Peri-operative Management of Patients with Altered Potassium Homeostasis

Abstract

P otassium 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.