Porth's Essentials of Pathophysiology, 4e

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Integrative Body Functions

U N I T 2

Disorders of Potassium Balance As the major intracellular cation, potassium is criti- cal to many body functions, including maintenance of the osmotic integrity of cells, acid–base balance, and the intricate chemical reactions that transform carbo- hydrates into energy and convert amino acids to pro- teins. Potassium also plays a critical role in conducting nerve impulses and controlling the excitability of skel- etal, cardiac, and smooth muscle. It does this by regu- lating the resting membrane potential, the opening of sodium channels that control the flow of current during the action potential, and the rate of repolarization. 30,33 Changes in nerve and muscle excitability are particu- larly important in the heart, where alterations in serum potassium levels can produce serious cardiac arrhyth- mias and conduction defects. Changes in serum potas- sium levels also affect the electrical activity of skeletal muscles and the smooth muscle in the blood vessels and gastrointestinal tract. The resting membrane potential is determined by the ratio of ECF to ICF potassium concentration (see Chapter 1, “Understanding Membrane Potentials”). A decrease in the ECF potassium concentration (hypo- kalemia) causes the resting membrane potential to become more negative, moving it further from the threshold for excitation (Fig. 8-11). Thus, it takes a greater stimulus to reach the threshold potential and open the sodium channels that are responsible for the action potential. An increase in serum potassium (hyperkalemia) has the opposite effect; it causes the resting membrane potential to become more positive, moving it closer to the threshold. With severe hyper- kalemia, the resting membrane potential approaches the threshold potential, causing sustained subthresh- old depolarization with a resultant inactivation of

the sodium channels and net decrease in excitability. 3 The rate of repolarization (return of the membrane potential toward its resting potential so it can undergo another action potential) also varies with serum potas- sium levels. It is more rapid in hyperkalemia and delayed in hypokalemia. Hypokalemia Hypokalemia refers to a decrease in serum potassium levels below 3.5 mEq/L (3.5 mmol/L). The causes of potassium deficit can be grouped into three categories: inadequate intake; excessive gastrointestinal, renal, and skin losses; and a shift between the ICF and ECF compartments. 3,30–33 Inadequate dietary intake is a frequent cause of hypo- kalemia. Insufficient dietary intake may result from the inability to obtain or ingest food or from a diet that is low in potassium-containing foods. Potassium intake is often inadequate in persons on fad diets and those who have eating disorders. Elderly persons are particularly likely to have potassium deficits. Excessive renal losses of potassium occur with diuretic therapy, metabolic alkalosis, magnesium depletion, trauma and stress, and an increase in aldo- sterone levels. Diuretic therapy, with the exception of potassium-sparing diuretics, is the most common cause of hypokalemia. Both thiazide and loop diuretics increase the loss of potassium in the urine. Magnesium depletion, which often coexists with potassium deple- tion due to diuretic therapy, produces additional uri- nary losses. Renal losses of potassium are accentuated by aldosterone. Primary aldosteronism, caused by either a tumor or hyperplasia of the cells of the adrenal cortex that secrete aldosterone, can produce severe losses by increasing potassium secretion in the distal renal tubule (see Chapter 32). Although potassium losses from the skin and the gas- trointestinal tract usually are minimal, these losses can become excessive under certain conditions. For exam- ple, burns increase surface losses of potassium. Intestinal secretions contain relatively large amounts of potassium (e.g., 85 to 90 mEq/L), thus diarrhea can produce large losses of potassium. 3 Hypokalemia can also be caused by intracellu- lar shifting of potassium from the ECF compartment (see Fig. 8-10). A wide variety of β 2 -adrenergic ago- nist drugs (e.g., decongestants and bronchodilators) produce an intracellular shift in potassium, causing a transient decrease in serum potassium levels. 37 Insulin also increases the movement of potassium into the cell. Because insulin increases the movement of glucose and potassium into cells, potassium deficit often develops during treatment of diabetic ketoacidosis. Manifestations. The manifestations of hypokalemia include alterations in neuromuscular, gastrointestinal, renal, and cardiovascular function 3,30–33 (Table 8-5). These manifestations reflect the effects of hypokale- mia on the electrical activity of excitable tissues such as those of the neuromuscular systems as well as the body’s

Resting membrane potential Threshold potential

Hyperkalemia Hypokalemia Normal

Normal Hypokalemia Hyperkalemia

FIGURE 8-11. Effect of changes in serum hypokalemia (red) and hyperkalemia (blue) on the resting membrane potential in relation to the threshold potential.