1. INTRODUCTION

Most students consider the discussion of physiological acid-base balance a mystery. This is mainly because of the way the topic has been presented. At first reading of any text book on acid-base balance they realise that what they are reading is not consistent with chemistry previously learnt. The terminology is not consistent and they are very suspicious as to whether the concepts themselves are consistent (Cresse et al, 1962). They conclude that the subject is too complicated and shelve it.

The presentation in this book has, as far as possible, avoided the historical approach. Historical and some complex aspects have been relegated to footnotes or appendices. At first reading, the footnotes and appendices should be omitted. Having fully understood the general text, the traditional approach can be read without fear of confusion.

Traditional Approach to Blood pH

The 'traditional' approach to blood pH or what is called acid-base balance is embodied in such things as the text by Davenport (1974) or the article "Serious Acid-Base Disorders" by Kassirer, 1974.

In these, control of HCO3 is assumed to be a primary parameter. Abnormalities in pH are assumed to be of primary physiological significance and clinical information is de-emphasized. It is assumed that empirically discovered statistical associations between particular laboratory results and certain clinical disorders, work in both directions, i.e. if a particular clinical disorder, e.g. chronic respiratory failure has a certain renal induced HCO3 increase, then if the [HCO3] lies outside this range, something other than pure chronic respiratory failure is present. Such an approach is impossible as the clinical disorder has to be defined before it can be used to set the criteria for the laboratory findings. Deciding what is chronic respiratory failure includes these laboratory findings.

In my approach, pH is seen as the end result of many physiological factors which alter addition and removal of acids and bases. Diagnosis is primarily clinical in that:

1) The clinical states suggests the possibility of a pH disorder, and limits the possible subdivision of such disorders. Then chemical tests are used to confirm, exclude and/or quantitate a disorder. Laboratory measurements are not made routinely but only after some clinical screening which suggests that an abnormal pH might be present.

2) Incidental finding of an abnormal HCO3 or one of its derivatives in a serum electrolyte estimate will cause clinical questions to be asked about possible causes of pH change and further laboratory studies to confirm or exclude a blood pH disorder.

The traditional approach attempts to match up empirical, clinical and laboratory findings with postulated pathological states. My approach is the opposite in that there is an initial postulation of a possible abnormality which one then attempts to exclude if the means are clinical (physiological) or confirm if the means are chemical.

Let us take as an example the following: a routine serum electrolytes gives a HCO3 of 8meq/litre or 50meq/litre in a healthy young patient with a clinical diagnosis of acute appendicitis with only abdominal symptoms. One might conclude there was a mistake, and may or may not repeat the test. One would not give treatment unless the finding was confirmed and corroborated.