Metabolic Alkalosis

Pathophysiology

• Saline-responsive etiologies require initiating event and maintenance factors, whereas saline-resistant etiologies develop from a variety of causes

• Initiating event loss of H from Gl tract or kidneys exogenous alkali contraction alkalosis: diuresis — excretion of HCOj-poor fluid extracellular fluid

"contracts" around fixed amount of HCO) -» Î HCOj concentration, posthypercapnia respiratory acidosis — renal compensation with HCOj retention: rapid correction of respiratory disorder (eg. with intubation) — transient excess HCOj

• Maintenance factors volume depletion — Î proximal reabsorption of NaHCOj and Î aldosterone (see next) hyperaldosteronism (either 1 ° or 2°) distal Na reabsorption in exchange for K ' and

H ' excretion (and consequent HCOj retention) hypokalemia . transcellular K ' H ' exchange: intracellular acidosis in renal proximal tubular cells promotes bicarbonate reabsorption and ammoniagenesis

Etiologies of Metabolic Alkalosis

Saline-responsive

Gl loss of H : vomiting, NGT drainage, villous adenoma

Diuretic use posthypercapnia

Saline-resistant

Hypertensive (mineralocorticoid excess)

1° hyperaldosteronism (eg.Conns)

2° hyperaldosteronism (eg. renovascular dis. renin-secredng tumor) non-aldo (eg. Cushing's. Liddle's. exogenous mineralocorticoids) Normotensive severe hypokalemia exogenous alkali load Bartter's syndrome. Gitelman s syndrome

Workup

• Check volume status and Uo

Uci <20 mEq L — saline-responsive

Uci >20 mEq L — saline-resistant (unless currently receiving diuretics) (U*, unreliable determinant of volume status as alkalemia -»t HCOj excretion tNa excretion; negatively charged HCO3 "drags" Na' along) If Ua >20 and volume replete. ✓ blood pressure

Figure 4-3 Approach to metabolic alkalosis

Metabolic Alkalosis

Saline-Responsive I

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