Acid-Base Physiology
References for Chapter 11 - Special Aspects of Acid-Base Physiology

Barela TD, Johnson JD & Hayek A. Metabolic Acidosis in the Newborn Period. Clin Endo Metab. 1983; 12: 429

Kreisberg R and Wood B. Drug and chemical-induced metabolic acidosis. Clin Endocrinol Metab 1983;12:391-411

Metabolic acidosis produced by drugs and/or chemicals can be conveniently divided into those with an increase in the anion gap (anion gap = Na- (Cl + HCO3)) and those with a normal anion gap. The increase in the anion gap is due to the accumulation of unmeasured organic anions, such as lactate or acetoacetate and beta-hydroxybutyrate, as occurs in ketoacidosis and lactic acidosis, or the accumulation of toxic anions such as formate or glycolate, as occurs with the ingestion of methanol or ethylene glycol. Increased
concentrations of lactic acid may also be present in the toxic forms of metabolic acidosis. The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide. In normal anion gap acidosis the reduction in bicarbonate is balanced by a reciprocal increase in the chloride concentration so that the sum of the two remains unchanged. Normal anion gap acidosis is caused by carbonic anhydrase inhibitors, hydrochloride salts of amino acids, toluene, amphotericin, spironolactone and non-steroidal anti-inflammatory drugs. The mechanism by which these substances produce metabolic acidosis and the therapy are discussed.

Lim VS et al. Acid-base Regulation in Pregnancy. Am J Physiol, 1976; 231: 1764.

Ozand PT & Gascon GG. Organic Acidurias: A Review. Part 1. J Child Neurol 1991; 6: 196-219.


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