Potassium Metabolism

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Potassium Balance.-The K+ content of the body depends on the balance of K+ intake and K+ loss. As K+ is an important constituent of all cells, animal and vegetable, any reasonably arranged diet will supply normal K+ needs. Excretion of K+^{Superscript text} occurs in the urine and some is lost in the faeces. A diet of pure carbohydrate and fat contains no K+ there is, of course, no K+ intake during starvation. The normal K+ ion concentration in serum is about 20 mg-%(5m.Eq./L); the concentration in the cells is far higher as K+ is the principal intracellular electrolyte. AS the surface membrane of most cells is between the K+ the great difference which are normally present between the K+ ion concentration in the intracellular and extra cellular fluids are maintained by the active cation transfer by the cells, the necessary energy being derived from metabolic processes; when cell metabolism is depressed, e.g. in stored red cells, K+ move passively out of the cells into intracellular K+ is combined with organic phosphate esters. In states of acidosis these esters undergo phosphorolysis releasing inorganic phosphate which. Together with K+ ions, passes into the plasma ; as some of the K+ is excreted in the urine as KH2PO4, acidosis leads to depletion of the K+ reserves of the tissues. In dehydration there is a loss of K+ from the cells Regulation of Serum K+-Our knowledge of factors which regulate the serum K+ level is still imperfect ; it is not clear to what extent K+ can be withdrawn from the plasma and stored in the cells when the serum K+ falls. Serum K+ depends to an important extent on the degree of K+ reabsorption which takes place in the renal tubules, which in turn depends on the level of adrenocorticoid activity. In Addison's disease serum K+ often rises ; conversely, serum K+ falls in hypercortism or after injection of DOCA, cortisone or ACTH. In familial periodic paralysis a fall of serum K+ occurs which is roughly proportional to the degree of muscular weakness. In renal disease serum K+ may rise from K+ retention (owing to decreased glomerular filtration) or fall from excessive excretion in the urine (owing to decreased reabsorption of K+ in the tubules). Severe K+ depletion occurs during the phase of recovery from diabetic coma ; if the K+ intake at this time is small, the serum K+ falls. Serum K+ may fall owing to K+ loss in severe vomiting, diarrhoea or steatorrhoea Function of Potassium- The role of K+ is still imperfectly understood. It is related to the excitability of nerve fiber and muscle fiber. It may be involved in transmission processes at the motor end plate and in autonomic ganglia. It modifies the action of heart muscle. Alteration in the electrocardiogram is a sensitive index of changes in the serum K+ level. A fall of serum K+ causes diminution, depression or occasional inversion of the T wave; the QT interval is prolonged, the ST segment is depressed. An abnormally high serum K+ level causes the T waves to become exaggerated and sharply peaked; eventually the P waves may disappear. The role of intracellular K+ as a buffer is considered in the case of the red cells and of the general tissue cells. Symptoms of Potassium Lack- The clinical findings are variable; muscular weakness and the e.c.g. changes mentioned above are the most regularly observed. Other symptoms noted in states of K+ lack and relieved by K+ therapy are: shallow rapid breathing, abdominal distention are mental changes, e.g. lethargy, apathy or delirium. K+ lack must be treated by giving potassium in amounts sufficient to restore not only the serum K+ level, but also the intracellular reserves ; the total loss of K+ which occurs in depleted patients may amount to 8-36 g. If the patient can take food by mouth, 3-5 g. of K+ (as KH2 PO4 and K2HPO4) may be added to each litre of milk or fruit drink ; if the flow of urine is adequate such treatment is safe. In urgent cases K+ may be given parenterally, e.g. in Butler’s solution or as Elkinton’s solution containing 4.5 g of K2HPO4, 1 g of KH2 PO4 and 5.5 g. of NaCl per litre. The rate of infusion should not exceed 20 m. Eq. (0.8 g.) of K+ per hour, corresponding to 300 c.c. per hour of Elkinton’s solution. Parental K+ therapy may be dangerous if the urinary output is low; the clinical state, the serum K+ level, and the e.c.g. appearances should be carefully watched for the first signs of potassium poisoning and appropriate measures taken.

Ref.: Elkinton and Tarail, Amer. J. Med., 1950, 9, 200 Hawkins et al.,5 Lancet, 1951, I, 318. Eliel et .al. New Engl. J. Med., 1950, 243, 471, 518