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.
·
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)
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.
