It is abundant in both plant and animal tissues and primary dietary deficiency is not observed. However, potassium depletion is encountered frequently in clinical medicine secondary to a number of pathologic states. The minimal daily requirement of potassium is not known but presumably is similar to that of sodium. Ingestion of excessive amounts of potassium leads to toxicity. Normal persons can take 6 gm. daily without danger but this amount may be harmful if there is renal damage or adrenal insufficiency.
Potassium is the principal cation of the cells, the concentration in extracellular fluids amounting to only a small per cent of the intracellular concentration. In the normal adult, the average level of potassium in serum is 4.2 mEq/1, in the cells, 112mEq/1. Total exchangeable potassium has been found to be 47 mEq/kg of body weight in the male, 40 mEq/kg in the female.
The important role of potassium in metabolism is indicated by the close relationship between cell growth and potassium accumulation and cell breakdown and potassium loss. Potassium is closely associated with protein and glycogen and functions in the cells in coniunction with phosphate, chloride and bicarbonate. The excitability of nerve tissue, the transmission of nerve impulses and the contractility of all types of muscles are influenced profoundly by potassium concentration. Paralysis of striated muscle is observed when the serum concentration is less than 2 to 2.5 mEq/1. Smooth muscle and cardiac muscle, likewise, are affected by potassium deficiency. Potassium is involved in a number of enzyme reactions. According to Greisheimer (67), the transport of potassium “across cell boundaries against existing ionic concentration gradients seems to be linked with the carbohydrate phosphorylation cycle.”
The kidney is largely responsible for maintaining a balance between the intake and output of potassium in a manner which resembles that for sodium except that during fasting or after tissue damage, potassium is released from the cells and excreted in the urine. Potassium leaves the cells with nitrogen in the ratio of about 2.7 mEq potassium per gram of nitrogen. Schwartz found that potassium excretion is increased under the following Conditions: when serum potassium concentration increases, in both acidosis and alkalosis, by administration of desoxycorticosterone, aldosterone, corticosterone, other corticoids or adrenocorticotropic hormone, or by activation of the adrenal cortex. Urine with a high level of sodium is usually high in potassium as well. The mercurial diuretics produce alkalosis that may or may not be accompanied by potassium deficit. In renal failure with oliguria, or when shock and dehydration are present, potassium may be retained and toxic levels may ensue. If urine volume is high, potassium excretion is usually maintained even in advanced renal insufficiency.
Moderate amounts of potassium are lost in the stools, about 2 millimoles per day being excreted by healthy infants. In infantile diarrhea, potassium loss in the stools may amount to 17 millimoles per day.
Potassium deficiency is likely to develop in acidosis and alkalosis and in conditions in which tissues are broken down with resultant loss of potassium in the urine. Such conditions include starvation, infections, tumors, diabetes mellitus and stress situations such as trauma or operative procedures. Potassium excretion may be increased by altered renal tubular function in alkalosis. Also, potassium deficiency alters renal function so that alkalosis appears or persists. Potassium deficiency may be induced by administration of diuretics and of adrenal cortical hormones. Loss of potassium in gastrointestinal secretions through diarrhea or vomiting may lead to depletion. Intravenous alimentation with solutions free of potassium may also result in deficiency. The expenditure of potassium under conditions of parenteral feeding varies from 1 to 3 mEq per 100 calories metabolized, usually 20 to 30 mEq per square meter of body surface in 24 hours.
The clinical features of potassium deficiency are dependent on decreased muscular irritability and disturbances of conduction and contractility of the heart muscle. Lassitude and general muscular weakness is followed by flaccid paralysis, lethargy and, at times, coma. Decreased tone of the smooth muscles produces gastric and intestinal distention, nausea, vomiting and paralytic ileus. Cardiac dilation, hypertension, congestive heart failure and cardiac arrest may ensue. Weakness of the respiratory muscles may be observed. Death may be the result of cardiac or respiratory failure or paralytic ileus. The paralysis of muscles, both smooth and skeletal, appears to be due to failure of myoneural conduction. The electrocardiogram often shows flat or inverted T-waves, prominent U waves, prolongation of the Q-T interval and RS-T segment depression.
Estimation of serum concentration of potassium is useful in evaluating the status of potassium nutrition if findings are interpreted in the light of certain basic considerations. Serum concentration of potassium reflects changes in serum pH and in concentration of potassium in cells (69). Scribner and Burnell (61h) suggest that potassium deficiency and excess be defined in terms of a ratio (Kr) between the total potassium content and the total potassium capacity of the body. The latter means “the sum total of all anions and other chemical groups outside the extracellular space capable of holding or binding potassium ions.” Potassium depletion represents a decrease in Kr; i. e., in the content-capacity ratio; potassium excess, an increase in this ratio. Interpretation of serum potassium concentration requires consideration of factors which can alter concentration independently of Kr. The most notable factor is change in extracellular pH. In severe alkalosis, serum potassium concentration may be low with an essentially normal content-capacity ratio, i. e., even if cell potassium is normal. Serum concentration is especially low when cellular potassium is decreased. In alkalosis, serum potassium concentration is not likely to be high unless renal function is impaired and cell potassium is relatively normal.
In severe acidosis, serum potassium concentration may be high with a normal Kr. Concentration may be either normal or high despite cellular defects. In fact, a normal serum potassium concentration in acidosis reflects a moderate potassium depletion while a low serum concentration reflects a profound depletion. Scribner and Burnell (61h) point out that water depletion, changes in the size of the extracellular space and changes in renal function do not cause significant changes in serum potassium concentration which do not reflect Kr. Accordingly, they state that “in the majority of clinical situations, the serum potassium concentration interpreted in the light of extra-cellular pH will reflect Kr. accurately and, therefore, the potassium needs of patients.”
Diabetic coma may be used to illustrate the above principles. Acidosis causes an initial hyperkalemia. The magnitude of potassium depletion can be estimated by the severity of the acidosis and the serum potassium concentration. When the initial serum potassium concentration is normal or low, initial potassium depletion has been moderate or marked. After administration of insulin, glycogen is deposited and potassium is drawn into the cells. Symptoms of deficiency may develop rapidly with restoration of metabolism if deficits have been marked (69). Appreciation of the magnitude of initial depletion and institution of proper therapy is of great importance in preventing serious deficiency from developing. Patients with alkalosis and hypokalemia, also, develop symptoms readily since alkalosis increases the tendency to transfer potassium from extracellular to intracellular fluids. In non-diabetic acidosis with potassium deficiency, hypokalemia develops more slowly due in part to retardation in transfer of potassium into the cells by the acidosis and to higher initial serum potassium concentration in most instances.
Potassium excess and an increase in serum potassium is less common than hypokalemia. It is encountered most often in advanced renal disease with oliguria or when renal function is impaired by shock or dehydration. It is also seen in adrenal insufficiency, or it may be due to the injudicious use of potassium salts. Clinical findings in hyperkalemia include mental confusion, weakness, numbness and tingling of the extremities, pallor, cold skin, disturbances in cardiac rhythm, and peripheral vascular collapse. A flaccid paralysis of skeletal muscle has been observed in advanced renal failure when serum concentration of potassium was high, resembling the paralysis seen in potassium deficiency (69). Electrocardiographic changes may appear at serum potassium concentrations above 6.5 mEq/1 and abnormalities roughly parallel the degree of potassium increase. There is alteration and peaking of the T waves and prolongation of the QRS and PR intervals. Finally, auricular standstill and delay in intraventricular conduction may occur ending ultimately in total arryhthmia and cardiac arrest.