[{"_1":2,"_3":-5,"_4":-5},"loaderData",{"_5":6,"_7":8},"actionData","errors","root",{"_109":110,"_111":112},"routes/embed.x.$handle.$name.$",{"_9":10,"_11":12,"_13":14,"_15":16,"_17":18,"_19":20,"_21":-5},"handle","dusty_medic","name","ekg-rhythm-practice","path","backend/rhythms-data.ts","project",{"_22":48,"_11":12,"_35":49,"_50":-5,"_51":44,"_52":53,"_54":53,"_55":56,"_57":-5,"_58":59,"_60":61,"_62":34,"_63":-5,"_64":-5,"_65":66,"_67":68,"_69":70,"_71":72,"_73":74,"_75":-5,"_76":77,"_78":77,"_79":80,"_81":80,"_82":80,"_83":77,"_84":77,"_85":86,"_87":88,"_89":90,"_91":44},"file",{"_22":23,"_11":24,"_25":26,"_27":28,"_29":30,"_31":32,"_33":34,"_35":36,"_37":38,"_39":40,"_41":42,"_43":44,"_45":-5,"_13":46},"permalink","https://www.val.town/x/dusty_medic/ekg-rhythm-practice/code/backend/rhythms-data.ts","extension","id","e865e48f-d5d4-4968-a6f5-300e4f67c971","rhythms-data.ts","fileId","fd91b3cc-a6f6-11f1-9d6d-1607ee4eb77e","parentId","64bd6515-b9fc-44a1-8fc2-785e7ebdd591","branchId","7029bff5-bb8a-442e-a4f2-805f0156bd56","branchVersion",55,"latest",true,"createdAt",["D",1788378459621],"version",13,"fileType","script","content","// Standard nursing/EMS EKG curriculum — 20 core rhythms.\n// free: true rhythms are visible without a Pro unlock.\nexport interface Question {\n prompt: string;\n choices: string[];\n correctIndex: number;\n explanation: string;\n}\n\n// Machine-readable description of what a rhythm strip looks like, used by\n// frontend/lib/waveform.ts to synthesize a fresh, slightly-randomized strip\n// on every practice round (not a literal clinical tracing — a teaching\n// approximation of rate, regularity, P-wave presence, and QRS width/shape).\nexport type WaveformPattern =\n | \"regular\"\n | \"ectopic\"\n | \"patternedEctopy\"\n | \"burstEctopy\"\n | \"parasystole\"\n | \"tachyBrady\"\n | \"failToCapture\"\n | \"failToSense\"\n | \"idioventricularCapture\"\n | \"afib\"\n | \"aflutter\"\n | \"wenckebach\"\n | \"type2block\"\n | \"thirdDegree\"\n | \"torsades\"\n | \"chaotic\"\n | \"flatline\"\n | \"pause\"\n | \"multifocal\";\n\nexport interface WaveformSpec {\n pattern: WaveformPattern;\n rateMin?: number;\n rateMax?: number;\n hasPWave?: boolean;\n wide?: boolean;\n prMs?: number;\n ectopicSubtype?: \"atrial\" | \"junctional\" | \"ventricular\";\n baseRateMin?: number;\n baseRateMax?: number;\n atrialRate?: number;\n ratios?: number[];\n startPrMs?: number;\n prIncrementMs?: number;\n cycleBeats?: number;\n dropEvery?: number;\n atrialRateMin?: number;\n atrialRateMax?: number;\n ventricularRateMin?: number;\n ventricularRateMax?: number;\n irregular?: boolean;\n delta?: boolean;\n pacedSpike?: boolean;\n // Extended fields for the expanded (100+) library — patterned/burst ectopy,\n // electrolyte/drug/device effects, and simple visual modifiers reused by\n // the 12-lead grid. All are optional teaching approximations, not literal\n // clinical tracings.\n count?: number; // how many ectopic beats to insert (unifocal/multifocal PVCs)\n unit?: number; // patternedEctopy: 2 = bigeminy, 3 = trigeminy\n burstLength?: number; // burstEctopy: couplet=2, triplet/NSVT=3+\n burstRateMin?: number;\n burstRateMax?: number;\n qDeep?: boolean; // exaggerated pathologic Q wave\n tAmpScale?: number; // T-wave amplitude multiplier (peaked/flattened T)\n tInvert?: boolean; // flip T-wave polarity\n qtOffsetMs?: number; // shift T-wave center (long/short QT)\n uWave?: boolean; // add a small U wave after the T\n stScoop?: boolean; // digoxin-effect ST sag\n stElevation?: boolean; // ST elevation bump\n stDepression?: boolean; // ST depression dip\n osbornWave?: boolean; // hypothermia J wave\n ampScale?: number; // global amplitude multiplier (low voltage)\n alternans?: boolean; // alternating beat-to-beat amplitude\n interference?: boolean; // fine AC-interference overlay\n}\n\nexport interface Rhythm {\n id: string;\n name: string;\n category: \"Sinus\" | \"Atrial\" | \"Junctional\" | \"AV Block\" | \"Ventricular\" | \"Other\";\n free: boolean;\n sortOrder: number;\n rate: string;\n regularity: string;\n pWave: string;\n prInterval: string;\n qrs: string;\n summary: string;\n clinicalNote: string;\n waveform: WaveformSpec;\n questions: Question[];\n}\n\nexport const RHYTHMS: Rhythm[] = [\n {\n id: \"nsr\",\n name: \"Normal Sinus Rhythm\",\n category: \"Sinus\",\n free: true,\n sortOrder: 1,\n rate: \"60-100 bpm\",\n regularity: \"Regular\",\n pWave: \"Present, upright, one before every QRS\",\n prInterval: \"0.12-0.20s, constant\",\n qrs: \"Narrow, <0.12s\",\n summary: \"The baseline rhythm every other rhythm is compared against — originates in the SA node, conducts normally through the AV node.\",\n clinicalNote: \"No intervention needed. This is the rhythm you're confirming is present, not absent, before worrying about anything else on the strip.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 100, hasPWave: true, wide: false, prMs: 160 },\n questions: [\n {\n prompt: \"A patient's monitor shows a rate of 78, regular, with an upright P wave before every QRS and a PR interval of 0.16s. What is this rhythm?\",\n choices: [\"Normal Sinus Rhythm\", \"Sinus Tachycardia\", \"First-Degree AV Block\", \"Junctional Rhythm\"],\n correctIndex: 0,\n explanation: \"Rate 60-100, regular, P before every QRS, normal PR interval — textbook NSR.\",\n },\n {\n prompt: \"Which feature, if it were missing, would rule OUT normal sinus rhythm?\",\n choices: [\"A narrow QRS\", \"An upright P wave before every QRS\", \"A rate under 150\", \"A regular rhythm\"],\n correctIndex: 1,\n explanation: \"Sinus rhythms are defined by the P wave originating from the SA node and preceding every QRS — lose that relationship and it's no longer sinus.\",\n },\n ],\n },\n {\n id: \"sinus-brady\",\n name: \"Sinus Bradycardia\",\n category: \"Sinus\",\n free: true,\n sortOrder: 2,\n rate: \"<60 bpm\",\n regularity: \"Regular\",\n pWave: \"Present, upright, one before every QRS\",\n prInterval: \"0.12-0.20s, constant\",\n qrs: \"Narrow, <0.12s\",\n summary: \"Same conduction pattern as NSR, just slower than 60. Can be normal (athletes, sleep) or pathologic (meds, sick sinus syndrome, hypothyroidism).\",\n clinicalNote: \"Only treat if symptomatic (hypotension, altered mental status, chest pain) — a healthy resting rate of 48 in a fit patient needs no intervention.\",\n waveform: { pattern: \"regular\", rateMin: 40, rateMax: 59, hasPWave: true, wide: false, prMs: 160 },\n questions: [\n {\n prompt: \"A rhythm strip shows a rate of 44, regular, normal P waves and PR interval, narrow QRS. The patient is alert, talking, and has a normal blood pressure. What's the priority action?\",\n choices: [\"Give atropine immediately\", \"Start transcutaneous pacing\", \"Monitor — this may not require treatment if asymptomatic\", \"Perform synchronized cardioversion\"],\n correctIndex: 2,\n explanation: \"Sinus bradycardia is only treated when it's causing symptoms. An asymptomatic, hemodynamically stable patient just gets monitored.\",\n },\n {\n prompt: \"Which of these is a common non-pathologic cause of sinus bradycardia?\",\n choices: [\"Third-degree AV block\", \"High level of physical conditioning (athlete's heart)\", \"Digoxin toxicity\", \"Hyperthyroidism\"],\n correctIndex: 1,\n explanation: \"Well-conditioned athletes often have resting rates in the 40s-50s from high vagal tone and stroke volume — a normal finding, not a block.\",\n },\n ],\n },\n {\n id: \"sinus-tach\",\n name: \"Sinus Tachycardia\",\n category: \"Sinus\",\n free: true,\n sortOrder: 3,\n rate: \">100 bpm\",\n regularity: \"Regular\",\n pWave: \"Present, upright, one before every QRS\",\n prInterval: \"0.12-0.20s, constant\",\n qrs: \"Narrow, <0.12s\",\n summary: \"Normal conduction, just faster than 100 — almost always a response to something else (pain, fever, dehydration, anxiety, blood loss), not a primary cardiac problem.\",\n clinicalNote: \"Treat the cause, not the rate — find and fix why the heart is compensating (fluids for dehydration, pain control, treat the fever) rather than trying to slow it directly.\",\n waveform: { pattern: \"regular\", rateMin: 101, rateMax: 150, hasPWave: true, wide: false, prMs: 140 },\n questions: [\n {\n prompt: \"A trauma patient's monitor shows a regular rhythm at 128 bpm with normal P waves and narrow QRS. What should you look for first?\",\n choices: [\"A drug that blocks the AV node\", \"A source of blood loss, pain, or hypoxia driving the rate up\", \"Evidence of a missed P wave\", \"A prolonged QT interval\"],\n correctIndex: 1,\n explanation: \"Sinus tach is almost always secondary to something — in trauma, think hemorrhage first. Slowing the rate directly (e.g. a beta blocker) without fixing the cause can be dangerous.\",\n },\n {\n prompt: \"What distinguishes sinus tachycardia from SVT on a monitor?\",\n choices: [\"Sinus tach has no visible P waves\", \"Sinus tach rarely exceeds 220 bpm and P waves are visible before each QRS\", \"Sinus tach always requires adenosine\", \"Sinus tach has a wide QRS\"],\n correctIndex: 1,\n explanation: \"Sinus tach retains normal P waves and typically tops out lower than SVT, which is often faster and can obscure or hide the P wave in the preceding T wave.\",\n },\n ],\n },\n {\n id: \"pac\",\n name: \"Premature Atrial Contraction (PAC)\",\n category: \"Atrial\",\n free: false,\n sortOrder: 4,\n rate: \"Underlying rhythm rate, with early beats\",\n regularity: \"Irregular (early beat interrupts the pattern)\",\n pWave: \"Early, and often a different shape than the sinus P wave\",\n prInterval: \"May be shorter or longer than normal\",\n qrs: \"Usually narrow (unless aberrantly conducted)\",\n summary: \"An ectopic focus in the atria fires before the SA node's next scheduled beat, causing an early beat with an abnormal-looking P wave.\",\n clinicalNote: \"Usually benign — caffeine, stress, and stimulants are common triggers. Frequent PACs can sometimes signal developing atrial fibrillation.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"atrial\", baseRateMin: 60, baseRateMax: 90 },\n questions: [\n {\n prompt: \"On an otherwise regular strip, one beat arrives early with a P wave that looks different from the others, followed by a normal QRS. What is this?\",\n choices: [\"Premature Ventricular Contraction\", \"Premature Atrial Contraction\", \"Second-degree AV block\", \"Atrial flutter\"],\n correctIndex: 1,\n explanation: \"An early beat with an abnormally-shaped (but present) P wave and a normal QRS is the signature of a PAC — the ectopic focus is atrial, not ventricular.\",\n },\n {\n prompt: \"A patient asks if their occasional PACs, found on a routine monitor, are dangerous. What's the most accurate response?\",\n choices: [\"They always require immediate cardioversion\", \"They're usually benign, often triggered by caffeine or stress, though frequent PACs are worth monitoring\", \"They mean the patient is in cardiac arrest\", \"They can only be caused by a heart attack\"],\n correctIndex: 1,\n explanation: \"Occasional PACs are common and usually harmless. It's a pattern of frequent PACs, not an isolated one, that occasionally warrants a closer look for developing afib.\",\n },\n ],\n },\n {\n id: \"afib\",\n name: \"Atrial Fibrillation\",\n category: \"Atrial\",\n free: true,\n sortOrder: 5,\n rate: \"Variable (ventricular response can be slow, controlled, or rapid)\",\n regularity: \"Irregularly irregular\",\n pWave: \"Absent — replaced by chaotic fibrillatory waves\",\n prInterval: \"Not measurable (no discrete P wave)\",\n qrs: \"Usually narrow\",\n summary: \"Multiple chaotic atrial foci fire simultaneously instead of one coordinated SA node signal, so the atria quiver rather than contract, and the ventricles respond irregularly.\",\n clinicalNote: \"The classic teaching point is 'irregularly irregular' with no true P waves. Stroke risk from atrial clot formation is the major long-term concern, not just the rhythm itself.\",\n waveform: { pattern: \"afib\", rateMin: 70, rateMax: 150 },\n questions: [\n {\n prompt: \"A strip shows no identifiable P waves, a chaotic baseline, and an R-R interval that varies with no repeating pattern. What is this rhythm?\",\n choices: [\"Sinus Arrhythmia\", \"Atrial Flutter\", \"Atrial Fibrillation\", \"Third-degree AV block\"],\n correctIndex: 2,\n explanation: \"Absent P waves plus an irregularly irregular rhythm (no predictable pattern at all, unlike flutter's often-regular ratios) is the defining picture of afib.\",\n },\n {\n prompt: \"Why is atrial fibrillation clinically significant beyond the rhythm itself?\",\n choices: [\"It always causes immediate cardiac arrest\", \"The quivering atria don't empty fully, raising the risk of clot formation and stroke\", \"It permanently damages the AV node\", \"It cannot occur in otherwise healthy people\"],\n correctIndex: 1,\n explanation: \"Blood pooling in the poorly-contracting atria can clot; if that clot embolizes, it can cause a stroke — this is why anticoagulation is a major part of afib management.\",\n },\n ],\n },\n {\n id: \"aflutter\",\n name: \"Atrial Flutter\",\n category: \"Atrial\",\n free: false,\n sortOrder: 6,\n rate: \"Atrial rate ~250-350 bpm; ventricular rate depends on conduction ratio\",\n regularity: \"Often regular (fixed conduction ratio) but can be irregular (variable conduction)\",\n pWave: \"Sawtooth ('flutter') waves, no isoelectric baseline\",\n prInterval: \"Not measurable in the usual sense\",\n qrs: \"Usually narrow\",\n summary: \"A single reentrant circuit in the atria fires very rapidly and regularly, producing the classic sawtooth pattern; the AV node protects the ventricles by only conducting a fraction of those impulses through (commonly 2:1, 3:1, or 4:1).\",\n clinicalNote: \"Look for the sawtooth pattern, most visible in leads II, III, and aVF — a 2:1 conduction ratio can be easy to mistake for sinus tach if you don't count carefully.\",\n waveform: { pattern: \"aflutter\", atrialRate: 300, ratios: [2, 3, 4] },\n questions: [\n {\n prompt: \"A strip shows a sawtooth-shaped baseline at roughly 300 bpm with every other flutter wave conducting to the ventricles, giving a ventricular rate near 150. What is this rhythm?\",\n choices: [\"Atrial Fibrillation\", \"Atrial Flutter with 2:1 conduction\", \"Sinus Tachycardia\", \"Ventricular Tachycardia\"],\n correctIndex: 1,\n explanation: \"The sawtooth pattern at ~300 with a 2:1 AV conduction ratio (every other impulse getting through) producing a ventricular rate near 150 is the classic atrial flutter picture.\",\n },\n {\n prompt: \"What structure is responsible for protecting the ventricles from the very fast atrial rate in atrial flutter?\",\n choices: [\"The SA node\", \"The AV node, by not conducting every atrial impulse through\", \"The bundle of His\", \"The Purkinje fibers\"],\n correctIndex: 1,\n explanation: \"The AV node's refractory period limits how many of the rapid atrial impulses actually reach the ventricles — that's why the ventricular rate is a fraction of the atrial rate.\",\n },\n ],\n },\n {\n id: \"svt\",\n name: \"Supraventricular Tachycardia (SVT)\",\n category: \"Atrial\",\n free: false,\n sortOrder: 7,\n rate: \"150-250 bpm\",\n regularity: \"Regular\",\n pWave: \"Often hidden in the preceding T wave or not visible\",\n prInterval: \"Not measurable if P waves aren't visible\",\n qrs: \"Narrow (unless aberrantly conducted)\",\n summary: \"An umbrella term for fast, regular rhythms originating above the ventricles, most commonly from a reentrant circuit involving the AV node — starts and stops abruptly.\",\n clinicalNote: \"Vagal maneuvers (bearing down, carotid massage by a trained provider) or adenosine are first-line treatments — both work by transiently blocking the AV node to interrupt the reentrant circuit.\",\n waveform: { pattern: \"regular\", rateMin: 150, rateMax: 220, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"A patient reports their heart 'suddenly took off' and the monitor shows a narrow-complex rhythm at 180 bpm, perfectly regular, with no visible P waves. What is the most likely rhythm?\",\n choices: [\"Sinus Tachycardia\", \"Supraventricular Tachycardia (SVT)\", \"Ventricular Tachycardia\", \"Atrial Flutter with 4:1 conduction\"],\n correctIndex: 1,\n explanation: \"The abrupt onset, rate over 150-180 with no visible P waves, and regular narrow QRS is classic SVT — sinus tach ramps up gradually and rarely reaches this rate with hidden P waves.\",\n },\n {\n prompt: \"Why does adenosine work as a treatment for SVT?\",\n choices: [\"It permanently destroys the reentrant pathway\", \"It briefly blocks conduction through the AV node, interrupting the reentrant circuit\", \"It increases the atrial rate to override the SVT\", \"It widens the QRS complex\"],\n correctIndex: 1,\n explanation: \"Adenosine causes a very brief, complete AV node block — long enough to break the reentry loop that's sustaining the SVT, often resetting the rhythm back to sinus.\",\n },\n ],\n },\n {\n id: \"pjc\",\n name: \"Premature Junctional Contraction (PJC)\",\n category: \"Junctional\",\n free: false,\n sortOrder: 8,\n rate: \"Underlying rhythm rate, with early beats\",\n regularity: \"Irregular (early beat interrupts the pattern)\",\n pWave: \"Absent, inverted, or after the QRS (retrograde)\",\n prInterval: \"Short if a retrograde P wave is present\",\n qrs: \"Narrow\",\n summary: \"An early beat originating from the AV junction rather than the SA node or atria — the junction can conduct upward into the atria (inverted/retrograde P) as well as down to the ventricles.\",\n clinicalNote: \"Distinguish from a PAC by the P wave: absent, inverted, or appearing after the QRS rather than a normal upright P wave before it.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"junctional\", baseRateMin: 60, baseRateMax: 90 },\n questions: [\n {\n prompt: \"An early narrow QRS appears with no visible P wave before it, but there's a small inverted deflection just after the QRS. What best explains this beat?\",\n choices: [\"Premature Atrial Contraction\", \"Premature Junctional Contraction with a retrograde P wave\", \"Third-degree AV block\", \"Premature Ventricular Contraction\"],\n correctIndex: 1,\n explanation: \"A junctional beat can conduct backward into the atria, producing an inverted P wave that shows up after (or hidden within) the QRS rather than before it.\",\n },\n {\n prompt: \"What differentiates a PJC from a PAC on a strip?\",\n choices: [\"PJCs have a wide QRS and PACs don't\", \"PJCs lack a normal upright P wave before the QRS; PACs have an abnormal but present upright P wave before it\", \"PJCs are always symptomatic and PACs never are\", \"There is no meaningful difference\"],\n correctIndex: 1,\n explanation: \"The key distinction is the P wave: a PAC still has one before the QRS (just oddly shaped), while a PJC's P wave is absent, inverted, or retrograde.\",\n },\n ],\n },\n {\n id: \"junctional\",\n name: \"Junctional Rhythm\",\n category: \"Junctional\",\n free: false,\n sortOrder: 9,\n rate: \"40-60 bpm\",\n regularity: \"Regular\",\n pWave: \"Absent, inverted, or after the QRS\",\n prInterval: \"Short or not measurable\",\n qrs: \"Narrow\",\n summary: \"The AV junction takes over as the heart's pacemaker when the SA node fails to fire or its impulse doesn't reach the ventricles — an intrinsic 'backup' rate of 40-60.\",\n clinicalNote: \"Treat the underlying cause (often SA node dysfunction) rather than the rhythm itself if the patient is stable; symptomatic patients may need atropine or pacing, same as symptomatic bradycardia.\",\n waveform: { pattern: \"regular\", rateMin: 40, rateMax: 60, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"A monitor shows a regular narrow-complex rhythm at 48 bpm with no visible P waves. What is the most likely rhythm?\",\n choices: [\"Sinus Bradycardia\", \"Junctional Rhythm\", \"Third-degree AV Block\", \"Idioventricular Rhythm\"],\n correctIndex: 1,\n explanation: \"A regular rate in the 40-60 range with a narrow QRS and no P waves points to the AV junction acting as the pacemaker, not the SA node (which would show P waves) or the ventricles (which would show a wide QRS).\",\n },\n {\n prompt: \"Why does a junctional rhythm typically run at 40-60 bpm rather than faster?\",\n choices: [\"That's the AV junction's own intrinsic backup pacing rate\", \"It's always a sign of digoxin toxicity\", \"The ventricles are pacing themselves at that rate\", \"It matches the SA node's normal rate\"],\n correctIndex: 0,\n explanation: \"The cardiac conduction system has tiered intrinsic backup rates — SA node fastest, AV junction next at 40-60, ventricles slowest — and junctional rhythm reflects the AV junction's own rate when it takes over.\",\n },\n ],\n },\n {\n id: \"accel-junctional\",\n name: \"Accelerated Junctional Rhythm\",\n category: \"Junctional\",\n free: false,\n sortOrder: 10,\n rate: \"60-100 bpm\",\n regularity: \"Regular\",\n pWave: \"Absent, inverted, or after the QRS\",\n prInterval: \"Short or not measurable\",\n qrs: \"Narrow\",\n summary: \"Same origin as a junctional rhythm, but the junction is firing faster than its normal 40-60 backup rate — often from irritability (ischemia, digoxin toxicity) rather than simple SA node failure.\",\n clinicalNote: \"A rate that's 'too fast' for a junctional escape rhythm (60-100 instead of 40-60) should prompt a look at digoxin levels and electrolytes.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 100, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"A regular narrow-complex rhythm at 75 bpm shows no P waves before the QRS. What distinguishes this from a plain junctional rhythm?\",\n choices: [\"The QRS is wide\", \"The rate (60-100) is faster than the typical junctional escape rate of 40-60, making this accelerated junctional\", \"There's a visible sawtooth pattern\", \"The PR interval is prolonged\"],\n correctIndex: 1,\n explanation: \"The mechanism (AV junction pacing, no true P wave before QRS) is identical to junctional rhythm — the only difference is the faster rate, which earns it the 'accelerated' label.\",\n },\n {\n prompt: \"Accelerated junctional rhythm is classically associated with which of the following?\",\n choices: [\"Athletic conditioning\", \"Digoxin toxicity or myocardial irritability\", \"Caffeine intake\", \"Normal aging\"],\n correctIndex: 1,\n explanation: \"Unlike a slow junctional escape rhythm (often benign SA node failure), an accelerated junctional focus is often irritable tissue — digoxin toxicity is a classic teaching association.\",\n },\n ],\n },\n {\n id: \"first-degree\",\n name: \"First-Degree AV Block\",\n category: \"AV Block\",\n free: false,\n sortOrder: 11,\n rate: \"Underlying rhythm rate\",\n regularity: \"Regular\",\n pWave: \"Present, one before every QRS\",\n prInterval: \"Prolonged, >0.20s, but constant\",\n qrs: \"Narrow (unless a separate bundle branch issue exists)\",\n summary: \"Every atrial impulse still reaches the ventricles, but conduction through the AV node is delayed — so the PR interval is stretched out but stays constant beat to beat.\",\n clinicalNote: \"Usually benign and often an incidental finding — it's a delay, not a dropped beat, so no beats are lost. Worth noting on the chart and monitoring for progression, but rarely urgent on its own.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 100, hasPWave: true, wide: false, prMs: 280 },\n questions: [\n {\n prompt: \"A strip shows a P wave before every QRS, a regular rhythm, but the PR interval measures 0.28s on every beat. What is this rhythm?\",\n choices: [\"Second-Degree AV Block Type I\", \"Third-Degree AV Block\", \"First-Degree AV Block\", \"Normal Sinus Rhythm\"],\n correctIndex: 2,\n explanation: \"A consistently prolonged (>0.20s) but unchanging PR interval, with every P wave still conducting to a QRS, is the definition of first-degree AV block.\",\n },\n {\n prompt: \"What is the key difference between first-degree AV block and normal sinus rhythm?\",\n choices: [\"First-degree block drops occasional QRS complexes\", \"First-degree block has a prolonged but constant PR interval; NSR's PR interval is normal (0.12-0.20s)\", \"First-degree block has no P waves\", \"There is no real difference\"],\n correctIndex: 1,\n explanation: \"The rhythm and P-QRS relationship look the same as NSR — the tell is a PR interval that's stretched past 0.20s but stays fixed beat to beat.\",\n },\n ],\n },\n {\n id: \"second-degree-1\",\n name: \"Second-Degree AV Block Type I (Wenckebach)\",\n category: \"AV Block\",\n free: false,\n sortOrder: 12,\n rate: \"Atrial rate normal; ventricular rate slightly slower due to dropped beats\",\n regularity: \"Irregular (patterned — groups of beats with a dropped QRS)\",\n pWave: \"Present, but one eventually isn't followed by a QRS\",\n prInterval: \"Progressively lengthens beat to beat until a QRS is dropped, then resets\",\n qrs: \"Narrow\",\n summary: \"The AV node conduction delay gets progressively worse with each beat until one impulse fails to conduct entirely, dropping a QRS — then the cycle resets and repeats ('longer, longer, longer, drop').\",\n clinicalNote: \"Usually a benign, often reversible pattern (inferior MI, medication effect, high vagal tone) — rarely progresses to complete block, and often just needs monitoring rather than pacing.\",\n waveform: { pattern: \"wenckebach\", rateMin: 60, rateMax: 90, startPrMs: 160, prIncrementMs: 40, cycleBeats: 4 },\n questions: [\n {\n prompt: \"On a strip, the PR interval gets progressively longer over three beats, then a P wave appears with no QRS after it, and the pattern restarts. What is this rhythm?\",\n choices: [\"First-Degree AV Block\", \"Second-Degree AV Block Type I (Wenckebach)\", \"Second-Degree AV Block Type II\", \"Third-Degree AV Block\"],\n correctIndex: 1,\n explanation: \"Progressive PR lengthening culminating in a dropped QRS, then a reset, is the hallmark 'longer, longer, longer, drop' pattern of Wenckebach.\",\n },\n {\n prompt: \"Compared to Type II second-degree block, Wenckebach (Type I) is generally considered:\",\n choices: [\"More dangerous and more likely to progress to complete block\", \"Less dangerous, often benign and reversible\", \"Identical in risk\", \"Only seen in pediatric patients\"],\n correctIndex: 1,\n explanation: \"Type I block is usually at the level of the AV node itself, tends to be transient, and rarely progresses — Type II (below the AV node) carries a higher risk of sudden progression to complete block.\",\n },\n ],\n },\n {\n id: \"second-degree-2\",\n name: \"Second-Degree AV Block Type II\",\n category: \"AV Block\",\n free: false,\n sortOrder: 13,\n rate: \"Atrial rate normal; ventricular rate depends on how many beats drop\",\n regularity: \"Irregular, but PR interval doesn't change beat to beat\",\n pWave: \"Present, with intermittently dropped QRS complexes\",\n prInterval: \"Constant on conducted beats — no progressive lengthening before the drop\",\n qrs: \"Often wide (block is usually below the AV node, in the bundle branches)\",\n summary: \"Unlike Wenckebach, the PR interval stays fixed on every conducted beat — a QRS just suddenly fails to follow a P wave with no warning lengthening beforehand. The block is typically lower in the conduction system.\",\n clinicalNote: \"Higher-risk than Type I — more likely to progress suddenly to complete heart block. Often needs a pacemaker even if currently stable.\",\n waveform: { pattern: \"type2block\", rateMin: 60, rateMax: 90, prMs: 180, dropEvery: 4, wide: true },\n questions: [\n {\n prompt: \"A strip shows a constant PR interval of 0.18s on every conducted beat, but every third P wave has no QRS following it, with no warning lengthening beforehand. What is this rhythm?\",\n choices: [\"Second-Degree AV Block Type I (Wenckebach)\", \"Second-Degree AV Block Type II\", \"First-Degree AV Block\", \"Sinus Arrhythmia\"],\n correctIndex: 1,\n explanation: \"A fixed PR interval with sudden, unpredictable dropped beats (no progressive lengthening) is the defining feature that separates Type II from Wenckebach.\",\n },\n {\n prompt: \"Why is Type II second-degree block generally treated more aggressively than Type I?\",\n choices: [\"It's always asymptomatic\", \"It carries a higher risk of sudden, unpredictable progression to complete heart block\", \"It only occurs in healthy young athletes\", \"It resolves on its own within minutes\"],\n correctIndex: 1,\n explanation: \"Because the block sits below the AV node (in the bundle branches), it's less stable and can progress abruptly and without warning to third-degree block — often prompting pacemaker placement even in stable patients.\",\n },\n ],\n },\n {\n id: \"third-degree\",\n name: \"Third-Degree (Complete) AV Block\",\n category: \"AV Block\",\n free: false,\n sortOrder: 14,\n rate: \"Atrial rate normal; ventricular rate slow (40-60 junctional or <40 ventricular escape)\",\n regularity: \"Both P waves and QRS complexes are regular, but independent of each other\",\n pWave: \"Present, marching out at their own regular rate\",\n prInterval: \"Not measurable — completely variable, no relationship between P and QRS\",\n qrs: \"Narrow (junctional escape) or wide (ventricular escape), depending on where the escape pacemaker sits\",\n summary: \"No atrial impulses reach the ventricles at all — the atria and ventricles are being paced completely independently ('AV dissociation'), with the ventricles relying entirely on a junctional or ventricular escape rhythm to keep beating.\",\n clinicalNote: \"This is a true emergency if the escape rate is too slow to maintain perfusion — transcutaneous pacing and/or a permanent pacemaker are typically needed. Do not give AV-node-blocking drugs.\",\n waveform: { pattern: \"thirdDegree\", atrialRateMin: 70, atrialRateMax: 100, ventricularRateMin: 30, ventricularRateMax: 50, wide: false },\n questions: [\n {\n prompt: \"A strip shows P waves marching out regularly at 90 bpm and QRS complexes marching out regularly at 38 bpm, with no consistent relationship between the two. What is this rhythm?\",\n choices: [\"Second-Degree AV Block Type II\", \"Sinus Arrhythmia\", \"Third-Degree (Complete) AV Block\", \"Atrial Fibrillation\"],\n correctIndex: 2,\n explanation: \"Two independently regular rates — one atrial, one ventricular — with no fixed PR relationship is the signature of complete AV dissociation.\",\n },\n {\n prompt: \"A patient in third-degree AV block with a ventricular rate of 32 and altered mental status needs which immediate intervention?\",\n choices: [\"Adenosine\", \"Vagal maneuvers\", \"Transcutaneous pacing\", \"Observation only\"],\n correctIndex: 2,\n explanation: \"A symptomatic, hemodynamically unstable bradycardia from complete heart block is a pacing emergency — adenosine and vagal maneuvers are for fast rhythms, not slow ones, and observation risks further deterioration.\",\n },\n ],\n },\n {\n id: \"pvc\",\n name: \"Premature Ventricular Contraction (PVC)\",\n category: \"Ventricular\",\n free: true,\n sortOrder: 15,\n rate: \"Underlying rhythm rate, with early wide beats\",\n regularity: \"Irregular (early beat interrupts the pattern)\",\n pWave: \"None associated with the early beat\",\n prInterval: \"Not applicable for the PVC itself\",\n qrs: \"Wide (>0.12s) and bizarre-looking, often followed by a compensatory pause\",\n summary: \"An ectopic focus in the ventricle fires early, bypassing the normal conduction pathway, producing a wide, oddly-shaped QRS with no preceding P wave.\",\n clinicalNote: \"Occasional PVCs are common and often benign. Frequent, multifocal, or PVCs falling on the T wave of the prior beat (R-on-T) raise concern for triggering a lethal rhythm and warrant closer attention.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"ventricular\", baseRateMin: 60, baseRateMax: 90 },\n questions: [\n {\n prompt: \"On an otherwise regular strip, a wide, bizarre-looking QRS appears early with no P wave before it, followed by a pause before the next normal beat. What is this?\",\n choices: [\"Premature Atrial Contraction\", \"Premature Junctional Contraction\", \"Premature Ventricular Contraction\", \"Second-degree AV block\"],\n correctIndex: 2,\n explanation: \"A wide, early QRS with no preceding P wave is the classic PVC picture — the wide complex reflects the impulse spreading through ventricular muscle directly, not the normal fast conduction pathway.\",\n },\n {\n prompt: \"Which finding about a patient's PVCs would be most concerning and worth flagging urgently?\",\n choices: [\"A single isolated PVC once during an 8-hour shift\", \"PVCs from multiple different ventricular sites (multifocal) or landing on the preceding T wave (R-on-T)\", \"A PVC that looks identical to the one seen an hour earlier\", \"PVCs only occurring while the patient is asleep\"],\n correctIndex: 1,\n explanation: \"Multifocal PVCs suggest more irritable ventricular tissue, and R-on-T PVCs can land during the heart's vulnerable repolarization window and trigger V-tach or V-fib — both are higher-risk patterns than an isolated, uniform PVC.\",\n },\n ],\n },\n {\n id: \"idioventricular\",\n name: \"Idioventricular Rhythm\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 16,\n rate: \"20-40 bpm\",\n regularity: \"Regular\",\n pWave: \"Absent\",\n prInterval: \"Not applicable\",\n qrs: \"Wide, >0.12s\",\n summary: \"When both the SA node and the AV junction fail to pace, the ventricles fall back on their own intrinsic, very slow escape rate — the pacemaker of last resort.\",\n clinicalNote: \"This rate is rarely enough to sustain adequate perfusion on its own — treat the underlying cause and prepare for pacing; this is often a peri-arrest rhythm.\",\n waveform: { pattern: \"regular\", rateMin: 20, rateMax: 40, hasPWave: false, wide: true },\n questions: [\n {\n prompt: \"A monitor shows a regular, wide-complex rhythm at 28 bpm with no identifiable P waves anywhere on the strip. What is the most likely rhythm?\",\n choices: [\"Junctional Rhythm\", \"Idioventricular Rhythm\", \"Ventricular Tachycardia\", \"Sinus Bradycardia\"],\n correctIndex: 1,\n explanation: \"A wide QRS at a very slow rate (20-40) with no P waves reflects the ventricles pacing themselves as the last-resort intrinsic pacemaker, after higher pacemakers have failed.\",\n },\n {\n prompt: \"Why is idioventricular rhythm considered a high-risk finding even if the patient currently has a pulse?\",\n choices: [\"It always means the patient is already in cardiac arrest\", \"The rate is usually too slow to maintain adequate perfusion and it can deteriorate further without intervention\", \"It's a completely normal variant in healthy adults\", \"It resolves without any treatment needed\"],\n correctIndex: 1,\n explanation: \"20-40 bpm is rarely enough cardiac output to perfuse the brain and organs adequately — it's often seen as a late, unstable rhythm needing urgent treatment of the underlying cause and likely pacing.\",\n },\n ],\n },\n {\n id: \"vtach\",\n name: \"Ventricular Tachycardia (Monomorphic)\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 17,\n rate: \">100 bpm, often 150-250\",\n regularity: \"Regular\",\n pWave: \"Absent (or dissociated, unrelated to the QRS)\",\n prInterval: \"Not applicable\",\n qrs: \"Wide, >0.12s, uniform shape from beat to beat ('monomorphic')\",\n summary: \"A run of three or more consecutive PVCs from the same ventricular focus at a fast, regular rate — a wide-complex tachycardia that can rapidly become unstable.\",\n clinicalNote: \"Treatment depends entirely on whether the patient has a pulse and is stable: pulseless V-tach is treated like V-fib (defibrillation, ACLS); stable V-tach with a pulse may get antiarrhythmics; unstable V-tach with a pulse needs synchronized cardioversion.\",\n waveform: { pattern: \"regular\", rateMin: 150, rateMax: 220, hasPWave: false, wide: true },\n questions: [\n {\n prompt: \"A monitor shows a regular, wide-complex rhythm at 180 bpm with a uniform QRS shape on every beat and no visible P waves. The patient has a pulse but is confused and hypotensive. What is this rhythm and the appropriate action?\",\n choices: [\"SVT with aberrancy — give adenosine\", \"Monomorphic V-tach with a pulse, unstable — prepare for synchronized cardioversion\", \"Normal sinus rhythm — no action needed\", \"Atrial fibrillation — start anticoagulation\"],\n correctIndex: 1,\n explanation: \"A fast, wide, regular, uniform rhythm with an unstable patient (altered mental status, hypotension) is unstable V-tach — synchronized cardioversion is indicated, not a rate-control drug.\",\n },\n {\n prompt: \"How is pulseless V-tach managed differently from stable V-tach with a pulse?\",\n choices: [\"Pulseless V-tach is treated exactly like a normal rhythm, no urgency\", \"Pulseless V-tach is treated like V-fib — immediate defibrillation and CPR per ACLS, not synchronized cardioversion\", \"Stable V-tach always requires immediate defibrillation\", \"There is no difference in management\"],\n correctIndex: 1,\n explanation: \"No pulse means no organized output regardless of what the monitor shows — pulseless V-tach is a cardiac arrest rhythm managed with immediate defibrillation and CPR, the same as V-fib.\",\n },\n ],\n },\n {\n id: \"torsades\",\n name: \"Torsades de Pointes\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 18,\n rate: \"150-250 bpm\",\n regularity: \"Irregular\",\n pWave: \"Absent\",\n prInterval: \"Not applicable\",\n qrs: \"Wide, with amplitude that twists around the baseline ('twisting of the points')\",\n summary: \"A distinctive polymorphic V-tach where the QRS complexes appear to spiral or twist around the isoelectric baseline — classically associated with a prolonged QT interval on the preceding baseline rhythm.\",\n clinicalNote: \"Magnesium sulfate is first-line treatment, unlike standard V-tach. Also review and stop any QT-prolonging medications contributing to the underlying cause.\",\n waveform: { pattern: \"torsades\", rateMin: 150, rateMax: 220 },\n questions: [\n {\n prompt: \"A wide-complex tachycardia shows QRS complexes that appear to twist in amplitude around the baseline, changing shape continuously rather than staying uniform. What is this rhythm?\",\n choices: [\"Monomorphic Ventricular Tachycardia\", \"Torsades de Pointes\", \"Ventricular Fibrillation\", \"Atrial Flutter\"],\n correctIndex: 1,\n explanation: \"The twisting, varying QRS amplitude (as opposed to monomorphic V-tach's uniform shape) is the defining visual feature that gives torsades its name.\",\n },\n {\n prompt: \"What is the first-line treatment for torsades de pointes, distinct from standard V-tach management?\",\n choices: [\"Amiodarone\", \"Magnesium sulfate\", \"Atropine\", \"Adenosine\"],\n correctIndex: 1,\n explanation: \"Torsades is strongly linked to a prolonged QT interval, and IV magnesium is first-line — it stabilizes the cardiac membrane even when magnesium levels are normal.\",\n },\n ],\n },\n {\n id: \"vfib\",\n name: \"Ventricular Fibrillation\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 19,\n rate: \"Not organized — no true rate\",\n regularity: \"Chaotic, no pattern\",\n pWave: \"Absent\",\n prInterval: \"Not applicable\",\n qrs: \"No identifiable QRS complexes — chaotic, disorganized waveform\",\n summary: \"Multiple ventricular sites fire chaotically and simultaneously, so the ventricles quiver instead of contracting — there is no organized electrical activity and no cardiac output whatsoever.\",\n clinicalNote: \"This is cardiac arrest. Immediate CPR and defibrillation are the only effective interventions — there is no pulse to check for or medication that substitutes for defibrillation.\",\n waveform: { pattern: \"chaotic\" },\n questions: [\n {\n prompt: \"A monitor shows a completely chaotic waveform with no identifiable P waves, QRS complexes, or any repeating pattern. The patient is unresponsive with no pulse. What is this rhythm and the immediate action?\",\n choices: [\"Asystole — begin transcutaneous pacing\", \"Ventricular Fibrillation — begin CPR and defibrillate immediately\", \"Sinus Arrhythmia — reassess in 5 minutes\", \"Atrial Fibrillation — control the rate with a beta blocker\"],\n correctIndex: 1,\n explanation: \"A chaotic, disorganized waveform with no pulse is V-fib — immediate CPR and defibrillation are the only interventions that restore organized electrical activity.\",\n },\n {\n prompt: \"Why does V-fib produce no pulse even though there's electrical activity on the monitor?\",\n choices: [\"The rate is simply too slow to generate a pulse\", \"The ventricles are quivering chaotically instead of contracting in a coordinated way, so no blood is being pumped\", \"The electrical activity is too fast to register a pulse manually\", \"V-fib patients always retain a weak pulse\"],\n correctIndex: 1,\n explanation: \"Effective pumping requires coordinated contraction — chaotic, disorganized electrical activity produces quivering muscle, not a mechanical pump stroke, so there's electrical activity but zero cardiac output.\",\n },\n ],\n },\n {\n id: \"asystole\",\n name: \"Asystole\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 20,\n rate: \"None\",\n regularity: \"Not applicable — flatline\",\n pWave: \"Absent (occasional P waves alone with no QRS can occur — 'P-wave asystole')\",\n prInterval: \"Not applicable\",\n qrs: \"None — no electrical activity\",\n summary: \"Complete absence of ventricular electrical activity — a flatline. Always confirm in more than one lead and check that leads are actually attached before treating as true asystole (a loose lead can mimic it).\",\n clinicalNote: \"Not a shockable rhythm — defibrillation does nothing for a flatline. Management is high-quality CPR, epinephrine, and searching for and treating a reversible cause (the H's and T's).\",\n waveform: { pattern: \"flatline\" },\n questions: [\n {\n prompt: \"A monitor shows a flat line with no electrical activity in any lead, confirmed with leads properly attached. The patient is unresponsive with no pulse. What is the appropriate immediate treatment?\",\n choices: [\"Immediate defibrillation\", \"High-quality CPR and epinephrine, while searching for a reversible cause — this is not a shockable rhythm\", \"Synchronized cardioversion\", \"Adenosine\"],\n correctIndex: 1,\n explanation: \"Asystole has no organized electrical activity for a shock to organize — defibrillating a flatline does nothing. CPR, epinephrine, and finding a reversible cause are the actual interventions.\",\n },\n {\n prompt: \"Before treating a flatline on the monitor as true asystole, what should always be checked first?\",\n choices: [\"The patient's blood pressure\", \"That the leads are properly attached and the rhythm is confirmed in more than one lead\", \"The patient's temperature\", \"The time of day\"],\n correctIndex: 1,\n explanation: \"A disconnected or loose lead can produce a flatline that looks exactly like asystole — always rule out an equipment/lead problem before committing to that diagnosis.\",\n },\n ],\n },\n {\n id: \"sinus-arrhythmia\",\n name: \"Sinus Arrhythmia\",\n category: \"Sinus\",\n free: false,\n sortOrder: 21,\n rate: \"60-100 bpm\",\n regularity: \"Irregular — rate cycles with breathing\",\n pWave: \"Present, upright, one before every QRS, normal shape\",\n prInterval: \"0.12-0.20s, constant\",\n qrs: \"Narrow, <0.12s\",\n summary: \"Vagal tone rises and falls with breathing, so the SA node speeds up on inspiration and slows on expiration even though it's still fully in charge of pacing.\",\n clinicalNote: \"A normal physiologic finding, especially in younger or athletic patients — no treatment needed. Non-respiratory variation in an older patient can be a clue to sinus node disease.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 100, hasPWave: true, wide: false, prMs: 160, irregular: true },\n questions: [\n {\n prompt: \"A strip shows a normal P wave before every narrow QRS and a constant PR interval, but the R-R interval visibly speeds up and slows down in a repeating pattern. What is this rhythm?\",\n choices: [\"Atrial Fibrillation\", \"Sinus Arrhythmia\", \"Second-Degree AV Block Type I\", \"Multifocal Atrial Tachycardia\"],\n correctIndex: 1,\n explanation: \"Sinus arrhythmia keeps a normal, unchanging P-QRS relationship — only the rate drifts, cycling with the respiratory pattern, unlike the chaotic irregularity of afib or MAT.\",\n },\n {\n prompt: \"What causes the cyclic rate change seen in sinus arrhythmia?\",\n choices: [\"A second competing pacemaker in the atria\", \"Vagal tone shifting with the breathing cycle, speeding the SA node on inspiration and slowing it on expiration\", \"Intermittent failure of the AV node to conduct\", \"Digoxin toxicity\"],\n correctIndex: 1,\n explanation: \"It's a normal autonomic effect — breathing modulates vagal tone, and the SA node responds by speeding up and slowing down in step with it.\",\n },\n ],\n },\n {\n id: \"sinus-pause\",\n name: \"Sinus Arrest / Sinus Pause\",\n category: \"Sinus\",\n free: false,\n sortOrder: 22,\n rate: \"Normal until the pause; escape rate depends on which pacemaker takes over\",\n regularity: \"Regular, interrupted by a pause that isn't a clean multiple of the normal P-P interval\",\n pWave: \"Normal in sinus beats; absent during the pause\",\n prInterval: \"Normal in sinus beats\",\n qrs: \"Narrow, unless a ventricular escape beat ends the pause\",\n summary: \"The SA node simply fails to fire for a beat or more. A gap under 2 seconds is called a pause; 2 seconds or longer is called an arrest — a lower pacemaker usually escapes to keep the heart beating.\",\n clinicalNote: \"Often vagally mediated and benign in a healthy young patient, but can reflect sick sinus syndrome, drug effect (beta-blockers, calcium channel blockers, digoxin), or ischemia. A long pause causing syncope is called an Adams-Stokes attack.\",\n waveform: { pattern: \"pause\", rateMin: 60, rateMax: 90, hasPWave: true, prMs: 160 },\n questions: [\n {\n prompt: \"An otherwise regular strip shows one unexpectedly long gap with no P wave or QRS, not matching any clean multiple of the normal beat-to-beat interval, before the rhythm resumes. What does this describe?\",\n choices: [\"Second-Degree AV Block Type II\", \"Sinus Arrest / Sinus Pause\", \"Atrial Flutter\", \"Third-Degree AV Block\"],\n correctIndex: 1,\n explanation: \"The SA node briefly fails to fire, producing a pause with no P wave at all — different from a block, where a P wave is present but simply fails to conduct.\",\n },\n {\n prompt: \"What is the key difference between a 'sinus pause' and 'sinus arrest'?\",\n choices: [\"Pauses only happen in children\", \"Arrest always requires a pacemaker; pauses never do\", \"They're defined by duration — a pause is under 2 seconds, arrest is 2 seconds or longer\", \"There is no real difference\"],\n correctIndex: 2,\n explanation: \"Both describe the same SA node failure — the terms just split by how long the gap lasts.\",\n },\n ],\n },\n {\n id: \"wap\",\n name: \"Wandering Atrial Pacemaker (WAP)\",\n category: \"Atrial\",\n free: false,\n sortOrder: 23,\n rate: \"<100 bpm\",\n regularity: \"Irregularly irregular\",\n pWave: \"At least 3 distinct P-wave shapes in the same view, varying beat to beat\",\n prInterval: \"Varies beat to beat along with the P wave\",\n qrs: \"Narrow\",\n summary: \"Pacemaker control shifts back and forth among the SA node, atrial tissue, and the AV junction, so each beat's P wave looks a little different depending on where it started.\",\n clinicalNote: \"Usually a benign, often incidental finding in young athletes or older adults with pulmonary disease — no treatment needed unless symptomatic.\",\n waveform: { pattern: \"multifocal\", rateMin: 60, rateMax: 95 },\n questions: [\n {\n prompt: \"A strip under 100 bpm shows P waves that change shape and size from beat to beat — at least three distinct forms — with a correspondingly variable PR interval. What is this rhythm?\",\n choices: [\"Multifocal Atrial Tachycardia\", \"Wandering Atrial Pacemaker\", \"Atrial Fibrillation\", \"Premature Atrial Contractions\"],\n correctIndex: 1,\n explanation: \"Multiple shifting P-wave shapes under 100 bpm is WAP — the same pattern above 100 bpm is called MAT instead.\",\n },\n {\n prompt: \"What's the practical difference between Wandering Atrial Pacemaker and Multifocal Atrial Tachycardia?\",\n choices: [\"WAP has a wide QRS and MAT doesn't\", \"They're the same underlying pattern, split purely by rate — under 100 bpm is WAP, over 100 bpm is MAT\", \"WAP only occurs in infants\", \"MAT always has a single P-wave shape\"],\n correctIndex: 1,\n explanation: \"Both show the same shifting-pacemaker P-wave pattern; the rate cutoff of 100 bpm is the only thing that separates the two names.\",\n },\n ],\n },\n {\n id: \"mat\",\n name: \"Multifocal Atrial Tachycardia (MAT)\",\n category: \"Atrial\",\n free: false,\n sortOrder: 24,\n rate: \"Usually 100-150 bpm, occasionally faster\",\n regularity: \"Irregularly irregular\",\n pWave: \"At least 3 distinct P-wave shapes in the same view\",\n prInterval: \"Variable; some P waves may not conduct\",\n qrs: \"Usually narrow\",\n summary: \"Multiple irritable atrial foci compete to pace the heart, each firing on its own, so no single organized P-wave pattern or rate emerges — often driven by hypoxia, a catecholamine surge, or an electrolyte disturbance.\",\n clinicalNote: \"Classically seen with a COPD exacerbation or decompensated heart failure — it's a marker of how sick the underlying illness is. Treat the underlying cause rather than the rhythm; AV nodal agents are used cautiously, and digoxin or cardioversion generally don't work.\",\n waveform: { pattern: \"multifocal\", rateMin: 100, rateMax: 150, irregular: true },\n questions: [\n {\n prompt: \"A COPD patient's monitor shows a chaotic rhythm at 130 bpm with at least three different P-wave shapes and a variable PR interval. What is this rhythm, and what should you focus treatment on?\",\n choices: [\"Atrial Flutter — synchronized cardioversion\", \"Multifocal Atrial Tachycardia — treat the underlying hypoxia/illness, not the rhythm directly\", \"Sinus Tachycardia — reassurance only\", \"SVT — adenosine\"],\n correctIndex: 1,\n explanation: \"MAT is a marker of underlying illness (classically COPD or heart failure) — cardioversion and digoxin generally don't work, and the priority is treating what's driving it.\",\n },\n {\n prompt: \"MAT and Wandering Atrial Pacemaker share the same multi-shaped P-wave pattern. What distinguishes MAT?\",\n choices: [\"A wide QRS\", \"A rate over 100 bpm\", \"The complete absence of P waves\", \"A fixed, unchanging PR interval\"],\n correctIndex: 1,\n explanation: \"The underlying mechanism — multiple competing atrial foci — is identical; MAT is simply the name used once the rate crosses 100 bpm.\",\n },\n ],\n },\n {\n id: \"junctional-tach\",\n name: \"Junctional Tachycardia\",\n category: \"Junctional\",\n free: false,\n sortOrder: 25,\n rate: \">100 bpm\",\n regularity: \"Regular\",\n pWave: \"Retrograde (inverted) if visible — may fall before, within, or after the QRS\",\n prInterval: \"Short (<0.12s) if a P wave precedes the QRS; often unmeasurable\",\n qrs: \"Narrow, unless a pre-existing bundle branch block is present\",\n summary: \"The AV junction fires faster than the SA node and takes over as pacemaker, sending impulses down to the ventricles normally but backward into the atria — producing the inverted P waves when they're visible at all.\",\n clinicalNote: \"Classically associated with digoxin toxicity; also seen with ischemia, myocarditis, or after cardiac surgery. Typically doesn't respond to vagal maneuvers, which helps distinguish it from a re-entrant SVT.\",\n waveform: { pattern: \"regular\", rateMin: 100, rateMax: 160, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"A monitor shows a regular, narrow-complex rhythm at 120 bpm with no clearly visible P waves, unresponsive to vagal maneuvers. Which cause should specifically come to mind?\",\n choices: [\"Caffeine intake\", \"Digoxin toxicity\", \"Athletic conditioning\", \"Dehydration\"],\n correctIndex: 1,\n explanation: \"Junctional tachycardia is a classic digoxin toxicity finding — it's also one of the clues that helps separate it from a re-entrant SVT, which usually does respond to vagal maneuvers.\",\n },\n {\n prompt: \"Why are P waves inverted (retrograde) in junctional tachycardia when they're visible at all?\",\n choices: [\"The SA node is firing backward\", \"The AV junction paces the ventricles normally but conducts backward up into the atria\", \"The atria are fibrillating\", \"The QRS is masking a normal upright P wave\"],\n correctIndex: 1,\n explanation: \"The junction sits between the atria and ventricles — when it takes over pacing, the impulse still reaches the ventricles normally but has to travel backward to reach the atria, producing an inverted P wave.\",\n },\n ],\n },\n {\n id: \"aivr\",\n name: \"Accelerated Idioventricular Rhythm (AIVR)\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 26,\n rate: \"40-100 bpm (some sources extend to 110-120)\",\n regularity: \"Regular\",\n pWave: \"Often dissociated from the QRS; occasional fusion/capture beats\",\n prInterval: \"Not applicable (P and QRS are dissociated) except at fusion beats\",\n qrs: \"Wide, bizarre, ventricular in origin\",\n summary: \"An irritable focus in the ventricle fires slightly faster than the SA node and briefly takes over pacing — 'accelerated' because it's faster than a normal ventricular escape rhythm (20-40) but not fast enough to call it V-tach.\",\n clinicalNote: \"A classic, usually benign finding after reperfusion (post-thrombolysis or PCI in a STEMI) — a 'reperfusion arrhythmia.' It's typically self-limited; treating it with antiarrhythmics is generally avoided since it can suppress the only functioning ventricular rhythm.\",\n waveform: { pattern: \"regular\", rateMin: 40, rateMax: 100, hasPWave: false, wide: true },\n questions: [\n {\n prompt: \"Shortly after a patient receives reperfusion therapy for a STEMI, the monitor shows a regular, wide-complex rhythm at 75 bpm. What is the most likely rhythm, and the appropriate response?\",\n choices: [\"Ventricular Tachycardia — synchronized cardioversion\", \"Accelerated Idioventricular Rhythm — usually benign, generally just observe\", \"Third-Degree AV Block — transcutaneous pacing\", \"Asystole — begin CPR\"],\n correctIndex: 1,\n explanation: \"AIVR classically shows up right after reperfusion and is usually a benign, self-limited finding — treating it aggressively can actually suppress the ventricular rhythm keeping the patient perfused.\",\n },\n {\n prompt: \"What separates AIVR from a slow Ventricular Tachycardia?\",\n choices: [\"AIVR always has a narrow QRS\", \"Rate is the main distinguishing feature, though the two can overlap — AIVR is generally under 100-120 bpm\", \"AIVR only occurs in children\", \"V-tach never has AV dissociation\"],\n correctIndex: 1,\n explanation: \"Both are wide-complex ventricular rhythms — rate is the main practical distinguishing feature, though sources acknowledge some overlap at the upper end of AIVR's range.\",\n },\n ],\n },\n {\n id: \"v-paced\",\n name: \"Ventricular Paced Rhythm\",\n category: \"Other\",\n free: false,\n sortOrder: 27,\n rate: \"Set by the pacemaker's programmed rate (commonly ~60-70 bpm baseline)\",\n regularity: \"Regular\",\n pWave: \"Absent or dissociated — a single-chamber ventricular pacemaker doesn't sense or pace the atrium\",\n prInterval: \"Not applicable for paced beats\",\n qrs: \"Wide, preceded by a sharp pacing spike; often resembles a left bundle branch block pattern\",\n summary: \"A wire in the right ventricle delivers an electrical stimulus directly to the heart muscle whenever the intrinsic rate drops below the device's set threshold, producing a wide, bizarre QRS with a pacing spike right before it.\",\n clinicalNote: \"This is the expected, normal appearance for a functioning single-chamber ventricular pacemaker. Standard STEMI criteria don't apply to paced beats — watch instead for failure to capture (a spike with no QRS following it) or failure to sense.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 72, hasPWave: false, wide: true, pacedSpike: true },\n questions: [\n {\n prompt: \"A strip shows a sharp vertical spike immediately before every wide, bizarre QRS, at a fixed rate of 70 bpm. What does this represent?\",\n choices: [\"Wolff-Parkinson-White pattern\", \"A functioning ventricular paced rhythm\", \"Torsades de Pointes\", \"First-Degree AV Block\"],\n correctIndex: 1,\n explanation: \"The pacing spike right before a wide QRS is the signature of a ventricular pacemaker firing — the device is generating the beat directly rather than the heart's own conduction system.\",\n },\n {\n prompt: \"A pacing spike appears on the strip but is NOT followed by a QRS complex. What does this indicate?\",\n choices: [\"Normal pacemaker function\", \"Failure to capture — the pacing stimulus isn't triggering a ventricular contraction\", \"Sinus arrhythmia\", \"First-degree AV block\"],\n correctIndex: 1,\n explanation: \"A spike with no resulting QRS means the electrical stimulus reached the tissue but failed to depolarize it — a pacemaker malfunction called failure to capture, worth flagging urgently.\",\n },\n ],\n },\n {\n id: \"wpw\",\n name: \"Wolff-Parkinson-White (WPW) Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 28,\n rate: \"Normal at baseline (WPW is a conduction pattern, not itself a tachycardia)\",\n regularity: \"Regular at baseline\",\n pWave: \"Normal sinus P wave\",\n prInterval: \"Short, <0.12s\",\n qrs: \"Wide, >0.12s, with a slurred, slowed initial upstroke (the 'delta wave')\",\n summary: \"An extra electrical connection between atria and ventricles (an accessory pathway) bypasses the AV node's normal delay, so part of the ventricle is activated early — producing the short PR interval and the slurred delta-wave upstroke where the early and normal wavefronts fuse.\",\n clinicalNote: \"Predisposes to re-entrant tachycardias and, critically, to very rapid ventricular rates if the patient develops atrial fibrillation, since the accessory pathway lacks the AV node's rate-limiting property. AV-node-blocking drugs (adenosine, beta-blockers, calcium channel blockers, digoxin) are contraindicated in pre-excited afib because they can paradoxically speed conduction down the bypass tract.\",\n waveform: { pattern: \"regular\", rateMin: 65, rateMax: 90, hasPWave: true, wide: true, prMs: 90, delta: true },\n questions: [\n {\n prompt: \"A resting strip shows a short PR interval and a QRS with a slurred, slowed initial upstroke before the sharp spike. What does this describe?\",\n choices: [\"First-Degree AV Block\", \"Wolff-Parkinson-White (WPW) pattern\", \"Right bundle branch block\", \"Sinus Tachycardia\"],\n correctIndex: 1,\n explanation: \"A short PR interval plus a delta wave — that slurred upstroke — is the defining ECG signature of pre-excitation from an accessory pathway.\",\n },\n {\n prompt: \"Why are adenosine, beta-blockers, and calcium channel blockers dangerous in a WPW patient who develops atrial fibrillation?\",\n choices: [\"They have no effect on the accessory pathway either way\", \"They slow the AV node, which can paradoxically push more of the fast atrial activity down the unprotected accessory pathway to the ventricles\", \"They only work in adults over 65\", \"They cure the accessory pathway permanently\"],\n correctIndex: 1,\n explanation: \"Unlike the AV node, the accessory pathway has no built-in rate limiter — blocking the AV node removes the 'safety valve' and can let dangerously fast atrial rates conduct straight to the ventricles, risking V-fib.\",\n },\n ],\n },\n {\n id: \"atrial-bigeminy\",\n name: \"Atrial Bigeminy\",\n category: \"Atrial\",\n free: false,\n sortOrder: 29,\n rate: \"Underlying sinus rate variable; every other beat is an early PAC, so overall rate often looks near-normal to mildly irregular\",\n regularity: \"Regularly irregular — patterned couplet of sinus beat + PAC repeating\",\n pWave: \"Alternating normal sinus P wave and a premature, differently-shaped ectopic P wave\",\n prInterval: \"Sinus beats normal (0.12-0.20s); ectopic P wave PR interval often shortened or variable\",\n qrs: \"Narrow (<0.12s) unless the PAC is aberrantly conducted\",\n summary: \"An irritable atrial focus fires prematurely after every normal sinus beat, producing a repeating two-beat pattern of 'normal-early, normal-early.'\",\n clinicalNote: \"Usually benign and related to caffeine, stress, or stretch (e.g., atrial enlargement); frequent bigeminy can herald atrial fibrillation and warrants clinical correlation, not automatic treatment.\",\n waveform: { pattern: \"patternedEctopy\", unit: 2, ectopicSubtype: \"atrial\", baseRateMin: 70, baseRateMax: 90 },\n questions: [\n {\n prompt: \"Atrial bigeminy describes a rhythm where:\",\n choices: [\"Every third beat is a PAC\", \"Every other beat is a PAC\", \"Two PACs occur in a row then a pause\", \"PACs occur randomly with no pattern\"],\n correctIndex: 1,\n explanation: \"Bigeminy means a 2-beat repeating pattern — one normal sinus beat followed by one premature atrial beat, repeating.\",\n },\n {\n prompt: \"A patient with new frequent atrial bigeminy should raise concern for eventual progression to:\",\n choices: [\"Third-degree AV block\", \"Atrial fibrillation\", \"Ventricular fibrillation\", \"Sinus arrest\"],\n correctIndex: 1,\n explanation: \"Frequent atrial ectopy, including bigeminy, is a recognized precursor pattern for atrial fibrillation.\",\n },\n ],\n },\n {\n id: \"atrial-trigeminy\",\n name: \"Atrial Trigeminy\",\n category: \"Atrial\",\n free: false,\n sortOrder: 30,\n rate: \"Variable underlying sinus rate\",\n regularity: \"Regularly irregular — repeating 3-beat group (two sinus beats + one PAC)\",\n pWave: \"Two consecutive normal P waves followed by one premature/abnormally-shaped P wave, repeating\",\n prInterval: \"Normal for sinus beats; variable for the ectopic beat\",\n qrs: \"Narrow unless aberrant conduction present\",\n summary: \"Similar mechanism to atrial bigeminy but the ectopic atrial focus fires every third beat instead of every other beat, creating a repeating triplet grouping.\",\n clinicalNote: \"Typically benign; assess for stimulant use, hyperthyroidism, electrolyte disturbance, or structural atrial disease if frequent or symptomatic.\",\n waveform: { pattern: \"patternedEctopy\", unit: 3, ectopicSubtype: \"atrial\", baseRateMin: 70, baseRateMax: 90 },\n questions: [\n {\n prompt: \"What distinguishes trigeminy from bigeminy?\",\n choices: [\"Trigeminy has 3 PACs in a row\", \"Trigeminy repeats every 3rd beat instead of every 2nd\", \"Trigeminy only occurs in the ventricles\", \"Trigeminy is always pathologic\"],\n correctIndex: 1,\n explanation: \"The repeating group size is three beats in trigeminy versus two in bigeminy.\",\n },\n {\n prompt: \"Isolated atrial trigeminy in an asymptomatic patient with no structural heart disease typically requires:\",\n choices: [\"Emergent cardioversion\", \"No specific treatment, address triggers\", \"Immediate pacemaker\", \"IV amiodarone\"],\n correctIndex: 1,\n explanation: \"Benign ectopy in a structurally normal heart is usually managed by addressing triggers (caffeine, stress) rather than pharmacologic or electrical intervention.\",\n },\n ],\n },\n {\n id: \"pvc-bigeminy\",\n name: \"PVC Bigeminy (Ventricular Bigeminy)\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 31,\n rate: \"Underlying rate variable; effective pulse rate may be lower if PVCs are non-perfusing\",\n regularity: \"Regularly irregular — repeating pattern of one normal beat then one PVC\",\n pWave: \"Normal sinus P wave on the sinus beat; no related P wave before the PVC\",\n prInterval: \"Normal on sinus beats; not applicable to the PVC\",\n qrs: \"Narrow on sinus beats; wide (>0.12s), bizarre-shaped on every other beat (the PVC)\",\n summary: \"A ventricular ectopic focus fires after every normal beat, producing an alternating pattern of one narrow sinus complex and one wide, premature ventricular complex.\",\n clinicalNote: \"Can occur in normal hearts but frequent bigeminy (especially with a PVC burden >10-15%) is associated with PVC-induced cardiomyopathy over time and warrants further workup.\",\n waveform: { pattern: \"patternedEctopy\", unit: 2, ectopicSubtype: \"ventricular\", baseRateMin: 65, baseRateMax: 85 },\n questions: [\n {\n prompt: \"On palpation, PVC bigeminy classically feels like:\",\n choices: [\"A perfectly regular pulse\", \"Every other beat is weak or dropped\", \"A slow, regular bradycardia\", \"No palpable pulse at all\"],\n correctIndex: 1,\n explanation: \"Because PVCs often don't generate an adequate stroke volume, alternating strong/weak beats can be felt.\",\n },\n {\n prompt: \"A sustained high PVC burden over months is most associated with:\",\n choices: [\"Improved ejection fraction\", \"PVC-induced cardiomyopathy\", \"Resolution of hypertension\", \"Guaranteed benign outcome\"],\n correctIndex: 1,\n explanation: \"Chronic, frequent PVCs can lead to a reversible dilated cardiomyopathy if the burden is high enough and untreated.\",\n },\n ],\n },\n {\n id: \"pvc-trigeminy\",\n name: \"PVC Trigeminy (Ventricular Trigeminy)\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 32,\n rate: \"Underlying sinus rate variable\",\n regularity: \"Regularly irregular — repeating 3-beat group (two normal beats + one PVC)\",\n pWave: \"Normal P waves precede the sinus beats; none associated with the PVC\",\n prInterval: \"Normal on sinus beats\",\n qrs: \"Narrow x2 then one wide, bizarre PVC, repeating\",\n summary: \"A ventricular ectopic focus discharges every third beat, producing a repeating triplet of two normal conducted beats followed by one premature wide complex.\",\n clinicalNote: \"Same clinical considerations as bigeminy — evaluate PVC burden, symptoms, and underlying structural heart disease or electrolyte abnormality (especially hypokalemia/hypomagnesemia).\",\n waveform: { pattern: \"patternedEctopy\", unit: 3, ectopicSubtype: \"ventricular\", baseRateMin: 65, baseRateMax: 85 },\n questions: [\n {\n prompt: \"A repeating pattern of two normal QRS complexes followed by one wide bizarre complex describes:\",\n choices: [\"PVC bigeminy\", \"PVC trigeminy\", \"Ventricular tachycardia\", \"Torsades de pointes\"],\n correctIndex: 1,\n explanation: \"The three-beat repeating group (2 normal + 1 PVC) is the defining feature of trigeminy.\",\n },\n {\n prompt: \"Which electrolyte disturbances commonly increase ventricular ectopy such as trigeminy?\",\n choices: [\"Hyperkalemia and hypercalcemia\", \"Hypokalemia and hypomagnesemia\", \"Hypernatremia and hypocalcemia\", \"None, electrolytes are unrelated\"],\n correctIndex: 1,\n explanation: \"Low potassium and low magnesium increase myocardial irritability and are classic reversible triggers for PVCs.\",\n },\n ],\n },\n {\n id: \"pvc-couplet\",\n name: \"PVC Couplet (Paired PVCs)\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 33,\n rate: \"Underlying sinus rate variable; the couplet itself occurs rapidly\",\n regularity: \"Irregular — two consecutive PVCs occur back-to-back\",\n pWave: \"None associated with either PVC\",\n prInterval: \"Not applicable to the couplet beats\",\n qrs: \"Two consecutive wide, bizarre complexes with no normal beat in between, followed by a compensatory pause\",\n summary: \"Two PVCs fire consecutively without an intervening sinus beat, representing a brief run of ventricular ectopy one beat short of being called a 'run' (three or more defines non-sustained VT).\",\n clinicalNote: \"Couplets are more concerning than isolated PVCs because they signal increased ventricular irritability and a higher likelihood of progressing to sustained ventricular tachycardia.\",\n waveform: { pattern: \"burstEctopy\", burstLength: 2, baseRateMin: 65, baseRateMax: 85, burstRateMin: 150, burstRateMax: 180 },\n questions: [\n {\n prompt: \"A PVC couplet is defined as:\",\n choices: [\"One PVC followed by a pause\", \"Two consecutive PVCs in a row\", \"Three or more consecutive PVCs\", \"A PVC that lands on a T wave\"],\n correctIndex: 1,\n explanation: \"A couplet is specifically two back-to-back PVCs; three or more in a row is termed a run.\",\n },\n {\n prompt: \"Compared to isolated unifocal PVCs, PVC couplets carry:\",\n choices: [\"The same clinical significance\", \"Lower risk of progressing to VT\", \"Higher risk of progressing to VT\", \"No clinical significance\"],\n correctIndex: 2,\n explanation: \"Couplets indicate greater myocardial irritability and a higher likelihood of degenerating into sustained ventricular arrhythmias.\",\n },\n ],\n },\n {\n id: \"pvc-triplet-nsvt\",\n name: \"PVC Triplet / Non-Sustained Ventricular Tachycardia (NSVT)\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 34,\n rate: \"Ventricular rate during the run typically 100-250 bpm\",\n regularity: \"The run itself is regular or near-regular; overall strip is irregular due to interruption of sinus rhythm\",\n pWave: \"None during the run; dissociated sinus P waves may be seen marching through\",\n prInterval: \"Not applicable during the run\",\n qrs: \"Three or more consecutive wide, bizarre complexes lasting <30 seconds and self-terminating\",\n summary: \"Three or more consecutive PVCs constitute a run of ventricular tachycardia; when it self-terminates within 30 seconds without hemodynamic collapse, it is classified as non-sustained VT.\",\n clinicalNote: \"NSVT in a structurally normal heart is often benign, but in the setting of prior MI, cardiomyopathy, or reduced ejection fraction it is a marker of increased risk for sudden cardiac death and warrants further evaluation.\",\n waveform: { pattern: \"burstEctopy\", burstLength: 5, baseRateMin: 65, baseRateMax: 85, burstRateMin: 160, burstRateMax: 220 },\n questions: [\n {\n prompt: \"How many consecutive PVCs are required to call a run \\\"ventricular tachycardia\\\" rather than a couplet?\",\n choices: [\"Two\", \"Three or more\", \"Five or more\", \"Ten or more\"],\n correctIndex: 1,\n explanation: \"Three or more consecutive ventricular beats at a rate over 100 bpm meets the definition of VT; a run lasting <30 seconds without collapse is termed non-sustained.\",\n },\n {\n prompt: \"NSVT is most clinically concerning when found in a patient with:\",\n choices: [\"A structurally normal heart and no symptoms\", \"Reduced ejection fraction after prior MI\", \"Well-controlled hypertension only\", \"Isolated caffeine use\"],\n correctIndex: 1,\n explanation: \"NSVT in structural heart disease, especially post-MI with reduced EF, is an independent risk marker for sudden cardiac death.\",\n },\n ],\n },\n {\n id: \"unifocal-pvcs\",\n name: \"Unifocal PVCs\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 35,\n rate: \"Underlying sinus rate variable\",\n regularity: \"Irregular due to premature beats\",\n pWave: \"None associated with the PVCs\",\n prInterval: \"Not applicable\",\n qrs: \"Wide, bizarre PVCs that are all identical in morphology to one another, arising from a single ventricular ectopic focus\",\n summary: \"All PVCs on the strip originate from the same irritable focus, so each one looks identical in shape, width, and axis.\",\n clinicalNote: \"Generally considered lower risk than multifocal PVCs because a single consistent focus is more predictable and often more benign, though burden and underlying heart disease still matter.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"ventricular\", count: 3, baseRateMin: 65, baseRateMax: 90 },\n questions: [\n {\n prompt: \"Unifocal PVCs are characterized by:\",\n choices: [\"Varying shapes from beat to beat\", \"Identical morphology from beat to beat\", \"Occurring only in pairs\", \"Always being asymptomatic\"],\n correctIndex: 1,\n explanation: \"\\\"Unifocal\\\" means one origin site, so every PVC has the same QRS morphology.\",\n },\n {\n prompt: \"Compared to multifocal PVCs, unifocal PVCs are generally considered:\",\n choices: [\"More dangerous\", \"Less concerning, arising from a single stable focus\", \"Impossible to distinguish clinically\", \"Always caused by digoxin toxicity\"],\n correctIndex: 1,\n explanation: \"A single consistent ectopic focus is typically viewed as lower risk than multiple competing irritable foci.\",\n },\n ],\n },\n {\n id: \"multifocal-pvcs\",\n name: \"Multifocal PVCs\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 36,\n rate: \"Underlying sinus rate variable\",\n regularity: \"Irregular\",\n pWave: \"None associated with the PVCs\",\n prInterval: \"Not applicable\",\n qrs: \"Wide, bizarre PVCs with varying morphology and axis from beat to beat, indicating more than one ventricular ectopic focus\",\n summary: \"PVCs arise from two or more different irritable ventricular sites, so their shape, width, and direction differ from one PVC to the next on the same strip.\",\n clinicalNote: \"Multifocal PVCs suggest a more diffusely irritable or diseased myocardium (ischemia, electrolyte disturbance, hypoxia) and are generally regarded as higher risk than unifocal PVCs.\",\n waveform: { pattern: \"multifocal\", wide: true, rateMin: 65, rateMax: 90, irregular: true },\n questions: [\n {\n prompt: \"Multifocal PVCs are identified by:\",\n choices: [\"Same shape every time\", \"Different QRS morphologies from beat to beat\", \"Occurring exactly every other beat\", \"A narrow QRS complex\"],\n correctIndex: 1,\n explanation: \"Multiple ectopic foci produce PVCs with varying shapes and axes on the same tracing.\",\n },\n {\n prompt: \"Multifocal PVCs are most concerning as a sign of:\",\n choices: [\"Normal aging only\", \"Diffuse myocardial irritability from ischemia, hypoxia, or electrolyte imbalance\", \"Excellent cardiac health\", \"Vagal tone\"],\n correctIndex: 1,\n explanation: \"Multiple competing ectopic foci suggest a broader insult to the myocardium and carry higher clinical concern than a single stable focus.\",\n },\n ],\n },\n {\n id: \"r-on-t-phenomenon\",\n name: \"R-on-T Phenomenon\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 37,\n rate: \"Underlying rate variable\",\n regularity: \"Irregular; the PVC falls during the vulnerable period of the preceding beat's T wave\",\n pWave: \"None associated with the PVC\",\n prInterval: \"Not applicable\",\n qrs: \"A PVC whose R wave lands directly on the peak/downslope of the preceding T wave\",\n summary: \"When a premature ventricular beat strikes during the relative refractory period marked by the T wave, it can trigger reentry and precipitate ventricular tachycardia or fibrillation.\",\n clinicalNote: \"R-on-T PVCs are considered a higher-risk ectopy pattern, particularly in the setting of acute ischemia or a prolonged QT interval, and clinicians should watch closely for degeneration into VT/VF or torsades.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"ventricular\", count: 1, baseRateMin: 65, baseRateMax: 85 },\n questions: [\n {\n prompt: \"R-on-T phenomenon describes a PVC that lands on:\",\n choices: [\"The P wave of the prior beat\", \"The T wave of the prior beat\", \"The QRS of the prior beat\", \"The isoelectric baseline\"],\n correctIndex: 1,\n explanation: \"The T wave represents the vulnerable period of ventricular repolarization; a PVC striking there risks precipitating a malignant arrhythmia.\",\n },\n {\n prompt: \"R-on-T is of greatest concern in a patient who also has:\",\n choices: [\"A short PR interval\", \"A prolonged QT interval or acute ischemia\", \"Sinus arrhythmia\", \"First-degree AV block\"],\n correctIndex: 1,\n explanation: \"A prolonged QT widens the vulnerable window, and acute ischemia increases myocardial irritability, both raising the risk that R-on-T triggers VT/VF or torsades.\",\n },\n ],\n },\n {\n id: \"ventricular-fusion-beat\",\n name: \"Ventricular Fusion Beat\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 38,\n rate: \"Underlying sinus rate variable\",\n regularity: \"Occurs as an isolated irregular beat within an otherwise regular rhythm\",\n pWave: \"A sinus P wave is present, conducting simultaneously with a competing ventricular ectopic impulse\",\n prInterval: \"May appear shortened or normal depending on timing\",\n qrs: \"A single complex with a morphology intermediate between a normal narrow QRS and a wide bizarre PVC\",\n summary: \"A fusion beat happens when a supraventricular impulse and a ventricular ectopic impulse depolarize the ventricles simultaneously, blending their two QRS morphologies into one hybrid complex.\",\n clinicalNote: \"Fusion beats are a classic supportive finding for diagnosing ventricular tachycardia (a 'Dressler beat'), helping distinguish VT from SVT with aberrancy.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"ventricular\", count: 1, baseRateMin: 65, baseRateMax: 85 },\n questions: [\n {\n prompt: \"A fusion beat results from:\",\n choices: [\"Two PVCs occurring simultaneously\", \"A sinus impulse and a ventricular ectopic impulse depolarizing the ventricle at the same time\", \"Complete AV block\", \"Atrial fibrillation with rapid response\"],\n correctIndex: 1,\n explanation: \"Fusion beats blend normal conduction with a competing ventricular ectopic focus into one intermediate-shaped complex.\",\n },\n {\n prompt: \"Finding fusion beats during a wide-complex tachycardia supports a diagnosis of:\",\n choices: [\"SVT with aberrancy\", \"Ventricular tachycardia\", \"Atrial flutter\", \"Sinus tachycardia\"],\n correctIndex: 1,\n explanation: \"Fusion (and capture) beats are classic AV dissociation clues that favor VT over SVT with aberrant conduction.\",\n },\n ],\n },\n {\n id: \"aberrantly-conducted-pac-ashman\",\n name: \"Aberrantly Conducted PAC (Ashman Phenomenon)\",\n category: \"Atrial\",\n free: false,\n sortOrder: 39,\n rate: \"Underlying sinus rate variable\",\n regularity: \"Irregular due to the premature beat\",\n pWave: \"A premature, differently-shaped P wave precedes the wide beat\",\n prInterval: \"Often shortened compared to sinus beats\",\n qrs: \"Wide and bizarre-looking (commonly RBBB morphology), mimicking a PVC, but preceded by a premature P wave\",\n summary: \"A PAC that arrives early, while part of the conduction system is still refractory from the preceding long cycle, conducts aberrantly and produces a wide QRS that mimics a PVC.\",\n clinicalNote: \"Recognizing Ashman phenomenon (classically a 'long-short' cycle sequence) prevents misdiagnosing a benign aberrantly conducted PAC as a dangerous PVC, and is frequently seen at the onset of atrial fibrillation.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"atrial\", wide: true, count: 1, baseRateMin: 70, baseRateMax: 90 },\n questions: [\n {\n prompt: \"Ashman phenomenon classically occurs after which cycle pattern?\",\n choices: [\"A short cycle followed by a long cycle\", \"A long cycle followed by a short cycle\", \"Two equal cycles in a row\", \"Complete pause with no preceding cycle\"],\n correctIndex: 1,\n explanation: \"A long R-R interval prolongs the refractory period of the bundle branches; a subsequent short-cycle beat can then conduct aberrantly.\",\n },\n {\n prompt: \"The key clue that a wide beat is an aberrantly conducted PAC rather than a true PVC is:\",\n choices: [\"A premature P wave preceding it with typical RBBB morphology\", \"A fully compensatory pause\", \"Absence of any P wave\", \"A fixed coupling interval\"],\n correctIndex: 0,\n explanation: \"Ashman-phenomenon beats are preceded by a premature ectopic P wave and often show a classic RBBB (rSR') pattern, distinguishing them from PVCs.\",\n },\n ],\n },\n {\n id: \"junctional-escape-beat\",\n name: \"Junctional Escape Beat\",\n category: \"Junctional\",\n free: false,\n sortOrder: 40,\n rate: \"A single beat occurring at the junctional escape rate (40-60 bpm) after a pause\",\n regularity: \"An isolated beat interrupting the underlying rhythm following a pause\",\n pWave: \"Absent, inverted, or retrograde\",\n prInterval: \"Short (<0.12s) if a retrograde P precedes the QRS, or not measurable if absent\",\n qrs: \"Narrow (<0.12s), normal in shape\",\n summary: \"When the sinus node fails to fire on time, the AV junction acts as a backup pacemaker and produces a single escape beat to prevent an excessively long pause.\",\n clinicalNote: \"A single junctional escape beat is a protective safety mechanism, not itself pathologic, but its presence signals underlying sinus node dysfunction that should be evaluated.\",\n waveform: { pattern: \"pause\", rateMin: 60, rateMax: 90, hasPWave: true, prMs: 160 },\n questions: [\n {\n prompt: \"A junctional escape beat occurs because:\",\n choices: [\"The junction is diseased and firing too fast\", \"The sinus node failed to fire on time and a backup pacemaker took over for one beat\", \"The patient has WPW\", \"It follows a PVC always\"],\n correctIndex: 1,\n explanation: \"Escape beats are a protective backup mechanism that fires after the sinus node pauses too long.\",\n },\n {\n prompt: \"A single junctional escape beat should prompt evaluation for:\",\n choices: [\"Nothing, it's always normal\", \"Underlying sinus node dysfunction\", \"Ventricular fibrillation risk\", \"Digoxin toxicity only\"],\n correctIndex: 1,\n explanation: \"While the escape beat itself is protective, its occurrence indicates the sinus node paused, warranting evaluation of sinus node function.\",\n },\n ],\n },\n {\n id: \"ventricular-escape-beat\",\n name: \"Ventricular Escape Beat\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 41,\n rate: \"A single beat at the ventricular escape rate (20-40 bpm) following a pause\",\n regularity: \"An isolated beat interrupting the underlying rhythm after a long pause\",\n pWave: \"Absent\",\n prInterval: \"Not applicable\",\n qrs: \"Wide (>0.12s), bizarre morphology, occurring late after a pause\",\n summary: \"When both the sinus node and the AV junction fail to initiate an impulse in time, a ventricular pacemaker cell fires as a last-resort backup to prevent asystole.\",\n clinicalNote: \"A ventricular escape beat is a life-sustaining safety mechanism; its appearance indicates significant conduction system disease and often precedes a need for pacing.\",\n waveform: { pattern: \"pause\", rateMin: 55, rateMax: 80, hasPWave: true, prMs: 160 },\n questions: [\n {\n prompt: \"A ventricular escape beat appears when:\",\n choices: [\"Both the SA node and AV junction fail to fire in time\", \"The atria are fibrillating\", \"A PVC lands on a T wave\", \"The patient is in normal sinus rhythm\"],\n correctIndex: 0,\n explanation: \"Ventricular escape is the heart's last line of defense, firing only when higher pacemakers (SA node, AV junction) fail to initiate an impulse.\",\n },\n {\n prompt: \"The presence of ventricular escape beats most strongly suggests the need to evaluate for:\",\n choices: [\"Simple sinus arrhythmia\", \"Significant conduction system disease requiring possible pacing\", \"Benign PACs\", \"Athletic heart syndrome\"],\n correctIndex: 1,\n explanation: \"Reliance on a ventricular escape mechanism reflects failure of both higher-order pacemakers and often signals a need for permanent pacing.\",\n },\n ],\n },\n {\n id: \"atrial-escape-beat\",\n name: \"Atrial Escape Beat\",\n category: \"Atrial\",\n free: false,\n sortOrder: 42,\n rate: \"A single beat occurring after a pause, originating from an ectopic atrial focus\",\n regularity: \"An isolated beat interrupting the underlying rhythm following a pause\",\n pWave: \"Present but abnormally shaped since it originates from an ectopic atrial site, not the SA node\",\n prInterval: \"May be normal or slightly different from sinus PR interval\",\n qrs: \"Narrow, normal conduction\",\n summary: \"When the SA node pauses, a subsidiary atrial pacemaker outside the sinus node fires to prevent a longer pause, producing a single beat with a differently shaped P wave but otherwise normal narrow QRS.\",\n clinicalNote: \"Like junctional escape, this is a protective mechanism reflecting transient SA node under-function rather than a primary arrhythmia requiring emergent treatment.\",\n waveform: { pattern: \"pause\", rateMin: 60, rateMax: 90, hasPWave: true, prMs: 150 },\n questions: [\n {\n prompt: \"An atrial escape beat differs from a PAC in that it:\",\n choices: [\"Comes early\", \"Comes late, after a pause, as a protective response\", \"Always has a wide QRS\", \"Never has a P wave\"],\n correctIndex: 1,\n explanation: \"A PAC is premature (early); an escape beat is, by definition, late — it fires only after the primary pacemaker fails to fire on time.\",\n },\n {\n prompt: \"The QRS of an atrial escape beat is typically:\",\n choices: [\"Wide and bizarre\", \"Narrow, since conduction through the AV node and ventricles is normal\", \"Absent entirely\", \"Always preceded by no P wave\"],\n correctIndex: 1,\n explanation: \"Since the impulse still originates above the ventricles and conducts normally through the His-Purkinje system, the QRS remains narrow.\",\n },\n ],\n },\n {\n id: \"hyperkalemia-ecg-changes\",\n name: \"Hyperkalemia ECG Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 43,\n rate: \"Variable; sinus rate may slow as severity increases\",\n regularity: \"Regular initially, progressing to irregular as severity worsens\",\n pWave: \"Flattened and widened, eventually disappearing as potassium rises further\",\n prInterval: \"Progressively prolonged, then P waves are lost\",\n qrs: \"Progressively widens; in severe hyperkalemia the QRS merges with the T wave (sine-wave pattern)\",\n summary: \"Rising extracellular potassium progressively depresses cardiac conduction velocity, producing a characteristic sequence from tall peaked T waves, to PR prolongation and flattened P waves, to QRS widening.\",\n clinicalNote: \"This is a true cardiac emergency — severity of ECG change (not the lab potassium value alone) should guide urgency of treatment with IV calcium, insulin/dextrose, and other potassium-lowering measures.\",\n waveform: { pattern: \"regular\", rateMin: 50, rateMax: 80, hasPWave: true, wide: true, prMs: 220, tAmpScale: 2.2 },\n questions: [\n {\n prompt: \"The earliest classic ECG change of hyperkalemia is:\",\n choices: [\"Widened QRS\", \"Tall, peaked, narrow-based T waves\", \"Sine wave pattern\", \"Prolonged QT\"],\n correctIndex: 1,\n explanation: \"Peaked, tented T waves are typically the earliest sign, appearing before P wave flattening and QRS widening.\",\n },\n {\n prompt: \"A sine-wave pattern on ECG in a hyperkalemic patient indicates:\",\n choices: [\"Mild, non-urgent hyperkalemia\", \"Life-threatening hyperkalemia requiring immediate treatment\", \"Normal variant\", \"Digoxin effect\"],\n correctIndex: 1,\n explanation: \"The sine-wave pattern represents merging of the widened QRS with the T wave and is a pre-terminal rhythm requiring emergent calcium administration and potassium-lowering therapy.\",\n },\n ],\n },\n {\n id: \"hypokalemia-ecg-changes\",\n name: \"Hypokalemia ECG Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 44,\n rate: \"Variable, underlying rhythm often sinus\",\n regularity: \"Usually regular unless ectopy or arrhythmia develops\",\n pWave: \"Normal, though may become more prominent\",\n prInterval: \"May be mildly prolonged\",\n qrs: \"Normal width, but ST depression, flattened/inverted T waves, and prominent U waves (sometimes exceeding T wave amplitude) are seen; severe cases show apparent QT prolongation actually representing T-U fusion\",\n summary: \"Low extracellular potassium increases the duration of ventricular repolarization, producing progressive ST depression, T wave flattening, and characteristically prominent U waves that can be mistaken for a prolonged QT interval.\",\n clinicalNote: \"Severe hypokalemia predisposes to ventricular ectopy and torsades de pointes; correction of potassium (and often concurrent magnesium) is required, and ECG changes may precede symptomatic weakness.\",\n waveform: { pattern: \"regular\", rateMin: 65, rateMax: 90, hasPWave: true, wide: false, prMs: 160, tAmpScale: 0.4, uWave: true },\n questions: [\n {\n prompt: \"The classic ECG hallmark of hypokalemia is:\",\n choices: [\"Peaked T waves\", \"Prominent U waves with flattened T waves\", \"Short QT interval\", \"Delta wave\"],\n correctIndex: 1,\n explanation: \"Hypokalemia flattens T waves and produces prominent U waves, sometimes larger than the T wave itself.\",\n },\n {\n prompt: \"What is frequently mistaken for QT prolongation in severe hypokalemia?\",\n choices: [\"ST elevation\", \"Fusion of the T and U waves creating an apparent long QT\", \"A delta wave\", \"Peaked T waves\"],\n correctIndex: 1,\n explanation: \"When the U wave merges with the T wave, it can be measured as an apparently prolonged QT interval (sometimes called QU interval).\",\n },\n ],\n },\n {\n id: \"digoxin-effect\",\n name: \"Digoxin Effect\",\n category: \"Other\",\n free: false,\n sortOrder: 45,\n rate: \"Usually normal sinus rate, no arrhythmia implied by the effect alone\",\n regularity: \"Regular\",\n pWave: \"Normal\",\n prInterval: \"Normal or mildly shortened\",\n qrs: \"Normal\",\n summary: \"Digoxin effect refers to characteristic, non-toxic ST-T changes — a downsloping 'scooped' or sagging ST segment sometimes called the 'Salvador Dali mustache' — seen at therapeutic drug levels and reflecting the drug's normal action on repolarization.\",\n clinicalNote: \"Digoxin effect is expected and does not indicate toxicity; it must be distinguished from digoxin toxicity, which presents with arrhythmias (e.g., PVCs, AV block, PAT with block) rather than isolated ST-T morphology changes.\",\n waveform: { pattern: \"regular\", rateMin: 65, rateMax: 90, hasPWave: true, wide: false, prMs: 150, stScoop: true },\n questions: [\n {\n prompt: \"The classic ST segment appearance of digoxin effect is often described as resembling:\",\n choices: [\"A tombstone\", \"A Salvador Dali mustache (scooped/sagging downslope)\", \"A camel hump\", \"A checkmark\"],\n correctIndex: 1,\n explanation: \"The gradual downsloping, scooped ST depression at therapeutic digoxin levels is classically nicknamed the 'Salvador Dali' or 'reverse tick' mustache sign.\",\n },\n {\n prompt: \"Digoxin effect (as opposed to digoxin toxicity) is:\",\n choices: [\"A dangerous emergency requiring reversal\", \"An expected, benign finding at therapeutic drug levels\", \"Always accompanied by arrhythmia\", \"Only seen in overdose\"],\n correctIndex: 1,\n explanation: \"Digoxin effect is a normal ECG finding at therapeutic doses and does not by itself indicate toxicity, which instead manifests as arrhythmias.\",\n },\n ],\n },\n {\n id: \"digoxin-toxicity\",\n name: \"Digoxin Toxicity\",\n category: \"Other\",\n free: false,\n sortOrder: 46,\n rate: \"Variable — can produce bradyarrhythmias or tachyarrhythmias\",\n regularity: \"Variable depending on the specific arrhythmia produced\",\n pWave: \"May show atrial tachycardia with block (P waves present but many are not conducted)\",\n prInterval: \"Variable — may be prolonged (AV block) or difficult to assess\",\n qrs: \"Variable; classic findings include PVCs (often bidirectional VT in severe cases), junctional rhythms, and paroxysmal atrial tachycardia with AV block\",\n summary: \"Digoxin toxicity impairs the Na-K-ATPase pump and increases vagal tone/automaticity, producing a wide range of arrhythmias — the combination of increased automaticity plus AV block (e.g., 'PAT with block') is considered classic.\",\n clinicalNote: \"Digoxin toxicity is a medical emergency, especially with hyperkalemia or bidirectional VT; treatment includes digoxin-specific antibody fragments (DigiFab) rather than standard antiarrhythmics alone.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"ventricular\", count: 3, baseRateMin: 55, baseRateMax: 85 },\n questions: [\n {\n prompt: \"A classic (though not exclusive) arrhythmia pattern of digoxin toxicity is:\",\n choices: [\"Atrial flutter with 2:1 block\", \"Paroxysmal atrial tachycardia with AV block\", \"Sinus tachycardia\", \"Wolff-Parkinson-White pattern\"],\n correctIndex: 1,\n explanation: \"The combination of an ectopic atrial tachycardia together with AV block is a well-recognized, classic (though not pathognomonic) presentation of digoxin toxicity.\",\n },\n {\n prompt: \"Severe digoxin toxicity can produce which distinctive ventricular arrhythmia?\",\n choices: [\"Torsades de pointes\", \"Bidirectional ventricular tachycardia\", \"Brugada pattern\", \"WPW-mediated AVRT\"],\n correctIndex: 1,\n explanation: \"Bidirectional VT, with beat-to-beat alternating QRS axis, is a rare but classic finding highly suggestive of digoxin toxicity.\",\n },\n ],\n },\n {\n id: \"hypercalcemia-short-qt\",\n name: \"Hypercalcemia (Short QT Pattern)\",\n category: \"Other\",\n free: false,\n sortOrder: 47,\n rate: \"Usually normal, though bradycardia can occur in severe cases\",\n regularity: \"Regular\",\n pWave: \"Normal\",\n prInterval: \"Normal, may be mildly prolonged in severe cases\",\n qrs: \"Normal width, but may show a very short or absent ST segment\",\n summary: \"Elevated extracellular calcium shortens the plateau phase of the cardiac action potential, most notably shortening or eliminating the ST segment, which shortens the overall QT interval.\",\n clinicalNote: \"Severe hypercalcemia can cause bradyarrhythmias and, rarely, Osborn (J) waves; treatment targets the underlying cause of hypercalcemia (e.g., malignancy, hyperparathyroidism) along with IV fluids and calcium-lowering therapy.\",\n waveform: { pattern: \"regular\", rateMin: 55, rateMax: 85, hasPWave: true, wide: false, prMs: 160, qtOffsetMs: -70 },\n questions: [\n {\n prompt: \"Hypercalcemia's classic ECG effect is:\",\n choices: [\"QT prolongation\", \"QT shortening due to a shortened ST segment\", \"Peaked T waves\", \"Widened QRS\"],\n correctIndex: 1,\n explanation: \"High calcium shortens the plateau phase of the action potential, shortening the ST segment and thus the overall QT interval.\",\n },\n {\n prompt: \"Severe hypercalcemia can occasionally also produce:\",\n choices: [\"Delta waves\", \"Osborn (J) waves and bradyarrhythmias\", \"Torsades de pointes only\", \"Right bundle branch block always\"],\n correctIndex: 1,\n explanation: \"While less common than in hypothermia, severe hypercalcemia has been associated with Osborn waves and bradyarrhythmias.\",\n },\n ],\n },\n {\n id: \"hypocalcemia-long-qt\",\n name: \"Hypocalcemia (Long QT Pattern)\",\n category: \"Other\",\n free: false,\n sortOrder: 48,\n rate: \"Usually normal\",\n regularity: \"Regular unless torsades develops\",\n pWave: \"Normal\",\n prInterval: \"Normal\",\n qrs: \"Normal width, but with a prolonged, often flat/featureless ST segment leading to a prolonged QT interval; T wave itself is usually normal shape\",\n summary: \"Low extracellular calcium prolongs the plateau phase of the cardiac action potential, lengthening the ST segment and therefore the QT interval, without typically changing T wave morphology.\",\n clinicalNote: \"Prolonged QT from hypocalcemia raises the risk of torsades de pointes, particularly when combined with other QT-prolonging drugs or electrolyte disturbances (low K+, low Mg2+); correcting calcium is first-line treatment.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 85, hasPWave: true, wide: false, prMs: 160, qtOffsetMs: 90 },\n questions: [\n {\n prompt: \"Hypocalcemia prolongs the QT interval primarily by lengthening the:\",\n choices: [\"PR interval\", \"ST segment\", \"QRS duration\", \"P wave\"],\n correctIndex: 1,\n explanation: \"Unlike other causes of long QT that widen the T wave itself, hypocalcemia characteristically prolongs the ST segment while T wave morphology stays normal.\",\n },\n {\n prompt: \"The major arrhythmic risk associated with hypocalcemia's QT prolongation is:\",\n choices: [\"Atrial fibrillation\", \"Torsades de pointes\", \"First-degree AV block\", \"Sinus tachycardia\"],\n correctIndex: 1,\n explanation: \"A prolonged QT interval from any cause, including hypocalcemia, increases susceptibility to the polymorphic VT known as torsades de pointes.\",\n },\n ],\n },\n {\n id: \"sick-sinus-syndrome\",\n name: \"Sick Sinus Syndrome (Tachy-Brady Syndrome)\",\n category: \"Sinus\",\n free: false,\n sortOrder: 49,\n rate: \"Alternates between periods of sinus bradycardia (or pauses) and paroxysmal atrial tachyarrhythmias (often atrial fibrillation or flutter)\",\n regularity: \"Irregular, with abrupt transitions between slow and fast rhythms\",\n pWave: \"Sinus P waves during bradycardic phases; absent/fibrillatory or flutter waves during tachycardic phases\",\n prInterval: \"Normal during sinus phases\",\n qrs: \"Narrow, unless aberrancy is present\",\n summary: \"Sinus node dysfunction causes the heart to swing between inappropriately slow sinus rates (or sinus pauses/arrest) and episodes of atrial tachyarrhythmia, most classically atrial fibrillation, reflecting a diseased sinoatrial node and surrounding atrial tissue.\",\n clinicalNote: \"Symptoms (syncope, presyncope, palpitations) often arise from the pauses following termination of the tachycardic phase; definitive treatment is usually a permanent pacemaker, often combined with rate/rhythm control medications for the tachy component.\",\n waveform: { pattern: \"tachyBrady\", rateMin: 40, rateMax: 160, hasPWave: true, irregular: true },\n questions: [\n {\n prompt: \"Sick sinus syndrome is also commonly known as:\",\n choices: [\"Wolff-Parkinson-White syndrome\", \"Tachy-brady syndrome\", \"Long QT syndrome\", \"Brugada syndrome\"],\n correctIndex: 1,\n explanation: \"The hallmark alternation between slow and fast rhythms gives this condition its common nickname, tachy-brady syndrome.\",\n },\n {\n prompt: \"Definitive treatment for symptomatic sick sinus syndrome typically involves:\",\n choices: [\"Beta-blockers alone\", \"Permanent pacemaker implantation, often with rate-control medication\", \"Cardiac ablation of the AV node only\", \"Observation with no treatment\"],\n correctIndex: 1,\n explanation: \"Because rate-control drugs for the tachy phase would worsen the bradycardia, a pacemaker is usually required before medications can be safely used.\",\n },\n ],\n },\n {\n id: \"rbbb-pattern\",\n name: \"Right Bundle Branch Block (RBBB) Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 50,\n rate: \"Underlying rate determined by the native rhythm (often sinus)\",\n regularity: \"Regular if underlying rhythm is sinus\",\n pWave: \"Normal, present before each QRS\",\n prInterval: \"Normal\",\n qrs: \"Widened (>0.12s) with an rSR' ('M-shaped') pattern in right-sided leads and wide slurred S waves in left-sided leads\",\n summary: \"Conduction through the right bundle branch is blocked or delayed, so the right ventricle depolarizes late via slower cell-to-cell spread from the left ventricle, widening the QRS and producing a characteristic terminal R' pattern.\",\n clinicalNote: \"RBBB can be a normal variant in an otherwise healthy heart or can indicate right heart strain (e.g., pulmonary embolism), prior right-sided injury, or conduction system disease; a new RBBB in the setting of chest pain warrants evaluation.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 90, hasPWave: true, wide: true, prMs: 160 },\n questions: [\n {\n prompt: \"The classic QRS pattern of RBBB is described as:\",\n choices: [\"A delta wave\", \"An rSR' ('M-shaped') pattern in the right precordial leads\", \"A sine wave\", \"A short PR with slurred upstroke\"],\n correctIndex: 1,\n explanation: \"RBBB produces a characteristic rSR' morphology, often nicknamed 'rabbit ears,' most visible in right-sided leads such as V1.\",\n },\n {\n prompt: \"RBBB found incidentally in an asymptomatic, healthy young adult is most often:\",\n choices: [\"An emergency requiring pacing\", \"A benign normal variant\", \"Always due to prior MI\", \"Diagnostic of WPW\"],\n correctIndex: 1,\n explanation: \"Isolated RBBB without other symptoms or structural disease is a common and generally benign incidental finding.\",\n },\n ],\n },\n {\n id: \"lbbb-pattern\",\n name: \"Left Bundle Branch Block (LBBB) Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 51,\n rate: \"Underlying rate determined by the native rhythm (often sinus)\",\n regularity: \"Regular if underlying rhythm is sinus\",\n pWave: \"Normal, present before each QRS\",\n prInterval: \"Normal\",\n qrs: \"Widened (>0.12s), broad monomorphic (often notched) R waves in left-sided leads, deep S waves in right-sided leads, with absent normal septal Q waves laterally\",\n summary: \"Conduction through the left bundle branch is blocked, so the left ventricle depolarizes late via slow spread from the right ventricle, producing a very wide, broad-notched QRS.\",\n clinicalNote: \"A new LBBB is more clinically significant than RBBB, as it is strongly associated with underlying structural heart disease (ischemia, cardiomyopathy) and can mask or mimic ST-elevation MI on ECG, requiring specific criteria (e.g., Sgarbossa) to evaluate for ischemia.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 90, hasPWave: true, wide: true, prMs: 160, tInvert: true },\n questions: [\n {\n prompt: \"A newly discovered LBBB is clinically significant primarily because it:\",\n choices: [\"Is always a benign normal variant\", \"Is strongly associated with underlying structural heart disease and can mask MI findings\", \"Only occurs in athletes\", \"Indicates hyperkalemia\"],\n correctIndex: 1,\n explanation: \"Unlike isolated RBBB, new LBBB usually signals underlying cardiac pathology and complicates the ECG diagnosis of acute MI.\",\n },\n {\n prompt: \"LBBB QRS morphology characteristically shows:\",\n choices: [\"An rSR' pattern in V1\", \"A broad, often notched R wave in the lateral leads with loss of normal septal Q waves\", \"A short QRS with delta wave\", \"Peaked T waves\"],\n correctIndex: 1,\n explanation: \"LBBB produces broad monomorphic (frequently notched) R waves laterally and loss of the small septal q waves normally seen in leads I, V5-V6.\",\n },\n ],\n },\n {\n id: \"atrial-standstill\",\n name: \"Atrial Standstill\",\n category: \"Atrial\",\n free: false,\n sortOrder: 52,\n rate: \"No atrial activity; ventricular rate reflects a junctional or ventricular escape rhythm\",\n regularity: \"Regular (escape rhythm) or absent if no escape occurs\",\n pWave: \"Completely absent — no atrial electrical activity is detectable\",\n prInterval: \"Not applicable, no P waves\",\n qrs: \"Narrow if a junctional escape rhythm is driving the ventricles, wide if a ventricular escape rhythm is present\",\n summary: \"The atria fail to depolarize entirely (electrically silent), and the ventricles are sustained only by a junctional or ventricular escape pacemaker, producing a rhythm with no P waves whatsoever.\",\n clinicalNote: \"A rare and serious finding, associated with severe hyperkalemia, extensive atrial fibrosis/myopathy, or neuromuscular disease; it usually requires pacemaker support since there is no reliable atrial contribution to cardiac output.\",\n waveform: { pattern: \"regular\", rateMin: 40, rateMax: 60, hasPWave: false, wide: false, prMs: 0 },\n questions: [\n {\n prompt: \"Atrial standstill is defined by:\",\n choices: [\"Very slow but present P waves\", \"Complete absence of detectable atrial electrical activity\", \"Fibrillatory waves only\", \"Flutter waves at 300/min\"],\n correctIndex: 1,\n explanation: \"In atrial standstill, the atria generate no electrical activity at all, unlike fibrillation or flutter where disorganized/organized atrial activity is still present.\",\n },\n {\n prompt: \"A recognized cause of atrial standstill is:\",\n choices: [\"Mild hypokalemia\", \"Severe hyperkalemia or advanced atrial myopathy/fibrosis\", \"Caffeine intake\", \"Sinus arrhythmia\"],\n correctIndex: 1,\n explanation: \"Severe hyperkalemia can paralyze atrial tissue, and diffuse atrial fibrosis/myopathy from various myopathic or infiltrative diseases can also silence the atria entirely.\",\n },\n ],\n },\n {\n id: \"atrial-paced-rhythm\",\n name: \"Atrial Paced Rhythm\",\n category: \"Other\",\n free: false,\n sortOrder: 53,\n rate: \"Set by the programmed pacemaker lower rate limit, typically 60-70 bpm unless programmed otherwise\",\n regularity: \"Regular\",\n pWave: \"A pacing spike immediately precedes each P wave, which may look somewhat different from a native sinus P wave\",\n prInterval: \"Normal or programmed AV delay follows the paced P wave to the native/intrinsic QRS\",\n qrs: \"Narrow and normal-looking, since the impulse still conducts normally through the native AV node and conduction system\",\n summary: \"A pacemaker lead in the right atrium delivers an electrical stimulus that is seen as a small pacing spike immediately before each P wave, after which the impulse conducts normally down the intrinsic conduction system to produce a normal narrow QRS.\",\n clinicalNote: \"Atrial pacing is used when the sinus node is diseased but AV conduction remains intact; it preserves the atrial kick and normal ventricular activation sequence, unlike ventricular pacing.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 70, hasPWave: true, wide: false, prMs: 160, pacedSpike: true },\n questions: [\n {\n prompt: \"In atrial paced rhythm, the QRS complex is typically:\",\n choices: [\"Wide and bizarre\", \"Narrow, since native AV/His-Purkinje conduction is intact\", \"Absent\", \"Always preceded by a delta wave\"],\n correctIndex: 1,\n explanation: \"Because pacing occurs only in the atrium and normal conduction to the ventricles is preserved, the QRS remains narrow.\",\n },\n {\n prompt: \"Atrial pacing is chosen over ventricular pacing when:\",\n choices: [\"AV conduction is completely blocked\", \"The sinus node is diseased but AV conduction is intact\", \"The patient has ventricular fibrillation\", \"The atria are in standstill\"],\n correctIndex: 1,\n explanation: \"Atrial pacing only makes sense if impulses can still travel normally through the AV node; complete heart block requires ventricular (or dual-chamber) pacing instead.\",\n },\n ],\n },\n {\n id: \"dual-chamber-paced-rhythm\",\n name: \"Dual-Chamber (AV Sequential) Paced Rhythm\",\n category: \"Other\",\n free: false,\n sortOrder: 54,\n rate: \"Set by the programmed pacemaker rate, commonly 60-70 bpm base rate\",\n regularity: \"Regular\",\n pWave: \"A pacing spike immediately precedes each P wave\",\n prInterval: \"A programmed AV delay (pacing spike to pacing spike) substitutes for the native PR interval\",\n qrs: \"A second pacing spike immediately precedes each QRS, which is wide and bizarre (paced morphology, typically resembling LBBB with a superior axis)\",\n summary: \"Leads in both the right atrium and right ventricle pace in sequence — the atrial spike triggers a paced P wave, followed after a programmed AV delay by a ventricular spike that triggers a wide paced QRS — mimicking normal AV synchrony in a heart with both sinus and AV conduction disease.\",\n clinicalNote: \"Dual-chamber pacing is used for patients needing both atrial and ventricular pacing support (e.g., complete heart block with sinus node dysfunction), preserving AV synchrony and the atrial contribution to cardiac output better than ventricular pacing alone.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 70, hasPWave: true, wide: true, prMs: 180, pacedSpike: true },\n questions: [\n {\n prompt: \"Dual-chamber paced rhythm shows how many pacing spikes per cardiac cycle?\",\n choices: [\"Zero\", \"One\", \"Two — one before the P wave, one before the QRS\", \"Three\"],\n correctIndex: 2,\n explanation: \"A dual-chamber pacemaker paces both the atrium and ventricle in sequence, producing two visible spikes per beat.\",\n },\n {\n prompt: \"A key advantage of dual-chamber over single-chamber ventricular pacing is:\",\n choices: [\"Lower battery cost\", \"Preservation of AV synchrony and the atrial contribution to cardiac output\", \"Faster heart rates\", \"No need for lead placement\"],\n correctIndex: 1,\n explanation: \"By pacing the atrium first and then the ventricle after a programmed delay, dual-chamber pacing better mimics normal physiologic AV timing.\",\n },\n ],\n },\n {\n id: \"pacemaker-failure-to-capture\",\n name: \"Pacemaker Failure to Capture\",\n category: \"Other\",\n free: false,\n sortOrder: 55,\n rate: \"Underlying intrinsic rate variable; paced rate as programmed\",\n regularity: \"Irregular due to missed captures\",\n pWave: \"Depends on intrinsic rhythm; may or may not be present independent of pacing spikes\",\n prInterval: \"Not applicable to the failed-capture beats\",\n qrs: \"A visible pacing spike is present but is NOT followed by a corresponding P wave or QRS complex — the electrical stimulus fails to depolarize the myocardium\",\n summary: \"The pacemaker fires an electrical stimulus (visible as a spike) but the myocardium fails to respond with a depolarization, meaning the spike is not followed by the expected P wave or QRS.\",\n clinicalNote: \"Failure to capture can result from lead dislodgement, elevated capture threshold, lead fracture, or battery depletion, and can cause dangerous bradycardia or asystole in a pacemaker-dependent patient — it requires urgent evaluation.\",\n waveform: { pattern: \"failToCapture\", rateMin: 60, rateMax: 70, hasPWave: false, wide: false, pacedSpike: true },\n questions: [\n {\n prompt: \"Failure to capture on a pacemaker ECG is recognized by:\",\n choices: [\"A pacing spike followed by a normal complex\", \"A pacing spike NOT followed by a corresponding depolarization\", \"No pacing spikes at all\", \"Two spikes per beat\"],\n correctIndex: 1,\n explanation: \"Capture means the pacing stimulus successfully triggers a depolarization; failure to capture means the spike appears but no P wave or QRS follows it.\",\n },\n {\n prompt: \"A common cause of pacemaker failure to capture is:\",\n choices: [\"Lead dislodgement or an elevated capture threshold\", \"Excessive potassium supplementation\", \"Normal battery function\", \"Sinus tachycardia\"],\n correctIndex: 0,\n explanation: \"Mechanical lead problems (dislodgement, fracture) and physiologic changes raising the capture threshold are classic causes of failure to capture.\",\n },\n ],\n },\n {\n id: \"pacemaker-failure-to-sense\",\n name: \"Pacemaker Failure to Sense (Undersensing)\",\n category: \"Other\",\n free: false,\n sortOrder: 56,\n rate: \"Native rate plus asynchronous pacing spikes\",\n regularity: \"Irregular due to inappropriately timed spikes\",\n pWave: \"Native P waves and QRS complexes present, with pacing spikes appearing inappropriately, sometimes within native beats\",\n prInterval: \"Normal for native beats\",\n qrs: \"Pacing spikes appear at their programmed intervals regardless of the patient's own intrinsic activity, sometimes landing within or shortly after native QRS complexes\",\n summary: \"The pacemaker fails to detect (sense) the patient's own intrinsic cardiac activity, so it continues firing at its programmed timing even when the heart has already depolarized on its own, potentially producing a spike that lands dangerously close to a native beat.\",\n clinicalNote: \"Undersensing risks delivering a pacing stimulus during the vulnerable period of a native beat's T wave, which could theoretically precipitate a malignant arrhythmia (an 'R-on-T'-like effect from the pacemaker itself); causes include lead displacement, low signal amplitude, or inappropriate sensitivity settings.\",\n waveform: { pattern: \"failToSense\", rateMin: 65, rateMax: 90, hasPWave: true, wide: false, pacedSpike: true },\n questions: [\n {\n prompt: \"Failure to sense (undersensing) is recognized on ECG by:\",\n choices: [\"Absent pacing spikes entirely\", \"Pacing spikes appearing inappropriately, ignoring the patient's own intrinsic beats\", \"A pacing spike followed by capture every time\", \"Complete heart block\"],\n correctIndex: 1,\n explanation: \"Undersensing means the device fails to recognize native cardiac activity and paces asynchronously, regardless of the heart's own rhythm.\",\n },\n {\n prompt: \"The theoretical major danger of failure to sense is:\",\n choices: [\"Battery depletion\", \"A pacing spike landing on a native T wave, risking a malignant arrhythmia\", \"Excessively slow pacing\", \"Loss of atrial kick\"],\n correctIndex: 1,\n explanation: \"An inappropriately timed spike falling during the vulnerable repolarization period can theoretically trigger ventricular tachycardia or fibrillation, similar to R-on-T.\",\n },\n ],\n },\n {\n id: \"pacemaker-mediated-tachycardia\",\n name: \"Pacemaker-Mediated Tachycardia (PMT)\",\n category: \"Other\",\n free: false,\n sortOrder: 57,\n rate: \"Rapid, typically at or near the pacemaker's programmed upper rate limit (often 120-180 bpm)\",\n regularity: \"Regular\",\n pWave: \"Retrograde P waves (from a PVC or PAC conducting backward to the atrium) are sensed by the atrial lead and mistaken for native atrial activity\",\n prInterval: \"Fixed, programmed AV delay follows each sensed/paced event\",\n qrs: \"Wide, paced ventricular morphology, repeating rapidly and regularly\",\n summary: \"In a dual-chamber pacemaker, a retrograde P wave from a PVC (or other event) is inappropriately sensed by the atrial lead, which then triggers the pacemaker to fire a ventricular paced beat, whose retrograde conduction again produces a retrograde P wave — creating a self-sustaining reentrant loop through the device itself.\",\n clinicalNote: \"PMT is terminated by applying a magnet over the device (which suspends sensing) or by reprogramming the post-ventricular atrial refractory period (PVARP) to prevent the device from tracking retrograde P waves.\",\n waveform: { pattern: \"regular\", rateMin: 120, rateMax: 180, hasPWave: true, wide: true, prMs: 160, pacedSpike: true },\n questions: [\n {\n prompt: \"Pacemaker-mediated tachycardia is caused by:\",\n choices: [\"A native atrial fibrillation episode\", \"The pacemaker tracking retrograde P waves and creating a self-sustaining reentrant loop\", \"Battery failure\", \"Lead fracture\"],\n correctIndex: 1,\n explanation: \"PMT is an endless-loop tachycardia where the device itself becomes part of the reentrant circuit by tracking retrograde atrial depolarization from a ventricular event.\",\n },\n {\n prompt: \"A rapid way to terminate pacemaker-mediated tachycardia in the field is to:\",\n choices: [\"Apply a magnet over the device\", \"Give adenosine\", \"Perform synchronized cardioversion first\", \"Administer atropine\"],\n correctIndex: 0,\n explanation: \"A magnet placed over most pacemakers suspends sensing and reverts the device to asynchronous pacing, breaking the reentrant loop.\",\n },\n ],\n },\n {\n id: \"ventricular-parasystole\",\n name: \"Ventricular Parasystole\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 58,\n rate: \"The parasystolic focus fires at its own independent, fixed intrinsic rate (commonly 20-50 discharges/min, though variable)\",\n regularity: \"The ectopic beats occur at variable coupling intervals to the preceding sinus beat, but the interval BETWEEN consecutive ectopic beats is a common multiple of a fixed base cycle length\",\n pWave: \"Normal sinus P waves for sinus beats; none for the ventricular ectopic beats\",\n prInterval: \"Normal for sinus beats\",\n qrs: \"Wide, bizarre ectopic beats with VARIABLE coupling intervals (unlike typical fixed-coupled PVCs) plus occasional fusion beats\",\n summary: \"A protected ventricular ectopic focus fires independently of the sinus node at its own steady inherent rate, 'protected' from being reset by conducted sinus impulses, producing ectopic beats whose timing relative to the sinus beat varies but whose own inter-ectopic intervals share a common mathematical denominator.\",\n clinicalNote: \"Parasystole is usually a benign electrophysiologic curiosity best recognized by variable coupling intervals plus fusion beats, distinguishing it from ordinary fixed-coupled PVCs, and rarely requires specific treatment.\",\n waveform: { pattern: \"parasystole\", baseRateMin: 65, baseRateMax: 85 },\n questions: [\n {\n prompt: \"The key distinguishing feature of parasystole compared with typical PVCs is:\",\n choices: [\"A fixed coupling interval to the preceding sinus beat\", \"A variable coupling interval, with inter-ectopic intervals sharing a common multiple\", \"Complete absence of fusion beats\", \"Occurrence only in pairs\"],\n correctIndex: 1,\n explanation: \"Unlike typical PVCs, which have a constant coupling interval, parasystolic beats fire independently, so their timing relative to sinus beats varies while their own spacing follows a mathematical pattern.\",\n },\n {\n prompt: \"Parasystole occurs because the ectopic focus is:\",\n choices: [\"Reset by every conducted sinus impulse\", \"'Protected' from being depolarized/reset by surrounding impulses\", \"Located in the SA node\", \"Only active during sleep\"],\n correctIndex: 1,\n explanation: \"An entrance block around the ectopic focus protects it from being reset by conducted impulses, allowing it to fire independently at its own steady rate.\",\n },\n ],\n },\n {\n id: \"isorhythmic-av-dissociation\",\n name: \"Isorhythmic AV Dissociation\",\n category: \"AV Block\",\n free: false,\n sortOrder: 59,\n rate: \"Atrial and ventricular (junctional) rates are nearly identical, commonly both around 60-100 bpm\",\n regularity: \"Both P waves and QRS complexes are individually regular but drift in and out of alignment with each other\",\n pWave: \"Present, marching through the strip independently of the QRS, sometimes appearing just before, within, or after the QRS as the two rates drift relative to one another\",\n prInterval: \"Variable/inconsistent since the P waves are not reliably conducting to the ventricles\",\n qrs: \"Narrow, driven by a junctional pacemaker at a rate very close to the sinus rate\",\n summary: \"The sinus node and the AV junction fire at nearly identical rates without true AV block, so the P waves and QRS complexes appear to march independently, with the P wave slowly sliding relative to the QRS across the strip rather than being fixed at one PR interval.\",\n clinicalNote: \"This is usually a benign, often transient finding (common with slight sinus slowing or accelerated junctional rates, e.g., from vagal tone or digoxin) and should be distinguished from complete heart block, since here the rates are similar rather than the ventricular rate being pathologically independent and slow.\",\n waveform: { pattern: \"thirdDegree\", atrialRateMin: 65, atrialRateMax: 75, ventricularRateMin: 65, ventricularRateMax: 75, hasPWave: true, wide: false },\n questions: [\n {\n prompt: \"Isorhythmic AV dissociation differs from third-degree AV block primarily because:\",\n choices: [\"The QRS is always wide\", \"The atrial and junctional rates are nearly equal rather than grossly different\", \"P waves are absent\", \"It always requires a pacemaker\"],\n correctIndex: 1,\n explanation: \"In isorhythmic AV dissociation the two pacemakers happen to fire at very similar rates, unlike complete heart block where the ventricular escape rate is markedly slower and unrelated to the atrial rate.\",\n },\n {\n prompt: \"Isorhythmic AV dissociation is often seen with:\",\n choices: [\"Severe hyperthyroidism only\", \"Slight sinus slowing or an accelerated junctional rhythm bringing the two rates close together\", \"Ventricular fibrillation\", \"WPW pattern\"],\n correctIndex: 1,\n explanation: \"When the sinus rate dips or the junctional rate rises so the two pacemakers become nearly matched, isorhythmic dissociation can appear, often transiently.\",\n },\n ],\n },\n {\n id: \"junctional-rhythm-retrograde-p\",\n name: \"Junctional Rhythm with Retrograde P Waves\",\n category: \"Junctional\",\n free: false,\n sortOrder: 60,\n rate: \"40-60 bpm (junctional rhythm range)\",\n regularity: \"Regular\",\n pWave: \"Inverted (retrograde) P waves in the inferior leads, occurring immediately before, buried within, or immediately after the QRS depending on the relative timing of atrial vs. ventricular activation\",\n prInterval: \"Short (<0.12s) if the retrograde P precedes the QRS; not measurable if buried or following\",\n qrs: \"Narrow, normal\",\n summary: \"The AV junction paces the heart and the impulse travels backward (retrograde) up into the atria as well as down into the ventricles, producing an inverted P wave whose position relative to the QRS depends on whether atrial or ventricular activation happens first.\",\n clinicalNote: \"Recognizing retrograde P wave position (before, during, or after the QRS) helps confirm a junctional origin and distinguish it from other narrow-complex rhythms; it is typically a benign, well-tolerated rhythm at these rates.\",\n waveform: { pattern: \"regular\", rateMin: 40, rateMax: 60, hasPWave: true, wide: false, prMs: 90 },\n questions: [\n {\n prompt: \"A retrograde P wave in a junctional rhythm appears inverted because:\",\n choices: [\"The atria are fibrillating\", \"Atrial depolarization travels backward from the AV junction toward the SA node\", \"The patient has WPW\", \"It represents ventricular repolarization\"],\n correctIndex: 1,\n explanation: \"Since the impulse originates in the AV junction and spreads upward into the atria, the direction of atrial depolarization is reversed, inverting the P wave in the inferior leads.\",\n },\n {\n prompt: \"If the retrograde P wave appears immediately after the QRS, this suggests:\",\n choices: [\"Atrial depolarization occurred before ventricular depolarization\", \"Ventricular depolarization occurred slightly before atrial depolarization\", \"Complete heart block\", \"Sinus rhythm\"],\n correctIndex: 1,\n explanation: \"The relative timing of the retrograde P wave to the QRS reflects whether the impulse reaches the ventricles or the atria first from the junctional focus.\",\n },\n ],\n },\n {\n id: \"artifact-mimicking-vfib\",\n name: \"Artifact Mimicking Ventricular Fibrillation\",\n category: \"Other\",\n free: false,\n sortOrder: 61,\n rate: \"Not a true rhythm — no organized cardiac electrical activity is actually occurring at the depicted 'rate'\",\n regularity: \"Chaotic, irregular baseline\",\n pWave: \"None identifiable, but this is due to signal noise, not true fibrillation\",\n prInterval: \"Not applicable\",\n qrs: \"No true QRS complexes; the tracing shows chaotic, irregular deflections from motion, loose leads, or patient movement (e.g., tooth-brushing, tremor, seizure activity) that visually resembles coarse VF\",\n summary: \"Electrical noise, patient movement, loose electrodes, or muscle tremor can produce a chaotic tracing that closely mimics ventricular fibrillation, even though the underlying cardiac rhythm is normal.\",\n clinicalNote: \"Always check the patient clinically (pulse, responsiveness, other monitor leads) before treating an apparent VF pattern — artifact has led to inappropriate defibrillation in documented cases; a patient who is awake, talking, or has a palpable pulse cannot be in true VF.\",\n waveform: { pattern: \"chaotic\", rateMin: 300, rateMax: 500 },\n questions: [\n {\n prompt: \"The single most important step before treating an apparent VF pattern on the monitor is to:\",\n choices: [\"Immediately defibrillate\", \"Assess the patient clinically — check responsiveness and pulse\", \"Increase the gain on the monitor\", \"Give epinephrine\"],\n correctIndex: 1,\n explanation: \"Because artifact can closely mimic VF, clinical correlation (checking for a pulse and responsiveness) is essential before delivering a shock.\",\n },\n {\n prompt: \"A common cause of artifact mimicking VF on a monitor is:\",\n choices: [\"True cardiac arrest\", \"Patient movement, tooth-brushing, tremor, or a loose lead\", \"Hyperkalemia\", \"Digoxin toxicity\"],\n correctIndex: 1,\n explanation: \"Motion artifact, loose electrodes, and activities like tooth-brushing or shivering are classic, well-documented causes of a chaotic tracing that resembles coarse VF.\",\n },\n ],\n },\n {\n id: \"artifact-mimicking-asystole\",\n name: \"Artifact/Lead Disconnection Mimicking Asystole\",\n category: \"Other\",\n free: false,\n sortOrder: 62,\n rate: \"Not a true rate — the flat line represents a disconnected or malfunctioning lead, not cardiac standstill\",\n regularity: \"Not applicable — flat, featureless line\",\n pWave: \"None visible, but due to lack of signal, not true absence of cardiac activity\",\n prInterval: \"Not applicable\",\n qrs: \"A flat or near-flat line, sometimes with a small step or artifact spike where a lead became loose or disconnected\",\n summary: \"A disconnected electrode, dead battery, or broken cable can produce a flat line on the monitor that looks identical to true asystole, even though the patient's heart is still beating.\",\n clinicalNote: \"Confirm true asystole in at least two leads and always check the patient (pulse, other vital signs, lead connections) before pronouncing cardiac arrest or beginning resuscitation based on monitor appearance alone — this is a core 'treat the patient, not the monitor' teaching point.\",\n waveform: { pattern: \"flatline\", rateMin: 0, rateMax: 0 },\n questions: [\n {\n prompt: \"A flat line on a single monitoring lead should always be confirmed by:\",\n choices: [\"Immediately calling a code with no further check\", \"Checking the patient and verifying in a second lead/confirming lead connections\", \"Increasing the defibrillator energy\", \"Assuming true asystole automatically\"],\n correctIndex: 1,\n explanation: \"Standard practice (and ACLS teaching) requires confirming asystole in more than one lead and ruling out equipment/lead problems before treating it as a true arrest rhythm.\",\n },\n {\n prompt: \"This teaching entry emphasizes the principle:\",\n choices: [\"Always trust the monitor without question\", \"Treat the patient, not the monitor\", \"Defibrillate any flat line immediately\", \"Artifact never occurs in modern monitors\"],\n correctIndex: 1,\n explanation: \"Clinical assessment of the actual patient always takes priority over an isolated monitor appearance, since technical problems can perfectly mimic a lethal rhythm.\",\n },\n ],\n },\n {\n id: \"sixty-cycle-interference\",\n name: \"60-Cycle (AC/Electrical) Interference Artifact\",\n category: \"Other\",\n free: false,\n sortOrder: 63,\n rate: \"The underlying cardiac rhythm can usually still be discerned beneath the interference\",\n regularity: \"The interference itself is a very fine, uniform, rapid oscillation superimposed on the real rhythm\",\n pWave: \"Usually still visible under close inspection, obscured by fine regular noise\",\n prInterval: \"Measurable once the artifact is mentally filtered out\",\n qrs: \"Normal underlying QRS, but the entire baseline shows a fine, regular, fast (60 Hz in the US; 50 Hz in many other countries) sinusoidal fuzz superimposed on it\",\n summary: \"Nearby AC-powered electrical equipment, poor grounding, or improperly applied electrodes can induce a fine, very regular high-frequency oscillation (60 Hz in North America) onto the ECG baseline, layered on top of the true underlying rhythm.\",\n clinicalNote: \"This is purely a technical artifact, not a cardiac abnormality — it is corrected by checking electrode contact, moving the patient away from electrical equipment, or ensuring proper grounding, rather than by any clinical intervention.\",\n waveform: { pattern: \"regular\", rateMin: 65, rateMax: 90, hasPWave: true, wide: false, prMs: 160, interference: true },\n questions: [\n {\n prompt: \"60-cycle interference on an ECG in North America is caused by:\",\n choices: [\"Ventricular fibrillation\", \"Nearby AC electrical equipment or poor electrode grounding\", \"Hyperkalemia\", \"Patient tremor\"],\n correctIndex: 1,\n explanation: \"Standard AC power in North America oscillates at 60 Hz, and inadequately grounded equipment or poor electrode contact can superimpose this frequency onto the ECG tracing.\",\n },\n {\n prompt: \"The correction for 60-cycle interference is:\",\n choices: [\"Administer antiarrhythmics\", \"Check electrode contact/grounding and move away from interfering equipment\", \"Defibrillate\", \"Begin CPR\"],\n correctIndex: 1,\n explanation: \"Because this is a technical/equipment artifact rather than a true arrhythmia, the fix is technical — improving electrode contact and grounding, not clinical treatment.\",\n },\n ],\n },\n {\n id: \"agonal-rhythm\",\n name: \"Agonal Rhythm\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 64,\n rate: \"Very slow, typically fewer than 20 wide complexes per minute, occurring irregularly and progressively decreasing\",\n regularity: \"Irregular, gradually decreasing in frequency\",\n pWave: \"Absent\",\n prInterval: \"Not applicable\",\n qrs: \"Wide, slow, bizarre complexes occurring at long, irregular intervals, progressively deteriorating in shape and frequency until they disappear entirely\",\n summary: \"Agonal rhythm represents the dying heart's last gasps of electrical activity — occasional, slow, wide, irregular complexes generated by the ventricles with no organized higher pacemaker activity, typically seen in the terminal minutes before asystole.\",\n clinicalNote: \"Agonal rhythm is a peri-arrest/pre-terminal pattern that does not produce a perfusing pulse; it should prompt immediate initiation or continuation of CPR per cardiac arrest protocols rather than being mistaken for a stable slow rhythm.\",\n waveform: { pattern: \"regular\", rateMin: 5, rateMax: 18, hasPWave: false, wide: true, irregular: true },\n questions: [\n {\n prompt: \"Agonal rhythm is best described as:\",\n choices: [\"A stable, well-perfusing bradycardia\", \"Occasional, slow, wide, irregular complexes representing the heart's last electrical activity before asystole\", \"A normal finding in healthy elderly patients\", \"A supraventricular rhythm\"],\n correctIndex: 1,\n explanation: \"Agonal rhythm is a pre-terminal, dying-heart pattern with sparse, progressively slowing wide complexes, not a stable perfusing rhythm.\",\n },\n {\n prompt: \"The appropriate management upon recognizing agonal rhythm in a pulseless patient is:\",\n choices: [\"Observe and reassess in 10 minutes\", \"Continue/initiate CPR per cardiac arrest protocol\", \"Administer oral medication\", \"Discharge the patient\"],\n correctIndex: 1,\n explanation: \"Agonal rhythm does not generate a perfusing pulse and is managed as cardiac arrest, following standard resuscitation protocols.\",\n },\n ],\n },\n {\n id: \"postural-vasovagal-sinus-arrest\",\n name: \"Vasovagal (Reflex) Sinus Arrest/Pause\",\n category: \"Sinus\",\n free: false,\n sortOrder: 65,\n rate: \"Normal sinus rate before and after the event, with a sudden pause of several seconds during the episode\",\n regularity: \"Regular except for the abrupt pause\",\n pWave: \"Normal sinus P waves before and after; absent during the pause\",\n prInterval: \"Normal on either side of the pause\",\n qrs: \"Normal narrow QRS before and after; absent during the pause (possibly followed by a junctional or ventricular escape beat)\",\n summary: \"A sudden surge in vagal (parasympathetic) tone — triggered by pain, emotional stress, standing suddenly, or a Valsalva-type maneuver — transiently suppresses SA node automaticity, producing an abrupt sinus pause or arrest that typically resolves spontaneously.\",\n clinicalNote: \"This is the electrophysiologic basis of vasovagal (neurocardiogenic) syncope, one of the most common causes of transient loss of consciousness; most episodes are self-limited and benign, though prolonged or recurrent pauses may need further evaluation (e.g., tilt-table testing, pacing in select cases).\",\n waveform: { pattern: \"pause\", rateMin: 60, rateMax: 85, hasPWave: true, prMs: 150 },\n questions: [\n {\n prompt: \"A vasovagal sinus pause is triggered by:\",\n choices: [\"A sudden increase in sympathetic tone\", \"A surge in vagal (parasympathetic) tone suppressing the SA node\", \"Digoxin toxicity only\", \"Ventricular ectopy\"],\n correctIndex: 1,\n explanation: \"Vagal surges (from pain, emotional stress, prolonged standing, or straining) transiently suppress sinus node automaticity, producing the characteristic pause.\",\n },\n {\n prompt: \"Vasovagal sinus arrest is most classically associated clinically with:\",\n choices: [\"Sudden cardiac death in athletes\", \"Neurocardiogenic (vasovagal) syncope\", \"Acute myocardial infarction\", \"Digoxin overdose\"],\n correctIndex: 1,\n explanation: \"This mechanism underlies common vasovagal syncope, typically triggered by situational or emotional stimuli, and is usually benign and self-limited.\",\n },\n ],\n },\n {\n id: \"pediatric-svt\",\n name: \"Supraventricular Tachycardia (SVT) in Infants/Children\",\n category: \"Other\",\n free: false,\n sortOrder: 66,\n rate: \"Typically 220-320 bpm in infants (markedly faster than adult SVT, which is usually 150-250 bpm)\",\n regularity: \"Regular\",\n pWave: \"Often not visible, buried in the preceding T wave, or retrograde if seen\",\n prInterval: \"Not measurable if P waves are not visible\",\n qrs: \"Narrow, unless aberrant conduction is present\",\n summary: \"SVT in infants and young children involves the same reentrant mechanisms (commonly AV reentry via an accessory pathway) as in adults, but presents at dramatically faster heart rates due to the smaller, faster pediatric conduction system.\",\n clinicalNote: \"Infants often present nonspecifically (poor feeding, irritability, tachypnea) rather than with palpitations, since they cannot verbalize symptoms; vagal maneuvers (e.g., ice to the face) and adenosine remain first-line treatments, with dosing weight-based and distinct from adult dosing.\",\n waveform: { pattern: \"regular\", rateMin: 220, rateMax: 300, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"Compared to adult SVT (150-250 bpm), infant SVT typically presents at rates of:\",\n choices: [\"100-140 bpm\", \"150-180 bpm\", \"220-320 bpm\", \"Under 100 bpm\"],\n correctIndex: 2,\n explanation: \"The pediatric conduction system supports much faster reentrant rates, so infant SVT classically runs 220-320 bpm, well above typical adult SVT rates.\",\n },\n {\n prompt: \"Infants with SVT most often present with:\",\n choices: [\"Complaints of palpitations\", \"Nonspecific signs like poor feeding, irritability, or tachypnea\", \"Chest pain radiating to the arm\", \"Syncope while exercising\"],\n correctIndex: 1,\n explanation: \"Preverbal infants cannot report palpitations, so SVT often manifests as nonspecific findings such as poor feeding, fussiness, pallor, or rapid breathing, sometimes only discovered incidentally.\",\n },\n ],\n },\n {\n id: \"pac-nonconducted-blocked\",\n name: \"Nonconducted (Blocked) PAC\",\n category: \"Atrial\",\n free: false,\n sortOrder: 67,\n rate: \"Underlying sinus rate with an apparent 'pause' where the blocked beat would have conducted\",\n regularity: \"Irregular due to the unexpected pause\",\n pWave: \"A premature P wave is visible, often distorting or hiding within the preceding T wave, but it is NOT followed by a QRS complex\",\n prInterval: \"Not applicable — the premature P wave fails to conduct entirely\",\n qrs: \"Absent after the early P wave, creating an apparent pause that can be mistaken for sinus arrest or a dropped beat from AV block\",\n summary: \"A PAC occurs so early that it arrives while the AV node is still refractory from the previous beat and therefore fails to conduct to the ventricles at all, producing an unexpected pause with no QRS, even though a premature P wave (often subtly deforming the preceding T wave) is present.\",\n clinicalNote: \"This is a key 'pause mimicker' — careful inspection of the T wave preceding a pause for a subtly hidden premature P wave distinguishes a benign nonconducted PAC from true sinus arrest or second-degree AV block, changing the clinical significance considerably.\",\n waveform: { pattern: \"pause\", rateMin: 65, rateMax: 90, hasPWave: true, prMs: 150 },\n questions: [\n {\n prompt: \"A nonconducted PAC produces a pause because:\",\n choices: [\"The SA node stopped firing\", \"A premature P wave arrives too early to conduct through a still-refractory AV node\", \"The AV node is completely blocked long-term\", \"A PVC occurred\"],\n correctIndex: 1,\n explanation: \"The PAC is early enough that the AV node is still in its refractory period from the prior beat and simply cannot conduct it, unlike true sinus arrest where no P wave is generated at all.\",\n },\n {\n prompt: \"The key clue that a pause is due to a nonconducted PAC rather than sinus arrest is:\",\n choices: [\"A completely flat baseline with no deflections\", \"A subtle deformity or extra bump in the T wave preceding the pause, representing a hidden early P wave\", \"A wide QRS after the pause\", \"A regular rhythm throughout\"],\n correctIndex: 1,\n explanation: \"Careful inspection often reveals the premature P wave distorting the shape of the preceding T wave, which is the giveaway that this is a blocked PAC rather than true sinus arrest.\",\n },\n ],\n },\n {\n id: \"pjc-with-aberrancy\",\n name: \"Premature Junctional Contraction with Aberrant Conduction\",\n category: \"Junctional\",\n free: false,\n sortOrder: 68,\n rate: \"Underlying sinus rate variable\",\n regularity: \"Irregular due to the premature beat\",\n pWave: \"Absent, inverted/retrograde, or hidden depending on timing\",\n prInterval: \"Short or not measurable\",\n qrs: \"Early, junctional-origin beat that conducts aberrantly through a still-partially-refractory bundle branch, producing a wide QRS that can be mistaken for a PVC\",\n summary: \"A junctional beat that fires prematurely can, like an early PAC, encounter a bundle branch still refractory from the preceding beat and conduct aberrantly, producing a wide-complex premature beat that originates above the ventricles despite its ventricular-like appearance.\",\n clinicalNote: \"This is a diagnostic pitfall similar to Ashman phenomenon — absence of a preceding P wave plus a retrograde or absent P around a premature wide beat should prompt consideration of aberrantly conducted PJC rather than automatically labeling it a PVC.\",\n waveform: { pattern: \"ectopic\", ectopicSubtype: \"junctional\", wide: true, count: 1, baseRateMin: 65, baseRateMax: 85 },\n questions: [\n {\n prompt: \"An aberrantly conducted PJC can be mistaken for a PVC because:\",\n choices: [\"Both always have identical fixed coupling\", \"Both can present as a wide, bizarre premature QRS complex\", \"PJCs never occur early\", \"PJCs always have a normal P wave before them\"],\n correctIndex: 1,\n explanation: \"When a premature junctional impulse encounters a still-refractory bundle branch, it conducts aberrantly and produces a wide QRS resembling a PVC, despite its supraventricular origin.\",\n },\n {\n prompt: \"A clue supporting a junctional (rather than ventricular) origin for a wide premature beat is:\",\n choices: [\"A fully compensatory pause with no other clues\", \"An associated retrograde/inverted P wave near the QRS\", \"A completely random coupling interval\", \"Absence of any T wave\"],\n correctIndex: 1,\n explanation: \"A retrograde P wave near the wide QRS suggests a supraventricular (junctional) origin conducting aberrantly, rather than a primary ventricular ectopic beat.\",\n },\n ],\n },\n {\n id: \"high-grade-av-block\",\n name: \"High-Grade (Advanced) Second-Degree AV Block\",\n category: \"AV Block\",\n free: false,\n sortOrder: 69,\n rate: \"Atrial rate normal; ventricular rate significantly slower due to multiple consecutive blocked P waves\",\n regularity: \"Regular or irregular depending on the conduction pattern (e.g., consistent 3:1 or 4:1 conduction, or varying)\",\n pWave: \"Regular, normal P waves, with two or more CONSECUTIVE P waves failing to conduct at a time (unlike single dropped beats in typical Mobitz I/II)\",\n prInterval: \"Constant for the P waves that do conduct\",\n qrs: \"Narrow or wide depending on the level of block; conducted beats look normal but occur infrequently\",\n summary: \"High-grade AV block is characterized by two or more consecutive non-conducted P waves (e.g., 3:1 or 4:1 conduction ratios) while at least some beats still conduct, placing it in severity between typical Mobitz II and complete heart block.\",\n clinicalNote: \"This pattern reflects significant conduction system disease and is generally considered an indication for pacemaker implantation, similar to Mobitz Type II, due to the risk of progression to complete heart block.\",\n waveform: { pattern: \"type2block\", atrialRate: 75, dropEvery: 4, hasPWave: true, wide: false },\n questions: [\n {\n prompt: \"High-grade AV block is defined by:\",\n choices: [\"A single dropped beat with prolonging PR intervals\", \"Two or more consecutive nonconducted P waves with some beats still conducting\", \"Complete absence of any conducted beats\", \"A 1:1 P to QRS ratio\"],\n correctIndex: 1,\n explanation: \"The hallmark of high-grade block is multiple consecutive blocked P waves — more severe than a single dropped beat but not a total block, since some P waves still conduct.\",\n },\n {\n prompt: \"High-grade AV block is generally managed with:\",\n choices: [\"Observation only, no intervention needed\", \"Pacemaker implantation given progression risk\", \"Beta-blocker therapy\", \"Increased physical activity\"],\n correctIndex: 1,\n explanation: \"Like Mobitz Type II, high-grade block reflects significant infranodal or nodal disease and carries meaningful risk of progressing to complete heart block, generally warranting pacing.\",\n },\n ],\n },\n {\n id: \"pea-electrical-narrow-complex\",\n name: \"Pulseless Electrical Activity (PEA) — Narrow Complex Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 70,\n rate: \"Variable, can appear as an otherwise normal or near-normal narrow-complex rhythm\",\n regularity: \"Regular or irregular depending on the organized rhythm displayed\",\n pWave: \"May be present and appear normal\",\n prInterval: \"May appear normal\",\n qrs: \"Narrow QRS complexes that look organized and near-normal on the monitor, despite the patient having no palpable pulse\",\n summary: \"PEA is not a distinct ECG waveform but a clinical state — organized electrical activity is present on the monitor (which can look essentially normal, narrow, and regular) while the patient has no palpable pulse, reflecting a failure of mechanical contraction or effective cardiac output despite intact electrical conduction.\",\n clinicalNote: \"PEA is diagnosed clinically (absence of a pulse despite organized electrical activity), not by the ECG waveform alone, and management focuses on rapidly identifying and reversing an underlying cause (the H's and T's: hypovolemia, hypoxia, hydrogen ion/acidosis, hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, thrombosis) alongside CPR.\",\n waveform: { pattern: \"regular\", rateMin: 70, rateMax: 100, hasPWave: true, wide: false, prMs: 160 },\n questions: [\n {\n prompt: \"PEA is defined by:\",\n choices: [\"A specific chaotic waveform on the monitor\", \"Organized electrical activity on the monitor with no palpable pulse\", \"Complete absence of any electrical activity\", \"Always a wide QRS pattern\"],\n correctIndex: 1,\n explanation: \"PEA is a clinical diagnosis — the monitor can show an essentially normal-looking organized rhythm, but the patient has no pulse, indicating a disconnect between electrical activity and effective mechanical pumping.\",\n },\n {\n prompt: \"Management of PEA focuses on:\",\n choices: [\"Immediate defibrillation\", \"High-quality CPR while identifying and treating a reversible underlying cause\", \"Cardioversion\", \"Observation only\"],\n correctIndex: 1,\n explanation: \"PEA is not a shockable rhythm; treatment is CPR combined with a rapid search for and correction of a reversible cause (the H's and T's).\",\n },\n ],\n },\n {\n id: \"focal-atrial-tachycardia\",\n name: \"Focal Atrial Tachycardia (FAT)\",\n category: \"Atrial\",\n free: false,\n sortOrder: 71,\n rate: \"100-250 bpm\",\n regularity: \"Regular, often with a 'warm-up' (gradual acceleration) and 'cool-down' (gradual slowing) at onset and offset\",\n pWave: \"Present before every QRS but with an abnormal morphology/axis compared to the sinus P wave, since the impulse originates from a single ectopic atrial focus outside the SA node\",\n prInterval: \"May be normal or mildly prolonged depending on the focus location and conduction time back to the AV node\",\n qrs: \"Narrow, unless aberrant conduction is present\",\n summary: \"A single irritable atrial focus outside the SA node discharges rapidly and regularly, producing a P wave that looks different from a sinus P wave (different axis/morphology) but is still followed 1:1 by a normal narrow QRS.\",\n clinicalNote: \"Unlike reentrant SVT, FAT often shows a gradual warm-up/cool-down rather than an abrupt start/stop, and it typically does NOT terminate with adenosine (though adenosine can transiently slow AV conduction to unmask the abnormal P waves for diagnosis); causes include structural heart disease, digoxin toxicity, and catecholamine excess.\",\n waveform: { pattern: \"regular\", rateMin: 130, rateMax: 220, hasPWave: true, wide: false, prMs: 140 },\n questions: [\n {\n prompt: \"Focal atrial tachycardia is distinguished from sinus tachycardia primarily by:\",\n choices: [\"A completely absent P wave\", \"A P wave with an abnormal morphology/axis different from the sinus P wave\", \"A wide QRS complex\", \"An irregularly irregular rhythm\"],\n correctIndex: 1,\n explanation: \"Because the ectopic focus is not the SA node, the P wave shape and axis differ from a normal sinus P wave even though the rhythm remains regular and 1:1 conducted.\",\n },\n {\n prompt: \"A classic feature that helps distinguish focal atrial tachycardia from reentrant SVT is:\",\n choices: [\"An abrupt, all-or-nothing onset and termination\", \"A gradual 'warm-up' and 'cool-down' in rate at onset and offset\", \"Complete resolution with adenosine every time\", \"A rate that is always below 100 bpm\"],\n correctIndex: 1,\n explanation: \"FAT often accelerates and decelerates gradually as the ectopic focus 'warms up' and 'cools down,' unlike the abrupt onset/offset typical of reentrant SVT.\",\n },\n ],\n },\n {\n id: \"atrial-flutter-variable-block\",\n name: \"Atrial Flutter with Variable Block\",\n category: \"Atrial\",\n free: false,\n sortOrder: 72,\n rate: \"Atrial rate ~250-350 bpm; ventricular rate irregular and dependent on the shifting conduction ratio\",\n regularity: \"Irregular — the AV conduction ratio changes beat to beat or in groups (e.g., alternating 2:1, 3:1, 4:1)\",\n pWave: \"Sawtooth flutter waves, no isoelectric baseline, with a variable, unpredictable number conducting to the ventricles\",\n prInterval: \"Not measurable in the usual sense\",\n qrs: \"Usually narrow\",\n summary: \"The same reentrant atrial circuit as typical atrial flutter, but the AV node's conduction ratio shifts unpredictably beat to beat instead of staying fixed, producing an irregularly irregular ventricular response that can be mistaken for atrial fibrillation at first glance.\",\n clinicalNote: \"Careful inspection for the underlying regular sawtooth flutter waves (best seen in II, III, aVF) distinguishes this from atrial fibrillation, which has no discrete, regular atrial waveform at all; management principles (rate/rhythm control, anticoagulation) otherwise mirror standard atrial flutter.\",\n waveform: { pattern: \"aflutter\", atrialRate: 300, ratios: [2, 3, 4], irregular: true },\n questions: [\n {\n prompt: \"Atrial flutter with variable block can be mistaken for atrial fibrillation because:\",\n choices: [\"Both have a wide QRS\", \"The unpredictable conduction ratio makes the ventricular response irregularly irregular\", \"Both lack any P waves\", \"The atrial rate is identical in both\"],\n correctIndex: 1,\n explanation: \"A shifting AV conduction ratio produces an irregular ventricular rate that can superficially resemble atrial fibrillation, unless the underlying regular sawtooth flutter waves are specifically identified.\",\n },\n {\n prompt: \"The key feature that distinguishes atrial flutter with variable block from atrial fibrillation is:\",\n choices: [\"A regular, organized sawtooth flutter wave pattern is still present in the atria\", \"A completely regular ventricular rate\", \"Absence of any atrial activity\", \"A QRS rate always over 150 bpm\"],\n correctIndex: 0,\n explanation: \"Even with variable AV block, the underlying atrial activity in flutter remains a single, regular, organized sawtooth circuit — unlike the chaotic, disorganized atrial activity of fibrillation.\",\n },\n ],\n },\n {\n id: \"junctional-tachycardia-nonparoxysmal\",\n name: \"Nonparoxysmal Junctional Tachycardia\",\n category: \"Junctional\",\n free: false,\n sortOrder: 73,\n rate: \"70-130 bpm, sometimes higher\",\n regularity: \"Regular\",\n pWave: \"Absent, retrograde, or dissociated from the QRS\",\n prInterval: \"Short or not measurable if a retrograde P is present; not applicable if dissociated\",\n qrs: \"Narrow, normal\",\n summary: \"Enhanced automaticity in the AV junction gradually accelerates the junctional pacemaker beyond its normal escape rate, producing a regular narrow-complex tachycardia that develops gradually rather than starting abruptly like a reentrant SVT.\",\n clinicalNote: \"Classically caused by digoxin toxicity, recent cardiac surgery (especially valve surgery), or inferior MI; because it results from increased automaticity rather than reentry, it does not respond to (and should not be treated with) cardioversion.\",\n waveform: { pattern: \"regular\", rateMin: 90, rateMax: 130, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"Nonparoxysmal junctional tachycardia most classically results from:\",\n choices: [\"A reentrant circuit in the AV node\", \"Enhanced automaticity of the AV junction, often from digoxin toxicity or recent cardiac surgery\", \"An accessory pathway\", \"Ectopic atrial focus with block\"],\n correctIndex: 1,\n explanation: \"Unlike reentrant junctional tachycardias, this rhythm arises from increased automaticity of junctional tissue, classically triggered by digoxin toxicity, inferior MI, or cardiac surgery.\",\n },\n {\n prompt: \"Why is synchronized cardioversion inappropriate for nonparoxysmal junctional tachycardia?\",\n choices: [\"It is always hemodynamically unstable\", \"The rhythm is due to automaticity, not reentry, so cardioversion will not terminate it and may worsen an underlying cause like digoxin toxicity\", \"It always requires defibrillation instead\", \"The QRS is too wide to synchronize\"],\n correctIndex: 1,\n explanation: \"Cardioversion works by interrupting reentrant circuits; an automaticity-driven rhythm simply resumes afterward, and if digoxin toxicity is the cause, cardioversion can precipitate dangerous ventricular arrhythmias.\",\n },\n ],\n },\n {\n id: \"lafb-pattern\",\n name: \"Left Anterior Fascicular Block (LAFB) Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 74,\n rate: \"Underlying rate determined by the native rhythm (often sinus)\",\n regularity: \"Regular if underlying rhythm is sinus\",\n pWave: \"Normal, present before each QRS\",\n prInterval: \"Normal\",\n qrs: \"Slightly widened but usually <0.12s; small q waves in leads I/aVL with small r waves in II/III/aVF, reflecting marked left-axis deviation\",\n summary: \"Conduction through the left anterior fascicle of the left bundle branch is blocked, so the left ventricle depolarizes via the remaining posterior fascicle first, swinging the QRS axis sharply leftward and superiorly (typically -45° to -90°) without significantly widening the QRS.\",\n clinicalNote: \"LAFB is primarily diagnosed by frontal-plane axis deviation across the full 12-lead ECG, which a single rhythm strip cannot show directly — this entry approximates the pattern's mildly widened QRS as a single-lead teaching reference; true confirmation requires a full 12-lead with calculated axis.\",\n waveform: { pattern: \"regular\", rateMin: 65, rateMax: 90, hasPWave: true, wide: false, prMs: 160 },\n questions: [\n {\n prompt: \"LAFB is fundamentally diagnosed by:\",\n choices: [\"A markedly widened QRS over 0.16s\", \"Left-axis deviation on the 12-lead ECG, with only mild QRS widening\", \"A sawtooth atrial pattern\", \"ST elevation in the precordial leads\"],\n correctIndex: 1,\n explanation: \"LAFB primarily causes marked left-axis deviation from selective loss of the anterior fascicle's conduction, while the QRS itself stays only mildly widened (usually <0.12s), unlike a complete bundle branch block.\",\n },\n {\n prompt: \"Why can't LAFB be reliably confirmed from a single rhythm strip lead alone?\",\n choices: [\"Because it requires calculating the frontal-plane axis, which needs multiple limb leads\", \"Because it never affects QRS morphology\", \"Because it only occurs in leads V1-V3\", \"Because it always causes a delta wave\"],\n correctIndex: 0,\n explanation: \"Diagnosing LAFB requires assessing the QRS axis across the limb leads (I, II, III, aVF), which a single monitoring strip cannot provide — a full 12-lead ECG is needed for a definitive diagnosis.\",\n },\n ],\n },\n {\n id: \"wpw-associated-avrt\",\n name: \"WPW-Associated AV Reentrant Tachycardia (Orthodromic AVRT)\",\n category: \"Other\",\n free: false,\n sortOrder: 75,\n rate: \"150-250 bpm\",\n regularity: \"Regular\",\n pWave: \"Often not visible, or a retrograde P wave appears shortly after the QRS as the impulse travels back up the accessory pathway\",\n prInterval: \"Not measurable during the tachycardia (no delta wave is seen during orthodromic AVRT, since conduction goes down the normal AV node)\",\n qrs: \"Narrow, since the impulse travels down the normal AV node/His-Purkinje system and back up the accessory pathway (orthodromic conduction)\",\n summary: \"In a patient with an underlying WPW accessory pathway, a premature beat can trigger a reentrant loop that conducts down the AV node (producing a normal narrow QRS, without the baseline delta wave) and back up the accessory pathway, sustaining a fast, regular narrow-complex tachycardia.\",\n clinicalNote: \"Because conduction is anterograde down the normal AV node in orthodromic AVRT, the QRS is narrow and looks like typical SVT — the WPW diagnosis is only apparent on a resting baseline ECG showing the short PR interval and delta wave once the tachycardia resolves; adenosine and vagal maneuvers are effective first-line treatments for this narrow-complex form.\",\n waveform: { pattern: \"regular\", rateMin: 160, rateMax: 220, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"During orthodromic AVRT in a WPW patient, the QRS is typically:\",\n choices: [\"Wide, with a delta wave visible\", \"Narrow, since conduction travels down the normal AV node and back up the accessory pathway\", \"Absent entirely\", \"Identical to atrial fibrillation\"],\n correctIndex: 1,\n explanation: \"Orthodromic AVRT conducts anterograde through the normal AV node/His-Purkinje system, producing a narrow QRS without a delta wave during the tachycardia itself.\",\n },\n {\n prompt: \"The WPW diagnosis in a patient who presents in orthodromic AVRT is typically confirmed by:\",\n choices: [\"The tachycardia strip alone\", \"A baseline (non-tachycardic) 12-lead ECG showing a short PR interval and delta wave\", \"A chest X-ray\", \"An elevated troponin\"],\n correctIndex: 1,\n explanation: \"Because the delta wave disappears during orthodromic AVRT (conduction is going down the normal pathway), the underlying WPW pattern is only visible on a baseline sinus-rhythm ECG.\",\n },\n ],\n },\n {\n id: \"hypothermia-osborn-waves\",\n name: \"Hypothermia with Osborn (J) Waves\",\n category: \"Other\",\n free: false,\n sortOrder: 76,\n rate: \"Bradycardic, often progressively slowing as core temperature drops\",\n regularity: \"Regular, though risk of atrial fibrillation and ventricular arrhythmias increases with worsening hypothermia\",\n pWave: \"Normal, though may become harder to distinguish from baseline artifact (shivering)\",\n prInterval: \"Often prolonged\",\n qrs: \"A distinctive extra positive deflection (the Osborn or 'J' wave) at the junction between the QRS and ST segment, with height that increases as core temperature falls further\",\n summary: \"As core body temperature drops, altered ion channel kinetics in hypothermic myocardium produce a characteristic hump-shaped positive deflection immediately after the QRS complex (the Osborn/J wave), alongside progressive bradycardia and prolonged intervals.\",\n clinicalNote: \"Osborn wave size roughly correlates with the severity of hypothermia and tends to resolve with rewarming; the hypothermic heart is also prone to atrial fibrillation and, in severe cases, ventricular fibrillation, so gentle handling and avoidance of unnecessary stimulation are important during rewarming.\",\n waveform: { pattern: \"regular\", rateMin: 35, rateMax: 55, hasPWave: true, wide: false, prMs: 200, osbornWave: true },\n questions: [\n {\n prompt: \"The Osborn (J) wave seen in hypothermia appears as:\",\n choices: [\"A slurred upstroke before the QRS\", \"A positive hump-shaped deflection at the junction of the QRS and ST segment\", \"A deeply inverted T wave\", \"A sawtooth baseline\"],\n correctIndex: 1,\n explanation: \"The Osborn wave is a distinctive extra positive deflection immediately following the QRS, at the J point, and its size tends to correlate with the degree of hypothermia.\",\n },\n {\n prompt: \"As a hypothermic patient is rewarmed, the Osborn wave typically:\",\n choices: [\"Grows larger\", \"Resolves as core temperature normalizes\", \"Converts immediately to a delta wave\", \"Has no expected change\"],\n correctIndex: 1,\n explanation: \"Osborn waves are a temperature-dependent finding and generally diminish and resolve as the patient is successfully rewarmed toward a normal core temperature.\",\n },\n ],\n },\n {\n id: \"brugada-pattern\",\n name: \"Brugada Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 77,\n rate: \"Usually normal at baseline (Brugada is a conduction/repolarization pattern, not itself a tachyarrhythmia)\",\n regularity: \"Regular at baseline\",\n pWave: \"Normal sinus P wave\",\n prInterval: \"Normal\",\n qrs: \"Normal duration in most leads, but a distinctive coved ('tombstone') ST-segment elevation in the right precordial leads is the defining feature\",\n summary: \"A sodium-channelopathy produces a characteristic coved ST-segment elevation followed by a negative T wave, classically in the right precordial leads, in a patient with a structurally normal heart who is nonetheless at risk for sudden ventricular arrhythmias, especially at rest or during fever.\",\n clinicalNote: \"Brugada pattern is a marker of risk for sudden cardiac death from polymorphic VT/VF, often presenting during sleep or with fever (which can unmask the pattern); management centers on risk stratification and, in higher-risk patients, an implantable cardioverter-defibrillator — avoid sodium-channel-blocking drugs and treat fever aggressively.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 85, hasPWave: true, wide: false, prMs: 160, stElevation: true, tInvert: true },\n questions: [\n {\n prompt: \"The classic ECG finding in Brugada pattern is:\",\n choices: [\"Diffuse concave ST elevation in all leads\", \"Coved ('tombstone') ST elevation followed by a negative T wave in the right precordial leads\", \"A sawtooth baseline\", \"A short PR with delta wave\"],\n correctIndex: 1,\n explanation: \"Brugada pattern shows a distinctive coved, downsloping ST elevation with a negative T wave, most classically seen in the right precordial leads (V1-V2).\",\n },\n {\n prompt: \"Brugada pattern is clinically significant primarily because it:\",\n choices: [\"Causes chronic hypertension\", \"Marks a risk for sudden cardiac death from polymorphic VT/VF, particularly with fever or at rest\", \"Always requires emergent cardioversion\", \"Is caused by coronary artery blockage\"],\n correctIndex: 1,\n explanation: \"Brugada pattern occurs in structurally normal hearts due to a sodium-channel abnormality and carries a risk of sudden death from ventricular arrhythmias, often triggered or unmasked by fever.\",\n },\n ],\n },\n {\n id: \"pericarditis-diffuse-st-elevation\",\n name: \"Acute Pericarditis (Diffuse ST Elevation)\",\n category: \"Other\",\n free: false,\n sortOrder: 78,\n rate: \"Often mildly elevated due to pain/inflammation\",\n regularity: \"Regular\",\n pWave: \"Normal\",\n prInterval: \"Often depressed (PR-segment depression), with reciprocal PR elevation in aVR\",\n qrs: \"Normal\",\n summary: \"Inflammation of the pericardium produces widespread, concave ('saddle-shaped') ST-segment elevation across most leads (rather than a single anatomic territory) along with PR-segment depression, reflecting diffuse rather than localized myocardial injury.\",\n clinicalNote: \"Distinguishing pericarditis from STEMI matters enormously: pericarditis shows diffuse concave ST elevation without reciprocal depression (except aVR/V1) and often improves when the patient leans forward, whereas STEMI shows convex ST elevation localized to a coronary territory with reciprocal changes; treatment is typically NSAIDs and colchicine rather than emergent catheterization.\",\n waveform: { pattern: \"regular\", rateMin: 80, rateMax: 105, hasPWave: true, wide: false, prMs: 150, stElevation: true },\n questions: [\n {\n prompt: \"Acute pericarditis classically produces ST elevation that is:\",\n choices: [\"Convex and localized to a single coronary territory\", \"Diffuse and concave ('saddle-shaped') across most leads\", \"Only present in the inferior leads\", \"Always accompanied by a wide QRS\"],\n correctIndex: 1,\n explanation: \"Pericarditis inflames the entire pericardial sac rather than a focal coronary territory, producing widespread concave ST elevation rather than the localized convex elevation of STEMI.\",\n },\n {\n prompt: \"A helpful ECG clue that favors pericarditis over STEMI is:\",\n choices: [\"ST elevation with reciprocal depression in a specific territory\", \"PR-segment depression with reciprocal PR elevation in aVR\", \"A new left bundle branch block\", \"Pathologic Q waves\"],\n correctIndex: 1,\n explanation: \"PR-segment depression (with reciprocal PR elevation in aVR) is a classic, relatively specific finding for pericarditis that is not typically seen in acute MI.\",\n },\n ],\n },\n {\n id: \"long-qt-syndrome-congenital\",\n name: \"Congenital Long QT Syndrome\",\n category: \"Other\",\n free: false,\n sortOrder: 79,\n rate: \"Usually normal at baseline\",\n regularity: \"Regular unless torsades develops\",\n pWave: \"Normal\",\n prInterval: \"Normal\",\n qrs: \"Normal width, but with a markedly prolonged QT interval (QTc typically >450-460ms), sometimes with abnormal T-wave morphology (e.g., notched T waves)\",\n summary: \"An inherited ion-channelopathy (commonly affecting potassium or sodium channels) delays ventricular repolarization, prolonging the QT interval on an otherwise structurally normal heart and predisposing to torsades de pointes, particularly with exertion, emotional stress, or auditory triggers depending on the specific genetic subtype.\",\n clinicalNote: \"Congenital long QT syndrome is a leading cause of unexplained syncope and sudden cardiac death in young, otherwise healthy people; management includes beta-blockers, avoidance of QT-prolonging medications, activity restrictions tailored to genotype, and an ICD in higher-risk patients.\",\n waveform: { pattern: \"regular\", rateMin: 60, rateMax: 85, hasPWave: true, wide: false, prMs: 160, qtOffsetMs: 120 },\n questions: [\n {\n prompt: \"Congenital long QT syndrome is primarily caused by:\",\n choices: [\"Coronary artery disease\", \"Inherited cardiac ion-channel abnormalities delaying ventricular repolarization\", \"Chronic hypertension\", \"Valvular disease\"],\n correctIndex: 1,\n explanation: \"Long QT syndrome arises from inherited mutations in cardiac ion channels (most often potassium channels) that slow ventricular repolarization, prolonging the QT interval.\",\n },\n {\n prompt: \"Congenital long QT syndrome is an important cause of:\",\n choices: [\"Chronic stable angina\", \"Unexplained syncope and sudden cardiac death in young, otherwise healthy patients\", \"Progressive heart failure over decades\", \"Atrial fibrillation only\"],\n correctIndex: 1,\n explanation: \"Because a markedly prolonged QT predisposes to torsades de pointes, this condition is a recognized cause of exertional or stress-triggered syncope and sudden death in young people with structurally normal hearts.\",\n },\n ],\n },\n {\n id: \"short-pr-lown-ganong-levine\",\n name: \"Short PR Interval (Lown-Ganong-Levine Pattern)\",\n category: \"Other\",\n free: false,\n sortOrder: 80,\n rate: \"Usually normal at baseline\",\n regularity: \"Regular\",\n pWave: \"Normal sinus P wave\",\n prInterval: \"Short, <0.12s\",\n qrs: \"Normal duration, with NO delta wave — this is the key feature distinguishing it from WPW\",\n summary: \"An accessory AV-nodal bypass connection (classically attributed to James fibers) allows the atrial impulse to reach the ventricles faster than through the normal AV node, shortening the PR interval, but the impulse still enters the normal His-Purkinje system, so the QRS remains narrow with no slurred delta-wave upstroke.\",\n clinicalNote: \"The short PR interval without a delta wave is what separates this pattern from WPW; patients with this pattern (historically termed Lown-Ganong-Levine syndrome when associated with palpitations) may still be predisposed to paroxysmal SVT, though the existence of a distinct anatomic bypass tract in every such case has been debated in more recent literature.\",\n waveform: { pattern: \"regular\", rateMin: 65, rateMax: 90, hasPWave: true, wide: false, prMs: 100 },\n questions: [\n {\n prompt: \"The key ECG feature that distinguishes a short-PR (LGL-type) pattern from WPW is:\",\n choices: [\"A wide QRS with a delta wave\", \"A short PR interval WITHOUT a delta wave, and a normal narrow QRS\", \"Absence of a P wave\", \"A sawtooth baseline\"],\n correctIndex: 1,\n explanation: \"Both patterns show a short PR interval, but WPW also shows a delta wave and widened QRS from ventricular pre-excitation, while this pattern conducts normally through the His-Purkinje system with a normal QRS.\",\n },\n {\n prompt: \"A patient with this ECG pattern who experiences palpitations may be at increased risk for:\",\n choices: [\"Ventricular fibrillation from the pattern alone\", \"Paroxysmal supraventricular tachycardia\", \"Complete heart block\", \"Torsades de pointes\"],\n correctIndex: 1,\n explanation: \"Accelerated AV conduction from a bypass connection has classically been associated with a predisposition to paroxysmal SVT in some patients with this pattern.\",\n },\n ],\n },\n {\n id: \"low-voltage-qrs\",\n name: \"Low-Voltage QRS Pattern\",\n category: \"Other\",\n free: false,\n sortOrder: 81,\n rate: \"Determined by the underlying rhythm (often sinus)\",\n regularity: \"Regular if underlying rhythm is sinus\",\n pWave: \"Normal, though may also appear diminished in amplitude\",\n prInterval: \"Normal\",\n qrs: \"Normal duration, but with markedly reduced overall amplitude compared to a typical strip\",\n summary: \"Something is attenuating or diluting the heart's electrical signal before it reaches the surface electrodes — commonly a pericardial effusion, obesity, COPD (hyperinflated lungs insulate the signal), or an infiltrative myocardial process such as amyloidosis — producing a QRS that appears smaller than expected throughout.\",\n clinicalNote: \"New low voltage, especially combined with electrical alternans, should raise concern for a large pericardial effusion and possible tamponade; other causes (obesity, COPD, myxedema, amyloid infiltration) are worked up based on the clinical context.\",\n waveform: { pattern: \"regular\", rateMin: 65, rateMax: 90, hasPWave: true, wide: false, prMs: 160, ampScale: 0.35 },\n questions: [\n {\n prompt: \"A globally diminished QRS amplitude across the strip should raise concern for which potentially serious cause?\",\n choices: [\"Hyperkalemia\", \"A large pericardial effusion with possible tamponade\", \"Digoxin effect\", \"Sinus tachycardia\"],\n correctIndex: 1,\n explanation: \"A pericardial effusion insulates and disperses the heart's electrical signal before it reaches the surface, and new low voltage is a classic warning sign that should prompt evaluation for tamponade physiology.\",\n },\n {\n prompt: \"Besides pericardial effusion, other recognized causes of low-voltage QRS include:\",\n choices: [\"Athletic training only\", \"Obesity, COPD, myxedema, and infiltrative diseases like amyloidosis\", \"Hyperthyroidism\", \"Acute anterior STEMI\"],\n correctIndex: 1,\n explanation: \"Body habitus, hyperinflated lungs, hypothyroidism, and myocardial infiltration by abnormal proteins (amyloid) are all recognized causes of attenuated QRS voltage on the surface ECG.\",\n },\n ],\n },\n {\n id: \"electrical-alternans\",\n name: \"Electrical Alternans\",\n category: \"Other\",\n free: false,\n sortOrder: 82,\n rate: \"Determined by the underlying rhythm, often sinus tachycardia\",\n regularity: \"Regular\",\n pWave: \"Normal, though amplitude may also alternate\",\n prInterval: \"Normal\",\n qrs: \"Beat-to-beat alternation in QRS amplitude (and sometimes axis), while the rate and rhythm otherwise stay constant\",\n summary: \"In a large pericardial effusion, the heart literally swings back and forth within the excess fluid with each beat, changing its distance and orientation to the surface electrodes and producing a QRS that alternates in size from beat to beat.\",\n clinicalNote: \"Electrical alternans combined with sinus tachycardia and low voltage is highly suggestive of cardiac tamponade and should prompt urgent bedside echocardiography; it can less commonly be seen with other conditions causing a swinging heart or severe tachyarrhythmias.\",\n waveform: { pattern: \"regular\", rateMin: 100, rateMax: 130, hasPWave: true, wide: false, prMs: 150, alternans: true, ampScale: 0.6 },\n questions: [\n {\n prompt: \"Electrical alternans occurs mechanically because:\",\n choices: [\"The AV node is diseased\", \"The heart swings back and forth within a large pericardial effusion, changing its position relative to the electrodes each beat\", \"The patient has WPW\", \"There is a bundle branch block\"],\n correctIndex: 1,\n explanation: \"A large effusion allows the heart to swing within the pericardial sac, altering its orientation to the surface leads beat to beat and producing the alternating QRS amplitude.\",\n },\n {\n prompt: \"The classic triad suggesting cardiac tamponade on ECG includes electrical alternans plus:\",\n choices: [\"Bradycardia and a short PR interval\", \"Sinus tachycardia and low QRS voltage\", \"A sawtooth baseline and a wide QRS\", \"ST elevation and Q waves\"],\n correctIndex: 1,\n explanation: \"Sinus tachycardia, low voltage, and electrical alternans together are a classic (though not universally present) ECG picture suggestive of pericardial tamponade.\",\n },\n ],\n },\n {\n id: \"idiopathic-vt-fascicular\",\n name: \"Idiopathic Fascicular Ventricular Tachycardia (Belhassen VT)\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 83,\n rate: \"150-200 bpm\",\n regularity: \"Regular\",\n pWave: \"None associated with the QRS; sinus P waves may be seen dissociated from the tachycardia\",\n prInterval: \"Not applicable during the tachycardia\",\n qrs: \"Wide but relatively narrow for VT (often 100-140ms), with a right-bundle-branch-block-like morphology and a superior (left-axis) frontal plane axis, reflecting its origin from the left posterior fascicle\",\n summary: \"A reentrant circuit involving Purkinje fibers near the left posterior fascicle produces a monomorphic ventricular tachycardia in a structurally normal heart, typically in young patients, with a QRS that is relatively narrower than most VT because much of the ventricle is still activated via the native conduction system.\",\n clinicalNote: \"This VT is classically verapamil-sensitive (unlike most other VTs, where verapamil is relatively contraindicated), which is both a diagnostic clue and a treatment option; it is generally well-tolerated hemodynamically and carries a favorable prognosis compared to VT associated with structural heart disease.\",\n waveform: { pattern: \"regular\", rateMin: 150, rateMax: 200, hasPWave: false, wide: true },\n questions: [\n {\n prompt: \"Idiopathic fascicular VT is notable for responding specifically to:\",\n choices: [\"Amiodarone only\", \"Verapamil\", \"Digoxin\", \"Atropine\"],\n correctIndex: 1,\n explanation: \"Unlike most other forms of VT, where calcium channel blockers are typically avoided, idiopathic fascicular VT arising near the left posterior fascicle is classically verapamil-sensitive.\",\n },\n {\n prompt: \"Compared to VT from structural heart disease, idiopathic fascicular VT typically occurs in:\",\n choices: [\"Older patients with prior MI\", \"Younger patients with structurally normal hearts\", \"Patients with severe cardiomyopathy only\", \"Patients with complete heart block\"],\n correctIndex: 1,\n explanation: \"This VT arises from a reentrant circuit in normal Purkinje/fascicular tissue, typically in young, otherwise healthy patients without underlying structural heart disease.\",\n },\n ],\n },\n {\n id: \"junctional-bradycardia\",\n name: \"Junctional Bradycardia\",\n category: \"Junctional\",\n free: false,\n sortOrder: 84,\n rate: \"<40 bpm\",\n regularity: \"Regular\",\n pWave: \"Absent, inverted (retrograde), or occurring after the QRS\",\n prInterval: \"Short or not measurable\",\n qrs: \"Narrow, normal\",\n summary: \"The AV junction paces the heart, as in a standard junctional rhythm, but at a rate slower than the typical 40-60 bpm junctional escape range, reflecting a junctional pacemaker that is itself depressed or suppressed.\",\n clinicalNote: \"This is a more concerning finding than a standard junctional rhythm, since it suggests both SA node failure and a depressed backup junctional pacemaker; causes include severe sinus node disease, hyperkalemia, hypothyroidism, and drug toxicity (beta-blockers, calcium channel blockers, digoxin), and symptomatic cases may require pacing.\",\n waveform: { pattern: \"regular\", rateMin: 25, rateMax: 39, hasPWave: false, wide: false },\n questions: [\n {\n prompt: \"Junctional bradycardia differs from a standard junctional (escape) rhythm in that:\",\n choices: [\"The QRS is wide\", \"The rate is slower than the typical 40-60 bpm junctional escape range\", \"P waves are always upright\", \"It never requires further workup\"],\n correctIndex: 1,\n explanation: \"The mechanism (AV junction pacing the ventricles) is the same as a junctional rhythm; junctional bradycardia specifically denotes a rate under the normal 40-60 bpm junctional range.\",\n },\n {\n prompt: \"Junctional bradycardia is a more concerning finding than a typical junctional rhythm because it suggests:\",\n choices: [\"A perfectly healthy conduction system\", \"Both SA node failure and depression of the backup junctional pacemaker itself\", \"Only mild vagal tone\", \"WPW pattern\"],\n correctIndex: 1,\n explanation: \"A junctional rate below the normal escape range indicates that even the backup pacemaker is underperforming, pointing to more significant conduction system depression or toxicity.\",\n },\n ],\n },\n {\n id: \"idioventricular-rhythm-with-capture\",\n name: \"Idioventricular Rhythm with Capture/Fusion Beats\",\n category: \"Ventricular\",\n free: false,\n sortOrder: 85,\n rate: \"20-40 bpm for the idioventricular escape rhythm, interrupted by faster capture/fusion beats\",\n regularity: \"Regular idioventricular rhythm interrupted by occasional early, differently-shaped beats\",\n pWave: \"None associated with the idioventricular beats; a sinus P wave precedes a capture beat and may partially precede a fusion beat\",\n prInterval: \"Normal preceding a full capture beat; not applicable for pure idioventricular or fusion beats\",\n qrs: \"Wide, slow, regular ventricular escape complexes, interrupted by an occasional narrow QRS (a 'capture' beat, when a sinus impulse fully conducts to the ventricles) or a hybrid-shaped complex (a 'fusion' beat, when the sinus impulse and the ventricular focus activate the ventricle simultaneously)\",\n summary: \"A slow ventricular escape pacemaker drives the heart because higher pacemakers are failing, but if a sinus impulse occasionally manages to conduct down to the ventricles between escape beats, it produces either a narrow 'capture' beat (fully conducted) or an intermediate-looking 'fusion' beat (blended with the ventricular focus), proving that AV conduction is intermittently still possible.\",\n clinicalNote: \"Recognizing capture and fusion beats within a slow ventricular rhythm is a classic teaching point confirming AV dissociation with intermittent conduction, and is also used diagnostically to help distinguish a ventricular rhythm from an aberrantly conducted supraventricular one during wide-complex tachycardia evaluation.\",\n waveform: { pattern: \"idioventricularCapture\", rateMin: 20, rateMax: 40, hasPWave: true, wide: true },\n questions: [\n {\n prompt: \"A 'capture beat' within an idioventricular rhythm occurs when:\",\n choices: [\"Two ventricular foci fire simultaneously\", \"A sinus impulse manages to fully conduct down to the ventricles between escape beats, producing a narrow QRS\", \"The rate suddenly increases to 150 bpm\", \"The patient is defibrillated\"],\n correctIndex: 1,\n explanation: \"A capture beat proves that AV conduction is still intermittently intact — a sinus impulse 'captures' the ventricles fully, producing a normal narrow QRS distinct from the surrounding wide escape beats.\",\n },\n {\n prompt: \"A fusion beat differs from a pure capture beat in that it:\",\n choices: [\"Has no relationship to 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