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 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. The sympathetic stimulation due to prolonged hypercapnia resulted in patients who were relatively vasoconstricted and volume depleted. 'Post hypercapnic alkalosis' (see below) may also contribute to the pathophysiology due to decreased myocardial contractility. The net result of such rapid correction of arterial pCO2 was hypotension. 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 inspiratory pressures and so decrease the risk of barotrauma.
If a chronically elevvated arterial pCO2 is returned to normal relatively quickly (as can happen if the patient is intubated and ventilated), then the patient is in the situation of having an elevated bicarbonate (due renal compensation) without there being the physiological need for it anymore. The elevated bicarbonate is typically slow to fall as return to normal requires renal excretion of the excess bicarbonate. The kidney normally has a large capacity to excrete bicarbonate but several factors, particularly chloride depletion, impairs this. Consequently, the bicarbonate level can remain persistently elevated; this state is referred to as ‘post-hypercapnic alkalosis’.
(See Case History 18 in Section 9.6)
The general factors causing maintenance of high bicarbonate levels in this situation 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 towards 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. These complex patients may also have other disorders which can themselves cause a metabolic alkalosis. In particular, the use of diuretics and loss of acidic gastric secretions (by nasogastric drainage) can be important factors in causing chloride depletion. Even with use of of H2-blockers (such as ranitidine), high nasogastric drainage can still result in significant chloride losses. These patients are often avidly retaining sodium in the kidneys and in the presence of low chloride levels, 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. Correction of fluid and chloride depletion leads to a fall in plasma bicarbonate levels.