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Abstract Potassium plays a key role in maintaining cell function. Almost all cells possess an Na+-K+-ATPase, which pumps Na+ out of the cell and K+ into the cell and leads to a K+ gradient across the cell membrane (K+ in>K+ out) that is partially responsible for maintaining the potential difference across the membrane which is critical to the function of cells, particularly in excitable tissues, such as nerve and muscle. The body has developed numerous mechanisms for K+ homeostasis. The kidney is primarily responsible for maintaining total body K+ content by matching K+ intake with K+ excretion. Adjustments in renal K+ excretion occur over several hours; therefore, changes in extracellular K+ concentration are initially buffered by movement of K+ into or out of skeletal muscle. The regulation of K+ distribution between the intracellular and extracellular space is referred to as internal K+ balance. The most important factors regulating this movement under normal conditions are insulin and catecholamines. Despite mechanisms to maintain K+ homeostasis, hypokalemia is frequently encountered in clinical practice. Transient causes of hypokalemia are due to cellular shift, whereas sustained hypokalemia can be manifested by either inadequate intake or excessive K+ loss. Hypokalemia resulting from excessive K+ loss can be due to renal or extrarenal losses. The cause and source of hypokalemia can be assessed by obtaining a clinical history and conducting a physical examination, with particular attention paid to volume and acid base status of the patient. The severity of the manifestations of hypokalemia tends to be proportionate to the degree and duration of the reduction in serum potassium. Symptoms generally do not become manifest until the serum potassium is below 3.0 meq/L, unless the serum potassium falls rapidly or the patient has a potentiating factor, such as a predisposition to arrhythmia due to the use of digitalis. Symptoms usually resolve with correction of the hypokalemia. Cellular redistribution is a more important cause of hyperkalemia than hypokalemia. It is important to note that as little as a 2% shift of intracellular K+ to the extracellular fluid will result in a serum K+of 8 mEq/l.Disturbances in serum K+ concentration due to cell shifts are generally transient in nature, whereas sustained hyperkalemia is due to impaired renal excretion. Metabolic acidosis promotes K+ exit from cells dependent upon the type of acid present. Mineral acidosis (NH4Cl or HCl) causes the greatest efflux of K+ from cells, whereas organic acidosis (i.e., lactic, β-hydroxybutyric, or methylmalonic acid) results in no significant efflux of K+. Hyperkalemia associated with lactic acidosis is the result of cell ischemia. The most serious manifestations of hyperkalemia are muscle weakness or paralysis, cardiac conduction abnormalities, and cardiac arrhythmias. These manifestations usually occur when the serum potassium concentration is ≥7.0 meq/L with chronic hyperkalemia or possibly at lower levels with an acute rise in serum potassium. Pseudohyperkalemia should be excluded before concluding that hyperkalemia is due to cell shift or abnormal renal K+ excretion. Pseudohyperkalemia is the result of release of K+ from cells during the phlebotomy procedure, or specimen processing, and is defined by a serum K+concentration 0.5 mEq/l greater than the plasma K+ concentration. The goals of therapy in hypokalemia are to prevent or treat life threatening complications (arrhythmias, paralysis, rhabdomyolysis, and diaphragmatic weakness), to replace the potassium deficit, and to diagnose and correct the underlying cause. The urgency of therapy depends upon the severity of hypokalemia, associated and/or comorbid conditions. The urgency of treatment of hyperkalemia varies with the presence or absence of the symptoms and signs associated with hyperkalemia, the severity of the potassium elevation, and the cause of hyperkalemia.Potassium a major intra cellular cation is intimately involved in the maintenance of resting membrane potential. Hypo or hyperkalemia can cause disturbances of muscle, nerve and cardiac cell excitability. These three excitable cells are closely associated with anaesthesia. The absolute levels of potassium, presence of symptoms, acute or chronic disturbance and associated risk factors should be borne in mind perioperatively. |