Porth's Essentials of Pathophysiology, 4e

181

Disorders of Fluid, Electrolyte, and Acid–Base Balance

C h a p t e r 8

R

Calcium, Phosphorus, and Magnesium Balance Calcium, phosphorus, and magnesium are the major divalent cations in the body. Most of these cations are deposited in bone, with only a small amount in the ECF. Homeostatic mechanisms that regulate serum calcium and phosphorus levels involve three organs—the intes- tine, kidney, and bone, principally through the complex interaction of parathyroid hormone and vitamin D 35–37 (Fig. 8-13). The main function of parathyroid hormone (PTH) is to maintain ECF calcium concentrations. 35,37 It does this by stimulating the release of calcium and phosphorus from bone into the ECF; increasing renal reabsorption of calcium and excretion of phosphorus; and enhancing the gastrointestinal absorption of calcium and phospho- rus through its effects on vitamin D synthesis. Vitamin D , which functions as a hormone, is synthesized by the skin and converted to its active form, calcitriol , in the kidney. The active form of vitamin D has several effects on the intestines, kidneys, and bone that increase serum levels of calcium and phosphorus and contribute to their of cells and acid–base balance, intricate chemical reactions that transform carbohydrates into energy, changing glucose into glycogen, and converting amino acids to proteins. Potassium also plays a critical role in conducting nerve impulses and controlling the excitability of skeletal, cardiac, and smooth muscles. ■■ Potassium is ingested in the diet and eliminated in the urine, with ICF and extracellular (ECF) levels being regulated by compartmental shifts between the ICF and ECF, and mechanisms that adjust renal excretion with dietary ingestion of potassium. ■■ Hypokalemia, or potassium deficit, can result from inadequate intake, excessive losses, or redistribution from the ECF to the ICF compartments. It is manifested by alterations in kidney, skeletal muscle, gastrointestinal, and cardiac function, reflecting the crucial role of potassium in cell metabolism and neuromuscular function. ■■ Hyperkalemia, or potassium excess, can result from decreased elimination of potassium by the kidney, a transcellular shift in potassium from the ICF into the ECF compartment, or excessively rapid intravenous administration of potassium. It is manifested by alterations in neuromuscular and cardiac function, the most serious being the development of serious and even fatal cardiac arrhythmias.

Delay in AV node

T

P

U

Q

A Normal

S

Depressed ST segment

Prominent U wave

PR prolongation

Low T

B Hypokalemia

Peaked T

Widening of QRS

PR prolongation

Low P wave

C Hyperkalemia

FIGURE 8-12. Comparison of the (A) normal electrocardiogram with electrocardiographic changes that occur with (B) hypokalemia and (C) hyperkalemia.

ICF compartment can be accomplished by the admin- istration of sodium bicarbonate, β -agonists (e.g., nebu- lized albuterol), or insulin to rapidly decrease the ECF concentration. 30 Less-emergent measures focus on decreasing or cur- tailing potassium intake or absorption, increasing renal excretion, and increasing cellular uptake. Decreased intake can be achieved by restricting dietary sources of potassium. The major ingredient in most salt substitutes is potassium chloride, and such substitutes should not be given to persons with kidney problems. Increasing potassium output often is more difficult. Persons with kidney failure may require hemodialysis or peritoneal dialysis to reduce serum potassium levels.

SUMMARY CONCEPTS

■■ Potassium is the second most abundant cation in the body, with 98% being located in the intracellular fluid (ICF) compartment.The high ICF concentration is required for many cell functions, including maintenance of the osmotic integrity