A Practical and Pathophysiologic Approach to Hypokalemia

Abstract

Hypokalemia is not an isolated disease but an associated finding in a vast number of different diseases; it poses a great challenge in correct diagnosis and proper management. Hypokalemia usually arises from a shift of potassium (K + ) into cells and/or a net loss of K + . Besides a detailed history and physical examination, measurement of K + excretion rate with freshly-voided and/or 24-hour urine and assessment of blood acid-base status can help discriminate between the various causes of hypokalemia. In patients with a low rate of K + excretion, hypokalemia can be due to an acute shift of K + into cells, intestinal/sweating K + loss, or prior renal K + excretion. In patients with a high rate of K + excretion, there may be either increased flow rate or increased K + secretion, seen with fast sodium (Na + ) or slow chloride (Cl − ) disorders, in the cortical collecting ducts (CCD). An increased flow rate in the CCD arises from increased osmole excretion (whether solutes or electrolytes). Patients with fast Na + disorders have a high extracellular fluid (ECF) volume and thus high blood pressure associated with a state of high mineralocorticoid activity. Measurement of renin activity, aldosterone, and cortisol levels in plasma helps distinguish between the causes. Patients with slow Cl − disorders usually have low to normal ECF volume and blood pressure and are usually associated with abnormal acid-base states. In patients with metabolic alkalosis, urine Na + and Cl − excretion rate reveal the basis for renal Na + wasting and distinguish it from non-renal Na + loss. In patients with hyperchloremic metabolic acidosis, an assessment of the ammonium excretion rate (NH 4 + ) separates those with renal tubular acidosis (low NH 4 + excretion) from those with other causes. The treatment of hypokalemia depends on the degree and timing of hypokalemia, clinical manifestations, underlying causes, and potential risks from associated conditions.