Discuss the treatment of hyperkalemia and its associated metabolic problems.
Patients with chronic renal failure experience an extraor-dinarily wide range of serum K+ levels ranging from 2.5 to 6.0 mEq/L. Acute hyperkalemia suppresses electrical con-duction and can ultimately cause cardiac arrest. Associated ECG changes include prolonged PR intervals, widened QRS complexes, and peaked T waves before ventricular fibrilla-tion actually occurs. Fatal dysrhythmias may occur without these gradual changes.
Extracellular acidosis results in an increased concentra-tion of hydrogen ion (H+), which moves into the cell along its concentration gradient. To preserve electrical neutrality, K+ moves out of the cell. In this way, extracellular acidosis promotes extracellular hyperkalemia. In acute metabolic acidosis, serum K+ increases approximately 0.5–0.8 mEq/L for every drop in pH of 0.1 units. Normally the ratio of intracellular to extracellular K+ concentration is approxi-mately 40:1 or 160:4 mEq/L in vivo. This is maintained by an energy-dependent Na+–K+-ATPase pump at the cell membrane, which brings K+ intracellularly against its concentration gradient.
In chronic renal failure patients, aggressive treatment of hyperkalemia is appropriate. The treatment for acute hyperkalemia consists of the intravenous administration of insulin 5–10 units with 25 mL of 50% dextrose, sodium bicarbonate 44.6 mEq/L, and calcium chloride 500 mg. Insulin promotes transmembrane cellular transport of K+ intracellularly, thus reducing serum levels of K+. Calcium chloride is given to reduce the arrhythmogenic potential.