A vital function of Ve is to regulate arterial pH at, or close to, normal.
This can be accomplished if PaCO2 is controlled to remain in proportion to the current [HCO3-] level.
The law of mass action enables us to calculate blood pH:
pH = pK'+ log ([HCO3-]/(alpha*PCO2))
pK' is a constant with a value of 6.1 in plasma
alpha is the solubility coefficient, relating PCO2 in mm Hg to [CO2] in mM/L, having a value in plasma at 37*C of 0.03.
This equation means that pH will be defined by the ratio of HCO3- to alpha*PCO2.
Any normal ratio of HCO3- to alpha*PCO2 will give a normal pH regardless of whether both HCO3- and alpha* PCO2 are normal, both are proportionally low, or both are proportionally high.
The normal ratio of [HCO3-] to alpha*PCO2 is 20:1, i.e., normal plasma [HCO3-] is 24 mM per L, PCO2 is 40 mm Hg and CO2 solubility alpha is 0.03 mM/L/mm Hg.
An acute metabolic acidosis, caused, for example, by a sudden, exercise-induced increase in [lactic acid], results in a reduction of arterial [HCO3-].
The consequent fall in pH leads to a rapid stimulation of Ve, causing PaCO2 to decrease, ideally until the ratio [HCO3-] / PaCO2 is returned to normal and pH is therefore restored.
Similarly, for an acute metabolic alkalosis (i.e., pH acutely increased, causing [HCO3-] to rise), Ve should be reduced sufficiently to cause PaCO2 to rise until [HCO3-] / PaCO2 is returned towards normal.
Arterial pH may also be affected by respiratory acid-base disturbances; i.e., resulting from ventilatory control mechanisms.
If, for example, PaCO2 is caused to rise owing to alveolar hypoventilation, [HCO3-] / PaCO2 - and hence pH - will be low.
This condition is an acute respiratory acidosis, and is compensated for by renal retention of HCO3- (a process that may take several days to complete).
Similarly, acute reduction in PaCO2 - consequent, for example, to hypoxemia or voluntary hyperventilation - induces an acute respiratory alkalosis.
Renal mechanisms compensate by increasing the excretion of HCO3-, thereby reducing blood [HCO3-] and restoring [HCO3-] / PaCO2 towards normal.
Chronic Lung Disease
Some patients with chronic lung disease exhibit a compensated respiratory acidosis with chronic hypoxemia, hypercapnia, renal HCO3- retention and a relatively normal blood pH.
These patients can become insensitive to the chronically elevated PaCO2 so that their ventilation is predominantly stimulated by hypoxia.
Giving oxygen to correct the hypoxia can reduce ventilatory drive leading to a further increase in PaCO2.
This type of patient typically develops pulmonary hypertension in response to hypoxemia which can lead on to right-sided heart failure (cor pulmonale).