Bench-to-bedside review: Treating acid–base abnormalities in the intensive care unit–the role of buffers
BK Gehlbach, GA Schmidt - Critical Care, 2004 - Springer
The recognition and management of acid–base disorders is a commonplace activity for
intensivists. Despite the frequency with which non-bicarbonate-losing forms of metabolic
acidosis such as lactic acidosis occurs in critically ill patients, treatment is controversial. This
article describes the properties of several buffering agents and reviews the evidence for their
clinical efficacy. The evidence supporting and refuting attempts to correct arterial pH through
the administration of currently available buffers is presented.
intensivists. Despite the frequency with which non-bicarbonate-losing forms of metabolic
acidosis such as lactic acidosis occurs in critically ill patients, treatment is controversial. This
article describes the properties of several buffering agents and reviews the evidence for their
clinical efficacy. The evidence supporting and refuting attempts to correct arterial pH through
the administration of currently available buffers is presented.
Bench-to-bedside review: Treating acid–base abnormalities in the intensive care unit–the role of renal replacement therapy
T Naka, R Bellomo - Critical Care, 2004 - Springer
Acid–base disorders are common in critically ill patients. Metabolic acid–base disorders are
particularly common in patients who require acute renal replacement therapy. In these
patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid–base
status using the Stewart–Figge methodology shows that these patients have greater
acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly
secondary to hyperphosphatemia, hyperlactatemia, and the accumulation of unmeasured …
particularly common in patients who require acute renal replacement therapy. In these
patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid–base
status using the Stewart–Figge methodology shows that these patients have greater
acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly
secondary to hyperphosphatemia, hyperlactatemia, and the accumulation of unmeasured …
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