The main principles are:
- Correct the primary cause of the disorder
- Correct those factors which maintain the disorder (esp chloride administration in the common Cl- deficient cases)
Repletion of chloride, potassium and ECF volume will promote renal bicarbonate excretion and return plasma bicarbonate to normal.
Must Give Chloride
Chloride administration1 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.
Rarely, it may be advantageous to institute treatments (hydrochloric acid infusion, or acetazolamide) that can return the bicarbonate level to normal more quickly. These are not routine components of management, and should not deflect attention from correcting the primary cause and from correcting a chloride deficiency, but may be useful for occasional patients with 'resistant' metabolic alkalosis managed in an Intensive Care Unit.
Proton pump inhibitors (eg omeprezole) have been successfully used to decrease gastric acid loss and prevent or ameliorate metabolic alkalosis 2,3,4
7.6.2: Hydrochloric Acid Infusion
An infusion of hydrochloric acid 5 can be given via a central line 6,7,8. The correct placement of the line very important. It is confirmed by the ability to easily withdraw blood AND by x-ray confirmation of the tip position. Continued vigilance of the tip position is required; extravasation of acid from a central line has caused death9.
The infusion will selectively correct the chloride deficiency and the infusion can be titrated to an end-point of a specific bicarbonate level of pH level. The H+ will consume HCO3- provided the excess CO2 can be ventilated off.
Studies have shown that improvement in gas exchange occurs 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 ventilation7,10. The probable cause 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.
A HCl infusion is a dramatic way of administering chloride but published reports 7,11,12 attest to its safety and successful use. An increase in arterial pO2 and a decrease in pCO2 generally occurs and may assist with weaning from mechaical ventilation. The administration of chloride in a small volume 12 may be useful in patients who are at risk of volume overload.
(Further details about hydrochloric acid infusions)
7.6.3: Use of Acetazolamide
Acetazolamide is a carbonic anhydrase inhibitor which has also been used to speed the rapidity of correction of alkalosis 13. 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:
- Renal losses of water, Na+ and K+ increase (so appropriate adjustments in IV fluids and K+ supplementation are necessary)
- It interferes with CO2 transport
- It is slower acting and more difficult to titrate to a given bicarbonate level
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.
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- Kinahan TJ, Khoury AE, McLorie GA, and Churchill BM. Omeprazole in post-gastrocystoplasty metabolic alkalosis and aciduria. J Urol 1992 Feb; 147(2) 435-7. PubMed
- Hixson R and Christmas D. Use of omeprazole in life-threatening metabolic alkalosis. Intensive Care Med 1999 Oct; 25(10) 1201. PubMed
- Hsu SC, Wang MC, Liu HL, Tsai MC, and Huang JJ. Extreme metabolic alkalosis treated with normal bicarbonate hemodialysis. Am J Kidney Dis 2001 Apr; 37(4) E31. PubMed
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- Marik PE, Kussman BD, Lipman J, and Kraus P. Acetazolamide in the treatment of metabolic alkalosis in critically ill patients. Heart Lung 1991 Sep; 20(5 Pt 1) 455-9. PubMed