Respiratory Compensation

RESPIRATORY COMPENSATION

Changes in alveolar ventilation responsible for the respiratory compensation of Paco₂ are medi-ated by chemoreceptors within the brainstem . These receptors respond to changes in cerebrospinal spinal fluid pH. Minute ventila-tion increases 1–4 L/min for every (acute) 1 mm Hg increase in Paco₂. In fact, the lungs are respon-sible for eliminating the approximately 15 mEq of CO₂ produced every day as a byproduct of carbo-hydrate and fat metabolism. Respiratory compen-satory responses are also important in defending against marked changes in pH during metabolic disturbances.

Respiratory Compensation During Metabolic Acidosis

Decreases in arterial blood pH stimulate medullary respiratory centers. The resulting increase in alveo-lar ventilation lowers Paco₂ and tends to restore arterial pH toward normal. The respiratory response to lower Paco₂ occurs rapidly but may not reach a predictably steady state until 12–24 hr; pH is never completely restored to normal. Paco₂ normally decreases 1–1.5 mm Hg below 40 mm Hg for every 1 mEq/L decrease in plasma [HCO ₃⁻].

Respiratory Compensation During Metabolic Alkalosis

Increases in arterial blood pH depress respiratory centers. The resulting alveolar hypoventilation tends to elevate Paco2 and restore arterial pH toward nor-mal. The respiratory response to metabolic alkalosis is generally less predictable than the respiratory response to metabolic acidosis. Hypoxemia, as a result of progressive hypoventilation, eventually activates oxygen-sensitive chemoreceptors; the latter stimulates ventilation and limits the compensatory respiratory response. Consequently, Paco2 usually does not increase above 55 mm Hg in response tometabolic alkalosis. As a general rule, Paco2 can be expected to increase 0.25–1 mm Hg foreach 1 mEq/L increase in [HCO₃⁻].