Untitled Document

Shedding Some "Lyte" on Potassium Replacement
Volume X, Issue 9
Harold J. DeMonaco, M.S., Director of Drug Therapy Management

The replenishment or maintenance of potassium stores in hospitalized patients represents one of the most common occurrences in routine clinical care. Unfortunately, it also represents one of the most dangerous therapeutic interventions in hospitals today.

Hypokalemia is arguably the most common electrolyte abnormality seen in clinical practice. Up to 20% of hospitalized patients may have a depletion of potassium stores. Interestingly, a study conducted in Austria in hospitalized patients suggests that up to 50% of patients with hypokalemia were normokalemic on admission.¹ This suggests that much of the hypokalemia encountered in hospitalized patients is iatrogenic either due to inadequate attention to intake (80-100 mmol/day in an adult), administration of drugs which alter the intracellular/extracellular ratio, or the use of potassium-wasting diuretics, such as furosemide.

Potassium is the most abundant cation in the body, with total body stores exceeding 4000 mmol. Intracellular potassium stores exceed extracellular stores by a factor of almost 50:1, with 98% of total stores in the intracellular fluid. Only about 60-80 mmol of potassium is present in extracellular fluid in the average adult. This intracellular/extracellular potassium ratio is responsible for the resting membrane potential of cells. Rapid shifts in the equilibrium alter the resting membrane potential until the equilibrium is renewed. Potassium balance is closely regulated by a complex system of feedback mechanisms. Insulin and beta-adrenergic catecholamines play critical roles in this homeostasis and, more importantly, in the intracellular/extracellular ratio.² Both increase intracellular potassium uptake.

Figure 1

Excretion

Extracellular Potassium Stores
80 mmol

Most hospitalized patients with hypokalemia have serum levels in the 3 to 3.5 mmol per liter (mEq/liter) range. These patients are usually asymptomatic and do not normally require intravenous therapy. Oral replacement of potassium stores is preferred. Patients with more severe hypokalemia can present with symptoms ranging from weakness and constipation to cardiac conduction disorders. The likelihood that a patient will experience symptoms is related to the degree of hypokalemia, the speed with which it developed and underlying factors such as concomitant drugs or diseases. Serum potassium decreases by roughly 0.3 mmol per liter for each 100 mmol reduction in total body stores. The total deficit in body stores should be calculated and replacement planned over an appropriate period of time. Oral potassium replacement is preferred unless the degree of hypokalemia is severe and symptoms are evident. Intravenous potassium replacement can only be done safely if the rate of replacement is less that the rate of extracellular-intracellular transport. If given at a rate that exceeds the rate of equilibrium, potassium serum levels will rise to dangerous levels.³

Hypokalemia is rarely a medical emergency. Before embarking on replacement, the underlying cause should be identified unless life-threatening arrhythmias are present. If serious ventricular arrhythmias do exist, therapy should be initiated first. Remember that the safety of replacement is directly related to the rate of administration. If the rate of potassium administration is greater than the rate of equilibration plus the rate of excretion, a rapid rise in serum potassium is likely. Extracellular potassium stores only equal 60-80 mmol. The administration of 80 mmol over a short period of time essentially doubles the serum level until equilibrium occurs. For that reason, potassium replacement should not exceed a rate of 20 mmol (mEq) per hour.