[box type=”download”] — Mode of transport of CO2 within plasma — Relation between CO2, carbonic acid and bicarbonate (detail of equation is required) — Chloride shift and the buffering effect of haemoglobin
— Carbaminohaemoglobin as a contributor to CO2 carriage [/box]
Blood can carry much more CO2 than O2, as can be seen in the CO2 dissociation curve.
This is also more linear than the O2 dissociation curve and does not plateau.
CO2 is transported as bicarbonate, carbamino compounds and simply dissolved in plasma.
Approximately 60% of CO2 is carried as bicarbonate.
Water and CO2 combine to form carbonic acid (H2CO3) and thence bicarbonate (HCO3-):
CO2 + H2O ⇔ H2CO3 ⇔ (HCO3– )+( H+).
The left side of the equation is normally slow, but speeds up dramatically in the presence of carbonic anhydrase, found in red cells.
Bicarbonate is therefore formed preferentially in red cells, from which it easily diffuses out.
Red cells are, however, impermeable to H+ ions, and Cl− enters the cell to maintain electrical neutrality (chloride shift).
H+ binds avidly to deoxygenated (reduced) haemoglobin (haemoglobin acts as a buffer), and so there is little increase in [H+] to impede further bicarbonate formation.
Oxygenated haemoglobin does not bind H+ as well, and so in the lungs H+ dissociates from haemoglobin and shifts the equation to the left, assisting CO2 unloading from the blood; the reverse occurs in the tissues.
Haldane effect – for any PCO2, the CO2 content of oxygenated blood is less than that of deoxygenated blood.
Formed by the reaction of CO2 with protein amino groups:
CO2 + protein-NH2 ⇔ protein-NHCOOH.
Haemoglobin forms carbaminohaemoglobin with CO2.
This occurs more readily for deoxygenated than oxygenated haemoglobin, contributing to the Haldane effect.
Carbamino compounds account for 30% of CO2 carriage.
Dissolved carbon dioxide.
CO2 is 20 times more soluble than O2 in plasma, and ∼10% of CO2 in blood is carried in solution.
Hyperventilation and hypoventilation
Doubling the rate of ventilation halves the alveolar and arterial PCO2.
Hyper and hypoventilation are defined in terms of arterial PCO2 (hyper: PCO2<5.3 kPa, and hypo: PCO2 >5.9 kPa).
Rapid breathing in exercise is not hyperventilation, as this is appropriate for increased CO2 production and PCO2 does not fall.
Hyperventilation cannot normally increase the O2 content, as arterial haemoglobin is already nearly fully saturated.
The fall in PCO2 (hypocapnia) during hyperventilation causes lightheadedness, visual disturbances due to cerebral vasoconstriction and muscle cramps (tetany).
Hyperventilation can be caused by pain, hysteria and strong emotion.
Hypoventilation causes a high PCO2 (hypercapnia) and a low PO2 (hypoxia), and may be caused by head injury or respiratory disease.