Hyperkalemia

ECG should be done on patients with hyperkalemia. ECG changes (see figure ) are frequently visible when serum potassium is > 5.5 mEq/L (> 5.5 mmol/L). Slowing of conduction is characterized by an increased PR interval and shortening of the QT interval. Tall, symmetric, peaked T waves are visible initially. Potassium > 6.5 mEq/L (> 6.5 mmol/L) causes further slowing of conduction with widening of the QRS interval, disappearance of the P wave, and nodal and escape ventricular arrhythmias. Finally, the QRS complex degenerates into a sine wave pattern, and ventricular fibrillation or asystole ensues.

Diagnosis of the cause of hyperkalemia requires a detailed history, including a review of medications, a physical examination with emphasis on volume status, and measurement of electrolytes, BUN (blood urea nitrogen), and creatinine. In cases in which renal failure is present, additional tests, including renal ultrasonography to exclude obstruction, are needed.

Patients with serum potassium < 6 mEq/L (< 6 mmol/L) and no ECG abnormalities may respond to diminished potassium intake or stopping potassium-elevating drugs. The addition of a loop diuretic enhances renal potassium excretion as long as volume depletion is not present.

Sodium polystyrene sulfonate in sorbitol can be given (15 to 30 g in 30 to 70 mL of 70% sorbitol orally every 4 to 6 hours). It acts as a cation exchange resin and removes potassium through the gastrointestinal mucosa. Sorbitol is administered with the resin to ensure passage through the gastrointestinal tract. Patients unable to take drugs orally because of nausea or other reasons may be given similar doses by enema. Enemas are not as effective at lowering potassium in patients with ileus. Enemas should not be used if acute abdomen is suspected. About 1 mEq (1 mmol) of potassium is removed per gram of resin given. Resin therapy is slow and often fails to lower serum potassium significantly in hypercatabolic states. Because sodium is exchanged for potassium when sodium polystyrene sulfonate is used, sodium overload (see Hypernatremia Hypernatremia Hypernatremia is a serum sodium concentration > 145 mEq/L (> 145 mmol/L). It implies a deficit of total body water relative to total body sodium, caused by water intake being less than water... read more ) may occur, particularly in patients with oliguria and preexisting volume overload.

In patients with recurrent hyperkalemia, avoidance of medications that can induce hyperkalemia (see table ) is generally all that is needed. In patients who need ACE inhibitors and angiotensin receptor blockers (eg, patients with chronic heart failure Heart Failure (HF) Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal... read more or diabetic nephropathy Diabetic Nephropathy Diabetic nephropathy is glomerular sclerosis and fibrosis caused by the metabolic and hemodynamic changes of diabetes mellitus. It manifests as slowly progressive albuminuria with worsening... read more ), the polymer resin patiromer can be taken daily to help decrease gut absorption of potassium and prevent hyperkalemia. Sodium zirconium cyclosilicate may also be used. It is a polymer matrix that binds to potassium in the gut. It decreases serum potassium over several hours and has few gastrointestinal adverse effects.

Serum potassium between 6 and 6.5 mEq/L (6 and 6.5 mmol/L) needs prompt attention, but the actual treatment depends on the clinical situation.

If no ECG changes are present and renal function is intact, maneuvers as for mild hyperkalemia are usually effective. Follow-up serum potassium measurements are needed to ensure that the hyperkalemia has been successfully treated.

If serum potassium is > 6.5 mEq/L (> 6.5 mmol/L), more aggressive therapy is required. Administration of regular insulin 5 to 10 units IV is followed immediately by or administered simultaneously with rapid infusion of 50 mL 50% glucose. Infusion of 10% dextrose in water should follow at 50 mL/hour to prevent hypoglycemia. The effect on serum potassium peaks in 1 hour and lasts for several hours.

If ECG changes include the loss of P-wave or widening of the QRS complex, treatment with IV calcium as well as insulin and glucose is indicated; 10 to 20 mL of 10% calcium gluconate (or 5 to 10 mL of 22% calcium gluceptate) is given IV over 5 to 10 minutes. If the ECG shows a sine wave pattern or asystole, calcium gluconate may be given more rapidly (5 to 10 mL IV over 2 minutes). Calcium antagonizes the effect of hyperkalemia on cardiac muscle. Calcium should be given with caution to patients taking digoxin because of the risk of precipitating hypokalemia-related arrhythmias. Calcium chloride can also be used but can be irritating to peripheral veins and cause tissue necrosis if extravasated. Calcium chloride should be given only through a correctly positioned central venous catheter.

The benefits of calcium occur within minutes but last only 20 to 30 minutes. Calcium infusion is a temporizing measure while awaiting the effects of other treatments or initiation of hemodialysis and may need to be repeated.

A high-dose beta 2-agonist, such as albuterol 10 to 20 mg inhaled over 10 minutes (5 mg/mL concentration), can lower serum potassium by 0.5 to 1.5 mEq/L (0.5 to 1.5 mmol/L) and may be a helpful adjunct. The peak effect occurs in 90 minutes. However, beta 2-agonists are contraindicated in patients with unstable angina or acute myocardial infarction.

Administration of IV sodium bicarbonate (NaHCO3) is frequently used to treat hyperkalemia, but evidence supporting its use is limited. It may lower serum potassium over several hours. Reduction may result from alkalinization or from the hypertonicity due to the concentrated sodium in the preparation. The amount of sodium contained in the infusion may be harmful for dialysis patients who also may have volume overload. Another possible complication of IV sodium bicarbonate is that it acts to acutely lower the ionized calcium concentration, which further exacerbates the cardiotoxicity of hyperkalemia. When sodium bicarbonate is given, the typical dose is 3 ampules of 7.5% sodium bicarbonate in one liter 5% dextrose in water infused over 2 to 4 hours. Bicarbonate therapy has little effect when used by itself in patients with severe renal insufficiency unless acidemia is also present.

In addition to strategies for lowering potassium by shifting it into cells, maneuvers to remove potassium from the body should also be done early in the treatment of severe or symptomatic hyperkalemia. Potassium can be removed via the gastrointestinal tract by administration of sodium polystyrene sulfonate Mild hyperkalemia Hyperkalemia is a serum potassium concentration > 5.5 mEq/L (> 5.5 mmol/L), usually resulting from decreased renal potassium excretion or abnormal movement of potassium out of cells. There... read more , but because the rate of potassium removal is somewhat unpredictable, close monitoring is needed.

Patiromer and sodium zirconium silicate are not recommended for use as an emergency treatment to acutely lower potassium because of these drugs' delayed onset of action.

Hemodialysis Hemodialysis In hemodialysis, a patient’s blood is pumped into a dialyzer containing 2 fluid compartments configured as bundles of hollow fiber capillary tubes or as parallel, sandwiched sheets of semipermeable... read more should be instituted promptly when emergency medical treatment is ineffective especially in patients with severe chronic kidney disease and/or acute kidney injury. Dialysis should be considered early in patients with end-stage renal disease and hyperkalemia because they are at increased risk of progression to more severe hyperkalemia and serious cardiac arrhythmias. Peritoneal dialysis is relatively inefficient at removing potassium acutely.