Stewart’s approach to acid base balance in critically ill patients

Abstract

Acid-base disorders are still a great problem in clinical practice, especially in emergency and intensive care units. Much of the confusion regarding acid-base chemistry relates the attempt to apply observational approaches, such as that of Henderson-Hasselbalch, and Schwartz and Brackett, to the entire spectrum of pathophysiologic processes. Many proposed theories for those disturbances have arisen over the years. In traditional acid-base theory, respiratory disorders are mediated by CO2 while metabolic derangements are caused by the production or removal of H⁺. In Stewart’s theory, respiratory disorders are also medicated by CO2. However, the three independent variables SID, [Atot] and PCO2 determine H⁺ and explain acid-base disturbances. A change in pH may be brought about only by a change in one or more of these variables and by no other means. The components of buffer base, HCO3⁻ and A⁻, are merely dependant variables and as such do not and cannot regulate H⁺. Unlike base excess, Stewart’s three independent variables may be used to both quantify and explain acid-base disorders. For example, Stewart’s model has been used to explain acid-base disturbances following the massive infusion of normal saline solution, albumin, and blood. Summary 72 Complex acid-base disorders are easier to understand, explain, and rationalize using Stewart’s methods compared with the traditional model. At the very least, Stewart’s variables are valid mathematically and may provide more useful clinical information than the older parameters such as base excess and anion gap. For these reasons, the Stewart approach has gained popularity in the intensive care unit setting. This “new approach” helps us to understand the underlying mechanisms of hyperchloremic acidosis, hyperalbuminemic acidosis, dilution acidosis, contraction alkalosis, and renal tubular acidosis leading to appropriate treatment. Physiologically, the kidney, intestine, and tissues each contribute to SID while the liver mainly determines Atot and the lungs PCO2. To examine the relationship between SID and Atot ,Wilkes et al.,1998 found that a low Atot was balanced by hyperchloremia, resulting in a low SID. In addition, Wilkes et al found a strong correlation between SID and PCO2. Together, these observations suggest that disturbances of SID are compensated by changes in PCO2 while disturbance of Atot are balanced by changes in SID. One may classify acid-base disorders based according to Stewart’s three independent variables. Acidosis results from an increase in PCO2 , Atot ,or temperature, or in a decrease in SID. Metabolic acidosis may be due to overproduction of organic acids (e.g., lactic acid, ketoacids, formic acid, salicylate, and Summary 73 sulfate), loss of cations (e.g., diarrhea), mishandling of ions (e.g., RTA) or administration of exogenous anions (e.g., poisoning). These all result in a low SID. Alkalosis results from a decrease in PCO2, Atot ,or temperature, or in an increase in SID. For example, metabolic alkalosis (e.g., due to vomiting) may be due to chloride loss resulting in a high SID