Gastrointestinale Ursachen von metabolischer Alkalose [Metabolic alkalosis in patients with gastrointestinal fluid loss]

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Item Type:	Article
Title:	Gastrointestinale Ursachen von metabolischer Alkalose [Metabolic alkalosis in patients with gastrointestinal fluid loss]
Creators Name:	Kettritz, R.
Abstract:	Buffer systems tightly regulate the extracellular H+-ion concentration to achieve a pH of 7.4 (40 nmol/l). Decreases in H+-ions result in alkalemia and the corresponding disease conditions are either metabolic or respiratory alkalosis. Metabolic alkalosis results from loss of acid, gain of bicarbonate or a combination of both. Acid loss is frequently caused by vomiting of acidic gastric fluid. Bicarbonate can be obtained from exogenous sources but is most often generated by the kidneys via aldosterone (mineralocorticoid effect). Diarrhea usually causes metabolic acidosis because of the bicarbonate loss; however, congenital or acquired enteropathy with chloridorrhea may result in bicarbonate excess and metabolic alkalosis. Metabolic alkaloses caused by gastrointestinal conditions will be discussed. The relationship of an acid-base disorder on the one hand and volume contraction, chloride and potassium deficit on the other hand will be highlighted. The alveolar- arterial pO2 gradient will be introduced to estimate the consequences of the respiratory compensation in patients with primary metabolic alkalosis.
Keywords:	Acid-Base Equilibrium, Metabolic Alkalosis, Volume Depletion, Chloridorrhea, Aldosterone
Source:	Nephrologe
ISSN:	1862-040X
Publisher:	Springer
Volume:	7
Number:	6
Page Range:	481-489
Date:	November 2012
Official Publication:	https://doi.org/10.1007/s11560-012-0668-1

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