The main principles are:
Repletion of chloride, potassium and ECF volume will promote renal bicarbonate excretion and return plasma bicarbonate to normal.
Chloride administration is essential for correction of chloride-depletion metabolic alkalosis and the alkalosis can be corrected with chloride even if volume depletion persists. Because of electroneutrality requirements it is not possible to give chloride alone, so 'giving chloride' is equivalent to 'giving saline' in most cases. (One exception to this is giving a dilute HCl infusion -see below)
Volume administration will not correct the alkalosis unless the administered fluid contains chloride. This is not difficult though as all available ECF replacement fluids contain chloride so administering these IV fluids to correct the volume deficiency must necessarily replenish chloride.
Maintenance IV fluids (eg 5% dextrose) are poor at replenishing IV volume and contain little or no chloride; they are not useful for this correction and should not be used.
Mineralocorticoid excess causes renal potassium wasting. This can maintain a metabolic alkalosis even in the absence of chloride depletion.
Rarely, it may be advantageous to institute treatments (eg HCl infusion; acetazolamide) that can return the bicarbonate level to normal more quickly.
An infusion of hydrochloric acid (HCl) can be given via a central line. This will selectively correct the deficiency of Cl- and H+ and the infusion can be titrated to an end-point of a specific bicarbonate level. The H+ will consume HCO3- provided the excess CO2 can be ventilated off.
Studies have shown that improvement in gas exchange results with a fall in arterial pCO2 and an increase in arterial pO2. These changes were originally considered to be due to the increase in ventilation that occurs (and the subsequent decrease in pulmonary microatelectasis) but the paO2 will increase even in patients maintained on constant ventilation! The probable reason is an improvement in ventilation-perfusion matching. Alkalosis impairs the efficiency of hypoxic pulmonary vasoconstriction so its correction could acutely result in improvements in the lung’s V/Q matching and an increase in arterial pO2.
The correction of alkalosis will also result in a right shift in the oxygen dissociation curve which will improve peripheral oxygen unloading.
(Further details about hydrochloric acid infusions)
Acetazolamide is a carbonic anhydrase inhibitor which has also been used to speed the rapidity of correction of alkalosis. It is usually more readily available than sterile hydrochloric acid solutions and is a more acceptable therapeutic option. It causes renal bicarbonate loss to increase and plasma bicarbonate levels fall. Only one or two doses probably should be used. Some problems with acetazolamide are:
Other sources of HCl have been used (eg lysine HCl, ammonium chloride). Hepatic metabolism of the ammonium generates hydrogen ions.
These ancillary measures may prove useful in a small number of patients but are not generally recommended.
1. Marik PE, Kussman BD, Lipman J, Kraus P. Acetazolamide in the treatment of metabolic alkalosis in critically ill patients. Heart Lung 1991;20(5 Pt1): 455-9
2. Rosen R, Julian B et al. On the mechanism by which chloride corrects metabolic alkalosis in man. Am J Med 1988 Mar; 84(3 Pt 1): 449-58