Treatment usually needs to be directed to correction of the primary cause if this is possible. In severe cases, intubation and mechanical ventilation will be necessary to restore alveolar ventilation.
The patient can deteriorate following intubation and ventilation which results in a rapid fall in pCO2 especially if the respiratory acidosis has been present for some time. This first became apparent when mechanical ventilation was instituted in the chronically hypercapnic patients during the polio epidemic in Copenhagen in about 1950. Rapid return of pCO2 towards normal was often accompanied by severe hypotension. Presumably the sympathetic stimulation due to hypercapnia resulted in patients who were relatively vasoconstricted and volume depleted. The acute drop in pCO2 decreased the sympathetic stimulation and hypotension resulted. These patients required significant fluid loading. (Incidentally, this epidemic and the experience in ventilating large numbers of patients resulted in the birth of ‘Respiratory Units’ which gradually evolved into the Intensive Care Unit of today. See Pontoppidan H et al. Respiratory Intensive Care. Anesthesiology. 1977; 47: 96-116 for more details)
In some other situations, it is preferable not to return arterial pCO2 to 40 mmHg with mechanical ventilation eg in patients with chronic CO2 retention from severe chronic obstructive airways disease. In some asthmatics presenting with severe bronchospasm (but not respiratory arrest), the problems associated with ventilation in this situation may suggest that administration of high oxygen concentrations to prevent hypoxaemia and tolerance of significant hypercapnia (‘permissive hypercapnia’) is a beneficial strategy. The idea is to adjust ventilation to allow adequate oxygenation using lower pressures which decrease the risk of barotrauma.
The correction of the elevated bicarbonate (renal compensation) associated with chronic respiratory acidosis may not be rapid. Return of plasma bicarbonate to normal requires renal excretion of the excess bicarbonate. The kidney has a large capacity to excrete bicarbonate but in certain abnormal conditions this capacity is impaired and the bicarbonate level remains elevated. This persistence of elevated bicarbonate despite resolution of the chronic respiratory acidosis is referred to by some as ‘post-hypercapnic alkalosis’. (See Case History 18 in Section 9.6)
The factors causing maintenance of high bicarbonate levels are the same as those involved in maintenance of a metabolic alkalosis. These factors are chloride depletion, potassium depletion, ECF volume depletion and reduction of GFR. (See Section 7.3 for discussion).
This situation occurs almost exclusively in ICU patients with chronic hypercapnia who are acutely ventilated back to a normal arterial pCO2. Chloride depletion occurring during the hypercapnia is probably the most important factor involved in the maintenance of the high bicarbonate levels. The coexistence of disorders which can cause a metabolic alkalosis is also important in many of these complicated ICU patients. The use of diuretics and loss of acidic gastric secretions (by nasogastric drainage) are usually the most important factors. It should be noted that high nasogastric drainage despite the use of H2-blockers such as ranitidine can still result in significant chloride losses which may not fully replaced by the IV fluids given to the patients. These patients are often avidly retaining sodium in the kidneys and this is associated with high levels of bicarbonate reabsorption. In general, bicarbonate levels in this situation are in the 30 to 45 mmol/l range.