Emergency Management of Hyperkalemia

Severe hyperkalemia is a life-threatening condition requiring emergent diagnosis and treatment. As such, it is well within the scope of practice for emergency physicians to be experts in the management of severe hyperkalemia.

The ratio of intracellular to extracellular potassium largely controls the electrical potential of the cell and thus controls the function of excitable tissue such as the myocardial cells. Very little change in the plasma concentration of potassium will easily effect this ratio. It is easy to understand why the body maintains potassium concentration (Pk) within a very narrow window.

Two physiologic systems are largely responsible for potassium balance. One system regulates the Pk across the cell membrane. This is effected by insulin, catecholamines, acid-base balance, and plasma tonicity. The other system effects the intake and elimination of potassium. In patients with normal renal function, the kidney eliminates 95% of the potassium load while the remainder is excreted by the gut.

Excess potassium effects many tissues. In the heart, potassium depolarizes the cellular membrane, slows ventricular conduction, and decreases the duration of the action potential. The classic EKG findings (in order of appearance) include peaked t waves, widening of the QRS, loss of the p wave, "sine wave" configuration, or ventricular fibrillation or asystole. Unfortunately, many factors influence the effect of Pk on the EKG and the EKG does not have the sensitivity that one would hope to find. Normal EKGs have been documented in patients with severe hyperkalemia, so do NOT depend on a normal EKG to diagnose a laboratory error (i.e. hemolysis).

Hyperkalemia effects nerve tissue as well. Patients may have paras emergently thesias, weakness, or flaccid paralysis that spares the diaphragm. Deep tendon reflexes will be depressed or absent.

Treatment includes stabilizing excitable membranes, redistributing potassium into the cells, and enhancing elimination of excess potassium. Hyperkalemia should be treatedfor all patients who either have a Pk >6.5 mmol/L or who have EKG changes consistent with hyperkalemia regardless of the Pk.

Calcium directly antagonizes the myocardial cells by reducing the threshold potential of the myocytes. The preferred dose is 10ml of IV 10% calcium gluconate over 10 minutes. Gluconate causes less tissue necrosis in the event of vascular extravasation. Onset of action is <3>

Insulin helps to redistribute potassium into the cell via activated of Na-K-ATPase. A dose of 10 units of regular insulin plus 25 gms of D50 lowers the Pk approximately 0.6 mmol/L within 15 minutes. An infusion of dextrose is recommended after the initial bolus in order to prevent hypoglycemia.

Albuterol also acts to redistribute potassium across the cellular membrane. Pk declines by 0.6 mmol/L after 10 mg of inhaled albuterol and by about 1 mmol/L after 20mg. Onset is approximately 30 minutes and lasts for 2 hours. Subcutaneous terbutaline exerts a similar effect at 60 minutes.

Bicarbonate has been widely used in the treatment of hyperkalemia. Recent studies have demonstrate little to no effect on the Pk until after 4 hours of continuous infusion. Reserve bicarbonate for other uses.

Elimination of potassium in patients with normal kidneys is accomplished by the use of diuretics. Thiazide and loop diuretics are both effective. Onset of both furosemide and bumetanide in approximately 15 minutes. Caution should be used in euvolemic patients as volume contraction will lead to decreased renal blood flow and thus reduced potassium elimination. Fluids may be needed in this patient population. In patients with renal failure, dialysis will lower Pk but approximately 2 mmol/l over 180 minutes. Some degree of a rebound rise in Pk will occur after dialysis due to redistribution of potassium. The degree of the rebound is proportional to the pre-dialysis Pk.

Sodium polystyrene (SPS, Kayexalate) is a cation exchange resin that is given orally or rectally. Each gram binds 0.65 mmol of potassium although the true effect is unpredictable. Due to its slow rate of onset and concerns over toxicity leading to intestinal necrosis, it is of little utility to the practicing emergency physician.

References:

Weisburg, LS. Management of Severe Hyperkalemia. Crit Care Med. 2008; 36(12): 3246-3251.