Orris

Explain me 10 common heart diseases with ECG changes and ECG images of those diseases

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STEMI ST elevation myocardial infarction ECG electrocardiogram

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atrial fibrillation ECG irregularly irregular no P waves

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ventricular tachycardia ECG wide complex tachycardia

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left bundle branch block LBBB ECG QRS morphology

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complete heart block third degree AV block ECG dissociation

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hypertrophic cardiomyopathy ECG left ventricular hypertrophy voltage criteria

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Wolff-Parkinson-White WPW ECG delta wave pre-excitation

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pericarditis ECG saddle-shaped ST elevation diffuse PR depression

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pulmonary embolism ECG S1Q3T3 right heart strain sinus tachycardia

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dilated cardiomyopathy ECG low voltage poor R wave progression sinus tachycardia

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The guide above covers all 10 diseases with dedicated ECG images sourced from peer-reviewed medical literature. Here's a quick recap of what was covered:
  1. STEMI — convex ST elevation, Q waves, reciprocal changes (two ECGs: anterior and inferolateral)
  2. NSTEMI/Unstable Angina — ST depression, T inversions, no Q waves
  3. Atrial Fibrillation — irregularly irregular rhythm, absent P waves, fibrillatory baseline
  4. Ventricular Tachycardia — wide QRS ≥120 ms, AV dissociation, fusion beats
  5. Complete (3rd Degree) AV Block — independent P waves and QRS, bradycardia
  6. LBBB — broad notched R waves laterally, QS in V1–V3, discordant ST-T changes
  7. WPW Syndrome — short PR, delta wave, pre-excitation pattern
  8. Acute Pericarditis — diffuse saddle-shaped ST elevation, PR depression, Spodick's sign
  9. Pulmonary Embolism — sinus tachycardia, S1Q3T3, right heart strain, T inversions V1–V4
  10. Hypertrophic Cardiomyopathy — LVH voltage, giant T-wave inversions (apical variant)
Let me know if you'd like deeper detail on any specific condition, treatment algorithms, or additional ECG variants.

Make printable pdf of above

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Running Command

ls /home/daytona/workspace/ 2>/dev/null || echo "workspace empty or missing"

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mkdir -p /home/daytona/workspace/heart-ecg-pdf && echo "done"

Writing File

~/heart-ecg-pdf/generate_pdf.py

#!/usr/bin/env python3
"""Generate a printable PDF: 10 Common Heart Diseases with ECG Changes & Images."""

import subprocess, sys

# Install weasyprint if not present
try:
    import weasyprint
except ImportError:
    subprocess.check_call([sys.executable, "-m", "pip", "install", "--user", "weasyprint"], stdout=subprocess.DEVNULL, stderr=subprocess.DEVNULL)
    import weasyprint

OUTPUT = "/home/daytona/workspace/heart-ecg-pdf/10_Heart_Diseases_ECG.pdf"

HTML = """<!DOCTYPE html>
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<!-- ══════════════════════════════════════════ COVER ══════════════════════════════════════════ -->
<div class="cover">
  <h1>10 Common Heart Diseases</h1>
  <div class="subtitle">ECG Changes &amp; Electrocardiographic Diagnosis</div>
  <div class="ecg-line"></div>
  <div class="toc-box">
    <h3>Contents</h3>
    <div class="toc-item"><span class="toc-num">1.</span><span>ST-Elevation Myocardial Infarction (STEMI)</span></div>
    <div class="toc-item"><span class="toc-num">2.</span><span>NSTEMI &amp; Unstable Angina</span></div>
    <div class="toc-item"><span class="toc-num">3.</span><span>Atrial Fibrillation (AF)</span></div>
    <div class="toc-item"><span class="toc-num">4.</span><span>Ventricular Tachycardia (VT)</span></div>
    <div class="toc-item"><span class="toc-num">5.</span><span>Complete (3rd Degree) AV Heart Block</span></div>
    <div class="toc-item"><span class="toc-num">6.</span><span>Left Bundle Branch Block (LBBB)</span></div>
    <div class="toc-item"><span class="toc-num">7.</span><span>Wolff-Parkinson-White (WPW) Syndrome</span></div>
    <div class="toc-item"><span class="toc-num">8.</span><span>Acute Pericarditis</span></div>
    <div class="toc-item"><span class="toc-num">9.</span><span>Pulmonary Embolism (PE)</span></div>
    <div class="toc-item"><span class="toc-num">10.</span><span>Hypertrophic Cardiomyopathy (HCM)</span></div>
    <div class="toc-item"><span class="toc-num">&#10003;</span><span>Quick Reference Summary Table</span></div>
  </div>
  <div class="footer-note">
    Sources: Harrison's Principles of Internal Medicine 22E (2025) · Braunwald's Heart Disease ·
    Tintinalli's Emergency Medicine · Goldman-Cecil Medicine · ECG images: PMC Clinical VQA
  </div>
</div>

<!-- ══════════════════════════════════════════ 1. STEMI ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 01</div>
    <div class="disease-title">ST-Elevation Myocardial Infarction (STEMI)</div>
    <div class="disease-subtitle">Acute transmural coronary occlusion with epicardial injury current</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> Complete occlusion of a coronary artery causes transmural ischemia. Severe ischemia lowers the resting membrane potential, creating a voltage gradient between normal and ischemic zones (current of injury). The ST vector shifts outward toward the epicardium, producing ST elevation in overlying leads and reciprocal depression in opposing leads.</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>ST elevation</td><td>Convex ("tombstone") ST elevation ≥1 mm in ≥2 contiguous leads</td></tr>
        <tr><td>Hyperacute T waves</td><td>Tall, broad, peaked T waves — earliest sign (minutes)</td></tr>
        <tr><td>Reciprocal ST depression</td><td>In leads electrically opposite the infarct zone</td></tr>
        <tr><td>Pathological Q waves</td><td>&gt;40 ms wide, &gt;25% of R-wave height — develop within hours, indicate necrosis</td></tr>
        <tr><td>T-wave inversions</td><td>Develop as infarct evolves (hours to days)</td></tr>
      </tbody>
    </table>

    <table>
      <thead><tr><th>Territory</th><th>Leads with ST elevation</th><th>Artery</th></tr></thead>
      <tbody>
        <tr><td>Anterior</td><td>V1–V4</td><td>LAD</td></tr>
        <tr><td>Inferior</td><td>II, III, aVF</td><td>RCA (or LCx)</td></tr>
        <tr><td>Lateral</td><td>I, aVL, V5–V6</td><td>LCx</td></tr>
        <tr><td>Posterior</td><td>Reciprocal ST↓ V1–V3 (mirror image)</td><td>RCA / LCx</td></tr>
        <tr><td>RV infarction</td><td>ST↑ V4R (right-sided leads)</td><td>Proximal RCA</td></tr>
      </tbody>
    </table>

    <div class="img-row">
      <div class="img-col">
        <div class="ecg-image-label">▶ ECG — Anterior STEMI (LAD Occlusion)</div>
        <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_646aa0cfb0d976b56d82780dedb4cd025e7f67b7aa7d1163a2f05a58a08c514e.jpg" alt="Anterior STEMI ECG"/>
        <div class="ecg-caption">Anterior STEMI: Convex "tombstoning" ST elevation in V2–V5, evolving QS waves in V2–V3 indicating necrosis. Classic LAD occlusion pattern.</div>
      </div>
      <div class="img-col">
        <div class="ecg-image-label">▶ ECG — Inferolateral STEMI</div>
        <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_3dee7a4a158b2ae0ff60150e6e2f63ffc7b5cab69ca1b45d2db4b86765c7720e.jpg" alt="Inferolateral STEMI ECG"/>
        <div class="ecg-caption">Inferolateral STEMI: ST elevation in II, III, aVF, V4–V6 with reciprocal ST depression in I, aVL, and V2–V3.</div>
      </div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 2. NSTEMI ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 02</div>
    <div class="disease-title">NSTEMI &amp; Unstable Angina</div>
    <div class="disease-subtitle">Subendocardial ischemia without complete coronary occlusion</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> Partial coronary occlusion or severe stenosis causes subendocardial ischemia. The ST vector shifts inward toward the subendocardium and ventricular cavity — producing ST depression in overlying leads and ST elevation in aVR. Unlike STEMI, the epicardium is relatively spared and Q waves do not form. Diagnosis depends on troponin elevation (NSTEMI) vs. normal troponin (unstable angina).</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>ST depression</td><td>Horizontal or downsloping ≥0.5 mm in ≥2 contiguous leads</td></tr>
        <tr><td>ST elevation in aVR</td><td>Indicates diffuse subendocardial ischemia or left main/proximal LAD disease</td></tr>
        <tr><td>T-wave inversions</td><td>Symmetric, deep — especially prominent in anterior leads</td></tr>
        <tr><td>Wellens' syndrome</td><td>Deep biphasic or inverted T waves in V2–V3 = critical LAD stenosis (high risk)</td></tr>
        <tr><td>No pathological Q waves</td><td>Key distinction from STEMI</td></tr>
        <tr><td>Normal ECG possible</td><td>In ~30% of NSTEMI; troponin elevation confirms diagnosis</td></tr>
      </tbody>
    </table>

    <div class="quote">
      "The diagnosis of NSTEMI depends on abnormal elevation of cardiac biomarkers but may include ECG changes not meeting criteria for STEMI."
      <cite>— Tintinalli's Emergency Medicine, A Comprehensive Study</cite>
    </div>

    <div class="patho" style="background:#fff0f0; border-color:#e94560;"><strong>⚠ Clinical Pearl:</strong> ST elevation ≥1 mm in aVR + diffuse ST depression in 8+ leads = left main or proximal LAD occlusion equivalent → urgent revascularization.</div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 3. AF ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 03</div>
    <div class="disease-title">Atrial Fibrillation (AF)</div>
    <div class="disease-subtitle">Disorganized atrial electrical chaos with irregular ventricular response</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> Multiple re-entrant wavelets or focal triggers (often pulmonary vein foci) create chaotic atrial depolarization at 300–600 impulses/min. The AV node conducts impulses irregularly, producing an irregularly irregular ventricular response. Absent coordinated atrial systole leads to blood stasis and thromboembolism risk.</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>Absent P waves</td><td>Replaced by chaotic fibrillatory (f) waves, best seen in V1 and II</td></tr>
        <tr><td>Irregularly irregular rhythm</td><td>The hallmark — no two R-R intervals are the same</td></tr>
        <tr><td>f-wave rate</td><td>300–600/min; variable in amplitude and morphology</td></tr>
        <tr><td>Narrow QRS</td><td>Usual; widened if aberrant conduction (BBB) or accessory pathway present</td></tr>
        <tr><td>Ventricular rate</td><td>Variable: 100–160 bpm (uncontrolled); 60–100 (rate-controlled)</td></tr>
      </tbody>
    </table>

    <div class="quote">
      "AF is characterized electrocardiographically by low-amplitude baseline oscillations (fibrillatory or f waves from the fibrillating atria) and an irregularly irregular ventricular rhythm. The f waves, 300 to 600 beats/min, are variable in amplitude and morphology."
      <cite>— Braunwald's Heart Disease, A Textbook of Cardiovascular Medicine</cite>
    </div>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Atrial Fibrillation</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_a8e7a35a18d282cc6de8c169a0213a6712f9fe9e4a7253f7828e22c867033097.jpg" alt="Atrial Fibrillation ECG"/>
      <div class="ecg-caption">AF: Absent P waves replaced by fine fibrillatory (f) waves visible along the baseline (best in V1). Irregularly irregular QRS complexes with narrow morphology indicating normal ventricular conduction.</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 4. VT ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 04</div>
    <div class="disease-title">Ventricular Tachycardia (VT)</div>
    <div class="disease-subtitle">Rapid arrhythmia originating in ventricular myocardium below the Bundle of His</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> VT arises from re-entry circuits or triggered activity within the ventricular myocardium — commonly on a substrate of scar tissue (post-MI), dilated cardiomyopathy, or channelopathies. Because depolarization bypasses the His-Purkinje system, conduction is slow, producing wide QRS complexes. The atria continue under sinus node control, creating AV dissociation.</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>Wide QRS complexes</td><td>≥120 ms (usually ≥140 ms); bizarre morphology</td></tr>
        <tr><td>Rapid rate</td><td>100–250 bpm, typically regular</td></tr>
        <tr><td>AV dissociation</td><td>P waves march independently at sinus rate — pathognomonic for VT</td></tr>
        <tr><td>Fusion beats</td><td>Hybrid P-wave conducting simultaneously with VT complex — diagnostic</td></tr>
        <tr><td>Capture beats</td><td>Narrow QRS within the wide complex rhythm — diagnostic of VT</td></tr>
        <tr><td>Concordance</td><td>All precordial leads positive (positive concordance) or negative — favors VT</td></tr>
        <tr><td>Northwest axis</td><td>QRS axis in "no man's land" (−90° to ±180°) strongly suggests VT</td></tr>
      </tbody>
    </table>

    <div class="quote">
      "The presence of fusion beats or AV dissociation during a wide-QRS complex tachycardia establishes the diagnosis of ventricular tachycardia."
      <cite>— Goldman-Cecil Medicine, International Edition</cite>
    </div>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Monomorphic Ventricular Tachycardia</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_d15a92de4e89b46f273b22d254d1e30fcd6a190c6d581b193e6dd338338c6bb6.jpg" alt="Ventricular Tachycardia ECG"/>
      <div class="ecg-caption">Monomorphic VT: Wide, high-amplitude QRS complexes at ~170 bpm with positive concordance across precordial leads. No visible P waves. Superior axis. Associated with structural heart disease (dilated cardiomyopathy / post-MI scar).</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 5. Complete Heart Block ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 05</div>
    <div class="disease-title">Complete (Third-Degree) AV Heart Block</div>
    <div class="disease-subtitle">Total failure of AV conduction — atria and ventricles beat independently</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> Complete failure of conduction through the AV node or His-Purkinje system. Atria are driven by the sinus node; ventricles rely on an escape pacemaker — junctional (40–60 bpm, narrow QRS) or ventricular (20–40 bpm, wide QRS). Causes include ischemia (inferior MI → nodal block; anterior MI → infra-Hisian), degenerative fibrosis, infiltrative disease, and drugs.</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>AV dissociation</td><td>P waves and QRS complexes completely independent; no fixed PR interval</td></tr>
        <tr><td>Regular P-P intervals</td><td>Atrial rate 60–100 bpm (sinus)</td></tr>
        <tr><td>Regular R-R intervals</td><td>Slow escape rhythm at its own constant rate</td></tr>
        <tr><td>Bradycardia</td><td>Ventricular rate 20–45 bpm (ventricular escape) or 40–60 bpm (junctional)</td></tr>
        <tr><td>QRS morphology</td><td>Narrow (junctional escape) or wide/bizarre (ventricular escape)</td></tr>
        <tr><td>P waves "march through"</td><td>P waves visible on T waves, within QRS complexes — all ignored by ventricle</td></tr>
      </tbody>
    </table>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Complete (3rd Degree) AV Block</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_8406f3f9d6a209bfd199f5a59f790f58cd2a726f5674a8e7fbed222b0a72b837.jpg" alt="Complete Heart Block ECG"/>
      <div class="ecg-caption">Third-degree heart block: P waves march at an independent atrial rate (faster). Wide, slow ventricular escape complexes occur at their own regular rate with no relationship to P waves. Complete AV dissociation. Requires urgent pacing.</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 6. LBBB ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 06</div>
    <div class="disease-title">Left Bundle Branch Block (LBBB)</div>
    <div class="disease-subtitle">Failure of left bundle conduction — abnormal ventricular depolarization sequence</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> Conduction block in the left bundle branch forces the left ventricle to depolarize slowly via cell-to-cell spread from the right ventricle. This widening and distortion of the QRS is accompanied by secondary repolarization abnormalities (discordant ST-T). New LBBB in the context of chest pain is treated as STEMI equivalent (Sgarbossa criteria apply).</div>

    <div class="ecg-table-title">ECG Changes (all 3 criteria must be present for complete LBBB)</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>Wide QRS</td><td>≥120 ms (complete LBBB)</td></tr>
        <tr><td>Broad monophasic R wave</td><td>In I, aVL, V5–V6 — with slurring or notching ("M" or "plateau" pattern)</td></tr>
        <tr><td>Deep QS pattern in V1–V3</td><td>rS or QS morphology in right precordial leads</td></tr>
        <tr><td>No septal Q waves</td><td>Absent in I and V5–V6 (reversed septal activation)</td></tr>
        <tr><td>Discordant ST-T changes</td><td>ST and T wave opposite to dominant QRS deflection (secondary repolarization)</td></tr>
        <tr><td>Left axis deviation</td><td>QRS axis leftward, common</td></tr>
      </tbody>
    </table>

    <div class="quote">
      "With bundle branch blocks, the T wave is typically opposite in polarity to the last deflection of the QRS. This discordance is caused by the altered sequence of repolarization."
      <cite>— Harrison's Principles of Internal Medicine 22E (2025)</cite>
    </div>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Left Bundle Branch Block</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_40539068af948d455bdd99bbaec214df9ffebcbb3690a9d5892ee0432bfb005a.jpg" alt="LBBB ECG"/>
      <div class="ecg-caption">LBBB: QRS duration 158 ms, broad "M-shaped" notched R waves in I, aVL, V5–V6, deep S waves in V1–V3, left axis deviation, and discordant ST-T changes. QTc 533 ms.</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 7. WPW ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 07</div>
    <div class="disease-title">Wolff-Parkinson-White (WPW) Syndrome</div>
    <div class="disease-subtitle">Ventricular pre-excitation via accessory pathway (Bundle of Kent)</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> An accessory muscular pathway (Bundle of Kent) connects atria to ventricles, bypassing the AV node's delay. Ventricular pre-excitation creates the delta wave. During tachyarrhythmias, impulses may use the accessory pathway antegradely (producing wide-complex tachycardia) or as part of an AVRT circuit. AF with rapid accessory pathway conduction can cause ventricular fibrillation.</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>Short PR interval</td><td>&lt;120 ms — AV node delay is bypassed</td></tr>
        <tr><td>Delta wave</td><td>Slurred upstroke at the beginning of the QRS complex</td></tr>
        <tr><td>Wide QRS</td><td>Total QRS &gt;120 ms due to fusion of pre-excitation + normal conduction</td></tr>
        <tr><td>Discordant ST-T changes</td><td>Secondary repolarization abnormalities opposite to delta wave polarity</td></tr>
        <tr><td>Pseudo-infarct pattern</td><td>Negative delta waves mimic pathological Q waves (inferior or lateral leads)</td></tr>
        <tr><td>Pathway localization</td><td>Delta wave polarity across leads localizes the accessory pathway location</td></tr>
      </tbody>
    </table>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Wolff-Parkinson-White Syndrome</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_53c53d9ed7100de15d6d512e52e2a269252a79c85c12a60e54a4ce2fc4d574ec.jpg" alt="WPW ECG"/>
      <div class="ecg-caption">WPW: Short PR interval (&lt;120 ms), delta waves at the onset of QRS (red arrows in II and III), widened QRS complexes. Anteroseptal accessory pathway suggested by the prominent R waves in V1. Classic pre-excitation pattern.</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 8. PERICARDITIS ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 08</div>
    <div class="disease-title">Acute Pericarditis</div>
    <div class="disease-subtitle">Pericardial inflammation causing diffuse subepicardial injury</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> Pericardial inflammation extends to the superficial myocardium (epicardium), causing diffuse subepicardial injury. Unlike MI, the injury is global — affecting all coronary territories simultaneously. Atrial inflammation causes PR segment depression. The 4-stage ECG evolution mirrors resolution of the inflammatory process.</div>

    <div class="ecg-table-title">ECG Changes — Four Stages</div>
    <table>
      <thead><tr><th>Stage</th><th>ECG Features</th><th>Timing</th></tr></thead>
      <tbody>
        <tr><td><span class="stage-label">Stage 1</span></td><td>Diffuse concave (saddle-shaped) ST elevation in nearly all leads except aVR &amp; V1; PR depression in II, V4–V6; PR elevation in aVR</td><td>Days 1–2</td></tr>
        <tr><td><span class="stage-label">Stage 2</span></td><td>ST normalizes; T waves flatten</td><td>Days 3–7</td></tr>
        <tr><td><span class="stage-label">Stage 3</span></td><td>T-wave inversions develop diffusely</td><td>Weeks 1–3</td></tr>
        <tr><td><span class="stage-label">Stage 4</span></td><td>ECG normalizes completely</td><td>Weeks–months</td></tr>
      </tbody>
    </table>

    <table>
      <thead><tr><th>Key Distinguishing Feature vs. STEMI</th><th>Pericarditis</th><th>STEMI</th></tr></thead>
      <tbody>
        <tr><td>ST distribution</td><td>Diffuse (all territories)</td><td>Regional (one territory)</td></tr>
        <tr><td>ST morphology</td><td>Concave upward (saddle)</td><td>Convex upward (tombstone)</td></tr>
        <tr><td>PR depression</td><td>Present</td><td>Absent</td></tr>
        <tr><td>Reciprocal changes</td><td>Only in aVR and V1</td><td>Prominent in multiple leads</td></tr>
        <tr><td>Q waves</td><td>Absent</td><td>Develop over hours</td></tr>
        <tr><td>Spodick's sign</td><td>Present (downsloping TP)</td><td>Absent</td></tr>
      </tbody>
    </table>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Acute Pericarditis</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_cd4008531c1b1a2a99ab6d9b4282dcdcedfcf77c302b6ecbb7f7e01c5c985cf9.jpg" alt="Acute Pericarditis ECG"/>
      <div class="ecg-caption">Acute pericarditis: Diffuse concave "saddle-shaped" ST elevation in I, II, III, aVF, V2–V6. PR depression in II; reciprocal ST depression and PR elevation in aVR. Spodick's sign present (downsloping TP segments). Sinus tachycardia consistent with systemic inflammation.</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 9. PE ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 09</div>
    <div class="disease-title">Pulmonary Embolism (PE)</div>
    <div class="disease-subtitle">Acute right heart strain from pulmonary vascular obstruction</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> Acute obstruction of pulmonary vasculature suddenly increases right ventricular afterload. The RV dilates, shifts the interventricular septum leftward, and stretches the right heart — reflected electrically as right axis deviation, RBBB, and right-sided strain pattern. Sinus tachycardia is the most common manifestation of sympathetic activation.</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th><th>Frequency</th></tr></thead>
      <tbody>
        <tr><td>Sinus tachycardia</td><td>Most common finding — sympathetic activation</td><td>~44%</td></tr>
        <tr><td>S1Q3T3 pattern</td><td>S wave in lead I + Q wave in III + inverted T wave in III (McGinn-White sign)</td><td>~12–20%</td></tr>
        <tr><td>T-wave inversions V1–V4</td><td>Right ventricular strain — most specific finding</td><td>~34%</td></tr>
        <tr><td>Incomplete/complete RBBB</td><td>Right ventricular conduction delay from dilation</td><td>~25%</td></tr>
        <tr><td>Right axis deviation</td><td>Rightward shift of QRS axis</td><td>~16%</td></tr>
        <tr><td>P pulmonale</td><td>Peaked P waves &gt;2.5 mm in II — right atrial enlargement</td><td>Variable</td></tr>
        <tr><td>Atrial fibrillation</td><td>May occur with large PE / right atrial distension</td><td>~8–10%</td></tr>
        <tr><td>Normal ECG</td><td>Does NOT exclude PE</td><td>~30%</td></tr>
      </tbody>
    </table>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Pulmonary Embolism with Right Heart Strain</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_7cfb4819f88c84d02f863ca2f948165b6f4f6fafd405ca0b0a7df41e2d8d8e2a.jpg" alt="Pulmonary Embolism ECG"/>
      <div class="ecg-caption">PE with right heart strain: Sinus tachycardia at 116 bpm. S1Q3T3 pattern (S wave in I, Q wave in III, T-wave inversion in III). T-wave inversions in V1–V3 and aVF indicating RV strain. Incomplete RBBB (QRS 110 ms). Consistent with acute pulmonary vascular obstruction.</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ 10. HCM ══════════════════════════════════════════ -->
<div class="disease">
  <div class="disease-header">
    <div class="disease-num">Disease 10</div>
    <div class="disease-title">Hypertrophic Cardiomyopathy (HCM)</div>
    <div class="disease-subtitle">Pathological myocardial hypertrophy with diastolic dysfunction and arrhythmia risk</div>
  </div>
  <div class="disease-body">
    <div class="patho"><strong>Pathophysiology:</strong> HCM involves asymmetric hypertrophy of the LV myocardium (predominantly the interventricular septum), causing diastolic dysfunction, LVOT obstruction, and myocardial fiber disarray. The increased muscle mass generates high-voltage ECG signals. In the apical variant (Yamaguchi syndrome), the apex is maximally hypertrophied, producing dramatic "giant" T-wave inversions pathognomonic for this subtype.</div>

    <div class="ecg-table-title">ECG Changes</div>
    <table>
      <thead><tr><th>Feature</th><th>Description</th></tr></thead>
      <tbody>
        <tr><td>LV hypertrophy (LVH)</td><td>High-voltage QRS — Sokolow-Lyon: SV1 + RV5/V6 ≥35 mm; Cornell: RaVL + SV3 ≥28 mm (men)</td></tr>
        <tr><td>Giant T-wave inversions</td><td>Deep (&gt;10 mm), symmetric inversions in V2–V6 — hallmark of apical HCM (Yamaguchi)</td></tr>
        <tr><td>ST depression</td><td>Horizontal/downsloping in lateral leads V4–V6</td></tr>
        <tr><td>Abnormal Q waves</td><td>Deep, narrow Q waves in inferior (II, III, aVF) and lateral leads — from septal hypertrophy</td></tr>
        <tr><td>Left axis deviation</td><td>Common due to septal hypertrophy and altered activation</td></tr>
        <tr><td>Atrial fibrillation</td><td>Occurs in ~20–25% — worsens hemodynamics significantly</td></tr>
        <tr><td>Non-specific IVCD</td><td>Widened QRS without classic BBB morphology</td></tr>
        <tr><td>P mitrale</td><td>Broad, notched P waves in II — left atrial enlargement from impaired filling</td></tr>
      </tbody>
    </table>

    <div class="ecg-image-block">
      <div class="ecg-image-label">▶ ECG — Apical Hypertrophic Cardiomyopathy (Yamaguchi Syndrome)</div>
      <img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_a4a1104644642cc1443b5c4973b34b81ddcd6755093b0251a607f6d12851205e.jpg" alt="HCM ECG"/>
      <div class="ecg-caption">Apical HCM (Yamaguchi syndrome): High QRS voltage meeting LVH criteria in V4–V6. Striking deep, symmetric "giant" T-wave inversions across V2–V6 and limb leads. Horizontal ST depression in lateral leads. This pattern is virtually diagnostic of apical HCM when LVH voltage is also present.</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════ SUMMARY TABLE ══════════════════════════════════════════ -->
<div class="summary-page">
  <h2>Quick Reference Summary</h2>
  <table class="summary-table">
    <thead>
      <tr>
        <th>#</th>
        <th>Disease</th>
        <th>Key ECG Hallmark</th>
        <th>Rate / Rhythm</th>
      </tr>
    </thead>
    <tbody>
      <tr>
        <td>1</td>
        <td>STEMI</td>
        <td>Convex ST elevation ≥1 mm in ≥2 leads; Q waves; reciprocal ST↓</td>
        <td>Sinus; various rates</td>
      </tr>
      <tr>
        <td>2</td>
        <td>NSTEMI / UA</td>
        <td>ST depression ≥0.5 mm; T inversions; no Q waves; ↑aVR</td>
        <td>Sinus; often tachycardia</td>
      </tr>
      <tr>
        <td>3</td>
        <td>Atrial Fibrillation</td>
        <td>Absent P waves; fibrillatory baseline; irregularly irregular rhythm</td>
        <td>Irregular; 60–160 bpm</td>
      </tr>
      <tr>
        <td>4</td>
        <td>Ventricular Tachycardia</td>
        <td>Wide QRS ≥120 ms; AV dissociation; fusion/capture beats</td>
        <td>Regular; 100–250 bpm</td>
      </tr>
      <tr>
        <td>5</td>
        <td>Complete Heart Block</td>
        <td>AV dissociation; independent P and QRS; slow escape rhythm</td>
        <td>Ventricular: 20–45 bpm</td>
      </tr>
      <tr>
        <td>6</td>
        <td>LBBB</td>
        <td>QRS ≥120 ms; broad R in I/V5–V6; QS in V1–V3; discordant ST-T</td>
        <td>Sinus; any rate</td>
      </tr>
      <tr>
        <td>7</td>
        <td>WPW Syndrome</td>
        <td>Short PR &lt;120 ms; delta wave; wide QRS; pseudo-Q waves</td>
        <td>Sinus; SVT/AF when arrhythmia</td>
      </tr>
      <tr>
        <td>8</td>
        <td>Acute Pericarditis</td>
        <td>Diffuse concave ST↑; PR↓ in II; PR↑ in aVR; Spodick's sign</td>
        <td>Sinus tachycardia common</td>
      </tr>
      <tr>
        <td>9</td>
        <td>Pulmonary Embolism</td>
        <td>S1Q3T3; T↓ V1–V4; RBBB; right axis deviation</td>
        <td>Sinus tachycardia (most common)</td>
      </tr>
      <tr>
        <td>10</td>
        <td>HCM</td>
        <td>LVH voltage; giant T inversions (apical); deep narrow Q waves</td>
        <td>Sinus; AF in ~20–25%</td>
      </tr>
    </tbody>
  </table>

  <div style="margin-top: 10mm; padding: 5mm 6mm; background: #f0f4fa; border-radius: 6px; border: 1px solid #c8d6ee;">
    <div style="font-weight:700; color:#0f3460; font-size:9.5pt; margin-bottom:3mm;">References</div>
    <div style="font-size:8.5pt; color:#333; line-height:1.8;">
      ● Harrison's Principles of Internal Medicine, 22nd Edition (2025). McGraw Hill Medical.<br/>
      ● Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. Elsevier.<br/>
      ● Tintinalli's Emergency Medicine: A Comprehensive Study Guide. McGraw Hill.<br/>
      ● Goldman-Cecil Medicine, International Edition. Elsevier.<br/>
      ● ECG images sourced from PMC Clinical VQA Database via Orris Medical Library.
    </div>
  </div>
</div>

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