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Mild acidosis causes a mass action shift of the bicarbonate equilibrium towards the production of CO₂, which is blown off in the lungs to raise blood pH. Should acidosis continue in spite of this, another mechanism that kicks in below pH 7.14 is the buffering action of H₂CO₃.

Bicarbonate Buffering System

CO2	+	H2O		[H2CO3]		H+	+	HCO3-
from metabolism (volatile)		always available		unstable intermediate		the pH term		major species in blood

Even though H₂CO₃ is an unstable intermediate (see equation above), it can still serve as the conduit for the conversion of HCO₃^- and excess H⁺ to CO₂ and water, a process which becomes accelerated as blood pH gets closer to its pK_a of 6.14.

The further pH falls toward the pK_a of 6.14, the more powerfully these pH changes are resisted by the buffering capacity of the bicarbonate system. Thus, the pK_a of carbonic acid can itself impose staunch resistance to a lowered value of blood pH below 7.

The problem is that, unlike mild acidosis, the consumption of HCO₃^- in acute metabolic acidosis can outstrip the body's metabolic replenishment of this vital blood buffer, such that, if the acidotic incident is prolonged, the buffering capacity of the blood can become seriously depleted. Thus, with severe metabolic acidosis (e.g. ingestion of large amounts of acid) infusion of bicarb may be necessary.