Figure 634

Changes in plasma anionic pattern, net acid excretion, and body electrolyte balance during development, maintenance, and correction of diuretic-induced metabolic alkalosis. Administration of a loop diuretic, such as furosemide, increases urine net acid excretion (largely in the form of ammonium) as well as the renal losses of chloride (Cl-), sodium (Na+), and potassium (K+). The resulting hyperbicarbonatemia reflects both loss of excess ammonium chloride in the urine and an element of contraction (consequent to diuretic-induced sodium chloride [NaCl] losses) that limits the space of distribution of bicarbonate. During the phase after diuresis (maintenance), and as long as the low-chloride diet is continued, a new steady state is attained in which the plasma bicarbonate concentration ([HCO3]) remains elevated, urine net acid excretion returns to baseline, and renal excretion of electrolytes matches intake. Addition of potassium chloride (KCl) in the correction phase repairs the chloride and potassium deficits, suppresses net acid excretion, and normalizes the plasma bicarbonate and chloride concentration ([Cl-]) levels [23,24]. If extracellular fluid volume has become subnormal folllowing diuresis, administration of NaCl is also required for repair of the metabolic alkalosis.

Maintenance of Cl -responsive metabolic alkalosis

Basic mechanisms Mediating factors

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