ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

For more than 15 years, an alternative view of the universe has been available for acid-base physiology. While conceptually new, this analysis, originally presented by Peter Stewart, is based on the same underlying fundamental principles used in more traditional treatments of acid-base. When properly translated, all approaches are mathematically interchangeable. The difference, however, is that the Stewart approach emphasizes mathematically independent and dependent variables. By this definition, bicarbonate and hydrogen ions are dependent variables and thus represent the effects rather than the causes of acid-base derangements. Neither bicarbonate nor pH can be regulated directly; rather, they are controlled by the independent variables. In blood plasma there are three independent variables: PCO2, weak acids, and the strong ion difference. The strong ion difference is the difference between completely dissociated cations (e.g.,Na+) and completely dissociated anions (e.g.,Cl–)

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Crystalloid solutions for intravenous use have complex physiologic effects. The acid-base approach of the late Peter Stewart is useful in analyzing some of these effects. The difference between the sum of the strong cations and the sum of the strong anions (strong ion difference) is an independent controlling factor of acid-base. Water acts as an acid, dissociating to supply hydrogen ions. Infusion of water induces a metabolic acidosis through a reduction in the strong ion difference. Dextrose infusion will also produce acidosis, which may be modified by the biochemical effects of glucose metabolism. Normal saline solutions produce perioperative acidosis through a reduction in strong ion difference. The acidosis is greater than the acidosis produced by solutions such as Ringer’s Lactate, which contain multicarbon anions. Intracellular uptake and metabolism of the multicarbon anions lead to alkalosis. All crystalloid infusions induce alkalosis by dilution of plasma weak acids, particularly albumin. The total concentration of weak acids is another independent controlling factor in the Stewart approach. Ringers’s Lactate also reduces plasma osmolality. Polyvinylchloride containers leach contaminants, such as phthalate derivatives, into the solutions. The physiologic importance of these effects is unclear.

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Colloids are an unusual state of matter of macromolecules with diameters between 1 and 100 nanometers. Macromolecules in clinical use include albumin, polygeline, and pentastarch. According to the approach of the late Peter Stewart, weak acids associated with these macromolecules will increase the total weak acid concentration. An increase in total weak acid concentration will increase plasma acidity. Electrolyte solutions accompanying the macromolecules in commercial preparations will further increase acidity by decreasing the strong ion difference. Controversial meta-analyses have suggested that colloid use leads to greater patient mortality. The acid-base effects of colloids are unlikely to be a major cause of increased mortality. Use of colloids with electrolyte solutions, including multicarbon anions such as lactate or acetate or both, may reduce the acidifying effect.

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Continuous hemofiltration techniques have a powerful effect on acid-base physiology. In patients with metabolic acidosis, hemofiltration techniques replace plasma water, which is low in bicarbonate concentration, with a solution, which contains either an above-normal bicarbonate concentration or a high concentration of a multi-carbon anion (lactate or acetate). Such anions are then transformed into CO2,which is removed by ventilation. This exchange contributes to the correction of acidosis. The conventional view of such changes in acid-base balance is that lactate and acetate correct acidosis by generating bicarbonate. An emerging view, however, is that such oxidizable anions probably alkalinize plasma by increasing the so-called strong ion difference in plasma water. An increase in the strong ion difference (cations – anions) then results in decreased plasma water dissociation and decreased hydrogen ion activity (Stewart’s approach). If such oxidizable anions are not fully taken up by the liver and, therefore, remain in plasma water, their ability to correct acidosis is lost. They accumulate in blood and fail to decrease the strong ion difference adequately, resulting in acidosis. This effect (iatrogenic hyperlactatemia with acidification of plasma water) is typically best seen in patients with liver failure. In such patients, bicarbonate-based replacement fluids or dialysate must be used to avoid uncontrolled metabolic acidosis. In addition, the effect of lactate-based replacement fluid on blood lactate concentration can be diagnostically confusing in septic patients with lactic acidosis. In these patients, the iatrogenic increase in lactate makes it very difficult to evaluate the effects of other therapies on the evolution of endogenous lactic acidosis. On the other hand, it appears that lactate clearance through the hemofilter is small compared to endogenous clearance. Accordingly, a falling lactate level in the setting of the recent initiation of hemofiltration is best interpreted as an actual improvement in the patient’s acid-base status. Clearly, the effects of hemofiltration on acid-base physiology need to be appreciated and understood if the intensive care physician is to avoid incorrect interpretations of the patient’s clinical progress and the consequences of misdirected therapeutic interventions.

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

In patients without functioning kidneys, alkali replenishment is accomplished by the addition of either HCO3-itself or a metabolic precursor of this anion, such as lactate, via dialysis solution. The body-base balance in peritoneal dialysis patients is self-regulated by the feedback between plasma bicarbonate concentration and dialytic base gain. Dialytic base gain is the only source of buffer for peritoneal dialysis patients, and this gain should counteract the metabolic acid production. Dialytic base gain depends on peritoneal buffer fluxes (lactate reabsorption minus bicarbonate lost). The level of plasma bicarbonate is determined by the dialytic base gain and the metabolic acid production. Bicarbonate buffered peritoneal dialysis solution provides some advantages to the conventional lactate buffered peritoneal dialysis solution, particularly in acute patients.

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Lactic acidosis is a common finding in critically ill patients during severe sepsis/septic shock, and a powerful predictor of mortality. Because of the knowledge that lactate is the end product of anaerobic glycolysis, the presence of hyperlactatemia in sepsis has been taken to indicate the development of anaerobic glycolysis within tissues. Such anaerobic glycolysis is understood to result from oxygen “debt” at cellular level. The metabolic acidosis frequently associated with hyperlactatemia has thus been ascribed to hydrogen ions released from adenosine triphosphate hydrolysis. This simplistic view of the pathogenesis and meaning of hyperlactatemia, however, is not supported by available data. Systemic oxygen transport is usually increased rather than decreased in septic patients. Whenever studied, tissue oxygenation is either preserved or increased in septic animals and humans. In addition, lactate levels may fluctuate in response to inotropic drugs and do not consistently decrease when tissue oxygen delivery is increased. Furthermore, there is strong evidence that large amounts of lactate can be produced and released under aerobic conditions and that the pathogenesis of hyperlactatemia in septic states is complex. Such pathogenesis may involve accelerated glycolytic fluxes, the inhibition of pyruvate dehydrogenase activity, and changes in intermediary metabolism. It may also involve the need to modulate the rate and efficiency of glycolytic flux by controlling the redox state of cytoplasm and mitochondria through lactate accumulation.Furthermore, recent investigations have attempted to establish which organs are responsible for lactate production in septic humans and endotoxemic animals. These studies suggest that the lung may be a major source of much of the excess lactate produced under these circumstances. They also suggest that decreased lactate elimination is also an important component of the pathogenesis of hyperlactatemia. Finally, the pathogenesis of the metabolic acidosis associated with hyperlactatemia is most likely to be related to the effect of the lactate ion on the strong ion difference and subsequently on the dissociation of plasma water into hydrogen ions.A great deal remains to be understood about the pathogenesis of lactic acidosis in sepsis. It is important, however, to understand that the concepts of “anaerobic glycolysis” and “unfettered adenosine triphosphate hydrolysis” are not convincingly supported by available evidence and probably represent an inaccurate and simplistic explanation of this complex phenomenon.

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The traditional acid-base paradigm used to address trauma patients is one of hypoperfusion-induced cellular hypoxia with the generation of lactate as a byproduct of anaerobic respiration. Evidence is mounting that the metabolic acidosis identified in trauma patients may be due only partly to lactate. Instead, the Stewartian method of acid-base evaluation allows one to identify uncharacterized anions as significant contributors to metabolic acidosis as well as to dissect the relative contribution of resuscitation fluid composition to the promotion of metabolic acidosis. Furthermore, such a paradigm enables the clinician to alter practice patterns to minimize iatrogenic derangements and to track those that are currently not under direct control. Regional evaluation of acid-base balance may provide earlier clues to tissue level dysoxia that are not reflected in standard acid-base parameters. Acid-base variables may suggest likely outcome after significant trauma. The interaction of acidosis with inflammatory mechanisms is reviewed as well.

ISSN:1070-5295    

出版商:OVID    

年代:1999

数据来源: OVID