Hyperkalemia


Article Author:
Leslie Simon
Muhammad Hashmi


Article Editor:
Mitchell Farrell


Editors In Chief:
Casey Ciresi


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
9/29/2019 7:54:09 PM

Introduction

Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L. While mild hyperkalemia is usually asymptomatic, high levels of potassium may cause life-threatening cardiac arrhythmias, muscle weakness or paralysis. Symptoms usually develop at levels higher levels, 6.5 mEq/L to 7 mEq/L, but the rate of change is more important than the numerical value. Patients with chronic hyperkalemia may be asymptomatic at increased levels, while patients with dramatic, acute potassium shifts may develop severe symptoms at lower ones. Infants have higher baseline levels than children and adults.

Pseudohyperkalemia is quite common and represents a false elevation in measured potassium due to specimen collection, handling, or other causes. Hyperkalemia should always be confirmed before aggressive treatment in cases where the serum potassium is elevated without explanation. True hyperkalemia may be caused by increased potassium intake, transcellular movement of intracellular potassium into the extracellular space, and decreased renal excretion. The urgency of therapy depends on symptoms, serum levels and explanation for hyperkalemia.[1][2][3][4]

Etiology

The most common cause of hyperkalemia is pseudohyperkalemia, which is not reflective of the true serum potassium levels. Pseudohyperkalemia is most commonly due to hemolysis of the sample causing intracellular potassium to be measured in the serum.  Hemolysis is more common when a syringe is used as compared to a vacuum device. The use of tourniquets and excessive fist-pumping during blood draw also increases the risk. Specimens drawn from patients with leukocytosis or thrombocytosis are also frequently associated with falsely elevated potassium concentrations.

Increased Potassium Intake

Increased potassium intake from food is a very uncommon cause of hyperkalemia in adult patients with normal renal function but can be an important cause in those with kidney disease. Foods with very high potassium content include dried fruits, seaweed, nuts, molasses, avocados, and Lima beans. Many vegetables that are also high in potassium include spinach, potatoes, tomatoes, broccoli, beets, carrots, and squash. High-potassium-containing fruits include kiwis, mangoes, oranges, bananas, and cantaloupe. Red meats are also rich in potassium. While generally safe to consume even in large quantities by patients with normal potassium homeostasis, these foods should be avoided in patients with the severe renal disease or other underlying conditions or medications that predispose them to hyperkalemia. Intravenous intake through high potassium-containing fluids, particularly total parenteral nutrition, medications with high potassium content and massive blood transfusions can significantly elevate serum potassium levels.

Intracellular Potassium Shifts

Cellular injury can release large quantities of intracellular potassium into the extracellular space. This can be due to rhabdomyolysis from a crush injury, excessive exercise, or other hemolytic processes. Metabolic acidosis may cause intracellular potassium to shift into the extracellular space without red cell injury.  Metabolic acidosis is most frequently caused by decreased, effective, circulating, arterial blood volume. Sepsis or dehydration may lead to hypotension and decreased tissue perfusion leading to metabolic acidosis with subsequent potassium elevation.  Insulin deficiency and diabetic ketoacidosis may cause dramatic extracellular shifts causing measured serum potassium to be elevated in the setting of whole-body potassium depletion. Certain medications, such as succinylcholine may cause severe, acute potassium elevations in patients with up-regulation of receptors, particularly in the setting of subacute neuromuscular disease. Tumor lysis syndrome, particularly in patients receiving chemotherapy for hematogenous malignancy, may cause acute hyperkalemia due to massive cancer cell death. Hyperkalemic periodic paralysis is a rare, autosomal dominant condition that causes potassium to shift into the extracellular space due to impaired sodium channel function in skeletal muscle.

Impaired Potassium Excretion

Acute or chronic kidney disease is a common cause of hyperkalemia. Hyperkalemia is usually not seen until the glomerular filtration rate falls below 30 ml/min. This is commonly due to primary renal dysfunction but maybe due to acute volume depletion from dehydration or bleeding or decreased circulating blood volume due to congestive heart failure or cirrhosis. Tubular dysfunction due to aldosterone deficiency or insensitivity can also cause hyperkalemia.

Epidemiology

Hyperkalemia is unusual in the general population, reported in less than 5% of the population, worldwide, but may affect up to 10% of all hospitalized patients. Most cases in hospitalized patients are due to medications and renal insufficiency. Diabetes, malignancy, extremes of age, and acidosis are other important causes in inpatients. Hyperkalemia is rare in children but may occur in up to 50% of premature infants. Hyperkalemia is more commonly reported in men than women perhaps due to increased muscle mass and higher rates of rhabdomyolysis and increased prevalence of neuromuscular disease.

Today there is a risk that empirical use of ACE inhibitors may cause hyperkalemia, which can be of concern in high risk populations like diabetics, and those with heart failure, and peripheral vascular disease.

Pathophysiology

Potassium is usually an intracellular cation. The sodium-potassium pump is responsible for maintaining potassium within the cells. Most potassium is excreted in urine through the kidneys with about 10% in sweat and stool. Inside the kidney, the excretion of potassium takes place in the distal convoluted and cortical collecting ducts.

Renal potassium excretion is influenced by elevated levels of:

  • Aldosterone
  • Diuretics (which deliver sodium to the distal tubule)
  • WNK1 and WNK4
  • High levels of serum potassium
  • A high flow of urine (osmotic diuresis)
  • Presence of negative ions in the distal tubule (bicarbonate)

History and Physical

Most patients are relatively asymptomatic with mild and even moderate hyperkalemia. Elevated potassium is often discovered on screening labs done in patients with nonspecific complaints or those with suspected electrolyte abnormalities due to infection, dehydration or hypoperfusion. Historical clues include the history of renal disease, diabetes, chemotherapy, major trauma, crush injury, or muscle pain suggestive of rhabdomyolysis. Medications that may predispose to the development of hyperkalemia include digoxin, potassium-sparing diuretics, non-steroidal anti-inflammatory drugs, ace-inhibitors or recent intravenous (IV) potassium, total parenteral nutrition, potassium penicillin or succinylcholine. Patients may complain of weakness, fatigue, palpitations, or syncope.

Physical exam findings may include hypertension and edema in the setting or renal disease. There may also be signs of hypoperfusion. Muscle tenderness may be present in patients with rhabdomyolysis. Jaundice may be seen in patients with hemolytic conditions. Patients may have muscle weakness, flaccid paralysis, or depressed deep tendon reflexes.

Evaluation

The first test that should be ordered in a patient with suspected hyperkalemia is an ECG since the most lethal complication of hyperkalemia is cardiac condition abnormalities which can lead to dysrhythmias and death.[5][6][7][8]

Elevated potassium causes ECG changes in a dose-dependent manner: 

  • K = 5.5 to 6.5 mEq/L ECG will show tall, peaked t-waves
  • K = 6.5 to 7.5 mEq/L ECG will show loss of p-waves
  • K = 7 to 8 ECG mEq/L will show widening of the QRS complex
  • K = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole

It should be noted that the rate of rising in serum potassium is a greater factor than the level. Patients with chronic hyperkalemia may have relatively normal EGCs even at high levels, and significant ECG changes may be present at much lower levels in patients with sudden spikes in serum potassium.ECG features of hyperkalemia include:

  • Small or absent P wave
  • Prolonged PR interval
  • Augmented R wave
  • Wide QRS
  • Peaked T waves

Additional laboratory testing should include serum blood urea nitrogen and creatinine to assess renal function, and urinalysis to screen for the renal disease. Urine potassium, sodium, and osmolality may also be helpful in evaluating the cause. In patients with the renal disease, the serum calcium level should also be checked because hypocalcemia may exacerbate the cardiac effects of hyperkalemia. Complete blood count to screen for leukocytosis or thrombocytosis may also be helpful. Serum glucose and blood gas analysis should be ordered in diabetics and patients with suspected acidosis. Lactate dehydrogenase should be ordered in patients with suspected hemolysis. Creatinine phosphokinases and urine myoglobin should be ordered in patients with suspected rhabdomyolysis. Uric acid and phosphorus should be ordered in patients with suspected tumor lysis syndrome. Digoxin toxicity may cause hyperkalemia so serum levels should be checked in patients on digoxin. If no other cause is found, consider cortisol and aldosterone levels to assess for mineralocorticoid deficiency.

Since pseudohyperkalemia is so common, confirmation should be obtained in asymptomatic patients without typical ECG changes prior to initiating aggressive therapy.

Treatment / Management

The urgency with which hyperkalemia should be managed depends on how rapidly the condition developed, the absolute serum potassium level, the degree of symptoms, and the cause.[9][10][11]

Patients with neuromuscular weakness, paralysis or ECG changes and elevated potassium of more than 5.5 mEq/L in patients at risk for ongoing hyperkalemia, or confirmed hyperkalemia of 6.5 mEq/L should have aggressive treatment. Exogenous sources of potassium should be immediately discontinued. Calcium therapy will stabilize the cardiac response to hyperkalemia and should be initiated first in the setting of cardiac toxicity. Calcium does not alter the serum concentration of potassium but is first-line therapy in hyperkalemia related arrhythmias and ECG changes.  Calcium chloride contains three times more elemental calcium than calcium gluconate but is more irritating to peripheral vessels and more likely to cause tissue necrosis with extravasation, so it is usually only given through central venous lines or peripherally in cardiac arrest. Thus, calcium gluconate is the usual initial drug of choice in patients with evidence of cardiac toxicity. Insulin and glucose, or insulin alone in hyperglycemic patients, will drive the potassium back into the cells, effectively lowering serum potassium. A common regimen is ten units of regular insulin given with 50 ml of a 50% dextrose solution (D50). Patients should be monitored closely for the development of hypoglycemia. A 10% dextrose infusion at 50-75 ml/hour is associated with less hypoglycemia than bolus dosing with D50. Beta-2 adrenergic agents such as albuterol will also shift potassium intracellularly. To be effective, beta-2 agonists are given in much higher doses than commonly used for bronchodilation. Sodium bicarbonate infusion may be helpful in patients with metabolic acidosis. Bolus dosing of sodium bicarbonate is less effective.

Loop or thiazide diuretics may be helpful in enhancing potassium excretion. They may be used in non-oliguric, volume overloaded patients but should not be used as monotherapy in symptomatic patients. Gastrointestinal cation exchangers such as patiromer may be helpful, particularly in patients with renal insufficiency who cannot receive immediate dialysis. Sodium polystyrene sulfonate, though commonly used, is falling out of favor due to lack of effectiveness and adverse effects, particularly bowel necrosis in elderly patients. If used due to lack of alternatives, it should not be given with sorbitol, which increases toxicity. Hemodialysis should be performed in patients with end-stage renal disease or severe renal impairment.

Complications of Treatment

  • Hypokalemia
  • Inability to control hyperkalemia
  • Hypocalcemia as a result of bicarbonate infusion
  • Hypoglycemia due to insulin
  • Metabolic alkalosis from bicarbonate therapy
  • Volume depletion from diuresis

Prognosis

For patients with mild transient hyperkalemia, the prognosis is excellent if the inciting cause is addressed and treated. Sudden onset, extreme hyperkalemia can cause cardiac arrhythmias that can be lethal in up to two-thirds of cases if not rapidly treated. Hyperkalemia is an independent risk factor for death in hospitalized patients.

Complications

  • Cardiac arrest
  • Weakness
  • Arrhythmias

Deterrence and Patient Education

Low salt diet

Avoid medications that cause hyperkalemia

Enhancing Healthcare Team Outcomes

The management of hyperkalemia is an interprofessional because of its potential to induce cardiac arrest and severe weakness. Once hyperkalemia is diagnosed, the primary condition must be treated. Patients with hyperkalemia need cardiac monitoring and nurses should be familiar with ECG features of hyperkalemia, which are often the first to appear. The pharmacist has to ensure that all nephrotoxic medications and agents that raise potassium are discontinued.

If hyperkalemia is severe, the nephrologist should be consulted. If ECG changes are present a cardiology consult should be made. Treatment to lower the high potassium should be ongoing. These patients need cardiac monitoring 24/7 until hyperkalemia has resolved. The dietitian should educate the patient on a low potassium diet. For those with renal dysfunction, continued to follow up with a nephrologist is recommended. Only through open communication between members of the interprofessional team can the morbidity of hyperkalemia be avoided.

Outcomes

The majority of patients have an excellent prognosis. However, patients with chronic disorders like end-stage renal failure may require continual blood work to monitor potassium.[12][13] (Level V)


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Hyperkalemia - Questions

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A 64-year-old male develops supraventricular arrhythmias after undergoing open-heart surgery. The laboratory measurements indicate that the potassium levels are 6.4. After administering calcium, what is the next step in management ?



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Which is true of hyperkalemia?



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Which of the following statements about potassium homeostasis is incorrect?



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A dialysis patient, with a serum potassium of 7.2, has peaked T waves and a widened QRS. Which of the following therapies would be most helpful in quickly stabilizing this patient?



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What is the earliest electrocardiographic sign of hyperkalemia?

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Which of the following is not used in the treatment of hyperkalemia?



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A cell will be hypopolarized and less negative with which electrolyte disturbance?



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In a patient with hyperkalemia, which of the following will not cause a lowering of potassium levels in blood?



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A postoperative open-heart patient has potassium of 7.5. Which of the following is the most beneficial treatment to protect the myocardium?



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In which electrolyte abnormality are peaked T waves commonly seen?

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What characteristic finding is seen on ECG in a patient with hyperkalemia?



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Which of the following is the most likely complication of hyperkalemia?



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Which is NOT a treatment for hyperkalemia in a patient with heart failure?



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Hyperkalemia can be treated with which medication?



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Which of the following is not a useful treatment for hyperkalemia?



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A 56-year-old with hyperkalemia is unlikely to present with which symptom?



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Which of the following would not acutely reduce serum potassium?



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Which of the following ECG changes is not associated with hyperkalemia?



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A 66-year-old develops arrhythmias on the night of his coronary bypass. Potassium has been administered and his urine output is 30 mL/h. Serum potassium level is now 6.6 mEq/L. Which of the following medications will oppose the harmful effects of potassium without lowering the potassium level?



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A 65-year-old develops acute renal failure following an emergency small bowel resection. Five days after surgery her serum electrolytes (mEq/L): Na 126, K 6.2, Cl 91, HCO3 14, Blood urea nitrogen 88 mg/dL, Serum creatinine 6.9 mg/dL. The patient has gained 3.5 kg since surgery and is now dyspneic at rest, with numerous PVCs on ECG. Which of the following is the most appropriate initial treatment in the management of this patient?



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A 58-year-old African American male with chronic, poorly controlled diabetes presents with new onset of swelling in his feet. He is insulin dependent and takes an ACE inhibitor. You note 3+ pitting edema along with a creatinine of 2.6 mg/dL and potassium 6 mg/dL. Past records indicate that his creatinine has been the same over the last two years. What should be your next step?



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A patient is suffering from end stage renal disease. His ECG shows peaked T waves. What is the most likely cause of this finding?



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The ECG of a patient with end-stage renal disease reveals peaked T waves and bradycardia. Which of the following should be the initial treatment?



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A patient with acute renal failure has a potassium of 6.9 mEq/L. What other diagnostic study should be done emergently?



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A patient has potassium of 6.3 mEq/L and EKG shows peaked T waves, shortened QT interval, and ST segment depression. What is the initial treatment?



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Which of the following can worsen hyperkalemia?



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Which of the following ECG findings are inconsistent with hyperkalemia?



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Which of the following can lower hyperkalemia quickly?



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Intravenous administration of which of the following is the most appropriate initial treatment for hyperkalemia with ECG changes of widened QRS?



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A patient with end-stage renal disease who has missed her last scheduled dialysis appointments presents to the emergency department with weakness, dyspnea, rales, and jugular venous distension. The monitor shows a wide complex bradycardia. Which medication is not indicated for her suspected electrolyte imbalance?



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Which of the following is an effective treatment of hyperkalemia?



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A patient is in the emergency department and is found to have a serum potassium of 6.8 mEq/L (normal range is 3.5-5.5 mEq/L). He is asymptomatic; the rhythm strip and ECG are normal. What is the most appropriate next treatment?



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A 65 -year-old male presents for preoperative evaluation for cataract removal. His preoperative laboratory evaluation revealed a serum potassium level of 5.7 mEq/L. He has no complaints except for increased thirst. Electrocardiogram revealed normal sinus rhythm without any acute changes. What is the next best step in the management of this patient?



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A 45-year-old African American female with past medical history of end-stage renal disease on hemodialysis Monday, Wednesday, and Friday presents to the emergency department with the chief complaint of heart palpitations. She has missed her last two sessions of hemodialysis due to feeling lethargic and weak. Laboratory studies are significant for potassium 6.8 mEq/L. Which of the following findings would be expected to seen on her electrocardiogram?



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A patient has acute hyperkalemia. Which of the following drugs might be used to lower serum potassium rapidly? Select all that apply.



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A novice nurse is caring for a client on the telemetry unit with a history of uncontrolled hypertension and renal insufficiency. The laboratory calls with a serum potassium of 6.2 mmol/L. Based on this lab result, what are the appropriate actions? Select all that apply.



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A patient presents to the emergency department having missed her last two dialysis appointments. Her blood work reveals a potassium of 6.6 mEq/L. What are the typical electrocardiogram (ECG) findings in the presence of hyperkalemia? Select all that apply.



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A client is in the emergency department with complaints of palpitations. Blood work reveals that he has hyperkalemia. Which of the following is a cause of this electrolyte disorder? Select all that apply.



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In a patient admitted with a diagnosis of hyperkalemia, which findings would be expected? Select all that apply.



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A client with renal failure has just been diagnosed with hyperkalemia in the emergency department and admitted to the hospital. What is the nursing management for this disorder? Select all that apply.



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Which of the following would cause tall, peaked T waves in the precordial leads, a shortened QT interval, and ST-segment depression on EKG?



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Hyperkalemia - References

References

Vieira A,Batista B,de Abreu TT, Iatrogenic Takotsubo Cardiomyopathy Secondary to Norepinephrine by Continuous Infusion for Shock. European journal of case reports in internal medicine. 2018;     [PubMed]
Fried L,Kovesdy CP,Palmer BF, New options for the management of chronic hyperkalemia. Kidney international supplements. 2017 Dec;     [PubMed]
Lytvyn Y,Godoy LC,Scholtes RA,van Raalte DH,Cherney DZ, Mineralocorticoid Antagonism and Diabetic Kidney Disease. Current diabetes reports. 2019 Jan 23;     [PubMed]
Flury G, [The 'Dangerous' ECG]. Praxis. 2019 Jan;     [PubMed]
Williams SM,Killeen AA, Tumor Lysis Syndrome. Archives of pathology     [PubMed]
Marti CN,Fonarow GC,Anker SD,Yancy C,Vaduganathan M,Greene SJ,Ahmed A,Januzzi JL,Gheorghiade M,Filippatos G,Butler J, Medication dosing for heart failure with reduced ejection fraction - opportunities and challenges. European journal of heart failure. 2018 Dec 10;     [PubMed]
Bayés-Genís A,Lupón J,Núñez J, No need for urgent revisiting of kalaemia levels in guidelines despite use of mineralocorticoid receptor antagonists: bring in more evidence. European journal of heart failure. 2018 Sep;     [PubMed]
Arnold R,Pianta TJ,Pussell BA,Endre Z,Kiernan MC,Krishnan AV, Potassium control in chronic kidney disease: Implications for neuromuscular function. Internal medicine journal. 2018 Sep 19;     [PubMed]
Campbell CA,Lam Q,Horvath AR, An evidence- and risk-based approach to a harmonized laboratory alert list in Australia and New Zealand. Clinical chemistry and laboratory medicine. 2018 Dec 19;     [PubMed]
Butler J,Vijayakumar S,Pitt B, Revisiting hyperkalaemia guidelines: rebuttal. European journal of heart failure. 2018 Sep;     [PubMed]
Butler J,Vijayakumar S,Pitt B, Need to revisit heart failure treatment guidelines for hyperkalaemia management during the use of mineralocorticoid receptor antagonists. European journal of heart failure. 2018 Sep;     [PubMed]
Formiga F,Chivite D,Corbella X,Conde-Martel A,Arévalo-Lorido JC,Trullàs JC,Silvestre JP,García SC,Manzano L,Montero-Pérez-Barquero M, Influence of potassium levels on one-year outcomes in elderly patients with acute heart failure. European journal of internal medicine. 2019 Feb;     [PubMed]
Linde C,Qin L,Bakhai A,Furuland H,Evans M,Ayoubkhani D,Palaka E,Bennett H,McEwan P, Serum potassium and clinical outcomes in heart failure patients: results of risk calculations in 21 334 patients in the UK. ESC heart failure. 2019 Jan 10;     [PubMed]

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