This is the first article in a new series on electrolytes and their imbalances in the body. The series begins with potassium, and will cover magnesium, calcium and phosphate, sodium and chloride, and bicarbonate in future articles. After a brief review of intracellular fluid (ICF) and extracellular fluid (ECF) compartments, the history and physiology of potassium, and the causes, signs and symptoms, and treatments of hyperkalemia and hypokalemia are covered.
The body is mostly liquid, with body fluids distributed between the ICF and ECF compartments.1 The ICF compartment is the larger of the two and consists of the fluid within each of the body's cells. The ECF compartment is composed of the fluid in the spaces outside of cells, including the interstitial or tissue spaces and the plasma in the blood vessels.1
ICF contains large amounts of potassium (the most abundant ICF electrolyte); moderate amounts of magnesium; small amounts of sodium, chloride, bicarbonate, and phosphorus; and minimal amounts of calcium. ECF contains large amounts of sodium and chloride; moderate amounts of bicarbonate; and small amounts of potassium, magnesium, calcium, and phosphorus.1 (See Concentrations of extracellular and intracellular electrolytes in adults.)
The cell membrane acts as the primary barrier to the movement of substances between the ICF and ECF compartments. Oxygen and carbon dioxide, which are lipid-soluble substances, can readily pass through the cell membrane; however, several ions, including sodium and potassium, need a transport mechanism, or pump, to move the ions across the cell membrane.1 Because the sodium (Na+)-potassium (K+) pump needs adenosine triphosphate (ATP) and the enzyme adenosine triphosphatase (ATPase) for energy, it is also known as the Na+/K+-ATPase membrane pump.1 (See Mechanisms regulating transcellular shifts of potassium and Glossary of helpful terms.)
Potassium was isolated chemically and named by Sir Humphrey Davy in 1807.2 He chose the name potassium after finding it in a substance known as potash, the substance that remains after burning wood and other plant material.3 Scientists after Davy chose to use the Latin name kalium instead of potassium when developing the periodic table of elements. As a result, the letter K is used to stand for potassium, and the words for high potassium (hyperkalemia) and low potassium (hypokalemia) are also derived from the Latin root.4,5
Potassium is one of the most abundant chemicals on earth and is found in all living cells. Commercially, it is used commonly in fertilizers, soaps, fireworks, explosives, and medications to keep patients' blood levels in the therapeutic range.6
Potassium is an element found in the form of a cation in the human body.6 This means that potassium in the body is not attached to other elements, and it has a positive electrical charge.7 Potassium is primarily found inside human cells, with intracellular concentrations usually between 140 and 150 mEq/L. In contrast, the serum concentration of potassium should average 4 mEq/L.8 Intracellular values of electrolytes are not measured clinically, so critical care nurses infer that patients have the normal amount of potassium inside their cells based on blood levels that are drawn. The normal serum potassium reference value range in adults is 3.5 to 5.0 mEq/L.1 However, texts vary somewhat on the normal serum values of potassium, with the upper normal value up to 5.6 mEq/L.1,5,7-12 These numbers can vary based on lab processing, so critical care nurses need to rely on the normal values posted by the lab in their facility.
To maintain appropriate potassium levels, a healthy adult should follow the dietary reference intakes and ingest approximately 4,700 mg of potassium each day.13 Many foods contain significant amounts of potassium. Oranges and bananas may be the best-known potassium-rich foods, but it is also found in beans, milk, carrots, leafy green vegetables, tomatoes, yams, fish, and nuts.13 Although some potassium is lost in stool or sweat, most ingested potassium is absorbed from the gastrointestinal (GI) tract into the bloodstream.1 Extra potassium is excreted by the kidneys; healthy kidneys are efficient in eliminating excess potassium from the blood.1
The hormone aldosterone also plays a role in keeping safe blood levels of potassium.1 Aldosterone is released from the adrenal gland when potassium levels are high. Aldosterone will cause sodium to be actively reabsorbed back into the bloodstream from the distal nephron in exchange for potassium. If serum potassium levels are too low, less aldosterone will be released, so less potassium will be excreted in the urine.1 In addition, if potassium levels are too high, this exchange process can be done with hydrogen (H+) ions instead of sodium. Hydrogen ions are positively charged, as are potassium ions. Thus, when hydrogen ions move into the cell, potassium moves out in exchange.1 If hydrogen ions are retained, this can result in metabolic acidosis.1
Another way in which potassium is regulated is by moving it into or out of the cells. For example, insulin increases the amount of potassium taken from the ECF into the cell, particularly after a meal.1
Nerve and muscle cells cannot function properly without a balance between intracellular and extracellular potassium. The body actively creates a situation in which sodium is moved outside of the cell and potassium is moved into the cell, in spite of having high concentration gradients that would normally lead to diffusion.1,8 In this polarized state, muscle and nerve cells generate and then transmit signals along nerve cells, enabling muscles to move. Without a balance of potassium in the body, this process is altered. In extreme situations, muscles can become fatigued, and the cardiac muscles in particular can become irritable, potentially resulting in life-threatening dysrhythmias.8
Hyperkalemia is present when the serum level of potassium is greater than 5.0 mEq/L.1 However, critical care nurses should refer to the values posted by the lab where the test was processed. An elevation in potassium should be promptly reported to the provider; it is important to determine the cause and quickly correct the potassium level before it increases any further.
Causes. According to the American Heart Association (AHA), the most common cause of hyperkalemia in the hospitalized patient is prior treatment with potassium replacements.11 The other major causes of hyperkalemia include decreased elimination of potassium by the kidneys, excessive potassium replacement, and transcellular shifts of potassium.1 (See Common causes of hyperkalemia.)
Signs and symptoms. The primary indication of hyperkalemia is an elevated serum potassium level. The nurse should have this information as soon as lab values are posted, and should take action accordingly. Typically, the first symptom associated with hyperkalemia is paresthesia.1 As the level climbs, patients with hyperkalemia may experience vague symptoms of nausea, vomiting, or muscle weakness. This can progress to respiratory muscle weakness and possibly paralysis. The patient's ECG will have pronounced or peaked T waves with a shortened QT interval (the earliest ECG change), flattened P waves, prolonged PR interval, widened QRS complexes, and finally ventricular fibrillation or asystole.7,11,12,14,16 (See ECG changes with hypokalemia and hyperkalemia.)
Although significant ECG changes associated with hyperkalemia should prompt immediate action, ECG changes by themselves are not diagnostic of high serum potassium.14 Changes noted on the cardiac monitor should prompt the critical care nurse to assess the patient for additional signs and symptoms of hyperkalemia and notify the provider of the findings and obtain an order for a serum potassium level so that treatment can be initiated.
Treatment. Medical treatment of hyperkalemia can include:
- removing potassium from the body
- moving potassium from the bloodstream into the cells
- administering calcium in an attempt to stabilize the cell membranes.1,12,14-16
Treatment is chosen based on the how fast the serum potassium level increased, and the signs and symptoms the patient is experiencing.
With mild hyperkalemia (may be defined as a potassium level of 5.0 to 5.5 mEq/L), removing potassium from the body may be as simple as adjusting the patient's diet or medications.1,16 This may include removing potassium from the I.V. fluid, decreasing or discontinuing an angiotensin-converting enzyme (ACE) inhibitor or changing other medications that are causing decreased kidney function. Though considered standard of care for heart failure, ACE inhibitors and angiotensin II receptor blockers (ARBs) are responsible for significant numbers of patients developing hyperkalemia.14 Loop diuretic therapy may be considered in patients with hypervolemia without severe kidney impairment.16 Advise patients not to use salt substitutes before talking with their healthcare provider because many of them contain potassium.1
With higher potassium levels the situation becomes more urgent and serum potassium levels need to be lowered within 6 to 12 hours.16 The patient may be given sodium polystyrene sulfonate orally or by enema. This substance eliminates potassium from the colon through ion exchange.1 If the patient with impaired kidney function has a dialysis catheter, or if one can be placed urgently, the patient may also be dialyzed. Both of these methods are effective because the excess potassium is actually removed from the body.1,14-16 Sodium polystyrene sulfonate should not be used in patients with an ileus, a small bowel obstruction, underlying bowel disease such as inflammatory bowel disease, or in those taking opioids.16
If the situation is still more urgent, requiring immediate treatment (severe hyperkalemia may be defined as a potassium level greater than 6.5 mEq/L), moving potassium from the bloodstream into the cells can be accomplished by giving regular insulin.16 If regular insulin therapy is chosen, the patient must be given glucose in conjunction with the insulin.16 However, insulin should be given without glucose if the patient has a blood glucose level of 250 mg/dL or greater.16 Blood glucose levels should be measured hourly for 6 hours after the administration of insulin to monitor the patient for hypoglycemia.16 Doses are determined by how high the potassium level is. While these measures work quickly to lower the serum level of potassium, they have potential adverse reactions, and the original cause of the elevated potassium must still be addressed.1,14,15 Sodium bicarbonate, a beta2-adrenergic agonist such as nebulized albuterol sulfate, or loop diuretic therapy are additional treatments that may be given, but should not be used as monotherapy.14,16
Calcium chloride or calcium gluconate can temporarily counteract the effects of potassium on cardiac cells. Calcium can stabilize the cell membranes by causing an exchange of calcium for potassium at the cellular level, but the duration of effect is only 30 to 60 minutes, and this treatment does not alter the serum potassium level.14 Therefore, calcium must be supported by other treatments and should only be used when significant changes on the ECG are present.1,12,14 (See Nursing considerations for hyperkalemia.)
The most recent Cochrane Review on hyperkalemia has a summary statement supporting the use of insulin and glucose and a beta2-adrenergic agonist (albuterol), but stated that none of the studies reviewed mentioned clinical outcomes. All studies looked at only potassium levels. Also, the review indicated that more randomized controlled trials are needed on the effectiveness of potassium-binding resins or calcium.17
Hypokalemia is defined as a serum potassium level less than 3.5 mEq/L.1 Hypokalemia can be just as life-threatening as hyperkalemia. According to the AHA, potassium levels less than 3.0 mEq/L are associated with 21% mortality.11
Causes. There are three major causes of hypokalemia: inadequate potassium intake; excessive GI, kidney, and skin losses of potassium; and transcellular shifts of potassium.10 (See Common causes of hypokalemia.)
Patients who cannot eat or have inadequate dietary intake will not consume the amount of potassium that is required each day and are at risk for hypokalemia.1,11 Similar to hyperkalemia, hypokalemia is frequently caused by medical interventions. The most common cause of hypokalemia is the use of diuretics, including both loop and thiazide diuretics.1 Nurses should not give any diuretic without checking the patient's potassium level. If the level is low, notify the patient's provider.
Patients who are vomiting or having diarrhea, as well patients on any form of GI suction are also at risk for hypokalemia. Consider whether increased GI output or lack of daily GI input is the issue.1,11,12,14
Hypokalemia also may be caused by situations in which too much potassium has moved into the cells. This can arise from iatrogenic causes such as administration of beta2-adrenergic agonist medications, or from the administration of insulin during treatment of diabetic ketoacidosis. It may also be attributed to hypomagnesemia or any condition that caused the patient to develop alkalosis.1,11,12
Signs and symptoms. Patients' signs and symptoms may be vague with mild hypokalemia. Patients may experience anorexia, nausea, vomiting, constipation, muscle weakness, or fatigue. This may progress to muscle cramps or even paralysis. Patients may also become confused.1 The ECG may show a smaller than usual T wave, and the patient may develop a U wave after the T wave or a depressed ST-segment.1 If the critical care nurse sees these changes on the cardiac monitor for a patient, a 12-lead ECG should be ordered and a serum potassium level should be run. As with hyperkalemia, a definitive diagnosis of hypokalemia cannot be made from a change on the cardiac monitor, but such changes should prompt further testing and assessment of the patient.11,12,14
Low potassium levels can also result in significant dysrhythmias such as ventricular tachycardia, or ventricular fibrillation. Cardiac arrest from ventricular fibrillation, asystole, or pulseless electrical activity can occur.11,14 However, inpatients should not reach this level if the nurse is thinking critically about medications, disease processes, and GI status.
Treatment. The best way to manage hypokalemia is to prevent it. However, if hypokalemia develops, treat the underlying cause and replace the potassium loss. When potassium replacement is necessary, the AHA recommends oral replacement if possible.11 According to The Joint Commission, injectable potassium is a high-alert medication and the facility's policy for high-alert medications must followed when potassium is given by I.V. infusion.18 The I.V. solution (usually 0.9% sodium chloride) with the potassium replacement dose must be given by infusion using an infusion pump. Potassium replacement is never given as an I.V. bolus of potassium, even during cardiac arrest.11 Assess the patient and monitor the patient's cardiac rhythm during the infusion.14 The serum potassium level should be repeated to determine the effectiveness of the therapy. See Nursing considerations for hypokalemia.
Potassium and BP. Although most healthcare providers are familiar with the association between dietary sodium and hypertension, research has shown an inverse relationship between potassium and hypertension that is not as well known. This was reported in detail by the National Academy of Medicine in 2005, which stated that adequate intake of potassium can lower BP and protect against stroke.19 Subsequent research supports this finding. In follow-up trials of hypertension prevention studies from 2009, researchers confirmed that adequate potassium intake can lower BP in hypertensive adults.20 Additional analysis showed that an even more accurate predictor of elevated BP is the sodium-to-potassium ratio.20
A more recent meta-analysis confirmed a positive link between potassium and other electrolytes in minimizing the risk of stroke.21 A study conducted by Blanch and colleagues specifically evaluated the effects of sodium and potassium on cardiovascular disease and found that potassium ingestion helps cardiovascular function by improving postprandial endothelial function.22 A study by Peng and colleagues showed that salt substitutes that contain more potassium and magnesium and less sodium can also contribute to lowering BP.23
Dietary intake of potassium. Research regarding the valuable role of potassium in preventing hypertension has led to various descriptive studies that have found widespread inadequacies in dietary intake of potassium. For example, pulling data from a national database, Drewnowski and colleagues reported in 2012 that less than 0.015% of the population met the combined recommended dietary requirements for lower sodium (less than 2,300 mg/day) and higher potassium (4,700 mg/day).24 Loftfield and colleagues studied New York City residents with similar findings.25 Low potassium intake was also confirmed to be a problem in children ages 7 months to 5 years.26 In 2012, diabetes educator Linda Antinoro published a statement indicating that white meats, fish, poultry, and a variety of fruits and vegetables are high in potassium content and should be consumed in greater quantities.27 Swiss chard was on the top of her list, with 961 mg of potassium/serving. Other research indicates that it may be time to reconsider moderate use of properly prepared lean red meat to make up dietary deficits of potassium and other nutrients.28
All of the recent articles on this topic indicate that healthcare providers should specifically focus on increasing their patients' dietary intake of potassium in addition to decreasing sodium consumption.
Physiology. A study from 2014 looked more specifically at the protection of muscle fibers that occurs in chronic heart failure.29 This study measured the release of amino acids that indicate muscle damage, and found that in the presence of low potassium, there was more muscle cell degradation.
I.V. infusion vs. enteral replacement for hypokalemia. One recent study confirmed prior findings regarding the efficacy of oral potassium. The study acknowledged that there seemed to be a preference for I.V. infusion potassium in the ICU, but postulated that it would be better to administer oral potassium. To that end, new protocols were written that focused more on oral replacement, and the findings were equivalent for patient outcomes.30
There is renewed attention to the role of potassium in the diet, and ongoing attention to the fact that serum potassium levels must be properly maintained and monitored. The critical care nurse should be aware of these issues, observe patients for signs of potassium abnormalities, and should add dietary potassium intake to any patient teaching about healthy diets.
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