Respiratory compensation to a primary metabolic alkalosis in humans

There is limited and disparate information about the extent of the respiratory compensation (hypoventilation) that occurs in response to a primary metabolic alkalosis in humans. Our aim was to examine the influence of the plasma bicarbonate concentration, the plasma base excess, and the arterial pH on the arterial carbon dioxide tension in 52 adult patients with primary metabolic alkalosis, mostly due to diuretic use or vomiting. Linear regression analysis was used to correlate degrees of alkalosis with arterial carbon dioxide tensions. In this alkalotic cohort, whose arterial plasma bicarbonate averaged 31.6 mEq/l, plasma base excess averaged 7.8 mEq/l, and pH averaged 7.48, both plasma bicarbonate and base excess correlated closely with arterial carbon dioxide tensions (r = 0.97 and 0.96, respectively; p < 0.0001), while there was little relationship between arterial pH and arterial carbon dioxide tensions (p = 0.08). The arterial carbon dioxide tension increased 1.2 torr for each 1.0 mEq/l increment in plasma bicarbonate or base excess (95% confidence interval, 1.1 - 1.3 torr). This 1.2 torr increase amounts to a ~ 50% greater degree of respiratory compensation (hypoventilation) to primary metabolic alkalosis than has been reported in prior smaller studies.