`, favicon, and body of `Root()` to\nmatch your app's existing `index.html`, and stamp anything else your shell\nreferences directly (images, css) with `immutableFileUrl()`.\n\n1. Create `frontend/root.tsx`:\n\n```tsx\n/** @jsxImportSource npm:hono@4/jsx */\nimport { raw } from \"npm:hono@4/html\";\nimport { immutableFileUrl } from \"https://esm.town/v/std/utils/index.ts\";\n\n// The HTML shell for the app. It is never cached, so immutableFileUrl can stamp\n// the current val version into each asset URL — the browser caches those\n// immutably, and publishing the val changes the URLs, refetching exactly once.\nexport function Root() {\n return (\n <>\n {raw(\"<!DOCTYPE html>\")}\n <html lang=\"en\">\n <head>\n <meta charSet=\"UTF-8\" />\n <meta name=\"viewport\" content=\"width=device-width, initial-scale=1.0\" />\n <title>React Hono Val Town Starter

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Reuses that file's\n// WaveformSpec/Question shapes and frontend/lib/waveform.ts's generateStrip\n// so each of the 12 leads renders through the exact same synthesis engine —\n// this file only supplies, per case, a base spec plus 12 per-lead overrides\n// (ST elevation/depression, T-wave inversion, amplitude/axis shifts, QRS\n// widening, etc.) hand-mapped to the real anatomical lead territories.\n//\n// Content is authored against clinical-education sources (LITFL, ECGwaves,\n// StatPearls, ACLS Medical Training) for teaching accuracy — these are\n// still synthesized teaching approximations, not literal clinical tracings.\nimport type { Question, WaveformSpec } from \"./rhythms-data.ts\";\n\nexport type LeadName = \"I\" | \"II\" | \"III\" | \"aVR\" | \"aVL\" | \"aVF\" | \"V1\" | \"V2\" | \"V3\" | \"V4\" | \"V5\" | \"V6\";\n\nexport const LEAD_ORDER: LeadName[] = [\"I\", \"II\", \"III\", \"aVR\", \"aVL\", \"aVF\", \"V1\", \"V2\", \"V3\", \"V4\", \"V5\", \"V6\"];\n\nexport interface TwelveLeadCase {\n id: string;\n name: string;\n category: \"STEMI\" | \"Ischemia\" | \"Conduction\" | \"Axis\" | \"Hypertrophy\" | \"Other\";\n sortOrder: number;\n rate: string;\n axis: \"Normal\" | \"Left\" | \"Right\" | \"Extreme\";\n summary: string;\n clinicalNote: string;\n // Shared base every lead starts from; leadFindings[lead] is merged on top.\n baseWaveform: WaveformSpec;\n leadFindings: Record>;\n questions: Question[];\n}\n\nconst NORMAL_BASE: WaveformSpec = { pattern: \"regular\", rateMin: 75, rateMax: 95, hasPWave: true, wide: false, prMs: 160 };\nconst BRADY_BASE: WaveformSpec = { pattern: \"regular\", rateMin: 48, rateMax: 62, hasPWave: true, wide: false, prMs: 160 };\nconst WIDE_BASE: WaveformSpec = { pattern: \"regular\", rateMin: 70, rateMax: 90, hasPWave: true, wide: true, prMs: 160 };\n\nconst NONE: Partial = {};\n\nexport const TWELVE_LEAD_CASES: TwelveLeadCase[] = [\n {\n id: \"anterior-stemi\",\n name: \"Anterior STEMI (LAD occlusion)\",\n category: \"STEMI\",\n sortOrder: 1,\n rate: \"80-100 bpm\",\n axis: \"Normal\",\n summary:\n \"Occlusion of the left anterior descending (LAD) artery infarcts the anterior and anteroseptal wall, producing ST-segment elevation across the precordial leads V1-V4 (often extending into V5-V6), with reciprocal ST depression in the inferior leads II, III, and aVF. Because the LAD supplies a large territory including the septum, anterior STEMI carries the highest risk of pump failure and new conduction disease among STEMI locations.\",\n clinicalNote:\n \"Activate the cath lab immediately. Watch closely for new LBBB or Mobitz II AV block, which signal extensive septal involvement and predict a rockier course.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: NONE,\n II: { stDepression: true },\n III: { stDepression: true },\n aVR: NONE,\n aVL: NONE,\n aVF: { stDepression: true },\n V1: { stElevation: true, qDeep: true },\n V2: { stElevation: true, qDeep: true },\n V3: { stElevation: true, qDeep: true },\n V4: { stElevation: true, qDeep: true },\n V5: { stElevation: true },\n V6: NONE,\n },\n questions: [\n {\n prompt:\n \"A 58-year-old with crushing chest pain has ST elevation in V1-V4 with reciprocal ST depression in II, III, and aVF. Which vessel is most likely occluded?\",\n choices: [\"Left anterior descending (LAD)\", \"Right coronary artery (RCA)\", \"Left circumflex (LCx)\", \"Posterior descending artery\"],\n correctIndex: 0,\n explanation: \"V1-V4 is the anteroseptal precordial territory supplied by the LAD; the inferior leads showing reciprocal depression confirm a precordial, not inferior, culprit.\",\n },\n {\n prompt: \"Why does anterior STEMI carry higher risk of cardiogenic shock than other STEMI locations?\",\n choices: [\n \"The LAD supplies a large territory including the septum, so infarct size and pump loss tend to be greater\",\n \"Anterior STEMI never causes chest pain, delaying treatment\",\n \"The LAD has no collateral circulation under any circumstance\",\n \"Anterior leads are technically hard to place correctly\",\n ],\n correctIndex: 0,\n explanation: \"The LAD is often called the 'widow maker' because it perfuses a large share of the left ventricle, including the septum — losing that territory more easily causes pump failure.\",\n },\n ],\n },\n {\n id: \"inferior-stemi\",\n name: \"Inferior STEMI (RCA/LCx occlusion)\",\n category: \"STEMI\",\n sortOrder: 2,\n rate: \"50-70 bpm (bradycardia common)\",\n axis: \"Normal\",\n summary:\n \"ST elevation in the inferior leads II, III, and aVF reflects occlusion of the right coronary artery (RCA) in roughly 80% of cases, or the left circumflex (LCx) in the remainder — elevation greater in III than II favors an RCA culprit. Reciprocal ST depression appears in I and aVL. Because the RCA usually also supplies the SA and AV nodes, inferior STEMI is frequently complicated by sinus bradycardia and AV block.\",\n clinicalNote:\n \"Check a right-sided lead (V4R) before giving nitrates — up to 40% of inferior STEMIs have concurrent RV infarction, which is preload-dependent and can develop profound hypotension with nitrates.\",\n baseWaveform: BRADY_BASE,\n leadFindings: {\n I: { stDepression: true },\n II: { stElevation: true, qDeep: true },\n III: { stElevation: true, qDeep: true },\n aVR: NONE,\n aVL: { stDepression: true },\n aVF: { stElevation: true, qDeep: true },\n V1: NONE,\n V2: NONE,\n V3: NONE,\n V4: NONE,\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"ST elevation in II, III, and aVF with reciprocal depression in I and aVL localizes ischemia to which wall?\",\n choices: [\"Inferior wall\", \"Anterior wall\", \"Lateral wall\", \"Posterior wall\"],\n correctIndex: 0,\n explanation: \"II, III, and aVF are the inferior limb leads, looking up at the diaphragmatic surface of the heart — the classic RCA/LCx territory.\",\n },\n {\n prompt: \"Why should nitrates be given cautiously in a patient with an inferior STEMI?\",\n choices: [\n \"Concurrent right ventricular infarction is common and is preload-dependent — nitrates can cause severe hypotension\",\n \"Nitrates always worsen AV block regardless of infarct location\",\n \"Inferior STEMI patients are never hypotensive\",\n \"Nitrates are contraindicated in every STEMI location equally\",\n ],\n correctIndex: 0,\n explanation: \"Because the RCA often perfuses the RV too, inferior STEMI carries a real risk of RV infarction — a preload-dependent state where venodilators like nitrates can crash the blood pressure.\",\n },\n ],\n },\n {\n id: \"lateral-stemi\",\n name: \"Lateral STEMI\",\n category: \"STEMI\",\n sortOrder: 3,\n rate: \"80-100 bpm\",\n axis: \"Normal\",\n summary:\n \"Lateral wall STEMI shows ST elevation in leads I, aVL, V5, and V6, from occlusion of the left circumflex artery or a diagonal/obtuse marginal branch. It's often subtle, low-amplitude, and frequently occurs alongside inferior or anterior involvement (infero-lateral or antero-lateral STEMI) rather than in true isolation.\",\n clinicalNote:\n \"Isolated lateral STEMI is easy to miss because the elevation is often small — compare I/aVL against a prior ECG, and treat a compelling clinical story as STEMI even with borderline elevation.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: { stElevation: true },\n II: { stDepression: true },\n III: { stDepression: true },\n aVR: NONE,\n aVL: { stElevation: true },\n aVF: { stDepression: true },\n V1: NONE,\n V2: NONE,\n V3: NONE,\n V4: NONE,\n V5: { stElevation: true },\n V6: { stElevation: true },\n },\n questions: [\n {\n prompt: \"Which lead pair, together with V5-V6, best identifies lateral wall ST elevation?\",\n choices: [\"I and aVL\", \"II and III\", \"V1 and V2\", \"aVR and aVF\"],\n correctIndex: 0,\n explanation: \"I and aVL are the high-lateral limb leads; together with V5-V6 (low-lateral precordial leads) they define the lateral wall territory.\",\n },\n {\n prompt: \"Lateral STEMI most commonly results from occlusion of which vessel?\",\n choices: [\"Left circumflex artery (or a diagonal/marginal branch)\", \"Right coronary artery only\", \"Left main coronary artery only\", \"Pulmonary artery\"],\n correctIndex: 0,\n explanation: \"The lateral wall is typically supplied by the left circumflex artery (via obtuse marginal branches) or a diagonal branch off the LAD.\",\n },\n ],\n },\n {\n id: \"posterior-stemi\",\n name: \"Posterior STEMI\",\n category: \"STEMI\",\n sortOrder: 4,\n rate: \"80-100 bpm\",\n axis: \"Normal\",\n summary:\n \"The posterior wall has no standard lead facing it directly, so posterior STEMI is diagnosed by mirror-image reciprocal changes in the anteroseptal leads V1-V3: ST depression, broadened R waves, and tall upright T waves — essentially an inverted view of what anterior elevation looks like. It results from LCx or distal RCA occlusion and very often accompanies inferior or lateral STEMI rather than occurring in isolation.\",\n clinicalNote:\n \"Confirm with posterior leads V7-V9 (≥0.5mm ST elevation is diagnostic there) — read alone as 'ST depression,' a posterior STEMI is easily mistaken for anterior ischemia rather than a STEMI-equivalent needing the cath lab.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: NONE,\n II: NONE,\n III: NONE,\n aVR: NONE,\n aVL: NONE,\n aVF: NONE,\n V1: { stDepression: true, tAmpScale: 1.4 },\n V2: { stDepression: true, tAmpScale: 1.4 },\n V3: { stDepression: true, tAmpScale: 1.3 },\n V4: NONE,\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"ST depression and tall, upright T waves isolated to V1-V3, with no obvious elevation elsewhere, should raise suspicion for which STEMI-equivalent?\",\n choices: [\"Posterior STEMI\", \"Anterior STEMI\", \"Pericarditis\", \"Left ventricular hypertrophy\"],\n correctIndex: 0,\n explanation: \"Because no standard 12-lead electrode faces the posterior wall, posterior infarction shows up as the mirror-image of ST elevation — depression, not elevation — in the opposing anteroseptal leads.\",\n },\n {\n prompt: \"How is a suspected posterior STEMI confirmed?\",\n choices: [\n \"Placing posterior leads V7-V9 and looking for ST elevation there\",\n \"Repeating troponin in 6 hours before doing anything else\",\n \"It cannot be confirmed by ECG under any circumstance\",\n \"Checking only lead aVR\",\n ],\n correctIndex: 0,\n explanation: \"V7-V9, placed around the left posterior chest wall, look directly at the posterior wall and will show true ST elevation confirming the diagnosis.\",\n },\n ],\n },\n {\n id: \"rv-stemi\",\n name: \"Right Ventricular (RV) STEMI\",\n category: \"STEMI\",\n sortOrder: 5,\n rate: \"50-70 bpm (bradycardia/AV block common)\",\n axis: \"Normal\",\n summary:\n \"Right ventricular infarction accompanies roughly 30-50% of inferior STEMIs, from proximal RCA occlusion cutting off flow before the RV marginal branches. The standard 12-lead shows the usual inferior pattern (ST elevation in II, III, aVF) plus a clue in V1 — the only standard precordial lead facing the right ventricle — where ST elevation, rather than the depression typical of posterior extension, points to RV involvement.\",\n clinicalNote:\n \"RV infarct patients are preload-dependent: avoid nitrates and diuretics, which can precipitate severe hypotension, and treat hypotension with IV fluid boluses instead.\",\n baseWaveform: BRADY_BASE,\n leadFindings: {\n I: { stDepression: true },\n II: { stElevation: true, qDeep: true },\n III: { stElevation: true, qDeep: true },\n aVR: NONE,\n aVL: { stDepression: true },\n aVF: { stElevation: true, qDeep: true },\n V1: { stElevation: true },\n V2: NONE,\n V3: NONE,\n V4: NONE,\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"In an inferior STEMI, ST elevation in V1 (instead of the depression seen with posterior extension) suggests which additional finding?\",\n choices: [\"Right ventricular infarction\", \"Anterior wall infarction\", \"Digoxin toxicity\", \"Benign early repolarization\"],\n correctIndex: 0,\n explanation: \"V1 is the precordial lead closest to the right ventricle — ST elevation there, in the setting of an inferior STEMI, points to RV involvement rather than posterior extension.\",\n },\n {\n prompt: \"Which medication class should be used cautiously (or avoided) in a patient with RV infarction?\",\n choices: [\"Nitrates\", \"Aspirin\", \"Beta blockers in a hemodynamically stable patient\", \"Heparin\"],\n correctIndex: 0,\n explanation: \"An infarcted, preload-dependent RV cannot compensate for the venodilation nitrates cause, so they can trigger a sharp, dangerous drop in blood pressure.\",\n },\n ],\n },\n {\n id: \"rbbb\",\n name: \"Right Bundle Branch Block (RBBB)\",\n category: \"Conduction\",\n sortOrder: 6,\n rate: \"70-90 bpm\",\n axis: \"Normal\",\n summary:\n \"Right bundle branch block delays right ventricular depolarization, widening the QRS to ≥120ms with a characteristic rsR' ('rabbit ears') pattern in V1-V2 and a wide, slurred S wave in the lateral leads I, aVL, and V6. It can be an incidental, benign finding or signal right heart strain, pulmonary embolism, or structural disease.\",\n clinicalNote:\n \"RBBB does not obscure inferior or anterior STEMI criteria the way LBBB can — standard ST-elevation criteria still apply — but it can distort V1-V3 morphology, so always compare against a prior tracing.\",\n baseWaveform: WIDE_BASE,\n leadFindings: {\n I: { wide: true },\n II: { wide: true },\n III: { wide: true },\n aVR: { wide: true },\n aVL: { wide: true },\n aVF: { wide: true },\n V1: { wide: true, tInvert: true },\n V2: { wide: true, tInvert: true },\n V3: { wide: true },\n V4: { wide: true },\n V5: { wide: true },\n V6: { wide: true },\n },\n questions: [\n {\n prompt: \"RBBB produces a QRS duration of at least how many milliseconds?\",\n choices: [\"120 ms\", \"80 ms\", \"40 ms\", \"200 ms\"],\n correctIndex: 0,\n explanation: \"A QRS ≥120ms is the threshold for a complete bundle branch block; RBBB widens the QRS because the right ventricle depolarizes late, via slow cell-to-cell conduction from the left ventricle.\",\n },\n {\n prompt: \"Where is the classic rsR' ('rabbit ears') pattern of RBBB best seen?\",\n choices: [\"V1-V2\", \"II and III\", \"aVL and aVF\", \"V5-V6\"],\n correctIndex: 0,\n explanation: \"V1-V2 face the right ventricle directly, so the delayed, unopposed right ventricular depolarization shows up there as a second, terminal R wave (R').\",\n },\n ],\n },\n {\n id: \"lbbb\",\n name: \"Left Bundle Branch Block (LBBB)\",\n category: \"Conduction\",\n sortOrder: 7,\n rate: \"70-90 bpm\",\n axis: \"Normal\",\n summary:\n \"Left bundle branch block widens the QRS to ≥120ms and abolishes the normal septal activation pattern, producing broad monophasic R waves in I, aVL, V5, and V6 and deep QS/rS complexes in V1-V3, with discordant ST-T changes — ST elevation opposite the deep S waves, ST depression/T-wave inversion opposite the tall R waves — that are a normal secondary finding, not ischemia.\",\n clinicalNote:\n \"New LBBB with a compatible clinical story is treated as a STEMI-equivalent; Sgarbossa criteria (concordant ST elevation ≥1mm, concordant depression in V1-V3, or markedly excessive discordant elevation) help find true ischemia hiding underneath a baseline LBBB.\",\n baseWaveform: WIDE_BASE,\n leadFindings: {\n I: { wide: true, stDepression: true, tInvert: true },\n II: { wide: true },\n III: { wide: true },\n aVR: { wide: true },\n aVL: { wide: true, stDepression: true, tInvert: true },\n aVF: { wide: true },\n V1: { wide: true, stElevation: true },\n V2: { wide: true, stElevation: true },\n V3: { wide: true, stElevation: true },\n V4: { wide: true },\n V5: { wide: true, stDepression: true, tInvert: true },\n V6: { wide: true, stDepression: true, tInvert: true },\n },\n questions: [\n {\n prompt: \"Discordant ST-T changes in LBBB — elevation opposite deep S waves, depression opposite tall R waves — represent what?\",\n choices: [\n \"A normal secondary repolarization change from the altered depolarization sequence, not ischemia\",\n \"Always an acute STEMI\",\n \"Evidence of digoxin toxicity specifically\",\n \"A sign the patient is in atrial fibrillation\",\n ],\n correctIndex: 0,\n explanation: \"Because depolarization travels an abnormal path in LBBB, repolarization (the ST-T segment) is expected to point opposite the QRS — that discordance is the baseline pattern, not a red flag by itself.\",\n },\n {\n prompt: \"What tool helps identify a true STEMI hiding underneath a baseline LBBB?\",\n choices: [\"Sgarbossa criteria\", \"The Ottawa ankle rules\", \"The Wells score\", \"The HEART score alone\"],\n correctIndex: 0,\n explanation: \"Sgarbossa criteria look for ST changes that are concordant (same direction as the QRS) or excessively discordant — patterns LBBB alone shouldn't produce — to flag true superimposed ischemia.\",\n },\n ],\n },\n {\n id: \"left-axis-deviation\",\n name: \"Left Axis Deviation (LAFB pattern)\",\n category: \"Axis\",\n sortOrder: 8,\n rate: \"70-90 bpm\",\n axis: \"Left\",\n summary:\n \"Left axis deviation (frontal-plane axis beyond -30°) most often results from left anterior fascicular block (LAFB): the anterior fascicle of the left bundle stops conducting, so the left ventricle depolarizes via the posterior fascicle first, swinging the axis superiorly and leftward. The QRS stays narrow (<120ms) unless paired with another conduction defect; look for a small Q in I/aVL with a small R and deeper S in II/III/aVF.\",\n clinicalNote:\n \"LAFB alone is usually benign, but paired with RBBB it forms a bifascicular block — a warning sign for progression to complete heart block, especially with a history of syncope.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: { ampScale: 1.3 },\n II: { ampScale: 0.6 },\n III: { ampScale: 0.55 },\n aVR: NONE,\n aVL: { ampScale: 1.3 },\n aVF: { ampScale: 0.6 },\n V1: NONE,\n V2: NONE,\n V3: NONE,\n V4: NONE,\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"Left axis deviation with a narrow QRS is most commonly caused by which conduction abnormality?\",\n choices: [\"Left anterior fascicular block (LAFB)\", \"Right bundle branch block\", \"WPW pattern\", \"Complete heart block\"],\n correctIndex: 0,\n explanation: \"LAFB, a block in only one of the left bundle's two fascicles, is the classic cause of an isolated left-axis QRS that remains narrow.\",\n },\n {\n prompt: \"Why is LAFB combined with RBBB (bifascicular block) clinically significant?\",\n choices: [\n \"Two of the heart's three conduction fascicles are now blocked, raising risk of progression to complete heart block\",\n \"It always requires emergent pacing regardless of symptoms\",\n \"It has no clinical significance and needs no follow-up\",\n \"It converts automatically to atrial fibrillation\",\n ],\n correctIndex: 0,\n explanation: \"The conduction system has three main fascicles (right bundle, left anterior, left posterior); losing two leaves only one fascicle carrying the impulse, one step from complete block.\",\n },\n ],\n },\n {\n id: \"right-axis-deviation\",\n name: \"Right Axis Deviation (RAD pattern)\",\n category: \"Axis\",\n sortOrder: 9,\n rate: \"70-90 bpm\",\n axis: \"Right\",\n summary:\n \"Right axis deviation (beyond +90°) shifts the mean QRS vector rightward and inferiorly, with lead III/aVF amplitude dominating over lead I. In adults it's usually pathologic — right ventricular hypertrophy, left posterior fascicular block, chronic lung disease, or acute right heart strain — rather than the normal variant it can be in children and thin, tall adults.\",\n clinicalNote:\n \"Correlate with the clinical picture: sudden new RAD with tachycardia and hypoxia should raise concern for acute pulmonary embolism (classically taught alongside the S1Q3T3 pattern) rather than being dismissed as incidental.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: { ampScale: 0.6 },\n II: { ampScale: 1.1 },\n III: { ampScale: 1.3 },\n aVR: NONE,\n aVL: { ampScale: 0.6 },\n aVF: { ampScale: 1.25 },\n V1: NONE,\n V2: NONE,\n V3: NONE,\n V4: NONE,\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"A sudden new right axis deviation in a tachycardic, hypoxic patient should prompt consideration of which diagnosis?\",\n choices: [\"Acute pulmonary embolism\", \"Normal sinus rhythm\", \"Benign early repolarization\", \"Sinus bradycardia\"],\n correctIndex: 0,\n explanation: \"Acute right heart strain from a large PE can acutely shift the axis rightward — a new, sudden finding that's a different clinical animal from the RAD seen at baseline in chronic lung disease.\",\n },\n {\n prompt: \"In right axis deviation, which limb lead typically shows the tallest R wave?\",\n choices: [\"III\", \"I\", \"aVL\", \"aVR\"],\n correctIndex: 0,\n explanation: \"As the axis rotates rightward toward +90-180°, lead III (which looks most directly at the inferior-right direction) picks up the dominant, tallest R wave.\",\n },\n ],\n },\n {\n id: \"lvh\",\n name: \"Left Ventricular Hypertrophy (LVH)\",\n category: \"Hypertrophy\",\n sortOrder: 10,\n rate: \"70-90 bpm\",\n axis: \"Left\",\n summary:\n \"Left ventricular hypertrophy — usually from longstanding hypertension or aortic stenosis — increases QRS voltage in the leads facing the thickened LV free wall (I, aVL, V5, V6) and often produces a 'strain pattern': downsloping ST depression with asymmetric T-wave inversion in those same lateral leads, reflecting altered repolarization of thickened myocardium rather than ischemia.\",\n clinicalNote:\n \"Voltage criteria (e.g., Sokolow-Lyon: S in V1 + R in V5/V6 > 35mm) plus a strain pattern strongly support LVH — but strain can look alarmingly like ischemia, so always correlate with symptoms before assuming ACS.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: { ampScale: 1.3, stDepression: true },\n II: NONE,\n III: NONE,\n aVR: NONE,\n aVL: { ampScale: 1.25, stDepression: true },\n aVF: NONE,\n V1: { ampScale: 0.7 },\n V2: { ampScale: 0.8 },\n V3: NONE,\n V4: NONE,\n V5: { ampScale: 1.6, stDepression: true, tInvert: true },\n V6: { ampScale: 1.5, stDepression: true, tInvert: true },\n },\n questions: [\n {\n prompt: \"The 'strain pattern' of LVH — ST depression with T-wave inversion in I, aVL, V5, and V6 — reflects what?\",\n choices: [\n \"Altered repolarization of hypertrophied myocardium, not active ischemia\",\n \"An acute STEMI in progress\",\n \"Digoxin toxicity exclusively\",\n \"Complete heart block\"],\n correctIndex: 0,\n explanation: \"Thickened LV muscle repolarizes abnormally even without ischemia — the resulting ST-T pattern is a secondary change from the hypertrophy itself.\",\n },\n {\n prompt: \"Which is a recognized voltage criterion for LVH?\",\n choices: [\n \"S wave in V1 + R wave in V5 or V6 greater than 35mm (Sokolow-Lyon)\",\n \"QRS duration greater than 200ms\",\n \"PR interval greater than 300ms\",\n \"A completely isoelectric QRS in all leads\",\n ],\n correctIndex: 0,\n explanation: \"Sokolow-Lyon voltage criteria sum the deepest S wave in V1 with the tallest R wave in V5/V6; a total over 35mm supports LVH.\",\n },\n ],\n },\n {\n id: \"rvh\",\n name: \"Right Ventricular Hypertrophy (RVH)\",\n category: \"Hypertrophy\",\n sortOrder: 11,\n rate: \"70-90 bpm\",\n axis: \"Right\",\n summary:\n \"Right ventricular hypertrophy — from pulmonary hypertension, congenital heart disease, or chronic lung disease — shifts the axis rightward and produces a dominant R wave in V1 (R greater than S) with a strain pattern of ST depression and T-wave inversion across V1-V3, the mirror image of the LV-facing findings seen in LVH.\",\n clinicalNote:\n \"A dominant R wave in V1 has a short differential — RVH, true posterior MI, RBBB, and WPW — so pair the ECG with the clinical context (chronic lung/heart disease vs. acute chest pain) before settling on RVH.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: { ampScale: 0.6 },\n II: NONE,\n III: { ampScale: 1.3 },\n aVR: NONE,\n aVL: NONE,\n aVF: { ampScale: 1.2 },\n V1: { ampScale: 1.5, stDepression: true, tInvert: true },\n V2: { ampScale: 1.3, tInvert: true },\n V3: NONE,\n V4: NONE,\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"A dominant R wave (R greater than S) in V1 with right axis deviation is characteristic of which condition?\",\n choices: [\"Right ventricular hypertrophy\", \"Left ventricular hypertrophy\", \"First-degree AV block\", \"Sinus arrhythmia\"],\n correctIndex: 0,\n explanation: \"V1 faces the right ventricle — when it hypertrophies enough to dominate the frontal precordial forces, V1 shows a tall R instead of its normal small r.\",\n },\n {\n prompt: \"What is a common cause of RVH in adults?\",\n choices: [\"Chronic pulmonary hypertension or COPD\", \"Isolated sinus bradycardia\", \"A single episode of PSVT\", \"Vagal syncope\"],\n correctIndex: 0,\n explanation: \"Chronic elevated pulmonary pressures — from COPD, pulmonary hypertension, or congenital shunts — force the right ventricle to hypertrophy against that afterload over time.\",\n },\n ],\n },\n {\n id: \"pericarditis\",\n name: \"Acute Pericarditis\",\n category: \"Other\",\n sortOrder: 12,\n rate: \"80-100 bpm\",\n axis: \"Normal\",\n summary:\n \"Acute pericarditis inflames the pericardium adjacent to the epicardium, producing diffuse, concave ('saddleback') ST elevation across most limb and precordial leads rather than the localized, convex elevation of a STEMI — plus PR-segment depression from atrial involvement, with reciprocal PR elevation and ST depression classically seen in aVR.\",\n clinicalNote:\n \"Distinguish from STEMI by the diffuse (non-territorial) ST elevation, the lack of reciprocal ST depression outside aVR, and a pleuritic/positional chest pain history — treat with NSAIDs/colchicine, not the cath lab.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: { stElevation: true },\n II: { stElevation: true },\n III: { stElevation: true },\n aVR: { stDepression: true },\n aVL: { stElevation: true },\n aVF: { stElevation: true },\n V1: NONE,\n V2: { stElevation: true },\n V3: { stElevation: true },\n V4: { stElevation: true },\n V5: { stElevation: true },\n V6: { stElevation: true },\n },\n questions: [\n {\n prompt: \"What distinguishes the ST elevation of acute pericarditis from a STEMI?\",\n choices: [\n \"It's diffuse and concave across most leads, without reciprocal depression outside aVR — rather than localized to one artery's territory\",\n \"It only ever appears in a single precordial lead\",\n \"It resolves within seconds without any treatment\",\n \"It is always accompanied by a wide QRS\"],\n correctIndex: 0,\n explanation: \"STEMI elevation is convex and confined to the leads over one coronary territory with reciprocal depression elsewhere; pericarditis inflames the whole pericardial surface, so the elevation is widespread and concave.\",\n },\n {\n prompt: \"Which lead classically shows PR-segment elevation (with reciprocal ST depression) in acute pericarditis?\",\n choices: [\"aVR\", \"V6\", \"III\", \"aVL\"],\n correctIndex: 0,\n explanation: \"aVR looks at the heart from an opposite vantage point to most other leads, so it shows the mirror-image reciprocal changes — PR elevation and ST depression — while the rest of the ECG shows PR depression and ST elevation.\",\n },\n ],\n },\n {\n id: \"hyperkalemia-12lead\",\n name: \"Hyperkalemia (12-lead pattern)\",\n category: \"Other\",\n sortOrder: 13,\n rate: \"60-90 bpm (varies with severity)\",\n axis: \"Normal\",\n summary:\n \"Rising serum potassium produces a progressive, dose-dependent sequence of diffuse ECG changes across all 12 leads: tall, narrow, symmetrically 'peaked' T waves first, followed by PR prolongation and flattening or loss of the P wave, then progressive QRS widening as severity worsens — eventually merging into the deadly sine-wave pattern that precedes cardiac arrest if untreated.\",\n clinicalNote:\n \"Treat the ECG, not just the lab value, in a symptomatic or unstable patient — IV calcium gluconate/chloride first to stabilize the cardiac membrane, then insulin/dextrose and albuterol to shift potassium intracellularly, with dialysis for definitive removal.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: { tAmpScale: 2.0, wide: true, hasPWave: false },\n II: { tAmpScale: 2.0, wide: true, hasPWave: false },\n III: { tAmpScale: 2.0, wide: true, hasPWave: false },\n aVR: { tAmpScale: 2.0, wide: true, hasPWave: false },\n aVL: { tAmpScale: 2.0, wide: true, hasPWave: false },\n aVF: { tAmpScale: 2.0, wide: true, hasPWave: false },\n V1: { tAmpScale: 2.0, wide: true, hasPWave: false },\n V2: { tAmpScale: 2.0, wide: true, hasPWave: false },\n V3: { tAmpScale: 2.0, wide: true, hasPWave: false },\n V4: { tAmpScale: 2.0, wide: true, hasPWave: false },\n V5: { tAmpScale: 2.0, wide: true, hasPWave: false },\n V6: { tAmpScale: 2.0, wide: true, hasPWave: false },\n },\n questions: [\n {\n prompt: \"Which ECG change is typically the earliest sign of rising potassium?\",\n choices: [\"Tall, narrow, peaked T waves\", \"A widened QRS\", \"Complete loss of the P wave\", \"A sine-wave pattern\"],\n correctIndex: 0,\n explanation: \"Peaked T waves appear first as potassium rises; PR prolongation/P-wave loss and QRS widening follow as hyperkalemia worsens, with the sine-wave pattern as a late, pre-arrest finding.\",\n },\n {\n prompt: \"What is the first-line treatment to stabilize the cardiac membrane in symptomatic hyperkalemia with ECG changes?\",\n choices: [\"IV calcium gluconate or calcium chloride\", \"Oral potassium binder alone\", \"Beta blocker\", \"Atropine\"],\n correctIndex: 0,\n explanation: \"IV calcium doesn't lower serum potassium — it directly stabilizes the cardiac cell membrane against potassium's effects, buying time while other therapies shift or remove potassium.\",\n },\n ],\n },\n {\n id: \"early-repolarization\",\n name: \"Early Repolarization\",\n category: \"Other\",\n sortOrder: 14,\n rate: \"60-90 bpm\",\n axis: \"Normal\",\n summary:\n \"Early repolarization is a common, usually benign variant most often seen in young, healthy patients — concave ST elevation with a notched or slurred J point, most prominent in the mid-precordial leads V2-V5, accompanied by tall, upright T waves and generally without reciprocal ST depression elsewhere.\",\n clinicalNote:\n \"Benign early repolarization is a diagnosis of exclusion in the ED — a new symptomatic patient still needs STEMI ruled out with serial ECGs/troponins and comparison to a prior baseline before being reassured.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: NONE,\n II: { tAmpScale: 1.1 },\n III: NONE,\n aVR: NONE,\n aVL: NONE,\n aVF: NONE,\n V1: NONE,\n V2: { stElevation: true, osbornWave: true, tAmpScale: 1.3 },\n V3: { stElevation: true, osbornWave: true, tAmpScale: 1.3 },\n V4: { stElevation: true, osbornWave: true, tAmpScale: 1.25 },\n V5: { stElevation: true, tAmpScale: 1.15 },\n V6: NONE,\n },\n questions: [\n {\n prompt: \"Early repolarization is most often seen in which patient population?\",\n choices: [\"Young, healthy patients\", \"Patients over 80 with known CAD\", \"Only patients on dialysis\", \"Only patients with a pacemaker\"],\n correctIndex: 0,\n explanation: \"Early repolarization is a common normal variant, classically found incidentally on ECGs of young, healthy, often athletic patients.\",\n },\n {\n prompt: \"Where is the notched/slurred J point of early repolarization most prominently seen?\",\n choices: [\"The mid-precordial leads (V2-V5)\", \"Lead aVR only\", \"V1 only\", \"The limb leads only\"],\n correctIndex: 0,\n explanation: \"The characteristic J-point notching and concave ST elevation of early repolarization is classically most visible in the mid-precordial leads.\",\n },\n ],\n },\n {\n id: \"wellens-syndrome\",\n name: \"Wellens Syndrome\",\n category: \"Ischemia\",\n sortOrder: 15,\n rate: \"60-80 bpm\",\n axis: \"Normal\",\n summary:\n \"Wellens syndrome is a pattern of deeply inverted or biphasic T waves in V2-V3 (sometimes extending into V1 and V4), seen during a pain-free interval after resolved anginal chest pain, that signals critical proximal LAD stenosis. The ST segment is characteristically normal or only minimally elevated — this is a warning sign of an impending large anterior MI, not an active STEMI.\",\n clinicalNote:\n \"Do not stress-test a Wellens pattern — it identifies a critical, unstable LAD lesion, and provocative testing can precipitate an anterior wall MI. These patients need prompt cardiology referral for catheterization.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: NONE,\n II: NONE,\n III: NONE,\n aVR: NONE,\n aVL: NONE,\n aVF: NONE,\n V1: { tInvert: true, tAmpScale: 1.1 },\n V2: { tInvert: true, tAmpScale: 1.6 },\n V3: { tInvert: true, tAmpScale: 1.6 },\n V4: { tInvert: true, tAmpScale: 1.2 },\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"Wellens syndrome — deeply inverted/biphasic T waves in V2-V3 with a pain-free patient and normal or minimal ST elevation — indicates what?\",\n choices: [\n \"Critical proximal LAD stenosis, an impending large anterior MI\",\n \"A completely normal, benign ECG\",\n \"Acute pericarditis\",\n \"Digoxin toxicity\"],\n correctIndex: 0,\n explanation: \"Wellens T-wave changes are a specific warning pattern for a critical LAD lesion that has recently reperfused — the artery is unstable and can re-occlude and cause a large anterior MI.\",\n },\n {\n prompt: \"Why is exercise/pharmacologic stress testing contraindicated in a patient with a Wellens pattern?\",\n choices: [\n \"It can provoke re-occlusion of the critically stenosed LAD and precipitate a large anterior MI\",\n \"Stress testing is always safe in Wellens syndrome\",\n \"It has no relationship to the LAD at all\",\n \"It is only contraindicated in pediatric patients\"],\n correctIndex: 0,\n explanation: \"Because the underlying lesion is a near-critical LAD stenosis, provoking demand ischemia with a stress test risks triggering the very large anterior infarct the pattern is warning about.\",\n },\n ],\n },\n {\n id: \"brugada-pattern\",\n name: \"Brugada Pattern\",\n category: \"Other\",\n sortOrder: 16,\n rate: \"60-80 bpm\",\n axis: \"Normal\",\n summary:\n \"Brugada Type 1 pattern shows a coved ('shark-fin') ST-segment elevation of at least 2mm in V1-V2 that descends into an inverted T wave, from a sodium-channelopathy affecting right ventricular outflow tract repolarization. It's typically an inherited condition (SCN5A mutation in many cases) that carries a real risk of sudden cardiac death from polymorphic VT/VF, especially during fever or at rest/sleep.\",\n clinicalNote:\n \"A Type 1 Brugada pattern with a history of syncope, family history of sudden cardiac death, or documented VT/VF is an indication for ICD referral — and fever should be treated aggressively in known Brugada patients, since it can unmask or worsen the pattern.\",\n baseWaveform: NORMAL_BASE,\n leadFindings: {\n I: NONE,\n II: NONE,\n III: NONE,\n aVR: NONE,\n aVL: NONE,\n aVF: NONE,\n V1: { stElevation: true, tInvert: true, wide: true },\n V2: { stElevation: true, tInvert: true, wide: true },\n V3: NONE,\n V4: NONE,\n V5: NONE,\n V6: NONE,\n },\n questions: [\n {\n prompt: \"Brugada Type 1 pattern is defined by which finding?\",\n choices: [\n \"Coved ST elevation ≥2mm in V1-V2 descending into an inverted T wave\",\n \"Diffuse ST elevation in every lead\",\n \"A short PR interval with a delta wave\",\n \"Peaked T waves with a widened QRS\"],\n correctIndex: 0,\n explanation: \"The coved, 'shark-fin' ST elevation confined to the right precordial leads V1-V2, sloping down into T-wave inversion, is the defining Type 1 morphology.\",\n },\n {\n prompt: \"What clinical trigger is classically associated with unmasking or worsening the Brugada pattern?\",\n choices: [\"Fever\", \"Cold exposure\", \"Hyperventilation\", \"Vigorous exercise only\"],\n correctIndex: 0,\n explanation: \"Fever is a well-recognized trigger that can unmask a latent Brugada pattern or worsen it in a known carrier, so it should be treated aggressively in these patients.\",\n },\n ],\n },\n];\n","createdAt",["D",1788376350327],"branchVersion","branchId","7029bff5-bb8a-442e-a4f2-805f0156bd56","id","4a26e4ff-5701-4f0e-a2d1-9b438dea196d","ekg-rhythm-practice",["D",1788371332863],"deletedAt","legacyEnvVars","privacy","public","httpPrivacy","description","EKG rhythm interpretation practice app for 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{ parseVal, serveImmutableFile } from \"https://esm.town/v/std/utils/index.ts\";\nimport { Hono } from \"npm:hono\";\nimport { Root } from \"./frontend/root.tsx\";\nimport { RHYTHMS } from \"./backend/rhythms-data.ts\";\n\nconst app = new Hono();\n\n// Serve the (never-cached) HTML shell at the root /\napp.get(\"/\", (c) => c.html(Root()));\n\n// Serve frontend files at the version-addressed URLs Root() stamps, cached immutably\napp.get(\"/__immutable/*\", (c) => serveImmutableFile(c.req.path));\n\n// View source redirect\napp.get(\"/source\", (c) => c.redirect(parseVal().links.self.val));\n\n// List all rhythms (summary only — no questions in the payload).\n// Every rhythm is unlocked content-wise; the free/Pro split is now a daily\n// practice cap enforced client-side, not a content paywall.\napp.get(\"/api/rhythms\", (c) => {\n const list = [...RHYTHMS]\n .sort((a, b) => a.sortOrder - b.sortOrder)\n .map(({ questions, ...summary }) => ({\n ...summary,\n locked: false,\n questionCount: questions.length,\n }));\n return c.json(list);\n});\n\n// Single rhythm detail — full content, including quiz questions, for everyone.\napp.get(\"/api/rhythms/:id\", (c) => {\n const rhythm = RHYTHMS.find((r) => r.id === c.req.param(\"id\"));\n if (!rhythm) return c.json({ error: \"not found\" }, 404);\n return c.json({\n ...rhythm,\n locked: false,\n });\n});\n\n// Unwrap and rethrow Hono errors as the original error\n// If you delete this, all errors will be \"Internal Server Error\"\napp.onError((err) => Promise.reject(err));\n\n// HTTP vals expect an exported \"fetch handler\"\n// This is how you \"run the server\" in Val Town with Hono\nexport default app.fetch;\n","label",[136],"f174df99-6739-437c-b218-528fe54153d7","README.md","01a0633c-efa7-770e-92de-f8c87a88692d",1,["D",1788371332863],"# React + Hono Starter\n\nA minimal starter template for building client-side React apps with a Hono\nbackend on Val Town. Click **Remix** to get your own copy.\n\n## Picking a starter\n\n| Starter | When to pick it |\n| --- | --- |\n| [`basic-html-starter`](https://www.val.town/x/templates/basic-html-starter) | Static HTML pages. Sprinkle of vanilla JS. No server-side rendering. |\n| [`hono-jsx-starter`](https://www.val.town/x/templates/hono-jsx-starter) | Dynamic server-rendered HTML with JSX. API routes. No React, no SPA. |\n| **[`react-hono-starter`](https://www.val.town/x/templates/react-hono-starter)** *(you're here)* | Client-side React SPA with a Hono API backend. |\n\n**Want to build UI?** Start writing React components in\n[`frontend/components/`](/frontend/components/). Import them into `App.tsx` and\nyou're good to go. Styling is [Twind](https://twind.style/) — just use Tailwind\nutility classes, zero config.\n\n**Want to add an API?** Add routes in [`index.ts`](/index.ts) (there's a\ncommented-out example). Fetch them from your React components.\n\n## Architecture\n\n```mermaid\ngraph LR\n Browser -->|\"GET /\"| Hono[\"index.ts
(Hono server)\"]\n Hono -->|serves| HTML[\"root.tsx\"]\n HTML -->|loads| Entry[\"index.tsx\"]\n Entry -->|renders| App[\"App.tsx\"]\n App -->|renders| Counter[\"Counter.tsx\"]\n```\n\n## File structure\n\n```\nindex.ts ← Hono backend (serves frontend + API routes)\nfrontend/\n root.tsx ← HTML shell (stamps immutable asset URLs)\n index.tsx ← React entrypoint (mounts )\n favicon.svg ← App icon\n components/\n App.tsx ← Root component (layout + view source link)\n Counter.tsx ← Example component with state\n```\n\n## How it works\n\n1. **`index.ts`** is the HTTP entrypoint — a Hono server that serves the\n frontend and any API routes you add.\n2. **`frontend/root.tsx`** is the HTML shell — it loads Twind and stamps\n immutable asset URLs for the favicon and React entrypoint.\n3. **`frontend/index.tsx`** mounts the React app.\n4. **`frontend/components/App.tsx`** is the root layout — add new components\n alongside it.\n5. **`frontend/components/Counter.tsx`** is an example stateful component —\n replace it with your own!\n\n## Next steps\n\n- Add API routes in `index.ts`\n- Add new components in `frontend/components/`\n- Add a SQLite database — see the\n [React Hono Example](https://www.val.town/x/stevekrouse/reactHonoExample) for\n a full-stack example with database, queries, and shared types\n\nTemplate updates and upgrade paths for existing remixes: [CHANGELOG.md](/CHANGELOG.md)\n",[147],"4d03780d-716e-4f3b-9cdf-f3d72852a379","CHANGELOG.md","01a0633c-efa7-770e-92de-f742abd282c5",["D",1788371332863],"# Changelog\n\n## 2026-07-30 — Immutable asset caching\n\nFrontend files are now served at version-addressed URLs\n(`/__immutable/45/frontend/index.tsx`) with\n`Cache-Control: public, max-age=31536000, immutable`, so repeat visits load the\nwhole client graph from the browser cache — roughly 3× faster (~665ms → ~157ms\nmeasured). Publishing your val bumps its version, which changes every URL, so\ncaches invalidate automatically. Old-version URLs return 404 after a publish\n(like Next.js build assets); a reload picks up the new version.\n\nWhat changed in the template:\n\n- `frontend/index.html` → [`frontend/root.tsx`](/frontend/root.tsx): the HTML\n shell is now JSX and stamps asset URLs with `immutableFileUrl()`\n- [`index.ts`](/index.ts): serves `Root()` at `/`, and one\n `app.get(\"/__immutable/*\", (c) => serveImmutableFile(c.req.path))` route\n serves all frontend files\n\n### Upgrading an existing remix\n\nYour copy of this template doesn't update automatically. Two options:\n\n**Minimal (most of the benefit):** point both routes at `serveImmutableFile` —\nyour existing bare URLs redirect into versioned space, the new route serves\nthem, and the whole module graph gets cached (costs one redirect per page view):\n\n```ts\nimport { serveImmutableFile } from \"https://esm.town/v/std/utils/index.ts\";\n\napp.get(\"/__immutable/*\", (c) => serveImmutableFile(c.req.path));\napp.get(\"/frontend/**/*\", (c) => serveImmutableFile(c.req.path)); // was serveFile\n```\n\n**Full upgrade (also removes the redirect):** three self-contained steps —\nno other files needed. Adjust the ``, favicon, and body of `Root()` to\nmatch your app's existing `index.html`, and stamp anything else your shell\nreferences directly (images, css) with `immutableFileUrl()`.\n\n1. Create `frontend/root.tsx`:\n\n```tsx\n/** @jsxImportSource npm:hono@4/jsx */\nimport { raw } from \"npm:hono@4/html\";\nimport { immutableFileUrl } from \"https://esm.town/v/std/utils/index.ts\";\n\n// The HTML shell for the app. It is never cached, so immutableFileUrl can stamp\n// the current val version into each asset URL — the browser caches those\n// immutably, and publishing the val changes the URLs, refetching exactly once.\nexport function Root() {\n return (\n <>\n {raw(\"<!DOCTYPE html>\")}\n <html lang=\"en\">\n <head>\n <meta charSet=\"UTF-8\" />\n <meta name=\"viewport\" content=\"width=device-width, initial-scale=1.0\" />\n <title>React Hono Val Town Starter\n

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