Medscape:

Practice Essentials
Hiperkalemia didefinisikan sebagai peningkatan level potassium lebih dari 5.5
mEq/L. [1] keadaan ini sulit di diagnosis secara klini karna gejala-gejalanya mungkin
samar atau bahkan tidak ada. Namun, fakta bahwa hiperkalemia dapat
menyebabkan kematian mendadak karna Aritmia jantung yang membutuhkan dokter
untuk segera menyadari hiperkalemia pada pasien berrisiko. [2, 3] Initial emergency
department care includes assessment of the ABCs and prompt evaluation of the
patient's cardiac status with an electrocardiogram (ECG). In patients in whom
hyperkalemia is severe (potassium >7.0 mEq/L) or symptomatic, treatment should
commence before diagnostic investigation of the underlying cause.
See the ECG below.

Widened QRS complexes in hyperkalemia.

See also Can't-Miss ECG Findings, Life-Threatening Conditions: Slideshow, a
Critical Images slideshow, to help recognize the conditions shown in various
tracings.
Signs and symptoms
Patients with hyperkalemia may be asymptomatic, or they may report the following
symptoms (cardiac and neurologic symptoms predominate):
 Generalized fatigue
 Weakness
 Paresthesias
 Paralysis
 Palpitations
Evaluation of vital signs is essential for determining the patient’s hemodynamic
stability and the presence of cardiac arrhythmias related to
hyperkalemia. [1] Additional important components of the physical exam may include
the following:
  Cardiac examination may reveal extrasystoles, pauses, or bradycardia
 Neurologic examination may reveal diminished deep tendon reflexes or
decreased motor strength
 In rare cases, muscular paralysis and hypoventilation may be observed
 Signs of renal failure, such as edema, skin changes, and dialysis sites, may be
present
 Signs of trauma may indicate that the patient has rhabdomyolysis, which is one
cause of hyperkalemia
See Clinical Presentation for more detail.
Diagnosis
Laboratory studies
The following lab studies can be used in the diagnosis of hyperkalemia:
 Potassium level: The relationship between serum potassium level and
symptoms is not consistent; for example, patients with a chronically elevated
potassium level may be asymptomatic at much higher levels than other
patients; the rapidity of change in the potassium level influences the symptoms
observed at various potassium levels
 Blood urea nitrogen (BUN) and creatinine levels: For evaluation of renal status
 Calcium level: If the patient has renal failure (because hypocalcemia can
exacerbate cardiac rhythm disturbances)
 Glucose level: In patients with diabetes mellitus
 Digoxin level: If the patient is on a digitalis medication
 Arterial or venous blood gas: If acidosis is suspected
 Urinalysis: To look for evidence of glomerulonephritis if signs of renal
insufficiency without a known cause are present
 Cortisol and aldosterone levels: To check for mineralocorticoid deficiency when
other causes are eliminated
Electrocardiography
Electrocardiography is essential and may be instrumental in diagnosing
hyperkalemia in the appropriate clinical setting. Electrocardiographic changes have a
sequential progression that roughly correlates with the patient’s potassium level.
Potentially life-threatening arrhythmias, however, can occur without distinct
electrocardiographic changes at almost any level of hyperkalemia.
See Workup for more detail.
Management
Prehospital care
Prior to reaching the emergency department, treatment of a patient with
hyperkalemia includes the following:
 A patient with known hyperkalemia or a patient with renal failure with suspected
hyperkalemia should have intravenous access established and should be
placed on a cardiac monitor [4]
 In the presence of hypotension or marked QRS widening, intravenous
bicarbonate, calcium, and insulin given together with 50% dextrose may be
appropriate
 Avoid calcium if digoxin toxicity is suspected; magnesium sulfate (2 g over 5
min) may be used alternatively in the face of digoxin-toxic cardiac arrhythmias
Inhospital care
Once the patient reaches the emergency department, assessment and treatment
include the following:
 Continuous ECG monitoring with frequent vital sign checks: When
hyperkalemia is suspected or when laboratory values indicative of hyperkalemia
are received
 Assessment of the ABCs and prompt evaluation of the patient's cardiac status
with an electrocardiogram (ECG)
 Discontinuation of any potassium-sparing drugs or dietary potassium
If the hyperkalemia is known to be severe (potassium >7.0 mEq/L) or if the patient is
symptomatic, begin treatment before diagnostic investigation of the underlying
cause. Individualize treatment based upon the patient's presentation, potassium
level, and ECG.
Dialysis is the definitive therapy in patients with renal failure or in whom
pharmacologic therapy is not sufficient. Any patient with significantly elevated
potassium levels should undergo dialysis, as pharmacologic therapy alone is not
likely to adequately bring down the potassium levels in a timely fashion.
Medications
Drugs used in the treatment of hyperkalemia include the following:
 Calcium (either gluconate or chloride): Reduces the risk of ventricular fibrillation
caused by hyperkalemia
 Insulin administered with glucose: Facilitates the uptake of glucose into the cell,
which results in an intracellular shift of potassium
 Alkalinizing agents: Increases the pH, which results in a temporary potassium
shift from the extracellular to the intracellular environment; these agents
enhance the effectiveness of insulin in patients with acidemia
 Beta2-adrenergic agonists: Promote cellular reuptake of potassium
 Diuretics: Cause potassium loss through the kidney
 Binding resins: Promote the exchange of potassium for sodium in the
gastrointestinal (GI) system
 Magnesium sulfate: Has been successfully used to treat acute overdose of
slow-release oral potassium

Background
Hyperkalemia is a potentially life-threatening illness that can be difficult to diagnose
because of a paucity of distinctive signs and symptoms. The physician must be quick
to consider hyperkalemia in patients who are at risk for this disease process.
Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any
suggestion of hyperkalemia requires an immediate ECG to ascertain whether
electrocardiographic signs of electrolyte imbalance are present.
Pathophysiology
Potassium is a major ion of the body. Nearly 98% of potassium is intracellular, with
the concentration gradient maintained by the sodium- and potassium-activated
adenosine triphosphatase (Na+/K+ –ATPase) pump. The ratio of intracellular to
extracellular potassium is important in determining the cellular membrane potential.
Small changes in the extracellular potassium level can have profound effects on the
function of the cardiovascular and neuromuscular systems. The normal potassium
level is 3.5-5.0 mEq/L, and total body potassium stores are approximately 50 mEq/kg
(3500 mEq in a 70-kg person).
Minute-to-minute levels of potassium are controlled by intracellular to extracellular
exchange, mostly by the sodium-potassium pump that is controlled by insulin and
beta-2 receptors. A balance of GI intake and renal potassium excretion achieves
long-term potassium balance.
Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L. [1] Ranges are
as follows:
 5.5-6.0 mEq/L - Mild
 6.1-7.0 mEq/L - Moderate
 7.0 mEq/L and greater - Severe
Hyperkalemia results from the following:
 Decreased or impaired potassium excretion - As observed with acute or chronic
renal failure [5] (most common), potassium-sparing diuretics, urinary obstruction,
sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)
 Additions of potassium into extracellular space - As observed with potassium
supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and
hemolysis (eg, blood transfusions, burns, tumor lysis)
 Transmembrane shifts (ie, shifting potassium from the intracellular to
extracellular space) - As observed with acidosis and medication effects (eg,
acute digitalis toxicity, beta-blockers, succinylcholine)
 Fictitious or pseudohyperkalemia - As observed with improper blood collection
(eg, ischemic blood draw from venipuncture technique), laboratory error,
leukocytosis, and thrombocytosis
Frequency
United States
Hyperkalemia is diagnosed in up to 8% of hospitalized patients. A retrospective
study by Betts et al estimated that in 2014, 3.7 million US adults (1.55%) had
hyperkalemia, an increase over 2010. Within the adult hyperkalemic population in
2014, chronic kidney disease (CKD) and/or heart failure existed in 48.43%, with the
annual prevalence of hyperkalemia in patients with CKD and/or heart failure that
year being 6.35%. [6]
Sex
The male-to-female ratio is 1:1.
Mortality/Morbidity
The primary cause of morbidity and death is potassium's effect on cardiac
function. [7, 8, 9] The mortality rate can be as high as 67% if severe hyperkalemia is
not treated rapidly. [10]
A study by Krogager et al indicated that in patients who need diuretic treatment
following a myocardial infarction, a potassium level above or below the 3.9-4.5
mmol/L range significantly increases the mortality risk, with the highest risk (38.3%
mortality rate at 90-day follow-up) found in patients with severe hyperkalemia (>5.5
mmol/L). [11]
A study by Norring-Agerskov indicated that hyperkalemia is associated with
increased 30-day mortality in hip-fracture patients, with a hazard ratio of 1.93. The
study included 7293 patients with hip fracture, aged 60 years or older. [12]

History
Hyperkalemia can be difficult to diagnose clinically because symptoms may be
vague or absent. The history is most valuable in identifying conditions that may
predispose to hyperkalemia.
Hyperkalemia frequently is discovered as an incidental laboratory finding.
Cardiac and neurologic symptoms predominate.
Patients may be asymptomatic or report the following:
 Generalized fatigue
 Weakness
 Paresthesias
 Paralysis
 Palpitations
Hyperkalemia is suggested in any patient with a predisposition toward elevated
potassium level. Potential potassium level elevation is observed in the following:
 Acute or chronic renal failure, especially in patients who are on dialysis
 Trauma, including crush injuries (rhabdomyolysis), or burns
 Ingestion of foods high in potassium (eg, bananas, oranges, high-protein diets,
tomatoes, salt substitutes). This alone is not likely to cause clinically significant
hyperkalemia in most people; it is often a contributing factor to an acute
potassium elevation.
 Medications - Potassium supplements, potassium-sparing diuretics,
nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers, digoxin,
succinylcholine, and digitalis glycoside
 Medication combinations (ie, spironolactone, ACE inhibitors) [13]
 Redistribution - Metabolic acidosis (diabetic ketoacidosis [DKA]), catabolic
states
Physical
Evaluation of vital signs is essential to determine hemodynamic stability and
presence of cardiac arrhythmias related to the hyperkalemia. [1]
Cardiac examination may reveal extrasystoles, pauses, or bradycardia.
Neurologic examination may reveal diminished deep tendon reflexes or decreased
motor strength.
In rare cases, muscular paralysis and hypoventilation may be observed.
Search for the stigmata of renal failure, such as edema, skin changes, and dialysis
sites.
Look for signs of trauma that could put the patient at risk for rhabdomyolysis.
Causes
Pseudohyperkalemia may result from the following:
 Hemolysis (in laboratory tube) most common
 Severe thrombocytosis
 Severe leukocytosis
 Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet
application)
Redistribution may result from the following:
 Acidosis
 Beta-blocker drugs
 Acute digoxin intoxication or overdose
 Succinylcholine [14]
 Arginine hydrochloride
 Hyperkalemic familial periodic paralysis
Excessive endogenous potassium load may result from the following:
 Hemolysis
 Rhabdomyolysis
 Internal hemorrhage
Excessive exogenous potassium load may result from the following:
 Parenteral administration
 Excess in diet
 Potassium supplements
 Salt substitutes
A study by Te Dorsthorst et al indicated that dietary hyperkalemia may not be a
condition of renal impairment. In an analysis of 35 case reports that included 44
incidences of hyperkalemia arising from oral intake, the investigators found no
kidney dysfunction in 17 patients. Salt substitutes and supplements were the primary
causes of hyperkalemia in patients with normal renal function. [15]
Diminished potassium excretion may result from the following:
 Decreased glomerular filtration rate (eg, acute or end-stage chronic renal
failure)
 Decreased mineral corticoid activity
 Defect in tubular secretion (eg, renal tubular acidosis II and IV)
 Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)
Laboratory error may be the cause of reported hyperkalemia, so if not consistent with
the clinical picture, repeat laboratory studies. [16]

Differential Diagnoses
 Hypocalcemia

Laboratory Studies
Potassium level
The relationship between the serum potassium level and symptoms is not consistent.
For example, patients with a chronically elevated potassium level may be
asymptomatic at much higher levels than other patients. The rapidity of change in
the potassium level influences the symptoms observed at various potassium levels.
BUN and creatinine level
For evaluation of renal status
Calcium level
If patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm
disturbances)
Glucose level
In patients with diabetes mellitus
Digoxin level
If patient is on a digitalis medication
Arterial or venous blood gas
If acidosis is suspected
Urinalysis
If signs of renal insufficiency without an already known cause are present (to look for
evidence of glomerulonephritis)
Other Tests
Continuous cardiac monitoring
Indicated for evaluation of rhythm disturbances
ECG
ECG is essential and may be instrumental in diagnosing hyperkalemia in the
appropriate clinical setting. ECG changes have a sequential progression of effects,
which roughly correlate with the potassium level.
ECG findings may be observed as follows:
 Early changes of hyperkalemia include peaked T waves, shortened QT interval,
and ST-segment depression.
 These changes are followed by bundle-branch blocks causing a widening of the
QRS complex, increases in the PR interval, and decreased amplitude of the P
wave (see the images below).

Widened QRS complexes in hyperkalemia.

View Media Gallery
 Widened QRS complexes in a patient whose serum potassium level was 7.8
mEq/L.
View Media Gallery
 These changes reverse with appropriate treatment (see the image below).

ECG of a patient with pretreatment potassium level of 7.8 mEq/L and widened
QRS complexes after receiving 1 ampule of calcium chloride. Notice narrowing
of QRS complexes and reduction of T waves.
View Media Gallery
 Without treatment, the P wave eventually disappears and the QRS morphology
widens to resemble a sine wave. Ventricular fibrillation or asystole follows.
 ECG findings generally correlate with the potassium level, but potentially life-
threatening arrhythmias can occur without distinct ECG changes at almost any
level of hyperkalemia.
Cortisol and aldosterone levels
To check for mineralocorticoid deficiency when other causes are eliminated

Prehospital Care
A patient with known hyperkalemia or a patient with renal failure with suspected
hyperkalemia should have intravenous access established and should be placed on
a cardiac monitor.[4] In the presence of hypotension or marked QRS widening,
intravenous bicarbonate, calcium, and insulin, given together with 50% dextrose,
may be appropriate, as discussed in Medication. Avoid calcium if digoxin toxicity is
suspected. Magnesium sulfate (2 g over 5 min) may be used alternatively in the face
of digoxin-toxic cardiac arrhythmias.
Emergency Department Care
Perform continuous ECG monitoring with frequent vital sign checks when
hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are
received.
Initial management includes assessment of the ABCs and prompt evaluation of the
patient's cardiac status with an ECG.
Discontinue any potassium-sparing drugs or dietary potassium.
If the hyperkalemia is known to be severe (potassium >7.0 mEq/L) or if the patient is
symptomatic, begin treatment before diagnostic investigation of the underlying
cause. Individualize treatment based upon the patient's presentation, potassium
level, and ECG. Not all patients should receive every medication listed in Medication.
Patients with mild hyperkalemia, for example, may need only excretion
enhancement.
Some studies are emerging that suggest sodium polystyrene sulfonate (SPS), also
known as Kayexalate, may be unhelpful in hyperkalemia and may increase the
chance of colonic necrosis (especially when used with sorbitol). [17, 18, 19, 20] A
retrospective study by Lee and Moffett, however, found SPS to be a safe and
effective treatment for hyperkalemia in most pediatric patients. However, the
investigators suggested that the drug may not be an appropriate first single-line
agent when patients with severe acute hyperkalemia need their serum potassium
level reduced by over 25% or when patients have a high cardiac arrhythmia
risk. [21] Generally, SPS is considered safe orally but is not recommended as a
retention enema, which has a higher rate of colonic necrosis. Effects are expected to
be minor and not adequate to reduce potassium levels to normal levels.
Phase II and III clinical trials have indicated that patiromer and sodium zirconium
cyclosilicate (ZS-9) have a dose-dependent ability to lower potassium levels. In
2015, patiromer (Veltassa) was approved by the US Food and Drug Administration
(FDA) for the treatment of hyperkalemia in adults, although its labeling specified that,
owing to its delayed onset of action, it "should not be used as an emergency
treatment for life-threatening hyperkalemia." In 2018, ZS-9 (Lokelma) became
FDA approved for adults with hyperkalemia as well, but like patiromer, it is also not
to be used for the emergency treatment of life-threatening hyperkalemia. [22, 23, 24, 25]
A study by Jacob et al of adult patients who received intravenous regular insulin
during emergency department treatment for hyperkalemia found the incidence of
hypoglycemia and severe hypoglycemia to be 19.8% and 5.2%, respectively. The
median blood glucose level at baseline was significantly lower in patients who
developed hypoglycemia than in those who did not. The investigators suggested that
standard insulin doses may not be suitable for hyperkalemic patients with low
baseline glucose. [26]
Consultations
Consult a nephrologist or the dialysis team for patients with either severe
symptomatic hyperkalemia or renal failure. Admit these patients to an ICU.
Medication Summary
Direct treatment is aimed at stabilizing the myocardium, shifting potassium from the
extracellular environment to the intracellular compartment, and promoting the renal
excretion and GI loss of potassium.
Electrolyte supplements
Class Summary
These agents are used to treat hyperkalemia and to reduce the risk of ventricular
fibrillation caused by hyperkalemia. They act quickly and can be lifesaving, thus they
are the first-line treatment for severe hyperkalemia when the ECG shows significant
abnormalities (eg, widening of QRS interval, loss of P wave, cardiac arrhythmias).
Calcium usually is not indicated when the ECG shows only peaked T waves.

Calcium chloride (Kalcinate)

 View full drug information
Calcium increases threshold potential, thus restoring normal gradient between
threshold potential and resting membrane potential, which is elevated abnormally in
hyperkalemia. One ampule of calcium chloride has approximately 3 times more
calcium than calcium gluconate. The onset of action is less than 5 min and lasts
about 30-60 minutes. Doses should be titrated with constant monitoring of ECG
changes during administration; repeat the dose if ECG changes do not normalize
within 3-5 minutes.
Antidotes
Class Summary
Insulin is administered with glucose to facilitate the uptake of glucose into the cell,
which results in an intracellular shift of potassium.

Dextrose (D-Glucose)
 View full drug information
Glucose and insulin temporarily shift K+ into cells; effects occur within first 30
minutes of administration.

Insulin (Humulin, Humalog, Novolin)

 View full drug information
Insulin stimulates cellular uptake of K+ within 20-30 minutes; administer glucose
along with insulin to prevent hypoglycemia (monitor blood glucose levels closely).
Alkalinizing agents
Class Summary
These agents increase the pH, which results in a temporary potassium shift from the
extracellular to the intracellular environment. These agents enhance the
effectiveness of insulin in patients with acidemia.

Sodium bicarbonate (Neut)

 View full drug information
Bicarbonate ions neutralize hydrogen ions and raise urinary and blood pH. The onset
of action is within minutes and lasts approximately 15-30 minutes. It is only likely to
be efficacious if underlying acidosis is present. Monitor blood pH to avoid excess
alkalosis.
Use 8.4% solution in adults and children and 4.2% solution in infants.
Beta2-adrenergic agonists
Class Summary
These agents promote cellular reuptake of potassium, possibly via the cyclic gAMP
receptor cascade.

Albuterol (Ventolin, Proventil)

 View full drug information
Albuterol is an adrenergic agonist that increases the plasma insulin concentration,
which may, in turn, help shift K+ into the intracellular space. It lowers K+ levels by
0.5-1.5 mEq/L. Albuterol can be very beneficial in patients with renal failure when
fluid overload is a concern. The onset of action is 30 minutes; the duration of action
is 2-3 hours.
Diuretics
Class Summary
These agents cause the loss of potassium through the kidney.

Furosemide (Lasix)
 View full drug information
Effects are slow and frequently take an hour to begin. Furosemide lowers the
potassium level by an inconsistent amount. Large doses may be needed in renal
failure.

Ethacrynic acid (Edecrin)

 View full drug information
Ethacrynic acid increases the excretion of water by interfering with the chloride-
binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption
in the ascending loop of Henle and distal renal tubule.
Binding resins
Class Summary
These agents promote exchange of potassium for sodium in GI system.

Sodium polystyrene sulfonate (Kayexalate)

 View full drug information
Sodium polystyrene sulfonate exchanges Na+ for K+ and binds it in the gut, primarily
in the large intestine, decreasing total body potassium. The onset of action after oral
administration ranges from 2-12 hours (longer when administered rectally). It lowers
K+ over 1-2 hours, with a duration of action of 4-6 hours. The potassium level drops
by approximately 0.5-1 mEq/L. Multiple doses are usually necessary.
Electrolytes
Class Summary
These agents have been successfully used in the treatment of acute SLOW released
oral potassium overdose.

Magnesium sulfate
 View full drug information
Magnesium sulfate is a nutritional supplement in hyperalimentation; it is a cofactor in
enzyme systems involved in neurochemical transmission and muscular excitability.
In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol of
phosphate per day may be necessary for an optimum metabolic response. Give
intravenously for acute suppression of torsade. Repeat doses are dependent upon
continuing the presence of a patellar reflex and adequate respiratory function.

Further Outpatient Care

Adjust diet to decrease potassium dietary load.
Adjust medications that predispose to or exacerbate hyperkalemia.
Repeat potassium level tests in 2-3 days.
Reevaluate renal function if signs of renal insufficiency are present.
Further Inpatient Care
Order continuous cardiac monitoring for patients who are hyperkalemic.
Definitive therapy is dialysis in patients with renal failure or when pharmacologic
therapy is not sufficient. Any patient with significantly elevated potassium levels
should undergo dialysis, as pharmacologic therapy alone is not likely to adequately
bring down the potassium levels in a timely fashion.
Monitor serial potassium levels.
Resolve acid-base problems.
Correct coexistent electrolyte disturbances.
Treat digoxin toxicity, if present.
Transfer
If unable to correct hyperkalemia with pharmacologic therapy and dialysis is
unavailable, stabilize the patient and transfer to a center where dialysis can be
performed.
Deterrence/Prevention
Avoid foods high in potassium.
Avoid medications that predispose to hyperkalemia.
Complications
Life-threatening cardiac arrhythmias may ensue.
Hypokalemia may result from the treatment of hyperkalemia.
Prognosis
Expect full resolution with correction of the underlying etiology.
Reduction of plasma potassium should begin within the first hour of initiation of
treatment.
Patient Education
Pursue diet modification.
Discontinue use of medications that may worsen hyperkalemia.
Encourage adherence to dialysis schedule if patient is noncompliant.

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Emergency Medicine Cases:
Cite this podcast as: Helman, A, Baimel, M, Etchells, E. Emergency Management of
Hyperkalemia. Emergency Medicine Cases. September,
2016. https://emergencymedicinecases.com/alcohol-withdrawal-delirium-tremens/. Accessed
[date].

General Approach to Emergency Management of Hyperkalemia

Place the patient on a cardiac monitor, establish IV access and obtain an ECG

If the patient is stable, consider the cause and rule out pseudohyperkalemia (from poor phlebotomy
technique, thrombocytosis or leucocytosis) and repeat the potassium to confirm hyperkalemia.

Stabilize the cardiac membrane with Calcium Gluconate 1-3 amps

(or Calcium Chloride 1 amp if peri-arrest/arrest) if:

a) K>6.5 or

b) wide QRS or

c) absent p waves or

d) peri-arrest/arrest

Drive K into cells with 2 amps D50W + Regular Insulin 10 units IV push

followed by B-agonists 20mg by neb or 8 puffs via spacer if:

a) K>5 with any hyperkalemia ECG changes or

b) K>6.5 regardless of ECG findings

Eliminate K through the kidneys and GI tract while achieving euvolemia and establish good urine
flow

Normal Saline IV boluses if hypovolemia

Furosemide IV only if hypervolemic

 PEG 3350 17g orally for alert patients remaining in your ED for prolonged period of time

Dialysis for arrest, peri-arrest, dialysis patient or severe renal failure

Monitor rythym strip, glucose at 30 mins, K and ECG at 60 mins

and repeat as needed until the K is below 6, ECG has normalized and/or dialysis has been started

Update 2017: A recent retrospective study suggested that in patients with renal
insufficiency and hyperkalemia, administration of 5 units of insulin rather than 10 units significantly
decreased the incidence of hypoglycemia while correcting potassium to a similar degree. For ED
patients with hyperkalemia and renal insufficiency, consider either lowering the initial dose of
insulin from 10 units to 5 units, or ensuring that 2 amps of D50W (rather than 1) is administered
concurrently to avoid hypoglycemia. Abstract

The ECG in Emergency Management of Hyperkalemia

The ECG changes associated with hyperkalemia do not always happen in a step-wise fashion with
predictable serum potassium levels. Although it is generally true that higher levels of potassium
correlate with progressive ECG changes, the more acute the hyperkalemia the more likely the ECG
changes occur. It is possible for a hyperkalemic patient to progress rapidly from a normal ECG to
ventricular fibrillation.

The classic ECG progression in hyperkalemia

1. Peaked T wave (K approx 5.5-6.5)

Peaked T waves reflect faster repolarization of the myosite. A sensitive sign is if the amplitude of the
T exceeds the amplitude of the R. This distinguishes peaked T waves of hyperkalemia from hyperacute
T waves of early MI which tend to have a broader base T wave.

Peaked T waves of Hyperkalemia. Note the amplitude of the T exceeds the amplitude of the R. Care of
Life in The Fast Lane blog.
 Hyperacute T waves of early MI. Note the broad-based T waves in the anterior leads to help
distinguish from peaked T waves of hyperkalemia. Care of Dr. Smith’s ECG blog.

2. Prolonged PR interval and flattening or disappearance of the P wave (K approx 6.5-

7.5)

The resting potential of myosite becomes more positive which slows depolarization.

Example of bradycardia with absent or flattened p waves in hyperkalemia. Care of Dr. Smith’s ECG
blog.

3. Widening of the QRS

The increasingly positive membrane potential leads to progressively slowed depolarization and
widening of the QRS.
 Widened QRS in severe hyperkalemia (Care of Dr. Melanie Baimel)

4. Sine Wave: pre-terminal rhythm

As the depolarization slows, the widening QRS begins to merge with the T wave. This is a pre-
terminal rhythm which can deteriorate rapidly into Ventricular Fibrillation.

Sine wave in severe hyperkalemia, a pre-arrest rhythm.

Hyperkalemia is the Great ECG Imitator

These ECG findings are not specific to hyperkalemia alone. Given the broad differential for these ECG
changes, hyperkalemia has been dubbed the “Great ECG Imitator”. It is important to consider the
patient’s presentation, clinical complaints and trends on the ECG.

PEARL: Hyperkalemia has been known to cause almost any dysrhythmia. Pay special attention to
patients in “slow VT” and wide-complex bradycardia and consider treating them empirically as
hyperkalemia.

Determine the Cause of Hyperkalemia

First rule out pseudohyperkalemia which accounts for 20% of hyperkalemia lab values.

Pseudohyperkalemia is caused by hemolyzed sample, poor phlebotomy technique leukocytosis or

thrombocytosis.
Then treat the underlying cause:

 Medications: ACEi, Potassium sparing diuretics, B-Blockers, NSAIDs, Trimethoprim (Septra)

and Non-prescription salt substitutes
 Renal Failure
 Cell death: Secondary to rhabdomyolisis, massive transfusion, crush or burn injuries.
 Acidosis: Consider Addisons crisis, primary adrenal insufficiency and DKA.

PEARL: If hyperkalemia cannot be explained by any other cause and the patient has
unexplained hypotension, draw a random cortisol and ACTH level and give 100 mg IV solucortef for
presumed adrenal insufficiency.

Medications in the Emergency Management of Hyperkalemia

Three main principles

1. Stabilize cardiac membrane

2. Shift potassium intracellularly
3. Eliminate potassium

There are specific treatments geared at targeting each of these three main principles, which we will
discuss below. Unfortunately, there is no clear evidence to guide exactly when to initiate specific
treatments for hyperkalemia. Our experts recommend using two factors to guide your management:

1. Serum potassium level and

2. ECG

with the following indications for immediate treatment of hyperkalemia in the ED:

Principle 1: Stabilize the cardiac membrane

There is no good literature to help guide whether calcium gluconate or calcium chloride is better for
stabilizing the cardiac membrane in hyperkalemia. The most important difference to remember is
that calcium chloride has 3 times more elemental calcium than calcium gluconate (6.8 mEq/10 mL vs
2.2 mEq/10 mL) and has greater bioavailability. However, calcium gluconate has less risk of local
tissue necrosis at the IV site. Therefore, if you decide to give calcium gluconate, ensure you are giving
sufficient doses of calcium since one amp may not be enough. Three amps of calcium gluconate
are often required to start to see the ECG changes of hyperkalemia resolve. Remember that
calcium does not lower the potassium level.

Our experts recommend using calcium chloride through a large well-flowing peripheral IV or central
line in the arrest or peri-arrest patient. Calcium gluconate is recommended for all other
patients given it’s lower risk for local tissue necrosis.

Routine use: 1 gram of 10% calcium gluconate (i.e. 10 ml mixed with 100cc of D5W or NS in a mini-
bag) over 5-10 minutes. Repeat as needed to achieve QRS <100ms and p waves re-appear.

Arrest or Pre-arrest: Push 1 amp (1 gram) of 10% calcium chloride through a large bore well-
running peripheral IV or central line (preferable). Repeat as needed to achieve QRS <100ms and p
waves re-appear.

In patients taking digoxin the traditional teaching is that calcium is contraindicated. The so-called
“stone heart” from the administration of calcium in patient with digoxin toxicity has been largely
debunked. A small case-controlled study found no mortality differences between 23 patients with
hyperkalemia and digitalis toxicity who were treated with calcium and 136 patients who were not.

If digoxin toxicity is suspected in the setting of severe hyperkalemia, our experts recommend giving
calcium cautiously, at a slower rate than usual: 1 gram of 10% calcium gluconate in 100 cc of D5W or
NS over 15-30 minutes (rather than 5 minutes).
Principle 2: Shifting potassium into cells:

The choices for shifting potassium into cells include intravenous insulin and glucose, beta-agonists
and bicarbonate. The indications for starting insulin and glucose include a K>5 mmol with ECG
changes or a K> 6.5 mmol regardless of ECG changes. Observational studies have shown that many
patients treated with insulin and glucose for hyperkalemia become hypoglycemic when given 1 amp
of D50W followed by 10 units of humulin R. Therefore, based on a recent systematic review our
experts recommend the following approach to initiating insulin and glucose therapy:

2 amps of D50W followed by 10 units IV humulin R (rapid injection)

Monitor glucose q30 minutes

Repeat K at 60 minutes

Beta agonists are also useful to rapidly shift potassium into cells. They act synergistically with
insulin and can lower serum potassium by 1.2 mmol in an hour. Paradoxically, one third of patients
will not have the predicted drop in serum potassium, and observational data has shown a very
transient initial rise in potassium up to 0.4 mmol after administration of beta agonists. Therefore, B-
agonists should NOT be used as mono-therapy and insulin/glucose be given first. The doses of beta
agonists for hyperkalemia are generally higher than what you would use in asthma:

Salbutamol 8 puffs by aerochamber or 20mg nebulized

Insulin and beta agonists will start to take effect within 15min with their peak effect being at 60min.

Pitfall: If B-agonists are given before insulin/glucose they may cause a transient rise in the
serum potassium level. Always give B-agonists after insulin/glucose.
Bicarbonate is also known to shift bicarbonate into cells. Our experts do not recommend the
routine use of bicarbonate in the treatment of hyperkalemia. It may have a role to play in a small
subset of patients who also have a non-anion gap metabolic acidosis such as those patients with renal
tubular acidosis.

Principle 3: Eliminate Potassium

The kidneys are the main route for eliminating of potassium. Ensuring euvolemia and appropriate
urine output is the mainstay of treatment. Inserting a foley catheter will allow you to monitor urine
output. Many patients will be hypovolemic and will need fluid resuscitation with crytalloid. If you
need to volume resuscitate your patient, the initial fluid of choice is Normal Saline even though with
huge doses hypercholoremic metabolic acidosis can occure. Ringer’s Lactate contains 4mmol/L of
potassium, which poses obvious risks of increasing serum potassium if appropriate renal
elimination has not started.

There is no role for diuretics in the routine management of hyperkalemia unless the patient is
hypervolemic.

Regarding potassium binding agents such as Kayexalate, a 2005 Cochrane review did not show any
evidence that they improve potassium levels. There have also been case reports of Kayexalate
causing GI necrosis and perforation. Our experts conclude that there is no role for Kayexalate in the
ED.

Consider PEG 3350 orally to help eliminate potassium through the GI tract if the patient is likely to
stay in your ED for a prolonged period of time.

Given that most patients with hyperkalemia will have some element of renal insufficiency it is
important to remember that milk of magnesia and fleet enemas are both contraindicated as they will
cause magnesium and phosphate toxicity, respectively.

Hyperkalemia in Cardiac Arrest

Based on the principles of treatment and indications discussed above, our experts recommend the
following approach to suspected hyperkalemia (based on patient history and rhythm strip) or
confirmed hyperkalemia (based on a point of care blood gas) in cardiac arrest in addition to usual
ACLS measures:

Push 1 amp calcium chloride in well running peripheral IV or central line and repeat until the
QRS is <100ms

Epinephrine 5-20 mcg q2-5 minutes (shifts K intracellularly)

Sodium Bicarbonate 1 amp IV (if suspect severe acidosis)

Bolus IV NS
 ↓

Shift potassium with Insulin and Glucose followed by B-agonist

Dialysis

Rebound Hyperkalemia

In cases of cardiac arrest due to hyperkalemia, perform CPR until the hyperkalemia is corrected. This
may be a much longer time than usual. When ROSC is achieved, it will be primarily due to the effects
of calcium rather than decreased potassium levels. The effect of calcium can last 20-30min. Since the
stabilizing effects of calcium will wear off, you must promptly work on shifting the potassium and
enhancing its elimination as described above. Consider repeating the calcium bolus if there are any
worsening ECG changes. Repeat serial potassium measurements to monitor for rebound
hyperkalemia, which occurs more often than we’d like.

PEARL: the patient in cardiac arrest with hyperkalemia should not be pronounced dead until their
potassium level is normalized

Intra-arrest Dialysis

In cardiac arrest, case reports have demonstrated successful ROSC and good neurologic outcomes
despite prolonged arrest when dialysis is initiated during CPR to correct hyperkalemia.

Future Directions in Emergency Management of Hyperkalemia

A new potassium binding drug, ZS-9 shows promise in the acute treatment of hyperkalemia and may
make it possible to avoid or postpone the most effective therapy, emergency hemodialysis.

For more on hyperkalemia on EM Cases:

Rapid Reviews Videos on Hyperkalemia
Best Case Ever 49 – Post-Arrest Hyperkalemia

Other FOAM Resources for Hyperkalemia:

Rebel EM on kayexalate and ECG changes in hyperkalemia

EMBasic on hyperkalemia

Life in the Fast Lane on hyperkalemia management

Academic Life in EM on preventing hypoglycemia from insulin in hyperkalemia

First10EM on initial management of hyperkalemia

Dr. Smith’s ECG blog on ECG changes with hyperkalemia

Dr. Etchelles, Dr. Bailel, Dr. Helman & Dr. Kilian have no conflicts of interest to declare.

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