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Electrolytes, in the right balance, are essential for regulating body functions and maintaining health. Even small deviations from normal electrolyte concentrations may cause significant problems. Hyperkalemia is acknowledged as one of the most dangerous electrolyte abnormalities. Symptoms are nonspecific and predominately related to cardiac or neuromuscular dysfunction, with potentially life-threatening consequences. Immediate and decisive treatment is necessary to lower the serum potassium level and to prevent a recurrence. This article reviews the pathophysiologic causes of hyperkalemia and discusses the manifestations, diagnostic tests, and various treatment options available to manage this electrolyte abnormality.
Fluids and electrolytes are vital for regulating and maintaining virtually every aspect of body function. This article will focus on the specific abnormality of hyperkalemia; however, a brief overview of fluid and electrolytes may be beneficial for understanding normal function.
Body fluid-mainly water-makes up about two-thirds of an adult's total body weight. The amount of fluid and how it is distributed in the body varies in relation to an individual's age, gender, and body build.
Lean body muscle mass is rich in water, while adipose, or fat, tissue is nearly water-free. The leaner the person, the greater the proportion of water in relation to total body weight. This concept aligns with gender and age as well. Women tend to have a lower water-percentage weight than men because of the higher concentration of fat content in their bodies. Similarly, as individuals age, they are predisposed to have a lower water-weight percentage overall as a result of a decrease in their muscle mass content.1-3
Fluid in the body is located in 2 major compartments: the intracellular space and the extracellular space. Extracellular fluids (ECFs) are further divided into intravascular fluid (blood plasma), transcellular fluids (water within epithelial-lined spaces), and interstitial fluid (tissue spaces surrounding the cells). Infants and children have a greater percentage of fluid in the interstitial spaces, which makes them more susceptible to fluid volume deficit problems.2,3
Electrolytes, or ions, are small, electrically charged elements located in body fluid, tissue, and blood. They are critical in maintaining proper cellular activity, facilitating oxygenation, controlling fluid and acid-base balance, and regulating many body functions. Common electrolytes include sodium, potassium, calcium, phosphorus, magnesium, chloride, and sodium bicarbonate.
Body fluids are electronically neutral; however, the distribution of electrolytes varies within the ECF and intracellular fluid (ICF). Like fluid, their levels are controlled by a variety of hormones, such as renin, aldosterone, and antidiuretic hormone (ADH). Electrolytes function optimally within a narrow range, and small shifts of any select electrolyte can have a significant effect on body function.
Sodium (Na+) is concentrated in the ECF, whereas potassium (K+) is concentrated in the ICF. Sodium and potassium share a unique reciprocal relationship with their ICF/ECF levels and movement. For example, following depolarization of cardiac cells, use of the sodium-potassium pump facilitates the return of these electrolytes to their respective fluid compartments during repolarization. In the repolarization process, sodium does not move back to the extracellular area passively, so energy use is required to facilitate this movement. As the sodium is transported into the ECF, potassium shifts back into the intracellular space to maintain overall electrolyte charge neutrality. Proper balance is essential for muscle coordination, cardiac function, fluid absorption and excretion, neuromuscular function, and appropriate mentation.3-5
Fluids and electrolytes are constantly moving between the compartments to maintain a homeostatic state. When the fluid spaces on either side of a membrane contain differing amounts of particles (solutes), a concentration gradient occurs. The body uses several means of moving fluid and/or particles to alter these concentrations and attain equilibrium. The 2 major types of movement for fluids and electrolytes include passive transport and active transport.
In passive transport, several mechanisms facilitate fluid and electrolyte shifts, including diffusion, osmosis, and filtration.3,4 Passive transport does not require energy to cause a fluid/electrolyte compartmental shift. No work is required because the movement is going down the concentration gradient in the natural flow.
The first type of passive transport, diffusion, is the movement of solute, including electrolytes, across a permeable membrane from a high concentration to a low concentration of that solute. The particles flow across the permeable membrane as they shift from a more crowded state to a lower-density area. This high-to-low, or "downhill," movement of the particles continues until a balance is achieved.3,4
Osmosis is the movement of fluid (solvent) from an area of higher fluid concentration (low solute concentration) to an area of lower fluid concentration (high solute concentration). Fluid is moving from an area with little solute to an area of more dense solute in an effort to "dilute" the latter. The movement occurs until the fluids on both sides of the permeable membrane contain equal concentrations of solute. No energy is required because the movement follows an ordinary flow on the gradient concentration and does not require assistance to occur.3,4
Filtration is the movement of fluid from 1 side of a membrane to another because of a difference in pressure exerted on the 2 sides of the membrane wall. The fluid compartment with the higher pressure forces the fluid across the membrane toward the fluid compartment exerting a lower pressure until equilibrium occurs. Although pressure is used, no energy is expended, so it is a form of passive transport.3,4
Active transport involves moving solutes from an area of low solute concentration to an area of high solute concentration, moving against a concentration gradient. Energy is required to help carry the molecules because it is forcing fluids and/or electrolytes to move against the natural concentration gradient flow ("uphill"). Energy is provided by adenosine triphosphate (ATP), a nucleoside triphosphate used in cells as a coenzyme. When generated by the metabolism of glucose or fat within a cell, chemical energy is released for physiologic function and needs of the body. Active transport requires the use of the energy produced by the hydrolysis of ATP to force the solute back across the membrane to where it needs to be.3,4 An example of an active transport mechanism in the body is the sodium-potassium pump. To maintain the normal resting potential, sodium has a high concentration extracellularly, and potassium has a high concentration intracellularly. The natural inclination is to move to equalize these electrolyte levels. For example, with cardiac depolarization, sodium shifts into the cell, causing potassium to shift out of the cell to facilitate contraction of the heart muscle. During repolarization, the electrolytes must be moved back to their original positions to be ready for the next needed shift. Because this movement requires the electrolytes to move against the concentration gradient, ATP energy is needed to force them back. Through active transport, the sodium-potassium pump transfers 3 sodium ions out of the cell in exchange for moving 2 potassium ions back into the cell. This is responsible for preserving the large concentration of sodium ions outside the cell and the large concentration of potassium ions inside.3,4
In addition to passive and active transport, hydrostatic pressure works reciprocally with osmotic pressure in the vascular space to preserve vascular fluid levels. Hydrostatic pressure is the pressure that fluid exerts on the walls of its container to leave the container. Osmotic pressure is the pressure required to prevent the flow of fluid across a semipermeable membrane. Osmotic pressure works to keep the fluid within the container. In blood vessels, for example, the fluid's hydrostatic pressure is pushing against the vessel wall to drive fluids out, while osmotic pressure (with plasma proteins like albumin) is pulling to maintain the fluid volume within the blood vessel. At the arteriole and early capillary level, hydrostatic pressure is higher than osmotic pressure. This pushes fluid, along with nutrients and oxygen, out of the blood vessels into the interstitial area for cellular use. As the fluid shifts out of the capillary, the albumin concentration in the blood vessels becomes higher. When the osmotic pressure surpasses the hydrostatic pressure, fluid is drawn back into the capillary bed. This fluid contains accumulated waste products and carbon dioxide.2,4
The major hormones affecting fluid and electrolyte balance are the ADH, aldosterone, and atrial natriuretic peptide (ANP). ADH, a hormone secreted by the posterior pituitary gland, is the primary controller of ECF volume. It is stimulated to secrete by an increase in blood osmolality, which indicates a state of water deficit. The release of ADH causes the kidneys to reabsorb more water in the distal convoluted tubules, which dilutes the blood and normalizes the serum osmolality. Thus, in the presence of ADH, water is reabsorbed and the ECF level remains high. When ADH secretion is suppressed, the kidneys secrete more water to maintain normal osmolality. Water is not reabsorbed and is excreted through the kidneys, lowering ECF volume.2,4
Fluid levels are also influenced through the renin-angiotensin-aldosterone feedback system. A decrease in the intravascular fluid volume stimulates the release of renin from the kidneys, which promotes the release of angiotensin I, a mild vasoconstrictor, from the liver. With the assistance of the angiotensin converting enzyme (ACE), angiotensin I is converted to angiotensin II, a powerful vasoconstrictor. The angiotensin II then stimulates the adrenal glands to secrete aldosterone. Aldosterone, a mineral corticoid produced by the adrenal cortex, works to regulate sodium balance as a part of this feedback system by dictating the amount of sodium that needs to be reabsorbed by the kidneys in order to maintain proper body fluid levels. An increase in aldosterone will promote the reabsorption of sodium in the distal tubules of the kidneys, which leads to water and chloride being reabsorbed as well. Aldosterone secretion causes the renal cortical collecting ducts to excrete potassium while preserving sodium. The constricting action of angiotensin II also causes constriction of vessels in the kidneys, which signals the posterior pituitary to secrete ADH to further conserve fluids. When the circulating levels of these substances in the bloodstream are decreased, the kidneys do not reabsorb as much sodium and water, allowing them to be excreted.2,4
Additional influence on the body's fluid and electrolyte regulation comes from ANP synthesis. This hormone is produced from atrial cells through the coronary sinus in response to increased vascular volume, increased pressure on the heart, and increased sodium levels (hypernatremia). Its effect on sodium and fluid balance is in opposition to aldosterone and ADH by blocking their production, initiating vasodilation, and stimulating kidney excretion of sodium and water. Thus, ANP production will promote a decrease in fluid volume through diuresis, providing a further check and counterbalance to the effects of ADH and aldosterone.4,5
Potassium is the most abundant cation in the ICF. Discovered by Sir Humphrey Davy in 1807, potassium is named for potash, the substance used as starting material in the identification, and is denoted in the periodic table by K+ for the Latin word kalium.6 Normal serum potassium levels range from 3.5 to 5.0 mEq/L, while normal ICF potassium levels are about 140 mmol/L. Ninety-eight percent of potassium is intracellular, leaving 2% in the ECFs. Because of its high concentration within the cell, potassium exerts some influence over intracellular osmolality and volume. Maintaining this great difference in potassium concentration between intracellular and ECF levels is imperative for excitable tissues to depolarize and generate action potentials. In addition to maintaining the cellular membrane potential, potassium is also involved in regular cellular maintenance, cell volume homeostasis/osmolality, and transmission of nerve impulses. Potassium is involved in cellular metabolism, regulating protein synthesis and glucose use and storage. It also affects the body's pH balance on the basis of its capacity to respond to and exchange with hydrogen ions. Acidic states will cause hydrogen ions to move intracellularly, forcing potassium ions to shift out of the cells to maintain intracellular electrical neutrality.1,3,7
Potassium is not easily stored in the body and requires daily consumption to maintain appropriate levels for body functions. Depending on diet, normal daily intake can vary. The majority of food products contain at least some potassium. Foods that are high in potassium include protein-rich foods, such as meat, fish, milk, almonds, and many fruits and vegetables, such as spinach, cantaloupe, bananas, oranges, mushrooms, and potatoes. Eggs, bread, and cereal grains have the lowest content.8,9 (See Table 1 for a more complete list of potassium-rich foods.)
The movement or shift of potassium in and out of the cells, while not changing overall potassium levels in the body, may influence serum levels of the electrolyte a great deal. Because potassium levels in the ECF compartments are so low, even small changes can seriously affect physiologic activities.3,10 To preserve appropriate electrolyte balance in the body, sodium and potassium are in perpetual fluctuation between the intracellular and extracellular body compartments. The sodium-potassium pump is the primary controller of the ECF potassium level, which works to move excess sodium out of the ICF and potassium from the ECF back into the cell.3,7 In addition, circulating insulin also helps maintain the level of potassium within the cells. Insulin facilitates potassium uptake into the liver and muscle cells by stimulating the sodium-potassium pump. Large increases in extracellular potassium concentration promote insulin secretion, which causes movement of excess potassium into the intracellular compartment.11 The kidneys are also regulators of body potassium, maintaining blood levels by controlling excretion, even as intake varies. Elimination of potassium from the body is performed primarily through the renal system (80%); other routes include the gastrointestinal tract and sweating.3,7 Kidney excretion is enhanced by aldosterone. Its role is to activate the basolateral Na+/K+-ATPase, which increases sodium and water reabsorption in the blood and excretion of potassium in the urine.11
Hyperkalemia is a potentially life-threatening situation in which the serum potassium level surpasses 5.0 mmol/L.7,12 It is further classified by severity as mild (5.5-6.5 mmol/L), moderate (6.5-7.5 mmol/L), and severe (>7.5 mmol/L) hyperkalemia.11 It may result from excessive intake of potassium and potassium-containing substances, impaired elimination of potassium, altered distribution shift from the intracellular to the extracellular spaces, or cellular injury.11,13,14
It is difficult for excessive intake of potassium to occur in patients with adequate renal function and intact other regulatory mechanisms. However, hyperkalemia may be induced with either ingestion or administration of excessive quantities of potassium. Individuals with impaired renal function may experience significant hyperkalemia with increased potassium consumption in foods and some salt substitutes. Oral and parenteral potassium supplements prescribed for patients to maintain adequate potassium levels have the potential to cause hyperkalemia if too much is administered or the body is unable to excrete the excess appropriately. Parenteral medications, such as penicillin and carbenicillin, and stored blood products contain significant amounts of potassium. Intravenous administration of these agents may contribute to the development of hyperkalemia.11,13
Impaired renal excretion from renal failure, tubular defects, or hypoaldosteronism affects the body's ability to remove potassium effectively. Renal insufficiency or failure (acute and chronic) is characterized by a decrease in glomerular filtration rate (GFR), the rate at which blood is filtered in the glomeruli of the kidney. This decrease in renal perfusion affects all the functions the kidneys perform for the body, among them the ability to excrete excess potassium. In addition to overall renal insufficiency, specific defects in renal tubule transport may elevate serum potassium levels. Medical conditions demonstrating tubular defects include sickle cell disease, obstructive uropathy, renal allograft, pyelonephritis, and interstitial nephritis.11,13
Because aldosterone helps regulate potassium levels and excretion, any condition that produces hypoaldosteronism will adversely affect potassium excretion. Primary adrenal insufficiency (Addison's disease) occurs when the adrenal glands are damaged and unable to produce the hormones cortisol and aldosterone. This loss of aldosterone hinders the body's ability to retain sodium and water and to excrete potassium. Other medical conditions that cause a secondary hypoaldosteronism, including renal tubular acidosis type 4 and congenital adrenal hyperplasia, will yield similar risks for the development of hyperkalemia.11,13
In addition, chronic constipation may interfere with normal intestinal excretion of potassium. Because about 20% of potassium is eliminated through the intestinal tract, long-term constipation issues may decrease enteral removal of potassium and cause hyperkalemia. Individuals with problems emptying their bowels secondary to myelodysplasia or VACTERL association are especially at risk for bowel-related potassium retention.9,11
Medications may interfere with normal excretion mechanisms of potassium. Potassium-sparing diuretics (spironolactone [Aldactone] and amiloride [Midamor]) facilitate the buildup of potassium in the body by blocking its excretion by the kidneys. Nonsteroidal anti-inflammatory drugs, including ibuprofen (Motrin) and naproxen (Aleve, Naprosyn), cause elevated potassium levels by a variety of mechanisms. They suppress prostaglandin synthesis, which reduces renal blood flow (GFR) and inhibits the systemic release of renin from the kidney. Their use also suppresses aldosterone synthesis in the adrenal gland. With this combination of effects, potassium levels can become dangerously high, especially in patients with renal insufficiency. Other medications, including cyclosporine (Neoral, Sandimmune), tacrolimus (Prograf), ACE inhibitors (lisinopril [Prinivil]), and angiotensin-II receptor antagonists (losartan [Cozaar], valsartan [Diovan]) also may cause a reduction in aldosterone and the GFR, facilitating the development of hyperkalemia.11,13,15 In addition, many herbal remedies will elevate potassium levels. Noni juice, dandelion, horsetail, and alfalfa have a high potassium content. Other herbals-such as lily of the valley, Hawthorne berry, dried toad skin, and Siberian ginseng-affect body functions such as insulin and aldosterone levels and kidney function. Patients should be questioned about any use of herbal supplements related to hyperkalemia.16,17 (Table 2 provides a more complete list of medications significant for contributing to hyperkalemia.)
Transcellular electrolyte shifts may induce elevated serum potassium levels in many situations, including acidosis, hypertonicity, cellular injury, and insulin deficiency. When managing hyperkalemia, it's important to recognize these pathophysiologic changes and their effects.
Acidosis, which occurs in a number of diseases, refers to an increase in the concentration of hydrogen ions in the bloodstream. The body attempts to correct the acidosis by pulling hydrogen ions into the cells by exchanging them with potassium ions, shifting potassium out of the cells and into the bloodstream. This can abnormally elevate the plasma's concentration of potassium ions.6,11
Hypertonicity, associated with an increase in ECF potassium, may occur as a result of conditions such as hyperglycemia, the administration of hypertonic saline or mannitol, and infusion of intravenous immunoglobulin. The body's need for balance in the ICF and ECF causes shifting of fluids and electrolytes in these compartments. Hypertonic states often present as an additional factor in patients with other underlying diseases that affect potassium levels, such as diabetes and low aldosterone.6,11
Hyperkalemia from transcellular shifts of potassium may be caused by cellular injury. Any process that leads to cellular/tissue injury can result in elevated serum levels because intracellular potassium is released by disruption of the cell membrane. Conditions that cause tissue damage include rhabdomyolysis (rapid breakdown of damaged muscle tissue from drugs, alcoholism, injury, coma, or infection), severe intravascular hemolysis, acute tumor lysis syndrome, burns, traumatic/crush injury, and surgery.11,13,15 During strenuous or prolonged exercise, potassium is released from active muscle, potentially elevating serum potassium to dangerous levels.11,13,15
Insulin enhances cellular potassium uptake and facilitates normal serum potassium levels through its ability to stimulate the sodium-potassium pump. Elevated extracellular potassium levels stimulate increased insulin secretion to promote the return of potassium to the cell. So an insulin deficiency reduces the body's ability to shift the potassium intracellularly, making the individual susceptible to hyperkalemia.
Many medications may cause elevated serum potassium levels by facilitating ICF-to-ECF shifts. For example, digoxin (Lanoxin) and beta-blockers, especially nonselective such as propranolol (Inderal), affect the sodium-potassium pump mechanism.11,13,15 Additional medications associated with ICF-to-ECF shifts include fluoride intoxication, succinylcholine, and propofol. Propofol infusion syndrome is a condition causing hyperkalemia associated with high-dosage and/or long-term use of propofol.18 (See Table 2 for medications causing hyperkalemia.) Other medical conditions causing transcellular hyperkalemia include malignant hyperthermia, an inherited muscle disorder triggered by anesthesia, and hyperkalemic periodic paralysis, a rare hereditary condition with heightened muscular sensitivity associated with transient potassium elevations.6,11,13
Diagnosis of hyperkalemia may be made with identification of elevated laboratory serum potassium levels, and reinforced through physical assessment findings, a thorough clinical history, and medication review. Additional blood testing should be ordered as appropriate to facilitate the differential diagnosis for the cause, including complete blood count, arterial blood gases, serum osmolality, electrolyte panel, blood urea nitrogen/creatinine, liver enzymes (ALT, LDH), glucose/HgbA1C, and renin, angiotensin, aldosterone, and cortisol levels. In addition, a complete urine analysis-including urine potassium, sodium, and creatinine levels, albumin, protein, and urine osmolality-should be performed.11 An electrocardiogram (ECG) will help confirm any cardiac rhythm changes related to hyperkalemia.2
When initial findings of hyperkalemia are identified, especially if the elevated serum potassium is found in an asymptomatic patient with no apparent cause, care should be given to rule out the possibility of pseudohyperkalemia. This occurs as a result of leakage of potassium from the blood cells during or following the drawing of blood samples, particularly in difficult blood sampling, such as pediatric blood draws and samples with hemolysis, lymphocytosis, or thrombocytosis.10,11,13,15 In addition, drawing blood from lines where potassium is being infused, technician error, fist clenching during phlebotomy, and traumatic venipuncture may cause a false elevation in serum potassium levels.15
Cardiovascular dysfunction and neurological alterations are the chief manifestations of hyperkalemia. In the heart, this dysfunction exhibits with ECG changes and cardiac dysrhythmias. The initial significant finding is peaked T waves. Increasing levels of potassium are associated with progressive ECG changes, including a widening PR interval, loss of P waves, ST segment changes, and a widening QRS. Potential hyperkalemic-induced dysrhythmias include second- and third-degree heart block, wide-complex tachycardia, ventricular fibrillation, asystole, and pulseless electrical activity. A sine wave, an EKG finding where the P wave disappears and the QRS complex and T wave merge in an oscillating pattern, may appear in severe hyperkalemia.2,11-13,19 Elevated potassium also may cause failure to capture in patients with pacemakers as a result of altered myocardial conduction patterns.20
The elevated potassium level modifies the impulse transmission to the nerves and muscles. Neurologically, the patient may demonstrate fatigue, irritability, and mental confusion. Neuromuscular manifestations include muscle cramps, weakness, speech problems, paresthesias (to the face, hand, feet, and tongue), tetany, and paralysis.2,11,13 The elevated potassium may also cause gastrointestinal hyperactivity, with the patient complaining of nausea, diarrhea, and abdominal cramping. In late stages of hyperkalemia, paralysis of the respiratory muscles may progress to respiratory arrest.1,2
Treatment for hyperkalemia centers on lowering the serum potassium level, preventing recurrences, and monitoring for patient safety. Therapeutic strategies need to be tailored for the individual while discerning the severity and cause of hyperkalemia. Appropriate treatment is determined by the speed of onset, severity level, and development of clinical findings.11
Potassium levels may be lowered by eliminating sources of potassium intake, including those that are ingested and administered parenterally. Providing a low-potassium diet-including foods such as apples, cherries, peaches, watermelon, carrots, cabbage, corn, white bread, white rice, chicken, and tuna-will help reduce the amount of potassium ingested.21 Enteral tube feeding formulas should be specially prepared to provide low potassium levels based on lab values. Oral potassium supplements should be withheld, and intravenous infusions containing potassium additives should be discontinued. In addition, any medications that might cause or aggravate hyperkalemia (eg, ACE inhibitors, digoxin, beta-blockers, penicillin, etc.) should be discontinued.3,11 For individuals with a functioning renal system, removing the sources of potassium and allowing the kidneys to excrete the excess may be sufficient to lower the extracellular potassium level. Patients with impaired renal function often require more intensive therapy to combat the hyperkalemia.
Medications that facilitate potassium's movement from extracellular to intracellular compartments help to reestablish the body's potassium balance. Though this shift will not actually eliminate potassium from the body, decreasing serum potassium levels by shifting it from the ECF to the ICF will facilitate a temporary improvement in hyperkalemia. Medications that force potassium from the extracellular to the ICF include calcium salts, bicarbonate, insulin/glucose, and beta agonists. Patients with moderate-to-severe hyperkalemia, particularly those with impaired renal function, may require a combination of medication. Such combinations simultaneously promote cellular potassium shifts and excretion from the body to effectively lower potassium levels and prevent hyperkalemia recurrences.11
The first treatment to shift potassium intracellularly involves intravenous administration of calcium salts (calcium gluconate, calcium carbonate). Patients with unstable dysrhythmias and/or hypotension may benefit from this treatment because the calcium has cardioprotective properties. Cardiac ECG changes reflecting normal sinus rhythm characteristics (from the potentially lethal rhythms identified with hyperkalemia) are often visible within 2 to 3 minutes of calcium administration. Multiple calcium ampoules (10 mL of a 10% solution) may be necessary to achieve the desired effect, and because of its short duration of action (20-40 minutes), other treatments should also be introduced quickly.11,13,19,22,23 Use of calcium products would be contraindicated in digoxin-intoxication and hypercalcemic states.11,23
Cellular uptake of potassium may be induced through use of the buffer sodium bicarbonate (NaHCO3), especially if the patient is acidotic. Sodium bicarbonate infusion will shift potassium intracellularly by increasing the blood pH, which reduces the level of hydrogen ions that are able to exchange with potassium forcing it out of the cell. One ampoule (44 mEq) should be administered intravenously over 5 to 15 minutes. Its duration of action is about 2 hours, which would allow time for the kidneys to excrete excess potassium and facilitate a more normal pH. Bicarbonate should be used with caution in patients where the risk of hypertonicity, fluid volume overload, or alkalosis would be deleterious to their health. As an additional caution, an elevation in pH may exacerbate hypocalcemia.11,13,22 Calcium carbonate will also offer some buffer activity for acidic hyperkalemia. It combines its cardioprotective qualities as a calcium agent with its alkaline "buffer" qualities as a carbonate to cause an intracellular shift of the potassium, while also protecting the heart from potentially life-threatening dysrhythmias.6,11,13
Using a regimen of intravenous insulin and glucose promotes a shift of potassium into the cells. Regular insulin (10-20 units) may be infused via bolus infusion to move the potassium into the cell. The insulin is usually accompanied by 50 mL of 50% dextrose solution in euglycemic patients and diabetic patients with a blood glucose level of less than 250 mg/dL to prevent hypoglycemia. If a patient is already hyperglycemic, supplemental glucose is not needed. Duration of action for this mixture is 4 to 6 hours. Caution should be used with rapid infusion of hypertonic glucose solution; the osmotic effect it exerts on the cells may transiently exacerbate the serum hyperkalemia.13,22
Use of beta-adrenergic agonists (inhaled, nebulized, or intravenous) will also help to move the potassium back into the cells. They stimulate potassium to move from the extracellular compartment to the intracellular compartment by the Na+/K+-ATPase mechanism. Use of nebulized albuterol (Ventolin) is administered in a dosage of 10 to 20 mg. Treatment with nebulized albuterol will lower the serum potassium level for more than 2 hours.13,19,22 The effect of beta2 agonists is additive to that of insulin administration, and they may be given together for an enhanced effect.19 Aminophylline administration also demonstrates some reduction in serum potassium levels, although this may potentiate tachycardia.22
Definitive treatment for hyperkalemia requires its removal from the body. The use of ion-exchange resins, such as sodium polystyrene sulphonate (Kayexalate), diuretics, and hemodialysis are methods that achieve this elimination. Exchange resins work by exchanging gut cations-most important, potassium-for sodium ions that are released from the resin. Each gram of Kayexalate, administered orally or rectally, may remove approximately 1.0 mEq of potassium. Exchange resins can cause significant constipation and are typically given in combination with a laxative such as sorbitol. Not only does a laxative prevent constipation, it also promotes the elimination of potassium from the gut once it binds to the resin. An oral dose of Kayexalate given with sorbitol, an osmotic cathartic, will produce results within 1 to 2 hours. Rectal enemas of 50 mg of Kayexalate, administered and then retained for 30 minutes, will produce effects in about half an hour. Patients with poor cardiovascular reserve should be monitored carefully because of the potential for exacerbating fluid volume overload.13 Although generally safe, the combination of a resin and sorbitol has been reported to cause intestinal necrosis. Because they are often packaged together as a single mixture, they should be administered cautiously and only when necessary.24
Diuretics, such as loop (furosemide [Lasix]) and, to a lesser degree, thiazides (hydrochlorothiazide), will remove potassium through the kidneys and renal system. They act by diminishing sodium reabsorption at different sites in the nephron, increasing urinary sodium, water, and potassium losses. In patients with functioning kidneys, this is a viable method for potassium removal. Even in patients with chronic renal failure, this treatment format has value if some residual renal function remains.11 In addition, the mineralocorticosteroid fludrocortisone (Florinef) may be beneficial in treating hyperkalemia. This agent facilitates excretion of potassium through the distal tubules of the kidneys. Caution should be observed, however, because it may cause increased retention of sodium and water.14,22
Dialysis is another option for potassium removal if the conservative measures listed above are ineffective. Dialysis corrects hyperkalemia rapidly and is indicated for unstable hyperkalemic patients with renal failure, severe rhabdomyolysis, and elevated potassium-induced cardiac arrest. In an emergency, hemodialysis is the preferred dialysis method because the rate of potassium removal is many times faster than that of peritoneal dialysis. Hemodialysis removes potassium from the blood only; rebound hyperkalemia may occur with ensuing efflux of intracellular potassium, following the completion of the treatment.13 Regardless of the chosen treatment modality, the potential for reemergence of hyperkalemia is a concern, so nurses must continue to monitor the patient for manifestations of the disorder. This is especially true if the original cause of the hyperkalemia has not been addressed.
In addition to treating the hyperkalemia, identification and treatment of the underlying cause for the elevated potassium level should be initiated. Examples of this may include treating rhabdomyolysis with intravenous fluids and bicarbonate; managing Addison's disease with intravenous fluids, corticosteroids, and glucose; treatment of digoxin toxicity with digoxin-binding antibodies such as digoxin immune fab (Digibind); or stopping the use of medications that may have contributed to the hyperkalemic state.13
Nursing care for patients with hyperkalemia is multifocused. Because potassium affects the functioning of all the body systems, it is important for the nurse to recognize abnormalities that may occur. Early identification of signs and symptoms of hyperkalemia is important for the nurse caring for the patient with hyperkalemia. A thorough head-to-toe nursing assessment is critical for patients diagnosed with hyperkalemia to determine any physiological changes in function and to alert the nurse to subtle changes that may indicate a rise in the serum potassium level. The nurse should assess the patient's cardiovascular status frequently, listening to heart sounds for irregularities, and assessing cardiac monitor patterns for any ECG changes/dysrhythmias related to hyperkalemia. Vascular perfusion should be monitored, with assessment of peripheral pulses and capillary refill. The nurse will want to perform a neurological assessment, observing for fatigue, sleepiness, altered level of consciousness, headache, muscle weakness/cramping, and paresthesias. For the respiratory system, the nurse should assess lung sounds, respiratory rate and depth, and oxygen saturation levels. Monitoring serum sodium and potassium levels, as well as other electrolyte and renal function laboratory values, is of extreme importance. Vital signs should be monitored regularly, and accurate intake/output measurements should be maintained. A health history should be obtained and a medication reconciliation performed, including all prescription and over-the-counter medications, and herbal and nutritional supplements. The nurse should be alert to and watch for signs and symptoms of hypokalemia, following interventions to reduce the potassium level. In addition, patients receiving insulin and glucose to treat the hyperkalemia should be monitored for manifestations of hypoglycemia.3
Patient education is an important component of nursing care in patients with hyperkalemia. Patients and their families should be provided education on the causes, clinical manifestations, and appropriate treatment options of this electrolyte abnormality. In addition, patients should be encouraged to limit oral intake of potassium and protein and to increase their fluid intake to promote adequate urinary output. The patient should be taught to avoid foods high in potassium and to read food labels on packaging to ascertain potassium content. They should also be careful about the use of salt substitute, which often contains potassium. A collaborative partnership between health care providers and patients promotes optimal management and health when patients are diagnosed with medical conditions that can potentially precipitate hyperkalemia.
Hyperkalemia is a complex medical issue with the potential to develop multisystem complications. Rapid identification and treatment of this electrolyte abnormality are essential to prevent the development of potentially fatal cardiac dysrhythmias. A comprehensive understanding of the predisposing clinical risk factors and pathophysiology of this disorder, cognizance of relevant medical treatment modalities, and appropriate nursing interventions are critical to providing optimal care for hyperkalemic patients. Incorporation of this knowledge, coupled with strong assessment skills, will provide the nurse with a strong foundation when caring for patients with elevated potassium levels.
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aldosterone; calcium gluconate; cardiac dysrhythmias; dialysis; diuretics; electrolytes; extracellular; hyperkalemia; insulin; intracellular; renal failure
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