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Source: Devlin JW, Matzke GR. Acid–base disorders. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861§ionid=146062232. Accessed March 3, 2017.
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Initiated by increased pH and HCO3− that can result from:
Loss of H+ via gastrointestinal (GI) tract (eg, nasogastric suctioning, vomiting) or kidneys (eg, diuretics, Cushing syndrome)
Gain of bicarbonate (eg, administration of bicarbonate, acetate, lactate, or citrate)
Maintained by abnormal renal function that prevents kidneys from excreting excess bicarbonate.
Primary compensation: respiratory response to metabolic alkalosis is increased in PaCO2 by hypoventilation.
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CLINICAL PRESENTATION
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MEANS OF CONFIRMATION AND DIAGNOSIS
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Blood gases, serum electrolytes, medical history, and clinical condition are the primary tools for determining the cause of acid–base disorders and for designing therapy.
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