Porth's Essentials of Pathophysiology, 4e

177

Disorders of Fluid, Electrolyte, and Acid–Base Balance

C h a p t e r 8

hydrogen exchange mechanism in the collecting tubules of the kidney. When serum potassium levels increase, K + is secreted into the urine and H + is reabsorbed, leading to a decrease in pH and metabolic acidosis; when potas- sium levels are low, K + is reabsorbed and H + is secreted in the urine, leading to an increase in pH and metabolic alkalosis. Among the factors that influence the ECF/ICF shift in potassium are serum osmolality, acid–base bal- ance, insulin, and increased sympathetic nervous sys- tem activity (Fig. 8-10). An acute increase in serum osmolality causes water to move out of the cell; this in turn prompts an increase in K + concentration that causes it to move out into the ECF. Acid–base disor- ders rely on an ECF to ICF cation shift for buffering of the H + ion. In metabolic acidosis, for example, H + moves into body cells for buffering, causing K + to leave and move into the ECF. Both insulin and epinephrine (a β -adrenergic sympathetic neurontransmitter) increase cellular uptake of K + by increasing the activity of the Na + /K + -adenosine triphosphatase (ATPase) membrane pump. 4,30–33 Normally, it takes 6 to 8 hours for the kidneys to eliminate half of potassium that has been ingested in the diet. 4 After a meal, insulin release not only serves to regulate blood glucose levels, but also serves to control serum potassium levels by temporarily shifting the excess into cells until it can be eliminated by the kidneys. Exercise can also produce compartmental shifts in potassium. Repeated muscle contraction causes potas- sium to be released into the ECF. Although the increase usually is small with modest exercise, it can be consid- erable during exhaustive exercise. Even the repeated clenching and unclenching of the fist during a blood draw can cause potassium to move out of cells causing an artificial elevation in serum potassium levels.

Potassium Balance Potassium (K + ) is the second most abundant cation in the body, with 98% located in the intracellular compart- ment, primarily in skeletal muscle. 30–32 Of the remaining 2% that is in the extracellular compartment, only about 0.4% is measurable in the plasma. This tiny amount is maintained at a fairly narrow serum concentration of 3.5 to 5.0 mEq/L (3.5 to 5.0 mmol/L). Regulation of Potassium Balance Potassium balance is normally regulated by dietary intake, urine output, and transcompartmental shifts between the ICF and ECF compartments. The kidneys are the main source of potassium loss. Approximately 80% to 90% of potassium loss occurs in the urine, with the remainder being lost in the stools from the gastroin- testinal tract and in sweat from the skin. 30–34 Potassium is filtered in the glomerulus, reabsorbed along with sodium and water in the proximal tubule and with sodium and chloride in the thick ascending loop of Henle, and then secreted into the late distal and collecting tubules for elimination in the urine. In con- trast to other electrolytes, the regulation of potassium elimination by the kidney is mainly controlled by its secretion from the blood into the tubular filtrate rather than through its reabsorption from the tubular filtrate into the blood (see Chapter 24). Aldosterone plays an essential role in regulating potassium elimination in the distal tubule of the kidney. In the presence of aldosterone, Na + is transported back into the blood and K + is secreted in the tubular filtrate for elimination in the urine. There is also a potassium/ proportionate changes in sodium and water. Isotonic fluid volume deficit (hypovolemia), which is characterized by a decrease in ECF volume, causes thirst, signs of decreased vascular volume, and a decrease in urine output along with an increase in urine specific gravity. Isotonic fluid volume excess (hypervolemia), which is characterized by an increase in ECF volume, is manifested by signs of increased vascular volume and edema. ■■ Hyponatremia (sodium deficit) and hypernatremia (sodium excess) are brought about by disproportionate losses or gains in ECF sodium concentration, which cause water to move in or out of body cells. Because of water movement, hyponatremia produces an increase in ICF water causing cells to swell;, whereas hypernatremia produces an ICF water deficit and cellular dehydration.

Intracellular

Extracellular

+

K

++

Na /K - ATPase pump

+

Na

+ +

Epinephrine Insulin

K +

+

H

FIGURE 8-10. Mechanisms regulating transcellular shifts in potassium.

Made with