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.
TABLE 1.Causes of Metabolic Alkalosis Differentiated on the Basis of Their Responsiveness to Sodium Chloride ||Download (.pdf) TABLE 1. Causes of Metabolic Alkalosis Differentiated on the Basis of Their Responsiveness to Sodium Chloride
|Sodium chloride–responsive (urinary chloride concentration <10 mEq/L [<10 mmol/L]) |
Villous adenoma of colon.
|Diuretic therapy |
|Correction of chronic hypercapnia |
|Cystic fibrosis |
|Excessive bicarbonate therapy of organic acidosis |
|Mild/moderate potassium deficiency |
|Sodium chloride–resistant (urinary chloride concentration >20 mEq/L [>20 mmol/L]) |
Excess mineralocorticoid activity.
|Excessive black licorice intake |
|Profound potassium depletion |
|Magnesium deficiency |
|Liddle syndrome |
|Estrogen therapy |
|Alkali administration |
|Milk-alkali syndrome |
|Massive blood or plasma protein fraction transfusion |
|Nonparathyroid hypercalcemia |
|Carbohydrate refeeding after starvation |
|Large doses of penicillin |
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.
MEANS OF CONFIRMATION AND DIAGNOSIS
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.