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    Subjects/Physiology/ECG — Waves and Intervals
    ECG — Waves and Intervals
    medium
    heart-pulse Physiology

    A 52-year-old man from Delhi presents to the emergency department with acute onset chest pain radiating to the left arm for 2 hours. He is diaphoretic and anxious. Vital signs: BP 128/82 mmHg, HR 102/min, RR 18/min. His ECG shows ST-segment elevation in leads II, III, and aVF with reciprocal ST depression in leads I and aVL. The PR interval measures 0.16 seconds, QRS duration 0.08 seconds, and QT interval 0.38 seconds. What is the primary abnormality indicated by the ST-segment changes?

    A. Acute anterior wall myocardial infarction due to left anterior descending artery occlusion
    B. Acute inferior wall myocardial infarction due to right coronary artery occlusion
    C. Acute left ventricular hypertrophy with secondary ST changes
    Acute pericarditis with diffuse ST-segment elevation
    D.

    Explanation

    Clinical Presentation and ECG Interpretation

    Key Point
    ST-segment elevation in the inferior leads (II, III, aVF) with reciprocal ST depression in the lateral leads (I, aVL) is pathognomonic for acute inferior wall myocardial infarction (IWMI).
    Anatomical Localization

    The inferior wall of the left ventricle is primarily supplied by the right coronary artery (RCA) in approximately 80% of the population. The ECG pattern of inferior STEMI is:

    Table
    Lead GroupFindingInterpretation
    II, III, aVFST elevationInferior wall infarction
    I, aVLST depressionReciprocal changes
    V1–V3Normal or depressionExcludes anterior STEMI
    Normal ECG Intervals in This Patient
    High-YieldNEET PG
    The PR interval (0.16 s), QRS duration (0.08 s), and QT interval (0.38 s) are all within normal limits:
    • PR interval: 0.12–0.20 seconds ✓
    • QRS duration: 0.06–0.10 seconds ✓
    • QT interval: corrected QT (QTc) = 0.38 s (normal for HR ~102) ✓

    These normal intervals rule out conduction abnormalities or prolongation that might suggest alternative diagnoses.

    Pathophysiology of STEMI
    1. 1.
      Acute coronary occlusion → transmural ischemia
    2. 2.
      Loss of repolarization voltage in infarcted zone
    3. 3.
      Current of injury flows from viable to infarcted tissue
    4. 4.
      Epicardial leads over infarct zone → ST elevation
    5. 5.
      Reciprocal leads → ST depression (opposite vector)
    Clinical Pearl
    Inferior STEMI carries a lower in-hospital mortality (3–5%) compared to anterior STEMI (5–10%), but right ventricular involvement (present in ~30% of inferior STEMI) can cause hemodynamic collapse if not recognized early.
    Management Implications

    Mnemonic: MONA — Morphine, Oxygen (if SpO₂ <90%), Nitrates, Aspirin (for STEMI management)

    This patient requires:

    • Immediate 12-lead ECG confirmation ✓ (already done)
    • Troponin and other cardiac biomarkers
    • Primary percutaneous coronary intervention (PCI) within 90 minutes (door-to-balloon time)
    • Dual antiplatelet therapy (aspirin + P2Y₁₂ inhibitor)
    • Beta-blocker and ACE inhibitor (post-reperfusion)
    Warning
    Do NOT delay reperfusion waiting for biomarker results; ST-elevation STEMI is a clinical diagnosis.

    Loading illustration…ECG — Waves and Intervals diagram

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