Hyperkalemia

Hyperkalemia Serum potassium > 5.0 mEq/L ( > 5.0 mmol/L)

 Myocyte action potential:

·         Depolarization of membrane potential

·         Decreased rate of Na influx (slope of phase 0) membrane potential determines the number of Na channels activated during depolarization. See figure below.  Causes a reduced rate of conduction and widened QRS.

·         Increased rate of K efflux (slope of phase 3); activation of Kir channels. Shortens repolarization time, leads to peaked T waves and shortening of QT interval.

·         

Regulation of SA node 

serum ion concentrations

Changes in the serum concentration of ions, particularly potassium, can cause changes in SA nodal firing rate.  Hyperkalemia induces bradycardia or can even stop SA nodal firing.  Hypokalemia increases the rate of phase 4 depolarization and causes tachycardia.  It apparently does this by decreasing gK during phase 4.

Hyperkalemia Revisited

Walter A. Parham, MD, Ali A. Mehdirad, MD, FACC, Kurt M. Biermann, BS, and Carey S. Fredman, MD, FACC

Tex Heart Inst J. 2006; 33(1): 40–47.

Skeletal Muscle (from Harrison’s)

Since the resting membrane potential is related to the ratio of the ICF to ECF K⁺ concentration, hyperkalemia partially depolarizes the cell membrane. Prolonged depolarization impairs membrane excitability and manifests as weakness, which may progress to flaccid paralysis and hypoventilation if the respiratory muscles are involved.

Acid Base

Hyperkalemia also inhibits renal ammoniagenesis and reabsorption of NH₄⁺ in the TALH. Thus, net acid excretion is impaired and results in metabolic acidosis, which may further exacerbate the hyperkalemia due to K⁺ movement out of cells.

Tx

Hyperkalemia: Treatment

The approach to therapy depends on the degree of hyperkalemia as determined by the plasma K⁺ concentration, associated muscular weakness, and changes on the electrocardiogram. Potentially fatal hyperkalemia rarely occurs unless the plasma K⁺ concentration exceeds 7.5 mmol/L and is usually associated with profound weakness and absent P waves, QRS widening, or ventricular arrhythmias on the electrocardiogram.

Severe hyperkalemia requires emergent treatment directed at minimizing membrane depolarization, shifting K⁺ into cells, and promoting K⁺ loss. In addition, exogenous K⁺ intake and antikaliuretic drugs should be discontinued. Administration of calcium gluconate decreases membrane excitability. The usual dose is 10 mL of a 10% solution infused over 2–3 min. The effect begins within minutes but is short-lived (30–60 min), and the dose can be repeated if no change in the electrocardiogram is seen after 5–10 min. Insulin causes K⁺ to shift into cells by mechanisms described previously and will temporarily lower the plasma K⁺ concentration. Although glucose alone will stimulate insulin release from normal pancreatic cells, a more rapid response generally occurs when exogenous insulin is administered (with glucose to prevent hypoglycemia). A commonly recommended combination is 10–20 units of regular insulin and 25–50 g of glucose. Obviously, hyperglycemic patients should not be given glucose. If effective, the plasma K⁺ concentration will fall by 0.5–1.5 mmol/L in 15–30 min, and the effect will last for several hours. Alkali therapy with intravenous NaHCO₃ can also shift K⁺ into cells. This is safest when administered as an isotonic solution of 3 ampules per liter (134 mmol/L NaHCO₃) and ideally should be reserved for severe hyperkalemia associated with metabolic acidosis. Patients with end-stage renal disease seldom respond to this intervention and may not tolerate the Na⁺ load and resultant volume expansion. When administered parenterally or in nebulized form, ₂-adrenergic agonists promote cellular uptake of K⁺ (see above). The onset of action is 30 min, lowering the plasma K⁺ concentration by 0.5 to 1.5 mmol/L, and the effect lasts 2–4 h.

Removal of K⁺ can be achieved using diuretics, cation-exchange resin, or dialysis. Loop and thiazide diuretics, often in combination, may enhance K⁺ excretion if renal function is adequate. Sodium polystyrene sulfonate is a cation-exchange resin that promotes the exchange of Na⁺ for K⁺ in the gastrointestinal tract. Each gram binds 1 mmol of K⁺ and releases 2–3 mmol of Na⁺. When given by mouth, the usual dose is 25–50 g mixed with 100 mL of 20% sorbitol to prevent constipation. This will generally lower the plasma K⁺ concentration by 0.5–1.0 mmol/L within 1–2 h and last for 4–6 h. Sodium polystyrene sulfonate can also be administered as a retention enema consisting of 50 g of resin and 50 mL of 70% sorbitol mixed in 150 mL of tap water. The sorbitol should be omitted from the enema in postoperative patients due to the increased incidence of sorbitol-induced colonic necrosis, especially following renal transplantation. The most rapid and effective way of lowering the plasma K⁺ concentration is hemodialysis. This should be reserved for patients with renal failure and those with severe life-threatening hyperkalemia unresponsive to more conservative measures. Peritoneal dialysis also removes K⁺ but is only 15–20% as effective as hemodialysis. Finally, the underlying cause of the hyperkalemia should be treated. This may involve dietary modification, correction of metabolic acidosis, cautious volume expansion, and administration of exogenous mineralocorticoid.