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Flashcards in Hyperkalemia Deck (24)
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Which patients would be defined as having a hyperkalemic emergency?

  • Patients who have clinical signs or symptoms of hyperkalemia
  • Patients with severe hyperkalemia (serum potassium greater than 6.5 mEq/L)
    • especially if there is concurrent tissue breakdown or gastrointestinal bleeding, even if there are no clinical signs or symptoms
  • Some patients with moderate hyperkalemia (>5.5 mEq/L) who have significant renal impairment and
    • marked, ongoing tissue breakdown (eg, rhabdomyolysis or crush injury
    • tumor lysis syndrome)
    • ongoing potassium absorption (eg, from substantial gastrointestinal bleeding)
    • or a significant non-anion gap
      metabolic acidosis or respiratory acidosis.


MoA of hyperK from 

  • tissue breakdown
  • GI bleed
  • acidosis

  • Tissue breakdown can release large amounts of potassium from cells, which can lead to rapid and substantial elevations in serum potassium.
  • Potassium absorption from the blood in the gastrointestinal tract or soft tissues can produce similar rapid increases in the serum potassium.
  • Patients with a non-gap acidosis or respiratory acidosis may develop severe hyperkalemia quickly if the acidosis worsens, or if they develop an additional superimposed metabolic or respiratory acidosis, particularly when renal function is impaired.


Most serious manifestations of hyperK?

The most serious manifestations of hyperkalemia:

  • muscle weakness or paralysis
  • cardiac conduction abnormalities (e.g. bundle branch blocks) 
  • cardiac arrhythmias, including sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystole

These manifestations usually occur when the serum potassium concentration is ≥7 mEq/L with chronic hyperkalemia, or possibly at lower levels in patients with an acute rise in serum potassium and/or underlying cardiac conduction disease.


EKG changes associated with hyperK: describe the abormalities at the following serum levels

  • 5.5 - 6.5
  • 6.5 - 7.5
  • 7.0 - 8.0
  • 8.0 - 10.0



  • Which patients may have chronic mild or moderate hyperK?
  • How do you treat these patients?

  • Most patients with hyperkalemia have chronic, mild (5.5 mEq/L) or moderate (5.5 to 6.5 mEq/L) elevations in serum potassium due to CKD or the use of medications that inhibit the renin-angiotensin-aldosterone system ([RAAS] or both).
  • Such patients do not require urgent lowering of the serum potassium and can often be treated with
    • dietary modification
    • use of diuretics (if otherwise appropriate)
    • treatment of chronic metabolic acidosis,
    • or reversal of factors that can cause hyperkalemia (eg, nonsteroidal antiinflammatory drugs, hypovolemia).
  • In some instances, drugs that inhibit the RAAS are reduced or discontinued, and drugs that remove potassium by gastrointestinal cation exchange are prescribed for chronic use.


Give therapies that can be used to treat hyperK emergency.

  • See table
  • Therapy to rapidly remove excess potassium from the body (ie, loop or thiazide diuretics if renal function is not severely impaired, a gastrointestinal cation exchanger, and/or dialysis [preferably hemodialysis] if renal function is severely impaired)
  • Treatment of reversible causes of hyperkalemia, such as correcting hypovolemia and discontinuing drugs that increase the serum potassium (eg, nonsteroidal antiinflammatory drugs, inhibitors of the renin-angiotensinaldosterone system)


How do you monitor patients with hyperK emergency?

  • Continuous cardiac monitoring and serial electrocardiograms (ECGs) are warranted in patients with hyperkalemia who require rapidly acting therapies.
  • The serum potassium should be measured at one to two hours after the initiation of treatment. The timing of further measurements is determined by the serum potassium concentration and the response to therapy.
  • Patients who receive insulin, with or without dextrose, should undergo hourly glucose measurements for up to six hours in order to monitor for hypoglycemia.


Calcium in hyperK emergencies

  • Why use Calcium in hyperK emergencies?
  • How quickly does IV Calcium act and how long does it last?
  • How often can it be repeated?
  • Give the dosages and infusion times of IV Calcium
  • Issues with IV Calcium?

  • Calcium directly antagonizes the membrane actions of hyperkalemia while hypocalcemia increases the cardiotoxicity of hyperkalemia. Hyperkalemia-induced depolarization of the resting membrane potential leads to inactivation of sodium channels and decreased membrane excitability. 
  • The effect of intravenous calcium administration begins within minutes but is relatively short lived (30 to 60 minutes). 
  • Administration of calcium can be repeated every 30 to 60 minutes if the hyperkalemic emergency persists and the serum calcium does not become elevated. The doses can also be repeated after five minutes if the ECG changes persist or recur.
  • Calcium can be given as either calcium gluconate or calcium chloride. Calcium chloride contains three times the concentration of elemental calcium compared with calcium gluconate The usual dose of calcium gluconate is 1000 mg (10 mL of a 10 percent solution) infused over two to three minutes, with constant cardiac monitoring. The usual dose of calcium chloride is 500 to 1000 mg (5 to 10 mL of a 10 percent solution), also infused over two to three minutes, with constant cardiac monitoring.
  • Concentrated calcium infusions (particularly calcium chloride) are irritating to veins, and extravasation can cause tissue necrosis. As a result, a central or deep vein is preferred for administration of calcium chloride. Calcium gluconate can be given peripherally, ideally through a small needle or catheter in a large vein. Calcium should not be given in bicarbonate-containing solutions, which can lead to the precipitation of calcium carbonate.


What do you do with hyperK due to Digitalis toxicity?

When hyperkalemia occurs in patients treated with digitalis, calcium should be administered for the same
indications as in patients not treated with digitalis (eg, widening of the QRS complex or loss of P waves) even
though hypercalcemia potentiates the cardiotoxic effects of digitalis. In such patients, a dilute solution can be
administered slowly, infusing 10 mL of 10 percent calcium gluconate in 100 mL of 5 percent dextrose in water over
20 to 30 minutes, to avoid acute hypercalcemia [1]. In patients with hyperkalemia due to digitalis toxicity, the
administration of digoxin-specific antibody fragments is the preferred therapy.


Insulin therapy with glucose in HyperK

  • MoA of insulin for reducing hyperK?
  • Should insulin ever be given alone?
  • Monitoring of glucose post insulin?
  • Regimens of insulin administration?
  • Should glucose infusion be given without insulin?
  • Time to see insulin repsonse? How long does it last?
  • How much does serum potassium drop with insulin therapy?
  • Repeat dosing/continuous infusion of insulin and glucose?

  • Insulin administration lowers the serum potassium concentration by driving potassium into the cells, primarily by enhancing the activity of the Na-K-ATPase pump in skeletal muscle
  • Glucose is usually given with insulin to prevent the development of hypoglycemia. However, insulin should be given alone if the serum glucose is ≥250 mg/dL (13.9 mmol/L)
  • The serum glucose should be measured every hour for five to six hours after the administration of insulin, given the risk of hypoglycemia.
  • One commonly used regimen for administering insulin and glucose is 10 to 20 units of regular insulin in 500 mL of 10 percent dextrose, given intravenously over 60 minutes. Another regimen consists of a bolus injection of 10 units of regular insulin, followed immediately by 50 mL of 50 percent dextrose (25 g of glucose).
    • This regimen may provide a greater early reduction in serum potassium since the potassium-lowering effect is greater at the higher insulin concentrations attained with bolus therapy.
    • However, hypoglycemia occurs in approximately 20 percent of patients treated with insulin and glucose
    • To avoid this complication, we recommend subsequent infusion of 10 percent dextrose at 50 to 75 mL/hour and close monitoring of blood glucose levels every hour for five to six hours.
    • Additional measures in appropriate patients include the use of only 5 units of insulin or the administration of 50 grams of dextrose along with insulin
  • The administration of glucose without insulin is not recommended, since the release of endogenous insulin can be variable and the attained insulin levels are generally lower with a glucose infusion alone. Furthermore, in susceptible patients (primarily diabetic patients with hyporeninemic hypoaldosteronism), hypertonic glucose in the absence of insulin may acutely increase the serum potassium concentration by raising the plasma osmolality, which promotes water and potassium movement out of the cells
  • The effect of insulin begins in 10 to 20 minutes, peaks at 30 to 60 minutes, and lasts for four to six hours.
  • In almost all patients, the serum potassium concentration drops by 0.5 to 1.2 mEq/L.
    • In particular, although patients with renal failure are resistant to the glucose-lowering effect of insulin, they are not resistant to the hypokalemic effect, because Na-K-ATPase activity is still enhanced.
  • Removal of excess potassium from the body (eg, with hemodialysis or a gastrointestinal cation exchanger) is sometimes not feasible or must be delayed.
    • Such patients can be treated with either a continuous infusion of insulin and glucose or bolus infusions of insulin with glucose, repeated every two to four hours, with serial monitoring of blood glucose levels.


3 available modalities for potassium removal are which?


3 available modalities for potassium removal:

  • diuretics
  • gastrointestinal cation exchangers (eg, patiromer, sodium polystyrene sulfonate [SPS], and zirconium cyclosilicate)
  • dialysis


In patients with a hyperkalemic emergency, diuretics should not be the only method used to remove potassium from the body.


Loop diuretics in HyperK emergency

  • MoA of loop diuretics in hyerpK
  • Why shouldnt it be the only means to remove K from the body?
  • Dosage of furosemide if no renal impairement
  • Dosage of furosemdie with renal impairment

  • Loop diuretics increase potassium loss in the urine in patients with normal or mild to moderately impaired renal function, particularly when combined with saline hydration to maintain distal sodium delivery and flow.
  • However, patients with persistent hyperkalemia typically have impaired renal potassium secretion, and there are no data demonstrating a clinically important short-term kaliuretic response to diuretic therapy. Thus, diuretics should not be used as the only means to remove potassium from the body in patients with a hyperkalemic emergency.
  • In hypervolemic patients with preserved renal function (eg, patients with heart failure), administer 40 mg of
    intravenous furosemide every 12 hours or a continuous furosemide infusion. In euvolemic or hypovolemic patients with preserved renal function, administer isotonic saline at a rate that is appropriate to replete hypovolemia and maintain euvolemia, followed by 40 mg of intravenous furosemide every 12 hours or a continuous furosemide infusion.
  • If renal function is not preserved, we use a combination of an intravenous isotonic bicarbonate or isotonic saline
    infusion plus intravenous furosemide at doses that are appropriate for the patient's renal function.


HyperK emergency - dialysis

  • when is it appropriate to use?
  • when would you administer gastrointestinal cation exchange therapy instead?

  • Hemodialysis is indicated in hyperkalemic patients with severe renal impairment, and is preferable to cation exchangers if the patient has functioning vascular access for dialysis and if the procedure can be performed without delay.
  • However, if hemodialysis cannot be performed promptly (eg, within six hours), we administer gastrointestinal cation exchange therapy (preferably not SPS) and then perform hemodialysis as soon as possible.


GI cation exchangers in hyperK

  • ]Dosages of Patiromer or Zirconium cyclosilicate in HyperK?
  • Reduction and time of onset of Zirconum cyclosilicate?

  • When using a cation exchanger in patients with a hyperkalemic emergency, we use patiromer (8.4 g, repeated daily as needed) or zirconium cyclosilicate (10 g three times daily for 48 hours), if these drugs are available, rather than SPS.
  • Although both patiromer and zirconium cyclosilicate may have a role in acutely reducing serum potassium in patients with hyperkalemic emergency, this has yet to be established.
  • However, the hypokalemic effect of zirconium cyclosilicate can be appreciated within one hour, with a mean reduction in serum potassium of 0.7 mEq/L four hours after a 10-gram dose. Our approach is based upon short-term effects of these drugs in a separate patient population (ie, those treated for chronic moderate hyperkalemia).


  • What is the rare but severe complication of SPS?
  • Describe patients who would be high risk for the complication?
  • What are precautions that should be taken if administering SPS?
  • Does sorbitol increase risk of complications with SPS?

  • Bowel necrosis
  • High risk patients for bowel necrosis
    • Postoperative patients
    • Patients with an ileus or who are receiving opiates
    • Patients with a large or small bowel obstruction
    • Patients with underlying bowel disease, eg, ulcerative colitis or Clostridioides (formerly Clostridium) difficile colitis
  • SPS in hyperK emergency may be considered in the following circumstances
    • Patient has potentially life-threatening hyperkalemia
      Dialysis is not readily available 
    • Newer cation exchangers (ie, patiromer or zirconium cyclosilicate) are not available
    • Other therapies to remove potassium (eg, diuretics, rapid restoration of kidney function) have failed or are not possible
    • If SPS is used, other orally administered drugs should be taken at least 3 hours before or 3 hours after the dose of SPS. SPS binds to and prevents the absorption of many common medications.
  • Controversial whether sorbitol increases risk but evidence shows that it should be avoided as much as possible. Despite this, many hospitals and pharmacies only stock sodium polystyrene sulfonate premixed in sorbitol. SPS alone is not always available and, when available, comes as a powder that must be reconstituted.
    • If given, SPS with or without sorbitol can be administered orally, and SPS without sorbitol can be administered as a retention enema. Oral dosing is probably more effective if intestinal motility is not impaired. The oral dose is usually 15 to 30 g, which can be repeated every four to six hours as necessary. Single doses are probably less effective


HyperK emergency - ß2 agonists

  • Why should ß2 agonists not be used in place of other hyperK treatments?
  • When should ß2 agonists be considered?
  • MoA of ß2 agonists?
  • Dosage of ß2 agonists?
  • Lowering K ability?
  • S-E of ß2 agonists?

  • Transient effect of ß2 agonists
  • can be considered as transient therapy in patients who have symptoms or serious ECG manifestations of hyperkalemia despite therapy with calcium and insulin with glucose, or in patients in whom dialysis is not appropriate or not feasible.
  • Like insulin, the beta-2-adrenergic agonists drive potassium into the cells by increasing the activity of the Na-K ATPase pump in skeletal muscle. ß2-adrenergic receptors in skeletal muscle also activate the inwardly directed Na-K-2Cl cotransporter, which may account for as much as one-third of the uptake response to catecholamines
  • Albuterol, which is relatively selective for the beta-2-adrenergic receptors, can be given as 10 to 20 mg in 4 mL of saline by nebulization over 10 minutes (which is 4 to 8 times the dose used for bronchodilation). Alternatively and where available, albuterol 0.5 mg can be administered by intravenous infusion. In patients who cannot tolerate nebulized albuterol, and if intravenous therapy is not available, subcutaneous terbutaline is a potential alternative. The peak effect is seen within 30 minutes with IV infusion and at 90 minutes with nebulization.
  • ß2-adrenergic agonists can be effective in the acute treatment of hyperkalemia, lowering the serum K concentration by 0.5 to 1.5 mEq/L
  • mild tachycardia and the possible induction of angina in susceptible patients. Avoid with CAD; monitor all patients with ESRD for subclinical or overt CAD.


Sodium Bicarbonate in HyperK emergencies

  • MoA of NAHCO3
  • efficacy?
  • Dosage?

  • Raising the systemic pH with sodium bicarbonate results in hydrogen ion release from the cells as part of the buffering reaction. This change is accompanied by potassium movement into the cells to maintain electroneutrality. The use of bicarbonate for the treatment of hyperkalemia was mainly based upon small uncontrolled clinical studies
  • Limited efficacy...
    • More applicable for patients in acidemia 
    • However, prolonged bicarbonate therapy appears to be beneficial in patients with metabolic acidosis, particularly when administered as an isotonic infusion rather than bolus ampules of hypertonic sodium bicarbonate
  • When bicarbonate is given in the acute setting, we recommend the administration of an isotonic solution (eg, 150 mEq in 1 L of 5 percent dextrose in water over two to four hours), assuming the patient can tolerate the volume load.
    • There is a potential hazard of giving hypertonic solutions, such as the standard ampule of 50 mEq of sodium bicarbonate in 50 mL. In addition, multiple doses can lead to hypernatremia.

Over the long term, in patients with CKD, there are a variety of benefits from treating metabolic acidosis, and alkali therapy is recommended to maintain a near-normal serum bicarbonate, independent of any effect on the serum potassium concentration.


Patients who do not have a hyperkalemic emergency can generally be divided into two groups, which are?

1) Those who, despite needing to have their potassium lowered promptly, do not require rapidly acting therapy
with calcium and insulin with glucose

  • Such patients with severe renal impairment are typically treated with dialysis (preferably hemodialysis) with or without the use of a gastrointestinal cation exchanger. 
  • In patients with normal renal function or mild to moderate renal impairment, correcting the cause of hyperkalemia (eg, drugs, hypovolemia) will generally suffice, in addition to treatment with saline infusion and loop diuretics.

2) Those who can safely have their serum potassium lowered slowly.

  • Such patients can usually be treated with therapies that gradually reduce the serum potassium, such as a low-potassium diet, loop or thiazide diuretics, or a reduction or cessation of medicines that can increase the serum potassium.
  • With the introduction of patiromer and zirconium cyclosilicate, it is anticipated that gastrointestinal cation exchangers will be utilized more frequently in these patients for chronic control of the serum potassium


Patients who need prompt reduction of hyperK  with renal impairment.

  • Dialysis can remove how much of K?
  • What can occur post-dialysis with serum K?

In patients with severe renal impairment who need prompt serum potassium reduction,

  • dialysis should be performed right away if it is logistically feasible (ie, regular working hours, availability of staff, and presence of a suitable vascular access).
  • Hemodialysis can normalize the serum potassium within four hours
    • Hemodialysis can remove 25 to 50 mEq of potassium per hour
  • A rebound increase in serum potassium concentration occurs after hemodialysis in all patients in whom potassium is removed since the reduction in serum potassium during dialysis creates a gradient for potassium movement out of the cells. 
    • Rapidly acting transient therapies given before dialysis, such as insulin with glucose or albuterol, have a twofold effect: Total potassium removal is reduced due to lowering of the serum potassium concentration; and the potassium rebound is greater because of the wearing off of the effect of the transient therapies.


Those without severe renal impairment and need prompt lowering of K.

  • Patients who have moderate hyperkalemia and either normal renal function or mild to moderate renal impairment can usually be managed without dialysis.
  • Treatment of such patients typically includes a GI cation exchanger in addition to reversing the cause of hyperkalemia.
  • As an example, a patient with moderate CKD treated with an RAAS inhibitor who presents with a serum potassium of 6.0 mEq/L may be treated with a cation exchanger (such as patiromer), temporary discontinuation of the RAAS inhibitor, as well as other therapies that are appropriate for the clinical setting (ie, bicarbonate therapy if the patient has metabolic acidosis, and diuretic therapy if the patient is hypervolemic).



  • Binds which cation in the GI tract for exchange?
  • What other electrolyte def can it cause?
  • What other drugs can it bind to in the GI tract? 

  • binds potassium in the colon in exchange for calcium
  • HypoMg
  • Clinically important interactions with ciprofloxacin, thyroxine, and metformin have been identified; these three drugs need to be administered more than three hours before or after patiromer


Sodium zirconium cyclosilicate

  • MoA?
  • S-E?

  • exchanges both sodium and hydrogen ions for potassium
    throughout its intestinal transit. The steepest decline in serum potassium with zirconium cyclosilicate occurred during the first four hours of therapy. This suggests an acute effect on intestinal potassium secretion, rather than simply a reduction in potassium absorption
  • Zirconium cyclosilicate is also effective for management of hyperkalemia among patients receiving maintenance
  • Higher edema rates with zirconium cyclosilicate are likely due to an increased sodium load


Which drugs cause hyperK?

Most common

  • ACEIs
  • ARBs
  • aldosterone antagonists
  • potassium sparing diuretics (eg. spironolactone, eplerenone, and amiloride)
  • digitalis
  • nonsteroidal antiinflammatory drugs


Give measures to help prevent hyperK

  • Avoid fasting (decreased insulin production)
    • Thus, nondiabetic patients with ESRD who are undergoing elective surgery should, if they
      are in the hospital, receive parenteral glucose-containing solutions when fasting overnight.
  • Avoid, if possible, drugs that raise the serum potassium concentration in patients with a serum potassium ≥5.5
  • Reduce dietary K if necessary