At first this seems like a silly thing to do, but intravenous infusions of hydrochloric acid are sometimes used in Intensive Care Units in patients with chronic respiratory acidosis and high plasma bicarbonate levels as a way to more rapidly return the bicarbonate towards normal levels.
As an example, consider the infusion via a central line of 100 mls of 1N hydrochloric acid solution in a healthy adult. This represents an acute acid load of 100 mmols of H+ which is sufficient to cause a metabolic acidosis. The defence against changes in [H+] involves buffering, compensation and correction.
Buffering is a rapid physicochemical process that involves titration of the acid by the body’s extracellular buffers (predominantly bicarbonate). Assuming a [HCO3-] of 24 mmols/l and an extracellular volume of 19 liters, this represents a bicarbonate pool in ECF of about 450 mmols. An acid load of 100 mmols of [H+] will titrate the bicarbonate buffer to about 18.7 mmol/l (ie 350/450 x 24) assuming all the buffering is by bicarbonate.
The metabolic acidosis will stimulate the peripheral chemoreceptors resulting in an increase in ventilation. The resultant hypocapnia is the physiological compensatory response which returns pH towards normal. This response starts early but can take 12 to 24 hours to reach its maximum value. Compensation will not return pH completely to normal. The expected pCO2 at maximum compensation is:
Expected pCO2 = 1.5 x [HCO3-] + 8
where pCO2 is arterial pCO2 in mmHg and [HCO3-] is arterial bicarbonate (in mmol/l) calculated from arterial blood gases.
The kidney will excrete the excess acid anion (Cl-) and this is equivalent to reabsorption of bicarbonate & excretion of acid. Normal acid-base status will be restored.