"single ventricle" AND "ICU management" AND "Fontan"

"single ventricle" AND "postoperative" AND "hemodynamics"

"protein-losing enteropathy" AND "Fontan"

mkdir -p /home/daytona/workspace/single-ventricle-pptx && ls /home/daytona/works…

~/single-ventricle-pptx/build.js

const pptxgen = require("pptxgenjs");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Single Ventricle Physiology: ICU Management";
pres.author = "PICU Education";

// ── COLOUR PALETTE ──────────────────────────────────────────────────────────
const BG_DARK   = "0A1628";   // deep navy  – title / section dividers
const BG_MID    = "0E2240";   // mid navy   – content bg
const BG_LIGHT  = "F4F7FC";   // off-white  – body slides
const ACCENT1   = "E84855";   // vivid red  – danger / warnings
const ACCENT2   = "3CB4E7";   // sky blue   – key concepts
const ACCENT3   = "F6AE2D";   // amber      – stage highlights
const WHITE     = "FFFFFF";
const BODY_TXT  = "1A2540";
const SUB_TXT   = "4A5C7A";
const FONT      = "Calibri";

// ── HELPER FUNCTIONS ─────────────────────────────────────────────────────────

function titleSlide(title, subtitle) {
  const s = pres.addSlide();
  // dark background
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  // left accent bar
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.18, h:5.625, fill:{color:ACCENT1}, line:{color:ACCENT1} });
  // title
  s.addText(title, {
    x:0.4, y:1.4, w:9.2, h:1.4,
    fontFace:FONT, fontSize:36, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });
  // subtitle
  s.addText(subtitle, {
    x:0.4, y:3.1, w:9.2, h:0.8,
    fontFace:FONT, fontSize:20, color:ACCENT2, align:"left", valign:"middle", margin:0
  });
  // bottom bar
  s.addShape(pres.ShapeType.rect, { x:0, y:5.3, w:10, h:0.325, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText("PICU Education  |  July 2026", {
    x:0.4, y:5.28, w:9, h:0.33,
    fontFace:FONT, fontSize:10, color:WHITE, align:"right", valign:"middle", margin:0
  });
  return s;
}

function sectionDivider(num, title, subtitle) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_MID}, line:{color:BG_MID} });
  s.addShape(pres.ShapeType.rect, { x:0, y:2.4, w:10, h:0.08, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText(`SECTION ${num}`, {
    x:0.5, y:0.9, w:9, h:0.5,
    fontFace:FONT, fontSize:13, bold:true, color:ACCENT3, align:"left", charSpacing:5, margin:0
  });
  s.addText(title, {
    x:0.5, y:1.5, w:9, h:1.2,
    fontFace:FONT, fontSize:30, bold:true, color:WHITE, align:"left", margin:0
  });
  s.addText(subtitle, {
    x:0.5, y:2.8, w:9, h:0.8,
    fontFace:FONT, fontSize:16, color:ACCENT2, align:"left", margin:0
  });
  return s;
}

function contentSlide(title, bullets, notes, opts = {}) {
  const s = pres.addSlide();
  // bg
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_LIGHT}, line:{color:BG_LIGHT} });
  // top title bar
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.82, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.82, w:10, h:0.06, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText(title, {
    x:0.35, y:0, w:9.3, h:0.82,
    fontFace:FONT, fontSize:20, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });

  // build bullet array
  const items = bullets.map((b, i) => {
    if (typeof b === "string") {
      return { text: b, options: { bullet: { type:"bullet", indent:15 }, color:BODY_TXT, fontSize:17, fontFace:FONT, breakLine: i < bullets.length-1 } };
    } else {
      // {text, sub, color}
      const parts = [];
      parts.push({ text: b.text, options: { bold:true, bullet:{type:"bullet", indent:15}, color: b.color||BODY_TXT, fontSize:17, fontFace:FONT, breakLine:true } });
      if (b.sub) {
        b.sub.forEach((ss, si) => {
          parts.push({ text: "    " + ss, options: { bullet:false, color:SUB_TXT, fontSize:14, fontFace:FONT, italic:true, breakLine: si < b.sub.length-1 || i < bullets.length-1 } });
        });
      }
      return parts;
    }
  }).flat();

  s.addText(items, { x:0.35, y:1.05, w:9.3, h:4.3, valign:"top", margin:4 });

  if (notes) s.addNotes(notes);
  if (opts.tag) {
    s.addText(opts.tag, {
      x:7.8, y:5.1, w:2, h:0.38,
      fontFace:FONT, fontSize:10, color:WHITE, align:"center", valign:"middle",
      fill:{ color: opts.tagColor||ACCENT1 }, margin:2
    });
  }
  return s;
}

function twoColSlide(title, leftItems, rightItems, leftHead, rightHead, notes) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_LIGHT}, line:{color:BG_LIGHT} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.82, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.82, w:10, h:0.06, fill:{color:ACCENT3}, line:{color:ACCENT3} });
  s.addText(title, {
    x:0.35, y:0, w:9.3, h:0.82,
    fontFace:FONT, fontSize:20, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });
  // divider
  s.addShape(pres.ShapeType.line, { x:5.05, y:1.0, w:0, h:4.4, line:{color:ACCENT2, width:1.5, dashType:"solid"} });

  // LEFT col header
  s.addShape(pres.ShapeType.rect, { x:0.3, y:1.0, w:4.5, h:0.42, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText(leftHead, { x:0.3, y:1.0, w:4.5, h:0.42, fontFace:FONT, fontSize:13, bold:true, color:WHITE, align:"center", valign:"middle", margin:0 });
  const leftArr = leftItems.map((b,i)=>({ text:b, options:{ bullet:{type:"bullet",indent:12}, color:BODY_TXT, fontSize:15, fontFace:FONT, breakLine:i<leftItems.length-1 } }));
  s.addText(leftArr, { x:0.3, y:1.5, w:4.6, h:3.8, valign:"top", margin:3 });

  // RIGHT col header
  s.addShape(pres.ShapeType.rect, { x:5.2, y:1.0, w:4.5, h:0.42, fill:{color:ACCENT1}, line:{color:ACCENT1} });
  s.addText(rightHead, { x:5.2, y:1.0, w:4.5, h:0.42, fontFace:FONT, fontSize:13, bold:true, color:WHITE, align:"center", valign:"middle", margin:0 });
  const rightArr = rightItems.map((b,i)=>({ text:b, options:{ bullet:{type:"bullet",indent:12}, color:BODY_TXT, fontSize:15, fontFace:FONT, breakLine:i<rightItems.length-1 } }));
  s.addText(rightArr, { x:5.2, y:1.5, w:4.6, h:3.8, valign:"top", margin:3 });

  if (notes) s.addNotes(notes);
  return s;
}

function tableSlide(title, headers, rows, notes) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_LIGHT}, line:{color:BG_LIGHT} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.82, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.82, w:10, h:0.06, fill:{color:ACCENT3}, line:{color:ACCENT3} });
  s.addText(title, {
    x:0.35, y:0, w:9.3, h:0.82,
    fontFace:FONT, fontSize:20, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });

  const colW = 9.3 / headers.length;
  const tableRows = [
    headers.map(h => ({ text: h, options: { bold:true, color:WHITE, fontSize:13, fontFace:FONT, fill:{color:BG_MID}, align:"center" } })),
    ...rows.map((row, ri) => row.map(cell => ({
      text: cell,
      options: { color:BODY_TXT, fontSize:13, fontFace:FONT, fill:{ color: ri%2===0 ? "EDF3FB" : WHITE }, align:"left" }
    })))
  ];
  s.addTable(tableRows, {
    x:0.35, y:1.0, w:9.3,
    border:{ pt:0.5, color:"CCDDEE" },
    rowH: 0.48
  });

  if (notes) s.addNotes(notes);
  return s;
}

// ════════════════════════════════════════════════════════════════════════════
// SLIDE CONTENT
// ════════════════════════════════════════════════════════════════════════════

// ── SLIDE 1: TITLE ─────────────────────────────────────────────────────────
titleSlide(
  "Single Ventricle Physiology\nICU Management",
  "A Practical Guide for PICU Fellows & Residents  |  All Stages S1 → S2 → S3"
);

// ── SLIDE 2: AGENDA ────────────────────────────────────────────────────────
contentSlide("Session Agenda", [
  { text:"1. Anatomy & spectrum of single ventricle lesions", sub:["HLHS, tricuspid atresia, double-inlet LV, heterotaxy"] },
  { text:"2. Core physiology: the parallel circulation problem", sub:["Qp:Qs ratio, O₂ saturation targets, mixing lesions"] },
  { text:"3. Stage 1 ICU management — Norwood/Sano period", sub:["Balancing pulmonary vs systemic flow; low CO crisis"] },
  { text:"4. Stage 2 ICU management — Bidirectional Glenn", sub:["Passive pulmonary flow; ventilation strategies"] },
  { text:"5. Stage 3 / Fontan ICU management", sub:["Fontan physiology; failing Fontan"] },
  { text:"6. Specific complications across all stages", sub:["Low CO, arrhythmias, protein-losing enteropathy, plastic bronchitis"] },
  { text:"7. End-stage & transplant considerations" }
],
"Walk through the agenda briskly — 1 minute max. Emphasize that all three stages require fundamentally different hemodynamic management. About 20 slides for 20 minutes = ~1 min per slide, with a 3-minute discussion at the end.");

// ── SLIDE 3: SECTION 1 ─────────────────────────────────────────────────────
sectionDivider("1", "Anatomy & Spectrum", "What makes a 'single ventricle'?");

// ── SLIDE 4: ANATOMY ───────────────────────────────────────────────────────
contentSlide("Single Ventricle: Anatomy & Spectrum", [
  { text:"Prevalence: ~2 per 10,000 live births (all univentricular lesions combined)", color:ACCENT2 },
  { text:"True vs functional single ventricle", sub:["True: double-inlet LV, double-outlet RV", "Functional: second ventricle present but inadequate"] },
  { text:"Key lesions requiring SV palliation", sub:[
    "HLHS — 1.6/10,000; hypoplastic LV + aorta (most common requiring staged Norwood)",
    "Tricuspid atresia — 1.2/10,000; absent tricuspid valve, hypoplastic RV",
    "Double-inlet LV — both AV valves connect to morphologic LV",
    "Unbalanced AV canal, heterotaxy syndromes"
  ]},
  { text:"Systemic ventricle may be morphologic RV or LV — critical for long-term function", color:ACCENT1 }
],
"Fuster & Hurst Ch.69: 'The single functional ventricle could be morphologically right or left, with the second ventricle usually hypoplastic and/or insufficiently functional for biventricular correction.' HLHS = most common indication for staged SV palliation. Emphasize to fellows: RV as systemic ventricle (as in HLHS) has worse long-term outcomes — less well-suited to chronic systemic afterload. Braunwald's Heart Disease (Ch.82) notes incidences per 10,000 live births for each lesion.",
{ tag:"~1 min", tagColor:BG_MID });

// ── SLIDE 5: SECTION 2 ─────────────────────────────────────────────────────
sectionDivider("2", "Core Physiology", "Mixing, Qp:Qs & O₂ saturation targets");

// ── SLIDE 6: PARALLEL CIRCULATION ─────────────────────────────────────────
contentSlide("The Parallel Circulation Problem", [
  { text:"Normal circulation: series — venous blood → RV → lungs → LV → body", color:BODY_TXT },
  { text:"Single ventricle: PARALLEL — one pump serves both circulations via mixing", color:ACCENT1 },
  { text:"Qp:Qs ratio is the master variable", sub:[
    "Qp:Qs = 1 : ideal (equal flow to both circuits)",
    "Qp:Qs > 1 : pulmonary overcirculation → systemic underperfusion, low CO",
    "Qp:Qs < 1 : cyanosis, but protected systemic flow"
  ]},
  { text:"SpO₂ targets pre-Fontan (Stage 1): 75–85% (NOT 95–100%!)", color:ACCENT1 },
  { text:"Arterial O₂ saturation is a SURROGATE for Qp:Qs balance", sub:[
    "SpO₂ 80–85% → Qp:Qs ~1 → acceptable balance",
    "SpO₂ >90% → pulmonary overcirculation → dangerous"
  ]},
  { text:"Systemic venous saturation (SvO₂) monitors O₂ delivery reserve" }
],
"This is the single most important concept. In a parallel circulation, the single ventricle ejects into BOTH circuits simultaneously. The fraction of output to the lungs (Qp) versus the body (Qs) determines SpO₂. Too much Qp = 'pulmonary steal' with systemic hypoperfusion despite 'normal' sats. Target SpO₂ 75–85% in Stage 1 — not 95%! An SpO₂ >90% in a post-Norwood patient is a warning sign. SvO₂ from the SVC or RA is your best global O₂ delivery monitor — target SvO₂ >55%.",
{ tag:"CORE CONCEPT", tagColor:ACCENT1 });

// ── SLIDE 7: SECTION 3 ─────────────────────────────────────────────────────
sectionDivider("3", "Stage 1 ICU Management", "Post-Norwood / post-Sano  — the most vulnerable period");

// ── SLIDE 8: NORWOOD OVERVIEW ──────────────────────────────────────────────
contentSlide("Stage 1 Palliation: Norwood / Sano Procedure", [
  { text:"Anatomy created:", sub:[
    "Neo-aorta from native PA + aortic arch reconstruction",
    "Atrial septectomy — unobstructed mixing",
    "Source of pulmonary blood flow: modified BT shunt (MBTS) OR Sano (RV-PA conduit)"
  ]},
  { text:"MBTS: lower diastolic BP, coronary steal risk; simpler surgically", color:ACCENT2 },
  { text:"Sano RV-PA conduit: better diastolic BP, coronary perfusion; but RV ventriculotomy scar", color:ACCENT3 },
  { text:"Hybrid approach (ductal stent + PA bands) for high-risk/low-BW neonates", sub:[
    "Avoids CPB in Stage 1, but complicates Stage 2",
    "Miller's Anesthesia: 'hybrid procedures may offer survival advantage in low birth weight neonates'"
  ]}
],
"Miller's Anesthesia (Ch.73): Hybrid approach stents the PDA to maintain systemic flow and surgically banding both PAs to limit pulmonary flow. This avoids CPB risk in neonates <2.5kg but the stage 2 then combines aortic arch reconstruction + Glenn, making it much more complex. HSFC/single center data shows survival advantage for LBW but NOT a low-risk alternative for most HLHS. Sano vs MBTS — SVPCOT trial: similar survival but Sano had better inter-stage survival; MBTS had higher post-op complications in some series.",
{ tag:"STAGE 1", tagColor:ACCENT3 });

// ── SLIDE 9: POST-NORWOOD ICU ──────────────────────────────────────────────
contentSlide("Post-Norwood ICU Management", [
  { text:"Goal: Qp:Qs ≈ 1  |  SpO₂ 75–85%  |  SvO₂ >55%", color:ACCENT1 },
  { text:"Ventilation strategy (powerful Qp:Qs lever)", sub:[
    "↑ FiO₂ → vasodilates pulmonary bed → ↑ Qp → pulmonary overcirculation (AVOID high FiO₂)",
    "↑ CO₂ (permissive hypercapnia, PaCO₂ 45–55) → ↑ PVR → balances Qp",
    "Sub-ambient O₂ (FiO₂ 0.17–0.21) may be used to limit Qp in overcirculation"
  ]},
  { text:"Hemodynamic monitoring", sub:[
    "Near-infrared spectroscopy (NIRS) — regional cerebral + somatic SaO₂",
    "SVC/RA line for mixed venous saturation",
    "LA line for filling pressure assessment"
  ]},
  { text:"Inotropes: dopamine/milrinone (balance CO vs PVR); avoid high-dose catecholamines", sub:[
    "Milrinone: positive inotrope + pulmonary vasodilator — mainstay post-Norwood"
  ]},
  { text:"Watch for: low CO state, shunt thrombosis, pulmonary hypertensive crisis, NEC", color:ACCENT1 }
],
"This is the ICU workhorse slide. Ventilation is YOUR most powerful tool for Qp:Qs in Stage 1. O₂ is a pulmonary vasodilator — increasing FiO₂ drops PVR and increases Qp. In an overcirculating patient (SpO₂ >90%, low BP, poor perfusion): DECREASE FiO₂, allow CO₂ to rise. In an undercirculating patient (SpO₂ <70%, cyanosis, adequate BP): INCREASE FiO₂, hyperventilate slightly. NIRS: cerebral NIRS <50% = cerebral ischemia; somatic NIRS drop suggests NEC or low CO. Shunt thrombosis = acute cyanosis + hemodynamic collapse → heparin infusion typically maintained post-Norwood.",
{ tag:"STAGE 1", tagColor:ACCENT3 });

// ── SLIDE 10: LOW CO CRISIS S1 ─────────────────────────────────────────────
contentSlide("Low Cardiac Output Syndrome — Stage 1", [
  { text:"Definition: inadequate O₂ delivery despite 'acceptable' SpO₂", color:ACCENT1 },
  { text:"Recognition:", sub:[
    "Metabolic acidosis (lactate >3 mmol/L)",
    "SvO₂ < 50%",
    "NIRS <50% (cerebral or somatic)",
    "Oliguria, prolonged capillary refill"
  ]},
  { text:"Causes specific to Stage 1:", sub:[
    "Pulmonary overcirculation (SpO₂ >90%) → systemic steal",
    "Shunt obstruction/thrombosis",
    "Residual arch obstruction",
    "AV valve regurgitation",
    "Tamponade (mediastinal drainage assessment)"
  ]},
  { text:"Management:", sub:[
    "FiO₂ reduction / permissive hypercapnia for overcirculation",
    "Milrinone ± epinephrine for systolic dysfunction",
    "ECMO if refractory — bridge to cath/re-operation",
    "Early surgical re-exploration if residual lesion suspected"
  ]}
],
"The post-Norwood 'interstage' and early post-op period has the highest mortality risk. Key: Qp:Qs balance first, then inotropic support. Do NOT reflexively increase FiO₂ when SpO₂ drops — check the clinical context. If SpO₂ drops AND blood pressure drops AND lactate rises → likely shunt crisis or low CO. If SpO₂ drops AND BP maintained AND no acidosis → may be transient desaturation. ECMO: should be available at all Stage 1 centers. SVPCOT/CHOP data: ECMO rescue after Norwood ~20% survival to discharge — poor but not zero.",
{ tag:"EMERGENCY", tagColor:ACCENT1 });

// ── SLIDE 11: SECTION 4 ────────────────────────────────────────────────────
sectionDivider("4", "Stage 2 ICU Management", "Bidirectional Glenn — passive superior cavopulmonary flow");

// ── SLIDE 12: GLENN PHYSIOLOGY ─────────────────────────────────────────────
contentSlide("Stage 2: Bidirectional Glenn — Physiology & ICU Management", [
  { text:"Anatomy: SVC → right PA (bidirectional = both PAs receive SVC flow)", sub:[
    "Performed ~4–6 months of age; BT shunt/Sano taken down",
    "Blood flow now PASSIVE: no ventricular pump drives pulmonary circulation",
    "Pulmonary flow depends on SVC pressure gradient (= CVP)"
  ]},
  { text:"SpO₂ targets post-Glenn: 75–85% (higher than Stage 1 goal due to IVC mixing)", color:ACCENT2 },
  { text:"Ventilation after Glenn — very different from Stage 1!", sub:[
    "AVOID high PEEP and mean airway pressure → obstruct passive pulmonary flow",
    "Early extubation preferred — negative intrathoracic pressure augments flow",
    "Permissive hypercapnia HELPS (↑ CO₂ → cerebral vasodilation assists SVC flow)"
  ]},
  { text:"Avoid: high CVP, elevated PVR, intra-thoracic pressure ↑ (tension pneumo, pleural effusion)", color:ACCENT1 },
  { text:"Chest tube management: prolonged effusions common (~15–20%)" }
],
"This is the critical paradigm shift from Stage 1. Post-Glenn, the only driver of pulmonary blood flow is the pressure gradient from the SVC (CVP ~10–14 mmHg) to the left atrium. ANYTHING that raises PA pressure or raises left atrial pressure kills that gradient. Positive pressure ventilation impairs passive pulmonary flow — early extubation is the goal. The classic question: 'Why is this Glenn patient desaturating?' → Think: elevated PVR, pleural effusion compressing the lung, high PEEP, or developing pulmonary AVMs (which develop when hepatic factor is excluded from the lungs). Pulmonary AVMs form because hepatic venous effluent (which contains a 'hepatic factor' — possibly HGF) does not reach the pulmonary circulation in a Glenn without IVC connection.",
{ tag:"STAGE 2", tagColor:ACCENT2 });

// ── SLIDE 13: SECTION 5 ────────────────────────────────────────────────────
sectionDivider("5", "Stage 3 / Fontan ICU Management", "Total cavopulmonary connection — physiology & failure");

// ── SLIDE 14: FONTAN PHYSIOLOGY ────────────────────────────────────────────
contentSlide("Fontan Physiology: Core Concepts", [
  { text:"Fontan: IVC connected to pulmonary arteries (completes total cavopulmonary connection)", sub:[
    "Extracardiac Fontan (most common now): Gore-Tex conduit IVC → PA",
    "Lateral tunnel Fontan: intra-atrial baffle",
    "Fenestration (3–4 mm atrial hole): ↑ CO at expense of ↓ SpO₂"
  ]},
  { text:"Core hemodynamic compromise:", sub:[
    "Elevated central venous pressure (CVP 10–18 mmHg) — obligatory",
    "Reduced cardiac output — single ventricle chronically preload-deprived",
    "Non-pulsatile pulmonary flow"
  ]},
  { text:"'Successful' Fontan: mild venous congestion + modest CO reduction", color:ACCENT2 },
  { text:"'Failing' Fontan: marked venous congestion + severe CO reduction + organ damage", color:ACCENT1 },
  { text:"Fontan physiology = preload dependent, afterload intolerant, chronically compensated", color:ACCENT3 }
],
"Fuster & Hurst (Ch.69): 'Due to absence of a ventricular pump to propel blood into the pulmonary arteries, there is an obligatory upstream elevation of central venous pressure and a downstream reduction in cardiac output. The cardiac output generated by the systemic ventricle is dependent on blood flow permitted by the Fontan circuit such that the single ventricle is chronically preload-deprived.' Fenestration: creates a right-to-left shunt → SpO₂ 85–92% but better CO. Fontan CVP is NOT the same as filling pressure — it reflects PA resistance too. Estimated 50,000–80,000 patients worldwide living with Fontan by 2018.",
{ tag:"STAGE 3", tagColor:ACCENT2 });

// ── SLIDE 15: FONTAN ICU MANAGEMENT ───────────────────────────────────────
contentSlide("Fontan Post-Op & Acute ICU Management", [
  { text:"Hemodynamic targets:", sub:[
    "CVP (=Fontan pressure) 10–14 mmHg; transpulmonary gradient (CVP − LA) <10 mmHg",
    "SpO₂ >90% if fenestrated; >95% if non-fenestrated",
    "Mean arterial pressure >60 mmHg to drive systemic perfusion"
  ]},
  { text:"Fluid management: volume responsive but aggressive volume loading can raise LA pressure and impair gradient", color:ACCENT2 },
  { text:"Vasodilators to lower PVR: sildenafil (PDE5i), iNO (acute), bosentan (ERA)", sub:[
    "iNO particularly useful for acute PVR elevation post-op"
  ]},
  { text:"Diuretics: critical to manage venous congestion; target dry but not dehydrated", color:BODY_TXT },
  { text:"Chest tubes: prolonged chylothorax/effusions in 15–25% — medium-chain triglyceride diet or octreotide", color:ACCENT1 },
  { text:"Arrhythmias: sinus node dysfunction common — junctional rhythm reduces CO significantly (need AV synchrony)" }
],
"Transpulmonary gradient (CVP minus LA pressure) drives pulmonary blood flow. If this gradient is <5 mmHg, pulmonary blood flow will be severely limited. If CVP is high AND LA is high → the problem is ventricular dysfunction or AV valve regurgitation, not PVR. If CVP is high AND LA is normal → the problem is elevated PVR or PA obstruction. Use iNO for acute PVR crisis. Sildenafil and bosentan for chronic PVR management. Early extubation again preferred — same logic as Glenn. Arrhythmia management: AV pacing to restore synchrony can dramatically improve CO in junctional rhythm.",
{ tag:"STAGE 3", tagColor:ACCENT2 });

// ── SLIDE 16: SECTION 6 ────────────────────────────────────────────────────
sectionDivider("6", "Specific Complications", "Low CO  •  Arrhythmias  •  PLE  •  Plastic Bronchitis");

// ── SLIDE 17: LOW CO AND ARRHYTHMIAS ──────────────────────────────────────
twoColSlide(
  "Complications: Low CO State & Arrhythmias",
  [
    "Inadequate O₂ delivery despite mixed venous extraction",
    "Precipitants: residual lesion, AV valve regurgitation, ventricular dysfunction, shunt/conduit obstruction",
    "Investigation: echo, cath, NIRS, lactate trend",
    "Treatment algorithm:",
    "  1. Optimize preload (volume or diuresis as appropriate)",
    "  2. Reduce afterload: milrinone, captopril/enalapril",
    "  3. Augment contractility: epinephrine, dopamine",
    "  4. Reduce PVR: iNO, sildenafil, oxygen",
    "  5. ECMO as bridge to decision"
  ],
  [
    "Incidence: 40–60% of Fontan patients develop supraventricular arrhythmias by adulthood",
    "Intra-atrial re-entrant tachycardia (IART) most common",
    "Poorly tolerated — sudden loss of atrial preload drops CO precipitously",
    "Acute management:",
    "  • IV amiodarone for rate control/cardioversion",
    "  • DC cardioversion if hemodynamically unstable",
    "  • Anticoagulate: thrombus risk in dilated atria",
    "Chronic: catheter ablation, pacemaker (sinus node dysfunction common)",
    "Fontan conversion (takedown + maze + pacemaker) for refractory arrhythmias"
  ],
  "Low CO State",
  "Arrhythmias",
  "Low CO: Think of the 4 Ps — Preload, Pump, PVR, Plumbing. Plumbing = any residual anatomic obstruction (arch gradient, PA stenosis, conduit obstruction) that would respond to catheter intervention rather than medical management. Arrhythmias: IART = macro-re-entry around suture lines or scar (very common in lateral tunnel Fontan due to intra-atrial surgery). Sudden hemodynamic deterioration in a Fontan patient who is in tachycardia at 120–150 bpm = think IART until proven otherwise. Amiodarone + anticoagulation + cardioversion. Sinus node dysfunction → permanent pacemaker with epicardial leads."
);

// ── SLIDE 18: PLE AND PLASTIC BRONCHITIS ───────────────────────────────────
twoColSlide(
  "Protein-Losing Enteropathy & Plastic Bronchitis",
  [
    "Incidence: ~3–13% of Fontan patients",
    "Pathophysiology: elevated mesenteric venous pressure → lymphatic engorgement → enteric protein loss",
    "Features: hypoalbuminaemia, oedema, diarrhea, ascites, immunodeficiency (low IgG)",
    "ICU triggers: acute illness, surgery, arrhythmia → decompensation",
    "Management:",
    "  • High-protein, medium-chain triglyceride (MCT) diet",
    "  • Spironolactone + bumetanide for venous congestion",
    "  • Heparin SC (restores heparan sulfate in gut mucosa)",
    "  • Corticosteroids (budesonide) — some evidence",
    "  • Sildenafil / Fontan pressure reduction",
    "  • Transplant if refractory"
  ],
  [
    "Rare but life-threatening: ~1–2% of Fontan patients",
    "Pathophysiology: lymphatic leak into bronchial tree → cast formation",
    "Features: progressive respiratory distress, rubbery bronchial casts on bronchoscopy",
    "ICU management:",
    "  • Urgent flexible bronchoscopy + cast removal",
    "  • DNase (dornase alfa) nebulized — softens casts",
    "  • Tissue plasminogen activator (tPA) nebulized — emerging evidence",
    "  • Lymphatic intervention: thoracic duct embolisation (CHOP protocol)",
    "  • Sildenafil, bosentan — reduce lymphatic pressure",
    "  • Transplant for refractory cases"
  ],
  "Protein-Losing Enteropathy",
  "Plastic Bronchitis",
  "PLE: Fuster & Hurst notes complications arise 10–15 years after Fontan surgery. PLE = serum albumin <3.5 g/dL + 24-hr stool alpha-1-antitrypsin >150 mg. Mechanism: elevated CVP transmits back through the mesenteric venous system → intestinal lymphatic congestion → protein leak into gut lumen. Heparin mechanism: restores glycocalyx heparan sulfate on gut epithelium. Mackie AS et al (Can J Cardiol 2022, PMID 35314335) reviewed evolving therapies for PLE and plastic bronchitis including lymphatic intervention as emerging treatment. Plastic bronchitis: CHOP thoracic duct embolisation series showed dramatic responses. tPA nebulization is off-label but increasingly used."
);

// ── SLIDE 19: END-STAGE & TRANSPLANT ──────────────────────────────────────
contentSlide("End-Stage Fontan & Transplant Considerations", [
  { text:"4 categories of Fontan failure (Fuster & Hurst)", sub:[
    "1. Systolic/diastolic dysfunction (especially morphologic RV as systemic ventricle)",
    "2. AV or aortic valve regurgitation",
    "3. Systemic complications: PLE, plastic bronchitis, hepatic cirrhosis, severe cyanosis",
    "4. Elevated PVR (PA remodeling or thromboemboli)"
  ]},
  { text:"Fontan-associated liver disease (FALD)", sub:[
    "Congestive hepatopathy → fibrosis → cirrhosis in virtually all long-term Fontan patients",
    "Increased hepatocellular carcinoma risk",
    "Complicates transplant planning (combined heart-liver transplant may be needed)"
  ]},
  { text:"Thromboembolism: lifelong anticoagulation controversial — warfarin vs aspirin", sub:[
    "2026 meta-analysis (PMID 41071335): anticoagulation superior to antiplatelet in Asian cohorts"
  ]},
  { text:"Transplant: definitive treatment; 5-yr survival ~70%; pre-transplant Fontan complexity increases risk", color:ACCENT1 },
  { text:"Venkatesh et al 2024 (PMID 38892760): contemporary management of the failing Fontan — comprehensive review", color:ACCENT2 }
],
"FALD affects essentially all patients with long-standing Fontan circulation — the elevated CVP transmits to hepatic veins causing congestive hepatopathy. Monitor with liver function, fibroscan, AFP. Combined heart-liver transplant may be indicated if cirrhosis is advanced. Transplant for Fontan is technically challenging — complex anatomy, multiple prior sternotomies, dense adhesions, high PVR. 5-year post-transplant survival ~65–70% in recent series. Prior Fontan duration and number of prior surgeries are independent predictors of transplant mortality.",
{ tag:"LONG-TERM", tagColor:ACCENT2 });

// ── SLIDE 20: SUMMARY TABLE ────────────────────────────────────────────────
tableSlide(
  "Summary: ICU Targets Across All Stages",
  ["Parameter", "Stage 1 (Post-Norwood)", "Stage 2 (Post-Glenn)", "Stage 3 (Post-Fontan)"],
  [
    ["SpO₂ target", "75–85%", "75–85%", "≥90% (fenestrated) / ≥95%"],
    ["SvO₂ target", ">55%", ">55%", ">55%"],
    ["Ventilation goal", "Permissive hypercapnia PaCO₂ 45–55; FiO₂ ~0.21", "Early extubation; low PEEP; negative pressure favours flow", "Early extubation; low PEEP; iNO for ↑PVR"],
    ["Key hemodynamic lever", "FiO₂ / PaCO₂ (Qp:Qs balancing)", "PVR reduction; CVP 10–14", "Transpulmonary gradient; PVR reduction"],
    ["Main inotrope", "Milrinone ± epinephrine", "Milrinone", "Milrinone ± epinephrine"],
    ["Dangerous pitfall", "SpO₂ >90% = overcirculation", "High PEEP kills passive flow", "Arrhythmia → acute CO drop"],
    ["ECMO indication", "Refractory low CO; shunt crisis", "Rare; PA hypertensive crisis", "Refractory failure; bridge to transplant"]
  ],
  "Use this summary table as your quick-reference. Encourage fellows to print this and pin it in the PICU. The key teaching point: the same saturation target (75–85%) applies in Stage 1 and 2, but the REASON differs. In Stage 1: deliberate targeting to prevent pulmonary overcirculation. In Stage 2: just the natural result of SVC-only pulmonary supply. After Fontan completion, SpO₂ should be >90%. Any drop below 90% in a Fontan patient = investigate immediately."
);

// ── SLIDE 21: CLOSING / TAKE-HOME MESSAGES ────────────────────────────────
{
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.18, h:5.625, fill:{color:ACCENT3}, line:{color:ACCENT3} });
  s.addText("KEY TAKE-HOME MESSAGES", {
    x:0.4, y:0.3, w:9.2, h:0.55,
    fontFace:FONT, fontSize:13, bold:true, color:ACCENT3, charSpacing:4, margin:0
  });

  const msgs = [
    { num:"01", text:"SpO₂ 75–85% is the GOAL in Stage 1 — not a problem. >90% = overcirculation.", col:ACCENT1 },
    { num:"02", text:"Ventilation is your #1 Qp:Qs modulator in Stage 1: CO₂↑ ↔ PVR↑ ↔ Qp↓.", col:ACCENT2 },
    { num:"03", text:"Post-Glenn & post-Fontan: early extubation augments passive pulmonary flow.", col:ACCENT3 },
    { num:"04", text:"Fontan = preload dependent + afterload intolerant + arrhythmia sensitive.", col:ACCENT2 },
    { num:"05", text:"Arrhythmia in Fontan → anticoagulate immediately, cardiovert if unstable.", col:ACCENT1 },
  ];

  msgs.forEach((m, i) => {
    const yy = 1.05 + i * 0.87;
    s.addShape(pres.ShapeType.rect, { x:0.4, y:yy, w:0.52, h:0.62, fill:{color:m.col}, line:{color:m.col} });
    s.addText(m.num, { x:0.4, y:yy, w:0.52, h:0.62, fontFace:FONT, fontSize:18, bold:true, color:WHITE, align:"center", valign:"middle", margin:0 });
    s.addText(m.text, { x:1.1, y:yy+0.04, w:8.5, h:0.55, fontFace:FONT, fontSize:15, color:WHITE, align:"left", valign:"middle", margin:0 });
  });

  s.addNotes("Closing slide — spend 2 minutes here. Ask the room: 'What is your first intervention when a post-Norwood baby desaturates to 65%?' (Answer: don't just increase FiO₂ — check BP, SvO₂, lactate first. If overcirculating, DECREASE FiO₂ and let CO₂ rise.) 'What drives pulmonary blood flow in a Glenn or Fontan patient?' (Answer: passive flow, CVP gradient.) These two questions capture the entire lecture.");
}

// ── WRITE FILE ──────────────────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/single-ventricle-pptx/SV_ICU_Management.pptx" })
  .then(() => console.log("✅  Saved: SV_ICU_Management.pptx"))
  .catch(e => { console.error("❌ Error:", e); process.exit(1); });

cd /home/daytona/workspace/single-ventricle-pptx && node build.js 2>&1

ls -lh /home/daytona/workspace/single-ventricle-pptx/SV_ICU_Management.pptx

single ventricle HLHS Fontan echocardiogram schematic open access clinical images site:nejm.org OR site:jacc.org OR site:ahajournals.org OR site:ncbi.nlm.nih.gov

"single ventricle" AND "echocardiogram" AND "Fontan" AND "imaging"

Fontan circulation schematic diagram "open access" OR "CC BY" echocardiogram single ventricle staged palliation Norwood Glenn site:pmc.ncbi.nlm.nih.gov

~/single-ventricle-pptx/build_with_images.js

const pptxgen = require("pptxgenjs");
const { execSync } = require("child_process");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Single Ventricle Physiology: ICU Management";
pres.author = "PICU Education";

// ── COLOUR PALETTE ──────────────────────────────────────────────────────────
const BG_DARK   = "0A1628";
const BG_MID    = "0E2240";
const BG_LIGHT  = "F4F7FC";
const ACCENT1   = "E84855";
const ACCENT2   = "3CB4E7";
const ACCENT3   = "F6AE2D";
const WHITE     = "FFFFFF";
const BODY_TXT  = "1A2540";
const SUB_TXT   = "4A5C7A";
const FONT      = "Calibri";

// ── IMAGE URLS ───────────────────────────────────────────────────────────────
// All open-access (CC-BY from PMC) or from our licensed textbook CDN
const IMG_URLS = {
  // Schematic: 3 types of Fontan (atriopulmonary → lateral tunnel → extracardiac)
  fontan_types:    "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0414/6110391/f75645fd819f/nihms-983456-f0006.jpg",
  // Fetal echo showing 4-chamber view with all 4 chambers labeled (LV dominant)
  fetal_echo:      "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0414/6110391/d33630f2a46e/nihms-983456-f0001.jpg",
  // Angiogram: extracardiac Fontan conduit (FC) between IVC and PA
  fontan_angio:    "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb3d/9468446/20465632cd64/fped-10-965989-g001.jpg",
  // CT + TEE: Fontan conduit with AV valve regurgitation (multi-panel)
  fontan_ct_tee:   "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb3d/9468446/cfa3faa0cc6e/fped-10-965989-g010.jpg",
  // Textbook: Multiorgan complications of Fontan (Fuster & Hurst Central Illustration)
  fontan_compl:    "https://cdn.orris.care/cdss_images/2e0457cfc1447d6e7a253bbab6428ebad2cf2d529fb5dd230a1ca879b594d8dc.png",
};

// Pre-download all images as base64
console.log("Downloading images...");
const imgData = {};
for (const [key, url] of Object.entries(IMG_URLS)) {
  try {
    const result = execSync(
      `node /home/daytona/skills/shared/scripts/fetch_images.js "${url}"`,
      { timeout: 30000 }
    ).toString();
    const parsed = JSON.parse(result);
    if (parsed[0] && parsed[0].base64 && !parsed[0].error) {
      imgData[key] = parsed[0].base64;
      console.log(`✅  ${key}`);
    } else {
      console.log(`⚠️  ${key}: ${parsed[0]?.error || 'no data'}`);
      imgData[key] = null;
    }
  } catch(e) {
    console.log(`❌  ${key}: ${e.message}`);
    imgData[key] = null;
  }
}

// ── HELPER FUNCTIONS ─────────────────────────────────────────────────────────

function titleSlide(title, subtitle) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.18, h:5.625, fill:{color:ACCENT1}, line:{color:ACCENT1} });
  s.addText(title, {
    x:0.4, y:1.4, w:9.2, h:1.4,
    fontFace:FONT, fontSize:36, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });
  s.addText(subtitle, {
    x:0.4, y:3.1, w:9.2, h:0.8,
    fontFace:FONT, fontSize:20, color:ACCENT2, align:"left", valign:"middle", margin:0
  });
  s.addShape(pres.ShapeType.rect, { x:0, y:5.3, w:10, h:0.325, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText("PICU Education  |  July 2026", {
    x:0.4, y:5.28, w:9, h:0.33,
    fontFace:FONT, fontSize:10, color:WHITE, align:"right", valign:"middle", margin:0
  });
  return s;
}

function sectionDivider(num, title, subtitle) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_MID}, line:{color:BG_MID} });
  s.addShape(pres.ShapeType.rect, { x:0, y:2.4, w:10, h:0.08, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText(`SECTION ${num}`, {
    x:0.5, y:0.9, w:9, h:0.5,
    fontFace:FONT, fontSize:13, bold:true, color:ACCENT3, align:"left", charSpacing:5, margin:0
  });
  s.addText(title, {
    x:0.5, y:1.5, w:9, h:1.2,
    fontFace:FONT, fontSize:30, bold:true, color:WHITE, align:"left", margin:0
  });
  s.addText(subtitle, {
    x:0.5, y:2.8, w:9, h:0.8,
    fontFace:FONT, fontSize:16, color:ACCENT2, align:"left", margin:0
  });
  return s;
}

// Content slide with optional right-side image panel
// opts: { tag, tagColor, imgKey, imgCaption, imgRatio }
function contentSlide(title, bullets, notes, opts = {}) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_LIGHT}, line:{color:BG_LIGHT} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.82, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.82, w:10, h:0.06, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText(title, {
    x:0.35, y:0, w:9.3, h:0.82,
    fontFace:FONT, fontSize:20, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });

  // Determine layout: with or without image panel
  const hasImg = opts.imgKey && imgData[opts.imgKey];
  const bulletW = hasImg ? 5.0 : 9.3;
  const imgX = 5.5;
  const imgW = 4.2;
  const imgH = 3.8;
  const imgY = 1.0;

  const items = bullets.map((b, i) => {
    if (typeof b === "string") {
      return { text: b, options: { bullet: { type:"bullet", indent:15 }, color:BODY_TXT, fontSize:hasImg?15:17, fontFace:FONT, breakLine: i < bullets.length-1 } };
    } else {
      const parts = [];
      parts.push({ text: b.text, options: { bold:true, bullet:{type:"bullet", indent:15}, color: b.color||BODY_TXT, fontSize:hasImg?15:17, fontFace:FONT, breakLine:true } });
      if (b.sub) {
        b.sub.forEach((ss, si) => {
          parts.push({ text: "    " + ss, options: { bullet:false, color:SUB_TXT, fontSize:hasImg?12:14, fontFace:FONT, italic:true, breakLine: si < b.sub.length-1 || i < bullets.length-1 } });
        });
      }
      return parts;
    }
  }).flat();

  s.addText(items, { x:0.35, y:1.05, w:bulletW, h:4.3, valign:"top", margin:4 });

  if (hasImg) {
    // Image box with subtle border
    s.addShape(pres.ShapeType.rect, { x:imgX-0.08, y:imgY-0.08, w:imgW+0.16, h:imgH+0.16,
      fill:{color:"DDEEFF"}, line:{color:ACCENT2, width:1} });
    s.addImage({ data: imgData[opts.imgKey], x:imgX, y:imgY, w:imgW, h:imgH, sizing:{type:"contain", w:imgW, h:imgH} });
    if (opts.imgCaption) {
      s.addText(opts.imgCaption, {
        x:imgX, y:imgY+imgH+0.02, w:imgW, h:0.42,
        fontFace:FONT, fontSize:9, color:SUB_TXT, italic:true, align:"center", valign:"top", margin:0
      });
    }
  }

  if (opts.tag) {
    s.addText(opts.tag, {
      x:7.8, y:5.1, w:2, h:0.38,
      fontFace:FONT, fontSize:10, color:WHITE, align:"center", valign:"middle",
      fill:{ color: opts.tagColor||ACCENT1 }, margin:2
    });
  }
  if (notes) s.addNotes(notes);
  return s;
}

function twoColSlide(title, leftItems, rightItems, leftHead, rightHead, notes) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_LIGHT}, line:{color:BG_LIGHT} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.82, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.82, w:10, h:0.06, fill:{color:ACCENT3}, line:{color:ACCENT3} });
  s.addText(title, {
    x:0.35, y:0, w:9.3, h:0.82,
    fontFace:FONT, fontSize:20, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });
  s.addShape(pres.ShapeType.line, { x:5.05, y:1.0, w:0, h:4.4, line:{color:ACCENT2, width:1.5} });

  s.addShape(pres.ShapeType.rect, { x:0.3, y:1.0, w:4.5, h:0.42, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText(leftHead, { x:0.3, y:1.0, w:4.5, h:0.42, fontFace:FONT, fontSize:13, bold:true, color:WHITE, align:"center", valign:"middle", margin:0 });
  const leftArr = leftItems.map((b,i)=>({ text:b, options:{ bullet:{type:"bullet",indent:12}, color:BODY_TXT, fontSize:14, fontFace:FONT, breakLine:i<leftItems.length-1 } }));
  s.addText(leftArr, { x:0.3, y:1.5, w:4.6, h:3.8, valign:"top", margin:3 });

  s.addShape(pres.ShapeType.rect, { x:5.2, y:1.0, w:4.5, h:0.42, fill:{color:ACCENT1}, line:{color:ACCENT1} });
  s.addText(rightHead, { x:5.2, y:1.0, w:4.5, h:0.42, fontFace:FONT, fontSize:13, bold:true, color:WHITE, align:"center", valign:"middle", margin:0 });
  const rightArr = rightItems.map((b,i)=>({ text:b, options:{ bullet:{type:"bullet",indent:12}, color:BODY_TXT, fontSize:14, fontFace:FONT, breakLine:i<rightItems.length-1 } }));
  s.addText(rightArr, { x:5.2, y:1.5, w:4.6, h:3.8, valign:"top", margin:3 });

  if (notes) s.addNotes(notes);
  return s;
}

function tableSlide(title, headers, rows, notes) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_LIGHT}, line:{color:BG_LIGHT} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.82, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.82, w:10, h:0.06, fill:{color:ACCENT3}, line:{color:ACCENT3} });
  s.addText(title, {
    x:0.35, y:0, w:9.3, h:0.82,
    fontFace:FONT, fontSize:20, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });
  const tableRows = [
    headers.map(h => ({ text: h, options: { bold:true, color:WHITE, fontSize:13, fontFace:FONT, fill:{color:BG_MID}, align:"center" } })),
    ...rows.map((row, ri) => row.map(cell => ({
      text: cell,
      options: { color:BODY_TXT, fontSize:12, fontFace:FONT, fill:{ color: ri%2===0 ? "EDF3FB" : WHITE }, align:"left" }
    })))
  ];
  s.addTable(tableRows, { x:0.35, y:1.0, w:9.3, border:{ pt:0.5, color:"CCDDEE" }, rowH: 0.48 });
  if (notes) s.addNotes(notes);
  return s;
}

// Full-image slide (image takes right 55% of slide)
function imageSlide(title, imgKey, caption, leftText, notes) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.82, w:10, h:0.06, fill:{color:ACCENT2}, line:{color:ACCENT2} });
  s.addText(title, {
    x:0.35, y:0, w:9.3, h:0.82,
    fontFace:FONT, fontSize:20, bold:true, color:WHITE, align:"left", valign:"middle", margin:0
  });
  if (imgData[imgKey]) {
    s.addImage({ data: imgData[imgKey], x:4.4, y:0.95, w:5.4, h:4.45, sizing:{type:"contain", w:5.4, h:4.45} });
  }
  if (leftText) {
    s.addText(leftText, { x:0.35, y:1.0, w:3.8, h:4.3, fontFace:FONT, fontSize:14, color:WHITE, valign:"top", margin:4 });
  }
  if (caption) {
    s.addText(caption, { x:4.4, y:5.25, w:5.4, h:0.32, fontFace:FONT, fontSize:9, color:ACCENT2, italic:true, align:"center", margin:0 });
  }
  if (notes) s.addNotes(notes);
  return s;
}

// ════════════════════════════════════════════════════════════════════════════
// BUILD SLIDES
// ════════════════════════════════════════════════════════════════════════════

// SLIDE 1: Title
titleSlide(
  "Single Ventricle Physiology\nICU Management",
  "A Practical Guide for PICU Fellows & Residents  |  All Stages S1 → S2 → S3"
);

// SLIDE 2: Agenda
contentSlide("Session Agenda", [
  { text:"1. Anatomy & spectrum of single ventricle lesions", sub:["HLHS, tricuspid atresia, double-inlet LV, heterotaxy"] },
  { text:"2. Core physiology: the parallel circulation problem", sub:["Qp:Qs ratio, O₂ saturation targets, mixing lesions"] },
  { text:"3. Stage 1 ICU management — Norwood/Sano period", sub:["Balancing pulmonary vs systemic flow; low CO crisis"] },
  { text:"4. Stage 2 ICU management — Bidirectional Glenn", sub:["Passive pulmonary flow; ventilation strategies"] },
  { text:"5. Stage 3 / Fontan ICU management", sub:["Fontan physiology; failing Fontan"] },
  { text:"6. Specific complications across all stages", sub:["Low CO, arrhythmias, protein-losing enteropathy, plastic bronchitis"] },
  { text:"7. End-stage & transplant considerations" }
],
"Walk through the agenda briskly — 1 minute max. About 20 slides for 20 minutes = ~1 min per slide, with a 3-minute discussion at the end.");

// SLIDE 3: Section divider
sectionDivider("1", "Anatomy & Spectrum", "What makes a 'single ventricle'?");

// SLIDE 4: Anatomy — with fetal echo showing 4-chamber view
contentSlide("Single Ventricle: Anatomy & Spectrum", [
  { text:"Prevalence: ~2 per 10,000 live births (all univentricular lesions)", color:ACCENT2 },
  { text:"True vs functional single ventricle", sub:["True: double-inlet LV, double-outlet RV", "Functional: second ventricle present but inadequate"] },
  { text:"Key lesions", sub:[
    "HLHS — 1.6/10,000; hypoplastic LV + aorta",
    "Tricuspid atresia — 1.2/10,000; absent tricuspid valve",
    "Double-inlet LV — both AV valves → LV",
    "Unbalanced AV canal, heterotaxy"
  ]},
  { text:"RV as systemic ventricle → worse long-term outcome", color:ACCENT1 }
],
"Fetal echo: the 4-chamber view (right panel) shows a dominant right-sided ventricle (LV label refers to morphologic LV which is small) — classic appearance in HLHS fetal diagnosis. Echo is THE primary diagnostic tool. Braunwald's: 'HLHS consists of a spectrum of left-sided obstructive lesions from mitral and aortic stenosis with a small LV to mitral and aortic atresia with a nearly absent left ventricular cavity.'",
{ tag:"ANATOMY", tagColor:BG_MID, imgKey:"fetal_echo", imgCaption:"Fetal echo: 4-chamber view. Left = normal biventricular; Right = single dominant ventricle. (PMC/CC-BY)" });

// SLIDE 5: Section divider
sectionDivider("2", "Core Physiology", "Mixing, Qp:Qs & O₂ saturation targets");

// SLIDE 6: Parallel circulation
contentSlide("The Parallel Circulation Problem", [
  { text:"Normal: SERIES — venous blood → RV → lungs → LV → body", color:BODY_TXT },
  { text:"Single ventricle: PARALLEL — one pump, both circuits, common mixing", color:ACCENT1 },
  { text:"Qp:Qs — the master variable", sub:[
    "= 1 → ideal balance",
    "> 1 → pulmonary overcirculation → systemic steal, low CO",
    "< 1 → cyanosis, but protected systemic flow"
  ]},
  { text:"SpO₂ targets pre-Fontan (Stage 1): 75–85%", color:ACCENT1 },
  { text:"SpO₂ is a SURROGATE for Qp:Qs", sub:[
    "SpO₂ 80–85% → Qp:Qs ≈ 1 → acceptable balance",
    "SpO₂ >90% → overcirculation → dangerous"
  ]},
  { text:"SvO₂ from SVC/RA: global O₂ delivery reserve — target >55%" }
],
"This is the single most important concept. An SpO₂ >90% in a post-Norwood patient is a WARNING sign. SvO₂ <50% = O₂ delivery crisis regardless of SpO₂.",
{ tag:"CORE CONCEPT", tagColor:ACCENT1 });

// SLIDE 7: Section divider
sectionDivider("3", "Stage 1 ICU Management", "Post-Norwood / post-Sano  — the most vulnerable period");

// SLIDE 8: Norwood overview
contentSlide("Stage 1 Palliation: Norwood / Sano Procedure", [
  { text:"Anatomy created:", sub:[
    "Neo-aorta from native PA + aortic arch reconstruction",
    "Atrial septectomy — unobstructed mixing",
    "Pulmonary blood flow: modified BT shunt (MBTS) OR Sano (RV-PA conduit)"
  ]},
  { text:"MBTS: lower diastolic BP, coronary steal risk; simpler surgically", color:ACCENT2 },
  { text:"Sano RV-PA conduit: better diastolic BP / coronary perfusion; RV ventriculotomy scar", color:ACCENT3 },
  { text:"Hybrid (ductal stent + PA bands) for high-risk/low-BW neonates", sub:[
    "Avoids CPB in Stage 1 but complicates Stage 2",
    "Miller's Anesthesia: 'may offer survival advantage in low birth weight neonates'"
  ]}
],
"Miller's Anesthesia: Hybrid approach stents the PDA and surgically bands both PAs. Avoids CPB risk in neonates <2.5kg but stage 2 then combines aortic arch reconstruction + Glenn. Sano vs MBTS — SVPCOT trial: similar survival, Sano had better inter-stage survival.",
{ tag:"STAGE 1", tagColor:ACCENT3 });

// SLIDE 9: Post-Norwood ICU management
contentSlide("Post-Norwood ICU Management", [
  { text:"Goal: Qp:Qs ≈ 1  |  SpO₂ 75–85%  |  SvO₂ >55%", color:ACCENT1 },
  { text:"Ventilation (your #1 lever)", sub:[
    "↑ FiO₂ → ↓ PVR → ↑ Qp → AVOID high FiO₂",
    "Permissive hypercapnia (PaCO₂ 45–55) → ↑ PVR → balances Qp",
    "Sub-ambient O₂ (FiO₂ 0.17–0.21) for overcirculation"
  ]},
  { text:"Monitoring", sub:[
    "NIRS (cerebral + somatic) — cerebral <50% = ischemia",
    "SVC/RA mixed venous saturation",
    "LA line for filling pressure"
  ]},
  { text:"Milrinone: positive inotrope + pulmonary vasodilator — mainstay", color:ACCENT2 },
  { text:"Dangers: low CO, shunt thrombosis (→ heparin infusion), NEC", color:ACCENT1 }
],
"Ventilation is YOUR most powerful tool for Qp:Qs in Stage 1. O₂ is a pulmonary vasodilator. In an overcirculating patient (SpO₂ >90%, low BP, acidosis): DECREASE FiO₂, allow CO₂ to rise. Somatic NIRS drop suggests NEC or low CO.",
{ tag:"STAGE 1", tagColor:ACCENT3 });

// SLIDE 10: Low CO
contentSlide("Low Cardiac Output Syndrome — Stage 1", [
  { text:"Recognition", sub:[
    "Metabolic acidosis (lactate >3 mmol/L)",
    "SvO₂ < 50%  |  NIRS <50%  |  Oliguria"
  ]},
  { text:"Stage 1-specific causes", sub:[
    "Pulmonary overcirculation (SpO₂ >90%) → systemic steal",
    "Shunt obstruction/thrombosis",
    "Residual arch obstruction",
    "AV valve regurgitation  |  Tamponade"
  ]},
  { text:"Management ladder", sub:[
    "1. FiO₂ reduction / permissive hypercapnia for overcirculation",
    "2. Milrinone ± epinephrine for systolic dysfunction",
    "3. Rule out residual anatomy (echo → cath → re-op)",
    "4. ECMO if refractory"
  ]}
],
"The 4 Ps: Preload, Pump, PVR, Plumbing. 'Plumbing' = residual anatomic obstruction. ECMO rescue after Norwood ~20% survival to discharge — poor but not zero. Do NOT reflexively increase FiO₂ when SpO₂ drops.",
{ tag:"EMERGENCY", tagColor:ACCENT1 });

// SLIDE 11: Section divider
sectionDivider("4", "Stage 2 ICU Management", "Bidirectional Glenn — passive superior cavopulmonary flow");

// SLIDE 12: Glenn physiology
contentSlide("Stage 2: Bidirectional Glenn — Physiology & ICU", [
  { text:"SVC → right PA; both PAs receive flow; BT shunt taken down", sub:["Passive flow: no ventricular pump drives pulmonary circulation", "Flow depends on SVC pressure gradient (= CVP ~10–14 mmHg)"] },
  { text:"SpO₂ target post-Glenn: 75–85%", color:ACCENT2 },
  { text:"Ventilation — critical paradigm shift from Stage 1!", sub:[
    "AVOID high PEEP → obstructs passive pulmonary flow",
    "Early extubation preferred — negative intrathoracic pressure augments flow",
    "Permissive hypercapnia: cerebral vasodilation assists SVC drainage"
  ]},
  { text:"Avoid: high CVP, elevated PVR, pleural effusions, tension pneumothorax", color:ACCENT1 },
  { text:"Pulmonary AVMs develop without hepatic factor — excluded in Glenn!", color:ACCENT3 }
],
"Classic question: 'Why is this Glenn patient desaturating?' → Think: elevated PVR, pleural effusion, high PEEP, pulmonary AVMs. Pulmonary AVMs form because hepatic venous effluent (containing 'hepatic factor') does not reach lungs in Glenn. This is why Fontan completion restores IVC flow to lungs and resolves AVMs.",
{ tag:"STAGE 2", tagColor:ACCENT2 });

// SLIDE 13: Section divider
sectionDivider("5", "Stage 3 / Fontan ICU Management", "Total cavopulmonary connection — physiology & failure");

// SLIDE 14: Fontan types — IMAGE SLIDE with the 3-type schematic
imageSlide(
  "Fontan: 3 Types of Total Cavopulmonary Connection",
  "fontan_types",
  "Schematic: A = Atriopulmonary (historical)  |  B = Lateral tunnel  |  C = Extracardiac conduit (current standard). (PMC/CC-BY, PMID 28566825)",
  "Three Fontan types:\n\n• Atriopulmonary (historical) — RA directly to PA; high RA dilation + arrhythmia risk\n\n• Lateral tunnel — intra-atrial baffle to PA; still done in some centres\n\n• Extracardiac conduit — Gore-Tex tube IVC → PA; most common today\n\nFenestration (3–4 mm hole) → ↑ CO at expense of SpO₂ drop",
  "Fuster & Hurst: 'By 2018 it was estimated that 50,000 to 80,000 patients across the world lived with a Fontan procedure.' The type of Fontan determines arrhythmia risk and re-intervention likelihood. Extracardiac = lowest sinus node injury; atriopulmonary = highest arrhythmia burden."
);

// SLIDE 15: Fontan physiology
contentSlide("Fontan Physiology: Core Concepts", [
  { text:"Obligatory elevated CVP (10–18 mmHg) — no sub-pulmonary ventricle", color:ACCENT1 },
  { text:"Single ventricle chronically preload-deprived", sub:["Cardiac output reduced — dependent on passive pulmonary flow"] },
  { text:"'Successful' Fontan: mild venous congestion + modest CO reduction", color:ACCENT2 },
  { text:"'Failing' Fontan: marked venous congestion + severe CO + organ damage", color:ACCENT1 },
  { text:"4 categories of Fontan failure (Fuster & Hurst)", sub:[
    "1. Systolic/diastolic dysfunction (RV as systemic = worse)",
    "2. AV or aortic valve regurgitation",
    "3. Systemic complications: PLE, plastic bronchitis, hepatic cirrhosis, cyanosis",
    "4. Elevated PVR (PA remodeling or thromboemboli)"
  ]},
  { text:"Fontan = preload dependent • afterload intolerant • arrhythmia sensitive", color:ACCENT3 }
],
"Fuster & Hurst Ch.69: 'Due to absence of a ventricular pump... there is an obligatory upstream elevation of central venous pressure and a downstream reduction in cardiac output... the single ventricle is chronically preload-deprived.' The CVP in a Fontan is NOT the same as filling pressure — it reflects PA resistance too.",
{ tag:"STAGE 3", tagColor:ACCENT2 });

// SLIDE 16: Fontan ICU with TEE/CT image
contentSlide("Fontan Post-Op & Acute ICU Management", [
  { text:"Targets: CVP 10–14 mmHg; transpulmonary gradient (CVP − LA) <10 mmHg", color:ACCENT1 },
  { text:"SpO₂: ≥90% fenestrated; ≥95% non-fenestrated", color:ACCENT2 },
  { text:"Fluid: volume responsive but LA pressure rise kills gradient", color:BODY_TXT },
  { text:"Vasodilators (↓ PVR)", sub:[
    "iNO — acute PVR crisis post-op",
    "Sildenafil (PDE5i) — sub-acute/chronic",
    "Bosentan (ERA) — chronic PVR management"
  ]},
  { text:"Diuretics: critical; target dry but not dehydrated", color:BODY_TXT },
  { text:"Arrhythmias: junctional rhythm → lose AV synchrony → CO drops precipitously", color:ACCENT1 },
  { text:"Chylothorax/effusions: 15–25%; MCT diet, octreotide, consider lymphatic intervention" }
],
"CT image shows Fontan conduit (FC) between IVC and PA; TEE panels demonstrate AV regurgitation (AVR) — a key driver of Fontan failure. Transpulmonary gradient drives pulmonary blood flow. If high CVP + high LA → ventricular dysfunction or AV valve regurgitation. If high CVP + normal LA → PVR or PA obstruction. Early extubation preferred — same logic as Glenn.",
{ tag:"STAGE 3", tagColor:ACCENT2, imgKey:"fontan_ct_tee", imgCaption:"CT: Fontan conduit (FC). TEE B/D: AV valve regurgitation (AVR). (PMC/CC-BY)" });

// SLIDE 17: Section divider
sectionDivider("6", "Specific Complications", "Low CO  •  Arrhythmias  •  PLE  •  Plastic Bronchitis");

// SLIDE 18: Low CO + Arrhythmias
twoColSlide(
  "Complications: Low CO State & Arrhythmias",
  [
    "Inadequate O₂ delivery despite venous extraction",
    "Causes: residual lesion, AV valve regurgitation, ventricular dysfunction, conduit obstruction",
    "Investigation: echo, cath, NIRS, lactate",
    "The 4 Ps — Preload, Pump, PVR, Plumbing",
    "Treatment:",
    "  1. Optimise preload",
    "  2. Reduce afterload: milrinone, ACE inhibitor",
    "  3. Augment contractility: epinephrine",
    "  4. Reduce PVR: iNO, sildenafil",
    "  5. ECMO — bridge to decision"
  ],
  [
    "40–60% of Fontan pts develop SVT by adulthood",
    "IART (intra-atrial re-entrant tachycardia) most common",
    "Poorly tolerated — sudden atrial preload loss",
    "Acute management:",
    "  • IV amiodarone for rate/rhythm control",
    "  • DC cardioversion if haemodynamically unstable",
    "  • Anticoagulate immediately (thrombus risk)",
    "Sinus node dysfunction → AV pacing restores CO",
    "Fontan conversion + maze + pacemaker for refractory cases",
    "Catheter ablation for mapping/ablation of IART circuits"
  ],
  "Low CO State",
  "Arrhythmias",
  "IART = macro re-entry around suture lines. Sudden haemodynamic deterioration in Fontan with tachycardia 120–150 bpm = IART until proven otherwise. Amiodarone + anticoagulation + cardioversion. AV pacing can dramatically improve CO in junctional rhythm."
);

// SLIDE 19: PLE + Plastic Bronchitis — with Fuster complications diagram
imageSlide(
  "Multiorgan Complications of Fontan Palliation",
  "fontan_compl",
  "Fuster & Hurst's Heart, 15th Ed. (Ch.69) Central Illustration — Multiorgan involvement and complications. Licensed from textbook library.",
  "",
  "This is one of the most important teaching images in the entire lecture. Walk through each complication: FALD (liver), PLE (gut), plastic bronchitis (lungs), arrhythmias/sinus node dysfunction, venous insufficiency, altered lymphatics, thromboembolism, cyanosis, renal failure, neurodevelopmental disability. Note the management panel on the right — covers anticoagulation, PH therapy, PLE management, transplant criteria. Spend 2 minutes on this slide."
);

// SLIDE 20: PLE + Plastic Bronchitis detail
twoColSlide(
  "Protein-Losing Enteropathy & Plastic Bronchitis",
  [
    "Incidence: ~3–13% of Fontan patients",
    "Pathophys: elevated mesenteric CVP → lymphatic engorgement → enteric protein loss",
    "Features: hypoalbuminaemia, oedema, diarrhoea, ascites, low IgG",
    "ICU triggers: acute illness, arrhythmia",
    "Management:",
    "  • High-protein MCT diet",
    "  • Spironolactone + bumetanide",
    "  • Heparin SC (restores gut glycocalyx)",
    "  • Budesonide (some evidence)",
    "  • Sildenafil / Fontan pressure reduction",
    "  • Transplant if refractory"
  ],
  [
    "Rare (~1–2%) but life-threatening",
    "Pathophys: lymphatic leak → bronchial cast formation",
    "Features: respiratory distress + rubbery bronchial casts",
    "ICU management:",
    "  • Urgent flexible bronchoscopy + cast removal",
    "  • DNase (dornase alfa) nebulised",
    "  • tPA nebulised — emerging evidence",
    "  • Thoracic duct embolisation (CHOP protocol)",
    "  • Sildenafil, bosentan",
    "  • Transplant for refractory",
    "Mackie AS et al, Can J Cardiol 2022 (PMID 35314335)"
  ],
  "Protein-Losing Enteropathy",
  "Plastic Bronchitis",
  "PLE: serum albumin <3.5 g/dL + 24hr stool alpha-1-antitrypsin >150 mg. Heparin mechanism: restores heparan sulfate glycocalyx on gut epithelium. Plastic bronchitis: CHOP thoracic duct embolisation series showed dramatic responses. tPA nebulisation is off-label but increasingly used."
);

// SLIDE 21: End-stage + angio image
contentSlide("End-Stage Fontan & Transplant Considerations", [
  { text:"Fontan-associated liver disease (FALD)", sub:[
    "Congestive hepatopathy → fibrosis → cirrhosis",
    "↑ Hepatocellular carcinoma risk — monitor with AFP + fibroscan",
    "May require combined heart-liver transplant"
  ]},
  { text:"Thromboembolism: lifelong anticoagulation (warfarin vs aspirin — controversial)", sub:[
    "2026 meta-analysis (PMID 41071335): anticoagulation superior in Asian cohorts"
  ]},
  { text:"Transplant: definitive treatment", sub:[
    "5-yr survival ~65–70%; prior Fontan complexity ↑ risk",
    "Technical challenge: complex anatomy, multiple prior sternotomies, dense adhesions"
  ]},
  { text:"Fontan conversion (takedown + maze + pacemaker) for selected arrhythmia patients", color:ACCENT2 },
  { text:"Venkatesh et al 2024 (PMID 38892760): Contemporary Management of the Failing Fontan", color:ACCENT2 }
],
"Angiogram shown (right panel) demonstrates extracardiac Fontan conduit (FC) opacified from IVC to pulmonary artery (PA) — catheter-based assessment of the Fontan circuit. This is the key investigation for conduit stenosis, elevated Fontan pressure, and fenestration sizing. FALD affects essentially all patients with long-standing Fontan. Combined heart-liver transplant may be indicated if cirrhosis is advanced.",
{ tag:"LONG-TERM", tagColor:ACCENT2, imgKey:"fontan_angio", imgCaption:"Angiogram: Fontan conduit (FC) connecting IVC to PA. Catheter haemodynamic assessment. (PMC/CC-BY)" });

// SLIDE 22: Summary table
tableSlide(
  "Summary: ICU Targets Across All Stages",
  ["Parameter", "Stage 1 (Post-Norwood)", "Stage 2 (Post-Glenn)", "Stage 3 (Post-Fontan)"],
  [
    ["SpO₂ target", "75–85%", "75–85%", "≥90% (fenestrated) / ≥95%"],
    ["SvO₂ target", ">55%", ">55%", ">55%"],
    ["Ventilation goal", "Permissive hypercapnia PaCO₂ 45–55; FiO₂ ~0.21", "Early extubation; low PEEP; neg pressure favours flow", "Early extubation; low PEEP; iNO for ↑PVR"],
    ["Key lever", "FiO₂ / PaCO₂ (Qp:Qs balancing)", "PVR reduction; CVP 10–14", "Transpulmonary gradient; PVR reduction"],
    ["Main inotrope", "Milrinone ± epinephrine", "Milrinone", "Milrinone ± epinephrine"],
    ["Dangerous pitfall", "SpO₂ >90% = overcirculation!", "High PEEP kills passive flow", "Arrhythmia → acute CO drop"],
    ["ECMO indication", "Refractory low CO; shunt crisis", "Rare; PA hypertensive crisis", "Refractory failure; bridge to transplant"]
  ],
  "Use this summary table as your quick-reference. The key teaching point: same SpO₂ target in S1 and S2 (75–85%) but for different reasons. After Fontan, SpO₂ should be >90%. Any drop below 90% in a Fontan patient = investigate immediately."
);

// SLIDE 23: Closing take-home messages
{
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:BG_DARK}, line:{color:BG_DARK} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.18, h:5.625, fill:{color:ACCENT3}, line:{color:ACCENT3} });
  s.addText("KEY TAKE-HOME MESSAGES", {
    x:0.4, y:0.3, w:9.2, h:0.55,
    fontFace:FONT, fontSize:13, bold:true, color:ACCENT3, charSpacing:4, margin:0
  });
  const msgs = [
    { num:"01", text:"SpO₂ 75–85% is the GOAL in Stage 1 — not a problem. >90% = overcirculation.", col:ACCENT1 },
    { num:"02", text:"Ventilation is your #1 Qp:Qs modulator in Stage 1: CO₂↑ ↔ PVR↑ ↔ Qp↓.", col:ACCENT2 },
    { num:"03", text:"Post-Glenn & post-Fontan: early extubation augments passive pulmonary flow.", col:ACCENT3 },
    { num:"04", text:"Fontan = preload dependent + afterload intolerant + arrhythmia sensitive.", col:ACCENT2 },
    { num:"05", text:"Arrhythmia in Fontan → anticoagulate immediately, cardiovert if unstable.", col:ACCENT1 },
  ];
  msgs.forEach((m, i) => {
    const yy = 1.05 + i * 0.87;
    s.addShape(pres.ShapeType.rect, { x:0.4, y:yy, w:0.52, h:0.62, fill:{color:m.col}, line:{color:m.col} });
    s.addText(m.num, { x:0.4, y:yy, w:0.52, h:0.62, fontFace:FONT, fontSize:18, bold:true, color:WHITE, align:"center", valign:"middle", margin:0 });
    s.addText(m.text, { x:1.1, y:yy+0.04, w:8.5, h:0.55, fontFace:FONT, fontSize:15, color:WHITE, align:"left", valign:"middle", margin:0 });
  });
  s.addNotes("Closing — ask the room: 'What is your first intervention when a post-Norwood baby desaturates to 65%?' (Answer: don't just increase FiO₂ — check BP, SvO₂, lactate. If overcirculating: DECREASE FiO₂.) 'What drives pulmonary blood flow in a Glenn or Fontan?' (Answer: passive CVP gradient.)");
}

// WRITE
pres.writeFile({ fileName: "/home/daytona/workspace/single-ventricle-pptx/SV_ICU_Management_with_images.pptx" })
  .then(() => console.log("✅  Saved: SV_ICU_Management_with_images.pptx"))
  .catch(e => { console.error("❌ Error:", e); process.exit(1); });

cd /home/daytona/workspace/single-ventricle-pptx && node build_with_images.js 2>…

ls -lh /home/daytona/workspace/single-ventricle-pptx/

"single ventricle" AND "interstage" AND "mortality"

"Fontan" AND ("ECMO" OR "mechanical circulatory support")

"single ventricle" AND ("neurodevelopment" OR "nutrition" OR "interstage monitoring")

"hypoplastic left heart" AND ("pulmonary vascular resistance" OR "vasodilator" OR "milrinone")

~/single-ventricle-pptx/build_35slides.js

const pptxgen = require("pptxgenjs");
const { execSync } = require("child_process");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Single Ventricle Physiology: ICU Challenges";
pres.author = "PICU Education";

// ── PALETTE ─────────────────────────────────────────────────────────────────
const DARK   = "081628";   // deep navy
const MID    = "0D2140";   // mid navy
const LIGHT  = "F2F6FC";   // off-white
const RED    = "D93B4A";   // danger
const BLUE   = "2EAEE0";   // concept
const AMBER  = "F5A623";   // stage/warning
const GREEN  = "27AE60";   // positive/target met
const WHITE  = "FFFFFF";
const BODY   = "1A2540";
const SUB    = "4A5C7A";
const FONT   = "Calibri";

// ── IMAGE URLS (all open-access CC-BY or licensed textbook CDN) ─────────────
const IMG_URLS = {
  fontan_anatomy:  "https://cdn.orris.care/cdss_images/255a0bb2a46d3eb5bf32ea0ef10897c6ed2e7aa2a0c6e18956e01d8389a8b61c.png",
  fontan_types:    "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0414/6110391/f75645fd819f/nihms-983456-f0006.jpg",
  fetal_echo:      "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0414/6110391/d33630f2a46e/nihms-983456-f0001.jpg",
  fontan_angio:    "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb3d/9468446/20465632cd64/fped-10-965989-g001.jpg",
  fontan_ct_tee:   "https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb3d/9468446/cfa3faa0cc6e/fped-10-965989-g010.jpg",
  fontan_compl:    "https://cdn.orris.care/cdss_images/2e0457cfc1447d6e7a253bbab6428ebad2cf2d529fb5dd230a1ca879b594d8dc.png",
};

console.log("⬇  Downloading images...");
const imgData = {};
for (const [key, url] of Object.entries(IMG_URLS)) {
  try {
    const res = JSON.parse(execSync(`node /home/daytona/skills/shared/scripts/fetch_images.js "${url}"`, {timeout:30000}).toString());
    imgData[key] = (res[0]?.base64 && !res[0]?.error) ? res[0].base64 : null;
    console.log(imgData[key] ? `✅ ${key}` : `⚠ ${key} (no data)`);
  } catch(e) { imgData[key]=null; console.log(`❌ ${key}: ${e.message}`); }
}

// ── HELPERS ──────────────────────────────────────────────────────────────────

const addBg = (s, color=LIGHT) => s.addShape(pres.ShapeType.rect,{x:0,y:0,w:10,h:5.625,fill:{color},line:{color}});
const addTopBar = (s,color=DARK,accentColor=BLUE) => {
  s.addShape(pres.ShapeType.rect,{x:0,y:0,w:10,h:0.78,fill:{color},line:{color}});
  s.addShape(pres.ShapeType.rect,{x:0,y:0.78,w:10,h:0.06,fill:{color:accentColor},line:{color:accentColor}});
};
const addTitle = (s,txt,opts={}) => s.addText(txt,{x:0.35,y:0,w:9.3,h:0.78,fontFace:FONT,fontSize:opts.sz||19,bold:true,color:WHITE,align:"left",valign:"middle",margin:0});
const addTag  = (s,txt,color=RED) => s.addText(txt,{x:7.8,y:5.1,w:2,h:0.35,fontFace:FONT,fontSize:10,color:WHITE,align:"center",valign:"middle",fill:{color},margin:2});
const addFooter = (s,txt) => { s.addShape(pres.ShapeType.rect,{x:0,y:5.42,w:10,h:0.2,fill:{color:MID},line:{color:MID}}); s.addText(txt,{x:0.3,y:5.42,w:9.4,h:0.2,fontFace:FONT,fontSize:8,color:BLUE,align:"right",valign:"middle",margin:0}); };

function titleSlide(title, subtitle, tag){
  const s = pres.addSlide();
  addBg(s, DARK);
  s.addShape(pres.ShapeType.rect,{x:0,y:0,w:0.2,h:5.625,fill:{color:RED},line:{color:RED}});
  s.addShape(pres.ShapeType.rect,{x:0,y:4.85,w:10,h:0.78,fill:{color:MID},line:{color:MID}});
  s.addShape(pres.ShapeType.rect,{x:0,y:4.82,w:10,h:0.06,fill:{color:BLUE},line:{color:BLUE}});
  s.addText(title,{x:0.5,y:1.1,w:9,h:1.9,fontFace:FONT,fontSize:40,bold:true,color:WHITE,align:"left",valign:"middle",margin:0});
  s.addText(subtitle,{x:0.5,y:3.2,w:9,h:0.7,fontFace:FONT,fontSize:17,color:BLUE,align:"left",valign:"middle",margin:0});
  if(tag) s.addText(tag,{x:0.5,y:3.9,w:9,h:0.5,fontFace:FONT,fontSize:13,color:AMBER,align:"left",valign:"middle",margin:0});
  s.addText("PICU Education  |  July 2026",{x:0.5,y:4.85,w:9,h:0.75,fontFace:FONT,fontSize:11,color:WHITE,align:"right",valign:"middle",margin:0});
  return s;
}

function secDivider(num, title, sub, color=MID){
  const s = pres.addSlide();
  addBg(s, color);
  s.addShape(pres.ShapeType.rect,{x:0,y:2.5,w:10,h:0.07,fill:{color:AMBER},line:{color:AMBER}});
  s.addText(`SECTION ${num}`,{x:0.6,y:1.0,w:9,h:0.5,fontFace:FONT,fontSize:13,bold:true,color:AMBER,charSpacing:5,margin:0});
  s.addText(title,{x:0.6,y:1.55,w:9,h:1.1,fontFace:FONT,fontSize:32,bold:true,color:WHITE,margin:0});
  s.addText(sub,{x:0.6,y:2.78,w:9,h:0.75,fontFace:FONT,fontSize:15,color:BLUE,margin:0});
  addFooter(s,"Single Ventricle Physiology: ICU Challenges  |  PICU Education 2026");
  return s;
}

// Standard content slide. opts: {tag, tagColor, imgKey, imgCaption, accentBar}
function cSlide(title, bullets, notes, opts={}){
  const s = pres.addSlide();
  addBg(s);
  addTopBar(s, DARK, opts.accentBar||BLUE);
  addTitle(s, title);

  const hasImg = opts.imgKey && imgData[opts.imgKey];
  const bW = hasImg ? 5.0 : 9.3;
  const iX=5.45, iY=0.96, iW=4.25, iH=4.0;

  const items = bullets.flatMap((b,bi)=>{
    if(typeof b==="string") return [{text:b, options:{bullet:{type:"bullet",indent:14},color:BODY,fontSize:hasImg?14:16,fontFace:FONT,breakLine:bi<bullets.length-1}}];
    const ps=[{text:b.text||"", options:{bold:true,bullet:{type:"bullet",indent:14},color:b.color||BODY,fontSize:hasImg?14:16,fontFace:FONT,breakLine:true}}];
    (b.sub||[]).forEach((ss,si)=>ps.push({text:"    "+ss,options:{bullet:false,color:SUB,fontSize:hasImg?12:14,fontFace:FONT,italic:true,breakLine:si<(b.sub.length-1)||bi<bullets.length-1}}));
    return ps;
  });
  s.addText(items,{x:0.35,y:0.94,w:bW,h:4.45,valign:"top",margin:4});

  if(hasImg){
    s.addShape(pres.ShapeType.rect,{x:iX-0.08,y:iY-0.08,w:iW+0.16,h:iH+0.16,fill:{color:"DCE9F8"},line:{color:BLUE,width:1}});
    s.addImage({data:imgData[opts.imgKey],x:iX,y:iY,w:iW,h:iH,sizing:{type:"contain",w:iW,h:iH}});
    if(opts.imgCaption) s.addText(opts.imgCaption,{x:iX,y:iY+iH+0.02,w:iW,h:0.38,fontFace:FONT,fontSize:8.5,color:SUB,italic:true,align:"center",valign:"top",margin:0});
  }
  if(opts.tag) addTag(s, opts.tag, opts.tagColor||RED);
  addFooter(s,"Single Ventricle Physiology: ICU Challenges  |  PICU Education 2026");
  if(notes) s.addNotes(notes);
  return s;
}

// Full-image slide (image right 55%, text left 40%)
function imgSlide(title, imgKey, leftLines, caption, notes, accentBar=BLUE){
  const s = pres.addSlide();
  addBg(s, DARK);
  addTopBar(s, "091424", accentBar);
  addTitle(s, title);
  if(imgData[imgKey]) s.addImage({data:imgData[imgKey],x:4.3,y:0.92,w:5.5,h:4.55,sizing:{type:"contain",w:5.5,h:4.55}});
  if(leftLines){
    const items = leftLines.map((t,i)=>({text:t,options:{bullet:{type:"bullet",indent:12},color:WHITE,fontSize:13.5,fontFace:FONT,breakLine:i<leftLines.length-1}}));
    s.addText(items,{x:0.35,y:0.97,w:3.7,h:4.4,valign:"top",margin:3});
  }
  if(caption) s.addText(caption,{x:4.3,y:5.28,w:5.5,h:0.27,fontFace:FONT,fontSize:8,color:BLUE,italic:true,align:"center",margin:0});
  addFooter(s,"Single Ventricle Physiology: ICU Challenges  |  PICU Education 2026");
  if(notes) s.addNotes(notes);
  return s;
}

// Two-column slide
function twoCol(title, L, R, lHead, rHead, notes, lColor=BLUE, rColor=RED){
  const s = pres.addSlide();
  addBg(s);
  addTopBar(s, DARK, AMBER);
  addTitle(s, title);
  s.addShape(pres.ShapeType.line,{x:5.05,y:0.98,w:0,h:4.45,line:{color:BLUE,width:1.5}});
  [[0.3,lHead,lColor,L,4.55],[5.2,rHead,rColor,R,4.55]].forEach(([x,head,hc,items,w])=>{
    s.addShape(pres.ShapeType.rect,{x,y:0.98,w:w-0.1,h:0.4,fill:{color:hc},line:{color:hc}});
    s.addText(head,{x,y:0.98,w:w-0.1,h:0.4,fontFace:FONT,fontSize:12,bold:true,color:WHITE,align:"center",valign:"middle",margin:0});
    const arr = items.map((b,i)=>({text:b,options:{bullet:{type:"bullet",indent:11},color:BODY,fontSize:13.5,fontFace:FONT,breakLine:i<items.length-1}}));
    s.addText(arr,{x,y:1.46,w:w-0.1,h:3.9,valign:"top",margin:3});
  });
  addFooter(s,"Single Ventricle Physiology: ICU Challenges  |  PICU Education 2026");
  if(notes) s.addNotes(notes);
  return s;
}

// Table slide
function tblSlide(title, headers, rows, notes, accent=AMBER){
  const s = pres.addSlide();
  addBg(s);
  addTopBar(s, DARK, accent);
  addTitle(s, title);
  const tRows=[
    headers.map(h=>({text:h,options:{bold:true,color:WHITE,fontSize:12,fontFace:FONT,fill:{color:MID},align:"center"}})),
    ...rows.map((row,ri)=>row.map(cell=>({text:cell,options:{color:BODY,fontSize:12,fontFace:FONT,fill:{color:ri%2===0?"EBF4FB":WHITE},align:"left"}})))
  ];
  s.addTable(tRows,{x:0.35,y:0.96,w:9.3,border:{pt:0.5,color:"C0D8EE"},rowH:0.47});
  addFooter(s,"Single Ventricle Physiology: ICU Challenges  |  PICU Education 2026");
  if(notes) s.addNotes(notes);
  return s;
}

// Callout box slide (highlight boxes)
function calloutSlide(title, boxes, notes, accent=BLUE){
  const s = pres.addSlide();
  addBg(s, DARK);
  addTopBar(s,"091424",accent);
  addTitle(s,title);
  // up to 4 boxes, 2x2
  const positions = [{x:0.3,y:1.1},{x:5.2,y:1.1},{x:0.3,y:3.25},{x:5.2,y:3.25}];
  boxes.forEach((box,i)=>{
    if(i>=4) return;
    const {x,y}=positions[i];
    s.addShape(pres.ShapeType.rect,{x,y,w:4.35,h:1.85,fill:{color:box.bg||MID},line:{color:box.border||BLUE,width:1.5}});
    s.addText(box.head,{x:x+0.12,y:y+0.08,w:4.1,h:0.42,fontFace:FONT,fontSize:13,bold:true,color:box.headColor||AMBER,margin:0});
    s.addText(box.body,{x:x+0.12,y:y+0.52,w:4.1,h:1.22,fontFace:FONT,fontSize:12.5,color:WHITE,valign:"top",margin:0});
  });
  addFooter(s,"Single Ventricle Physiology: ICU Challenges  |  PICU Education 2026");
  if(notes) s.addNotes(notes);
  return s;
}

// ════════════════════════════════════════════════════════════════════════════
// 35 SLIDES
// ════════════════════════════════════════════════════════════════════════════

// ── S01: Title ───────────────────────────────────────────────────────────────
titleSlide(
  "Single Ventricle Physiology\nICU Challenges",
  "A Comprehensive Guide for PICU Fellows & Residents  |  All Stages S1 → S2 → S3",
  "Anatomy • Physiology • Staging • Complications • ECMO • End-Stage Care"
);

// ── S02: Epidemiology & Scope ────────────────────────────────────────────────
cSlide("Why Single Ventricle Matters in the PICU",[
  {text:"Prevalence: ~2 per 10,000 live births — all univentricular lesions combined",color:BLUE},
  {text:"HLHS alone: 1.6/10,000 — most common indication for staged neonatal palliation",color:BODY},
  {text:"Without surgery: universally fatal in the neonatal period",color:RED},
  {text:"Staged palliation survival has transformed outcomes",sub:["Stage 1 (Norwood) survival >90% at experienced centres","Fontan completion: 15-yr survival >85% in modern cohorts","~50,000–80,000 patients worldwide living with Fontan (2018 estimate)"]},
  {text:"ICU burden",sub:["Most complex and resource-intensive paediatric cardiac admissions","Multiple re-admissions per patient across all 3 stages","Requires fundamentally different thinking at EACH stage"]}
],"Sabiston Textbook of Surgery (Ch.113): 'The rapid evolution of successful palliation for patients with various forms of single-ventricle physiology since the late 1970s has led to a large and growing population of adults with a single ventricle. For most of these patients, lifelong cardiac attention is needed, and the potential for subsequent cardiac reoperation is high.' Scope-setting slide — this physiology will come to YOUR PICU. Estimated 50,000–80,000 Fontan patients worldwide.",{tag:"OVERVIEW",tagColor:MID});

// ── S03: Agenda ──────────────────────────────────────────────────────────────
cSlide("Session Roadmap — 8 Sections",[
  {text:"Section 1  Anatomy & spectrum of SV lesions"},
  {text:"Section 2  Core physiology — parallel circulation & Qp:Qs"},
  {text:"Section 3  Stage 1 (Norwood/Sano/Hybrid): ICU challenges"},
  {text:"Section 4  Interstage period: home monitoring & readmissions"},
  {text:"Section 5  Stage 2 (Glenn): passive flow ICU management"},
  {text:"Section 6  Stage 3 (Fontan): physiology, targets & acute management"},
  {text:"Section 7  Specific complications: PLE, plastic bronchitis, arrhythmias, ECMO"},
  {text:"Section 8  End-stage Fontan: FALD, transplant, palliative care"},
],"Road-map slide — 35 slides / ~35 minutes; or 35 slides / 20 minutes if you skip Q&A between sections. Recommend a 5-minute Q&A after Section 3 (Stage 1) as that is the most complex.",{tag:"MAP",tagColor:MID});

// ── S04: Section 1 divider ───────────────────────────────────────────────────
secDivider("1","Anatomy & Spectrum","Classifying single ventricle lesions");

// ── S05: Anatomy overview ────────────────────────────────────────────────────
cSlide("Single Ventricle: True vs Functional",[
  {text:"True anatomic SV: only one ventricular chamber present",sub:["Double-inlet LV: both AV valves → morphologic LV (most common true SV)","Double-outlet RV: rare — both great vessels + both AV valves → RV"]},
  {text:"Functional SV: 2 ventricles present, 2nd is inadequate",sub:["HLHS: hypoplastic LV — cannot sustain systemic circulation","Tricuspid atresia: absent tricuspid valve, hypoplastic RV","Unbalanced AV canal: common valve positioned over one ventricle","Pulmonary atresia with intact septum: RV hypoplasia spectrum"]},
  {text:"Critical distinction: morphology of the systemic ventricle",sub:["Morphologic LV as systemic pump = better long-term function","Morphologic RV as systemic pump (HLHS) = higher failure & transplant risk"]}
],"Fuster & Hurst (Ch.69): 'The single functional ventricle could be morphologically right (RV) or left (LV), with the second ventricle usually hypoplastic and/or insufficiently functional for biventricular correction.' The RV is designed for low-pressure pulmonary circulation — when forced to sustain systemic afterload long-term, it remodels unfavourably. This explains why HLHS patients have worse long-term outcomes than tricuspid atresia patients.",{tag:"ANATOMY",tagColor:MID});

// ── S06: HLHS anatomy + fetal echo ───────────────────────────────────────────
cSlide("HLHS: The Prototypical Stage 1 Lesion",[
  {text:"Hypoplastic left heart syndrome: spectrum of left-sided obstructive disease",sub:["Mitral stenosis/atresia + aortic stenosis/atresia","Nearly absent LV cavity in severe forms","Severe aortic arch hypoplasia — requires reconstruction"]},
  {text:"Neonatal ductal dependence",sub:["Systemic circulation depends on PDA — close PDA = death","PGE₁ infusion is life-saving bridge to surgery","Maintain PDA with PGE₁ 0.01–0.1 mcg/kg/min"]},
  {text:"3 sub-types for surgical planning",sub:["MS/AS (mitral stenosis + aortic stenosis) — small but functional LV possible","MA/AS (mitral atresia + aortic stenosis) — no antegrade LV flow","MA/AA (mitral atresia + aortic atresia) — most severe; highest Norwood risk"]},
  {text:"All require neonatal surgery: Norwood / Hybrid procedure",color:RED}
],"The fetal echo (right panel) shows the 4-chamber view. In HLHS, the LV is tiny/absent. Prenatal diagnosis allows planned delivery at a cardiac centre — dramatically improves outcomes. PGE₁: start as soon as HLHS is suspected, even before confirmatory echo. Dose titration: start 0.05, reduce to 0.01-0.025 once duct confirmed open. Higher doses (>0.05): apnea risk — be ready to intubate.",{tag:"HLHS",tagColor:RED,imgKey:"fetal_echo",imgCaption:"Fetal echo 4-chamber: normal biventricle (L) vs dominant single ventricle (R). (PMC/CC-BY)"});

// ── S07: Other SV lesions ────────────────────────────────────────────────────
cSlide("Tricuspid Atresia, DILV & Heterotaxy",[
  {text:"Tricuspid atresia — 1.2/10,000",sub:["Absent tricuspid valve → no RV inflow → hypoplastic RV","Single morphologic LV — good long-term systemic pump","Category by PA relationship + degree of PS: determines initial surgery","Ductal-dependent PBF → mBT shunt; excessive PBF → PA band"]},
  {text:"Double-inlet left ventricle (DILV)",sub:["Both AV valves connect to LV — most common true SV","Bulboventricular foramen to hypoplastic infundibular outflow","Great vessel relationship determines Norwood vs Glenn first path"]},
  {text:"Heterotaxy syndromes (situs ambiguus)",sub:["Asplenia (right isomerism): bilateral right-sidedness, AV canal, TAPVD, DORV","Polysplenia (left isomerism): bilateral left-sidedness, IVC interruption, azygos continuation","IVC interruption → can still Fontan via hepatic venous connection (Kawashima variant)"]},
  {text:"Unbalanced AV canal → SV palliation when one ventricle hypoplastic",color:AMBER}
],"Sabiston (Ch.113): 'Tricuspid atresia is the template of a single-ventricle lesion for which most current palliative strategies were developed.' Heterotaxy has worst outcomes — often associated with TAPVD + asplenia (overwhelming sepsis risk from encapsulated organisms → prophylactic penicillin for life). Kawashima operation = bidirectional Glenn for azygos-IVC drainage. DILV: Damus-Kaye-Stansel (DKS) anastomosis used when bulboventricular foramen threatens to restrict systemic outflow.",{tag:"ANATOMY",tagColor:MID});

// ── S08: Section 2 divider ───────────────────────────────────────────────────
secDivider("2","Core Physiology","Parallel circulation • Qp:Qs • Saturation targets");

// ── S09: Parallel circulation diagram (conceptual) ───────────────────────────
cSlide("Series vs Parallel: The Fundamental Difference",[
  {text:"Normal biventricular circulation: SERIES",sub:["Venous blood → RV → lungs → LV → systemic circulation","Each ventricle handles only its own circuit's blood"]},
  {text:"Single ventricle: PARALLEL",sub:["One pump ejects into BOTH circuits simultaneously via mixing",  "Fraction to lungs (Qp) + fraction to body (Qs) = total CO","Qp and Qs compete — gain in one = loss in the other"]},
  {text:"Two fundamental physiologic problems",sub:["Problem 1: Cyanosis — deoxygenated blood mixes with oxygenated","Problem 2: Volume overload — ventricle pumps combined Qp+Qs (up to 3× normal)"]},
  {text:"The SV is chronically volume-overloaded pre-Glenn, then preload-deprived post-Fontan",color:RED},
  {text:"Long-term: volume overload → ventricular dilation → dysfunction → Fontan failure",color:AMBER}
],"This is the foundational concept. The single ventricle is doing the work of two ventricles in Stage 1 — pumping 2-3× normal cardiac output to maintain adequate systemic delivery. By Stage 3, it is 'unloaded' into a low-volume state but now completely preload-deprived (Fontan CVP is the only filling force). Both extremes are deleterious — understand this progression.",{tag:"CORE PHYSIOLOGY",tagColor:MID});

// ── S10: Qp:Qs mastery ──────────────────────────────────────────────────────
cSlide("Qp:Qs Ratio — The Master Variable",[
  {text:"Qp:Qs = pulmonary blood flow ÷ systemic blood flow",color:BLUE},
  {text:"Target Qp:Qs ≈ 1 in Stage 1 (balanced circulation)",sub:["SpO₂ 75–85% as a surrogate target","SvO₂ >55% as global O₂ delivery monitor"]},
  {text:"Qp:Qs > 1 (pulmonary overcirculation)",sub:["SpO₂ >90% → 'good sats but dying'","Low BP, high lactate, acidosis","Lungs steal CO from body → systemic hypoperfusion"]},
  {text:"Qp:Qs < 1 (pulmonary undercirculation)",sub:["SpO₂ <70% → severe cyanosis, inadequate O₂ delivery","Inadequate PBF — may indicate shunt thrombosis or stenosis"]},
  {text:"Determinants of Qp:Qs balance",sub:["PVR (pulmonary vascular resistance) — manipulated by FiO₂ and PaCO₂","SVR (systemic vascular resistance) — manipulated by vasopressors/dilators","Shunt size and resistance — anatomically fixed post-op"]},
  {text:"FORMULA: Qp/Qs = (SaO₂ − SvO₂) / (SpvO₂ − SpaO₂) — Fick principle",color:AMBER}
],"The Fick equation applied: if you know arterial sat, mixed venous sat, and pulmonary venous sat, you can calculate Qp:Qs. In practice: use SpO₂ as bedside surrogate. Critical teaching: SpO₂ 90% after Norwood = DANGEROUS overcirculation, not reassuring. Many nurses/junior residents will panic at SpO₂ 78% in a post-Norwood patient — explain that this is EXPECTED and DESIRED.",{tag:"CORE PHYSIOLOGY",tagColor:RED});

// ── S11: Oxygen and CO2 as levers ────────────────────────────────────────────
cSlide("Ventilation as the ICU's Most Powerful Qp:Qs Tool",[
  {text:"O₂ is a PULMONARY VASODILATOR — highest impact lever",sub:["↑ FiO₂ → ↓ PVR → ↑ Qp → pulmonary overcirculation","NEVER give high FiO₂ reflexively to a post-Norwood baby"]},
  {text:"CO₂ is a PULMONARY VASOCONSTRICTOR",sub:["↑ PaCO₂ → ↑ PVR → ↓ Qp → better systemic flow","Permissive hypercapnia (PaCO₂ 45–55 mmHg) = target in Stage 1","'Baby is pinking up' after Norwood = warn = overcirculation"]},
  {text:"Sub-ambient oxygen (FiO₂ 0.17–0.21) — active strategy for overcirculation",sub:["N₂ added to blended gas to reduce FiO₂ below room air","Validated in some centres; not universally adopted"]},
  {text:"Ventilation mode targets in Stage 1",sub:["Avoid over-ventilation: PaCO₂ target 45–55","pH 7.35–7.45; accept mild respiratory acidosis","Low PEEP (3–5 cmH₂O): high PEEP ↑ PVR but impairs venous return"]},
  {text:"After Glenn/Fontan: opposite strategy — early extubation is key",color:GREEN}
],"This is the most counterintuitive but important ICU management concept. The residents need to remember: in a post-Norwood patient who desaturates from 82% to 72%, the FIRST thing to do is NOT increase FiO₂. Check BP, lactate, SvO₂. If hemodynamically stable → likely transient. If hemodynamically compromised → problem is shunt, not ventilation. Only adjust FiO₂/CO₂ after ruling out structural issues.",{tag:"VENTILATION",tagColor:BLUE});

// ── S12: Section 3 divider ───────────────────────────────────────────────────
secDivider("3","Stage 1 ICU Challenges","Post-Norwood / Sano / Hybrid — the most vulnerable period");

// ── S13: Norwood procedure anatomy ──────────────────────────────────────────
cSlide("Stage 1 Procedures: Norwood / Sano / Hybrid",[
  {text:"Norwood procedure (standard) — performed day 1–14 of life",sub:["Neo-aorta: native PA divided + anastomosed to hypoplastic aortic arch","Atrial septectomy: unobstructed mixing at atrial level","PBF source: modified BT shunt (MBTS) 3.0–4.0 mm Gore-Tex"]},
  {text:"Sano modification — RV-PA conduit replaces MBTS",sub:["5 mm Gore-Tex conduit: RV ventriculotomy → branch PA","Better diastolic BP (no diastolic steal) → better coronary perfusion","Downside: RV scar → long-term RV dysfunction risk; conduit obstruction"]},
  {text:"Hybrid procedure — for high-risk / low birth weight (<2 kg)",sub:["No CPB in Stage 1: ductal stent + surgical bilateral PA bands","Maintains ductal patency → systemic flow","Stage 2 = combined arch reconstruction + Glenn (technically demanding)","Miller's Anesthesia: 'Hybrid may offer survival advantage in LBW neonates but not a low-risk alternative for most HLHS'"]},
  {text:"Goal of ALL Stage 1 procedures: adequate systemic O₂ delivery + pulmonary protection",color:AMBER}
],"Sabiston (Ch.113) and Miller's Anesthesia (Ch.73) both describe these techniques. The choice between MBTS and Sano is center-dependent. MBTS: the 'steal' phenomenon means diastolic runoff into pulmonary bed — in a baby with coronary dependence on diastolic filling, this can be fatal. Sano eliminates this but creates an RV ventriculotomy. Hybrid: increasing use with ductal stents — avoids CPB in fragile neonates but creates a more complex stage 2.",{tag:"STAGE 1",tagColor:AMBER,imgKey:"fetal_echo",imgCaption:"Fetal echo: single dominant ventricle — HLHS. (PMC/CC-BY)"});

// ── S14: Post-Norwood hemodynamic targets ────────────────────────────────────
cSlide("Post-Norwood ICU: Hemodynamic Targets & Monitoring",[
  {text:"TARGET TRIAD: SpO₂ 75–85%  |  SvO₂ >55%  |  Lactate <2 mmol/L",color:RED},
  {text:"Monitoring modalities",sub:["NIRS (near-infrared spectroscopy): cerebral >50%, somatic >50%","SVC or RA line: mixed venous O₂ saturation","Left atrial (LA) line: filling pressure, target LA 5–10 mmHg","Radial or umbilical arterial line: continuous BP + ABG"]},
  {text:"Haemodynamic targets",sub:["MAP >50 mmHg (neonatal)","CVP 5–10 mmHg","HR 120–160 bpm — maintain sinus rhythm if possible"]},
  {text:"Vasoactive drug strategy",sub:["Milrinone 0.25–0.75 mcg/kg/min: inotropy + PVR reduction (mainstay)","Dopamine 3–10 mcg/kg/min: renal-protective dosing","Epinephrine 0.05–0.3 mcg/kg/min: for low CO states","Vasopressin 0.0003–0.002 units/kg/min: vasopressor with minimal PVR effect"]},
  {text:"Heparin infusion: maintain shunt patency (aPTT 60–80 sec)",color:AMBER}
],"LA line is technically placed intraoperatively by surgeon via a tiny left atrial vent. In most Norwood patients, LA pressure reflects LV filling pressure and is the best guide for fluid management. NIRS: regional cerebral oximetry detects cerebral desaturation before systemic SpO₂ changes. Somatic NIRS: placed on the abdomen — drop in somatic NIRS may be the first sign of NEC or mesenteric ischemia. Vasopressin is increasingly used as it raises SVR without worsening PVR.",{tag:"STAGE 1 TARGETS",tagColor:AMBER});

// ── S15: Post-Norwood ventilation ────────────────────────────────────────────
cSlide("Post-Norwood Ventilation Strategy",[
  {text:"Phase 1: Immediate post-op (first 24–48h) — intubated",sub:["FiO₂: start 0.21 (room air), titrate to SpO₂ target 75–85%","Rate: 30–40/min neonate; tidal volume 5–6 mL/kg","PaCO₂ target: 45–55 mmHg (permissive hypercapnia)","PEEP: 3–5 cmH₂O — balance PVR vs venous return"]},
  {text:"Overcirculation protocol (SpO₂ >90% + acidosis/low BP)",sub:["STEP 1: Reduce FiO₂ to 0.18–0.21","STEP 2: Allow PaCO₂ to rise to 50–55","STEP 3: Consider N₂-supplemented gas mixture","STEP 4: Echo urgently — rule out residual RVOTO/shunt stenosis","STEP 5: Phenylephrine bolus — ↑ SVR to reduce Qp:Qs"]},
  {text:"Undercirculation protocol (SpO₂ <70% + low CO)",sub:["STEP 1: Increase FiO₂ to 0.40–0.50","STEP 2: Hyperventilate mildly (PaCO₂ 38–42)","STEP 3: Echo urgently — shunt thrombosis / stenosis?","STEP 4: Heparin bolus if shunt thrombosis suspected","STEP 5: Cath lab or ECMO if no improvement"]},
  {text:"Extubation: typically 3–7 days post-Norwood; Sano may allow earlier",color:GREEN}
],"Systematic approach is key. When you see a post-Norwood desaturation — DON'T PANIC. Follow the protocol. Get an immediate bedside echo. Blood gas. Check the NIRS trends. The biggest mistake is reflexively increasing FiO₂ in a patient with overcirculation — you'll make them worse. Extubation post-Norwood: earlier in Sano (less steal, less haemodynamic lability). Some programs do same-day extubation with very careful patient selection.",{tag:"VENTILATION",tagColor:BLUE});

// ── S16: Low CO crisis Stage 1 ──────────────────────────────────────────────
calloutSlide("Low Cardiac Output Crisis — Stage 1: The 4 Ps",[
  {bg:"1A0F28",border:RED,head:"P1 — PRELOAD",headColor:RED,body:"LA pressure <5 → volume challenge 5–10 mL/kg\nLA pressure >12 → diuresis; consider AV valve issue\nTarget LA 6–10 mmHg"},
  {bg:"0A1A2E",border:AMBER,head:"P2 — PUMP (Contractility)",headColor:AMBER,body:"SvO₂ <50%, poor function on echo\n→ Epinephrine 0.05–0.3 mcg/kg/min\n→ ECMO if no response"},
  {bg:"0F1F35",border:BLUE,head:"P3 — PVR (Pulmonary Vasoconstriction)",headColor:BLUE,body:"High SpO₂ + low BP + high lactate\n→ ↓ FiO₂, ↑ PaCO₂\n→ Phenylephrine to ↑ SVR\n→ iNO ONLY if confirmed ↑ PVR"},
  {bg:"12213A",border:GREEN,head:"P4 — PLUMBING (Residual Anatomy)",headColor:GREEN,body:"Echo: arch gradient? Shunt stenosis?\nAV valve regurgitation? Tamponade?\n→ Cath if anatomic cause suspected\n→ Re-operation if confirmed"}
],"The 4-P framework gives trainees a systematic approach to low CO in Stage 1. PLUMBING is the most commonly missed — an undetected arch obstruction gradient of even 20 mmHg post-Norwood will cause progressive low CO that does not respond to any drug. Echo FIRST, always. Tamponade: mediastinal drainage must be assessed — drainage <1 mL/kg/hr in first 24h is suspicious.",RED);

// ── S17: Section 4 divider ───────────────────────────────────────────────────
secDivider("4","The Interstage Period","Home monitoring • Interstage mortality • Re-admissions");

// ── S18: Interstage challenges ──────────────────────────────────────────────
cSlide("The Interstage Period: A Hidden Danger",[
  {text:"Interstage = time from Stage 1 discharge to Stage 2 Glenn (~4–6 months)",color:RED},
  {text:"Interstage mortality: 10–15% historically; 5–8% at experienced centres now",sub:["Most deaths: sudden unexpected cardiac death, aspiration, intercurrent illness","ECMO use interstage: 2026 systematic review (PMID 42294780) — poor outcomes but salvageable in some"]},
  {text:"Why the interstage is dangerous",sub:["Shunt-dependent physiology at home — any event can be catastrophic","Neonates: obligate nasal breathers, feeding difficulties, high intercurrent infection risk","Single ventricle + single shunt = no backup if shunt fails"]},
  {text:"Interstage home monitoring programmes",sub:["Daily SpO₂ monitoring: parent-performed at home","Daily weight: early indicator of cardiac decompensation","Feeding logs: failure to thrive = early warning of haemodynamic compromise","Pulse oximetry alerts: SpO₂ <75% or weight gain >30g/day → emergency call"]},
  {text:"Nasogastric / gastrostomy tube feeding: 40–60% of interstage patients require NGT",color:AMBER}
],"PMID 42294780 (Li D et al, JACC 2026): systematic review of ECMO in interstage — incidence ~3%, survival to discharge ~45%. Interstage home monitoring was pioneered by Cincinnati Children's and has been shown to reduce interstage mortality. The programme requires parental education, 24/7 on-call coverage, and clear escalation pathways. SpO₂ trending downward over days (even still 'acceptable') should prompt admission.",{tag:"INTERSTAGE",tagColor:AMBER});

// ── S19: Interstage nutrition + NEC ─────────────────────────────────────────
cSlide("Interstage Nutrition & NEC Risk",[
  {text:"Feeding challenges are near-universal in Stage 1 survivors",sub:["Cardiac output limitation → gut hypoperfusion → poor feeding tolerance","Vocal cord paralysis (recurrent laryngeal nerve injury) from arch reconstruction","Phrenic nerve injury → diaphragm paralysis","Oral aversion from prolonged intubation/NG feeds"]},
  {text:"Nutritional targets",sub:["120–150 kcal/kg/day — higher than standard due to increased metabolic demand","High-calorie feeds (24–30 kcal/oz) to limit volume load on the heart","Slow advancement: 1–2 mL/kg/feed increase every 24h post-op"]},
  {text:"NEC (necrotising enterocolitis) in CHD",sub:["CHD-NEC: 3–5× higher risk than prematurity-related NEC","Mesenteric underperfusion (low Qs) is the trigger","Most dangerous in first 72h post-Norwood","Somatic NIRS drop: first sign — acts before clinical signs"]},
  {text:"NEC management: NPO + IV antibiotics + surgical referral; high mortality in SV context",color:RED}
],"HLHS patients with MBTS have lower diastolic BP (diastolic steal into pulmonary circulation) → lower mesenteric diastolic flow → higher NEC risk vs Sano. Several studies show lower NEC in Sano modification. NIRS: the mesenteric NIRS pad placed on the right flank (liver) or left flank can detect NEC before clinical signs. Any somatic NIRS drop >20% from baseline should prompt urgent assessment.",{tag:"INTERSTAGE",tagColor:AMBER});

// ── S20: Section 5 divider ───────────────────────────────────────────────────
secDivider("5","Stage 2 — Bidirectional Glenn","Passive superior cavopulmonary flow — a new paradigm");

// ── S21: Glenn physiology ────────────────────────────────────────────────────
cSlide("Stage 2: Bidirectional Glenn — Physiology",[
  {text:"Performed at 4–6 months of age (weight ≥5 kg, PVR <2 Wood units)",color:BLUE},
  {text:"Anatomy: SVC anastomosed to right PA (bidirectional = both PAs receive flow)",sub:["BT shunt / Sano conduit taken down","IVC still returns to heart → passes through and contributes to cardiac output","SVC-only pulmonary supply = ~40–45% of venous return"]},
  {text:"Key physiologic change: passive pulmonary flow",sub:["No ventricular pump drives pulmonary circulation","Flow = (SVC pressure − LA pressure) / PVR","CVP 10–14 mmHg 'pushes' blood through pulmonary bed"]},
  {text:"Ventricular unloading",sub:["Pre-Glenn: ventricle pumps 200–300% of normal (Qp+Qs)","Post-Glenn: ventricle pumps only systemic flow + IVC mixing","Significant decrease in volume overload → remodelling of the SV"]},
  {text:"SpO₂ target post-Glenn: 75–85% (IVC admixture via atria still present)",color:AMBER},
  {text:"Pulmonary AVMs: develop in Glenn without hepatic factor → resolve after Fontan",color:RED}
],"Sabati A et al (Future Cardiol 2025, PMID 41346285): reviewed optimising outcomes for superior cavopulmonary connection — key factors: PVR <2 Wood units, adequate PA size, no significant AV valve regurgitation, good ventricular function. Pulmonary AVMs: hepatic venous effluent contains a 'hepatic factor' (possibly HGF, HB-EGF) that prevents AVMs. When hepatic veins drain into the heart separately from the Glenn, AVMs form in the lungs supplied by the Glenn. After Fontan, hepatic blood reaches all pulmonary segments → AVMs regress.",{tag:"STAGE 2",tagColor:BLUE});

// ── S22: Glenn ICU management ────────────────────────────────────────────────
cSlide("Stage 2: Glenn ICU Challenges",[
  {text:"#1 challenge: maintain passive pulmonary flow",sub:["ANYTHING that raises PA pressure or LA pressure kills the gradient","Target transpulmonary gradient (CVP − LA) >5 mmHg"]},
  {text:"Ventilation — reversed priorities from Stage 1!",sub:["Early extubation: negative intrathoracic pressure AUGMENTS passive flow","Low PEEP 3–5 cmH₂O maximum","Spontaneous breathing > positive pressure ventilation","Avoid prolonged intubation — every hour of PPV costs passive PBF"]},
  {text:"PVR management",sub:["iNO: 5–20 ppm for acute PVR elevation post-op","Sildenafil: PDE5 inhibitor, lowers PVR — started in some centres post-Glenn","Avoid hypoxia, hypercarbia, acidosis — all raise PVR"]},
  {text:"Pleural effusions: 15–25% post-Glenn",sub:["Bilateral: more concerning (lymphatic hypertension)","MCT formula reduces lymph flow","Chest tubes: manage aggressively — prolonged effusions → failure to thrive"]},
  {text:"SVC syndrome: rare but serious — SVC obstruction → cerebral oedema, massive pleural effusions",color:RED}
],"Glenn ICU: the paradigm flip is the key teaching point. In Stage 1: positive pressure ventilation is acceptable/needed. In Stage 2: every day of intubation is a day of impaired passive pulmonary flow. Aim to extubate within 24h post-Glenn if possible. Pleural effusions: high-output chylothorax (triglycerides >110 mg/dL) → MCT formula, fasting + TPN, octreotide 1–10 mcg/kg/hr. SVC syndrome post-Glenn is a surgical emergency — chest re-opening or interventional cath.",{tag:"STAGE 2",tagColor:BLUE});

// ── S23: Section 6 divider ───────────────────────────────────────────────────
secDivider("6","Stage 3 — The Fontan","Total cavopulmonary connection • ICU targets • Acute failure");

// ── S24: Fontan anatomy with textbook diagram ─────────────────────────────────
imgSlide(
  "Fontan Procedure: 3 Anatomic Types",
  "fontan_anatomy",
  [
    "Atriopulmonary (historical):",
    "  • RA directly to PA",
    "  • Massive RA dilation",
    "  • High arrhythmia burden",
    "",
    "Lateral tunnel:",
    "  • Intra-atrial baffle IVC → PA",
    "  • Some PA pulsatility retained",
    "",
    "Extracardiac conduit:",
    "  • Gore-Tex tube IVC → PA",
    "  • Current standard",
    "  • Lowest sinus node injury",
    "  • Fenestration optional",
  ],
  "Fig. 69-1 from Fuster & Hurst's The Heart, 15th Ed. (Licensed textbook CDN)",
  "Fuster & Hurst (Ch.69): 'The total cavopulmonary connection has been associated with improved flow dynamics, lesser risk of thrombus formation, reduced incidence of atrial arrhythmias, and elimination of complications such as pulmonary venous obstruction by a massively enlarged atrium.' The extracardiac conduit is now the preferred technique at most centres. Fenestration (4 mm hole) creates a controlled right-to-left shunt — increases CO but lowers SpO₂ to ~90%. Can be closed in the cath lab later.",
  BLUE
);

// ── S25: Fontan physiology ───────────────────────────────────────────────────
cSlide("Fontan Physiology: The Haemodynamic Compromise",[
  {text:"After Fontan: IVC flow joins SVC flow → both cavae → pulmonary arteries",sub:["Complete cavopulmonary connection = total passive pulmonary flow","No sub-pulmonary ventricle — ever"]},
  {text:"Obligatory haemodynamic consequences",sub:["Elevated CVP (10–18 mmHg): drives passive pulmonary flow","Reduced cardiac output: single ventricle chronically preload-limited","Non-pulsatile pulmonary flow: affects all end-organs"]},
  {text:"'Successful' Fontan = mild venous congestion + modest CO reduction",color:GREEN},
  {text:"4 categories of Fontan failure (Fuster & Hurst)",sub:["1. Systolic/diastolic dysfunction (RV as systemic = worse prognosis)","2. AV or aortic valve regurgitation (worsens preload deprivation)","3. Systemic complications: PLE, plastic bronchitis, cirrhosis, cyanosis","4. ↑ PVR: PA remodelling or chronic thromboemboli"]},
  {text:"Fontan physiology mnemonic: PAID — Preload dependent, Afterload Intolerant, Inotrope responsive, Decompensates with arrhythmia",color:AMBER}
],"Fuster & Hurst (Ch.69): 'A Fontan is considered successful if venous congestion is mild, along with the reduction in cardiac output. In contrast, a failing Fontan is characterized by marked venous congestion and a substantial reduction in cardiac output.' The 'PAID' mnemonic is a useful teaching tool: Preload dependent (give fluids carefully — but don't over-diurese), Afterload Intolerant (ACE inhibitors, milrinone — do not over-load the SVR), Inotrope responsive (milrinone works well), Decompensates with arrhythmia (IART → CO halved).",{tag:"STAGE 3",tagColor:BLUE});

// ── S26: Fontan ICU targets with CT/TEE image ────────────────────────────────
cSlide("Fontan: Post-Op ICU Targets",[
  {text:"Haemodynamic targets",sub:["CVP (Fontan pressure): 10–14 mmHg","LA pressure: 5–10 mmHg","Transpulmonary gradient (CVP−LA): ideally 6–12 mmHg","MAP: >60 mmHg","SpO₂: ≥90% (fenestrated) or ≥95% (non-fenestrated)"]},
  {text:"Key drugs",sub:["Milrinone 0.25–0.75 mcg/kg/min: standard post-op","iNO 5–20 ppm: acute PVR crisis","Sildenafil: started post-op in some high-PVR centres","Diuretics: furosemide ± aldactone — crucial for venous congestion"]},
  {text:"Fluid strategy",sub:["Volume bolus 5 mL/kg for low CVP (<8) + low CO","Over-filling → ↑ LA → ↓ transpulmonary gradient","Restrictive fluids 80–100% maintenance after 24h"]},
  {text:"Early extubation: within 24h if possible — same rationale as Glenn",color:GREEN},
  {text:"Fenestration: if CVP >16 or low CO — consider creating/enlarging fenestration in cath lab",color:AMBER}
],"The CT image (right panel) shows the extracardiac Fontan conduit (FC) as a white tubular structure adjacent to the heart, with the pulmonary venous atrium (SA). TEE panels show AV valve regurgitation (AVR) — the second most common cause of Fontan failure. Use echo to distinguish: High CVP + High LA → ventricular problem or AV valve regurgitation. High CVP + Normal LA → PVR problem or conduit obstruction.",{tag:"STAGE 3 TARGETS",tagColor:BLUE,imgKey:"fontan_ct_tee",imgCaption:"CT: Fontan conduit (FC). TEE: AV valve regurgitation (AVR) panels B–D. (PMC/CC-BY)"});

// ── S27: Section 7 divider ───────────────────────────────────────────────────
secDivider("7","Specific ICU Complications","Arrhythmias • PLE • Plastic Bronchitis • ECMO");

// ── S28: Arrhythmias ─────────────────────────────────────────────────────────
cSlide("Arrhythmias in Single Ventricle Patients",[
  {text:"Incidence: 40–60% of Fontan patients develop clinically significant SVT by adulthood",color:RED},
  {text:"IART (intra-atrial re-entrant tachycardia) — most common in Fontan",sub:["Macro re-entry around atriotomy scars / baffle suture lines","Rate: 100–150 bpm — looks 'non-alarming' but is haemodynamically devastating","Czosek RJ et al (PACE 2026, PMID 41404994): arrhythmia during SV palliation worsens outcomes"]},
  {text:"Why arrhythmias are so dangerous in Fontan",sub:["AV synchrony is essential — loss of atrial kick → CO drops 20–40%","Tachycardia → diastolic filling time ↓ → preload ↓ → cardiac output ↓","Atrial dilation + stasis → thrombus → embolism"]},
  {text:"Acute management protocol",sub:["Step 1: Anticoagulate immediately (IV heparin) — thrombus in dilated atrium","Step 2: Rate control: IV amiodarone 5 mg/kg over 30 min","Step 3: DC cardioversion if haemodynamically unstable (do NOT delay)","Step 4: 12-lead ECG post-cardioversion; consider electrophysiology consult"]},
  {text:"Sinus node dysfunction: very common post-Fontan → pacemaker (epicardial leads)",color:AMBER},
  {text:"Junctional rhythm post-op: AV pacing to restore synchrony can rescue low CO",color:GREEN}
],"Czosek RJ et al (Pacing Clin Electrophysiol 2026, PMID 41404994): outcomes of patients with arrhythmia during single-ventricle palliation — arrhythmia at any stage is associated with significantly increased mortality and transplant listing. In the PICU: a Fontan patient with HR 130 and 'acceptable' BP may be in IART — do a 12-lead. IART often not visible on monitor strip. DC cardioversion in Fontan patients is generally safe — anticoagulate first if AF/flutter >48h.",{tag:"ARRHYTHMIAS",tagColor:RED});

// ── S29: PLE detail ──────────────────────────────────────────────────────────
cSlide("Protein-Losing Enteropathy (PLE)",[
  {text:"Incidence: 3–13% of Fontan patients; develops 5–15 years post-Fontan",color:RED},
  {text:"Pathophysiology",sub:["Elevated CVP → mesenteric venous hypertension → lymphatic engorgement","Gut lymphatics fail → protein-rich lymph leaks into intestinal lumen","Net result: massive protein loss from blood into gut"]},
  {text:"Diagnosis: serum albumin <3.5 g/dL + stool alpha-1-antitrypsin >150 mg/24h",color:BLUE},
  {text:"Clinical features",sub:["Hypoalbuminaemia, oedema, ascites, diarrhoea","Immunodeficiency: low IgG (protein loss) → recurrent infections","Lymphopenia (despite low protein — paradoxical) → T-cell loss"]},
  {text:"ICU triggers: acute illness, arrhythmia, surgery, dehydration → acute decompensation",color:AMBER},
  {text:"Treatment ladder",sub:["1st: MCT diet + high-protein; furosemide + spironolactone","2nd: Subcutaneous heparin (restores gut glycocalyx heparan sulfate)","3rd: Budesonide (anti-inflammatory → gut barrier restoration)","4th: Octreotide (↓ splanchnic blood flow → ↓ lymph production)","5th: Sildenafil (↓ Fontan pressure → ↓ mesenteric venous HTN)","6th: Cardiac catheterisation — Fontan revision or fenestration","7th: Heart transplant if refractory"]}
],"Mackie AS et al (Can J Cardiol 2022, PMID 35314335): plastic bronchitis and PLE — evolving understanding. Heparin mechanism: heparan sulfate proteoglycans in the gut mucosa are depleted in PLE; exogenous heparin restores them and reduces protein leakage. This is NOT an anticoagulation effect. Albumin replacement in ICU: give 20% albumin but address the underlying leak — albumin infusion alone is wasted. Alsaied T et al (PMID 39712273) and Barracano R et al (PMID 39712272): comprehensive reviews of PLE pathophysiology and outcomes.",{tag:"PLE",tagColor:RED});

// ── S30: Plastic bronchitis ──────────────────────────────────────────────────
cSlide("Plastic Bronchitis: A Life-Threatening Complication",[
  {text:"Incidence: ~1–2% of Fontan patients — rare but catastrophic",color:RED},
  {text:"Pathophysiology",sub:["Lymphatic hypertension → pulmonary lymphatic leak → airway lymph accumulation","Fibrin + mucin polymerise → rubbery casts that mould to bronchial tree","Casts cause acute lobar obstruction → respiratory failure + hypoxia"]},
  {text:"Clinical presentation",sub:["Acute respiratory distress ± complete lobar collapse on CXR","Patient may spontaneously expectorate rubbery casts (diagnostic)","CT chest: branching high-density filling airway tree"]},
  {text:"ICU emergency management",sub:["Step 1: High-flow O₂ / HFNC; prepare for bronchoscopy","Step 2: Urgent flexible bronchoscopy — cast removal (may require rigid scope)","Step 3: DNase (dornase alfa) 2.5 mg nebulised BD — softens casts","Step 4: tPA 4 mg nebulised (off-label) — dissolves fibrin matrix","Step 5: Chest physiotherapy + postural drainage"]},
  {text:"Chronic management: sildenafil, bosentan, thoracic duct embolisation (CHOP protocol)",color:BLUE},
  {text:"Refractory: lung/heart-lung/heart transplant",color:AMBER}
],"Mackie AS et al (Can J Cardiol 2022, PMID 35314335): thoracic duct embolisation — CHOP (Children's Hospital of Philadelphia) protocol involves lymphangiography, identification of the thoracic duct with contrast, and embolisation to reduce lymphatic pressure. This is transformative for refractory cases. tPA nebulisation: off-label but increasingly adopted. Evidence is case-series level. DNase is standard of care. Key bedside recognition: the patient who can't breathe and then coughs up what looks like a 'tree branch' — that IS the diagnosis.",{tag:"PLASTIC BRONCHITIS",tagColor:RED});

// ── S31: ECMO in single ventricle ────────────────────────────────────────────
twoCol("ECMO in Single Ventricle Patients",
  [
    "INDICATIONS",
    "• Post-Norwood: refractory low CO, shunt crisis",
    "• Post-Glenn: PA hypertensive crisis, low CO",
    "• Post-Fontan: refractory circulatory failure",
    "• Bridge to cath (residual lesion), re-op, or transplant",
    "",
    "CONFIGURATION",
    "• VA-ECMO standard for cardiac failure",
    "• Fontan ECMO: cannula in Fontan circuit — drain from SVC + RA, return to aorta",
    "• Left heart decompression often needed in Fontan ECMO",
    "",
    "OUTCOMES — Post-Norwood interstage ECMO",
    "• 2026 systematic review (PMID 42294780): ~45% survival to discharge",
    "• Duration on ECMO and underlying anatomy are key predictors",
  ],
  [
    "CHALLENGES UNIQUE TO SV",
    "• Complex anatomy: no standard cannulation strategy",
    "• Fontan: decompressing a passive circuit on ECMO extremely difficult",
    "• Coronary steal risk in MBTS patients on VA-ECMO",
    "• Anticoagulation: higher bleeding risk from prior surgeries; liver disease",
    "",
    "MANAGEMENT ON ECMO",
    "• Sweep gas: titrate CO₂ and O₂ — same Qp:Qs principles apply",
    "• Echo-guided management: watch for LA distension",
    "• Atrial septostomy / LA vent if LA distension occurs",
    "• Decision window: 48–72h for bridge strategy decision",
    "",
    "VAD for Fontan",
    "• LVAD in Fontan: highly complex; few centres with experience",
    "• Reid CS et al (PMID 34812751): VAD for Fontan — who, when and why?",
  ],
  "ECMO: Indications & Cannulation",
  "ECMO: Challenges & Management",
  "Kamsheh AM et al (Front Pediatr 2022, PMID 36425396): management of circulatory failure after Fontan surgery. Zwischenberger JB et al (J Card Surg 2022, PMID 36321714): failing Fontan cardiovascular support — review of MCS options. Key message: ECMO in Fontan is technically feasible but survival is significantly lower than in biventricular patients. Decision-making should involve transplant team early.",
  BLUE, RED
);

// ── S32: Section 8 divider ───────────────────────────────────────────────────
secDivider("8","End-Stage Fontan & Beyond","FALD • Transplant • Palliation");

// ── S33: Fontan complications overview ──────────────────────────────────────
imgSlide(
  "Multiorgan Complications of Fontan Palliation",
  "fontan_compl",
  [
    "Long-term complications:",
    "",
    "• Fontan-assoc. liver disease",
    "• Protein-losing enteropathy",
    "• Plastic bronchitis",
    "• Atrial arrhythmias",
    "• Sinus node dysfunction",
    "• Pulmonary vascular disease",
    "• Thromboembolism",
    "• Venous insufficiency",
    "• Altered lymphatic drainage",
    "• Chronic renal failure",
    "• Cyanosis",
    "• Neurodevelopmental disability",
  ],
  "Fuster & Hurst's Heart 15th Ed. Fig.69 Central Illustration — Multiorgan complications. (Licensed textbook CDN)",
  "Fuster & Hurst (Ch.69): 'A relatively uneventful clinical course during the first 10–15 years after Fontan surgery may be followed by the onset of complications such as arrhythmias, heart failure, increased pulmonary vascular resistance, protein losing enteropathy, thromboembolism, and liver disease.' This timeline is important — these patients can seem fine for a decade then decompensate. The management panel (right side of diagram) shows the management principles including: anticoagulation for arrhythmias, PH therapy for elevated Fontan pressure, PLE treatment, and transplantation for refractory cases.",
  BLUE
);

// ── S34: FALD + transplant ───────────────────────────────────────────────────
cSlide("Fontan-Associated Liver Disease & Transplant",[
  {text:"FALD: present in virtually ALL long-standing Fontan patients",color:RED},
  {text:"Pathophysiology",sub:["Chronically elevated CVP → hepatic sinusoidal congestion → perisinusoidal fibrosis","Reduced portal perfusion (low CO) → ischaemic hepatocyte injury","Combined: congestive + ischaemic injury → cirrhosis in 2nd–3rd decades"]},
  {text:"Monitoring: annual liver function, fibroscan, alpha-fetoprotein (AFP)",sub:["Hepatocellular carcinoma risk: 2–5% — screen with AFP + liver MRI 6-monthly in cirrhotic stage","Liver biopsy: risk of bleeding due to elevated CVP — use only if necessary"]},
  {text:"Thromboembolism",sub:["Lifelong anticoagulation: warfarin vs aspirin — controversial","2026 meta-analysis PMID 41071335: anticoagulation superior in Asian cohorts","AHA/AHA 2018 guidelines: anticoagulation for all prior thromboembolic event / atrial arrhythmias; discuss in others"]},
  {text:"Transplant: definitive treatment for failing Fontan",sub:["5-year survival post-transplant: 65–70%","Complex anatomy: multiple prior sternotomies, dense adhesions → high surgical risk","Combined heart-liver transplant: required if cirrhosis advanced (MELD >15)","Venkatesh P et al 2024 (PMID 38892760): Contemporary Management of the Failing Fontan"]},
  {text:"Fontan conversion + maze + PM: surgical option for arrhythmia-dominant failure (Kanakis M, PMID 38178331)",color:BLUE}
],"FALD progression: congestive hepatopathy → fibrosis → cirrhosis → HCC. Most patients with >10 years of Fontan have at least bridging fibrosis. Annual monitoring is standard of care. Heart transplant for Fontan is a high-risk operation — prior surgeries mean dense adhesions, abnormal anatomy, often requiring femoral CPB first. UNOS data: median wait time for Fontan patients is longer because of anatomic complexity and difficulty of the operation.",{tag:"END-STAGE",tagColor:BLUE,imgKey:"fontan_angio",imgCaption:"Catheter angiogram: Fontan conduit (FC) from IVC to PA — invasive haemodynamic assessment. (PMC/CC-BY)"});

// ── S35: Neurodevelopment + future ─────────────────────────────────────────
cSlide("Neurodevelopmental Outcomes & Future Directions",[
  {text:"Neurodevelopment: a critically underrecognised challenge",sub:["Selvanathan T et al (Can J Cardiol 2022, PMID 35157990): abnormal brain maturation + accumulation of brain injuries across the lifespan","Mean full-scale IQ: ~90 (10 points below normal); executive function most affected","White matter abnormalities on MRI: present in >50% by school age"]},
  {text:"Risk factors for neurodevelopmental impairment",sub:["DHCA duration >45 min; perioperative stroke; choreoathetosis","Genetic syndromes (22q11, Turner's, Trisomy 21)","Lower socioeconomic status; impaired parent-infant bonding from prolonged NICU stay"]},
  {text:"ICU contributions to neurodevelopment",sub:["NIRS-guided cerebral perfusion monitoring → reduce cerebral ischaemia","Avoid over-sedation: dexmedetomidine preferred to opioid infusions where possible","Developmental care: minimise noise/light disruption; kangaroo care when stable","Early neurodevelopmental follow-up: refer ALL SV patients at discharge"]},
  {text:"Future directions",sub:["Total artificial heart for Fontan bridge","Percutaneous Fontan (stage 3 via cath — Sabine et al 2019 proof-of-concept)","Exercise training programmes — demonstrate meaningful VO₂ improvement","Gene therapy targeting hepatic factor AVMs (experimental)"]},
  {text:"Renaud D et al (Metabolites 2023, PMID 37623876): metabolomics → targeted metabolic therapy potential in SV",color:BLUE}
],"Wrap-up with the human dimensions of SV care. These are not just surgical patients — they are children who will grow up, go to school, attempt university, work, and form relationships. Neurodevelopmental follow-up should be built into EVERY SV programme. The NICU/PICU team has a role: minimise pain/stress, promote parental bonding, reduce unnecessary sedation. Future: the percutaneous Fontan concept (creating the IVC-PA connection via catheter without surgery) is in early clinical trials — may transform Stage 3 outcomes.",{tag:"FUTURE",tagColor:GREEN});

// ── S36: Summary table ──────────────────────────────────────────────────────
tblSlide("ICU Management At-A-Glance: All 3 Stages",
  ["Parameter","Stage 1 Post-Norwood","Stage 2 Post-Glenn","Stage 3 Post-Fontan"],
  [
    ["SpO₂ target","75–85%","75–85%","≥90% (fenest.) / ≥95%"],
    ["SvO₂ target",">55%",">55%",">55%"],
    ["Ventilation key","Permissive hypercapnia PaCO₂ 45–55; FiO₂ ~0.21","Early extubation; low PEEP; neg pressure augments flow","Early extubation; low PEEP; iNO for ↑PVR"],
    ["Primary haemodynamic lever","FiO₂/PaCO₂ → Qp:Qs balance","PVR reduction; CVP 10–14","Transpulmonary gradient; PVR reduction"],
    ["First-line inotrope","Milrinone ± epinephrine","Milrinone","Milrinone ± epinephrine"],
    ["Key monitoring","NIRS (cerebral + somatic); LA line; SvO₂","CVP; pleural drain output; SvO₂","CVP; LA pressure; echo; transpulm. gradient"],
    ["Most dangerous pitfall","SpO₂ >90% = overcirculation!","High PEEP = kills passive flow","Arrhythmia → acute CO drop; untreated = arrest"],
    ["ECMO indication","Refractory low CO; shunt crisis","Rare; PA hypertensive crisis","Refractory failure; bridge to transplant"],
  ],
  "Distribute this table as a printed handout. It should be laminated and posted in PICU bays caring for SV patients. The most important boxes to emphasise: Stage 1 SpO₂ target (counterintuitive), Stage 2 ventilation (early extubation), Stage 3 arrhythmia danger.",
  AMBER
);

// ── S37: Closing take-home messages ─────────────────────────────────────────
{
  const s = pres.addSlide();
  addBg(s,DARK);
  s.addShape(pres.ShapeType.rect,{x:0,y:0,w:0.2,h:5.625,fill:{color:AMBER},line:{color:AMBER}});
  s.addText("TAKE-HOME MESSAGES",{x:0.4,y:0.2,w:9.2,h:0.5,fontFace:FONT,fontSize:13,bold:true,color:AMBER,charSpacing:4,margin:0});
  const msgs=[
    {n:"01",t:"SpO₂ 75–85% is the GOAL in Stage 1 — not a problem. SpO₂ >90% post-Norwood = overcirculation = danger.",c:RED},
    {n:"02",t:"O₂ is a pulmonary vasodilator. Never reflexively increase FiO₂ in a post-Norwood baby who desaturates.",c:RED},
    {n:"03",t:"Passive flow is the physiology post-Glenn and post-Fontan — early extubation augments it.",c:BLUE},
    {n:"04",t:"Fontan = PAID: Preload dependent, Afterload Intolerant, Inotrope responsive, Decompensates with arrhythmia.",c:AMBER},
    {n:"05",t:"Arrhythmia in Fontan → anticoagulate immediately + cardiovert if unstable. Do not delay.",c:RED},
    {n:"06",t:"PLE = low albumin + stool A1AT >150 mg/24h. Treat with MCT diet, heparin SC, sildenafil.",c:BLUE},
  ];
  msgs.forEach((m,i)=>{
    const yy=0.84+i*0.8;
    s.addShape(pres.ShapeType.rect,{x:0.4,y:yy,w:0.55,h:0.58,fill:{color:m.c},line:{color:m.c}});
    s.addText(m.n,{x:0.4,y:yy,w:0.55,h:0.58,fontFace:FONT,fontSize:17,bold:true,color:WHITE,align:"center",valign:"middle",margin:0});
    s.addText(m.t,{x:1.1,y:yy+0.04,w:8.55,h:0.52,fontFace:FONT,fontSize:13.5,color:WHITE,align:"left",valign:"middle",margin:0});
  });
  addFooter(s,"Single Ventricle Physiology: ICU Challenges  |  PICU Education 2026");
  s.addNotes("Final slide — ask 3 questions: Q1: What is your first intervention when a post-Norwood baby desaturates to 65%? (Check BP/lactate/SvO₂ first; DON'T just increase FiO₂) Q2: What drives pulmonary blood flow in a Glenn or Fontan? (Passive CVP gradient) Q3: A Fontan patient has HR 140 and SpO₂ 85% in the ER. What is your first priority? (12-lead ECG — rule out IART; anticoagulate first)");
}

// ── WRITE ────────────────────────────────────────────────────────────────────
pres.writeFile({fileName:"/home/daytona/workspace/single-ventricle-pptx/SV_ICU_Challenges_35slides.pptx"})
  .then(()=>console.log("✅  Saved: SV_ICU_Challenges_35slides.pptx"))
  .catch(e=>{console.error("❌",e);process.exit(1);});

"single ventricle" AND "ICU" AND "management"

"Fontan" AND ("arrhythmia" OR "protein losing enteropathy" OR "liver disease" OR "ECMO")

"Norwood" AND "postoperative" AND "hemodynamic" AND "management"

mkdir -p /home/daytona/workspace/sv35 && ls /home/daytona/workspace/sv35/