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Hyperkalemia (Nursing)
Leslie V. Simon; Muhammad F. Hashmi; Mitchell W. Farrell; Rojeena Chapagain.

Author Information and Affiliations

Last Update: February 19, 2023.

Learning Outcome

1. List the causes of hyperkalemia

2. Describe the ECG features of hyperkalemia

3. Summarize the treatment of hyperkalemia

4. Provide the nurse diagnosis of hyperkalemia

Introduction
Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L.
While mild hyperkalemia is usually asymptomatic, high potassium levels may cause life-threatening cardiac arrhythmias, muscle weakness, or
paralysis. Symptoms usually develop at higher levels, 6.5 mEq/L to 7 mEq/L, but the rate of change is more important than the numerical value.
Patients with chronic hyperkalemia may be asymptomatic at increased levels, while patients with dramatic, acute potassium shifts may develop
severe symptoms at lower ones. Infants have higher baseline levels than children and adults.

Pseudohyperkalemia is quite common and represents a false elevation in measured potassium due to specimen collection, handling, or other causes.
Hyperkalemia should always be confirmed before aggressive treatment in cases where the serum potassium is elevated without explanation. True
hyperkalemia may be caused by increased potassium intake, transcellular movement of intracellular potassium into the extracellular space, and
decreased renal excretion. The urgency of therapy depends on symptoms, serum levels, and underlying reasons for hyperkalemia.[1][2][3][4]

Nursing Diagnosis

Weakness, fatigue

Risk of adverse cardiac events

Inadequate urine output

Palpitations

Fluid retention due to renal dysfunction

Anxiety

Causes
The most common cause of hyperkalemia is pseudohyperkalemia, which is not reflective of the true serum potassium levels. Pseudohyperkalemia is
most commonly due to hemolysis of the sample, causing intracellular potassium to be measured in the serum. Hemolysis is more common when a
syringe is used than a vacuum device. Using tourniquets and excessive fist pumping during blood draw also increases the risk. Specimens drawn
from patients with leukocytosis or thrombocytosis are also frequently associated with falsely elevated potassium concentrations.

Increased Potassium Intake

Increased potassium intake from food is a very uncommon cause of hyperkalemia in adult patients with normal renal function but can be an
important cause in those with kidney disease. Foods with very high potassium content include dried fruits, seaweed, nuts, molasses, avocados, and
Lima beans. Many vegetables that are also high in potassium include spinach, potatoes, tomatoes, broccoli, beets, carrots, and squash. High-
potassium-containing fruits include kiwis, mangoes, oranges, bananas, and cantaloupe. Red meats are also rich in potassium. While generally safe
to consume even in large quantities by patients with normal potassium homeostasis, these foods should be avoided in patients with severe renal
disease or other underlying conditions or medications predisposing them to hyperkalemia. Intravenous intake through high potassium-containing
fluids, particularly total parenteral nutrition, medications with high potassium content, and massive blood transfusions can significantly elevate
serum potassium levels.

Intracellular Potassium Shifts

Cellular injury can release large quantities of intracellular potassium into the extracellular space. This can be due to rhabdomyolysis from a crush
injury, excessive exercise, or other hemolytic processes. Metabolic acidosis may cause intracellular potassium to shift into the extracellular space
without red cell injury. Metabolic acidosis is most frequently caused by decreased, effective circulating arterial blood volume. Sepsis or dehydration
may lead to hypotension and decreased tissue perfusion leading to metabolic acidosis with subsequent potassium elevation. Insulin deficiency and
diabetic ketoacidosis may cause dramatic extracellular shifts causing measured serum potassium to be elevated in the setting of whole body
potassium depletion. Certain medications, such as succinylcholine, may cause severe, acute potassium elevations in patients with up-regulation of
receptors, particularly in the setting of subacute neuromuscular disease. Tumor lysis syndrome, particularly in patients receiving chemotherapy for
hematogenous malignancy, may cause acute hyperkalemia due to massive cancer cell death. Hyperkalemic periodic paralysis is a rare, autosomal
dominant condition that causes potassium to shift into the extracellular space due to impaired sodium channel function in skeletal muscle.

Impaired Potassium Excretion

Acute or chronic kidney disease is a common cause of hyperkalemia. Hyperkalemia is usually not seen until the glomerular filtration rate falls
below 30 ml/min. This is commonly due to primary renal dysfunction but may be from acute volume depletion from dehydration or bleeding or
decreased circulating blood volume due to congestive heart failure or cirrhosis. Tubular dysfunction due to aldosterone deficiency or insensitivity
can also cause hyperkalemia.

Risk Factors
Hyperkalemia is unusual in the general population, reported in less than 5% of the population worldwide, but may affect up to 10% of all
hospitalized patients. Most cases in hospitalized patients are due to medications and renal insufficiency. Diabetes, malignancy, extremes of age, and
acidosis are other important causes in inpatients. Hyperkalemia is rare in children but may occur in up to 50% of premature infants. Hyperkalemia is
more commonly reported in men than women, perhaps due to increased muscle mass and higher rates of rhabdomyolysis, and increased prevalence
of neuromuscular disease.

Assessment
Most patients are relatively asymptomatic with mild and even moderate hyperkalemia. Elevated potassium is often discovered on screening labs
done in patients with nonspecific complaints or those with suspected electrolyte abnormalities due to infection, dehydration, or hypoperfusion.
Historical clues include the history of renal disease, diabetes, chemotherapy, major trauma, crush injury, or muscle pain suggestive of
rhabdomyolysis. Medications that may predispose to the development of hyperkalemia include digoxin, potassium-sparing diuretics, non-steroidal
anti-inflammatory drugs, ace-inhibitors or recent intravenous (IV) potassium, total parenteral nutrition, potassium penicillin or succinylcholine.
Patients may complain of weakness, fatigue, palpitations, or syncope.

Physical exam findings may include hypertension and edema in the setting or renal disease. There may also be signs of hypoperfusion. Muscle
tenderness may be present in patients with rhabdomyolysis. Jaundice may be seen in patients with hemolytic conditions. Patients may have muscle
weakness, flaccid paralysis, or depressed deep tendon reflexes.

Evaluation

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The first test that should be ordered in a patient with suspected hyperkalemia is an ECG since the most lethal complication of hyperkalemia is
cardiac condition abnormalities which can lead to dysrhythmias and death.[5][6][7][8]

Elevated potassium causes ECG changes in a dose-dependent manner:

K = 5.5 to 6.5 mEq/L ECG will show tall, peaked t-waves

K = 6.5 to 7.5 mEq/L ECG will show loss of p-waves

K = 7 to 8 ECG mEq/L will show widening of the QRS complex

K = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole

It should be noted that the rate of rising serum potassium is a more significant factor than the level. Patients with chronic hyperkalemia may have
relatively normal EGCs, even at high levels. Significant ECG changes may be present at much lower levels in patients with sudden spikes in serum
potassium.

Additional laboratory testing should include serum blood urea nitrogen and creatinine to assess renal function and urinalysis to screen for renal
disease. Urine potassium, sodium, and osmolality may also help evaluate the cause. In patients with renal disease, the serum calcium level should
also be checked because hypocalcemia may exacerbate the cardiac effects of hyperkalemia. A complete blood count to screen for leukocytosis or
thrombocytosis may also be helpful. Serum glucose and blood gas analysis should be ordered in diabetics and patients with suspected acidosis.
Lactate dehydrogenase should be ordered in patients with suspected hemolysis. Creatinine phosphokinases and urine myoglobin should be ordered
in patients with suspected rhabdomyolysis. Uric acid and phosphorus should be ordered in patients with suspected tumor lysis syndrome. Digoxin
toxicity may cause hyperkalemia, so serum levels should be checked in patients on digoxin. If no other cause is found, consider cortisol and
aldosterone levels to assess for mineralocorticoid deficiency.

Since pseudohyperkalemia is so common, confirmation should be obtained in asymptomatic patients without typical ECG changes before initiating
aggressive therapy.

Medical Management
The urgency with which hyperkalemia should be managed depends on how rapidly the condition develops, the absolute serum potassium level, the
degree of symptoms, and the cause.[9][10][11]

Patients with neuromuscular weakness, paralysis, or ECG changes and elevated potassium of more than 5.5 mEq/L in patients at risk for ongoing
hyperkalemia or confirmed hyperkalemia of 6.5 mEq/L should have aggressive treatment. Exogenous sources of potassium should be immediately
discontinued. Calcium therapy will stabilize the cardiac response to hyperkalemia and should be initiated first in the setting of cardiac toxicity.
Calcium does not alter the serum concentration of potassium but is a first-line therapy in hyperkalemia-related arrhythmias and ECG changes.

Calcium chloride contains three times more elemental calcium than calcium gluconate but is more irritating to peripheral vessels and more likely to
cause tissue necrosis with extravasation, so it is usually only given through central venous lines or peripherally in cardiac arrest. Thus, calcium
gluconate is the usual initial drug of choice in patients with evidence of cardiac toxicity. Insulin and glucose, or insulin alone in hyperglycemic
patients, will drive the potassium back into the cells, effectively lowering serum potassium. A common regimen is ten units of regular insulin given
with 50 ml of a 50% dextrose solution (D50). Patients should be monitored closely for the development of hypoglycemia. A 10% dextrose infusion
at 50-75 ml/hour is associated with less hypoglycemia than bolus dosing with D50. Beta-2 adrenergic agents such as albuterol will also shift
potassium intracellularly. To be effective, beta-2 agonists are given in much higher doses than commonly used for bronchodilation. Sodium
bicarbonate infusion may be helpful in patients with metabolic acidosis. Bolus dosing of sodium bicarbonate is less effective.

Loop or thiazide diuretics may help enhance potassium excretion. They may be used in non-oliguric, volume overloaded patients but should not be
used as monotherapy in symptomatic patients. Gastrointestinal cation exchangers such as patiromer may be helpful, particularly in patients with
renal insufficiency who cannot receive immediate dialysis. Sodium polystyrene sulfonate, though commonly used, is falling out of favor due to lack
of effectiveness and adverse effects, particularly bowel necrosis in elderly patients. If used due to a lack of alternatives, it should not be given with
sorbitol, which increases toxicity. Hemodialysis should be performed in patients with end-stage renal disease or severe renal impairment.

Nursing Management

Monitor ins and outs

Check serum potassium levels

Follow ECG closely to look for peaked T waves

Educate patient on hyperkalemia

Administer diuretics as ordered

Administer insulin to lower potassium as ordered

Check blood glucose when administering insulin

Check BUN and creatinine levels

Educate the patient on a low potassium diet

Encourage the patient to follow closely with the clinician

Educate the patient on renal dysfunction and hyperkalemia

Ensure the patient is on no medications that can cause hyperkalemia or renal dysfunction

When To Seek Help

If ECG evidence of hyperkalemia

Unstable hemodynamics

High serum potassium

Cardiac arrest

Unresponsive

Outcome Identification
The majority of patients have an excellent prognosis. However, patients with chronic disorders like end-stage renal failure may require continual
blood work to monitor potassium.[12][13] [Level 5]

Monitoring
The management of hyperkalemia is multidisciplinary because of its potential to induce cardiac arrest and severe weakness. Once hyperkalemia is
diagnosed, the primary condition must be treated. Patients with hyperkalemia need cardiac monitoring, and nurses should be familiar with ECG
features of hyperkalemia, which are often the first to appear. The pharmacist has to ensure that all nephrotoxic medications and agents that raise
potassium are discontinued.

If the hyperkalemia is severe, the nephrologist should be consulted. If ECG changes are present, a cardiology consult should be made. Treatment to
lower the high potassium should be ongoing. These patients need cardiac monitoring 24/7 until the hyperkalemia has resolved. The dietitian should
educate the patient on a low potassium diet. For those with renal dysfunction, continued follow-up with a nephrologist is recommended. Only
through open communication between members of the interprofessional team can the morbidity of hyperkalemia be avoided.

Coordination of Care

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10/3/23, 9:01 PM Hyperkalemia (Nursing) - StatPearls - NCBI Bookshelf
The management of hyperkalemia is multidisciplinary because of its potential to induce cardiac arrest. Once hyperkalemia is diagnosed, the primary
condition must be treated. If the hyperkalemia is severe, the nephrologist should be consulted. If ECG changes are present, a cardiology consult
should be made. Treatment to lower the high potassium should be ongoing. These patients need cardiac monitoring 24/7 until the hyperkalemia has
resolved. The majority of patients have an excellent prognosis. However, patients with chronic disorders like end-stage renal failure may require
continual blood work to monitor potassium.[12][13] [Level 5]

Health Teaching and Health Promotion

Encourage a low potassium diet

Educate patient on hyperkalemia

Discharge Planning
Patients need to understand the potential perils of hyperkalemia. They can be instructed to limit high potassium foods, and the pharmacist should
perform a thorough medication reconciliation to screen for drugs that may contribute to their condition. Home pulse screening should be performed
if possible, and the patient must understand the importance of keeping their follow-up appointments and expect to have their potassium levels
checked regularly.

Review Questions

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References
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Disclosure: Leslie Simon declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Hashmi declares no relevant financial relationships with ineligible companies.

Disclosure: Mitchell Farrell declares no relevant financial relationships with ineligible companies.

Disclosure: Rojeena Chapagain declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

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