Two experiments, deliberately separated
The labeled free-particle scene is a fixed inlet-pressure snapshot across an alveolar–capillary interface. The content chart and capacity rack add a separate oxygen-only reference-pass model. Moving carriers now carry two magnified exchange cues: green for O₂ and pink for CO₂. The tissue scene is a whole-body metabolic ratio. It is not a coupled cardiopulmonary simulator. Decorative vehicles, cells, and particles are schematic and do not represent measured volumes or transit times.
Pressure gradients and Fick’s law
ΔPO₂ = PAO₂ − PincomingO₂
ΔPCO₂ = PincomingCO₂ − PACO₂
V̇gas ∝ Dgas × (A/T) × ΔP
For each gas, diffusion conductance depends on its own diffusivity D, exchange area A, and barrier thickness T. Positive displayed O₂ gradients point toward blood; positive displayed CO₂ gradients point toward air. Negative gradients reverse those directions. At zero gradient, random exchange continues in both directions with no net transfer.
The normal teaching snapshot uses alveolar PO₂ 100 and PCO₂ 40 mmHg; incoming capillary PO₂ 40 and PCO₂ 46 mmHg. These are rounded illustrative values, not reference intervals. The oxygen slider spans 0–115 mmHg, matching the preceding oxygen-curve notebook; this is an interface range, not the full physiological range.
M = (selected area / 100%) / relative thickness
O₂ transfer index = 100 × M × |ΔPO₂| / 60
CO₂ transfer index = 100 × M × |ΔPCO₂| / 6
Each index compares one gas with its own normal example. Within each gas, D is held fixed and cancels from the relative calculation. The two 100% values are not equal molar fluxes. CO₂ has much greater solubility than O₂; neither its physical diffusion coefficient nor its equilibration time can be read from particle speed. The colored bars saturate visually at 200%, while their numerical labels remain unclipped.
The visual net-particle rate is proportional to its gas’s index up to a display cap; a minimum and maximum crossing duration keep the motion visible. Gas directions, displayed pressures, and index calculations are not altered for styling. Smaller active area localizes the visible crossings to the remaining interface. At zero area there is no transmembrane passage, although particles continue moving on either side.
RQ and its inputs
RQ = V̇CO₂ / V̇O₂
V̇CO₂ = RQ × V̇O₂
Default: 0.80 × 250 = 200 mL/min
Inputs use consistent gas-volume units (conceptually STPD). RQ is dimensionless. Presets are fat ≈0.70, a mixed-substrate example of 0.80, and carbohydrate 1.00. This model restricts RQ to 0.70–1.00 to teach common oxidative-substrate examples; it does not assert that every physiological or measured ratio must fall within those bounds.
The token diagram is normalized to 10 O₂ volume units. CO₂ units = 10 × RQ. Changing V̇O₂ changes calculated V̇CO₂ and the conceptual metabolic flow animation, but not that normalized ratio. RQ is not the ratio of gas partial pressures, inhaled/exhaled total volumes, or local snapshot diffusion indices.
The gas-exchange ratio measured at the mouth is RER. In a suitable metabolic and gas-store steady state, RER approximates tissue RQ. Transient ventilation, bicarbonate buffering, and CO₂ storage changes can separate them. The page does not infer diet, nutrition adequacy, or clinical status from an RQ value.
Where the analogy stops
The membrane is not an open loading gate; gases diffuse through a thin tissue–fluid barrier. Hemoglobin carries most blood oxygen, whereas much blood CO₂ is carried chemically as bicarbonate. Molecular CO₂, not a bicarbonate ion, diffuses into alveolar air. Carrier count schematically represents the selected Hb amount, not a cell count or hematocrit. The moving green strips show magnified O₂ change from the separate oxygen-loading model below; they no longer display total Hb saturation. Pink strips are schematic CO₂ unloading cues, not Hb-bound CO₂ or total CO₂ content. The particle scene still illustrates the inlet pressure snapshot; it does not count the amount of oxygen loaded into each moving cell.
The oxygen-only loading extension uses a fixed-affinity content curve and a simplified reference-pass profile. No alveolar gas equation, systemic arterial mixing, shunt, V̇/Q̇ distribution, perfusion adjustment, pH or temperature adjustment, CO₂ content or buffering kinetics, or tissue oxygen delivery is computed. Alveolar and incoming-blood pressures stay at the selected values. The labeled free particles and transfer indices refer to those inlet pressures; they are not a map of local gradients throughout the capillary. Only the separate O₂-loading model computes a reference end-capillary state. It is not a prediction of systemic arterial blood gases. The thick-wall and reduced-area buttons isolate membrane effects rather than simulate all effects of edema, fibrosis, or emphysema.
Hemoglobin capacity and the oxygen-loading extension
Anemia and polycythemia examples change Hb to 7 and 20 g/dL, respectively; the reference is 15 g/dL. They are demonstration values, not diagnostic cutoffs. The combined high-Hb/low-diffusion example additionally sets membrane thickness to 4×. Polycythemia itself is not assigned a membrane defect. Measured DLCO can be higher with more Hb and lower with anemia; it must not be equated with the area/thickness factor used here. [6,7]
Hb capacity = 1.34 × Hb
S(P) = (P³ + 150P) / (P³ + 150P + 23400)
C(P,Hb) = 1.34 × Hb × S(P) + 0.003 × P
S is a fraction, not a percentage. C is mL O₂ per dL of blood, Hb is g/dL, and P is mmHg. The normal-affinity Severinghaus approximation connects pressure with saturation. It does not shift when Hb changes. The 1.34 and 0.003 constants are conventional teaching approximations. The outlined cargo rack is Hb capacity only; dissolved O₂ is displayed separately. [7,8]
M = (area / 100%) / relative thickness
dC/du = K × M × [PAO₂ − P(u)]
K = 0.30 mL O₂ / (dL · mmHg) per reference pass
u = 0 → 1; C(0) = C(PincomingO₂,Hb)
This content-balance model has a fixed, dimensionless reference contact opportunity. K is an illustrative model parameter, not a measured diffusing capacity or a validated disease calibration. It makes the baseline sample nearly equilibrate with 100 mmHg air by the end of the reference pass. Inverse content is solved by monotonic bisection in 400 implicit steps, bounded between incoming and alveolar pressures. A lower M slows loading. More Hb increases capacity and the oxygen amount needed for a given saturation change. An intact reference membrane can still nearly fully equilibrate in the polycythemia-only example.
The profile is a content calculation, so O₂ gained = exit content − incoming content; it can be negative when the O₂ gradient is reversed. Zero area gives no uptake and preserves incoming content. The dashed reference uses Hb 15, normal area/thickness, and the same selected incoming/alveolar O₂ pressures. The current path, exit saturation, content, and green exchange cues use the same lookup profile. The capacity rack below the animation still compares bound oxygen only and does not silently include dissolved gas in Hb capacity. The moving green strips instead magnify the change in total O₂ content during this pass; they are not saturation meters.
Neither anemia compensation, viscosity effects, cardiac output, nor capillary recruitment is simulated. Do not use higher calculated content to conclude that polycythemia improves tissue oxygen delivery. CO₂ transport remains the original independent inlet snapshot; altered Hb does not calculate a Haldane effect. RQ, oxygen consumption, and CO₂ production are not fed back into these imposed lung pressures.
Reading the green and pink bars
In the usual lung example, the green strip begins almost empty on the left and grows; the pink strip starts high and shrinks. This is a magnified view of the change during the pass, not an assertion that incoming blood has almost no oxygen or that exiting blood has almost no carbon dioxide. Existing incoming O₂ content, saturation, exit values, and the Hb-capacity rack are unchanged.
O₂ display progress = clamp(|C(u) − C(0)| / [C(100,Hb) − C(40,Hb)], 0, 1)
CO₂ display progress = clamp(u × CO₂ inlet transfer index / 100, 0, 1)
Loading cue = 8% + 84% × display progress
Unloading cue = 92% − 84% × display progress
The 8% and 92% limits are visual margins, not physiological percentages. O₂ uses the existing modeled content change relative to a fixed 40-to-100 mmHg reference change at the selected Hb. This makes impaired loading visible instead of scaling every curve to a full bar. The pink cue is a deliberately simple linear illustration tied to the selected CO₂ inlet gradient, membrane factor, and position. It does not calculate CO₂ content, removal fraction, local capillary PCO₂, bicarbonate kinetics, or a CO₂ equilibration time. The two progress scales are independent; matching lengths are not equal gas amounts, and they are not linked to RQ.
Reversing a gas gradient reverses that bar’s change. Equal pressures give no net change for that gas. Zero active area freezes both bars at their entry state. More Hb still means more schematic carriers. The pink strip is associated with a moving blood sample for illustration; it does not imply that all CO₂ is physically carried on hemoglobin. The quantitative O₂-capacity panel remains the place to read actual modeled content and saturation.
Sources and further reading
References support the physiology. The illustration, user interface, normalized indices, and demonstration presets are original teaching constructions, not clinically validated models.
- National Heart, Lung, and Blood Institute. How the Lungs Work: What Breathing Does for the Body. Overview of oxygen delivery and carbon dioxide removal.
- National Library of Medicine. Gas exchange. Alveoli, capillary blood flow, and gas exchange.
- OpenStax. Anatomy and Physiology 2e, §22.4: Gas Exchange. Partial pressures, diffusion, and relative gas solubility. §22.5: Transport of Gases. Hemoglobin and bicarbonate transport.
- Price, E. R., & Mager, E. M. (2020). Respiratory quotient: Effects of fatty acid composition. Journal of Experimental Zoology Part A, 333(9), 613–618. doi:10.1002/jez.2422. Substrate dependence and the approximate nature of fat RQ.
- Ramos-Jiménez, A., et al. (2008). The respiratory exchange ratio is associated with fitness indicators both in trained and untrained men. Clinical Medicine: Circulatory, Respiratory and Pulmonary Medicine, 2, 1–9. doi:10.4137/ccrpm.s449.
- Burgess, J. H., & Bishop, J. M. (1963). Pulmonary diffusing capacity and its subdivisions in polycythemia vera. Journal of Clinical Investigation, 42, 997–1006. doi:10.1172/JCI104804.
- High Oxygen Partial Pressure Decreases Anemia-Induced Heart Rate Increase Equivalent to Transfusion. Original human hemodilution study; discussion distinguishes Hb-bound and dissolved oxygen.
- Severinghaus, J. W. (1979). Simple, accurate equations for human blood O₂ dissociation computations. Journal of Applied Physiology, 46, 599–602. doi:10.1152/jappl.1979.46.3.599.
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