How the model works
What each slider sets, and why the final numbers can move together.
Baseline controls are physiological experiments. They set reference inputs before the full treatment and rhythm calculation; they are not fluid doses, measured valve areas or guaranteed achievable cardiac outputs.
Pressure calculations retain decimal precision. Display rounding never feeds back into the circulation. A visible wedge target can differ from the final mean wedge after disease-specific waves, rhythm, treatment, respiration and transmitted chest pressure have been applied.
| Control | Range | Meaning |
|---|---|---|
| Ventricular rate | 0–240 bpm | Rhythm-specific ventricular timing; zero removes native organized ejection. |
| Filling pressure | 0–60 mmHg | Reference wedge target. Related chamber filling shifts preserve lesion-specific offsets until lower bounds apply. |
| Forward output | 0.5–15 L/min | Reference flow at the disease reference rate; not a prescribed inotrope or measured CO. |
| PVR | 0.25–20 WU | Pulmonary resistance; changes RV load, flow and PA pressure. |
| SVR | 200–3200 dyn·s/cm⁵ | Systemic resistance; changes pressure, LV afterload and forward flow. |
Reducing the target reduces reference flow according to the bounded ratio (new wedge + 1)/(baseline wedge + 1), with a flow-factor floor of 0.25. Raising it does not automatically recruit extra forward flow. RAP, RVEDP and LVEDP shift with the target, subject to lower limits; MS and other anatomic pressure differences are retained where possible.
The target is a model loading control. Mean wedge includes atrial-wave and respiratory effects and is recalculated downstream. PEEP can raise measured wedge while reducing transmural filling. Compare the reference target, final wedge and LVEDP rather than treating their difference as a display error.
For one steady forward circulation: MAP − RAP = CO × SVR / 80; mean PA − PAWP = CO × PVR. With a shunt, pulmonary resistance uses Qp and systemic resistance uses Qs. MCS also distinguishes native and circuit paths internally; it does not label bypass flow as a congenital shunt.
Changing resistance can change output: the model uses bounded, phenotype-dependent loading sensitivities. RV failure is more sensitive to PVR; LV pump failure and fixed regurgitation are more sensitive to SVR; preload-limited or constrained states have less recruitment. Very low perfusion pressure can further limit output. These are algebraic sensitivities, not measured elastance or vascular autoregulation.
The native rate response uses the ratio of selected rate to the phenotype reference rate. Its ordinary flow term is ratio^0.3 with an exponential penalty for additional rate above 120 bpm; the selected vagal example uses ratio^0.8 to represent recovery of a slow rate. AS/HOCM add a grade-dependent penalty for tachycardia above the reference rate. These exponents and rate boundaries are synthetic response choices.
Mitral and tricuspid stenosis have independent rate-related upstream pressure terms; faster rate does not add the same pressure to both sides of a stenotic AV valve. AR uses a longer-diastole loading/runoff term at slower rate. Very rapid rates can also impair filling.
Manual BP changes are interpreted through a chosen pulse-pressure/stroke-volume and afterload relationship. The flow factor includes the selected/reference pulse-pressure ratio, an exponential afterload penalty and the rate term, with protective numerical bounds. Disease-specific sensitivities change filling. The model does not treat a manually chosen BP as an independent immutable output once rhythm and therapies act.
The output control preserves reference resistance and ventricular filling while changing pressure gradients and pulse pressure under an assumed compliance. Stenotic valve gradients vary approximately with flow squared; mitral/tricuspid upstream burdens are recalculated. Severe unsupported tamponade retains its flow ceiling.
Reset Vitals restores the scenario reference controls. The full simulator Reset restores the normal baseline and clears the selected disease/intervention experiment. Neither represents a physiological recovery mechanism.