Metabolic alkalosis is a very common primary acid–base disturbance associated with increased plasma HCO3. Increased extracellular HCO3 is due to net loss of H+ and/or addition of HCO3. The most common cause of metabolic alkalosis is gastrointestinal acid loss because of vomiting or nasogastric suctioning; the resulting hypovolemia leads to secretion of renin and aldosterone and enhanced absorption of HCO3.Diuretics are another common cause of metabolic alkalosis. Thiazides (e.g., hydrochlorothiazide) and loop diuretics (e.g., furosemide) induce a net loss of chloride and free water, without altering bicarbonate excretion, and can cause a volume “contraction” alkalosis. When metabolic alkalosis is persistent, it usually reflects an inability of the kidney to excrete HCO3. Rare inherited renal causes of metabolic alkalosis exist (e.g., Bartter syndrome). A typical respiratory response to all types of metabolic alkalosis is hypoventilation leading to a pH correction towards normal.
Increases in arterial blood pH depress respiratory centers. The resulting alveolar hypoventilation tends to elevate PaCO2 and restore arterial pH toward normal. The pulmonary response to metabolic alkalosis is generally less predictable than the response to metabolic acidosis. Hypoxemia, as a result of progressive hypoventilation, eventually activates oxygen-sensitive chemoreceptors; the latter stimulates ventilation and limits the compensatory pulmonary response. Consequently, PaCO2 usually does not rise above 55 mm Hg in response to metabolic alkalosis. As a general rule, PaCO2 can be expected to increase 0.25–1 mm Hg for each 1 mEq/L increase in [HCO3–].