The total body potassium (K+) content in a normal adult is approximately 3,000 to 4,000 meq, 98% of which is intracellular. The normal serum potassium concentration ranges from 3.5 to 5meq/L, whereas that inside the cell is approximately 150 meq/L. Thus, the ECF compartment from which we measure the serum K+ level contains only 2% of the total body potassium. The results therefore are misleading as to the degree of total K+ deficit or excess. With the major effector organ of potassium excretion being the kidney, its balance is regulated primarily by two physiologic stimuli; aldosterone and K+ concentration itself.
Hypokalemia or low serum potassium occurs as a result of three main mechanism a.) A shift of K+ to the ICF, b.) Inappropriate renal wasting and c.) Extrarenal K+ loss. In the critically ill patients these etiologies are of special importance. 1.) Transcellular shift : movement of K+ into cells may transiently decrease the plasma K+ without altering the total body K+ content. The magnitude of the change is relatively small, often <1meq/L, but it may amplify hypokalemia from other causes. Triggers of intracellular shift include alkalemia, insulin and catecholamines( either produced endogenously through the stress response or administered exogenously.) Marked anabolism can also result in K+ translocation into cells. The most common example of this occurs with the refeeding syndrome, when nutritional support is initiated after a long period of starvation. 2) Gastrointestinal K+ loss : In general, gastrointestinal fluids have a significant K+ content and excessive enteral losses may result in hypokalemia. When lower GI tract is the source of the loss, there is a concominant metabolic acidosis from bicarbonate loss. When losses are from the upper GI tract , metabolic alkalosis is usually present. 3.) Renal K+ loss: Urinary K+ wasting may be caused by factors that augment the distal nephron tubular flow rate or by factors that increase the distal tubular fluid [K+]. Augmented distal flow occurs with thiazide and loop diuretic use, osmotic diuresis, hyperaldosteronism of any cause, the urinary excretion of anions which causes coexcretion of cations including K+, hypomagnesemia and amphotericin B. Hypokalemia seen in diabetic ketoacidosis result from glucosuria, volume depletion and intracellular shift due to insulin therapy.
Treatment of hypokalemia consists of rapid correction when symptoms or electrocardiographic changes are present. In these cases when patients are unable to take enteral medications, IV repletion is appropriate. Otherwise it is generally safer to correct hypokalemia via the enteral route bcoz larger doses can be administered orally given the limitations on the rate of IV infusion of K+. KCL is usually the preparation of choice regardless of the route of administration as it promotes more rapid correction of hypokalemia and associated metabolic alkalosis than the other preparations. Potassium citrate or bicarbonate may be useful in correcting hypokalemia and acidosis associated with chronic diarrhea or renal tubular acidosis. Hypomagnesemia should be sought in all hypokalemic patients and corrected prior to, or concurrently with K+ repletion. Without Mg+ repletion, reduced renal K+ absorption in the loop of Henle and collecting duct would result in the prompt loss of administered potassium. Although there are rules to estimate the total K+ deficit present, mechanism of transcellular shift are difficult to predict and the degree of K+ depletion does not correlate well with the serum[K+]. The serum K+ should therefore be monitored closely and frequently during therapy .