Porth's Essentials of Pathophysiology, 4e

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Disorders of Fluid, Electrolyte, and Acid–Base Balance

C h a p t e r 8

controlling HCO 3 – loss is the chloride/bicarbonate anion exchange that occurs in association with Na + reabsorp- tion. Chloride is absorbed along with Na + throughout the tubules. In situations of volume depletion due to vomiting and Cl – depletion, the kidney is forced to sub- stitute HCO 3 – for the Cl – anion, thereby increasing its absorption of HCO 3 – . Both reabsorption of HCO 3 – and excretion of acid are accomplished through H + secretion as the urine fil- trate moves through the tubular structure of the kidney. The epithelial cells of the proximal tubule, the thick ascending limb of Henle, and distal tubule all secrete H + nto the tubular fluid by the Na + /H + counter-transport mechanism (see Chapter 24). The potassium/hydrogen exchange system in the collecting tubules functions in H + secretion by substituting the reabsorption of K + for excretion of H + Acidosis tends to increase H + elimi- nation and decrease K + elimination, with a resultant increase in serum potassium levels, whereas alkalosis tends to decrease H + elimination and increase K + elimi- nation, with a resultant decrease in serum potassium levels. 64–66 Generation of New Bicarbonate. Another impor- tant but more complex buffer system that facilitates the excretion of H + and generation of new HCO 3 – is the ammonia buffer system. Renal tubular cells are able to use the amino acid glutamine to synthesize ammonia (NH 3 ) and secrete it into the tubular fluid. Hydrogen ions then combine with the NH 3 to form ammonium ions (NH 4 + ). The NH 4 + ions, in turn, combine with Cl – ions that are present in the tubular fluid to form ammonium chloride (NH 4 Cl), which is then excreted in the urine. Under normal conditions, the amount of H + ion eliminated by the ammonia buffer system is about 50% of the acid excreted and new HCO 3 – regen- erated. However, with chronic acidosis, it can become the dominant mechanism for H + excretion and new HCO 3 – generation. Phosphate Buffer System. Because extremely acidic urine (pH 4.0 to 4.5) would be damaging to structures in the urinary tract, the elimination of H + requires a buf- fer system. There are two important intratubular buffer systems: the phosphate buffer system and the previously described ammonia buffer system. The phosphate buf- fer system uses HPO 4 2– and H 2 PO 4 – that are present in the tubular filtrate to buffer H + . Because HPO 4 2– and H 2 PO 4 – are poorly absorbed, they become more concen- trated as they move through the tubules. LaboratoryTests Laboratory tests that are used in assessing acid–base balance include arterial blood gases and serum electro- lytes, base excess or deficit, and anion gap. Although useful in determining whether acidosis or alkalosis is present, the pH measurements of the blood provide little information about the cause of an acid–base disorder.

Arterial blood gases provide a means of assessing the respiratory component of acid–base balance. H 2 CO 3 levels are determined from arterial PCO 2 levels and the solubility coefficient for CO 2 (normal arterial PCO 2 is 38 to 42 mm Hg). Arterial blood gases are used because venous blood gases are highly variable, depending on metabolic demands of the various tissues that empty into the vein from where the sample is being drawn. Laboratory tests are used to measure serum electro- lytes, CO 2 content, and HCO 3 – . These measurements are determined by adding a strong acid to a blood sample and measuring the amount of CO 2 that is produced. More than 70% of the CO 2 in the blood is in the form of bicarbonate. The serum bicarbonate is then determined from the total CO 2 content of the blood. Base excess or deficit is a measure of the HCO 3 – excess or deficit. It describes the amount of a fixed acid or base that must be added to a blood sample to achieve a pH of 7.4 (nor- mal ± 2.0 mEq/L). 60 A base excess indicates metabolic alkalosis, and a base deficit indicates metabolic acidosis. The anion gap describes the difference between the serum concentration of the major measured cation (Na + ) and the sum of the measured anions (Cl – and HCO 3 – ). This difference represents the concentration of unmea- sured anions, such as phosphates, sulfates, organic acids, and proteins (Fig. 8-18). Normally, the anion gap ranges between 8 and 12 mEq/L (a value of 16 mEq/L is normal if both Na + and K + concentrations are used in the calcu- lation). The anion gap is increased in conditions such as lactic acidosis and ketoacidosis that result in a decrease in HCO 3 , and it is normal in hyperchloremic acidosis, where Cl – replaces the HCO 3 – anion. 1 Disorders of Acid–Base Balance The terms acidosis and alkalosis describe the clinical conditions that arise as a result of changes in dissolved CO 2 and HCO 3 – concentrations. 64 There are two types

mEq/L

150

Acidosis due to excess chloride levels

Acidosis due to excess organic acids

Normal

140

130

12 mEq/L

12 mEq/L

Anion gap

Anion gap

120

Anion gap 25 mEq/L

110

Sodium 142 mEq/L

Sodium 142 mEq/L

Sodium 142 mEq/L

Chloride 116 mEq/L

Chloride 103 mEq/L

Bicarbonate 14 mEq/L

Bicarbonate 27 mEq/L

100

Chloride 103 mEq/L

Bicarbonate 14 mEq/L

FIGURE 8-18. The anion gap in acidosis due to excess metabolic acids and excess serum chloride levels. Unmeasured anions such as phosphates, sulfates, and organic acids increase the anion gap because they replace bicarbonate.This assumes there is no change in sodium content.