The kidneys are the main way the body regulates potassium levels. When potassium levels are too high, the kidneys will excrete excess potassium. When the kidneys don’t work like they should and can’t filter out the excess potassium like usual, this is really the primary reason you’ll see potassium levels rise significantly in the blood. This can be from acute or chronic kidney disease.

Certain medications can cause an increase in serum potassium levels, such as lisinopril, potassium-sparing diuretics (like Spironolactone), and even NSAIDs. These impact how the kidneys normally excrete potassium. Beta-blockers even can increase potassium levels, but to a lesser degree (usually < 0.5 mEq/L elevation).

Acidosis, when a buildup of hydrogen ions in the blood, causes a potassium shift from inside to outside the cells, leading to hyperkalemia.

Insulin and aldosterone both impact potassium levels.

A deficiency in insulin (such as with DKA) leads to potassium accumulation outside the cell.

In hypoaldosteronism (Addison’s disease), there is not enough aldosterone. Aldosterone normally promotes potassium excretion in the kidney. So not having enough leads to higher potassium levels.

You’ll see later that we can utilize one of these hormones in the actual treatment for hyperkalemia!

When a cell lyses or splits open, its contents are released into the extracellular space. As we discussed, potassium concentration is much higher in the cells.

Whenever a condition or injury leads to massive destruction and lysis of cells, this can lead to hyperkalemia.

These conditions include major trauma, crush injuries, tumor-lysis syndrome, rhabdomyolysis, major burns, and hemolytic anemia.

Blood sample hemolysis usually occurs when drawing blood draw from mechanical trauma. This often occurs if the catheter is against the vein wall and causes red blood cell lysis during the draw. This blood can have a red tint due to released hemoglobin.

Repeated fist-clenching can cause potassium to shift out of the muscles temporarily. This can lead to elevations by more than 1-2 mEq/L in that forearm.

Significant elevations in platelet levels and very high WBCs (in the setting of chronic lymphocytic leukemia) can cause false potassium elevations, since the white blood cells are very fragile and break after the draw.

Certain forms of hereditary pseudohyperkalemia exist due to potassium shifting out of red blood cells.

Muscle weakness can also be a sign of hyperkalemia, just as it can be a sign of hypokalemia. As potassium levels rise, there can initially be increased contractions and cause spasms and twitches.

However, as the potassium level continues to rise, skeletal muscle excitability decreases, resulting in muscle weakness and even paralysis.

Symptoms of cardiac arrhythmias may occur if the patient is experiencing an arrhythmia, such as palpitations, chest pain, Shortness of breath, dizziness, or syncope.

High potassium levels can affect the smooth muscles of the GI tract, leading to nausea, vomiting, and possibly abdominal pain/cramping or diarrhea.

Like with hypokalemia, hyperkalemia can also cause numbness or tingling, typically in the extremities or the face.

This is usually only in severe cases with severe muscle fatigue of the respiratory muscles, and the patient may even need to be intubated.

High potassium levels can also agitate the central nervous system, leading to anxiety or restlessness.

• HR: May be fast or slow, depending on any arrhythmias. It may also be abnormal.
• BP: Severe hyperkalemia can cause hypotension.
• Respirations: usually normal, but may be increased or decreased if respiratory failure is present
• SPO2: Usually normal
• Temp: Normal

• Abdominal distention or bloating
• Bradycardia or arrhythmias on the monitor
• Respiratory distress in severe cases
• Patient may appear anxious or irritable, restless, or even confused

• Listen for slow or irregular heart rhythm, which may be caused by ectopy or arrhythmia from the hyperkalemia. May also have diminished or absent S3 and S4 heart sounds.

• Muscle weakness in the lower or upper extremities, particularly in the legs. These muscles may be tender to palpation.
• Weak or thready pulses in the extremities (radial pulse)
• Abdominal tenderness or discomfort

Identifying and addressing the underlying causes of hyperkalemia. The first thing would be to look at their renal function on their labs – if it is elevated, the high potassium level is likely true. Ensure it is true hyperkalemia instead of pseudohyperkalemia as above.

Avoid potassium supplements or foods rich in potassium until the potassium has normalized. All medications which can worsen hyperkalemia should be stopped.

Calcium is a very important part of the treatment for hyperkalemia. When given, it stabilizes cardiac conduction and decreases the risk of arrhythmias such as Vfib or VTACH.

Calcium gluconate is preferred, with the dose being 1,000mg (10mL of 10% solution) infused over 2-3 minutes. This dose can be repeated if ECG changes persist.

As with any electrolyte, your patient should be on the cardiac monitor during this infusion.

IV insulin is given to all patients (not just patients with diabetes) with moderate to severe hyperkalemia when dialysis is not readily available/indicated, since insulin drives potassium into the cells. This is a temporary fix but will decrease potassium levels by about 1 mEq/L pretty quickly, lasting for about 4-6 hours. The dose may need to be repeated at that time.

Please note this should be given with dextrose so it doesn’t cause hypoglycemia. Patients who’s glucose is > 250 can receive the insulin alone.

Glucose monitoring should be monitored every hour for 5-6 hours.

Dextrose is given with insulin to prevent hypoglycemia but can also lead to endogenous insulin secretion, which further enhances the potassium-reducing effect.

The dosage is typically 25gm, or 1 full amp (the total amount in the code cart). This is pushed slowly and is very thick and sticky.

Even with one amp given, hypoglycemia still occurs in many patients. It’s recommended to start a 10% dextrose infusion at 50-75ml/hr until 5-6 hours after administering the insulin.

Beta-agonists, such as albuterol, are sometimes used as a treatment for hyperkalemia to cause a shift of potassium into the cells (similar to the effect of insulin). This is not always ordered but should be considered in patients with significant symptoms or ECG changes despite the above treatment.

Beta-agonists can reduce potassium levels by 0.5 – 1.5 mEq/L, and is usually given in an hour-long treatment. SubQ Terbutaline is an alternative to albuterol.

This will also increase heart rate, and patients with heart disease and at risk for cardiac complications may be better off not getting a beta-agonist.

Sodium bicarbonate can reduce potassium levels in patients with metabolic acidosis. 1 amp (50 mEq) can be given in 50ml, or alternatively 150mEq can be given in 1 L of 5% Dextrose over 2-4 hours.

This treatment for hyperkalemia should be limited to patients with metabolic acidosis, and multiple doses can lead to hypernatremia.

Potassium levels will be redrawn and assessed depending on the severity and what type of treatment for hyperkalemia was ordered.

Mild to moderate levels can be rechecked in 4-6 hours, but severe hyperkalemia may need to be checked more frequently.

If insulin is given, glucose levels must be checked hourly for 4-6 hours, as hypoglycemia is common (even if you administer dextrose).

Closely monitor the patient’s renal function (BUN & Creatinine), other electrolytes, and acid-base balance (CO2).

As discussed, high potassium levels can lead to bradycardia and arrhythmias. Continuous cardiac monitoring should be maintained, and intermittent ECGs may also be warranted.

Severe hyperkalemia can cause respiratory failure, so monitoring their breathing, lung sounds, respiratory rate, and pulse ox is important.

Vital signs should be checked per facility protocol.

Monitoring urine output is important, especially in patients where loop diuretics are given, and potassium is being wasted through the kidneys.