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Introduction

Regulation of [H+] is of crucial importance for maintenance of normal cellular functions. The normal [H+] is maintained at about 40 nEq/L. When there is even a small change in the [H+], intracellular proteins gain or lose H+ ions resulting in alterations in charge distribution which may affect molecular structure and protein function. The hydrogen ion concentration in bodily fluids is largely regulated by the ratio of the concentrations of carbon dioxide and bicarbonate. This is predicated upon the relationship demonstrated in the Henderson–Hasselbalch equation:

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where pH = −log[H+] (the H+ concentration measured in moles per liter) and pKa = 6.10. The lungs are responsible for modulating arterial PCO2, whereas the kidneys are primarily responsible for modulating the concentration of bicarbonate in plasma. In concert, these organs maintain a stable extracellular acid–base milieu that is readily assessed by measuring arterial pH.

The normal internal environment is maintained within narrow limits: The arterial blood pH is kept remarkably close to 7.40, the bicarbonate concentration is maintained around 24.5 mEq/L, and the PCO2 is maintained at about 40 mm Hg. Deviations of the pH with accompanying changes in the PCO2 and [HCO3] result in the four major categories denoted in Table 17-1. Metabolic acidosis is characterized by acidemia (pH < 7.35) that is due to reduced plasma [HCO3]. Metabolic alkalosis is characterized by an alkalemia (pH > 7.45) that results from an elevation in the plasma [HCO3]. Respiratory acidosis is due to hypoventilation resulting in a net increase in PCO2 (hypercapnia) and a concomitant fall in pH. Respiratory alkalosis is due to primary hyperventilation leading to a fall in PCO2 (hypocapnia) and a rise in pH.

Table 17-1Patterns of PCO2 and HCO3 Changes in Acid–Base Disorders

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