Sources & model details
Where the teaching comes from, how far it has been checked, and what the simulation leaves out. These are three different questions, kept apart on purpose.
1. Content review status
Whether people with the right expertise have checked the teaching statements, parameter values and answer keys. At present, 0 of 25 lessons, 0 of 30 cases and 0 of 37 source claims have been expert reviewed. All of it is proposed teaching content; no reviewer approvals are recorded. 37 claims still lack an exact passage locator, which blocks release.
2. Simulation testing status
Whether the equations are solved correctly and behave as stated: volume conservation, step-size convergence, repeatable runs, a normal baseline, and the expected direction of each intervention and phenotype. The core model is recorded as quantitatively tested; the device circuits are proposed (device curves are placeholders, not manufacturer data). Passing these tests does not mean that any lesson, case answer or normal range has been expert reviewed.
3. Limitations
Each lesson, case and topic lists the limitations that matter for it under its own “Sources & model details”. General ones: no real recordings are included; the baroreflex is an optional first-order teaching controller; remodelled states are authored parameter sets, not simulated time courses; oxygen transport is a steady-state teaching model. The full list is in What the simulator covers.
No dangling source references. 37 claims are registered, 37 proposed and 0 source mapped.
Technical detailsversions and model records
App 0.5.0 · content 0.5.0 · model fh-closed-loop 0.4.0.
Model records
Finding Hemo closed-loop lumped-parameter model
- Equations
- docs/science/MODEL.md
- Implementation
- src/engine/model.ts, src/engine/simulator.ts, src/engine/valve.ts, src/engine/activation.ts
- Licence
- Original implementation (project licence). S01/S02 cited as precedent only; no code or parameters copied.
- Solver
- RK4, dt = 0.2 ms, output 1 kHz; settling = 3 consecutive beats within 0.5% on 8 summary metrics; max 80 beats. Ramped interventions interpolate parameters linearly over N beats.
- Error metrics
- Volume drift < 1e-9 relative over 100 beats; core stable metrics change < 1% at dt/2.
- Calibration
- None. Parameters hand-tuned to textbook resting ranges (CL-normal-resting-ranges).
- Benchmarks
- VF-normal-baseline; tests/science/controlled-changes.test.ts (directional); tests/science/phenotypes.test.ts (qualitative phenotype patterns); tests/science/drugs.test.ts (directional drug effects); tests/science/clamps-oxygen-migration.test.ts; tests/science/observation.test.ts
- Excluded physiology
- Baroreflex and other reflexes; Ventricular interdependence via septum; Inertance / wave reflection; Afterload- or ischaemia-dependent contractility; Device circuits; Dynamic outflow obstruction; Remodelling and drug kinetics; Regional oxygen extraction (ScvO2)
- Reviewer
- none — Software, conservation and qualitative pattern tests pass. Not expert reviewed; normal ranges and phenotype parameter sets are proposed teaching values. 0.2.0 adds isolated-physiology clamps (LA, RA, systemic arterial pressure with explicit reservoir accounting), a steady-state Fick oxygen teaching model (no hemodynamic feedback), ramped interventions, and uses the exponential pericardium in the RV-failure, biventricular and PE phenotypes.
Device circuits: IABP, microaxial pump, VA-ECMO, intracardiac shunts
- Equations
- docs/science/MODEL.md section 16
- Implementation
- src/engine/model.ts (devices), src/engine/simulator.ts (IABP scheduler)
- Licence
- Original implementation. Pressure–flow characteristics are explicit placeholder parameters, not manufacturer data.
- Solver
- Same RK4 integrator; IABP balloon volume ramps over the transition time; pump flows evaluated at every stage.
- Error metrics
- Closed-loop volume conserved to floating precision with all circuits active; native + device flow equals mean systemic flow within 2% at steady state.
- Calibration
- None.
- Benchmarks
- tests/science/devices.test.ts (conservation, timing errors, head dependence, suction, distension, flow balance)
- Excluded physiology
- Manufacturer pressure–flow curves (placeholders in use); Haemolysis, cannula resistances, circuit oxygenator physics; Spatial oxygen mixing (differential oxygenation); Right-sided support and durable LVADs
- Reviewer
- none — Explanatory/teaching device circuits. Device-specific validation against manufacturer data is a release gate and has NOT been done.
Claims
| ID | Claim | Sources / passage | Status |
|---|---|---|---|
| CL-normal-resting-ranges | Typical resting adult hemodynamics: aortic pressure about 100–140/60–90 mmHg, mean PA pressure 9–18 mmHg, PAWP 4–12 mmHg, RAP 0–6 mmHg, LVEDV 100–160 mL, LVEF 55–70%, cardiac output 4–7 L/min, cardiac index 2.2–4.0 L/min/m², SVR 10–20 Wood units, PVR 0.5–2.0 Wood units. Healthy resting adults · Supine rest; teaching ranges, not diagnostic cut-offs. | TXT-physiology TODO: map to specific textbook/guideline tables. | Teaching approximation Proposed |
| CL-sv-definition | Total chamber stroke volume is end-diastolic minus end-systolic volume and includes any regurgitant volume; forward stroke volume is the volume ejected through the outlet valve. General · Any | TXT-physiology TODO | Clinical reference Proposed |
| CL-forward-flow | Forward valve flow is the time integral of positive flow through the valve; regurgitant volume is the integral of retrograde flow. In regurgitation, shunts or MCS, forward output must be derived from the appropriate flow signal rather than chamber excursion. General · Any | TXT-physiology TODO | Clinical reference Proposed |
| CL-ef-not-contractility | Ejection fraction is load dependent and is not a measure of contractility; end-systolic elastance (Ees) is the model contractility parameter. General · Any | TXT-physiology TODO | Clinical reference Proposed |
| CL-co-definition | In an unsupported, steady circulation without shunts, cardiac output equals forward stroke volume times heart rate; cardiac index is CO divided by body surface area. General · No shunt, no device | TXT-physiology TODO | Clinical reference Proposed |
| CL-svr-pvr | SVR = (MAP − RAP) / systemic flow; PVR = (mPAP − PAWP) / pulmonary flow; in Wood units (mmHg·min/L), multiplied by 80 for dyn·s·cm⁻⁵. Resistance should not be calculated from negligible or invalid flow. General · Valid flow measurement | S07, TXT-physiology S07: TODO exact section | Clinical reference Proposed |
| CL-pawp-alias | Pulmonary artery wedge pressure (PAWP) and pulmonary capillary wedge pressure (PCWP) refer to the same measurement; the mean wedge approximates mean left atrial pressure under stated assumptions. General · Correct catheter position; no pulmonary venous obstruction | S07 TODO | Clinical reference Proposed |
| CL-ea-definition | Effective arterial elastance Ea is end-systolic pressure divided by stroke volume; it is a lumped afterload index, not SVR, and the standard definition assumes an unsupported circulation without major regurgitation. General · No major regurgitation or device | TXT-physiology TODO: modern coupling reviews required | Clinical reference Proposed |
| CL-ees-identifiability | A single ordinary PV loop does not identify Ees; estimating it clinically requires a multi-beat loading manoeuvre or single-beat approximations with stated assumptions. In the simulator Ees is a known model parameter. General · Any | TXT-physiology TODO | Teaching approximation Proposed |
| CL-stroke-work | Stroke work is the area enclosed by the pressure–volume loop (∮P dV); 1 mmHg·mL = 1.333×10⁻⁴ J. General · Closed loop (steady beat) | TXT-physiology TODO | Clinical reference Proposed |
| CL-cpo | Cardiac power output = MAP × CO / 451 (W). No single threshold is a universal treatment target. General · Any | S08 TODO | Clinical reference Proposed |
| CL-papi | PAPi = (PA systolic − PA diastolic) / RAP. Interpretation is context dependent. General · RAP measurable and not near zero | S09 TODO | Clinical reference Proposed |
| CL-fluid-stressed-volume | Venous return is driven by the gradient between mean systemic filling pressure and right atrial pressure; mean systemic filling pressure depends on stressed volume and venous compliance. Fluid adds stressed volume; venoconstriction converts unstressed to stressed volume without changing total volume. General · Closed circulation | TXT-physiology TODO: Guyton venous-return literature | Clinical reference Proposed |
| CL-afterload-ees-shift | With a pure increase in arterial resistance, end-systolic volume rises along the ESPVR and stroke volume falls; because the arterial compliance fills over several beats, aortic pressure and ESV change little on the first beat and build to a new steady state. General · No reflexes; constant Ees and preload | TXT-physiology TODO | Clinical reference Proposed |
| CL-starling-filling | Increasing end-diastolic volume increases stroke volume (Frank–Starling); on an exponential EDPVR the filling-pressure cost rises more steeply as volume increases. General · Constant contractility and afterload | TXT-physiology TODO | Clinical reference Proposed |
| CL-fick-oxygen | Arterial oxygen content ≈ 1.34 × Hb × SaO₂; oxygen delivery = CaO₂ × CO × 10; by the Fick principle at steady state VO₂ = CO × (CaO₂ − CvO₂), so mixed venous saturation falls as delivery falls for a fixed consumption. ScvO₂ and SvO₂ are different measurements. General · Any | S07, TXT-physiology TODO | Clinical reference Proposed |
| CL-hfref-pattern | Systolic heart failure shows a reduced ejection fraction with a rightward-shifted, enlarged pressure–volume loop and raised filling pressures; chronic eccentric remodelling increases chamber volume and compliance compared with an acute loss of contractility. General · Any | TXT-physiology TODO | Clinical reference Proposed |
| CL-hfpef-pattern | HFpEF phenotypes show raised filling pressures with a preserved ejection fraction; passive stiffness (steep EDPVR) and impaired active relaxation are distinct mechanisms with different rate dependence. General · Any | TXT-physiology TODO | Clinical reference Proposed |
| CL-shock-phenotypes | Shock phenotypes differ in output, filling pressures and vascular resistance even at similar mean arterial pressure: cardiogenic (low output, high filling pressure, high resistance), hypovolaemic (low output, low filling pressure, high resistance), distributive (normal/high output, low resistance), obstructive (low output with high right-sided pressure) and mixed forms. General · Any | S08, TXT-physiology S08: TODO exact section | Clinical reference Proposed |
| CL-drug-mechanisms-qualitative | Vasoactive and inotropic drugs act on several targets at once (arteriolar tone, venous tone, contractility, rate, relaxation); their hemodynamic effect depends on the phenotype. The simulator maps each named drug to qualitative multi-target effects without doses or kinetics. General · Any | S08, TXT-physiology TODO: pharmacology references required per drug | Teaching approximation Proposed |
| CL-gradient-definitions | Instantaneous peak, peak-to-peak and mean gradients are different quantities; for a fixed orifice the gradient scales with the square of flow, so low-flow states understate severity and transmitral gradients rise with shorter diastole. General · Any | S03, S07 TODO | Clinical reference Proposed |
| CL-v-wave | The atrial v wave reflects filling against a closed AV valve and depends on atrial compliance and inflow; a large wedge v wave is not a stand-alone MR severity classifier. General · Any | S07 TODO | Clinical reference Proposed |
| CL-transmural-pressure | Chamber distension depends on transmural pressure (intracavitary minus external); pleural and pericardial pressure make measured filling pressures differ from the distending pressure. General · Any | TXT-physiology, S06 TODO | Clinical reference Proposed |
| CL-hocm-dynamic-obstruction | Dynamic LVOT obstruction in HCM depends on cavity size, contractility and afterload: it increases with reduced preload, reduced afterload, increased contractility and post-extrasystolic potentiation (Brockenbrough–Braunwald–Morrow sign: post-PVC gradient rises while aortic pulse pressure falls). General · Any | S04 TODO | Clinical reference Proposed |
| CL-pva-energetics | Pressure–volume area (stroke work plus potential energy) relates to myocardial oxygen consumption in experimental preparations; the relation is not a clinical measurement and efficiency cannot be read from one loop. General · Any | TXT-physiology TODO: Suga ventricular energetics literature | Teaching approximation Proposed |
| CL-pericardial-physiology | Tamponade raises intrapericardial pressure so that diastolic pressures equalise and inspiratory RV filling occurs at the expense of LV filling (pulsus paradoxus); constriction shields the heart from pleural pressure (dissociation of intrathoracic and intracardiac pressures) and produces discordant respiratory variation of LV and RV systolic pressures, whereas restriction produces concordant variation. Equalised pressures or a dip-and-plateau alone do not establish constriction. General · Any | S06 TODO | Clinical reference Proposed |
| CL-ph-classification | Pulmonary hypertension is defined hemodynamically by mPAP, PAWP and PVR thresholds stored in the rule set RS-ph-hemodynamic-classification (2022 ESC/ERS); a hemodynamic classification does not establish aetiology or justify a pulmonary vasodilator. General · Any | S05 TODO: exact table | Clinical reference Proposed |
| CL-ppv-svv-limits | Pulse pressure and stroke volume variation predict fluid responsiveness only under controlled ventilation with adequate tidal volume, regular rhythm and no spontaneous effort; they are unreliable with arrhythmia, spontaneous breathing, low tidal volume or RV dysfunction. General · Any | S08 TODO | Clinical reference Proposed |
| CL-baroreflex | The arterial baroreflex counters a fall in arterial pressure within seconds to a minute by raising heart rate, contractility, arteriolar resistance and venous tone; the simulator implements it as an explicit first-order option with stated gains and time constant. General · Any | TXT-physiology TODO | Teaching approximation Proposed |
| CL-force-interval | A premature beat is weaker and the beat after a compensatory pause is stronger (post-extrasystolic potentiation) with a longer filling time; in a normal heart aortic pulse pressure rises after the pause, in dynamic obstruction it falls. General · Any | S04, TXT-physiology TODO | Clinical reference Proposed |
| CL-exercise-hemodynamics | Exercise raises heart rate, contractility and venous return and lowers systemic resistance; the slope of mean PA pressure (and PAWP) against cardiac output during exercise carries information beyond resting values, with published thresholds depending on protocol and population. General · Any | S05, TXT-physiology TODO: exercise hemodynamics literature | Clinical reference Proposed |
| CL-mcs-flow-accounting | Under mechanical support, flows that enter the systemic arteries in parallel (native aortic ejection, a microaxial pump from the LV, an ECMO return) add to total systemic output; flows through serial segments of one circuit must not be added. Native and device contributions should be displayed separately. General · Any | S09 TODO | Clinical reference Proposed |
| CL-shunt-oxygen | A left-to-right intracardiac shunt raises the oxygen saturation of the chamber it enters (step-up) and makes pulmonary flow exceed systemic flow; Qp/Qs is derived from the saturations at the systemic arterial, mixed venous and pulmonary arterial sites. General · Any | S07, TXT-physiology TODO | Clinical reference Proposed |
| CL-iabp-timing | Counterpulsation inflates at aortic valve closure (dicrotic notch) and deflates just before ejection; early inflation and late deflation raise LV afterload, late inflation and early deflation lose augmentation and unloading. Counterpulsation is not a continuous addition of cardiac output. General · Any | S09 TODO | Clinical reference Proposed |
| CL-va-ecmo-lv | Peripheral VA-ECMO returns blood retrograde into the arterial tree, raising LV afterload; a weak LV may fail to open the aortic valve, distend and raise pulmonary pressures, which is the rationale for LV venting or unloading (e.g. ECPELLA). Favourable unloading does not by itself establish survival benefit or device preference. General · Any | S09 TODO | Clinical reference Proposed |
| CL-impella-performance | Microaxial pump flow depends on the pressure head between aorta and LV and on the speed setting; the nominal maximum is not delivered at every head, and inadequate LV filling causes suction. General · Any | S09 TODO: manufacturer performance curves required per model | Clinical reference Proposed |
| CL-structural-remodelling | Relief of a valve lesion changes loading immediately; chamber remodelling follows over months. Removing a regurgitant outlet can unmask afterload mismatch in a dilated ventricle, so the immediate response is case specific. General · Any | S03 TODO | Clinical reference Proposed |
Sources
- S01 CVSim: An Open-Source Cardiovascular Simulator for Teaching and Research (2011)Use: Educational lumped-parameter model precedent and review of model structure. No code or parameters were copied; licence not verified. Rights: Not reused. Cited as precedent only. Note: Identity from the spec seed register; passage mapping pending. Accessed: not yet
- S02 Closed-loop real-time simulation model of hemodynamics and oxygen transport in the cardiovascular system (2013)Use: Model equation precedent, coupled physiology and stated validation limitations. No code or parameters were copied. Rights: Not reused. Cited as precedent only. Note: Passage mapping pending. Accessed: not yet
- S03 2025 ESC/EACTS Guidelines for the management of valvular heart disease (2025)Use: Valve definitions and clinical interpretation (later milestones). Rights: Not reproduced. Note: Add ACC/AHA valve guidance and identify rule differences. Accessed: not yet
- S04 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy (2024)Use: HCM terminology, provocation and clinical context (later milestones). Rights: Not reproduced. Accessed: not yet
- S05 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension (2022)Use: Pulmonary hemodynamic definitions and provocative testing context (later milestones). Rights: Not reproduced. Note: Check for subsequent updates before encoding thresholds. Accessed: not yet
- S06 2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Diagnosis and Management of Pericarditis (2025)Use: Pericardial disease and invasive assessment context (later milestones). Rights: Not reproduced. Accessed: not yet
- S07 Practical Guidance for Hemodynamic Assessment by Right Heart Catheterization in Management of Heart Failure (2024)Use: Acquisition, measurement quality and interpretation (M11). Rights: Not reproduced. Accessed: not yet
- S08 ESICM guidelines on circulatory shock and hemodynamic monitoring 2025 (2025)Use: Shock assessment and monitoring context (M12). Rights: Not reproduced. Accessed: not yet
- S09 Escalating and De-escalating Temporary Mechanical Circulatory Support in Cardiogenic Shock: A Scientific Statement From the American Heart Association (2022)Use: Device strategies, escalation and weaning context (M13). Rights: Not reproduced. Accessed: not yet
- TXT-physiology Standard cardiovascular physiology textbook material (placeholder record)Use: Resting normal ranges and classical pressure–volume / venous-return teaching relationships used while passage-mapped primary sources are being acquired. Rights: No text or figures reproduced. Note: PLACEHOLDER. Must be replaced by specific, passage-mapped sources before any claim it supports can leave 'proposed'. Accessed: not yet
For reviewers and editors: editorial sign-in.