Hyperkalemia is an elevated potassium level that can have serious consequences if left untreated. In this article, learn what causes hyperkalemia, clinical signs and symptoms, how it is treated, and how at-risk patients can prevent it.

The role of potassium in the body

Potassium is the most abundant intracellular cation in the body, meaning that most of it lives within the cell. The higher concentration of potassium inside the cell forms an electrochemical gradient that is maintained by the sodium-potassium ATPase transporter. This gradient is essential for nerve transmission and muscle contraction, including cardiac muscle contraction. Potassium also plays a key role in intracellular fluid volume and has a close relationship with sodium, which is the main regulator of extracellular fluid volume.

Potassium is an essential nutrient that is acquired through nutrition as well as PO or IV supplementation when needed. It is primarily excreted in the urine, though small amounts can be excreted in the stool. A normal potassium level is about 3.5 to 5 mmol/L.

Dangers of hyperkalemia

When potassium levels are dangerously high, severe complications can occur including cardiac arrest, serious cardiac dysrhythmias, and significant muscle weakness or even flaccid paralysis that (thankfully) does not affect the diaphragm. Prompt recognition of hyperkalemia is crucial for improving patient outcomes. In fact, in-hospital mortality for patients with hyperkalemic emergencies is 4.5 times higher than patients with normal potassium levels.

Causes of hyperkalemia

Common causes of hyperkalemia are impaired excretion due to kidney disease or the use of medications that inhibit the RAAS pathway. However, in some cases, hyperkalemia can be due to the movement of potassium from the intracellular to the extracellular space (this is called redistributive hyperkalemia), such as in cases of acidosis or uncontrolled hyperglycemia.

Common meds that can cause hyperkalemia

Another cause of hyperkalemia is tissue breakdown, such as in rhabdomyolysis. This is due to the fact that potassium is most abundant within the cell. As the cells die, they spill their contents into the bloodstream, which can lead to hyperkalemia. This may also occur in tumor lysis syndrome and crush injuries.

Gastrointestinal bleeding can also lead to hyperkalemia due to the potassium in blood being absorbed via the GI tract. 

Hyperkalemic emergency

When potassium levels are significantly elevated the patient can experience dangerous signs and symptoms such as: 

  • Cardiac arrhythmias, which can range from bradycardia to ventricular tachycardia or even ventricular fibrillation and asystole
  • Cardiac conduction defects such as bundle branch blocks
  • Muscle weakness or paralysis

On the ECG, hyperkalemia’s classic sign is a tall, peaked T-wave. You could also see a shortened QT interval, progressively lengthening PR intervals and widening QRS. Eventually, without treatment, the QRS widens to the point of asystole.

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How is hyperkalemia treated?

Hyperkalemia treatment depends on the severity of the condition, the patient’s symptoms, and the presence or absence of underlying renal disease. Treatment for hyperkalemia follows a three-pronged approach: remove excess potassium from the body, drive potassium into the cell, and antagonize the effects of hyperkalemia on cardiac cells.

Remove excess potassium from the body:

  • Hemodialysis – Patients with ESRD or significant renal dysfunction may get emergent dialysis to remove excess potassium from the body.
  • Diuretics – Provided renal function is adequate, loop or thiazide diuretics may be used to cause increased renal excretion of potassium. Patients may receive IV fluids to prevent hypovolemia and maintain renal perfusion.
  • Gastrointestinal cation exchangers – Kayexalate and other gastrointestinal cation exchangers, bind up potassium in the GI tract so it can be excreted in the stool. Because this therapy does not depend on renal function, it may be utilized in patients with renal impairment. Note this can take several hours so it is not used as monotherapy in severe hyperkalemia.

Drive potassium into the cell:

  • IV insulin and dextrose – Insulin drives potassium into the cells by enhancing the Na-K-ATPase pump in skeletal muscle. Dextrose is added to prevent hypoglycemia in patients without elevated blood glucose levels. A patient receiving IV insulin for hyperkalemia should have hourly blood glucose checks for up to six hours to watch for hypoglycemia. In addition, a dextrose infusion may be initiated to prevent hypoglycemia during that time frame. Studies show that in most patients, the serum potassium level drops by 0.5 to 1.2 mEq/L when administered 10 units of insulin IV.
  • Beta-2-adrenergic agonists – Inhaled albuterol can temporarily shift potassium into the cell, but should not be used in place of insulin/glucose therapy. When used along with insulin/glucose, albuterol can lower the potassium level by approximately 1.2 to 1.5 mEq/L. 
  • Sodium bicarbonate – Since acidosis can cause hyperkalemia, an alkaline environment can help drive the potassium into the cell. Note this is not used as monotherapy, but instead may be utilized with other treatments.

Antagonize the effects of hyperkalemia on cardiac cells:

  • IV calcium – Calcium does not cause potassium excretion or drive potassium into the cell. Instead, calcium is “cardioprotective” meaning it helps counteract the effects of hyperkalemia on cardiac tissue. Note the effects of calcium only last about 30 to 60 minutes, so this treatment is not used in isolation. It will always be combined with another method to lower potassium levels. IV calcium is administered slowly over several minutes, typically about 1 to 1.5 ml per minute (always go by your facility policy).

In addition to utilizing one or more of these therapies, it’s also important to treat reversible causes of hyperkalemia such as discontinuing medications that increase serum potassium levels or correcting hypovolemia. 

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How can hyperkalemia be prevented?

Patients with chronic kidney disease are advised to take measures to help avoid hyperkalemia. This can include:

  • Dietary modification – The renal diet limits foods high in potassium such as avocado, banana, oranges and orange juice, beets, tomatoes, and legumes.
  • Avoid periods of fasting – Fasting can cause the body to shift potassium out of the cell. This is because low blood glucose causes reduced insulin secretion. With reduced insulin secretion, potassium shifts out of the cell. So, nondiabetic patients with ESRD who must fast for surgery may receive IV dextrose to avoid this shift.
  • Avoid certain medications – Patients with ESRD may need to avoid medications that contribute to hyperkalemia such as ACE inhibitors, angiotensin receptor blockers, NSAIDs , some beta blockers, and potassium-sparing diuretics.

Review hyperkalemia for your exams, clinicals, and NCLEX while you’re on the go by tuning in to episode 347 of the Straight A Nursing podcast. Tune in wherever you get your podcast fix, or straight from the website here.

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