Although the human diet is essentially neutral with respect to its pH, various aerobic and anaerobic metabolic processes create large amounts of acid daily from the catabolism of carbohydrates, fats, and proteins. The body maintains a constant [H⁺] such that blood and extracellular pH is near 7.4 and intracellular pH is about 7.1. The buffer most responsible for this is the HCO^–₃/H₂CO₃ system, regulated by the coordinated behavior of the lungs and kidneys. Aerobic metabolism yields gaseous CO₂ that combines with water to form volatile carbonic acid, H₂CO₃. The lungs are primarily responsible for elimination of CO₂. Anaerobic metabolism of glucose and fat, as well as some protein catabolism yield fixed or nonvolatile acids such as lactic acid, sulfuric acid, and phosphoric acid, most being excreted by the kidneys. In one 24-hour period, a 70-kg person produces 70-100 mmol of such nonvolatile acids versus 20 moles CO₂, all without appreciable change in plasma pH. An effective V̇_A controls CO₂ excretion, while the kidneys excrete nonvolatile acids and reabsorb or regenerate HCO^–₃. The lungs and kidneys maintain a balance of CO₂ and HCO^–₃, and thus pH_a near 7.4 (Fig. 17.1).

Acidosis and alkalosis are terms that describe primary processes modulating [H⁺] in patient populations. Each may be metabolic or respiratory in origin, based on whether the primary deviation is in arterial [HCO^–₃] or P_aco₂, respectively. Respiratory disorders are caused by inappropriate excretion of CO₂ that raises or lowers [H₂CO₃] in body fluids. Metabolic disorders reflect primary changes in plasma [HCO^–₃] due to excessive intake, production, or loss of HCO^–₃ or inappropriate handling of H⁺ and anions from dissociated nonvolatile acids. Primary acid-base disorders and the compensations that must follow to restore pH to normal are shown in Table 17.1.

In respiratory acidosis, excessive CO₂ raises blood Pco₂, and produces by the mass action principle more H₂CO₃ which then dissociates into H⁺ and HCO^–₃ to reduce pH_a (Fig. 17.2). Compensation for this drop in pH_a is attempted in the kidneys through reabsorption of filtered HCO^–₃ to restore pH_a toward 7.4. In respiratory alkalosis, a reduced P_aco₂ forces by mass action the resynthesis of H₂CO₃ from free H⁺ and HCO^–₃ and thereby raises pH_a (Fig. 17.2). Compensation for the rise in pH_a is attempted in the kidneys by excretion of more anion, including HCO^–₃.

In metabolic acidosis, excess H⁺ from various nonvolatile acids causes pH_a to fall below 7.4, even as blood [HCO^–₃] decreases due to its recombination with those protons (Fig. 17.3). Respiratory compensation requires hyperventilation to excrete the added acid burden and restore pH_a to 7.4, although this response simultaneously lowers P_aco₂. In metabolic alkalosis, the blood [HCO^–₃] is abnormally elevated, raising pH_a above 7.4. Respiratory compensation attempts to increase P_aco₂ by hypoventilation, which then acts to restore pH_a downward toward 7.4 by forming more H₂CO₃.

Laboratory assessment of a patient’s acid-base status involves quantifying components of this HCO^–₃/H₂CO₃ buffer system. Arterial blood gas (ABG

Stay updated, free articles. Join our Telegram channel

Join