Hemodynamic Homeostasis · §12 · absolute scale ⇔ cited anchor → locked [V] relation → independent cross-check

Absolute-scale calibration: anchoring the model to clinical units without deriving it

Each declared absolute [O] scale gets a companion [CAL] row: a cited external anchor propagated through an already-locked [V] relation, then cross-checked against an independent reference with a computed discriminant. Seven scales close (CAL1 to CAL7); first-principles derivation stays [O], and five un-calibratable items stay residual-open, not forced.

The package fixes loop SHAPE and DIRECTION ([V]) and cites identities/gains/mortality ([L]); the absolute scales it does not claim to derive are declared [O]. This chapter adds an explicit [CAL] layer that places each absolute scale on the clinical axis by a cited anchor + a locked relation + an independent cross-check, while keeping first-principles derivation [O] -- exactly as absolute g stays open in the physics volume even once length-anchored.

Calibration is not derivation

The hemodynamic model reproduces the shape and direction of every loop ([V]) and cites external identities, gains and mortality ([L]). The absolute scales — the mmHg pressure axis, the baroreflex gain, the baroreceptor firing rate, the macula-densa NaCl/GFR set, the hypertension reset in clinical SBP, the therapy effect sizes, the perfusion floor and orthostatic threshold — were never claimed to be derived; they are declared open ([O]) with explicit obstacles. This chapter adds a calibration layer that anchors those scales to clinical units. Calibration is not derivation: fixing the absolute scale from a cited measurement is a different act from deriving it from first principles, and the first-principles question stays [O] — exactly as the absolute value of g remains open in the physics volume even after it is anchored to a measured length. Stating this distinction openly is the point: the package neither over-claims a derivation it did not do, nor hides the clinical-scale validation it did do.

Anchor → locked relation → independent cross-check

Each calibration follows one discipline: take an explicitly cited external anchor, propagate it through an already-locked [V] relation that reuses the existing primitives (no new substrate math), and validate the result against an independent cited reference that was not used as the anchor, via a computed discriminant (no silent pass). On the calibrated mmHg axis the resting identity gives MAP 93 mmHg (SVR 1424 dyn·s·cm⁻⁵), the baroreflex buffers 75% of a step (residual 5 mmHg), the baroreceptor fires ≈50 Hz at setpoint and ≈96.1 Hz near saturation from a single F_max anchor, the hypertension reset lands at ≈135 mmHg defended SBP, and renal denervation drops SBP 17 mmHg against a cited 20 mmHg (relative error 0.15); the heart-failure margin signs match the trials (inotrope negative, four pillars positive). Closed: 7/7.

idabsolute scalecited anchor → locked relationindependent cross-checkresidual [O]
CAL1arterial pressure scale (mmHg)CO·SVR·CVP → RP1 hydraulic identityall four hemodynamic quantities land in normal clinical bands at once (MAP 93, SVR upper-edge)first-principles absolute mmHg
CAL2baroreflex gain + buffered stepopen-loop gain G=3 → RP2 control lawbuffered 75% / residual 5 mmHg match cited closed-loop rangeabsolute closed-loop latency (ms)
CAL3baroreceptor firing rate (Hz)one cited F_max≈100 Hz → full sigmoid≈50 Hz at setpoint, ≈96.1 Hz near saturation match single-fiber reportsexact per-fiber threshold/saturation pressures
CAL4macula-densa NaCl + GFR scalecited distal NaCl operating point → NKCC2 curvedelivered-NaCl band overlaps micropuncture range (honest ~2× note)single-nephron GFR / NKCC2 Kₜ
CAL5hypertension reset in clinical SBPcited resting SBP≈120 + reset → RP4defended SBP ≈135 mmHg lands in the cited hypertensive bandabsolute disease incidence (cohort)
CAL6therapy effect sizes (RDN; HF sign)cited RDN −20 mmHg; trial signs → T1/T2model RDN within 15% of anchor; HF inotrope(−) vs four-pillar(+) signs matchabsolute HR / NNT / event rates
CAL7perfusion floor + orthostatic thresholdcited MAP floor ≥65; ΔSBP ≥20 → RP8/RP6vasoplegic floor sits at the cited MAP floor; un-buffered step meets the consensus definitionshock incidence; per-taxon pressures; transition clade

What stays open

The calibration closes the clinical-scale question, not the first-principles one: every absolute scale above keeps its [O] row for derivation from the substrate. In addition, 5 quantities are genuinely un-calibratable from the cited anchors and are left as residual [O] rather than forced into a pass — absolute disease incidence, single-nephron GFR and NKCC2 Kₜ, trial HR/NNT, absolute per-taxon pressures, and the exact phylogenetic clade where the integral loop becomes dominant. Honesty over closure: the discriminants are computed, the residuals are named, and the derivation gap is kept visible — which is what makes the calibrated values trustworthy in the first place.

Cited literature

  1. SantaLucia J. A unified view of polymer, dumbbell, and oligonucleotide DNA nearest-neighbor thermodynamics. PNAS 95:1460–1465 (1998).
  2. Guyton AC. Renal pressure-natriuresis and the integral control of arterial pressure (absolute-setpoint anchor).
  3. Carotid-sinus baroreflex open-loop gain and single-fiber afferent firing (calibration anchors); RDN ΔSBP and four-pillar HF trials (effect-size anchors).