Orris

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

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Now let me run parallel searches across the medical library for ECG changes in key heart diseases:
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Good, I have key file paths. Now let me read the relevant ECG sections and search for images in parallel:
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Reading File
Searching Images

STEMI ST elevation myocardial infarction ECG electrocardiogram

Excellent! Now let me search for ECG images for the remaining diseases in parallel:
Searching Images

atrial fibrillation ECG irregularly irregular no P waves

Searching Images

ventricular tachycardia ECG wide complex tachycardia

Searching Images

left bundle branch block LBBB ECG QRS morphology

Searching Images

complete heart block third degree AV block ECG dissociation

Excellent! Now let me search for the remaining diseases:
Searching Images

hypertrophic cardiomyopathy ECG left ventricular hypertrophy voltage criteria

Searching Images

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

Searching Images

pericarditis ECG saddle-shaped ST elevation diffuse PR depression

Searching Images

pulmonary embolism ECG S1Q3T3 right heart strain sinus tachycardia

I have excellent images and content. Let me get one more image search for dilated cardiomyopathy and also read the key Harrison's section for additional clinical detail:
Searching Images

dilated cardiomyopathy ECG low voltage poor R wave progression sinus tachycardia

Reading File
I now have comprehensive information and images for all 10 diseases. Let me compile the full response:Here is a comprehensive overview of 10 common heart diseases with their ECG changes and representative ECG images.

10 Common Heart Diseases: ECG Changes & Images

1. ST-Elevation Myocardial Infarction (STEMI)

Pathophysiology: Complete occlusion of a coronary artery causes transmural ischemia. The outer (epicardial) layers are injured, creating a current of injury directed outward — producing ST elevation in overlying leads.

ECG Changes

FeatureDescription
ST elevationConvex ("tombstone") ST elevation ≥1 mm in ≥2 contiguous leads
Hyperacute T wavesTall, broad T waves — earliest sign
Reciprocal ST depressionIn leads opposing the infarct zone
Pathological Q wavesDevelop within hours; indicate necrosis (>40 ms wide, >25% of R-wave height)
T-wave inversionsAppear as infarct evolves
Localization:
  • Anterior: V1–V4 (LAD occlusion)
  • Inferior: II, III, aVF (RCA occlusion)
  • Lateral: I, aVL, V5–V6 (LCx occlusion)
  • Posterior: Reciprocal ST depression V1–V3
Anterior STEMI — tombstone ST elevation in V2–V5 with LAD occlusion
Anterior STEMI: Prominent convex "tombstoning" ST elevation in V2–V5, evolving QS waves, consistent with LAD occlusion.
Inferolateral STEMI with reciprocal changes
Inferolateral STEMI: ST elevation in II, III, aVF, V4–V6 (green circles) with reciprocal ST depression in I, aVL, V2–V3 (yellow arrows).

2. Non-ST-Elevation Myocardial Infarction (NSTEMI) / Unstable Angina

Pathophysiology: Partial coronary occlusion causes subendocardial ischemia. The ST vector shifts toward the subendocardium — producing ST depression (and ST elevation in aVR).

ECG Changes

FeatureDescription
ST depressionHorizontal or downsloping ≥0.5 mm in ≥2 contiguous leads
ST elevation in aVRIndicates diffuse subendocardial ischemia or left main/proximal LAD disease
T-wave inversionsParticularly deep symmetric inversions (Wellens' syndrome = critical LAD stenosis)
No pathological Q wavesDistinguishes from STEMI
Normal ECG possibleIn ~30% of NSTEMI; diagnosis depends on troponin elevation
"The diagnosis of NSTEMI depends on abnormal elevation of cardiac biomarkers but may include ECG changes not meeting criteria for STEMI." — Tintinalli's Emergency Medicine

3. Atrial Fibrillation (AF)

Pathophysiology: Chaotic, disorganized atrial electrical activity at 300–600 impulses/min, with variable conduction through the AV node producing an irregular ventricular response.

ECG Changes

FeatureDescription
Absent P wavesReplaced by chaotic fibrillatory (f) waves, best seen in V1
Irregularly irregular rhythmThe hallmark — no two R-R intervals are the same
Narrow QRSUnless aberrant conduction or bundle branch block is present
Fibrillatory baselineUndulating baseline at 350–600 waves/min
"AF is characterized electrocardiographically by low-amplitude baseline oscillations (fibrillatory or f waves) and an irregularly irregular ventricular rhythm." — Braunwald's Heart Disease
Atrial fibrillation — irregularly irregular rhythm, absent P waves, fibrillatory baseline
AF: Absent P waves replaced by fine f-waves (most visible in V1), irregularly irregular QRS intervals, narrow complexes.

4. Ventricular Tachycardia (VT)

Pathophysiology: A rapid arrhythmia originating in the ventricular myocardium (below the Bundle of His), producing wide QRS complexes. Often occurs on a background of structural heart disease (prior MI, cardiomyopathy).

ECG Changes

FeatureDescription
Wide QRS complexes≥120 ms (usually ≥140 ms in VT)
Rapid rate100–250 bpm, regular
AV dissociationP waves "march through" QRS at their own rate — pathognomonic
Fusion beatsHybrid P-wave + QRS complex — diagnostic of VT
Capture beatsNarrow QRS amid wide complex — diagnostic
ConcordanceAll precordial leads positive or negative
"The presence of fusion beats or AV dissociation during a wide-QRS complex tachycardia establishes the diagnosis of VT." — Goldman-Cecil Medicine
Monomorphic ventricular tachycardia — wide complex tachycardia, AV dissociation
Monomorphic VT: Wide, high-amplitude QRS complexes at ~170 bpm, positive concordance in precordial leads, absent P waves.

5. Complete (Third-Degree) AV Heart Block

Pathophysiology: Total failure of conduction through the AV node. Atria and ventricles depolarize independently — the ventricles rely on an escape pacemaker (junctional at 40–60 bpm; ventricular at 20–40 bpm).

ECG Changes

FeatureDescription
AV dissociationP waves and QRS complexes independent; no fixed PR interval
Regular P-P intervalAtrial rate faster (~60–100 bpm)
Regular R-R intervalVentricular escape rhythm, slower
Wide QRSIf infra-Hisian escape (ventricular origin); narrow if junctional
BradycardiaVentricular rate 20–45 bpm
Complete heart block — AV dissociation, independent atrial and ventricular rhythms
Third-degree AV block: P waves march through at a faster, independent rate; wide, slow ventricular escape complexes with no PR relationship.

6. Left Bundle Branch Block (LBBB)

Pathophysiology: Failure of conduction in the left bundle branch — ventricular depolarization travels abnormally through the myocardium, widening and distorting the QRS. Frequently indicates underlying coronary artery disease, hypertensive heart disease, or cardiomyopathy.

ECG Changes

FeatureDescription
Wide QRS≥120 ms
Broad monophasic R in I, aVL, V5–V6With slurring/notching ("M" pattern)
Deep QS in V1–V3rS or QS pattern
No septal Q wavesAbsent in I, V5–V6 (normally present)
Discordant ST-T changesST/T opposite to dominant QRS deflection (secondary changes)
Left axis deviationCommon
"With bundle branch blocks, the T wave is typically opposite in polarity to the last deflection of the QRS. New LBBB in the context of chest pain should be treated as STEMI equivalent." — Harrison's Principles of Internal Medicine 22E
LBBB — widened QRS, broad notched R in lateral leads, deep S waves in V1–V3
LBBB: QRS ≥158 ms, broad "M-shaped" R waves in I, aVL, V5–V6, deep S waves in V1–V3, discordant ST-T changes, left axis deviation.

7. Wolff-Parkinson-White (WPW) Syndrome

Pathophysiology: An accessory pathway (Bundle of Kent) bypasses the AV node, pre-exciting the ventricles. This produces the characteristic delta wave and short PR interval. Can cause life-threatening arrhythmias (SVT, AF with rapid ventricular response).

ECG Changes

FeatureDescription
Short PR interval<120 ms (AV node bypassed)
Delta waveSlurred upstroke at start of QRS
Wide QRSDue to fusion of pre-excitation + normal conduction
Secondary ST-T changesDiscordant repolarization
Pseudo-infarct patternNegative delta waves mimic Q waves (inferior or lateral leads)
"Prolongation of QRS duration may be due to pre-excitation of the ventricles via a bypass tract, as in Wolff-Parkinson-White (WPW) patterns." — Harrison's Principles of Internal Medicine 22E
WPW — short PR interval, delta wave, widened QRS with pre-excitation
WPW: Short PR (<120 ms), prominent delta waves (red arrows in II and III), widened QRS complexes — classic ventricular pre-excitation pattern.

8. Acute Pericarditis

Pathophysiology: Inflammation of the pericardium produces diffuse subepicardial injury affecting multiple leads simultaneously (unlike MI, which is territory-specific). PR depression reflects atrial inflammation.

ECG Changes (4 Stages)

StageECG Finding
Stage 1Diffuse concave ("saddle-shaped") ST elevation in nearly all leads except aVR and V1; PR depression in II, aVF, V4–V6; PR elevation in aVR
Stage 2ST normalizes; T waves flatten
Stage 3T-wave inversions develop
Stage 4ECG normalizes
Key distinguishing features from STEMI:
  • ST elevation is diffuse (not in one coronary territory)
  • ST morphology is concave upward (not convex)
  • PR depression present
  • No reciprocal changes (except aVR)
  • Spodick's sign — downsloping TP segment
Acute pericarditis — diffuse saddle-shaped ST elevation, PR depression, Spodick's sign
Acute pericarditis: Diffuse concave 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.

9. Pulmonary Embolism (PE)

Pathophysiology: Acute obstruction of pulmonary vasculature causes sudden right ventricular pressure overload and right heart strain, reflected electrically as right axis deviation and right-sided changes.

ECG Changes

FeatureDescription
Sinus tachycardiaMost common finding (~44%)
S1Q3T3 patternS wave in I, Q wave in III, inverted T wave in III (McGinn-White sign)
Right axis deviationShift to right
Incomplete/complete RBBBRight ventricular conduction delay
T-wave inversions V1–V4Right ventricular strain
P pulmonalePeaked P waves in II — right atrial enlargement
Atrial fibrillationMay occur with large PE
Note: ECG is abnormal in ~70% of PE cases, but the findings are non-specific. Normal ECG does not exclude PE.
Pulmonary embolism — S1Q3T3, sinus tachycardia, right heart strain, T-wave inversions V1–V3
PE with right heart strain: Sinus tachycardia at 116 bpm, S1Q3T3 pattern, T-wave inversions in V1–V3 and aVF, incomplete RBBB pattern (QRS 110 ms).

10. Hypertrophic Cardiomyopathy (HCM)

Pathophysiology: Pathological myocardial hypertrophy (especially the interventricular septum) produces high-voltage QRS complexes, repolarization abnormalities, and, in the apical variant (Yamaguchi syndrome), dramatic "giant" T-wave inversions.

ECG Changes

FeatureDescription
Left ventricular hypertrophy (LVH)High-voltage QRS (Sokolow-Lyon: SV1 + RV5/V6 ≥35 mm)
Deep T-wave inversions"Giant" symmetric inversions in V2–V6 (apical HCM)
Left axis deviationCommon
Abnormal Q wavesDeep narrow Q waves in inferior and lateral leads (septal hypertrophy)
ST depressionLateral leads V4–V6
Atrial fibrillationOccurs in ~20–25% of HCM patients
Non-specific IVCDWidened QRS without classic BBB pattern
Apical HCM (Yamaguchi) — giant T-wave inversions V2–V6, LVH voltage criteria
Apical HCM: High QRS voltage meeting LVH criteria, striking deep symmetric "giant" T-wave inversions across V2–V6 and limb leads — hallmark of Yamaguchi syndrome.

Quick Reference Summary

#DiseaseKey ECG Hallmark
1STEMIST elevation ≥1 mm in ≥2 leads, Q waves, reciprocal changes
2NSTEMI/UAST depression, T-wave inversions, no Q waves
3Atrial FibrillationIrregularly irregular rhythm, absent P waves
4Ventricular TachycardiaWide QRS ≥120 ms, AV dissociation, fusion beats
5Complete Heart BlockIndependent P waves and QRS (AV dissociation), bradycardia
6LBBBWide QRS, broad R in I/V5–V6, QS in V1–V3
7WPW SyndromeShort PR, delta wave, wide QRS
8Acute PericarditisDiffuse concave ST elevation, PR depression, Spodick's sign
9Pulmonary EmbolismSinus tachycardia, S1Q3T3, RV strain, T inversions V1–V4
10HCMLVH voltage, giant T inversions (apical), deep Q waves
Sources: Harrison's Principles of Internal Medicine 22E (2025); Braunwald's Heart Disease (Textbook of Cardiovascular Medicine); Tintinalli's Emergency Medicine; Goldman-Cecil Medicine; ECG images from PMC Clinical VQA database via Orris Medical Library.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

Reading File
Running Command

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

Running Command

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

I'll generate a polished PDF using WeasyPrint (HTML→PDF) with all ECG images embedded. Let me write the script:
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>
<html lang="en">
<head>
<meta charset="UTF-8"/>
<style>
  @page {
    size: A4;
    margin: 18mm 15mm 18mm 15mm;
    @bottom-center {
      content: "Page " counter(page) " of " counter(pages);
      font-size: 9pt;
      color: #666;
    }
  }
  * { box-sizing: border-box; }
  body {
    font-family: 'Helvetica Neue', Arial, sans-serif;
    font-size: 10pt;
    color: #1a1a2e;
    line-height: 1.5;
    margin: 0;
  }

  /* ── Cover page ── */
  .cover {
    page: cover;
    height: 267mm;
    background: linear-gradient(145deg, #0f3460 0%, #16213e 60%, #1a1a2e 100%);
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    font-size: 14pt;
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    margin: 0 0 14mm 0;
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  .cover .ecg-line {
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    padding: 8mm 12mm;
    text-align: left;
    color: #cde;
    font-size: 9.5pt;
    line-height: 1.9;
    margin-top: 8mm;
    width: 90%;
  }
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    color: #e94560;
    font-size: 10pt;
    margin: 0 0 4mm 0;
    text-transform: uppercase;
    letter-spacing: 2px;
  }
  .cover .toc-item { display: flex; gap: 6mm; }
  .cover .toc-num { color: #e94560; font-weight: 700; min-width: 18px; }
  .cover .footer-note {
    color: rgba(200,220,240,0.5);
    font-size: 7.5pt;
    margin-top: 12mm;
  }

  /* ── Disease cards ── */
  .disease {
    page-break-before: always;
    padding: 0;
  }
  .disease-header {
    background: linear-gradient(to right, #0f3460, #16213e);
    color: white;
    padding: 6mm 8mm 5mm 8mm;
    border-radius: 6px 6px 0 0;
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  }
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    font-weight: 700;
    letter-spacing: 2px;
    text-transform: uppercase;
    margin-bottom: 1mm;
  }
  .disease-title {
    font-size: 18pt;
    font-weight: 800;
    margin: 0;
    line-height: 1.2;
  }
  .disease-subtitle {
    font-size: 9pt;
    color: #a8d8ea;
    margin: 2mm 0 0 0;
  }

  .disease-body {
    border: 1px solid #dde4f0;
    border-top: none;
    border-radius: 0 0 6px 6px;
    padding: 6mm 7mm;
    background: #fafcff;
  }

  /* Pathophysiology */
  .patho {
    background: #eef4ff;
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    padding: 3mm 5mm;
    border-radius: 0 4px 4px 0;
    margin-bottom: 5mm;
    font-size: 9.5pt;
    color: #1a2a4a;
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  .patho strong { color: #0f3460; }

  /* ECG table */
  .ecg-table-title {
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    font-weight: 700;
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    color: #5a4000;
    margin: 3mm 0 5mm 0;
  }
  .quote cite { font-style: normal; font-size: 8pt; color: #888; display: block; margin-top: 1mm; }

  /* ECG image */
  .ecg-image-block {
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    object-fit: contain;
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    padding: 0.5mm 2mm;
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    display: inline-block;
  }
</style>
</head>
<body>

<!-- ══════════════════════════════════════════ 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>

</body>
</html>
"""

print("Generating PDF...")
from weasyprint import HTML as WH, CSS
doc = WH(string=HTML, base_url="https://cdn.orris.care")
doc.write_pdf(OUTPUT)
print(f"PDF saved to: {OUTPUT}")
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