Protective effects of acidosis

Abstract

The recent paper (Story et al. Anaesthesia 2001; 56: 530–3) provides a welcome demonstration of the utility of the Stewart approach to the analysis of acid–base disorders in critically ill patients. The authors are to be commended on their clear illustration of the potential of this methodology to offer mechanistic insights not readily attained with the more traditional Henderson–Hasselbach approach. The demonstration that decreases in plasma albumin, a common finding in critically ill patients, may have contributed to the alkalosis seen in their patients is of particular interest. The authors suggest that an acidifying effect of increasing plasma albumin concentration may play a role in the apparent adverse effect of albumin therapy reported in a recent meta-analysis [1]. This contention reveals a common and important misconception regarding acidosis and outcome from illness. While acidosis is clearly associated with poor outcome, this does not imply causation. Acidosis, particularly lactic acidosis, may indicate tissue hypoxia; however, acidosis per se is not necessarily harmful [2]. In fact, there is abundant evidence in the literature that acidaemia may exert protective effects in the context of acute organ injury. Acidosis, metabolic and/or respiratory, is protective in a variety of animal models of neurologic [3], cardiac [4] and pulmonary injury [5]. The mechanisms underlying the protective effects of acidosis are becoming increasingly clear, and include attenuation of key components of the inflammatory process, and reduction of cellular respiration and oxygen consumption [2]. A recent novel hypothesis [8], pointing out that acidosis protects against ongoing tissue production of further organic acids (by a negative feedback loop), provides a mechanism for cellular metabolic shutdown at times of nutrient shortage, e.g. ischaemia. This distinction between cause and association is of particular importance in regard to the practice of buffering, which remains a common, if controversial, practice [9, 10]. The physiological rationale for this practice is based on the concept that acidosis is directly harmful and therefore must be treated. However, there exist few if any data to support the practice of buffering acidosis. In fact, there is evidence from laboratory models of lung injury that buffering may abolish the protective effects of acidosis [7]. In summary, in the light of current evidence, it may be timely to re-evaluate our traditional concepts regarding acidosis.