarct Locations

<aside> ‼️ Make sure to know the blood supply!

• leads affected in STEMI:
  • anterior wall
    • anteroseptal → LAD→ V1-V2
    • anteroapical → distal LAD→ V3-V4
  • lateral wall
    • anterolateral → LAD or LCX → V5-V6
    • LCX → I, aVL, V5-6
  • inferior wall → PDA (from RCA 90%, 10% LCX — dominance) → II, III, aVF
  • ST elevations in aVR + diffuse depressions → massive MI (left main occlusion)
  • posterior MI → involves only PDA (isolated) → ST depressions in leads V1-V3 → diagnosed by posterior leads V7-V9 (not NSTEMI!)
  • isolated RV myocardial infarction (MI) can occur due to RCA occlusion in a patient with left-dominant circulation
• ECG leads & corresponding blood supply (anatomy)
• ECG Changes in NSTEMI & UA
• ECG Changes in STEMI
• STEMI Equivalents
• Practice ECGs </aside>

Pathological Tissue Changes in MI

Biochemical Changes in Ischemic Injury

<aside> 🫀 treatment: NSTEMI & UA

• MONA + BASH:
  • Mophine
  • Oxygen
  • Nitroglycerin
  • Aspirin
  • β blocker
  • ACE inhibitor
  • Statin
  • Heparin
  • Clopidogrel
• invasive therapy (high risk ACS):
  • non-emergent angioplasty → within 12-48hrs
  • MONA + heparin (UFH)
  • clopidogrel/ticagrelor → 1-9 months </aside>

<aside> 🫀 treatment: STEMI

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MI Complications

• Sudden cardiac death
• Papillary muscle rupture (day 2-7)
• Acute post-MI pericarditis (< 1 week post MI)
• Re-infarction