Respiratory Acid-Base Control

Overview
  • The lungs can exert significant control over the extracellular fluid pH by modulating the partial pressure of arterial carbon dioxide (PaCO2). This capacity can be used for medium-term correction of acid-base disturbances; however, such processes do not represent a long-term solution as the requisite changes in respiration cannot be maintained indefinitely without consequences.
Mechanism
  • As discussed on the Bicarbonate Buffer page, the overall ECF pH is largely determined by the ratio between the arterial partial pressure of CO2 (PaCO2) and the ECF concentration of bicarbonate (HCO3-). The lungs can rapidly modify the PaCO2 of the arterial blood by changing their rate of alveolar ventilation (See: Alveolar Ventilation). By doing so, the lungs can exert powerful control over the ECF pH simply by changing the ratio of PaCO2 to ECF bicarbonate.
  • In contexts of acidosis, the alveolar ventilation rate is increased, reducing the PaCO2, and thus increasing the ECF pH. In contrast, when alkalosis is encountered, the alveolar ventilation is decreased, increasing the PaCO2, and thus reducing the ECF pH.
  • A less technical conceptualization may reference the fact that the Weak Acid form of the bicarbonate buffer is essentially dissolved gaseous CO2 (See: Bicarbonate Buffer). Because the lungs are able to "Breathe off" this acidic form of the bicarbonate buffer, the lungs can powerfully modulate the ECF pH. Increased breathing and in turn boosted alveolar ventilation reduce CO2 levels, thus increasing ECF pH; in contrast, reduced breathing with concomitant reduced alveolar ventilation allows build up of CO2, thus reducing ECF pH.
Regulation