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The potassium ion is the principal intracellular cation of most body tissues. Potassium ions participate in a number of essential physiological processes, including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal, and smooth muscle, and the maintenance of normal renal function.
The intracellular concentration of potassium is approximately 150 to 160 mEq/L. The normal adult plasma concentration is 3.5-5.0 mEq/L. An active ion transport system maintains this gradient across the plasma membrane.
Potassium is a normal dietary constituent; under steady-state conditions, the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. The usual dietary intake of potassium is 50 to 100 mEq per day.
Potassium depletion may occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Such depletion usually develops slowly as a consequence of prolonged therapy with oral diuretics, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Depletion can develop rapidly with severe diarrhea, especially if associated with vomiting. Potassium depletion due to these causes is usually accompanied by a concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. Potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent U waves in the electrocardiogram, and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine.
If potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long-term diuretic therapy, supplemental potassium in the form of high-potassium food or potassium chloride may be able to restore normal potassium levels.
In rare circumstances (e.g., patients with renal tubular acidosis) potassium depletion may be associated with metabolic acidosis and hyperchloremia. In such patients potassium replacement should be accomplished with potassium salts other than the chloride, such as potassium bicarbonate, potassium citrate, potassium acetate, or potassium gluconate.
The potassium chloride in Slow-K (potassium chloride) is completely absorbed before it leaves the small intestine. The wax matrix is not absorbed and is excreted in the feces; in some instances the empty matrices may be noticeable in the stool. When the bioavailability of the potassium ion from Slow-K (potassium chloride) is compared to that of a true solution the extent of absorption is similar.
The extended-release properties of Slow-K (potassium chloride) are demonstrated by the finding that a significant increase in time is required for renal excretion of the first 50% of the Slow-K (potassium chloride) dose as compared to the solution.
Increased urinary potassium excretion is first observed 1 hour after administration of Slow-K (potassium chloride) , reaches a peak at 4 hours, and extends up to 8 hours. Mean daily steady-state plasma levels of potassium following daily administration of Slow-K (potassium chloride) cannot be distinguished from those following administration of a potassium chloride solution or from control plasma levels of potassium ion.
Last reviewed on RxList: 4/13/2009
This monograph has been modified to include the generic and brand name in many instances.
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