Learn Lesson 19 of 25
Shock phenotypes
Two patients have a MAP of 62 mmHg. Patient A has CI 3.8 and SVR 9 WU; patient B has CI 2.0 and SVR 20 WU with a wedge of 24. Which pairing is right?
Experiment: Normal adult at rest · unchanged from its starting state
Shock phenotypes at their preset state (same MAP can hide very different perfusion)
Computing phenotype table…
Units: MAP mmHg, HR bpm, CI L/min/m², SV mL, EF %, PAWP and RAP mmHg, SVR WU, CPO W, DO₂ mL/min, SvO₂ %. Compensation (tachycardia, vasoconstriction, venoconstriction) is part of each phenotype's fixed parameter set; no live reflex runs. Urine output, lactate and organ injury are not readouts of these numbers.
Named drugs: qualitative multi-target mappings (not doses)
| Drug | Class | Mechanism targets at medium strength | |
|---|---|---|---|
| Norepinephrine | α1 > β1 agonist | α1 arteriolar constriction (×1.6)α venoconstriction (recruits unstressed volume) (-200)β1 inotropy (modest) (×1.15) | |
| Epinephrine | β1/β2 and α agonist | β1 inotropy (×1.5)β1 chronotropy (+20)β2 vasodilation at low strength, α constriction at high (×1.1)venoconstriction (-200)β1 lusitropy (×0.9) | |
| Phenylephrine | Pure α1 agonist | α1 arteriolar constriction (×1.6)venoconstriction (-200) | |
| Vasopressin | V1 agonist | V1 arteriolar constriction (pulmonary resistance relatively spared) (×1.5) | |
| Dobutamine | β1 > β2 agonist | β1 inotropy (×1.5)β1 chronotropy (+10)β2 arteriolar dilation (mild) (×0.9)β1 lusitropy (×0.9) | |
| Milrinone | PDE-3 inhibitor (inodilator) | inotropy (cAMP) (×1.35)systemic arteriolar dilation (×0.75)pulmonary arteriolar dilation (×0.75)venodilation (+200)lusitropy (×0.9) | |
| Nitroprusside | Balanced arterial and venous NO donor | arteriolar dilation (×0.6)venodilation (+300) | |
| Nitroglycerin | Predominantly venous NO donor | venodilation (dominant) (+400)arteriolar dilation (weaker, higher strength) (×0.9)pulmonary vasodilation (mild) (×0.9) | |
| β-blocker | β1 antagonist | negative inotropy (×0.75)negative chronotropy (-20)slower relaxation (loss of catecholamine lusitropy) (×1.1) | |
| Cardiac myosin inhibitor | Mavacamten-type | reduced contractility (×0.8)improved relaxation (×0.9) Dynamic obstruction is not modelled; only the generic contractility and relaxation effects are shown. |
Current beat: MAP — mmHg, CI —, PAWP —, DO₂ — mL/min. Read the interpretation panel for the confirmed effects and the trade-offs.
Key measurements
Inspect beats and technical detailsbeat selection, transient versus settled, timings
Early beats after a change are transient: the circulation is still re-balancing. A beat is called settled when three consecutive windows agree within the tolerance. Playback speed only moves the cursor over the finished simulation; it never changes the heart rate.
Compare scenariosbaseline, snapshots, axes, export
Baseline
No baseline is set.
Comparison snapshots
Keep up to three snapshots of states you want to compare with the baseline and the current state.