Focus On... Critical Decisions: Hyperkalemia
By Camiron L. Pfennig, MD, Sage Whitmore, MD, and Corey Slovis, MD, FACEP
From the EM Model
5.0 Endocrine, Metabolic, and Nutritional Disorders
5.3 Fluid and Electrolyte Disturbances
Camiron L. Pfennig, MD, Sage Whitmore, MD, and Corey Slovis, MD, FACEP, wrote “Hyperkalemia.” Dr. Pfennig is assistant professor of emergency medicine and director of undergraduate medical education in the Department of Emergency Medicine at Vanderbilt University in Nashville, Tennessee. Dr. Whitmore is a clinical instructor and critical care fellow in the Department of Emergency Medicine at the University of Arizona College of Medicine. Dr. Slovis is professor of medicine and emergency medicine, chairman of the Department of Emergency Medicine at Vanderbilt University School of Medicine, and medical director of the Nashville Fire Department and International Airport in Nashville. Robert C. Solomon, MD, is Medical Editor of ACEP News and editor of the “Focus On… Critical Decisions” series, core faculty in the emergency medicine residency at Allegheny General Hospital, Pittsburgh, Pennsylvania, and assistant professor in the Department of Emergency Medicine at Temple University School of Medicine, Philadelphia. Mary Anne Mitchell is an ACEP staff member who reviews and manages the ACEP “Focus On… Critical Decisions” series.
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Dr. Pfennig, Dr. Whitmore, Dr. Slovis , Dr. Solomon, and Ms. Mitchell have disclosed that they have no significant relationships with or financial interests in any commercial companies that pertain to this article. There is no commercial support for this activity.
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"Focus On… Critical Decisions: Hyperkalemia" is approved by the American College of Emergency Physicians for 1 ACEP Category I credit.
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Questionnaire Is Available Online
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The participant should, in order, review the learning objectives, read the article, and complete the CME post-test/evaluation form to receive up to 1 ACEP Category I credit and 1 AMA PRA Category 1 CreditTM. You must score at least 70% to receive credit. You will be able to print your CME certificate immediately.
This article was published online September 1, 2013. The credit for this CME activity expires August 31, 2016.
On completion of this lesson, you should be able to:
1. List common disease states that place patients at risk for hyperkalemia.
2. Describe the classic signs and symptoms of hyperkalemia.
3. Describe the emergency treatments for hyperkalemia.
4. Discuss the ECG changes that are characteristic of hyperkalemia.
Hyperkalemia, defined as a serum potassium level of more than 5 mEq/L, is the most common electrolyte abnormality leading to life-threatening arrhythmias and cardiac arrest.1 Hyperkalemia has vague and varied symptoms; in fact, it can be totally asymptomatic, or the initial presentation may be sudden death. The correct and early diagnosis of hyperkalemia requires attention to risk factors, especially a history of renal failure and medication that can cause potassium retention, as well as a search for ECG changes consistent with elevated potassium. Hyperkalemia can be rapidly progressive, and lifesaving interventions must be instituted at the earliest suspicion of toxicity.
A 51-year-old woman with a history of diabetes mellitus, hypertension, peripheral vascular disease, and hemodialysis-dependent end-stage renal disease presents by ambulance because of dizziness, weakness, abdominal pain, vomiting, and diarrhea. Her symptoms began 3 days ago and have been worsening. She did not feel well enough to go to her dialysis appointment yesterday and has not been able to afford any of her medications this week.
On physical examination, the patient appears lethargic and very ill. Her initial vital signs are supine blood pressure 98/66, pulse rate 98, respiratory rate 26, oral temperature 36.7°C (98°F), and oxygen saturation 96% on room air. She has a patent airway and an unremarkable HEENT examination. Her chest examination reveals mild bibasilar crackles and normal heart sounds with a grade II/VI systolic murmur. Her abdomen is soft but diffusely tender. She has a weak radial pulse in the right arm; there is an AV fistula with a palpable thrill medial to the left biceps. Her lower extremities are cool, dry, and shiny, with 1+ pitting pretibial edema bilaterally.
By department protocol, in light of the patient’s initial vital signs and lethargy, weakness, and ill appearance, she was placed on a cardiac monitor and an ECG was performed immediately. The ECG and the rhythm on the monitor revealed a junctional tachycardia without P waves, a wide QRS, and peaked T waves. Blood was obtained by peripheral butterfly stick, and a stat chemistry panel revealed sodium 129, potassium 8.2, chloride 88, bicarbonate 5, BUN 48, creatinine 3.9, glucose 422, and venous pH 7.11.
Table 1, below, organizes five of the most common causes of hyperkalemia. A history of one of these conditions may be the lone clue to the diagnosis because symptoms do not reliably appear with any particular serum potassium level.1
The ECG can be helpful in making the diagnosis of hyperkalemia. Peaked T waves appear as serum potassium levels exceed 5.5 to 6.5 mEq/L; P-wave disappearance and PR prolongation occur with levels above 6.5 to 7.5 mEq/L; and QRS prolongation occurs when levels rise above 7 to 8 mEq/L.1-3 These ECG changes occur in only half of patients with hyperkalemia, but recognizing these changes, when they are present, is vital to rapid diagnosis and initiation of lifesaving treatment.4 A serum potassium level above 5 mEq/L is diagnostic of hyperkalemia, but the value itself does not always predict ECG changes or the degree of cardiotoxicity.5
Patients with suspected or known hyperkalemia should have an intravenous line established and should be placed on continuous cardiac monitoring. The treatment of hyperkalemia is based on the clinical scenario combined with the 12-lead ECG and the laboratory potassium value. The treatment strategy consists of three main steps: 1) stabilizing the cardiac membrane, 2) shifting potassium into the cells, and 3) removing potassium from the body.
When should intravenous calcium be administered in patients with hyperkalemia?
Administration of calcium as either calcium chloride or calcium gluconate for hyperkalemia is controversial.1 Some authors advocate administering calcium for any ECG changes associated with hyperkalemia, including isolated peaked T waves. We believe that there are only three indications for administering calcium in hyperkalemia, as follows: 1) a widening QRS including a sine wave, 2) a cardiac arrest that is believed to be due to hyperkalemia, or 3) signs of rapidly progressing hyperkalemia in the face of tumor lysis syndrome, massive hemolysis, or rhabdomyolysis where a normal ECG has rapidly progressed through tall peaked T waves and loss of the P wave. In this situation, calcium could be given “prophylactically” while other methods are used to stop potassium release, drive already released potassium into the cell, and begin emergent dialysis to remove potassium from the body.
Because intravenous calcium can cause tachycardia, hypertension, and arrhythmias, as well as hypercalcemia, we urge that calcium not be given routinely for hyperkalemia in an otherwise stable patient with a normal QRS or just isolated, peaked T waves. In the context of digitalis toxicity, intravenous calcium should still be used for life-threatening hyperkalemia with a widening QRS while awaiting the administration and effects of digoxin Fab fragments.
Calcium restores the electrical and chemical gradient of the cardiac myocyte, thus narrowing the QRS.5 Calcium does not decrease serum potassium levels, and its effect is rapid but transient. The dose is one ampule, or 10 mL of 10% calcium chloride solution, with a maximum dose of two ampules or 20 mL. Some authors prefer calcium gluconate to calcium chloride based on the reduced risk of tissue necrosis should it extravasate at the injection site.6 Calcium gluconate may also be preferred in pediatric cases and in more chronic, less emergent hyperkalemic patients when a slow infusion is desired. It has about a third the amount of free calcium (13.6 mEq/10 mL for calcium chloride versus 4.6 mEq/10 mL for calcium gluconate).
What medications should be considered for patients with hyperkalemia to drive potassium into the cell, after the immediate need for intravenous calcium has been determined?
A β2-agonist, insulin and glucose, in some cases sodium bicarbonate, and saline can be given to shift potassium into cells. Sodium bicarbonate alone does not lower serum potassium in patients with hyperkalemia and is unreliable at best in combination with other agents. It should be reserved for patients who are severely acidemic.3,7,8 Sodium bicarbonate should not be used in patients with a pH above 7.3 as it is hyperosmolar and will not lower potassium values in the nonacidotic patient. Patients with a pH value below 7.2 or 7.3 will benefit from 100 mL or 50 mL of sodium bicarbonate, respectively.
Nebulized albuterol by face mask begins to take measurable effect after 15 to 20 minutes and lowers the serum potassium level by up to 1 mEq/L, depending on the dose. β-Agonists are safe despite the side effect of tachycardia.9,10 Insulin, given intravenously in combination with glucose, also results in a similar fall in the potassium level after 20 to 30 minutes and also lowers levels by up to 1 mEq/L. The combination of nebulized albuterol and intravenous insulin with glucose appears to be additive, lowering serum potassium by a mean of 1.21 mEq/L or more.11 Adult hyperkalemic patients who have ECG changes should receive continuous nebulized albuterol and 50 grams of intravenous dextrose plus 10 units of intravenous regular insulin.
Most patients with hyperkalemia have impaired or no renal function. However, even a few hundred milliliters of normal saline can help move potassium intracellularly via the sodium-potassium pump. Prior to the use of saline, the patient’s nephrologist should be consulted and emergent hemodialysis scheduled. For patients with normal or near normal renal function such as those with rhabdomyolysis or tumor lysis syndrome, aggressive saline diuresis supplemented by furosemide may be all that is required to treat the patient’s hyperkalemia, thus avoiding dialysis.
Cation exchange resins, such as sodium polystyrene sulfonate have not been shown to decrease the serum potassium level within the first 4 hours of treatment and should not be used alone in the acute management of hyperkalemia.12
When should hemodialysis be initiated in a hyperkalemic patient?
Emergent hemodialysis is the most reliable method of definitively lowering serum potassium in patients with renal failure. Hemodialysis reliably decreases serum potassium levels by at least 1 mEq/L in the first hour and another 1 mEq/L over the next 2 hours.7,9,10 It should be instituted early on in the treatment of life-threatening hyperkalemia in patients with renal failure.10 Hemodialysis should also be the treatment of choice for hyperkalemic patients who have impaired renal function and pulmonary edema caused by fluid overload.
Hemodialysis via central venous access can be used during ongoing cardiopulmonary resuscitation to acutely lower the serum potassium level and may result in return of spontaneous circulation with intact neurologic status despite prolonged resuscitative efforts and failure of conventional medications and defibrillation.13
In patients with intact renal function, medical management alone may be sufficient even in extreme cases, and hemodialysis may not be necessary unless multiple medical modalities fail.8 These patients should initially be treated medically and hemodialysis delayed until it appears that medical management alone has failed.
On recognizing life-threatening hyperkalemia in this dialysis-dependent woman, the emergency physician ensured that intravenous access was immediately obtained. Based on the patient’s hyperkalemia with a wide QRS, severe acidemia, and renal failure, she was given one 10-mL ampule of 10% calcium chloride, 10 units of insulin (no glucose was immediately administered because the patient was already hyperglycemic), and one 50-mL ampule of sodium bicarbonate. Nephrology was consulted for emergent hemodialysis.
Electrolyte abnormalities are very common in emergency medicine practice and rarely occur in isolation. Emergency physicians must be able to identify common disease states that place patients at risk for serious hyperkalemia and initiate appropriate emergency treatment when needed.
Table 1. Five most common causes of hyperkalemia
Spurious elevation--Hemolysis while drawing or storing the laboratory sample
Renal failure--Acute or chronic
Acidosis--Diabetic ketoacidosis, Addison disease, adrenal insufficiency, type 4 renal tubular acidosis
Cell death--Rhabdomyolysis, tumor lysis syndrome, burns, massive hemolysis or transfusion, crush injury
Drugs--β-Blockers, acute digitalis toxicity, succinylcholine, ACE inhibitors, angiotensin receptor blockers, nonsteroidal anti-inflammatory drugs, spironolactone, amiloride
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10. Mahoney BA, Smith WA, Lo DS, et al. Emergency interventions for hyperkalaemia. Cochrane Database of Syst Rev. 2005;(2):CD003235.
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12. Gruy-Kapral C, Emmett M, Santa Ana CA, et al. Effect of single dose resin-cathartic therapy on serum potassium concentration in patients with end-stage renal disease. J Am Soc Nephrol. 1998;9(10):1924–1930.
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