Carbon Dioxide Transport

NCERT grounding

NCERT Class XI, Chapter 14 (§14.4.2 Transport of Carbon dioxide) fixes three numbers that the NEET paper recycles every cycle. Carbon dioxide is carried by haemoglobin as carbamino-haemoglobin (about 20–25 per cent), the binding being related to the partial pressures of CO2 and O2; nearly 70 per cent travels as bicarbonate (HCO3-) generated through the carbonic anhydrase reaction inside the erythrocyte; and the remaining slim fraction of about 7 per cent is physically dissolved in plasma. The NIOS Biology lesson on Respiration and Elimination of Nitrogenous Wastes (§14.2.4) adds the third route explicitly, with figures of 5–7 per cent dissolved, 21–23 per cent as carbamino compound and 75–80 per cent as bicarbonate. The NCERT closing line of the section is the one NEET likes to lift verbatim: every 100 ml of deoxygenated blood delivers approximately 4 ml of CO2 to the alveoli.

Three forms, one journey from tissue to alveolus

Active tissues burn glucose, fats and amino acids, and CO2 is the universal exhaust of that catabolism. A working cell maintains an intracellular pCO2 that is higher than the venous-blood pCO2, so CO2 diffuses outward across the cell membrane, through the interstitial fluid and into the systemic capillary. The capillary endothelium offers no barrier — CO2 is roughly 20 to 25 times more soluble in lipid bilayers than O2, which is why the small driving gradient at the tissue–blood interface still moves a large flux. Once CO2 is in the blood the body must store it stably for the seconds-long trip to the lungs, where it must come out again with equal speed.

That storage problem is solved by splitting the load three ways. A minor portion remains as free dissolved gas in plasma; a second portion is sequestered on the protein chains of haemoglobin; and the majority is converted chemically into bicarbonate. Each route has its own NCERT-fixed percentage, its own chemistry and its own NEET-favoured cue word.

Route 1 — Dissolved in plasma (~7 per cent)

Some CO2 simply stays as dissolved gas, obeying Henry's law: the amount of gas physically dissolved in a liquid is proportional to its partial pressure above the liquid. Because CO2 is significantly more soluble than O2 — Bunsen-coefficient ratios of roughly 20–25:1 — even a venous pCO2 of around 45 mm Hg dissolves more CO2 per millilitre of plasma than a similar pO2 would dissolve as O2. Even so, the dissolved fraction caps at only 5–7 per cent of the total CO2 the blood needs to carry. The dissolved pool is what actually sets the measurable pCO2 reading on a blood-gas analyser, and it is the pool that equilibrates first across the alveolar membrane.

Route 2 — Carbamino-haemoglobin (20–25 per cent)

CO2 also binds directly to haemoglobin, but at a different site from the one that holds O2. Oxygen sits on the iron (Fe2+) of the haem group; CO2 attaches to the free amino (-NH2) groups of the globin chains, forming a carbamino linkage and releasing a proton. The product is carbamino-haemoglobin (carbaminoHb), and the binding is reversible. NCERT states the binding is related to the partial pressure of CO2, with pO2 a major factor that influences it. When pCO2 is high and pO2 is low — exactly the chemistry of the tissues — more CO2 binds to Hb; when pCO2 is low and pO2 is high — exactly the chemistry of the alveoli — carbamino-haemoglobin dissociates and unloads CO2.

The HbO2 / carbaminoHb antagonism is the Haldane effect: deoxygenated haemoglobin is a better carbamino carrier and a better H+ buffer than oxygenated haemoglobin. Oxygenation at the lungs sharply lowers Hb's affinity for both CO2 and protons, helping to expel both. The Haldane effect is the CO2-side mirror of the Bohr effect (which describes how H+ and CO2 reduce O2 affinity at the tissues), and the two operate in unison: O2 loading drives CO2 unloading and vice versa.

Route 3 — Bicarbonate via carbonic anhydrase (~70 per cent)

The dominant route is chemical conversion. Inside every RBC sits a high concentration of the zinc-containing enzyme carbonic anhydrase (CA); minute quantities are also present in the plasma. NCERT identifies CA explicitly and writes the reaction it catalyses in both directions:

At a systemic capillary the sequence is precise. CO2 diffuses from tissue into plasma and from plasma across the RBC membrane. Inside the RBC, CA hydrates CO2 to carbonic acid (H2CO3); H2CO3 immediately dissociates into a proton (H+) and a bicarbonate ion (HCO3-). The proton does not stay free — it is buffered onto deoxy-haemoglobin, which acts as a strong buffer (this is one half of why deoxygenated Hb carries more CO2 — the Haldane effect again). The bicarbonate is now in surplus inside the RBC, so it diffuses outward into plasma down its concentration gradient through the band-3 anion exchanger. To preserve electrical neutrality the exchanger imports a chloride ion (Cl-) from plasma in return. This Cl- ↔ HCO3- swap is the chloride shift, also called the Hamburger shift after Hartog Jakob Hamburger who described it in 1892. The net effect: most of the CO2 leaves the RBC dressed up as HCO3- in plasma, while the Cl- that entered the RBC is held there as the counter-ion.

The cascade in order

Reversal at the alveoli

When venous blood reaches the pulmonary capillary the gradient flips. Alveolar pCO2 is approximately 40 mm Hg while incoming venous pCO2 is approximately 45 mm Hg, so CO2 diffuses out of the blood and into the alveolar air. As the dissolved CO2 fraction is removed, every other equilibrium shifts to compensate. Carbamino-haemoglobin dissociates because pCO2 has fallen and Hb is being simultaneously oxygenated (Haldane effect — oxy-Hb is a poor carbamino carrier). HCO3- diffuses from plasma back into the RBC; chloride leaves the RBC, reversing the Hamburger shift. Inside the RBC, HCO3- combines with the H+ released from oxy-Hb's buffering sites, reforms H2CO3 and — under the same CA enzyme — dehydrates to CO2 + H2O. The CO2 then leaves the RBC, crosses the alveolar membrane and exits with the next expired breath. The NCERT closing accounting line: every 100 ml of deoxygenated blood delivers approximately 4 ml of CO2 to the alveoli.

Partial-pressure accounting at each site

Two features of this table earn dedicated NEET-style questions. First, the tissue–alveolus pCO2 gradient is only about 5 mm Hg — modest compared to the 60 mm Hg drop for O2 — yet it suffices because CO2 is so much more diffusible. Second, atmospheric pCO2 of 0.3 mm Hg is essentially negligible; the gradient from alveolar air to atmosphere is generated almost entirely by expiration.

Comparing the two simultaneous shifts

Why ~70 per cent, not 100 per cent?

A common doubt is why the body does not push the whole CO2 load through the bicarbonate route, since it has the largest capacity. The simplest answer is rate of equilibration. The bicarbonate pathway depends on CO2 first crossing into the RBC, getting hydrated, and then HCO3- diffusing out. That sequence — though enzyme-accelerated — still takes finite time. The dissolved and carbamino pools, by contrast, equilibrate almost instantaneously and act as fast-response buffers. The 7 / 20–25 / 70 split is the steady-state outcome of all three routes operating in parallel under physiological conditions; it is not a fixed quota engineered by the cell. If CA were inhibited (for example by acetazolamide), the bicarbonate pathway would slow, CO2 would back up in the tissues and blood pH would drop — exactly the clinical picture of mild respiratory acidosis.

Worked examples

Common confusion & NEET traps