Pathophysiology and therapeutic strategy of respiratory acidosis

Out of 15–30 × 10–3 moles/day of protons derived from the hydration of CO2 only 40–60 × 10–9 moles/day remain unbounded in the plasma. If the CO2 production exceeds the excretion, the CO2 content in plasma and tissue rises (respiratory acidosis) until a new equilibrium is reached. In fact, doubling the PCO2 may compensate the halving of alveolar ventilation with unchanged excretion of the CO2 metabolically produced. Body reacts to respiratory acidosis increasing the secretion of chloride associated with ammonium. The process leads to an increase of bicarbonate in the plasma with an associated increase of pH. All the steps described may be altered in critically-ill patients due to hyper-metabolism, decreased excretion, decreased content of buffering proteins and impaired kidney response. Several options are available for therapy, from mechanical ventilation to artificial lung, up to lung transplant, depending on the severity of clinical conditions and their possible reversibility.