CO₂ diffuses from the RBC into the plasma, then into the alveoli, and is exhaled.
4.1 Quick‑Reference Box
CO₂ distribution in blood
≈ 70 % as HCO₃⁻ (plasma) – primary transport route
≈ 23 % as carbamino‑Hb (inside RBCs)
≈ 7 % dissolved directly in plasma
5. Quantitative Relationship (Henry’s Law)
The amount of CO₂ dissolved in plasma (\(C\)) is directly proportional to its partial pressure (\(p{\text{CO}2}\)):
\[
C = kH \times p{\text{CO}_2}
\]
where \(k_H\) is Henry’s constant for CO₂ in blood. This explains why a rise in tissue pCO₂ leads to a proportional increase in dissolved CO₂, which then drives the hydration‑bicarbonate pathway.
6. Clinical Relevance (Brief)
Hypercapnia – elevated pCO₂ raises H⁺, causing respiratory acidosis; the bicarbonate buffer system (plasma HCO₃⁻) mitigates the fall in pH.
Chronic obstructive pulmonary disease (COPD) – impaired CO₂ removal stresses the plasma bicarbonate system, often leading to compensatory renal retention of HCO₃⁻.
Electrolyte disturbances – conditions that alter plasma Cl⁻ (e.g., massive transfusion, diuretics) affect the chloride shift and can modify CO₂ transport efficiency.
7. Summary of Key Points
≈ 70 % of CO₂ is carried in plasma as bicarbonate ion; this is why plasma is essential for CO₂ transport.
Carbonic anhydrase, located inside red blood cells, accelerates the conversion of CO₂ ↔ H₂CO₃.
H⁺ produced during hydration is buffered by haemoglobin, forming haemoglobinic acid (Hb‑H⁺).
The chloride shift moves HCO₃⁻ into plasma and Cl⁻ into RBCs, preserving electrical neutrality and cell volume.
Only ~7 % of CO₂ is transported dissolved directly in plasma; the rest is as carbamino‑Hb (≈23 %) and HCO₃⁻ (≈70 %).
O₂ is carried bound to Hb; its release is controlled by the sigmoid oxygen‑dissociation curve.
The Bohr effect (low pH/high pCO₂) and other right‑shift factors (temperature, 2,3‑BPG) promote O₂ release where metabolic demand is greatest.
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