Metabolic alkalosis: Respiratory compensation

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–].