Mechanisms for acid–base balance

Respiratory regulation

The lungs provide rapid, minute-to-minute acid-base regulation by adjusting CO2 excretion via alveolar ventilation - the fast-acting partner to the kidney's slower bicarbonate-based regulation
Respiratory compensation for a metabolic disturbance occurs within minutes to hours, far faster than the kidney's 1-3 day response to a respiratory disturbance

CO2 + H2O <-> H2CO3 <-> H+ + HCO3- (carbonic anhydrase-catalysed) - increased ventilation blows off CO2, shifting the equation left and consuming H+ (raising pH); reduced ventilation retains CO2, shifting right and generating H+ (lowering pH)
Central chemoreceptors (medulla, sensing CSF pH/PaCO2) and peripheral chemoreceptors (carotid/aortic bodies, sensing PaO2 predominantly, and PaCO2/pH) drive ventilatory drive
Chronic CO2 retainers (severe COPD) progressively lose central CO2 responsiveness and become relatively more dependent on hypoxic drive via peripheral chemoreceptors - the physiological basis for cautious, titrated oxygen therapy in this group

Expected respiratory compensation for a metabolic acidosis/alkalosis can be calculated (Winter's formula for metabolic acidosis) - a measured PaCO2 outside the predicted range indicates a mixed acid-base disorder, not compensation alone

Mechanical ventilation settings are titrated using this relationship (increase minute ventilation to correct acidosis, and vice versa)
Permissive hypercapnia is deliberately tolerated in some ventilation strategies (e.g. ARDS lung-protective ventilation) to avoid the harms of high tidal volumes

COPD (chronic CO2 retention, hypoxic drive), metabolic acidosis compensation, ARDS ventilation strategy

Loss of central CO2 sensitivity in chronic retainers is why controlled, titrated oxygen (not high-flow) is used in COPD exacerbations at risk of hypercapnic respiratory failure

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