In ARDS, when acidosis complicates LPV, the goal of alkali therapy is to maintain arterial pH at a safe level (> or = 7.20). A pure respiratory acidosis generally does not require alkali therapy. If the Pplat is greater than 30 cm H2O, and the respiratory rate equals the upper limit (35-40 breaths/minute), then V(E) is slowly titrated down by approximately 1 L/hour, so that PaCO2 increases by 10 mm Hg/hour or less. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on the type of acidosis, cardiorespiratory status, and lung mechanics. Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. Using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation. Under these circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. When renal failure is present, CRRT is indicated to manage acidosis. When ARDS is complicated by traumatic or hemorrhagic shock, overresuscitation with Cl(-)-rich solutions should be avoided to prevent metabolic acidosis.