Overview
Low, Medium and High are bounded effect levels, not administered doses. The vascular model generally normalizes these levels to one-third, two-thirds and full effect. Multiple drugs can contribute to a shared resistance, filling or contractility term; their labels remain available in the paused intervention reference.
There is no general pharmacokinetic simulation. Infusion onset, renal clearance, accumulation, receptor saturation, changing electrolytes, lactate and toxicity are not predicted. Turning a drug off reverses its modeled effect rather than waiting for a biological half-life.
Families and coupled responses
| Family | Modeled action and important interactions |
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| Norepinephrine, phenylephrine, vasopressin | Raise systemic vascular tone. Higher pressure may accompany lower native output when LV afterload or RV delivery limits ejection. Phenylephrine has a pulmonary-load term; HOCM can benefit from increased afterload. |
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| Dobutamine, epinephrine, dopamine, milrinone | Increase contractile support with differing systemic/pulmonary tone effects. Fixed obstruction limits recruitment; dynamic obstruction, depletion or hypotension can reverse benefit. Epinephrine/dopamine use nonlinear dose-level tone terms. |
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| Isoproterenol, ephedrine, atropine | Alter rate and/or vascular tone through distinct pathways. Atropine improves selected vagal sinus/AV-node responses but is not a universal cure for distal block or vasodepression. |
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| Nitroglycerin, nitroprusside, amyl nitrite | Reduce vascular tone and/or filling. Depletion, external constraint and dynamic obstruction can worsen. Selected well-perfused high-afterload LV failure or AR can gain forward flow; this is not a blanket treatment rule. |
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| Inhaled nitric oxide, IV epoprostenol | Reduce pulmonary resistance, with systemic dilation for IV epoprostenol. Greater pulmonary return can increase wedge when the left heart cannot accept additional flow. Benefit depends on coexisting valve/pump reserve. |
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| Fluids, furosemide | Change filling with phenotype-dependent forward response. Underfilled states may recruit flow; already congested/limited ventricles can gain pressure with little flow. No cumulative intake, urine output or bleeding balance is integrated. |
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| Metoprolol, digoxin | Rate/conduction changes are handled separately from negative or modest positive inotropy. Beta blockade opposes selected catecholamine effects; both can worsen protective bradycardia/escape or pre-excited AF scenarios. |
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How combined medications are resolved
Systemic resistance starts from the current vascular state and is multiplied by a combined drug factor. Pulmonary resistance receives a separate factor. Nominal flow receives a bounded, phenotype-specific multiplier; filling pressures receive preload and contractility contributions. The engine then resolves PA pressure, RV gradient and systemic pressure from the resulting flow/resistance.
Severe valve penalties use independent valve burdens. Mild disease does not inherit a full severe-stenosis penalty. A pulmonary vasodilator does not guarantee systemic improvement when severe MS, AS or LV failure constrains flow. Drug effects are not a list of independent fixed BP changes.
Selected response assumptions
The nitroprusside branch permits a monitored high-afterload LV-failure/AS example to improve flow when starting pressure is adequate and competing risk is absent. The AR branch can reduce modeled recirculation as forward flow improves. These branches represent selected study-informed directions; their numerical coefficients are original teaching choices.
All medication pages describe mechanism, route, example clinical dosing information, cautions and monitoring separately from simulator effect levels. Read the cited reference rather than translating a Low/Medium/High setting into a dose.
References & further reading