POTASSIUM PHYSIOLOGY

Potassium is the most abundant positive ion in the intracellular fluid. In the short term (minutes), potassium balance is influenced by insulin, pH, β-adrenergic agonists, and bicarbonate concentration. Long-term regulation of potassium excretion and balance primarily involves the kidney and aldosterone. Several factors cause the potassium concentration to average 0.4 to 0.5 mEq/L lower when measured on heparinized arterial samples compared with clotted venous samples.

Elevations in potassium intake increase renal excretion of potassium through a variety of cellular mechanisms. In response to increases in extracellular potassium levels, aldosterone is secreted from the zona glomerulosa of the adrenal gland and acts on cortical collecting ducts to increase potassium secretion into the tubular fluid and therefore increase potassium excretion.

Many of the effects seen during alterations in normal potassium levels result from potassium's importance in the membrane potential of cells. Potassium is the principal intracellular cation, with more than 98% of the body's potassium found within the intracellular water. In the resting state, cell membrane conductance is higher for potassium than sodium. This increased conductance leads to transmembrane potential being closer to the transmembrane value of potassium (-90 mV). Alterations in extracellular potassium concentration alter the resting membrane potential, which may cause the cell to be unresponsive or overresponsive to sodium shifts into the cell. High or low potassium levels can result in potentially lethal problems in excitatory tissue, particularly cardiac tissue.

Multiple factors regulate the normal maintenance of the transmembrane potassium gradient. The most important

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Potassium requirements vary with age and growth. The typical term baby requires 2 to 3 mEq/kg/day,^[39] whereas the adult uses 1.0 to 1.5 mEq/kg/day. Potassium demands are related to metabolic rate (2.0 mEq/100 kcal). In this regard, the requirement increases dramatically during cell growth after establishment of nutrition in previously starved individuals. Extremely high or low levels of potassium can be life threatening.

Hypokalemia

Hypokalemia (<3.5 mEq/L) may occur because of an absolute deficiency or redistribution into the intracellular space. A reduction in serum potassium of 1 mEq/L indicates a net loss of 100 to 200 mEq of potassium in a normal adult. Hypokalemia in the range of 2 to 2.5 mEq/L is likely to cause muscular weakness, arrhythmias, and electrocardiographic abnormalities, including sagging of the ST segment, depression of the T wave, and U-wave elevation. These morphologic changes do not correlate with the severity of potassium depletion. However, cardiac dysrhythmias are more predictable and most frequently involve atrial fibrillation and premature ventricular systoles.

The four most common causes of hypokalemia include reduced intake, gastrointestinal losses, excessive renal losses of potassium (e.g., with excess of mineralocorticoids

TABLE 46-8 -- Major causes of hypokalemia

Causes	Mechanisms
Inadequate intake	Anorexia nervosa, starvation, alcoholism, mineralocorticoid excess (primary and secondary hyperaldosteronism)
Excess renal loss	Bartter's syndrome; diuresis: diuretics with a pre-late distal locus osmotic diuresis, chronic metabolic alkalosis; impermeant anion antibiotics: carbenicillin, penicillin, nafcillin, or ticarcillin; renal tubular acidosis; hypomagnesemia; myelomonocytic leukemia
Gastrointestinal losses	Vomiting; diarrhea, particularly secretory diarrheas; villous adenoma
Shifts of extracellular fluid (ECF) to intracellular fluid (ICF) with altered internal potassium balance	β2 -Agonists, acute alkalosis, hypokalemic periodic paralysis, insulin therapy, vitamin B12 therapy, lithium overdose
Adapted from Andreoli TE: Disorders of fluid volume, electrolyte, and acid-base balance. In Wyngaarden JB, Smith LH Jr (eds): Cecil Textbook of Medicine, 17th ed. Philadelphia, WB Saunders, 1985, p 532.

or diuretics), and potassium shifts from the extracellular to the intracellular fluid. These shifts can occur with acute alkalosis, insulin therapy, stress-related catecholamine activity, and hypokalemic periodic paralysis. Surgical stress may reduce the serum potassium concentration by 0.5 mEq/L, and the administration of exogenous catecholamines such as isoproterenol, terbutaline, epinephrine, and ritodrine also decreases potassium levels.^{[40] [41] [42] [43]} Clinically, this includes pregnant patients on tocolytic therapy or respiratory treatment with β₂ -agonists and critically ill patients requiring pharmacologic cardiovascular support.

No studies demonstrate increased morbidity or mortality for patients undergoing anesthesia with a potassium level of at least 2.6 mEq/L. Even though administration of supplemental potassium chloride is a common practice for the anesthesiologist, studies demonstrate that in many instances therapy is ineffective, with most of the supplemental potassium being excreted in the urine despite continued hypokalemia. ^{[44] [45]} If therapy is indicated, the anesthesiologist uses intravenous potassium chloride. Because the rate of administration of potassium must be adjusted for the rate of distribution through the extracellular space before entry into the intracellular space, the rate of potassium administration is limited to 0.5 to 1.0 mEq/kg/hour. The typical replacement rate is 10 to 20 mEq/hour for a normal adult with constant monitoring of the electrocardiogram ^{[46] [47]} ( Table 46-8 ).