1 Patient

Clinical state

Weight (kg)

BSA (m²)

Baroreflex

2 Drugs (up to 3)

Or load a teaching scenario

Advanced model settings

Baroreflex strength 0.35

In-vivo potency shift ×41

β receptor density 100%

β G-protein coupling 100%

Density lowers the maximum response only. Coupling lowers the maximum and shifts the EC₅₀. The clinical states above set both.

Patient-to-patient drug level typical

3 Hemodynamics

How the drug gets there

4 Plasma level

5 Receptor response

Bar = response with the drug. Tick = resting tone. Red bar = potency is an estimate.

6 Effect on the circulation

Behind the model

How well is it calibrated?

Trace the SVR back to its sources

Spare receptors: why binding K_D is the wrong number

Drug and receptor

Drugs this model cannot simulate

References

What the vasopressor and inotrope simulator does

Most vasoactive-drug references are grids of plus signs and arrows: norepinephrine gets α1 +++ and β1 ++, dobutamine gets β1 +++ and α1 +, and the fellow is left to guess what that means for a mean arterial pressure. Most cardiovascular simulators, on the other side, have real physiology and no drugs at all. This page closes the gap. It carries an infusion through four explicit stages, each with its own visible intermediate: the dose in micrograms per kilogram per minute, the plasma concentration that dose produces, the fraction of each receptor that concentration drives, and the change in systemic resistance, stressed volume, end-systolic elastance, heart rate and relaxation that follows. The last stage feeds a closed-loop cardiovascular engine — a time-varying-elastance left ventricle coupled to a lumped Guyton circulation — so that the pressure-volume loop, the arterial pressure trace, the venous-return and cardiac-function intersection, and the cath-lab readout are all read off one steady state rather than drawn independently.

Why the arterial baroreflex is on by default

A vasoactive simulator without a reflex teaches something false. Phenylephrine given to a patient with an intact reflex raises the pressure and slows the heart; without the reflex the model shows a pressor response and no bradycardia at all, which is the opposite of the lesson. The reflex equations and gains are taken from CVSim, the open-source cardiovascular model published by Heldt, Mukkamala, Moody and Mark at MIT — an external research model, not another CathMath tool. It senses a saturating mean-pressure error and drives four effectors: R-R interval, lumped systemic resistance, venous unstressed volume and end-systolic compliance. You can switch it off, and the page will show you the difference the reflex makes on every number.

Functional EC₅₀, never binding K_D — the spare-receptor trap

Catecholamine binding affinity at the α-adrenoceptors is measured in tens to hundreds of micromolar, while functional potency is measured in nanomolar. For epinephrine at α1A the binding log K_D is −5.09 and the functional log EC₅₀ is −9.09 — four orders of magnitude apart. Plasma norepinephrine during a clinical infusion sits in the single-digit to low-hundreds nanomolar range, so an occupancy model built on K_D would read essentially zero percent occupied at every dose a patient ever receives. The response layer here therefore runs on functional EC₅₀. The discrepancy is not hidden; it has its own panel (Spare receptors), where the occupancy curve and the response curve are drawn together and the horizontal gap between them is labelled the spare-receptor reserve.

Where the numbers come from, and where they stop

Affinity and functional potency at the α1 and α2 subtypes are measured human values from Proudman and Baker. Pharmacokinetics come from the regulatory labels and from the one good human intensive-care norepinephrine dataset. Measured human β1 and β2 agonist potencies (Baker 2010; Hoffmann 2004) were not available when the model was built, so every β potency is a placeholder on the published rank order and is tagged as an estimate. There is likewise no published transfer function anywhere in the literature that maps receptor occupancy onto a change in systemic vascular resistance or end-systolic elastance in humans. One effect size is fitted to a named clinical observation; the rest are teaching estimates and are tagged as such. Two quantities — pulmonary vascular resistance and the pulmonary artery pulsatility index — are not shown, because this model lumps the pulmonary artery, pulmonary veins and left atrium into a single reservoir and so has neither a pulmonary resistance nor a pulmonary artery pulse to measure.

Drugs that do not fit the model

Ephedrine and hydralazine are on the page precisely because they cannot be simulated. Ephedrine is an indirect sympathomimetic whose defining behaviour — tachyphylaxis as the presynaptic vesicular stores deplete — is a state variable of the nerve terminal and not a receptor occupancy; no gain setting in an occupancy engine reproduces it. Hydralazine has no receptor to occupy, its mechanism is genuinely unsettled, and its twelve-hour effect is dissociated from its plasma half-life, so a concentration-driven model gives the wrong offset whatever gain is chosen. Naming the two assumptions each drug breaks teaches more than a fabricated grid row would.

Intended use

This is a teaching tool for cardiology and critical-care trainees. It is not a dosing calculator, not validated against any patient, and must never be used to choose or titrate a drug for a real person. Doses shown are the ranges printed on the United States prescribing information, reproduced for teaching; they are not a recommendation.