Diarrhea, Hypokalemia, and Refractory Weakness

Potassium is the main intracellular cation, and the resting membrane potential depends largely on the potassium gradient across the cell membrane. A low serum potassium increases the gradient between intracellular and extracellular potassium, so more potassium leaves the cell and the inside of the cell becomes more negative. This is hyperpolarization. A hyperpolarized cell is farther from threshold, so a stimulus that would normally trigger an action potential may not do so. In skeletal muscle this produces weakness, cramps, and reduced deep tendon reflexes. In smooth muscle of the bowel it produces decreased motility and constipation. The ECG changes reflect delayed repolarization: flattened T waves, a prominent U wave, and premature ventricular contractions. The reasoning is that the symptoms are not merely low potassium in the blood but altered excitability of muscle and cardiac cells. Severe hypokalemia can also cause ileus and life-threatening arrhythmias.

Magnesium is a cofactor for the sodium-potassium pump and helps regulate potassium channels in the kidney. When magnesium is low, potassium leaks out of cells and is wasted in the urine through channels that magnesium normally blocks. Giving potassium without correcting magnesium often leaves the serum potassium low because the kidney continues to excrete it. That is why the magnesium of 1.2 mg/dL must be replaced. IV potassium is dangerous because it can raise serum potassium abruptly and cause arrhythmias, including ventricular tachycardia and fibrillation. It must be infused at a controlled rate using a pump, never as a bolus, and usually through a central line at higher concentrations because peripheral administration can cause phlebitis. Cardiac monitoring is required. The nurse should verify the rate, concentration, and route, and check the potassium level before and after infusion. The reasoning is that the therapeutic margin for IV potassium is narrow.

About 98% of body potassium is intracellular, so the serum level reflects only a small fraction of total body stores. A serum potassium of 2.8 mEq/L usually represents a large total-body deficit because potassium has moved out of cells or been lost, and the serum level falls only after those reserves are depleted. In diarrhea, potassium is lost in the stool, and aldosterone and ADH effects can increase renal loss. Acid-base status, insulin, and beta-adrenergic activity also shift potassium between compartments without changing total body content. Therefore the serum value can appear only mildly low while the intracellular deficit is severe, and it can fall further as treatment shifts potassium back into cells. The reasoning is that treatment must replace the deficit gradually and monitor for changes, rather than relying on a single serum value.