Critical Care and Resuscitation 1999
fluids which on infusion have entirely different effects on metabolic acid-base status. The term ‘post infusion acidosis’ seems merely confusing. Dr Story et al, also object to my contention that Plasmalyte, which has an intrinsic SID of around 50 mEq/L after metabolism of the contained acetate and gluconate, is unlikely to cause a metabolic acidosis unless these organic anions are incompletely metabolised. They refer to a study involving patients subjected to cardiopulmonary bypass. This study is unpublished at the time of writing and thus it is hard to comment without knowledge of the detail. Nevertheless, we were originally informed that in patients for whom the pump had been primed with Plasmalyte, the median arterial base excess post-bypass increased by 1.1 mEq/L compared with pre-bypass values. Dr Story et al, now tell us that in these same patients, standard base excess initially fell by 4.4 mEq/L on commencement of bypass. If the original information is correct, they can not claim that priming with Plasmalyte produced a metabolic acidosis post-bypass. In fact the trend was towards a metabolic alkalosis. I can only assume that the authors were able to show that the transient reduction in base excess while on cardiopulmonary bypass was not due to my suggested mechanism – namely incomplete metabolism of acetate and gluconate. If that was not shown, I do not understand the objection. I await the paper with interest. x
fluids which on infusion have entirely different effects on metabolic acid-base status. The term ‘post infusion acidosis’ seems merely confusing. Dr Story et al, also object to my contention that Plasmalyte, which has an intrinsic SID of around 50 mEq/L after metabolism of the contained acetate and gluconate, is unlikely to cause a metabolic acidosis unless these organic anions are incompletely metabolised. They refer to a study involving patients subjected to cardiopulmonary bypass. This study is unpublished at the time of writing and thus it is hard to comment without knowledge of the detail. Nevertheless, we were originally informed that in patients for whom the pump had been primed with Plasmalyte, the median arterial base excess post-bypass increased by 1.1 mEq/L compared with pre-bypass values. Dr Story et al, now tell us that in these same patients, standard base excess initially fell by 4.4 mEq/L on commencement of bypass. If the original information is correct, they can not claim that priming with Plasmalyte produced a metabolic acidosis post-bypass. In fact the trend was towards a metabolic alkalosis. I can only assume that the authors were able to show that the transient reduction in base excess while on cardiopulmonary bypass was not due to my suggested mechanism – namely incomplete metabolism of acetate and gluconate. If that was not shown, I do not understand the objection. I await the paper with interest. Finally there is the question of ‘hypoproteinaemic alkalosis’. Many advocates of the Stewart approach, including Dr Story and colleagues, insist that this is a clinical entity. However the evidence for its existence in vivo is at best slim. The in vitro study referred to merely confirms that alteration of ATOT (which in plasma is primarily albumin) changes the normal range of SID (but not PCO2). This is no surprise. 3 However it does not mean that hypoalbuminaemia causes metabolic alkalosis in vivo. For example, one of the most dramatic acute reductions in plasma albumin concentrations occurs in burns patients resuscitated with crystalloid 4mL/kg/% burn in the first day. At the end of that time total protein concentrations are often halved and plasma albumin almost disappears. The only metabolic acidbase disturbance seen under these circumstances is metabolic acidosis and hyperchloraemia, (usually without elevation of plasma lactate concentrations or renal dysfunction). If acute hypoproteinaemia is a genuine cause of metabolic alkalosis, why don’t we see it in any of these extreme examples? All of this aside, it should be pointed out that the appropriate reference compartment in vivo for acid-base status is not plasma – it is the extracellular space. The stability of standard base excess (an extracellular space parameter) in acute respiratory acid-base disturbances
