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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.
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−].
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−].
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