Printed from acutecaretesting.org
April 2008
Acid-base balance - one for the novice, one for the expert
Summarized from Edwards S. Pathophysiology of acid-base balance: the theory practice relationship. Intensive and Critical Care Nursing 2008; 24: 28-40 Morris CG, Low J. Metabolic acidosis in the critically ill: Part 1. Classification and pathophysiology. Anaesthesia. 2008; 63: 294-01. Part 2 Causes and treatment. Anaesthesia 2008; 63: 396-411.
Two very different reviews of acid-base pathophysiology are recently published. The first, written by a nurse educator is a comprehensive overview and serves as an introduction to the topic. The approach is familiar and reflects standard physiology texts.
After a very brief synthesis of the significance of respiratory and renal systems for maintenance of blood pH and explanation of the concept of partial pressure of a gas, the bicarbonate buffer system is introduced. The rest of the article focuses in turn on each of the four categories of acid-base disturbance: respiratory acidosis, metabolic acidosis, respiratory alkalosis and metabolic alkalosis.
For each of these there is discussion of the causes and the compensatory mechanisms they invoke to maintain normal blood pH. Consideration is given to how the results of arterial blood gas analysis (pH, pCO2 and bicarbonate) are used to identify each of the four disturbances.
Whilst this first review is clearly aimed at the student with little or no previous knowledge of acid-base physiology, that cannot be said of the second, which assumes a considerable grounding in the subject on the part of the reader.
Aimed at clinicians (anaesthetists, intensivists) who have to make treatment decisions on behalf of patients suffering acid-base disturbance, this two-part review is confined to metabolic acidosis, a common feature of critical illness.
Discussion goes well beyond that available in standard texts, and includes not only the familiar CO2/HCO3– model of acidosis based on the Henderson-Hasselbach equation, but also the physiochemical model based on strong ion difference (SID) attributed to Stewart. Clinical utility and limitations of base excess and the anion gap are discussed.
The argument for anion gap to be corrected for serum albumin in critically ill patients is made. In the second part of the review, three broad causes of metabolic acidosis: lactic acidosis, ketoacidosis and acidosis induced by drugs and toxins are discussed in some detail.
Finally treatment options based on identifying the cause of acidosis are considered. With a total of 252 references, this two-part review is a considerable resource for those with a clinical interest in metabolic acidosis.
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