mkdir -p /home/daytona/workspace/md-medicine-notes && ls /home/daytona/workspace…

~/md-medicine-notes/create_notes.js

const {
  Document, Packer, Paragraph, TextRun, Table, TableRow, TableCell,
  HeadingLevel, AlignmentType, BorderStyle, WidthType, ShadingType,
  PageBreak, TableOfContents, VerticalAlign
} = require('docx');
const fs = require('fs');

// ─── Helper functions ────────────────────────────────────────────────────────

function heading1(text) {
  return new Paragraph({
    text,
    heading: HeadingLevel.HEADING_1,
    spacing: { before: 400, after: 200 },
    shading: { type: ShadingType.SOLID, color: '1F3864', fill: '1F3864' },
  });
}

function heading2(text) {
  return new Paragraph({
    text,
    heading: HeadingLevel.HEADING_2,
    spacing: { before: 300, after: 150 },
  });
}

function heading3(text) {
  return new Paragraph({
    text,
    heading: HeadingLevel.HEADING_3,
    spacing: { before: 200, after: 100 },
  });
}

function body(text, bold = false, color = '000000') {
  return new Paragraph({
    children: [new TextRun({ text, bold, color, size: 22 })],
    spacing: { before: 60, after: 60 },
  });
}

function bullet(text, level = 0) {
  return new Paragraph({
    children: [new TextRun({ text, size: 22 })],
    bullet: { level },
    spacing: { before: 40, after: 40 },
  });
}

function boldBullet(label, value, level = 0) {
  return new Paragraph({
    children: [
      new TextRun({ text: label + ': ', bold: true, size: 22 }),
      new TextRun({ text: value, size: 22 }),
    ],
    bullet: { level },
    spacing: { before: 40, after: 40 },
  });
}

function pageBreak() {
  return new Paragraph({ children: [new PageBreak()] });
}

function colorBox(text, bgColor = 'E8F4FD') {
  return new Paragraph({
    children: [new TextRun({ text, size: 22, bold: true })],
    shading: { type: ShadingType.SOLID, color: bgColor, fill: bgColor },
    spacing: { before: 100, after: 100 },
    indent: { left: 360 },
  });
}

function divider() {
  return new Paragraph({
    border: { bottom: { color: '1F3864', size: 6, style: BorderStyle.SINGLE } },
    spacing: { before: 100, after: 100 },
  });
}

function noteBox(text) {
  return new Paragraph({
    children: [new TextRun({ text: '📝 EXAM TIP: ' + text, size: 20, color: '7B2D8B', bold: true })],
    shading: { type: ShadingType.SOLID, color: 'F5E6FA', fill: 'F5E6FA' },
    spacing: { before: 80, after: 80 },
    indent: { left: 360 },
  });
}

// Simple text-based flowchart row
function flowRow(text, bgColor = 'D6E4F0') {
  return new Paragraph({
    children: [new TextRun({ text, bold: true, size: 22, color: '1A1A1A' })],
    alignment: AlignmentType.CENTER,
    shading: { type: ShadingType.SOLID, color: bgColor, fill: bgColor },
    spacing: { before: 40, after: 0 },
    border: {
      top: { color: '2E75B6', size: 4, style: BorderStyle.SINGLE },
      bottom: { color: '2E75B6', size: 4, style: BorderStyle.SINGLE },
      left: { color: '2E75B6', size: 4, style: BorderStyle.SINGLE },
      right: { color: '2E75B6', size: 4, style: BorderStyle.SINGLE },
    },
  });
}

function flowArrow() {
  return new Paragraph({
    children: [new TextRun({ text: '▼', size: 22, color: '2E75B6', bold: true })],
    alignment: AlignmentType.CENTER,
    spacing: { before: 0, after: 0 },
  });
}

function flowDiamond(text) {
  return new Paragraph({
    children: [new TextRun({ text: '◆ ' + text + ' ◆', bold: true, size: 22, color: 'FFFFFF' })],
    alignment: AlignmentType.CENTER,
    shading: { type: ShadingType.SOLID, color: 'C00000', fill: 'C00000' },
    spacing: { before: 40, after: 0 },
    border: {
      top: { color: 'C00000', size: 4, style: BorderStyle.SINGLE },
      bottom: { color: 'C00000', size: 4, style: BorderStyle.SINGLE },
      left: { color: 'C00000', size: 4, style: BorderStyle.SINGLE },
      right: { color: 'C00000', size: 4, style: BorderStyle.SINGLE },
    },
  });
}

// Table helper
function makeTable(headers, rows, colWidths) {
  const headerCells = headers.map((h, i) =>
    new TableCell({
      children: [new Paragraph({
        children: [new TextRun({ text: h, bold: true, color: 'FFFFFF', size: 20 })],
        alignment: AlignmentType.CENTER,
      })],
      width: { size: colWidths[i], type: WidthType.PERCENTAGE },
      shading: { type: ShadingType.SOLID, color: '1F3864', fill: '1F3864' },
      verticalAlign: VerticalAlign.CENTER,
    })
  );

  const dataRows = rows.map((row, ri) =>
    new TableRow({
      children: row.map((cell, ci) =>
        new TableCell({
          children: [new Paragraph({
            children: [new TextRun({ text: cell, size: 20 })],
          })],
          width: { size: colWidths[ci], type: WidthType.PERCENTAGE },
          shading: {
            type: ShadingType.SOLID,
            color: ri % 2 === 0 ? 'F2F2F2' : 'FFFFFF',
            fill: ri % 2 === 0 ? 'F2F2F2' : 'FFFFFF',
          },
        })
      ),
    })
  );

  return new Table({
    rows: [new TableRow({ children: headerCells }), ...dataRows],
    width: { size: 100, type: WidthType.PERCENTAGE },
  });
}

// ─── DOCUMENT CONTENT ────────────────────────────────────────────────────────

const children = [];

// =================== TITLE PAGE ===================
children.push(new Paragraph({
  children: [new TextRun({ text: 'MD MEDICINE UNIVERSITY EXAM NOTES', bold: true, size: 48, color: '1F3864' })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 1400, after: 200 },
}));
children.push(new Paragraph({
  children: [new TextRun({ text: 'Cardiology Module', bold: true, size: 32, color: '2E75B6' })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 0, after: 200 },
}));
children.push(new Paragraph({
  children: [new TextRun({ text: 'Long Question Answers', size: 28, color: '595959' })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 0, after: 100 },
}));
children.push(new Paragraph({
  children: [new TextRun({ text: 'July 2026', size: 24, color: '595959' })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 0, after: 800 },
}));
children.push(divider());
children.push(new Paragraph({
  children: [new TextRun({ text: 'Contents', bold: true, size: 28, color: '1F3864' })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 400, after: 200 },
}));
children.push(bullet('Q1. Approach to Broad QRS Tachycardia & Management'));
children.push(bullet('Q2. Pathophysiology of ACS with Physiology of Coagulation'));
children.push(pageBreak());

// =================== QUESTION 1 ===================
children.push(new Paragraph({
  children: [new TextRun({ text: 'QUESTION 1', bold: true, size: 32, color: 'FFFFFF' })],
  alignment: AlignmentType.CENTER,
  shading: { type: ShadingType.SOLID, color: '1F3864', fill: '1F3864' },
  spacing: { before: 200, after: 0 },
}));
children.push(new Paragraph({
  children: [new TextRun({ text: 'Approach to a Case with Broad QRS Tachycardia & Its Management', bold: true, size: 28, color: 'FFFFFF' })],
  alignment: AlignmentType.CENTER,
  shading: { type: ShadingType.SOLID, color: '2E75B6', fill: '2E75B6' },
  spacing: { before: 0, after: 300 },
}));

// DEFINITION
children.push(heading2('1. DEFINITION'));
children.push(body('Broad (wide) QRS tachycardia is defined as a tachycardia (HR > 100 bpm) with a QRS duration ≥ 120 ms (≥ 0.12 s or ≥ 3 small squares on ECG).'));
children.push(noteBox('Threshold for "broad" QRS = 120 ms. In exam, if QRS > 0.14 s → strongly suggests VT over SVT.'));

// CAUSES
children.push(heading2('2. CAUSES / CLASSIFICATION'));
children.push(body('Broad QRS tachycardia has three main etiological categories:', true));

children.push(heading3('A. Ventricular Tachycardia (VT) — Most Common (80%)'));
children.push(boldBullet('Monomorphic VT', 'All QRS complexes have same morphology. Most common. Usually from scar-related re-entry after MI.'));
children.push(boldBullet('Polymorphic VT', 'QRS morphology varies beat to beat. Includes Torsades de Pointes (TdP).'));
children.push(boldBullet('Ventricular Flutter', 'Rate 250-350 bpm, sine-wave morphology, haemodynamically unstable.'));

children.push(heading3('B. SVT with Aberrant Conduction (~15-20%)'));
children.push(boldBullet('SVT + RBBB / LBBB', 'Pre-existing or rate-dependent bundle branch block widens QRS.'));
children.push(boldBullet('SVT + Metabolic', 'Hyperkalaemia, antiarrhythmic drug toxicity (Class Ic, tricyclics) widens QRS.'));

children.push(heading3('C. Pre-excitation Syndromes (~1-5%)'));
children.push(boldBullet('WPW with AF/AFL', 'Delta wave + rapid ventricular rate + irregular RR. Extremely dangerous — can degenerate to VF.'));
children.push(boldBullet('Antidromic AVRT', 'Wide QRS (fully pre-excited) tachycardia via accessory pathway.'));

children.push(divider());

// KEY CLINICAL RULE
children.push(new Paragraph({
  children: [
    new TextRun({ text: '⚠ GOLDEN RULE: ', bold: true, size: 22, color: 'C00000' }),
    new TextRun({ text: 'All broad QRS tachycardias should be treated as VT until proven otherwise.', size: 22, bold: true }),
  ],
  shading: { type: ShadingType.SOLID, color: 'FFE4E1', fill: 'FFE4E1' },
  spacing: { before: 100, after: 200 },
  indent: { left: 360 },
}));

// CLINICAL APPROACH
children.push(heading2('3. SYSTEMATIC CLINICAL APPROACH'));

// FLOWCHART 1 — Initial Assessment
children.push(heading3('Flowchart 1: Initial Assessment of Broad QRS Tachycardia'));
children.push(new Paragraph({ spacing: { before: 100, after: 0 } }));

children.push(flowRow('PATIENT PRESENTS WITH BROAD QRS TACHYCARDIA (QRS ≥ 120ms, HR > 100 bpm)'));
children.push(flowArrow());
children.push(flowDiamond('HAEMODYNAMICALLY STABLE?'));
children.push(new Paragraph({
  children: [
    new TextRun({ text: 'YES → Proceed to diagnosis               ', bold: true, color: '2E75B6', size: 22 }),
    new TextRun({ text: 'NO → IMMEDIATE ELECTRICAL CARDIOVERSION', bold: true, color: 'C00000', size: 22 }),
  ],
  alignment: AlignmentType.CENTER,
  spacing: { before: 40, after: 40 },
}));
children.push(flowArrow());
children.push(flowRow('ECG ANALYSIS → Brugada / Griffith / Vereckei Criteria'));
children.push(flowArrow());
children.push(flowDiamond('VT vs SVT with Aberrancy vs Pre-excitation?'));
children.push(flowArrow());
children.push(flowRow('TARGETED TREATMENT BASED ON DIAGNOSIS'));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));

// HAEMODYNAMIC STATUS
children.push(heading2('4. HAEMODYNAMIC STATUS — FIRST ASSESSMENT'));
children.push(body('Assess IMMEDIATELY on patient contact:'));
children.push(boldBullet('Signs of HAEMODYNAMIC INSTABILITY (any one → immediate cardioversion):', ''));
children.push(bullet('Hypotension (SBP < 90 mmHg)', 1));
children.push(bullet('Altered consciousness / syncope', 1));
children.push(bullet('Signs of pulmonary oedema / acute heart failure', 1));
children.push(bullet('Severe chest pain / ongoing ischaemia', 1));
children.push(bullet('HR > 200 bpm', 1));

children.push(divider());

// ECG DIAGNOSIS
children.push(heading2('5. ECG DIAGNOSIS — DISTINGUISHING VT FROM SVT'));

children.push(heading3('Brugada 4-Step Algorithm (Gold Standard)'));
children.push(body('Answer each question in sequence. If "YES" at any step → VT. Only "NO" to ALL 4 → SVT.'));

const brugadaRows = [
  ['Step 1', 'Is there ABSENCE of RS complex in ALL precordial leads (V1-V6)?', 'YES → VT', 'NO → next step'],
  ['Step 2', 'Is the RS interval (nadir of S) > 100 ms in any precordial lead?', 'YES → VT', 'NO → next step'],
  ['Step 3', 'Is there AV dissociation?', 'YES → VT', 'NO → next step'],
  ['Step 4', 'Are VT morphology criteria met in V1 & V6?', 'YES → VT', 'NO → SVT'],
];
children.push(makeTable(['Step', 'Question', 'YES', 'NO'], brugadaRows, [10, 50, 20, 20]));
children.push(new Paragraph({ spacing: { before: 100, after: 100 } }));
children.push(noteBox('Brugada criteria: Sensitivity 98.7%, Specificity 96.5% for VT. However, Class I drugs (flecainide) reduce reliability.'));

children.push(heading3('Key ECG Features Favouring VT'));
const vtEcgFeatures = [
  ['QRS Duration', '> 140 ms (RBBB pattern) or > 160 ms (LBBB pattern)', 'Usually < 140 ms'],
  ['QRS Axis', 'Extreme left axis (-90° to ±180°)', 'Normal / near-normal'],
  ['AV Dissociation', 'P waves independent of QRS (pathognomonic of VT)', 'P before each QRS'],
  ['Fusion Beats', 'Hybrid QRS — sinus + ectopic (PATHOGNOMONIC)', 'Absent'],
  ['Capture Beats', 'Narrow QRS during tachycardia (PATHOGNOMONIC)', 'Absent'],
  ['Precordial Concordance', 'All V1-V6 positive or all negative', 'Variable'],
  ['V1 morphology (RBBB)', 'R, qR, or RS (monophasic/biphasic)', 'Triphasic rSR' (rabbit ears)'],
  ['V6 morphology (RBBB)', 'S, rS, or QS pattern', 'qRS'],
];
children.push(makeTable(['Parameter', 'Ventricular Tachycardia', 'SVT + Aberrancy'], vtEcgFeatures, [22, 39, 39]));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));

// CLINICAL FEATURES COMPARISON
children.push(heading2('6. CLINICAL FEATURES: VT vs SVT'));
const clinicalRows = [
  ['Age', '≥ 50 years', '≤ 35 years'],
  ['H/O Ischaemic Heart Disease', 'Common (post-MI, CHF, CABG)', 'Usually absent'],
  ['Previous VT', 'Present', 'Absent (previous SVT)'],
  ['Cannon A waves (JVP)', 'Present (AV dissociation)', 'Absent'],
  ['Arterial pulse variation', 'Yes (beat-to-beat variation)', 'No variation'],
  ['S1 variability', 'Variable intensity', 'Constant intensity'],
  ['Response to Adenosine', 'No effect (or minor change)', 'Slows / terminates SVT'],
  ['Response to Valsalva', 'No effect', 'May slow or terminate'],
];
children.push(makeTable(['Parameter', 'VT', 'SVT + Aberrancy'], clinicalRows, [30, 35, 35]));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));

// SPECIAL SCENARIOS
children.push(heading2('7. SPECIAL SCENARIOS'));
children.push(heading3('A. Pre-excitation (WPW) with Broad QRS Tachycardia'));
children.push(boldBullet('Antidromic AVRT', 'Delta wave + fully pre-excited wide QRS. Regular rhythm.'));
children.push(boldBullet('WPW + AF', 'IRREGULAR broad QRS tachycardia. Rate > 200 bpm. Life-threatening.'));
children.push(new Paragraph({
  children: [
    new TextRun({ text: '⚠ DANGER: ', bold: true, color: 'C00000', size: 22 }),
    new TextRun({ text: 'AV nodal blockers (adenosine, verapamil, digoxin, beta-blockers) are ABSOLUTELY CONTRAINDICATED in WPW+AF — they can accelerate accessory pathway conduction and cause VF.', size: 22 }),
  ],
  shading: { type: ShadingType.SOLID, color: 'FFE4E1', fill: 'FFE4E1' },
  spacing: { before: 80, after: 80 },
  indent: { left: 360 },
}));

children.push(heading3('B. Torsades de Pointes (TdP)'));
children.push(boldBullet('Definition', 'Polymorphic VT with QRS complexes twisting around baseline. "Twisting of the points."'));
children.push(boldBullet('Substrate', 'Prolonged QT interval (acquired or congenital — Long QT Syndrome)'));
children.push(boldBullet('Causes', 'Drugs (quinidine, amiodarone, antihistamines, macrolides, haloperidol), hypokalaemia, hypomagnesaemia'));
children.push(boldBullet('Treatment', 'IV Magnesium sulfate 2g over 10 min (DOC). Withdraw offending drug. Pacing to suppress.'));
children.push(noteBox('TdP mnemonic: "CQUA" — Class Ia/III drugs, QT prolongation, Underlying hypo-K/Mg, Atypical polymorphic VT with "twisting."'));

children.push(divider());

// MANAGEMENT FLOWCHART
children.push(heading2('8. MANAGEMENT OF BROAD QRS TACHYCARDIA'));

children.push(heading3('Flowchart 2: Management Algorithm'));
children.push(new Paragraph({ spacing: { before: 80, after: 0 } }));
children.push(flowRow('BROAD QRS TACHYCARDIA CONFIRMED'));
children.push(flowArrow());
children.push(flowDiamond('PULSELESS?'));
children.push(new Paragraph({
  children: [new TextRun({ text: 'YES → CPR + Unsynchronised Defibrillation (VF/pulseless VT) — Follow ACLS', bold: true, color: 'C00000', size: 22 })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 40, after: 40 },
}));
children.push(flowArrow());
children.push(flowDiamond('HAEMODYNAMICALLY UNSTABLE? (Hypotension, Altered consciousness, Pulmonary oedema, Severe chest pain)'));
children.push(new Paragraph({
  children: [new TextRun({ text: 'YES → Immediate Synchronised Electrical Cardioversion (100J biphasic, escalate if needed)', bold: true, color: 'C00000', size: 22 })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 40, after: 40 },
}));
children.push(flowArrow());
children.push(flowRow('HAEMODYNAMICALLY STABLE — ECG DIAGNOSIS'));
children.push(flowArrow());
children.push(flowDiamond('VT CONFIRMED (or cannot exclude VT)?'));
children.push(new Paragraph({
  children: [new TextRun({ text: 'YES → Pharmacological Cardioversion: Amiodarone or Procainamide', bold: true, color: '2E75B6', size: 22 })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 40, after: 40 },
}));
children.push(flowArrow());
children.push(flowDiamond('SVT + Aberrancy CONFIRMED?'));
children.push(new Paragraph({
  children: [new TextRun({ text: 'YES → Adenosine IV 6mg rapid bolus (if no pre-excitation)', bold: true, color: '375623', size: 22 })],
  alignment: AlignmentType.CENTER,
  spacing: { before: 40, after: 40 },
}));
children.push(new Paragraph({ spacing: { before: 80, after: 200 } }));

// PHARMACOLOGICAL MANAGEMENT
children.push(heading2('9. PHARMACOLOGICAL MANAGEMENT'));
children.push(heading3('A. Confirmed / Presumed VT'));
const vtDrugs = [
  ['Amiodarone', '150 mg IV over 10 min, then 1 mg/min × 6h, then 0.5 mg/min × 18h', 'First-line for haemodynamically stable VT. Safe in structural heart disease.'],
  ['Procainamide', '15-17 mg/kg IV at ≤50 mg/min', 'Effective for VT and WPW. Avoid in heart failure.'],
  ['Lidocaine', '1-1.5 mg/kg IV bolus', 'Adjunct. Preferred in ischaemic VT (post-MI). Less effective than amiodarone.'],
  ['Sotalol', '100 mg IV over 5 min', 'Alternative; avoid in QT prolongation.'],
  ['MgSO4', '2 g IV over 10 min', 'DRUG OF CHOICE for Torsades de Pointes.'],
];
children.push(makeTable(['Drug', 'Dose', 'Notes'], vtDrugs, [20, 40, 40]));
children.push(new Paragraph({ spacing: { before: 100, after: 100 } }));

children.push(heading3('B. SVT with Aberrancy (once VT excluded)'));
const svtDrugs = [
  ['Adenosine', '6 mg rapid IV bolus → 12 mg → 18 mg if needed', 'DOC for AVNRT/AVRT. Avoid in pre-excitation (WPW).'],
  ['Verapamil', '5-10 mg IV slow over 2 min', 'Alternative for SVT without pre-excitation. CONTRAINDICATED in VT.'],
  ['Beta-blockers', 'Metoprolol 5 mg IV over 5 min', 'Rate control. Avoid in decompensated HF.'],
  ['Flecainide', 'Oral for paroxysmal SVT, NOT for structural heart disease', 'Sodium channel blocker.'],
];
children.push(makeTable(['Drug', 'Dose', 'Notes'], svtDrugs, [20, 40, 40]));
children.push(new Paragraph({ spacing: { before: 100, after: 100 } }));

children.push(heading3('C. WPW with Broad QRS Tachycardia'));
children.push(boldBullet('Drug of Choice', 'Procainamide IV or Ibutilide IV (block accessory pathway)'));
children.push(boldBullet('If unstable', 'Immediate DC cardioversion'));
children.push(new Paragraph({
  children: [
    new TextRun({ text: 'CONTRAINDICATED: ', bold: true, color: 'C00000', size: 22 }),
    new TextRun({ text: 'Adenosine, Verapamil, Diltiazem, Digoxin, IV Amiodarone in WPW+AF (all can cause VF)', size: 22 }),
  ],
  shading: { type: ShadingType.SOLID, color: 'FFE4E1', fill: 'FFE4E1' },
  spacing: { before: 80, after: 80 },
  indent: { left: 360 },
}));

children.push(divider());

// NON-PHARMACOLOGICAL / LONG-TERM
children.push(heading2('10. NON-PHARMACOLOGICAL & LONG-TERM MANAGEMENT'));
children.push(boldBullet('Implantable Cardioverter-Defibrillator (ICD)', 'Primary prevention (EF ≤ 35%, NYHA II/III on optimal medical therapy) and secondary prevention (survivor of VF/VT)'));
children.push(boldBullet('Catheter Ablation', 'Radiofrequency ablation for recurrent VT, WPW (accessory pathway), bundle branch re-entry VT'));
children.push(boldBullet('Treat Reversible Causes', 'Correct hypokalaemia, hypomagnesaemia, withdraw QT-prolonging drugs, treat ischaemia'));
children.push(boldBullet('Beta-blockers', 'Reduce recurrent VT post-MI; reduce mortality'));
children.push(boldBullet('Anti-ischaemic therapy', 'Revascularisation (PCI/CABG) for VT in context of ischaemia'));

children.push(heading3('Surgical Options'));
children.push(bullet('Surgical ablation/aneurysmectomy for scar-related VT'));
children.push(bullet('Surgical disconnection of accessory pathway in WPW (historical; now replaced by catheter ablation)'));

children.push(noteBox('ICD indications (exam): EF ≤ 35% + NYHA II-III on optimal medical therapy for ≥ 3 months (primary prevention). Survivor of VF/cardiac arrest (secondary prevention).'));
children.push(divider());

// EXAMPLE
children.push(heading2('11. CLINICAL EXAMPLE'));
children.push(new Paragraph({
  children: [new TextRun({ text: 'Case Vignette:', bold: true, size: 22, color: '2E75B6' })],
  spacing: { before: 80, after: 40 },
}));
children.push(body('A 62-year-old man with known anterior MI 3 years ago presents with sudden-onset palpitations and presyncope. HR 160 bpm. BP 85/60 mmHg. ECG shows broad QRS (0.18 s), positive concordance in V1-V6, AV dissociation.'));
children.push(body('Diagnosis: Monomorphic VT — haemodynamically unstable.'));
children.push(body('Management:', true));
children.push(bullet('Immediate IV sedation (Midazolam 2.5mg IV)'));
children.push(bullet('Synchronised DC cardioversion — 100J biphasic'));
children.push(bullet('Post-cardioversion: IV Amiodarone infusion'));
children.push(bullet('Assess EF (Echo) → if EF ≤ 35% → ICD'));
children.push(bullet('Optimise medical therapy: BB, ACEi, Aldosterone antagonist'));

children.push(pageBreak());

// =================== QUESTION 2 ===================
children.push(new Paragraph({
  children: [new TextRun({ text: 'QUESTION 2', bold: true, size: 32, color: 'FFFFFF' })],
  alignment: AlignmentType.CENTER,
  shading: { type: ShadingType.SOLID, color: '1F3864', fill: '1F3864' },
  spacing: { before: 200, after: 0 },
}));
children.push(new Paragraph({
  children: [new TextRun({ text: 'Pathophysiology of Acute Coronary Syndrome with Physiology of Coagulation', bold: true, size: 28, color: 'FFFFFF' })],
  alignment: AlignmentType.CENTER,
  shading: { type: ShadingType.SOLID, color: '2E75B6', fill: '2E75B6' },
  spacing: { before: 0, after: 300 },
}));

// INTRODUCTION
children.push(heading2('1. INTRODUCTION & SPECTRUM OF ACS'));
children.push(body('Acute Coronary Syndrome (ACS) is a spectrum of clinical conditions from unstable angina (UA) to NSTEMI and STEMI, all sharing the same underlying mechanism: acute disruption of a coronary artery atherosclerotic plaque leading to thrombus formation and myocardial ischaemia.'));

const acsSpectrum = [
  ['Unstable Angina (UA)', 'No troponin rise, no ST elevation', 'Partial occlusion; no necrosis', 'Non-occlusive thrombus'],
  ['NSTEMI', 'Troponin RISE, no persistent ST elevation', 'Subendocardial necrosis', 'Non-occlusive / occlusive with collaterals'],
  ['STEMI', 'Troponin RISE + persistent ST elevation (>20 min)', 'Transmural necrosis', 'Occlusive thrombus'],
];
children.push(makeTable(['Type', 'Biomarkers / ECG', 'Pathology', 'Thrombus Type'], acsSpectrum, [20, 30, 25, 25]));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));

// NORMAL CORONARY ARTERY
children.push(heading2('2. NORMAL CORONARY ARTERY vs ATHEROSCLEROSIS'));
children.push(boldBullet('Intima', 'Single layer of endothelium resting on basal lamina. Key barrier.'));
children.push(boldBullet('Media', 'Smooth muscle cells — maintain vasomotor tone.'));
children.push(boldBullet('Adventitia', 'Outer connective tissue layer.'));
children.push(body('Healthy endothelium: anti-thrombotic, anti-inflammatory, produces NO (vasodilator) and prostacyclin (anti-platelet).'));

// ATHEROSCLEROSIS DEVELOPMENT
children.push(heading2('3. ATHEROSCLEROSIS — STEP BY STEP PATHOGENESIS'));
children.push(heading3('Flowchart 3: Formation of Atherosclerotic Plaque'));
children.push(new Paragraph({ spacing: { before: 80, after: 0 } }));
children.push(flowRow('RISK FACTORS: Hypertension, Dyslipidaemia, Diabetes, Smoking, Obesity, Family History'));
children.push(flowArrow());
children.push(flowRow('ENDOTHELIAL DYSFUNCTION — Loss of protective barrier; reduced NO; increased ICAM-1, VCAM-1'));
children.push(flowArrow());
children.push(flowRow('LDL enters intima → OXIDISED LDL (oxLDL) by reactive oxygen species'));
children.push(flowArrow());
children.push(flowRow('oxLDL → Monocyte recruitment via MCP-1 → Differentiation to MACROPHAGES'));
children.push(flowArrow());
children.push(flowRow('Macrophages engulf oxLDL via Scavenger Receptors → FOAM CELLS → FATTY STREAK'));
children.push(flowArrow());
children.push(flowRow('Smooth Muscle Cell migration from media → Collagen secretion → FIBROUS CAP'));
children.push(flowArrow());
children.push(flowRow('FIBROUS PLAQUE: Fibrous cap + Lipid core + Inflammatory cells + Calcification'));
children.push(new Paragraph({ spacing: { before: 80, after: 200 } }));

// PLAQUE VULNERABILITY
children.push(heading2('4. VULNERABLE PLAQUE — KEY CONCEPT'));
children.push(body('Not all plaques are equal. The VULNERABLE PLAQUE is the one that precipitates ACS.'));
const plaqueRows = [
  ['Stable Plaque', 'Thick fibrous cap', 'Small lipid core', 'Few inflammatory cells', 'Causes stable angina when stenosis > 70%'],
  ['Vulnerable Plaque', 'THIN fibrous cap (< 65 μm)', 'LARGE necrotic lipid core (> 40% of plaque volume)', 'Many macrophages / T cells', 'Ruptures at stenosis often < 50% — "non-flow-limiting"'],
];
children.push(makeTable(['Type', 'Cap', 'Core', 'Inflammation', 'Clinical Impact'], plaqueRows, [20, 20, 20, 20, 20]));
children.push(new Paragraph({ spacing: { before: 100, after: 100 } }));
children.push(noteBox('Key exam point: 2/3 of AMI culprit lesions had < 50% stenosis prior to rupture — unstable plaques, not the most severely stenosed!'));

// TRIGGERS OF PLAQUE RUPTURE
children.push(heading2('5. TRIGGERS OF PLAQUE RUPTURE'));
children.push(boldBullet('Intrinsic factors', 'Thin fibrous cap; large necrotic core; MMP activity by macrophages (degrade collagen); high lipid content'));
children.push(boldBullet('Extrinsic factors', 'High shear stress at plaque shoulder; systemic inflammation (CRP, IL-6, TNF); sympathetic surges (morning peak)'));
children.push(boldBullet('Plaque erosion', 'NO RUPTURE — endothelial cell apoptosis/loss exposes subendothelial matrix; more common in women, younger patients, smokers'));
children.push(boldBullet('MMP (Matrix Metalloproteinases)', 'Collagenases elaborated by macrophages that degrade Type I/III collagen in fibrous cap → destabilise plaque'));

children.push(divider());

// PHYSIOLOGY OF COAGULATION (DETAILED)
children.push(heading2('6. PHYSIOLOGY OF COAGULATION — DETAILED'));
children.push(body('Coagulation is the process by which soluble fibrinogen is converted to insoluble fibrin, forming a stable clot. It involves PRIMARY hemostasis (platelet plug) and SECONDARY hemostasis (coagulation cascade).'));

children.push(heading3('A. Primary Haemostasis — The Platelet Plug'));
children.push(heading3('Flowchart 4: Primary Haemostasis'));
children.push(new Paragraph({ spacing: { before: 80, after: 0 } }));
children.push(flowRow('VASCULAR INJURY → Subendothelial collagen & vWF EXPOSED'));
children.push(flowArrow());
children.push(flowRow('Platelet GpIb binds vWF → PLATELET ADHESION'));
children.push(flowArrow());
children.push(flowRow('PLATELET ACTIVATION: Shape change (disc → spiky spheroid) + Granule release'));
children.push(new Paragraph({
  children: [
    new TextRun({ text: 'Dense granules: ADP, Serotonin (5-HT), Ca²⁺   |   Alpha granules: Fibrinogen, vWF, P-selectin, Factor V', size: 20 }),
  ],
  alignment: AlignmentType.CENTER,
  shading: { type: ShadingType.SOLID, color: 'E8F4FD', fill: 'E8F4FD' },
  spacing: { before: 20, after: 20 },
}));
children.push(flowArrow());
children.push(flowRow('ADP + TXA₂ → GpIIb-IIIa receptor conformational change → Fibrinogen bridges platelets'));
children.push(flowArrow());
children.push(flowRow('PRIMARY HAEMOSTATIC PLUG formed (fragile, platelet-rich, "white clot")'));
children.push(new Paragraph({ spacing: { before: 80, after: 200 } }));

children.push(heading3('Platelet Activation Pathways (Summary)'));
const plateletRows = [
  ['Collagen', 'GPVI receptor', 'Adhesion, TXA₂ generation, platelet activation'],
  ['ADP', 'P2Y1 (Gq) + P2Y12 (Gi)', 'Amplifies aggregation; P2Y12 is target of Clopidogrel/Ticagrelor'],
  ['Thromboxane A₂ (TXA₂)', 'TP receptor', 'Potent platelet activator & vasoconstrictor; target of Aspirin'],
  ['Thrombin', 'PAR-1 + PAR-4 (protease-activated)', 'Most potent physiologic platelet activator'],
  ['Epinephrine', 'α2-adrenergic receptor', 'Synergistic activator'],
];
children.push(makeTable(['Agonist', 'Receptor', 'Effect'], plateletRows, [25, 35, 40]));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));

children.push(heading3('B. Secondary Haemostasis — The Coagulation Cascade'));
children.push(body('The coagulation cascade generates THROMBIN (Factor IIa), which converts fibrinogen to fibrin, consolidating the platelet plug.'));
children.push(new Paragraph({ spacing: { before: 80, after: 0 } }));

children.push(flowRow('TISSUE FACTOR (TF/Factor III) Exposed at injury site (subendothelial cells: fibroblasts, smooth muscle cells)'));
children.push(flowArrow());
children.push(flowRow('TF + Factor VIIa → TF-VIIa Complex (Extrinsic Tenase)'));
children.push(flowArrow());
children.push(flowRow('TF-VIIa activates Factor X → Xa   AND   Factor IX → IXa'));
children.push(flowArrow());
children.push(flowRow('INTRINSIC PATHWAY: Factor IXa + VIIIa (Intrinsic Tenase) → more Factor Xa'));
children.push(new Paragraph({
  children: [new TextRun({ text: '       (Contact activation XII → XI → IX supplements but NOT essential in vivo)', size: 20, color: '595959' })],
  spacing: { before: 10, after: 10 },
}));
children.push(flowArrow());
children.push(flowRow('COMMON PATHWAY: Factor Xa + Va (Prothrombinase complex) → Prothrombin (II) → THROMBIN (IIa)'));
children.push(flowArrow());
children.push(flowRow('THROMBIN: Fibrinogen → Fibrin monomers → Fibrin polymer + Factor XIII → CROSSLINKED FIBRIN CLOT'));
children.push(new Paragraph({ spacing: { before: 80, after: 200 } }));

// KEY COAGULATION FACTORS TABLE
children.push(heading3('Key Coagulation Factors'));
const factorRows = [
  ['I', 'Fibrinogen', 'Substrate for fibrin formation', 'PT, aPTT'],
  ['II', 'Prothrombin', 'Becomes Thrombin (IIa)', 'PT, aPTT'],
  ['III', 'Tissue Factor', 'Initiates extrinsic pathway', '-'],
  ['IV', 'Calcium (Ca²⁺)', 'Cofactor for multiple steps', '-'],
  ['V', 'Labile factor (Cofactor)', 'Accelerates Xa → IIa conversion', 'PT, aPTT'],
  ['VII', 'Proconvertin', 'Extrinsic pathway; shortest half-life', 'PT only'],
  ['VIII', 'Anti-haemophilic factor A', 'Cofactor for IXa; deficient in Haemophilia A', 'aPTT only'],
  ['IX', 'Christmas factor', 'Intrinsic tenase; deficient in Haemophilia B', 'aPTT only'],
  ['X', 'Stuart-Prower factor', 'Common pathway — prothrombinase complex', 'PT, aPTT'],
  ['XI', 'PTA', 'Contact activation pathway', 'aPTT only'],
  ['XII', 'Hageman factor', 'Contact activation; not essential in vivo', 'aPTT only'],
  ['XIII', 'Fibrin stabilising factor', 'Crosslinks fibrin monomers', 'Neither (special test)'],
];
children.push(makeTable(['Factor', 'Name', 'Function', 'Lab Test'], factorRows, [10, 25, 45, 20]));
children.push(new Paragraph({ spacing: { before: 100, after: 100 } }));
children.push(noteBox('Vitamin K-dependent factors: II, VII, IX, X (+ Protein C, S). Remember: "1972" → factors 1, 9, 7, 2 (reverse) or mnemonic "Ten Two Nine Seven."'));

// ANTICOAGULANT MECHANISMS
children.push(heading3('C. Natural Anticoagulant Mechanisms'));
children.push(boldBullet('Antithrombin III (AT-III)', 'Inhibits Thrombin, Xa, IXa, XIa, XIIa. Enhanced 1000x by Heparin (clinical use!).'));
children.push(boldBullet('Protein C + Protein S', 'Vitamin K-dependent. Thrombomodulin-Thrombin complex activates Protein C → inactivates Va and VIIIa.'));
children.push(boldBullet('Tissue Factor Pathway Inhibitor (TFPI)', 'Inhibits TF-VIIa complex and Xa. Limits extent of extrinsic pathway activation.'));
children.push(boldBullet('Fibrinolysis (t-PA / u-PA)', 'Endothelial cells release t-PA → Plasminogen → PLASMIN → digests fibrin → FDPs/D-dimers.'));
children.push(noteBox('Heparin works via AT-III (enhances it). Warfarin inhibits Vitamin K epoxide reductase → reduces II, VII, IX, X, Protein C & S.'));

children.push(divider());

// LINKING COAGULATION TO ACS
children.push(heading2('7. HOW COAGULATION CAUSES ACS — INTEGRATED PATHOPHYSIOLOGY'));
children.push(heading3('Flowchart 5: Integrated ACS Pathophysiology'));
children.push(new Paragraph({ spacing: { before: 80, after: 0 } }));
children.push(flowRow('CHRONIC ATHEROSCLEROSIS: Vulnerable Plaque in Coronary Artery'));
children.push(flowArrow());
children.push(flowRow('TRIGGER: Haemodynamic stress / Inflammation / MMP activation'));
children.push(flowArrow());
children.push(flowRow('PLAQUE RUPTURE or EROSION → Subendothelial collagen + Tissue Factor EXPOSED to flowing blood'));
children.push(flowArrow());
children.push(flowRow('PRIMARY HAEMOSTASIS: Platelet adhesion (GpIb-vWF) → Activation → GpIIb-IIIa → Platelet aggregation'));
children.push(flowArrow());
children.push(flowRow('SECONDARY HAEMOSTASIS: TF → Extrinsic pathway → Thrombin → Fibrin → THROMBUS'));
children.push(flowArrow());
children.push(flowDiamond('DEGREE OF OCCLUSION?'));
children.push(new Paragraph({
  children: [
    new TextRun({ text: 'Partial → NSTEMI/UA          |          Complete → STEMI', bold: true, size: 22, color: '1F3864' }),
  ],
  alignment: AlignmentType.CENTER,
  spacing: { before: 40, after: 40 },
}));
children.push(flowArrow());
children.push(flowRow('Myocardial Ischaemia → Necrosis → Troponin release → Cardiac biomarker elevation'));
children.push(new Paragraph({ spacing: { before: 80, after: 200 } }));

// CONSEQUENCES OF ISCHAEMIA
children.push(heading2('8. CELLULAR CONSEQUENCES OF ISCHAEMIA'));
const ischemiaRows = [
  ['0-2 min', 'ATP depletion begins; K⁺ efflux; Na⁺/Ca²⁺ influx starts', 'Reversible; contractile dysfunction'],
  ['2-20 min', 'Cellular swelling; glycogen depletion; anaerobic glycolysis; lactic acid', 'Reversible with reperfusion'],
  ['20-40 min', 'Irreversible injury threshold; mitochondrial dysfunction; Ca²⁺ overload', 'POINT OF NO RETURN'],
  ['> 1 hour', 'Coagulation necrosis begins; myocyte death; enzyme release (Troponin, CK-MB)', 'Transmural necrosis if sustained'],
  ['6-24 hours', 'Neutrophil infiltration; early inflammatory changes', 'Macroscopic infarct area visible'],
  ['1-3 days', 'Macrophage infiltration; phagocytosis of dead cells', 'Infarct expansion risk'],
  ['1-2 weeks', 'Granulation tissue; collagen deposition begins', 'Remodelling phase'],
  ['Weeks-months', 'Dense fibrous scar formation', 'Completed healing / dysfunction'],
];
children.push(makeTable(['Time', 'Cellular Event', 'Clinical Significance'], ischemiaRows, [18, 47, 35]));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));

// BIOMARKERS
children.push(heading2('9. CARDIAC BIOMARKERS IN ACS'));
const biomarkerRows = [
  ['Cardiac Troponin I/T (cTnI/T)', '3-6 hrs', '12-24 hrs', '7-14 days', 'GOLD STANDARD; most sensitive & specific; detected by hs-Troponin assay at 1 hr'],
  ['CK-MB', '3-6 hrs', '12-24 hrs', '48-72 hrs', 'Reinfarction detection (early return); less specific than troponin'],
  ['Myoglobin', '1-3 hrs', '6-9 hrs', '24-36 hrs', 'Earliest marker; NOT cardiac specific; useful for EARLY RULE-OUT'],
  ['LDH (LDH1)', '24-48 hrs', '3-6 days', '14 days', 'Historical; LDH1 > LDH2 ("flip") = MI. Rarely used now.'],
];
children.push(makeTable(['Marker', 'Rises At', 'Peaks At', 'Returns to Normal', 'Notes'], biomarkerRows, [25, 12, 13, 20, 30]));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));
children.push(noteBox('h-Troponin (high-sensitivity): Rise ≥ 5 ng/L within 1 hour = high-sensitivity protocol. HEART Score > 6 = high risk ACS.'));

// MANAGEMENT OF ACS
children.push(heading2('10. MANAGEMENT OF ACS — OVERVIEW'));
children.push(heading3('A. General Initial Management (ALL ACS)'));
children.push(bullet('Aspirin 300 mg loading (irreversibly inhibits COX-1 → reduces TXA₂ → anti-platelet)'));
children.push(bullet('P2Y12 Inhibitor loading: Ticagrelor 180 mg OR Clopidogrel 300-600 mg (dual antiplatelet therapy — DAPT)'));
children.push(bullet('Anticoagulation: Heparin (UFH IV) or LMWH (enoxaparin SC) or Fondaparinux'));
children.push(bullet('Nitrates: GTN sublingual / IV for pain + vasodilation'));
children.push(bullet('Oxygen: if O₂ saturation < 94%'));
children.push(bullet('Morphine: cautiously (may reduce drug absorption)'));
children.push(bullet('Beta-blockers: if no contraindications (reduces myocardial O₂ demand)'));

children.push(heading3('B. STEMI — Reperfusion Strategy'));
children.push(boldBullet('Primary PCI (PPCI)', 'Preferred if door-to-balloon time < 90 min (or < 120 min from first medical contact). Gold standard.'));
children.push(boldBullet('Thrombolysis (Fibrinolysis)', 'If PPCI not available within 120 min. Use Tenecteplase or Streptokinase. Benefit if given within 12 hours of symptom onset.'));
children.push(boldBullet('Post-PCI care', 'DAPT for 12 months; Statin (high-intensity); ACEi/ARB; Eplerenone if EF ≤ 40%; ICD if EF remains ≤ 35% at 40 days'));

children.push(heading3('C. NSTEMI/UA — Risk Stratification & Management'));
children.push(boldBullet('High Risk (TIMI ≥ 3, GRACE > 140)', 'Early invasive strategy within 24 hours (PCI)'));
children.push(boldBullet('Intermediate Risk', 'Invasive strategy within 25-72 hours'));
children.push(boldBullet('Low Risk', 'Medical management; non-invasive stress test'));

// ANTIPLATELET / ANTICOAGULANT TABLE
children.push(heading3('D. Antiplatelet & Anticoagulant Drugs in ACS'));
const antiRows = [
  ['Aspirin', 'COX-1 inhibitor → ↓TXA₂', 'All ACS (loading + maintenance)', 'Bleeding, GI upset'],
  ['Clopidogrel', 'P2Y12 (ADP receptor) blocker — irreversible prodrug', 'DAPT with Aspirin', 'Slow onset; variable response (CYP2C19)'],
  ['Ticagrelor', 'P2Y12 blocker — direct, reversible', 'Preferred over Clopidogrel (PLATO trial)', 'Dyspnoea (bradycardia via adenosine)'],
  ['Prasugrel', 'P2Y12 blocker — irreversible prodrug (faster)', 'STEMI with known anatomy', 'Higher bleeding risk (avoid in stroke/TIA)'],
  ['Abciximab / Eptifibatide', 'GpIIb-IIIa inhibitor', 'Adjunct during PCI (high thrombus burden)', 'Major bleeding'],
  ['UFH (Unfractionated Heparin)', 'AT-III → inhibits Thrombin + Xa', 'During PCI; Dose by aPTT', 'HIT, variable dosing'],
  ['LMWH (Enoxaparin)', 'AT-III → mainly anti-Xa', 'NSTEMI/UA; predictable dosing', 'No HIT antidote'],
  ['Fondaparinux', 'Selective anti-Xa', 'NSTEMI/UA preferred (OASIS-5)', 'Do NOT use as sole agent during PCI'],
  ['Bivalirudin', 'Direct Thrombin Inhibitor', 'Alternative to Heparin during PCI', 'Lower bleeding vs Heparin+GPIIb/IIIa'],
];
children.push(makeTable(['Drug', 'Mechanism', 'Indication in ACS', 'Key Side Effects'], antiRows, [20, 25, 25, 30]));
children.push(new Paragraph({ spacing: { before: 100, after: 200 } }));

// PATHOPHYSIOLOGY INTEGRATION DIAGRAM
children.push(heading2('11. INTEGRATED SUMMARY DIAGRAM'));
children.push(heading3('Flowchart 6: ACS Pathophysiology to Management — At a Glance'));
children.push(new Paragraph({ spacing: { before: 80, after: 0 } }));
children.push(flowRow('RISK FACTORS (HTN + DM + Dyslipidaemia + Smoking + Obesity)'));
children.push(flowArrow());
children.push(flowRow('ATHEROSCLEROSIS: Foam cells → Fatty streak → Fibrous plaque → Vulnerable plaque'));
children.push(flowArrow());
children.push(flowRow('PLAQUE RUPTURE / EROSION (MMP activity, thin cap, large core)'));
children.push(flowArrow());
children.push(flowRow('COAGULATION CASCADE ACTIVATED: Primary (platelet plug) + Secondary (fibrin clot)'));
children.push(flowArrow());
children.push(flowDiamond('COMPLETE OCCLUSION?'));
children.push(new Paragraph({
  children: [
    new TextRun({ text: 'YES = STEMI (transmural MI)      |      NO = NSTEMI or UA', bold: true, size: 22, color: '1F3864' }),
  ],
  alignment: AlignmentType.CENTER,
  spacing: { before: 40, after: 40 },
}));
children.push(flowArrow());
children.push(flowRow('TREATMENT: DAPT + Anticoagulation + Reperfusion (PPCI or Thrombolysis for STEMI)'));
children.push(flowArrow());
children.push(flowRow('LONG-TERM: BB + Statin + ACEi/ARB + DAPT 12 months + ICD if EF ≤ 35%'));
children.push(new Paragraph({ spacing: { before: 80, after: 200 } }));

// COMPLICATIONS
children.push(heading2('12. COMPLICATIONS OF ACS (EXAM KEY POINTS)'));
const compRows = [
  ['< 24 hours', 'Arrhythmias', 'VF, VT (most common cause of death early); AF; Bradyarrhythmias (inferior MI — AV block)'],
  ['1-3 days', 'Acute LV failure / Cardiogenic Shock', 'Loss > 40% myocardium; IABP / Mechanical support'],
  ['2-5 days', 'Myocardial rupture — Free wall', 'Sudden haemopericardium & tamponade — fatal'],
  ['3-7 days', 'Papillary muscle rupture', 'Acute severe MR, pulmonary oedema, emergency surgery'],
  ['3-14 days', 'VSR (Ventricular Septal Rupture)', 'New loud pansystolic murmur; haemodynamic collapse'],
  ['Days-weeks', 'Pericarditis', 'Dressler syndrome at 2-10 weeks (immune-mediated)'],
  ['Weeks-months', 'LV Remodelling / Aneurysm', 'Persistent ST elevation; mural thrombus → embolism; HF'],
];
children.push(makeTable(['Time', 'Complication', 'Notes'], compRows, [18, 30, 52]));

children.push(new Paragraph({ spacing: { before: 100, after: 100 } }));
children.push(noteBox('Dressler Syndrome: Post-MI pericarditis at 2-10 weeks. Autoimmune. Treat with NSAIDs/Aspirin. Avoid corticosteroids (impairs scar healing).'));
children.push(noteBox('Rupture sequence: Free wall (1-3 days peak) → Papillary muscle (3-7 days) → Ventricular septum (3-14 days).'));

children.push(divider());

// FINAL SUMMARY TABLE
children.push(heading2('13. QUICK REVISION: KEY POINTS FOR EXAM'));
children.push(bullet('Broad QRS tachycardia (> 120 ms + HR > 100): always treat as VT unless proven otherwise'));
children.push(bullet('Brugada criteria — best algorithm for VT diagnosis; 4 steps'));
children.push(bullet('VT management: unstable → DC cardioversion; stable → Amiodarone IV'));
children.push(bullet('TdP = polymorphic VT + QT prolongation → MgSO4 IV is DOC'));
children.push(bullet('WPW + AF → CONTRAINDICATED: Adenosine, Verapamil, Digoxin; use Procainamide/DC cardioversion'));
children.push(bullet('ACS mechanism: Vulnerable plaque rupture → TF exposed → Coagulation → Thrombus → Ischaemia'));
children.push(bullet('Vitamin K factors: II, VII, IX, X → remember "1972" or "Ten Two Nine Seven"'));
children.push(bullet('Primary haemostasis = platelet plug (GpIb-vWF adhesion, GpIIb-IIIa aggregation)'));
children.push(bullet('Secondary haemostasis = coagulation cascade → Thrombin → Fibrin clot'));
children.push(bullet('t-PA mechanism: Plasminogen → Plasmin → Fibrin degradation → FDPs + D-dimers'));
children.push(bullet('STEMI: Primary PCI < 90 min; else Thrombolysis if < 12 h symptom onset'));
children.push(bullet('Post-ACS: DAPT 12 months + High-intensity Statin + ACEi + BB + Aldosterone antagonist if EF ≤ 40%'));

// References
children.push(divider());
children.push(new Paragraph({
  children: [new TextRun({ text: 'SOURCES & REFERENCES', bold: true, size: 24, color: '1F3864' })],
  spacing: { before: 200, after: 100 },
}));
children.push(bullet('Robbins & Kumar Basic Pathology — Hemostasis, Thrombosis, Acute Coronary Syndrome, Myocardial Infarction'));
children.push(bullet("Rosen's Emergency Medicine — Broad Complex Tachycardia, Brugada Algorithm, Ventricular Tachycardia Management"));
children.push(bullet("Braunwald's Heart Disease — VT vs SVT differentiation, Pre-excitation, WPW"));
children.push(bullet("Goldman-Cecil Medicine — ACS Pathophysiology, Plaque Rupture, Anticoagulation"));
children.push(bullet("Lippincott Illustrated Reviews Pharmacology — ACS drugs, Coagulation"));
children.push(bullet("Fuster & Hurst's The Heart — Thin-cap fibroatheroma, Plaque Rupture"));

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cd /home/daytona/workspace/md-medicine-notes && node create_notes.js 2>&1

~/md-medicine-notes/create_notes.js

Successfully replaced 1 instance(s) of the string in '/home/daytona/workspace/md-medicine-notes/create_notes.js'

cd /home/daytona/workspace/md-medicine-notes && node create_notes.js 2>&1

ls -lh /home/daytona/workspace/md-medicine-notes/ && python /home/daytona/worksp…

python3 -c " import zipfile with zipfile.ZipFile('/home/daytona/workspace/md-med…