Most of the clinical abnormalities of acid-base balance are self-limited. They relate either to an increase in the number of hydrogen ions entering the extracellular fluid (ECF) or to an extracorporeal loss of base. Sustained abnormalities most often result from disease of one of the two major organs concerned with acid-base regulation, the lung or the kidney.
A rational approach to the diagnosis and management of acid-base abnormalities requires an understanding of the physiologic processes concerned with hydrogen ion regulation. Conceptual clarity in this area has been abetted by the widespread utilization of the Bronsted-Lowry concept of acids and bases. In this view, simply stated, an acid is a proton donor and a base is a proton acceptor.1 Buffers minimize changes in hydrogen ion concentration by converting strong (completely ionized) acids and bases into weaker (less completely dissociated) acids and bases, respectively. In man, the major physiologically active buffer