This mirrors the citations already sitting in the model's own code comments (the Live monitor tab's The math panel shows the live-substituted formulas themselves). Sources tagged loaded in this chat are documents Kyle supplied directly; sources tagged web-verified were located and checked against the model's constants during grounding passes on 2026-08-28 and 2026-09-10 — the full record is in the project's frc-ppl-pra-grounding.md and lagged-cvp-model-notes.md notes.

1. [1]Kenny JE. An Approach to Mechanical Heart-Lung Interaction, 1st ed.loaded in this chat
   The model's primary textbook. Grounds the Campbell-diagram/FRC concept (ch.1); the mmHg↔cmH₂O conversion 1 mmHg = 1.36 cmH₂O (ch.2, PPL_TO_MMHG); the Eq.12 transmission fraction fPpl=CL/(CL+CCW) and Crs=CL·CCW/(CL+CCW) (ch.1); the end-expiration CVP-measurement rationale (ch.7) and the three-simultaneous-effects passage on inspiration and Pra (ch.7); the Starling-resistor venous-return floor, ≈atmospheric (ch.2/ch.10); the "cardiac-function curve's x-intercept tracks intrathoracic pressure" mechanism behind shiftAndSeptalAt() (ch.8, citing Guyton and Marini); mean pulmonary artery pressure ≈14 mmHg at rest, citing ref [329] (ch.10, used for PA0); the ventricular-interdependence/septal-bowing mechanism, citing Jardin's status-asthmaticus study (ch.5–6); and the "pulmonary" vs. "extra-pulmonary" ARDS distinction (ch.9 p.289: in pulmonary ARDS the lung accounts for ≈80% of total respiratory-system stiffness, chest wall essentially preserved), used to set ards's chest-wall compliance equal to the model's own normal baseline (ccw:150 as of the 2026-09-16 Kenny-calibrated rescale — see the constants index below).
2. [2]Enfield KB. "Pulses Paradoxus — An Introduction to Heart-Lung Interactions" (talk), slide 17.Kyle's own talk
   "Actual vs. relative pressure" framing at FRC: 760 mmHg/0 cmH₂O at the airway opening vs. 756 mmHg/−4 cmH₂O in the pleural space. This is the model's own Ppl-at-FRC anchor in both breathing modes (respState()) and the diagram's initial Ppl/Pmsf placeholder labels — the 2026-09-10 recalibration moved the model from −5 to this exact number.
3. [3]Del Rio-Pertuz G, Nugent K, Argueta-Sosa E. "Right heart catheterization in clinical practice: a review of basic physiology and important issues relevant to interpretation." Am J Cardiovasc Dis 2023;13(3):122–137.loaded in this chat
   Table 2: clinical normal ranges — RAP 0–6 mmHg, PCWP 6–12 mmHg, mPAP 10–20 mmHg (via [PASP+2·PADP]/3). Grounds PA0=15, PCWP0=9, and the cvp0=7 Normal-preset baseline (sits at the top of this RAP range).
4. [4]Fujimoto N, Shibata S, Hastings JL, Carrick-Ranson G, Bhella PS, Palmer D, Fu Q, Levine BD. "Effects of pericardial constraint and ventricular interaction on left ventricular hemodynamics in the unloaded heart." Am J Physiol Heart Circ Physiol 2011;300:H1688–H1695.loaded in this chat
   Table 1: measured baseline RAP = 8.0±1.9 mmHg, PCWP = 11.4±2.3 mmHg in 50 healthy supine volunteers — real measured data, not an illustrative diagram value. Grounds PCWP0=9 and the cvp0=7 Normal-preset baseline (just under this measured mean). Also defines LVTMP = PCWP−RAP, an independent pericardial-constraint parallel to the deck's own Ppl/P_ra,tm transmural-pressure argument (discussed in frc-ppl-pra-grounding.md §5, not yet a modeled constant).
5. [5]Whelton PK, et al. "2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults." Hypertension 2018;71:e13–e115.web-verified
   Normal blood pressure defined as <120/<80 mmHg. Grounds SBP0=118, DBP0=76.
6. [6]Kussmaul A. "Ueber schwielige Mediastino-pericarditis und den paradoxen Puls." 1873.web-verified
   Original description of pulsus paradoxus in constrictive/effusive pericardial disease — "pulse simultaneously slight and irregular, disappearing during inspiration and returning upon expiration." Source of the classic >10 mmHg pulsus-paradoxus flag threshold in the readouts panel.
7. [7]Jardin F, et al. Circulation 1982;66(4):887.web-verified
   Status-asthmaticus septal-shift data — already Kenny's own reference [280]. Grounds the ventricular-interdependence/septalShift mechanism (interdep, tamponade and asthma presets).
8. [8]Yang F, et al. Front Physiol 2021. DOI: 10.3389/fphys.2021.639761.web-verified
   Echocardiographic cohort, 99 healthy adults measured at 500 m and again ~15 h after ascent to 4100 m: mPAP 14.4→18.1 mmHg (Δ3.7), PCWP 9.9→8.9 (Δ−1.0), brachial SBP/DBP 117/73→121/81. Grounds HPV_PA_BUMP=3.7, HPV_PCWP_DROP=1.0, HPV_SBP_BUMP=4, HPV_DBP_BUMP=8 — the hpvGain=1 anchor for the High-altitude preset.
9. [9]"Clinical review: Guyton — the role of mean circulatory filling pressure and right atrial pressure in controlling cardiac output." Critical Care 2010. DOI: 10.1186/cc9247.web-verified
   Notes that Guyton's theoretical zero RA-pressure intercept "had not been measured in a functioning cardiovascular system in humans," and that measured mean systemic filling pressure (Maas et al., 18.8 mmHg euvolemic supine) runs well above the classic teaching value. Context/caveat for the cvp0 recalibration decision, not a specific-constant citation.
10. [10]"Physiology, Central Venous Pressure." StatPearls (NBK519493).web-verified
    Clinically-cited normal CVP ≈8–12 mmHg — corroborates Fujimoto's [4] measured value. Supporting source for cvp0=7.
11. [11]Forbes LM, Bull TM, Lahm T, et al. "Right ventricular performance during acute hypoxic exercise." J Physiol 2024;602(21):5523–5537. DOI: 10.1113/JP284943.loaded in this chat
    Invasive haemodynamics in 10 healthy adults at rest and exercise under acute hypoxia (F_iO₂=0.12): mPAP rose to 20 [15–33] mmHg and RVSP to 54 [49–59] mmHg at hypoxic exercise, with RV contractility rising appropriately in step (afterload rises, contractile reserve is not the limiting factor). Citing Maggiorini et al. 2001, Forbes also reports mean PA pressures spanning "high teens to low 30s" in healthy adults at this same F_iO₂. Supporting source for the HAPE preset's hpvGain=3.5 target of mean PA in the low-30s.
12. [12]Müller J, Mayer L, Schneider SR, et al. "Pulmonary haemodynamics and right heart function during exercise at high versus low altitude in patients with pulmonary vascular disease: a randomised crossover trial." Heart 2026;112:28–36. DOI: 10.1136/heartjnl-2024-325605.loaded in this chat
    27 patients with PAH/CTEPH at high (2500 m) vs. low (470 m) altitude: resting systolic PAP significantly higher at altitude, total pulmonary resistance significantly higher at altitude (rest through peak exercise), and RV-arterial coupling lower at rest. A diseased population, distinct from the healthy-ascent physiology [8] the altitude preset is calibrated to — used here as qualitative support for the HAPE preset's "frankly pulmonary-hypertensive, afterload-stressed RV" framing at hpvGain=3.5, not as a direct calibration anchor.
13. [13]Michard F, Boussat S, Chemla D, et al. "Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure." Am J Respir Crit Care Med 2000;162(1):134–138.web-verified
    Cited by name in the deck's own walkthrough text as one source for the ≈12–13% SPV/PPV fluid-responsiveness threshold used to flag the readouts panel's SPV%.
14. [14]Marik PE, Cavallazzi R, Vasu T, Hirani A. "Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature." Crit Care Med 2009;37(9):2642–2647.web-verified
    Cited alongside [13] for the same ≈12–13% SPV/PPV threshold.
15. [15]Behazin N, Jones SB, Cohen RI, Loring SH. "Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity." J Appl Physiol 2009;108(1):212–218.web-verified
    51 obese vs. 10 nonobese anesthetized, paralyzed subjects: Crs and CL lower in obese, principally from lower lung volume, not lower chest-wall compliance (Ccw not significantly different); pleural pressure at relaxation volume higher in obese (12.5±3.9 vs. 6.9±3.1 cmH₂O). Grounds the Respiratory & Circulatory Curves tool's "Restrictive load" mechanism (positional shift of the chest-wall curve, not its slope) and slide s14's obesity discussion.
16. [16]Pelosi P, Ravagnan I, Giurati G, et al. "Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis." Anesthesiology 1999;91(5):1221–1231.web-verified
    PEEP 0 vs. 10 cmH₂O in obese vs. normal postoperative patients: PEEP improved elastance/compliance and oxygenation (r=0.81 with recruitment) in the obese group only — a recruitable, low-lung-volume picture, not fixed tissue stiffening. Supporting citation for slide s14's PEEP-reversibility point (the model itself does not yet make compliance a function of PEEP/operating volume — see the review notes).
17. [17]Broseghini C, Brandolese R, Poggi R, et al. "Respiratory mechanics during the first day of mechanical ventilation in patients with pulmonary edema and chronic airway obstruction." Am Rev Respir Dis 1988;138(2):355–361.web-verified
    Mean static respiratory-system compliance 35±5 mL/cmH₂O in ARDS patients on day 1 of ventilation. Grounds the ards preset's cl:46, ccw:150 (reproduces this Crs almost exactly — 35.2 vs. the literature's 35 — via the series formula, with chest wall left at the model's Kenny-calibrated normal per Kenny [1] ch.9's "pulmonary ARDS" phenotype).