The elevated SID leads to a decrease in (increase in pH). The alkaline tide refers to the Cl −-depleted plasma that leaves the stomach. Cl − is pumped into the stomach, reducing SID in the stomach and increasing the (decreasing the pH) and, at the same time, causing the alkaline tide in the blood (increasing SID) that occurs at the beginning of a meal when gastric acid secretion is maximal. Their ability to manipulate SID complexly is a direct result of the fact that strong ions are handled differently in different portions of the gastrointestinal tract. The organs of the gastrointestinal tract are underappreciated regulators of acid-base balance. 7, 8 Nonetheless, it has yet to be demonstrated that treating acidosis improves outcome. However, acidosis itself has been shown to produce harm in animal models 5–8-especially in models of sepsis, where decreased survival time and hypotension appear to be attributable to exogenous acid loading. Dissecting out the effects of acidosis itself from the causes that underlie it is difficult in patients. Treating the lactic acidosis without addressing the underlying cause of the lactic acidosis in this scenario is certain to fail. For instance, bowel infarction is lethal, and only surgical resection is curative. Common forms of acidemia may be associated with significant mortality because of the disease processes that underlie them, not necessarily because of the actual.
Frequently, when treating critically ill patients, it is easy to blur the lines between supportive measures and therapeutic interventions. 4 However, supporting respiratory compensation when feasible and avoiding acidosis when possible seems a prudent course of action in most clinical scenarios. Indeed, the existing evidence does not support the use of sodium bicarbonate for the purpose of correcting the pH in most conditions of acute acidosis, 3 and some animal experiments even suggest harm. This is not to say that we believe that correcting an acid-base disorder is always appropriate. Philadelphia, Saunders, 1999, Chapter 76, pp 839–853, with permission. Source: Adapted from Kellum JA: Diagnosis and treatment of acid-base disorders, in Grenvik A, Shoemaker PK, Ayers S, Holbrook (eds): Textbook of Critical Care. *Animal studies have shown both increased and decreased coronary artery blood flow. Hypophosphatemia Impaired enzyme function Potential Clinical Effects of Metabolic Acid-Base Disorders Metabolic AcidosisĬatecholamine, PTH, and aldosterone stimulation
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