Recognition and Management of a Critical Electrolyte Disturbance

The Art and Science of Infusion Nursing Ann H. Crawford , PhD, RN, CNS, CEN

Hyperkalemia: Recognition and Management of a Critical Electrolyte Disturbance

luids and electrolytes are vital for regulating ABSTRACT and maintaining virtually every aspect of Electrolytes, in the right balance, are essential for body function. This article will focus on the regulating body functions and maintaining health. specific abnormality of hyperkalemia; how- Even small deviations from normal electrolyte ever, a brief overview of fluid and electro- concentrations may cause significant problems. Flytes may be beneficial for understanding normal Hyperkalemia is acknowledged as one of the function. most dangerous electrolyte abnormalities. Body fluid—mainly water—makes up about two- Symptoms are nonspecific and predominately thirds of an adult’s total body weight. The amount of related to cardiac or neuromuscular dysfunction, fluid and how it is distributed in the body varies in rela- with potentially life-threatening consequences. tion to an individual’s age, gender, and body build. Lean body muscle mass is rich in water, while adi- Immediate and decisive treatment is necessary to pose, or fat, tissue is nearly water-free. The leaner the lower the serum potassium level and to prevent person, the greater the proportion of water in relation a recurrence. This article reviews the to total body weight. This concept aligns with gender pathophysiologic causes of hyperkalemia and and age as well. Women tend to have a lower water- discusses the manifestations, diagnostic tests, percentage weight than men because of the higher con- and various treatment options available to centration of fat content in their bodies. Similarly, as manage this electrolyte abnormality. individuals age, they are predisposed to have a lower Key words: aldosterone , calcium gluconate , water-weight percentage overall as a result of a decrease cardiac dysrhythmias , dialysis , diuretics , in their muscle mass content. 1-3 electrolytes , extracellular , hyperkalemia , insulin , Fluid in the body is located in 2 major compart- intracellular , renal failure ments: 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 Author Affiliation: Professor, College of Nursing, University of and children have a greater percentage of fluid in the Mary Hardin-Baylor, Belton, Texas. interstitial spaces, which makes them more susceptible Ann H. Crawford, PhD, RN, CNS, CEN, is a professor of nursing to fluid volume deficit problems. 2 , 3 at the University of Mary Hardin-Baylor. She serves on the under- graduate and graduate faculties. Dr. Crawford earned her bachelor’s and master’s degrees at the University of North Dakota. She obtained her doctorate in education at Texas A&M University. In addition to ELECTROLYTES teaching, Dr. Crawford works in the emergency department of a local hospital, McLane Children’s Baylor Scott & White, in Temple, Texas. Electrolytes, or ions, are small, electrically charged The author of this article has no conflicts of interest to disclose. elements located in body fluid, tissue, and blood. They Corresponding Author: Ann H. Crawford, PhD, RN, CNS, CEN, University of Mary Hardin-Baylor, 900 College Street, PO Box 8015, are critical in maintaining proper cellular activity, Belton, TX 76513 ( [email protected]). facilitating oxygenation, controlling fluid and acid-base DOI: 10.1097/NAN.0000000000000036 balance, and regulating many body functions. Common

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 116767 33/24/14/24/14 8:118:11 AMAM electrolytes include sodium, potassium, calcium, phos- (high solute concentration). Fluid is moving from an phorus, magnesium, chloride, and sodium bicarbonate. area with little solute to an area of more dense solute in Body fluids are electronically neutral; however, the an effort to “dilute” the latter. The movement occurs distribution of electrolytes varies within the ECF and until the fluids on both sides of the permeable mem- intracellular fluid (ICF). Like fluid, their levels are con- brane contain equal concentrations of solute. No energy trolled by a variety of hormones, such as renin, aldos- is required because the movement follows an ordinary terone, and antidiuretic hormone (ADH). Electrolytes flow on the gradient concentration and does not require function optimally within a narrow range, and small assistance to occur. 3 , 4 shifts of any select electrolyte can have a significant Filtration is the movement of fluid from 1 side of a effect on body function. membrane to another because of a difference in pressure Sodium (Na + ) is concentrated in the ECF, whereas exerted on the 2 sides of the membrane wall. The fluid potassium (K + ) is concentrated in the ICF. Sodium and compartment with the higher pressure forces the fluid potassium share a unique reciprocal relationship with across the membrane toward the fluid compartment their ICF/ECF levels and movement. For example, fol- exerting a lower pressure until equilibrium occurs. lowing depolarization of cardiac cells, use of the Although pressure is used, no energy is expended, so it sodium-potassium pump facilitates the return of these is a form of passive transport.3 , 4 electrolytes to their respective fluid compartments dur- Active transport involves moving solutes from an ing repolarization. In the repolarization process, sodium area of low solute concentration to an area of high sol- does not move back to the extracellular area passively, ute concentration, moving against a concentration gra- so energy use is required to facilitate this movement. As dient. Energy is required to help carry the molecules the sodium is transported into the ECF, potassium shifts because it is forcing fluids and/or electrolytes to move back into the intracellular space to maintain overall against the natural concentration gradient flow electrolyte charge neutrality. Proper balance is essential (“uphill”). Energy is provided by adenosine triphos- for muscle coordination, cardiac function, fluid absorp- phate (ATP), a nucleoside triphosphate used in cells as tion and excretion, neuromuscular function, and appro- a coenzyme. When generated by the metabolism of priate mentation. 3-5 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 FLUID AND ELECTROLYTE hydrolysis of ATP to force the solute back across the MOVEMENT membrane to where it needs to be. 3 , 4 An example of an active transport mechanism in the body is the sodium- Fluids and electrolytes are constantly moving between potassium pump. To maintain the normal resting poten- the compartments to maintain a homeostatic state. tial, sodium has a high concentration extracellularly, When the fluid spaces on either side of a membrane and potassium has a high concentration intracellularly. contain differing amounts of particles (solutes), a con- The natural inclination is to move to equalize these centration gradient occurs. The body uses several means electrolyte levels. For example, with cardiac depolariza- of moving fluid and/or particles to alter these concen- tion, sodium shifts into the cell, causing potassium to trations and attain equilibrium. The 2 major types of shift out of the cell to facilitate contraction of the heart movement for fluids and electrolytes include passive muscle. During repolarization, the electrolytes must be transport and active transport. moved back to their original positions to be ready for In passive transport, several mechanisms facilitate the next needed shift. Because this movement requires fluid and electrolyte shifts, including diffusion, osmosis, the electrolytes to move against the concentration gradi- and filtration.3 , 4 Passive transport does not require ent, ATP energy is needed to force them back. Through energy to cause a fluid/electrolyte compartmental shift. active transport, the sodium-potassium pump transfers No work is required because the movement is going 3 sodium ions out of the cell in exchange for moving 2 down the concentration gradient in the natural flow. potassium ions back into the cell. This is responsible for The first type of passive transport, diffusion, is the preserving the large concentration of sodium ions out- movement of solute, including electrolytes, across a side the cell and the large concentration of potassium permeable membrane from a high concentration to a ions inside. 3 , 4 low concentration of that solute. The particles flow In addition to passive and active transport, hydro- across the permeable membrane as they shift from a static pressure works reciprocally with osmotic pressure more crowded state to a lower-density area. This high- in the vascular space to preserve vascular fluid levels. to-low, or “downhill,” movement of the particles con- Hydrostatic pressure is the pressure that fluid exerts on tinues until a balance is achieved. 3 , 4 the walls of its container to leave the container. Osmotic Osmosis is the movement of fluid (solvent) from an pressure is the pressure required to prevent the flow of area of higher fluid concentration (low solute fluid across a semipermeable membrane. Osmotic pres- con centration) to an area of lower fluid concentration sure works to keep the fluid within the container. In

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 116868 33/24/14/24/14 8:118:11 AMAM blood vessels, for example, the fluid’s hydrostatic pres- Additional influence on the body’s fluid and electro- sure is pushing against the vessel wall to drive fluids lyte regulation comes from ANP synthesis. This hor- out, while osmotic pressure (with plasma proteins like mone is produced from atrial cells through the coronary albumin) is pulling to maintain the fluid volume within sinus in response to increased vascular volume, increased the blood vessel. At the arteriole and early capillary pressure on the heart, and increased sodium levels level, hydrostatic pressure is higher than osmotic pres- (hypernatremia). Its effect on sodium and fluid balance sure. This pushes fluid, along with nutrients and oxy- is in opposition to aldosterone and ADH by blocking gen, out of the blood vessels into the interstitial area for their production, initiating vasodilation, and stimulating cellular use. As the fluid shifts out of the capillary, the kidney excretion of sodium and water. Thus, ANP pro- albumin concentration in the blood vessels becomes duction will promote a decrease in fluid volume through higher. When the osmotic pressure surpasses the hydro- diuresis, providing a further check and counterbalance static pressure, fluid is drawn back into the capillary to the effects of ADH and aldosterone.4 , 5 bed. This fluid contains accumulated waste products 2,4 and carbon dioxide. POTASSIUM

HORMONAL INFLUENCE Potassium is the most abundant cation in the ICF. Discovered by Sir Humphrey Davy in 1807, potassium The major hormones affecting fluid and electrolyte bal- is named for potash, the substance used as starting mate- ance are the ADH, aldosterone, and atrial natriuretic rial in the identification, and is denoted in the periodic peptide (ANP). ADH, a hormone secreted by the poste- table by K+ for the Latin word kalium .6 Normal serum rior pituitary gland, is the primary controller of ECF potassium levels range from 3.5 to 5.0 mEq/L, while volume. It is stimulated to secrete by an increase in normal ICF potassium levels are about 140 mmol/L. blood osmolality, which indicates a state of water defi- Ninety-eight percent of potassium is intracellular, leav- cit. The release of ADH causes the kidneys to reabsorb ing 2% in the ECFs. Because of its high concentration more water in the distal convoluted tubules, which within the cell, potassium exerts some influence over dilutes the blood and normalizes the serum osmolality. intracellular osmolality and volume. Maintaining this Thus, in the presence of ADH, water is reabsorbed and great difference in potassium concentration between the ECF level remains high. When ADH secretion is intracellular and ECF levels is imperative for excitable suppressed, the kidneys secrete more water to maintain tissues to depolarize and generate action potentials. In normal osmolality. Water is not reabsorbed and is addition to maintaining the cellular membrane potential, excreted through the kidneys, lowering ECF volume. 2 , 4 potassium is also involved in regular cellular mainte- Fluid levels are also influenced through the renin- nance, cell volume homeostasis/osmolality, and trans- angiotensin-aldosterone feedback system. A decrease in mission of nerve impulses. Potassium is involved in the intravascular fluid volume stimulates the release of cellular metabolism, regulating protein synthesis and renin from the kidneys, which promotes the release of glucose use and storage. It also affects the body’s pH angiotensin I, a mild vasoconstrictor, from the liver. With balance on the basis of its capacity to respond to and the assistance of the angiotensin converting enzyme exchange with hydrogen ions. Acidic states will cause (ACE), angiotensin I is converted to angiotensin II, a hydrogen ions to move intracellularly, forcing potassium powerful vasoconstrictor. The angiotensin II then stimu- ions to shift out of the cells to maintain intracellular lates the adrenal glands to secrete aldosterone. electrical neutrality.1 , 3 , 7 Aldosterone, a mineral corticoid produced by the adre- Potassium is not easily stored in the body and nal cortex, works to regulate sodium balance as a part of requires daily consumption to maintain appropriate this feedback system by dictating the amount of sodium levels for body functions. Depending on diet, normal that needs to be reabsorbed by the kidneys in order to daily intake can vary. The majority of food products maintain proper body fluid levels. An increase in aldos- contain at least some potassium. Foods that are high in terone will promote the reabsorption of sodium in the potassium include protein-rich foods, such as meat, fish, distal tubules of the kidneys, which leads to water and milk, almonds, and many fruits and vegetables, such as chloride being reabsorbed as well. Aldosterone secretion spinach, cantaloupe, bananas, oranges, mushrooms, causes the renal cortical collecting ducts to excrete potas- and potatoes. Eggs, bread, and cereal grains have the sium while preserving sodium. The constricting action of lowest content. 8 , 9 (See Table 1 for a more complete list angiotensin II also causes constriction of vessels in the of potassium-rich foods.) kidneys, which signals the posterior pituitary to secrete The movement or shift of potassium in and out of ADH to further conserve fluids. When the circulating the cells, while not changing overall potassium levels levels of these substances in the bloodstream are in the body, may influence serum levels of the electro- decreased, the kidneys do not reabsorb as much sodium lyte a great deal. Because potassium levels in the ECF and water, allowing them to be excreted.2 , 4 compartments are so low, even small changes can

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 116969 33/24/14/24/14 8:118:11 AMAM HYPERKALEMIA TABLE 1 High-Potassium Foods Hyperkalemia is a potentially life-threatening situation in which the serum potassium level surpasses 5.0 Meats and Other mmol/L. 7 , 12 It is further classified by severity as mild Fruits Vegetables Sources (5.5-6.5 mmol/L), moderate (6.5-7.5 mmol/L), and Apricots Artichokes Almonds severe ( > 7.5 mmol/L) hyperkalemia.11 It may result Avocados Asparagus Roast beef from excessive intake of potassium and potassium- Bananas Beans (black, kidney, Salmon containing substances, impaired elimination of potassi- pinto, white, etc.) um, altered distribution shift from the intracellular to 11,13,14 Dates Beets Turkey (dark meat) the extracellular spaces, or cellular injury. It is difficult for excessive intake of potassium to occur Figs Brussels sprouts Chocolate in patients with adequate renal function and intact other Grapefruit Mushrooms Lentils regulatory mechanisms. However, hyperkalemia may be Kiwi Potato (sweet and Milk induced with either ingestion or administration of exces- white) sive quantities of potassium. Individuals with impaired Mangos Pumpkin Nuts renal function may experience significant hyperkalemia with increased potassium consumption in foods and Melons (cantaloupe, Tomato, tomato juice Peanuts honeydew, etc.) some salt substitutes. Oral and parenteral potassium supplements prescribed for patients to maintain adequate Nectarines Spinach Salt substitutes potassium levels have the potential to cause hyperkalemia Oranges, orange Squash Yogurt if too much is administered or the body is unable to juice excrete the excess appropriately. Parenteral medications, Papayas Turnips such as penicillin and carbenicillin, and stored blood Pears Yams products contain significant amounts of potassium. Zucchini Intravenous administration of these agents may contrib- ute to the development of hyperkalemia.11 , 13 Sources: Academy of Nutrition and Dietetics. Kidney disease: high- and low- potassium foods. http://www.eatright.org. Accessed December 20, 2012; O’Neill P. Impaired renal excretion from renal failure, tubular Helping your patient to restrict potassium. Nursing. 2007;37(4):64hn6-64hn8. 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 seriously affect physiologic activities.3 , 10 To preserve blood is filtered in the glomeruli of the kidney. This appropriate electrolyte balance in the body, sodium decrease in renal perfusion affects all the functions the and potassium are in perpetual fluctuation between the kidneys perform for the body, among them the ability intracellular and extracellular body compartments. to excrete excess potassium. In addition to overall renal The sodium-potassium pump is the primary controller insufficiency, specific defects in renal tubule transport of the ECF potassium level, which works to move may elevate serum potassium levels. Medical conditions excess sodium out of the ICF and potassium from the demonstrating tubular defects include sickle cell disease, ECF back into the cell. 3 , 7 In addition, circulating insu- obstructive uropathy, renal allograft, pyelonephritis, lin also helps maintain the level of potassium within and interstitial nephritis. 11 , 13 the cells. Insulin facilitates potassium uptake into the Because aldosterone helps regulate potassium levels liver and muscle cells by stimulating the sodium- and excretion, any condition that produces hypoaldo- potassium pump. Large increases in extracellular steronism will adversely affect potassium excretion. potassium concentration promote insulin secretion, Primary adrenal insufficiency (Addison’s disease) occurs which causes movement of excess potassium into the when the adrenal glands are damaged and unable to intracellular compartment.11 The kidneys are also reg- produce the hormones cortisol and aldosterone. This ulators of body potassium, maintaining blood levels by loss of aldosterone hinders the body’s ability to retain controlling excretion, even as intake varies. Elimination sodium and water and to excrete potassium. Other of potassium from the body is performed primarily medical conditions that cause a secondary hypoaldo- through the renal system (80%); other routes include steronism, including renal tubular acidosis type 4 and the gastrointestinal tract and sweating.3 , 7 Kidney congenital adrenal hyperplasia, will yield similar risks excretion is enhanced by aldosterone. Its role is to acti- for the development of hyperkalemia. 11 , 13 vate the basolateral Na+ /K + -ATPase, which increases In addition, chronic constipation may interfere with sodium and water reabsorption in the blood and excre- normal intestinal excretion of potassium. Because about tion of potassium in the urine.11 20% of potassium is eliminated through the intestinal

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 117070 33/24/14/24/14 8:118:11 AMAM tract, long-term constipation issues may decrease enteral Hyperkalemia from transcellular shifts of potassium removal of potassium and cause hyperkalemia. Individuals may be caused by cellular injury. Any process that leads with problems emptying their bowels secondary to myelo- to cellular/tissue injury can result in elevated serum levels dysplasia or VACTERL association are especially at risk because intracellular potassium is released by disruption for bowel-related potassium retention.9 , 11 of the cell membrane. Conditions that cause tissue dam- Medications may interfere with normal excretion age include rhabdomyolysis (rapid breakdown of dam- mechanisms of potassium. Potassium-sparing diuretics aged muscle tissue from drugs, alcoholism, injury, coma, (spironolactone [Aldactone] and amiloride [Midamor]) or infection), severe intravascular hemolysis, acute tumor facilitate the buildup of potassium in the body by block- lysis syndrome, burns, traumatic/crush injury, and ing its excretion by the kidneys. Nonsteroidal anti- surgery.11 , 13 , 15 During strenuous or prolonged exercise, inflammatory drugs, including ibuprofen (Motrin) and potassium is released from active muscle, potentially naproxen (Aleve, Naprosyn), cause elevated potassium elevating serum potassium to dangerous levels.11 , 13 , 15 levels by a variety of mechanisms. They suppress prosta- Insulin enhances cellular potassium uptake and facili- glandin synthesis, which reduces renal blood flow (GFR) tates normal serum potassium levels through its ability and inhibits the systemic release of renin from the kidney. to stimulate the sodium-potassium pump. Elevated Their use also suppresses aldosterone synthesis in the extracellular potassium levels stimulate increased insulin adrenal gland. With this combination of effects, potassi- secretion to promote the return of potassium to the cell. um levels can become dangerously high, especially in So an insulin deficiency reduces the body’s ability to patients with renal insufficiency. Other medications, shift the potassium intracellularly, making the individual including cyclosporine (Neoral, Sandimmune), tacroli- susceptible to hyperkalemia. mus (Prograf), ACE inhibitors (lisinopril [Prinivil]), and Many medications may cause elevated serum potas- angiotensin-II receptor antagonists (losartan [Cozaar], sium levels by facilitating ICF-to-ECF shifts. For exam- valsartan [Diovan]) also may cause a reduction in aldos- ple, digoxin (Lanoxin) and beta-blockers, especially terone and the GFR, facilitating the development of nonselective such as propranolol (Inderal), affect the hyperkalemia. 11 , 13 , 15 In addition, many herbal remedies sodium-potassium pump mechanism. 11 , 13 , 15 Additional will elevate potassium levels. Noni juice, dandelion, medications associated with ICF-to-ECF shifts include horsetail, and alfalfa have a high potassium content. fluoride intoxication, succinylcholine, and propofol. Other herbals—such as lily of the valley, Hawthorne Propofol infusion syndrome is a condition causing berry, dried toad skin, and Siberian ginseng—affect body hyperkalemia associated with high-dosage and/or long- functions such as insulin and aldosterone levels and kid- term use of propofol. 18 (See Table 2 for medications ney function. Patients should be questioned about any causing hyperkalemia.) Other medical conditions caus- use of herbal supplements related to hyperkalemia.16 , 17 ing transcellular hyperkalemia include malignant hyper- (Table 2 provides a more complete list of medications thermia, an inherited muscle disorder triggered by significant for contributing to hyperkalemia.) anesthesia, and hyperkalemic periodic paralysis, a rare Transcellular electrolyte shifts may induce elevated hereditary condition with heightened muscular sensitiv- serum potassium levels in many situations, including aci- ity associated with transient potassium elevations. 6 , 11 , 13 dosis, hypertonicity, cellular injury, and insulin deficiency. When managing hyperkalemia, it’s important to recog- Diagnosis nize these pathophysiologic changes and their effects. Acidosis, which occurs in a number of diseases, refers Diagnosis of hyperkalemia may be made with identifica- to an increase in the concentration of hydrogen ions in tion of elevated laboratory serum potassium levels, and the bloodstream. The body attempts to correct the aci- reinforced through physical assessment findings, a thor- dosis by pulling hydrogen ions into the cells by exchang- ough clinical history, and medication review. Additional ing them with potassium ions, shifting potassium out of blood testing should be ordered as appropriate to facili- the cells and into the bloodstream. This can abnormally tate the differential diagnosis for the cause, including elevate the plasma’s concentration of potassium ions.6 , 11 complete blood count, arterial blood gases, serum Hypertonicity, associated with an increase in ECF osmolality, electrolyte panel, blood urea nitrogen/ potassium, may occur as a result of conditions such as creatinine, liver enzymes (ALT, LDH), glucose/HgbA1C, hyperglycemia, the administration of hypertonic saline and renin, angiotensin, aldosterone, and cortisol levels. or mannitol, and infusion of intravenous immunoglobu- In addition, a complete urine analysis—including urine lin. The body’s need for balance in the ICF and ECF potassium, sodium, and creatinine levels, albumin, pro- causes shifting of fluids and electrolytes in these com- tein, and urine osmolality—should be performed.11 An partments. Hypertonic states often present as an addi- electrocardiogram (ECG) will help confirm any cardiac tional factor in patients with other underlying diseases rhythm changes related to hyperkalemia.2 that affect potassium levels, such as diabetes and low When initial findings of hyperkalemia are identified, aldosterone.6 , 11 especially if the elevated serum potassium is found in an

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 117171 33/24/14/24/14 8:118:11 AMAM TABLE 2 Medications Causing Hyperkalemia Medication Mechanisms Causing Hyperkalemia Reduces adrenal aldosterone biosynthesis ACE inhibitors (lisinopril [Prinivil]) Reduces effective glomerulofiltration rate Angiotensin receptor blockers (ARBs) (losartan [Cozaar]), Reduces adrenal aldosterone biosynthesis (valsartan [Diovan]) Reduces effective glomerulofiltration rate Antifungals (ketoconazole, fluconazole, itraconazole) Inhibits adrenal steroid synthesis, decreasing mineralocorticoid production Inhibits renin secretion Beta-blockers (propranolol, nadolol) Decreases cellular potassium uptake Calcium channel blockers (nifedipine, amlodipine) Inhibits adrenal aldosterone biosynthesis Antibiotics (carbenicillin, penicillin G [high dose]) Medications contain significant amount of potassium Inhibits adrenal aldosterone biosynthesis Immunosuppressants (cyclosporine [Neoral, Sandimmune]) Induces chloride channel shunt Increases potassium efflux from cells Digoxin (Lanoxin) Inhibits Na +/K +-ATPase Aldosterone antagonist (eplerenone [Inspra]) Inhibits adrenal aldosterone biosynthesis Inhibits adrenal aldosterone biosynthesis Anticoagulant (heparin) Decreases number and affinity of angiotensin II receptors Hypertonic infusion Hypertonic infusions (mannitol, glucose) Causes extracellular potassium shift NSAIDs (naproxen [Naprosyn]), ibuprofen [Motrin]) Inhibits renal prostaglandin synthesis, inducing hypoaldosteronism Pentamidine (Nebupent) Blocks sodium channels of principal cells Potassium-sparing diuretics (amiloride [Midamor]) Blocks sodium channels of principal cells Spironolactone (Aldactone), triamterene (Dyrenium) Mineralocorticoid receptor antagonist (competes with aldosterone) Succinylcholine Causes potassium efflux through cellular membrane depolarization Inhibits adrenal aldosterone biosynthesis; induces chloride channel shunt; Tacrolimus (Prograf) increases potassium efflux from cells Trimethoprim Blocks sodium channels of principal cells Yasmin Mineralocorticoid receptor antagonist (competes with aldosterone) Sources: Family Practice Notebook;20 Lehnhart and Kemper, 2011;12 Miller and Graham, 2006.15

asymptomatic patient with no apparent cause, care should this dysfunction exhibits with ECG changes and cardiac be given to rule out the possibility of pseudohyperkalemia. dysrhythmias. The initial significant finding is peaked This occurs as a result of leakage of potassium from the T waves. Increasing levels of potassium are associated blood cells during or following the drawing of blood with progressive ECG changes, including a widening PR samples, particularly in difficult blood sampling, such interval, loss of P waves, ST segment changes, and a wid- as pediatric blood draws and samples with hemolysis, ening QRS. Potential hyperkalemic-induced dysrhythmias lymphocytosis, or thrombocytosis.10 , 11 , 13 , 15 In addition, include second- and third-degree heart block, wide-com- drawing blood from lines where potassium is being infused, plex tachycardia, ventricular fibrillation, asystole, and technician error, fist clenching during phlebotomy, and pulseless electrical activity. A sine wave, an EKG finding traumatic venipuncture may cause a false elevation in where the P wave disappears and the QRS complex and serum potassium levels. 15 T wave merge in an oscillating pattern, may appear in severe hyperkalemia.2 , 11-13 , 19 Elevated potassium also may Manifestations cause failure to capture in patients with pacemakers as a result of altered myocardial conduction patterns.20 Cardiovascular dysfunction and neurological alterations The elevated potassium level modifies the impulse are the chief manifestations of hyperkalemia. In the heart, transmission to the nerves and muscles. Neurologically,

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 117272 33/24/14/24/14 8:118:11 AMAM the patient may demonstrate fatigue, irritability, and those with impaired renal function, may require a com- mental confusion. Neuromuscular manifestations include bination of medication. Such combinations simultane- muscle cramps, weakness, speech problems, paresthesias ously promote cellular potassium shifts and excretion (to the face, hand, feet, and tongue), tetany, and from the body to effectively lower potassium levels and paralysis.2 , 11 , 13 The elevated potassium may also cause prevent hyperkalemia recurrences.11 gastrointestinal hyperactivity, with the patient complain- The first treatment to shift potassium intracellularly ing of nausea, diarrhea, and abdominal cramping. In late involves intravenous administration of calcium salts stages of hyperkalemia, paralysis of the respiratory mus- (calcium gluconate, calcium carbonate). Patients with cles may progress to respiratory arrest.1 , 2 unstable dysrhythmias and/or hypotension may benefit from this treatment because the calcium has cardioprotective properties. Cardiac ECG changes reflecting TREATMENT normal sinus rhythm characteristics (from the potentially lethal rhythms identified with hyperkalemia) are Treatment for hyperkalemia centers on lowering the often visible within 2 to 3 minutes of calcium adminis- serum potassium level, preventing recurrences, and tration. Multiple calcium ampoules (10 mL of a 10% monitoring for patient safety. Therapeutic strategies solution) may be necessary to achieve the desired effect, need to be tailored for the individual while discerning and because of its short duration of action (20-40 min- the severity and cause of hyperkalemia. Appropriate utes), other treatments should also be introduced treatment is determined by the speed of onset, severity quickly. 11,13,19,22,23 Use of calcium products would be level, and development of clinical findings. 11 contraindicated in digoxin-intoxication and hypercal- cemic states.11 , 23 K + Source Removal Cellular uptake of potassium may be induced through use of the buffer sodium bicarbonate Potassium levels may be lowered by eliminating sources (NaHCO3), especially if the patient is acidotic. Sodium of potassium intake, including those that are ingested and bicarbonate infusion will shift potassium intracellu- administered parenterally. Providing a low-potassium larly by increasing the blood pH, which reduces the diet—including foods such as apples, cherries, peaches, level of hydrogen ions that are able to exchange with watermelon, carrots, cabbage, corn, white bread, white potassium forcing it out of the cell. One ampoule rice, chicken, and tuna—will help reduce the amount of (44 mEq) should be administered intravenously over 5 potassium ingested.21 Enteral tube feeding formulas to 15 minutes. Its duration of action is about 2 hours, should be specially prepared to provide low potassium which would allow time for the kidneys to excrete levels based on lab values. Oral potassium supplements excess potassium and facilitate a more normal pH. should be withheld, and intravenous infusions containing Bicarbonate should be used with caution in patients potassium additives should be discontinued. In addition, where the risk of hypertonicity, fluid volume overload, any medications that might cause or aggravate hyper- or alkalosis would be deleterious to their health. As an kalemia (eg, ACE inhibitors, digoxin, beta-blockers, additional caution, an elevation in pH may exacerbate penicillin, etc.) should be discontinued. 3 , 11 For individu- hypocalcemia.11 , 13 , 22 Calcium carbonate will also offer als with a functioning renal system, removing the some buffer activity for acidic hyperkalemia. It com- sources of potassium and allowing the kidneys to bines its cardioprotective qualities as a calcium agent excrete the excess may be sufficient to lower the extra- with its alkaline “buffer” qualities as a carbonate to cellular potassium level. Patients with impaired renal cause an intracellular shift of the potassium, while also function often require more intensive therapy to combat protecting the heart from potentially life-threatening the hyperkalemia. dysrhythmias.6 , 11 , 13 Using a regimen of intravenous insulin and glucose ECF-to-ICF Shift promotes a shift of potassium into the cells. Regular insulin (10-20 units) may be infused via bolus infusion Medications that facilitate potassium’s movement from to move the potassium into the cell. The insulin is usu- extracellular to intracellular compartments help to rees- ally accompanied by 50 mL of 50% dextrose solution tablish the body’s potassium balance. Though this shift in euglycemic patients and diabetic patients with a will not actually eliminate potassium from the body, blood glucose level of less than 250 mg/dL to prevent decreasing serum potassium levels by shifting it from the hypoglycemia. If a patient is already hyperglycemic, ECF to the ICF will facilitate a temporary improvement supplemental glucose is not needed. Duration of action in hyperkalemia. Medications that force potassium for this mixture is 4 to 6 hours. Caution should be used from the extracellular to the ICF include calcium salts, with rapid infusion of hypertonic glucose solution; the bicarbonate, insulin/glucose, and beta agonists. Patients osmotic effect it exerts on the cells may transiently exac- with moderate-to-severe hyperkalemia, particularly erbate the serum hyperkalemia. 13 , 22

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 117373 33/24/14/24/14 8:118:11 AMAM Use of beta-adrenergic agonists (inhaled, nebulized, Dialysis is another option for potassium removal if or intravenous) will also help to move the potassium the conservative measures listed above are ineffective. back into the cells. They stimulate potassium to move Dialysis corrects hyperkalemia rapidly and is indicated from the extracellular compartment to the intracellular for unstable hyperkalemic patients with renal failure, compartment by the Na + /K + -ATPase mechanism. Use severe rhabdomyolysis, and elevated potassium-induced of nebulized albuterol (Ventolin) is administered in a cardiac arrest. In an emergency, hemodialysis is the dosage of 10 to 20 mg. Treatment with nebulized preferred dialysis method because the rate of potassium albuterol will lower the serum potassium level for more removal is many times faster than that of peritoneal than 2 hours.13 , 19 , 22 The effect of beta2 agonists is addi- dialysis. Hemodialysis removes potassium from the tive to that of insulin administration, and they may be blood only; rebound hyperkalemia may occur with given together for an enhanced effect. 19 Aminophylline ensuing efflux of intracellular potassium, following the administration also demonstrates some reduction in completion of the treatment. 13 Regardless of the chosen serum potassium levels, although this may potentiate treatment modality, the potential for reemergence of tachycardia.22 hyperkalemia is a concern, so nurses must continue to monitor the patient for manifestations of the disorder. Excretion This is especially true if the original cause of the hyperkalemia has not been addressed. Definitive treatment for hyperkalemia requires its In addition to treating the hyperkalemia, identifica- removal from the body. The use of ion-exchange resins, tion and treatment of the underlying cause for the ele- such as sodium polystyrene sulphonate (Kayexalate), vated potassium level should be initiated. Examples of diuretics, and hemodialysis are methods that achieve this may include treating rhabdomyolysis with intrave- this elimination. Exchange resins work by exchanging nous fluids and bicarbonate; managing Addison’s dis- gut cations—most important, potassium—for sodium ease with intravenous fluids, corticosteroids, and glu- ions that are released from the resin. Each gram of cose; treatment of digoxin toxicity with digoxin-binding Kayexalate, administered orally or rectally, may remove antibodies such as digoxin immune fab (Digibind); or approximately 1.0 mEq of potassium. Exchange resins stopping the use of medications that may have contrib- can cause significant constipation and are typically uted to the hyperkalemic state. 13 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 NURSING CONSIDERATIONS once it binds to the resin. An oral dose of Kayexalate given with sorbitol, an osmotic cathartic, will produce Nursing care for patients with hyperkalemia is multifo- results within 1 to 2 hours. Rectal enemas of 50 mg of cused. Because potassium affects the functioning of all the Kayexalate, administered and then retained for 30 min- body systems, it is important for the nurse to recognize utes, will produce effects in about half an hour. Patients abnormalities that may occur. Early identification of signs with poor cardiovascular reserve should be monitored and symptoms of hyperkalemia is important for the nurse carefully because of the potential for exacerbating fluid caring for the patient with hyperkalemia. A thorough volume overload. 13 Although generally safe, the combi- head-to-toe nursing assessment is critical for patients nation of a resin and sorbitol has been reported to cause diagnosed with hyperkalemia to determine any physio- intestinal necrosis. Because they are often packaged logical changes in function and to alert the nurse to subtle together as a single mixture, they should be adminis- changes that may indicate a rise in the serum potassium tered cautiously and only when necessary. 24 level. The nurse should assess the patient’s cardiovascular Diuretics, such as loop (furosemide [Lasix]) and, to a status frequently, listening to heart sounds for irregulari- lesser degree, thiazides (hydrochlorothiazide), will ties, and assessing cardiac monitor patterns for any ECG remove potassium through the kidneys and renal sys- changes/dysrhythmias related to hyperkalemia. Vascular tem. They act by diminishing sodium reabsorption at perfusion should be monitored, with assessment of different sites in the nephron, increasing urinary sodi- peripheral pulses and capillary refill. The nurse will want um, water, and potassium losses. In patients with func- to perform a neurological assessment, observing for tioning kidneys, this is a viable method for potassium fatigue, sleepiness, altered level of consciousness, head- removal. Even in patients with chronic renal failure, this ache, muscle weakness/cramping, and paresthesias. For treatment format has value if some residual renal func- the respiratory system, the nurse should assess lung tion remains.11 In addition, the mineralocorticosteroid sounds, respiratory rate and depth, and oxygen saturation fludrocortisone (Florinef) may be beneficial in treating levels. Monitoring serum sodium and potassium levels, as hyperkalemia. This agent facilitates excretion of potas- well as other electrolyte and renal function laboratory sium through the distal tubules of the kidneys. Caution values, is of extreme importance. Vital signs should be should be observed, however, because it may cause monitored regularly, and accurate intake/output measure- increased retention of sodium and water. 14 , 22 ments should be maintained. A health history should be

JJIN-D-13-00027R1.inddIN-D-13-00027R1.indd 117474 33/24/14/24/14 8:118:11 AMAM obtained and a medication reconciliation performed, 4. Morton PG , Fontaine DK . Critical Care Nursing: A Holistic including all prescription and over-the-counter medica- Approach . 10th ed. Philadelphia, PA: Lippincott, Williams & tions, and herbal and nutritional supplements. The nurse Wilkins ; 2013 : 261-262, 630 . should be alert to and watch for signs and symptoms of 5. Porth CM. Essentials of Pathophysiology Concepts of Altered Health States . 3rd ed . Philadelphia, PA : Lippincott, Williams & hypokalemia, following interventions to reduce the Wilkins ; 2010 : 786-789. potassium level. In addition, patients receiving insulin 6. Segal A . Potassium and dyskalemias. In: Mount DB , Sayegh MH , and glucose to treat the hyperkalemia should be moni- Singh AK , eds. Core Concepts in the Disorders of Fluid, 3 tored for manifestations of hypoglycemia. Electrolytes, and Acid-Base Balance . New York, NY: Springer ; Patient education is an important component of 2013 : 49-102 . nursing care in patients with hyperkalemia. Patients and 7. Lazzari M . A harmful banana? Med Lab Observ . April 2009 : their families should be provided education on the 50-52 . causes, clinical manifestations, and appropriate treat- 8. Academy of Nutrition and Dietetics . Kidney disease: high- and ment options of this electrolyte abnormality. In addi- low-potassium foods. http://www.eatright.org . Accessed December tion, patients should be encouraged to limit oral intake 20, 2012. of potassium and protein and to increase their fluid 9. O’Neill P . Helping your patient to restrict potassium. Nursing . 2007 ; 37 ( 4 ): 64hn6-64hn8 . intake to promote adequate urinary output. The patient 10. Stover J . Issues in renal nutrition: nondietary causes of hyper- should be taught to avoid foods high in potassium and kalemia . Nephr Nurs J. 2006 ; 33 ( 2 ): 221-222. to read food labels on packaging to ascertain potassium 11. Lehnhardt A , Kemper MJ . Pathogenesis, diagnosis, and manage- content. They should also be careful about the use of ment of hyperkalemia. Pediatr Nephrol. 2011 ; 26 : 377-384 . salt substitute, which often contains potassium. A col- 12. Humphreys M . Potassium disturbances and associated electrocar- laborative partnership between health care providers diogram changes . Emerg Nurs . 2007 ; 15 ( 5 ): 28-34 . and patients promotes optimal management and health 13. Gibbs MA , Tayal VS . Electrolyte disturbances. In: Marx JA , when patients are diagnosed with medical conditions Hockberger RS , Walls RM , eds. Rosen’s Emergency Medicine: that can potentially precipitate hyperkalemia. Concepts and Clinical Practice . 7th ed. Philadelphia, PA: Elsevier; 2010 : 1618-1622 . 14. Hsieh M , Power DA . Abnormal renal function and electrolyte CONCLUSION disturbances in older people. J Pharm Pract Res . 2009 ; 39 ( 3 ): 230-234 . 15. Miller W , Graham MG . Life-threatening electrolyte abnormalities. Hyperkalemia is a complex medical issue with the Pt Care . December 2006 : 19-27 . http://www.nwprimarycare.com/ potential to develop multisystem complications. Rapid Journal%20Articles/electrolyte%20abnormalities.pdf. Accessed identification and treatment of this electrolyte abnor- February 21, 2014. mality are essential to prevent the development of 16. Combest W , Newton M , Combest A , Kosier H . Effects of herbal potentially fatal cardiac dysrhythmias. A comprehen- supplements on the kidney. Urol Nurs . 2005 ; 25 ( 5 ): 381-386 . sive understanding of the predisposing clinical risk fac- 17. Family Practice Notebook . Hyperkalemia due to medications. tors and pathophysiology of this disorder, cognizance of http://fpnotebook.com. Accessed December 20, 2012. relevant medical treatment modalities, and appropriate 18. Kam PCA , Cardone D . Propofol infusion syndrome. Anaesthesia . 2007 ; 62 ( 7 ): 690-701. nursing interventions are critical to providing optimal 19. Krost WS , Mistovich JJ , Limmer DD . Beyond the basics: elec- care for hyperkalemic patients. Incorporation of this trolyte disturbances. Emerg Med Services . April 2009 ; 38 ( 4 ): knowledge, coupled with strong assessment skills, will 47-55 . provide the nurse with a strong foundation when caring 20. Barold SS , Leonelli F , Herweg B . Hyperkalemia during cardiac for patients with elevated potassium levels. pacing . PACE . 2007 ; 30 ( 1 ): 1-3 . 21. National Kidney Foundation . Potassium and your CKD diet. REFERENCES http://www.kidney.org/atoz/content/potassium.cfm. Accessed July 25, 2013. 1. Crawford A , Harris H . Balancing act: Na + sodium K + potassi- 22. Elliott MJ , Ronksley PE , Clase CM , Ahmed SB , Hemmelgarn BR . um . Nursing . 2011 ; 41 ( 7 ): 44-50. Management of patient with acute hyperkalemia . CMAJ. 2. Hankins J . Fluids and electrolytes. In: Alexander M , Corrigan A , 2010 ; 182( 15 ): 1631-1635 . Gorski L , Hankins J , Perucca R , eds. Infusion Nursing: An 23. Weisberg LS . Management of severe hyperkalemia. Crit Care Evidence-Based Approach . 3rd ed. St Louis, MO: Saunders/ Med . 2008 ; 36 ( 12 ): 1-6 . Elsevier; 2010 : 178-203 . 24. Sterns RH , Rojas M , Bernstein P , Chennupati S . Ion-exchange 3. Ignatavicius D , Workman M . Medical-Surgical Nursing. Patient- resins for the treatment of hyperkalemia: are they safe and effec- Centered Collaborative Care . 6th ed . St Louis, MO : Saunders/ tive? JASN . 2010; 21 ( 5 ): 733-735 . http://jasn.asnjournals.org/. Elsevier; 2009 : 169-186 . Accessed January 15, 2014.

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