Potassium is one of the few electrolytes whose disturbances can be lethal. Hyperkalemia is defined when potassium levels in the blood rise above the normal permissible levels. Treatment guidelines for moderate and severe hyperkalemia vary with the severe degree being treated with utmost monitoring and aggressiveness.
The aggressiveness of the treatment for hyperkalemia will depend on how rapidly the serum potassium level has risen, the level of serum potassium and presence of any complications such as cardiotoxicity. Luckily, most cases of elevated potassium are of mild nature.
Severe hyperkalemia can kill. It increases the overall mortality risk by 10%. Once diagnosed, close monitoring and treatment are initiated.
And, you should know that neither the ECG nor the serum potassium levels are a correct index of the urgency of hyperkalemia. The clinical picture must be considered when assessing the severity of the hyperkalaemic patient.
Moderate hyperkalemia management
A moderate increase in potassium level in a healthy individual can be corrected by its increased removal from the body through urine with the help of diuretics.
The cause of the potassium rise due to increased intake should also be eliminated. It could be an increased intake of potassium foods, oral supplements or parenteral administration in the hospital.
Drugs that induce hyperkalemia should be discontinued and safer alternatives instituted. Reading what the various reasons that cause hyperkalemia are, would be good here.
Severe hyperkalemia means having too much potassium in the blood with serum potassium levels defined as more than serum 7.0 mEq/L.
The clinical severity is determined by the speed of its onset, the extent of the severity, and the development of clinical findings.
Levels greater than 7 mEq/L of severe hyperkalemia can lead to significant complications in the hemodynamic and neurologic functions.
Potassium levels exceeding 8.5 mEq/L can lead to respiratory paralysis or cardiac arrest and can immediately be fatal. Sudden death due to hyperkalemia is the fear uppermost in the mind of the treating doctor.
Treatment is always an emergency and is instituted in the ICU.
The guidelines to treat severe hyperkalemia consist of three essential steps:
1. Stabilizing the cardiac membrane to protect against arrhythmias (irregular and rapid heartbeat)
2. Rapidly shifting potassium from the blood into the cells, and
3. Eliminating the extra potassium from the body.
Potassium levels are measured 1, 2, 4, 6, and 24 hours after diagnosis and treatment of hyperkalemia is initiated.
Stabilizing the cardiac membrane with calcium gluconate
The first step in treating high potassium blood levels is to stabilize the cardiac membrane.
In hyperkalemia, there is a shift of potassium from the intracellular compartment to the extracellular compartment (which is the bloodstream). This causes a change in the voltage of the cell membrane.
Muscle cells, particularly of the heart become more excitable, which causes irregular beating of the heart (arrhythmias) and corresponding ECG changes.
Calcium directly acts against the hyperkalemia effects on heart muscle without lowering serum potassium.
Calcium for injection is available as its chloride or gluconate salt. Calcium gluconate is preferred as it is less likely to cause tissue necrosis.
Calcium gluconate dose
Twenty ml of 10% Ca gluconate is given intravenously in adults over 5–10 minutes and may be repeated as necessary because though its onset of action is immediate, its duration of action lasts only for a 30 to 60 minutes.
Calcium reduces the threshold potential of cardiac myocytes, which restores the gradient with the resting membrane potential to normalcy.
Improvement in the ECG changes is usually seen within two to three minutes after administration of calcium.
In patients on digoxin
In hyperkalaemic patients on digoxin, calcium should be given as a slow infusion over 20 to 30 minutes. This avoids the possibility of hypercalcemia that may potentiate the myocardial toxicity of digitalis.
However, if digoxin toxicity is suspected, avoid calcium totally. Magnesium sulfate (2 g over 5 minutes) can be safely given for patients with cardiac arrhythmias due to digitalis toxicity.
Shifting potassium back into the cells with insulin and albuterol
Shifting potassium back into the cells is achieved using insulin and/or a beta2 agonist. Insulin stimulates the sodium/potassium pump, which promotes the shift of potassium into the cells.
The onset of action is 20-30 minutes, and the duration ranges from 2 to 6 hours. Repeated doses can be given if the potassium level remains elevated.
Insulin (short-acting) is administered as 10 units intravenously with 50 mL of 50 percent glucose. This is done to counteract hypoglycemia that may present.
Blood glucose and potassium levels are measured every two hours for fear of hypoglycemia especially in patients with reduced kidney function.
If severe acidosis develops, use parenteral sodium bicarbonate.
Inhaled beta2 agonists: Albuterol
Inhaled beta2 agonists through a nebulizer act rapidly. The effect of beta2 agonists is synergistic with that of insulin, and they can be given together.31 Nebulized albuterol or salbutamol (Ventolin) is taken in a dose of 10 to 20 mg.
Eliminating potassium from the body
Renal excretion of potassium is achieved in patients with normal kidney function by administering IV saline accompanied by a loop diuretic (e.g. furosemide).
More of potassium excretion through the gastrointestinal tract can be achieved in people with normal bowel function through the use of cation exchange resins such as sodium polystyrene sulfonate (SPS), which can be administered orally or rectally (as a retention enema).
Hemodialysis is indicated in patients who have potentially lethal hyperkalemia that is not responding to conservative measures and in patients with renal failure.