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Pathophysiology and causes of metabolic acidosis in the critically ill 

Pathophysiology and causes of metabolic acidosis in the critically ill
Pathophysiology and causes of metabolic acidosis in the critically ill

Patrick J. Neligan

and Clifford S. Deutschman

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date: 04 July 2022

Critical illness is typically characterized by changes in the balance of water and electrolytes in the extracellular space, resulting in the accumulation of anionic compounds that manifests as metabolic acidosis. Metabolic acidosis manifests with tachypnoea, tachycardia, vasodilatation, headache and a variety of other non-specific symptoms and signs. It is caused by a reduction in the strong ion difference (SID) or an increase in weak acid concentration (albumin or phosphate). Increased SID results from hyperchloraemia, haemodilution or accumulation of metabolic by-products. A reduction in SID results in a corresponding reduction is serum bicarbonate. There is a corresponding increase in alveolar ventilation and reduced PaCO2. Lactic acidosis results from increased lactate production or reduced clearance. Ketoacidosis is associated with reduced intracellular glucose availability for metabolism, and is associated with insulin deficiency and starvation. Hyperchloraemic acidosis is associated with excessive administration of isotonic saline solution, renal tubular acidosis and ureteric re-implantation. Renal acidosis is associated with hyperchloraemia, hyperphosphataemia, and the accumulation of medley nitrogenous waste products.

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