Hipercalemia.pdf

▼Emergency

By Carolyn M. Burger, MSN, RN,BC, AOCN, OCN

Hyperkalemia When serum K+ is not okay.

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eventy-seven-year-old Martha White is watching a baseball game at a major sports stadium when she begins to experience palpitations and weakness. Her husband brings her to the firstaid station, where she immediately loses consciousness; she has no pulse and isn’t breathing. The emergency staff begins cardiopulmonary resuscitation and attaches an automated external defibrillator, which reveals ventricular fibrillation (VF). The area is cleared and the defibrillator delivers a countershock. For a few minutes, Ms. White’s rhythm converts to sinus tachycardia but then returns to VF. This cycle—VF, countershock, revival, return to VF—repeats a few times. Her cardiac cells aren’t responding as expected. Furthermore, the nurse notices, during Ms. White’s brief episodes of sinus tachycardia, her T wave is narrow and peaked. These two factors provide important clues to Ms. White’s problem, and her nurse immediately seeks out Ms. White’s husband, who is waiting anxiously in the adjoining room. From him, the nurse learns that Ms. White is, in fact, on nighttime home peritoneal dialysis, which increases the nurse’s suspicion that her patient is suffering from hyperkalemia (defined by Stedman’s Medical Dictionary, 27th edition, as “a greater than normal concentration of potassium ions in the circulating blood”), which is a common consequence of chronic kidney failure. After collecting a serum sample for electrolyte analysis, the nurse confirmed with Ms. White’s husband that she isn’t taking digoxin (Lanoxin) (calcium can potentiate the effects of digoxin, resulting in digitalis toxicity). Finally, after consultation with the physician—who agrees that Ms. White’s symptoms suggest hyperkalemia—the nurse administers IV calcium gluconate 10% solution at less than 2 mL/minute, a rate unlikely to induce bradycardia, hypotension, or cardiac arrest.1 Calcium gluconate helps to calm the irritable myocardium by decreasing cardiac cell–membrane excitability, in addition to having a positive inotropic action (increased myocardial contraction and force).

Carolyn M. Burger is an assistant professor at the Miami University Department of Nursing, Middletown, OH. Emergency is coordinated by Mary Jo Koschel, MSN, RN: [email protected].

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People with advancing hyperkalemia may not be symptomatic until cardiac symptoms arise. And complaints can be vague. Fortunately, after the initial dose, Ms. White converts immediately from VF to sustained sinus tachycardia. She is transported to a nearby ED, where the diagnosis of hyperkalemia is confirmed when the laboratory results reveal that her serum potassium level had been 7.6 mEq/L. Ms. White remains hospitalized for four days. Upon discharge, she says she’s looking forward to attending her next baseball game. When an emergency occurs, nurse becomes sleuth—discovering problems and suggesting interventions. This role is especially important when electrolyte imbalances such as hyperkalemia are concerned. Potassium is required for transmitting and conducting nerve impulses, including contractions of cardiac, skeletal, and smooth muscles. It’s also the body’s primary intracellular cation. As the case of Ms. White makes clear, cardiac cells are especially sensitive to changes in levels of potassium. But what are the causes of hyperkalemia? What are its signs and symptoms? What interventions are appropriate? A nurse who can recognize and treat hyperkalemia can help to avert serious, potentially lethal, problems. POTASSIUM: AN OVERVIEW Much of the body’s functioning relies on maintaining a proper balance of electrolytes. Ninety-eight percent of the potassium in the human body, for example, exists in the intracellular fluid; the remaining 2% is in the intravascular and interstitial spaces.2 Even small changes in this balance can significantly alter the actions of cardiovascular and neuromuscular tissue. http://www.nursingcenter.com

The normal serum potassium concentration is 3.5 to 5 mEq/L; in intracellular fluid, the normal range is 140 to 150 mEq/L. The sodium–potassium pump actively transports sodium and potassium across the cell membrane. Sodium, the primary extracellular cation, is forced into the cell, while the potassium is forced out. This exchange stimulates depolarization and activity of neuron and muscle cells. When the sodium shifts back into the serum and potassium returns into the cell, repolarization occurs. In this way, the sodium–potassium pump maintains water balance and neuromuscular activity. Dextrose, insulin, and bicarbonate also facilitate the active transport of potassium into the cells. DIAGNOSTICS While the levels of potassium deemed normal vary slightly by laboratory, in general, values of between 5.1 and 5.5 mEq/L are considered indicative of the onset of hyperkalemia. In some patients, gradual increases in potassium levels may not be manifested symptomatically until the serum level reaches approximately 8 mEq/L.3 However, when potassium levels increase abruptly, clinical signs and symptoms of hyperkalemia may be obvious at serum levels of 6 to 7 mEq/L.4 Cardiac arrest may occur with serum potassium concentrations lower than 2.5 mEq/L or higher than 7 mEq/L, although levels that are lower than 3 mEq/L and higher than 5.3 mEq/L can be lethal and require timely intervention.5 Signs and symptoms. People with advancing hyperkalemia may not be symptomatic until cardiac symptoms arise. And complaints can be vague. Signs and symptoms may include weakness, areflexia, nausea, hyperactive bowel sounds, explosive diarrhea, and intermittent intestinal pain or cramping. Respiratory depression or failure may also occur. Twitching and tingling usually ascend from the lower extremities and evolve into muscle weakness that can lead to flaccid paralysis. Electrocardiographic changes. Tachycardia can be present at the onset of hyperkalemia. Narrow, tall, peaked T waves constitute early electrocardiographic evidence of hyperkalemia. Other indicative electrocardiographic changes are a prolonged PR interval and, possibly, the extinguishing of the P wave and a prolonged QRS interval as the potassium level continues to rise. Precordial leads from V1 to V4 are usually best for detecting and analyzing these changes. In severe hyperkalemia, bradycardia leading to VF or asystole can follow. [email protected]

Tall tented T wave

Wide QRS

Prolonged PR interval

ST segment depression

Electrocardiographic changes resulting from an elevated serum potassium level.

CAUSES OF HYPERKALEMIA Hyperkalemia can result from a decrease in potassium excretion, an increase in intake, or the release of potassium already present in cells into the blood. Renal failure, acute or chronic, is the most common cause of hyperkalemia, which rarely occurs when the kidneys are functioning normally. Serum potassium levels rise when the kidneys, which excrete up to 90% of potassium (the rest is lost through stool and perspiration), are unable to excrete the electrolyte. In the presence of chronic renal failure, the glomerular filtration rate before the onset of hyperkalemia is usually below 10 mL/min.2 (The rate is normally 125 mL/min.) In addition to the serum potassium concentration, laboratory tests should include the serum creatinine level (the value most specifically reflecting renal function) and the blood urea nitrogen level. However, the latter may be elevated with dehydration, upper gastrointestinal bleeding, or increased protein intake, even when renal function is not impaired. Excessive intake. Potassium supplements or salt substitutes can contribute to excessive serum levels of the electrolyte, although they don’t usually cause hyperkalemia in people with normal renal function. In fact, the Institute of Medicine recently stated that “in otherwise healthy individuals (those without impaired urinary potassium excretion from a medical condition or drug therapy) there have been no reports of hyperkalemia resulting from acute or chronic ingestion of potassium naturally occuring in food.”6 AJN ▼ October 2004

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▼Emergency Pseudohyperkalemia When what you see is not what you get.

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hile elevated serum potassium levels usually support a diagnosis of hyperkalemia, there are exceptions. Damage to blood specimens cause falsely elevated potassium levels, a phenomenon referred to as pseudohyperkalemia. Hemolysis resulting in intracellular potassium release into the serum can occur during or after collection; for this reason, The Merck Manual of Diagnosis and Therapy, 17th edition, warns practitioners not to “rapidly aspirate blood through a narrow gauge needle or excessively agitate samples of blood.” Other causes of pseudohyperkalemia include traumatic venipunctures, thrombocytosis, a tourniquet that is too constricting or worn too long, fist clenching during blood sampling, or delays in testing the specimen. Finally, a specimen drawn above an IV infusion with a potassium supplement can also result in pseudohyperkalemia. If any of the practices listed above were observed during the sampling procedure, pseudohyperkalemia should be suspected. In addition, retesting may be appropriate if results show elevated potassium levels that aren’t congruent with a patient’s medical problems or clinical manifestations.

IV administration of potassium can have serious, even lethal, consequences when inappropriately administered. Potassium is never administered as an IV push or a bolus, nor should it be added to an existing hanging IV solution because it can gravitate to a port and be delivered in a higher concentration. Potassium is an irritant to vessels, and the risk of phlebitis can be reduced with central venous, rather than peripheral, administration. Further, because potassium can cause tissue necrosis and sloughing, it’s never administered intramuscularly or subcutaneously. Potassium should always be diluted and administered as an infusion, preferably through a central line on an infusion pump. When potassium chloride is added to IV solutions for peripheral administration, it’s recommended that the amount be no more than 40 mEq/L. Ignatavicius and colleagues recommend “a dilution of no more than 1 mEq/10 mL of solution.”7 Too-rapid administration can lead to cardiac arrest. Most often the rate is 5 to 10 mEq/hour, but it can be as high as 20 mEq/hour. If potassium chloride is administered at a rate greater than 20 mEq/hour, continuous electrocardiographic monitoring is required and potassium levels should be checked every four

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to six hours.8 Potassium infused at a rate greater than 20 mEq/hour for 24 hours or longer can result in hyperkalemia.9 When potassium supplements are given, urinary output needs to be at least 600 mL daily.10 Cellular destruction resulting from trauma, rhabdomyolysis, burns, or crush injuries can cause a sudden release of potassium from damaged cells into extracellular spaces. Gastrointestinal bleeding also causes potassium to be released into the serum. Release of potassium into the extracellular space can also occur in hyperuricemia, the accumulation of uric acids that are the end product of catabolism. Further, uric acid crystals can be deposited in the urinary tract, causing renal dysfunction, which can interfere with the excretion of potassium. Hyperuricemia is seen most often in oncology patients receiving chemotherapy or radiation, when rapid necrosis of cells occurs. Hypoaldosteronism. As stated above, the sodium–potassium pump maintains an electrical balance between the cations potassium and sodium; when the level of one decreases, the level of the other increases. When serum sodium is low, as occurs in hypoaldosteronism, potassium is not excreted as the body tries to maintain cation balance. This phenomenon is seen in Addison disease and in other disorders of adrenal insufficiency. Medications implicated in hyperkalemia can impair the renal excretion of potassium or influence how it moves between the intracellular fluid and the intravascular and interstitial spaces. Drugs that interfere with renal potassium excretion (particularly in renal impairment). Heparin, nonsteroidal antiinflammatory drugs such as ibuprofen (Advil and others) and indomethacin (Indocin), angiotensin-converting enzyme inhibitors, aldosterone-inhibiting or angiotensin II receptor antagonists, potassium-sparing diuretics such as triamterene (Dyrenium) and spironolactone (Aldactone), trimethoprim (Proloprim, Trimplex) (and trimethoprim–sulfamethoxazole [Bactrim, Septra]), cyclosporine (Sandimmune and others), and potassium-containing drugs such as penicillin K and potassium phosphate enemas. Drugs that cause transcellular shifts. These include β-blockers; succinylcholine (Anectine, Quelicin); drugs that act on the central nervous system, such as amphetamines, barbiturates, heroin, and narcotics; digitalis; chemotherapeutic agents, which can cause tumor lysis syndrome; and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, such as atorvastatin (Lipitor), pravastatin (Pravachol), and simvastatin (Zocor), which may cause rhabdomyolysis. http://www.nursingcenter.com

Metabolic acidosis. When acidemia occurs, especially in metabolic acidosis, there is an increase in hydrogen ions circulating in the blood. Because potassium and hydrogen are both cations, they can cross cell membranes without altering the serum electrical charge. As an early buffering response to acidemia (to prevent or minimize it), the intracellular potassium is, in essence, kicked out of the cell to make room for hydrogen ions. This switch of cations results in an increase in the pH that ameliorates the acidosis. There is a limit to the amount of cation shifting that can occur, and such a shift can cause a temporary relative hyperkalemia, specifically: the increase in serum potassium doesn’t represent an actual increase in the body’s overall potassium level but represents instead a change in the ratio of extracellular and intracellular potassium as room is made in the cells for the hydrogen. Hyperkalemia would be expected during this interval. (In fact, under these circumstances, a serum potassium level that remains within normal limits actually indicates a potassium deficit.) Once the body or therapeutic interventions have been successful in restoring pH balance in the blood, the hydrogen ions that had been sequestered in the cell are free to return to the blood. The excess potassium ions in the blood now can return to the intracellular spaces. Blood transfusion. As packed red blood cells age and hemolysis occurs, the cell membranes can break down, releasing potassium. As a result, by the time blood has been stored for three weeks, the serum potassium level can be as high as 25 mEq/L.11, 12 While such high levels in transfused blood raise the recipient’s risk of hyperkalemia, it is in fact a rare occurrence in adults—primarily because red blood cells contain little plasma and because during transfusion, potassium moves quickly into the recipient’s cells. However, in patients who are already hyperkalemic, multiple transfusions can increase the hyperkalemia. If available, more recently collected units of packed red blood cells can be infused to minimize the risk. To avoid hemolysis during transfusion, large bore IV access can be used; the blood administration set is primed with normal saline, and care is taken to ensure that the fluid in the drip chamber covers the filter so the red blood cells don’t splatter. The container of packed red blood cells shouldn’t be squeezed or shaken. Malignant hyperthermia can occur when a person with a genetic predisposition to this metabolic disorder is given certain muscle relaxants or anesthetics; agents known to induce hyperthermia include succinylcholine (Anectine), a muscle [email protected]

Table 1. Clinical Manifestations of Hyperkalemia Muscle weakness

• Flaccid muscles • Respiratory distress (from weakened breathing muscles)

Changes in affect

• Irritability • Anxiety

Hyperreflexia

• Twitching • Paresthesias

Hyperactivity of smooth muscles

• Intestinal colic or abdominal cramping • Diarrhea • Nausea or vomiting

Decreased cardiac contractility

• Tachycardia early, bradycardia later • Heart block • Palpitations • Ventricular fibrillation • Cardiac arrest

Electrocardiographic changes

• • • •

Renal signs

• Oliguria • Anuria

Peaked, narrow T wave Prolonged PR interval Disappearance of P wave Widened QRS interval

ant, and inhalation anesthetics, including halothane (Fluothane) and enflurane (Ethrane). A defect in the muscle cell membrane causes an increase in muscle metabolism and the subsequent release of potassium from the muscle cells into the blood. INTERVENTIONS According to The Merck Manual of Diagnosis and Therapy, 17th edition, “The absolute level of potassium should not be the sole determinant of the urgency of initiation of therapy. The presence of electrocardiographic changes dictates the mode of therapy.” In milder states of hyperkalemia (serum potassium levels of 5.1 to 5.6 mEq/L), it may be enough to simply restrict potassium intake. If renal function is adequate, loop or thiazide diuretics may be prescribed to increase potassium excretion. AJN ▼ October 2004

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▼Emergency When implementing IV interventions, the nurse needs to assess for bradycardia and hypotension while monitoring the electrocardiograph continuously. The following intravenous treatments may be considered when the patient’s potassium level is 5.6 to 6.0 mEq/L or when symptoms become more extreme. • Dextrose 10% to 50% in water with regular insulin.13 Glucose with insulin moves potassium into the cells. The effect lasts about six hours, and subsequent administrations usually produce less effective results. • Sodium bicarbonate infused intravenously over four to eight hours at 2 to 5 mEq/kg, not to exceed 50 mEq/hour. In cardiac arrest, 1 mEq/kg of a 7.5% or 8.4% solution is given as an IV push. Half that dose may be repeated every 10 minutes depending on arterial blood gas results.14 Intravenous sodium bicarbonate acts immediately, creating alkalemia that causes a temporary intracellular shift of serum potassium to allow intracellular hydrogen to move into the serum. The duration of its effects is not known. • 10% calcium gluconate. Calcium gluconate is generally preferred over calcium chloride because of the hyperchloremia that usually accompanies hyperkalemia. The effects of calcium last approximately 30 to 60 minutes and the dose may be repeated in five to 10 minutes if there are no electrocardiographic changes.15 When implementing IV interventions, the nurse needs to assess for bradycardia and hypotension while monitoring the electrocardiograph continuously. All of these interventions may provide only temporary effects if the underlying cause of hyperkalemia isn’t treated, in which case more aggressive and long-term therapy, such as dialysis and ultrafiltration, may be required. In severe hyperkalemia, in which renal function is impaired, cation-exchange resins with sodium polystyrene sulfonate (Kayexalate and others) and sorbitol 70% are administered orally or rectally. Sorbitol 70% is also an osmotic laxative. These agents promote cation exchange by increasing the 70

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serum sodium level, prompting renal excretion of the cation potassium. The time to onset with oral administration is two to 12 hours with six to 24 hours’ duration. With rectal administration, retention needs to be 20 to 30 minutes with onset in two to 12 hours. These effects last four to six hours.16 Approximately 0.5 to 1 mEq/L of potassium is eliminated per enema.15 Since the cation exchange may take several hours to effect a decrease in the serum potassium level, dialysis and ultrafiltration may be necessary. Peritoneal dialysis and continuous renal replacement therapy remove more potassium than hemodialysis because the dialysate used in hemodialysis contains potassium. (Therefore, between hemodialysis treatments, potassium may need to be restricted.) ▼ REFERENCES 1. Shannon M, et al. Health professionals drug guide. Upper Saddle River, NJ: Prentice-Hall; 2003. p. 212. 2. Salem M, Batlle D. Hyperkalemia and hypokalemia. 2001. http://merck.micromedex.com/index.asp?page=bpm_ brief&article_id=CPM01NP258. 3. Rhyme L. Potassium balances and imbalances. In: Hogan M, Wane D, editors. Fluids and electrolytes and acid–base balance. Upper Saddle River, NJ: Prentice Hall; 2003. p. 178-9. 4. Rhyme L. Potassium balances and imbalances. In: Hogan M, Wane D, editors. Fluids and electrolytes and acid–base balance. Upper Saddle River, NJ: Prentice Hall; 2003. p. 73. 5. Kee J, et al. Fluids and electrolytes with clinical applications. a programmed approach. Clifton Park, NJ: Thomson Learning, Inc.; 2004. p. 111. 6. Institue of Medicine. Dietary reference intakes for water, potassium, sodium chloride, and sulfate. 2004. http:// www.nap.edu/books/0309091691/html. 7. Ignatavicius D, Workman M. Medical–surgical nursing: critical thinking for collaborative care. Philadelphia: W.B. Saunders; 2002. p. 176. 8. Rhyme L. Potassium balances and imbalances. In: Hogan M, Wane D, editors. Fluids and electrolytes and acid–base balance. Upper Saddle River, NJ: Prentice Hall; 2003. p. 72. 9. Kee J, et al. Fluids and electrolytes with clinical applications. a programmed approach. Clifton Park, NJ: Thomson Learning, Inc.; 2004. p. 108. 10. Kee J, et al. Fluids and electrolytes with clinical applications. a programmed approach. Clifton Park, NJ: Thomson Learning, Inc.; 2004. p. 129. 11. Kee J, et al. Fluids and electrolytes with clinical applications. a programmed approach. Clifton Park, NJ: Thomson Learning, Inc.; 2004. p. 107. 12. Kee J, et al. Fluids and electrolytes with clinical applications. a programmed approach. Clifton Park, NJ: Thomson Learning, Inc.; 2004. p. 135. 13. Ignatavicius D, Workman M. Medical–surgical nursing: critical thinking for collaborative care. Philadelphia: W.B. Saunders; 2002. p. 180. 14. Smeltzer S, Bare B. Brunner and Suddarth’s textbook of medical–surgical nursing. Philadelphia: Lippincott, Williams and Wilkins; 2000. p. 221. 15. Sommers M, Johnson S. Diseases and disorders: a nursing therapeutics manual. Philadelphia: F. A. Davis; 2002. p. 470. 16. Deglin J, Vallerand A. Davis’s drug guide for nurses. Philadelphia: F. A. Davis; 2003. p. 947. http://www.nursingcenter.com