Treatment of Hyperkalemia
Recognition and treatment of hyperkalemia is crucial to avoid serious complications, such as death. The urgency needed to address this problem is based on a few factors: how fast the hyperkalemia developed, the current serum potassium level, the degree of signs/symptoms, and the underlying cause. Severe hyperkalemia is define as a serum potassium level of greater than or equal to 5.5 mEq/L. Concerning signs and symptoms include ECG changes (ie. peaked T waves, widened QRS, prolonged PR interval), neuromuscular weakness, and/or paralysis.
The standard of care for treating life-threatening hyperkalemia involves 3 approaches:
Cardiomyocytes stabilization
Transcellular Shift
Excretion
For cardiomyocytes stabilization, most providers will use 1 gram of calcium gluconate. Typically it is bolused slowly (3-4 intermittent pushes totaling 1 gram) to avoid sudden hypertension. Calcium gluconate is usually preferred over calcium chloride because the later tends to be more irritating to peripheral vessels and more likely to cause tissue necrosis with extravasation. That’s why calcium chloride is usually reserved for when a patient has central line access. “Stabilizing” the cardiac membrane refers to the lowering of the resting action potential of cardiomyocytes, closer to their typical resting potential when potassium levels are normal (-90 mEv).
There are three main drugs used for shifting potassium back into cells. The first is insulin. We typically give 10u of IV insulin along with 25-50ml of D50 to avoid hypoglycemia. Insulin stimulates the sodium-hydrogen antiporter, leading to sodium influx. This increase in intracellular sodium then triggers the sodium-potassium ATPase transporter, which causes an efflux of sodium out of the cell and an influx of potassium into the cell. The second drugs of choice is albuterol. Albuterol is a beta-2 agonist that creates a release of glucose, thus stimulating insulin release and uses the same mechanism that I previously mentioned. The typical dose is 10-20mg of nebulized albuterol. The third choice for shifting potassium into cells is bicarbonate. This is typically dosed as a bolus of 1 mEq/kg. The mechanism is a rise in serum pH, causing cells to shift potassium into cells in an attempt to buffer the change in pH.
Lastly, the ultimate treatment for hyperkalemia is excretion of excess potassium from the body. The body gets rid of potassium via the kidneys (90%) and colonic system (10%). Lasix is a great option for patients who make urine. In fact, many patients who are on Lasix for heart failure will need potassium supplementation because they pee out so much potassium. If a patient does not make urine, then urgent dialysis may be necessary. This may seem like a drastic treatment option, but it can be life saving and should be considered when dealing with severe hyperkalemia with EKG changes. Kayexalate (sodium polystyrene) or Lokelma (sodium zirconium cyclosilicate) are potassium binds in the colonic system that usually take a couple days to work but can effectively lower serum potassium levels in patients who are able to make bowel movements. Occasionally these medications can cause constipation and need to be administered with a stool softener.
