Ventilatory Responses
Ventilation is quantitatively the most important mechanism of acid removal, given the enormous daily production of volatile acid compared to nonvolatile acid.
Ventilatory responses cannot return pH to 7.4 when a metabolic abnormality is responsible for the acid-base disturbance (intensity of the stimulus responsible for increases or decreases in alveolar ventilation will begin to diminish as pH returns toward 7.4).
Most patients cannot hyperventilate to below 20 mm Hg.
It is likely that the insult causing severe metabolic acidosis will also adversely affect respiratory muscle function, thus compromising the respiratory response.
Renal Responses
The day-to-day renal contribution to acid-base regulation is directed toward the conservation of bicarbonate and the excretion of hydrogen ions.
Almost all filtered bicarbonate must be reabsorbed from the glomerular filtrate to maintain the normal plasma bicarbonate concentration (25 mEq/L) and plasma pH.
Carbonic anhydrase facilitates the dissociation of carbonic acid into water and carbon dioxide that both enter the renal tubular cell. Inhibition of carbonic anhydrase by acetazolamide interferes with the reabsorption of bicarbonate ions from renal tubular fluid. As a result, excess bicarbonate ions are lost in the urine and the plasma bicarbonate concentration is decreased (Fig. 26-4).
Hydrogen ions are secreted into renal tubules by epithelial cells lining proximal renal tubules, distal renal tubules, and collecting ducts (facilitated by aldosterone).
Active hydrogen ion transport is inhibited when the urinary pH drops below 4.0. Thus, hydrogen ions must combine with ammonia and phosphate buffers in the renal tubular lumen to prevent the pH from decreasing below this critical level (Fig. 26-5).
The value of renal regulation of hydrogen ion concentration is not its rapidity but instead its ability to nearly completely neutralize any excess acid or alkali that enters the body fluids.