November 2016

Evidence-Based Management Volume 18, Number 11

Of Potassium Disorders In The

Authors

John Ashurst, DO, MSc

Director of Emergency Medicine Residency Research, Duke Lifepoint

Emergency Department Conemaugh Memorial Medical Center, Johnstown, PA

Shane R. Sergent, DO
Department of Emergency Medicine, Conemaugh Memorial Hospital,
Johnstown, PA
Abstract
Benjamin J. Wagner, DO
Department of Emergency Medicine, Conemaugh Memorial Hospital,
Hypokalemia and hyperkalemia are the most common elec- Johnstown, PA
trolyte disorders managed in the emergency department. The Peer Reviewers
diagnosis of these potentially life-threatening disorders is chal- Camiron L. Pfennig, MD, MHPE
lenging due to the often vague symptomatology a patient may Associate Professor of Emergency Medicine, University of South Carolina
express, and treatment options may be based upon very little School of Medicine; Emergency Medicine Residency Program Director,
Greenville Health System, Greenville, SC
data due to the time it may take for laboratory values to return.
Corey M. Slovis, MD, FACP, FACEP
This review examines the most current evidence with regard to Professor and Chair, Department of Emergency Medicine, Vanderbilt
the pathophysiology, diagnosis, and management of potassium University Medical Center, Nashville, TN
disorders. In this review, classic paradigms, such as the use of CME Objectives

sodium polystyrene and the routine measurement of serum Upon completion of this article, you should be able to:
magnesium, are tested, and an algorithm for the treatment of 1. Identify the etiology of the depletion of potassium in patients with
hypokalemia.
potassium disorders is discussed.
2. Identify and manage the etiology and underlying causes of hyperkalemia.
3. Describe the algorithmic management of hypokalemia and
hyperkalemia.
Prior to beginning this activity, see Physician CME Information
on the back page.

Editor-In-Chief Daniel J. Egan, MD Eric Legome, MD Robert Schiller, MD International Editors

Andy Jagoda, MD, FACEP
Professor and Chair, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, Medical
Director, Mount Sinai Hospital, New
York, NY
Associate Editor-In-Chief
Kaushal Shah, MD, FACEP
Associate Professor, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY
Editorial Board
Saadia Akhtar, MD
Associate Professor, Department of
Emergency Medicine, Associate Dean Steven A. Godwin, MD, FACEP
for Graduate Medical Education,
Program Director, Emergency
Medicine Residency, Mount Sinai
Beth Israel, New York, NY
William J. Brady, MD
Professor of Emergency Medicine
and Medicine; Chair, Medical
Emergency Response Committee;
Medical Director, Emergency
Management, University of Virginia
Medical Center, Charlottesville, VA
Calvin A. Brown III, MD
Director of Physician Compliance,
Credentialing and Urgent Care
Services, Department of Emergency
Medicine, Brigham and Women's
Hospital, Boston, MA
Peter DeBlieux, MD Alfred Sacchetti, MD, FACEP
Professor of Clinical Medicine,
Interim Public Hospital Director
of Emergency Medicine Services,
Louisiana State University Health
Science Center, New Orleans, LA
Associate Professor, Department
of Emergency Medicine, Program
Director, Emergency Medicine
Residency, Mount Sinai St. Luke's
Roosevelt, New York, NY
Nicholas Genes, MD, PhD
Assistant Professor, Department of
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY
Michael A. Gibbs, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Carolinas
Medical Center, University of North
Carolina School of Medicine, Chapel
Hill, NC
Professor and Chair, Department
of Emergency Medicine, Assistant
Dean, Simulation Education,
University of Florida COM-
Jacksonville, Jacksonville, FL
Gregory L. Henry, MD, FACEP
Clinical Professor, Department of
Emergency Medicine, University
of Michigan Medical School; CEO,
Medical Practice Risk Assessment,
Inc., Ann Arbor, MI
John M. Howell, MD, FACEP
Clinical Professor of Emergency
Medicine, George Washington
University, Washington, DC; Director
of Academic Affairs, Best Practices,
Inc, Inova Fairfax Hospital, Falls
Church, VA
Shkelzen Hoxhaj, MD, MPH, MBA
Chief of Emergency Medicine, Baylor
College of Medicine, Houston, TX
Chief of Emergency Medicine,
Kings County Hospital; Professor of Beth Israel Medical Center; Senior
Clinical Emergency Medicine, SUNY
Downstate College of Medicine,
Brooklyn, NY
Keith A. Marill, MD
Research Faculty, Department of Chair, Department
Emergency Medicine, University
of Pittsburgh Medical Center,
Pittsburgh, PA
Charles V. Pollack Jr., MA, MD,
FACEP
Professor and Senior Advisor for
Interdisciplinary Research and
Clinical Trials, Department of
Emergency Medicine, Sidney Kimmel
Medical College of Thomas Jefferson
University, Philadelphia, PA
Michael S. Radeos, MD, MPH
Associate Professor of Emergency
Medicine, Weill Medical College
of Cornell University, New York; Associate Professor of Emergency
Research Director, Department of
Emergency Medicine, New York
Hospital Queens, Flushing, NY
Ali S. Raja, MD, MBA, MPH
Vice-Chair, Emergency Medicine,
Massachusetts General Hospital,
Boston, MA
Robert L. Rogers, MD, FACEP,
FAAEM, FACP
Assistant Professor of Emergency
Medicine, The University of
Maryland School of Medicine,
Baltimore, MD
Assistant Clinical Professor,
Department of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA
Chair, Department of Family Medicine,
Peter Cameron, MD
Academic Director, The Alfred
Faculty, Family Medicine and
Emergency and Trauma Centre,
Community Health, Icahn School of
Monash University, Melbourne,
Medicine at Mount Sinai, New York, NY
Australia
Scott Silvers, MD, FACEP
of Emergency Giorgio Carbone, MD
Medicine, Mayo Clinic, Jacksonville, FL Chief, Department of Emergency
Medicine Ospedale Gradenigo,
Corey M. Slovis, MD, FACP, FACEP Torino, Italy
Professor and Chair, Department
Suzanne Y.G. Peeters, MD
of Emergency Medicine, Vanderbilt
Emergency Medicine Residency
University Medical Center, Nashville, TN
Director, Haga Teaching Hospital,
Ron M. Walls, MD The Hague, The Netherlands
Professor and Chair, Department of
Hugo Peralta, MD
Emergency Medicine, Brigham and
Chair of Emergency Services, Hospital
Women's Hospital, Harvard Medical
Italiano, Buenos Aires, Argentina
School, Boston, MA
Dhanadol Rojanasarntikul, MD
Critical Care Editors Attending Physician, Emergency
Medicine, King Chulalongkorn
William A. Knight IV, MD, FACEP Memorial Hospital, Thai Red Cross,
Thailand; Faculty of Medicine,
Medicine and Neurosurgery, Medical
Chulalongkorn University, Thailand
Director, EM Midlevel Provider
Program, Associate Medical Director, Stephen H. Thomas, MD, MPH
Neuroscience ICU, University of Professor & Chair, Emergency
Cincinnati, Cincinnati, OH Medicine, Hamad Medical Corp.,
Weill Cornell Medical College, Qatar;
Scott D. Weingart, MD, FCCM
Emergency Physician-in-Chief,
Associate Professor of Emergency
Hamad General Hospital, Doha, Qatar
Medicine, Director, Division of ED
Critical Care, Icahn School of Medicine Edin Zelihic, MD
at Mount Sinai, New York, NY Head, Department of Emergency
Medicine, Leopoldina Hospital,
Senior Research Editors Schweinfurt, Germany
James Damilini, PharmD, BCPS
Clinical Pharmacist, Emergency
Room, St. Josephs Hospital and
Medical Center, Phoenix, AZ
Joseph D. Toscano, MD
Chairman, Department of Emergency
Medicine, San Ramon Regional
Medical Center, San Ramon, CA
Case Presentations
An elderly woman presents with 4 days of generalized
weakness and fatigue secondary to diarrhea. On examina-
tion, she appears dehydrated. During your workup, you
find that she is in acute renal failure and is suffering from
hyperkalemia, with a serum potassium of 6.5 mEq/L. Her
ECG shows mild peaked T waves. During discussion with
the admitting physician, you are asked to give the patient
sodium polystyrene. You seem to recall some controversy
regarding this treatment and wonder if it is really indi-
cated for this patient.
Your next patient is a 24-year-old woman with diar-
rhea and vomiting. During your workup, you find that
she has hypokalemia, with a potassium level of 2.2 mEq/L,
an ECG with a prolonged QT interval, and a serum
magnesium of 1.9 mEq/L. The patients internist recom-
mends treatment with an antiemetic, oral potassium, and
discharge home. You wonder if this is the best manage-
ment plan.
Your third patient is a dialysis-dependent 56-year-old
man who presents with shortness of breath and weakness.
His serum potassium is 6.9 mEq/L, and there is evidence
of fluid overload on the chest radiograph. You contact re-
nal to arrange emergent dialysis and they recommend that
you administer a new potassium-binding agent and
discharge the patient for his regularly scheduled dialysis
appointment later in the day. You wonder what these new
agents are and whether best practice has recently changed
without your being aware of it.
Introduction
Potassium disorders are common and potentially
deadly, which makes early recognition and treatment
fundamental to quality emergency care. The symp-
toms that a patient may experience with these disor-
ders are typically vague and difficult to distinguish.
The emergency clinician must have a heightened
index of suspicion and a low threshold for testing
and treating. Recent literature has questioned several
age-old practices and has challenged the emergency
clinician to assess new practice paradigms, includ-
ing the routine ordering of serum magnesium levels
in patients with hypokalemia, redrawing potassium
levels in a hemolyzed sample, proper blood-drawing
techniques, and the utility of sodium polystyrene
sulfonate and bicarbonate in the treatment of acute
hyperkalemia. This issue of Emergency Medicine
Practice provides a systematic review of the newest
evidence regarding the pathophysiology, diagnosis,
and management of potassium-related emergencies.
Critical Appraisal Of The Literature
A MEDLINE search for randomized controlled tri-
als since 2010 was conducted using the search terms
hyperkalemia and hypokalemia. MEDLINE was also
Copyright 2016 EB Medicine. All rights reserved. 2
queried using the terms hyperkalemia and hypokalemia
and therapy or treatment in order to identify studies
that have not yet reached the randomized controlled
trial phase. A total of 281 articles were identified and
reviewed, with 118 being for hyperkalemia and 163
articles for hypokalemia. The literature reviewed
had numerous large retrospective studies but very
few randomized controlled trials for either hyperka-
lemia or hypokalemia. Moreover, very few articles
reviewed dealt with new management strategies
of these disease processes. The National Guideline
Clearinghouse (www.guideline.gov) was searched
and no recommendations for the treatment of hyper-
kalemia or hypokalemia were found. The Cochrane
Database of Systematic Reviews was also queried.
No reviews have been published for hypokalemia; a
review was published in 2009 for hyperkalemia, but
it has not been updated.
Pathophysiology Of Potassium Regulation
Potassium is the most abundant ion in the body,
with about 98% of it located intracellularly. Cellular
potassium levels range between 140 and 150 mmol/L,
while the extracellular fluid potassium concentration
ranges between 3.5 and 5 mmol/L. The cellular gradi-
ent of potassium is maintained by the sodium-po-
tassium adenosine triphosphatase (Na+/K+-ATPase)
pump in the cell membrane, which actively transports
potassium into and sodium out of the cell.1 The large
potassium gradient between the intracellular and
extracellular compartments is fundamental to several
vital cellular functions, including the excitability of
nerves and muscle, cardiac pacemaker activity, and
the resting cell membrane potential.
Various mechanisms promote the movement of
potassium both into and out of the cell. The bodys
primary mechanism of transcellular potassium shift
is through the upregulation or downregulation of
Na+/K+-ATPase activity. A postprandial release of
insulin stimulates the insertion of the glucose trans-
porter protein 4 (GLUT 4), which causes an upregu-
lation of the Na+/K+-ATPase activity. This increased
activity allows potassium from the extracellular
space to enter the intracellular space.
Magnesium also plays a crucial role in the man-
agement of potassium regulation. Homeostasis is
managed primarily by intestinal diet absorption, re-
nal reabsorption, and excretion. A total of 60% of all
magnesium is stored in bone, with only 2% available
in the extracellular fluid. A magnesium deficiency
causes impairment of the Na+/K+-ATPase pump
and thus decreases cellular uptake of potassium.1
The increase in extracellular potassium signals the
kidney to excrete an increased amount of potassium
through aldosterone secretion, which can lead to
refractory hypokalemia. A second mechanism for the
role of magnesium in the regulation of potassium
Reprints: www.ebmedicine.net/empissues
lies within activation of the renal outer medullary
potassium (ROMK) channel. Magnesium binds to
the ROMK channel and prevents the efflux of potas-
sium out of the cell and prevents hypokalemia.1
Catecholamines can also cause changes in potas-
sium uptake and removal from the cell. Alpha ad-
renergic receptors impair the transport of potassium
intracellularly while an upregulation of beta recep-
tors stimulates Na+/K+-ATPase activity. Additional
acute potassium shifts occur most often secondary to
disruption of the acid/base state. As pH changes (eg,
secondary to hyperventilation or a decrease in partial
pressure of carbon dioxide [PCO2]), potassium will
adjust at about 0.1 to 0.3 mEq/L for each 0.1 pH unit
change. Sudden changes in potassium homeostasis
secondary to acid-base changes are very complicated
and dependent on the underlying cause.
Homeostasis of potassium is mainly regulated
through excretion by the kidney, which accounts for
80% of the daily potassium loss. A total of 15% of
potassium excretion occurs through the gastrointes-
tinal system, except for patients with end-stage renal
disease, and the remaining is excreted through sweat
loss. In patients with end-stage renal disease, up to
25% of daily potassium excretion can occur through
the gut secondary to an upregulation of high-con-
ductance calcium-sensitive potassium channels.
Etiologies Of Hypokalemia
Hypokalemia is a condition referring to the deple-
tion of serum potassium < 3.5 mEq/L, and is char-
acterized as being either mild, moderate, or severe.2
(See Table 1.) Hypokalemia is one of the most
common electrolyte abnormalities, with a preva-
lence of up to 21% in hospitalized patients.3-5 In an
observational cohort study of almost 12,000 patients,
hypokalemia was associated with increased mortal-
ity in patients admitted without severe heart or renal
disease.6 Although excessive loss is the most com-
mon etiology for hypokalemia, inadequate potas-
sium intake and transcellular shifts of potassium can
also be causes of hypokalemia. (See Table 2.)
Inadequate Intake
Inadequate potassium intake is defined as intake of
< 1 gram of potassium per day.2 The condition is rare,
because in otherwise healthy patients, the kidneys are
able to compensate for decreased intake by decreas-
ing potassium excretion to < 15 mEq/L per day. This
Table 1. Severity Classifications Of
Hypokalemia And Hyperkalemia
Condition Mild Moderate Severe
(mEq/L) (mEq/L) (mEq/L)
Hypokalemia 3.0-3.5 2.5-2.9 < 2.5
Hyperkalemia 5.5-6.4 6.5-7.5 > 7.5
November 2016 www.ebmedicine.net
response sustains total body stores for 2 to 3 weeks
before levels fall < 3 mEq/L. However, alcoholics and
patients in a chronically malnourished state are most
likely to have inadequate intake and develop symp-
tomatic hypokalemia.
Renal Loss
The most common site of potassium loss occurs
in the renal system, which can account for a 5 to
10 mEq loss per day.7 The renal tubules are able to
reabsorb about 90% of the potassium that is excret-
ed. Most losses are secondary to increased urinary
flow or increased sodium delivery to the distal
nephron. This phenomenon commonly occurs from
drug-related involvement, as seen with diuretics.
Diuretic-induced hypokalemia is usually mild, and
it is dose-dependent. Thiazide and loop diuretics
increase sodium and chloride to the distal collecting
duct, and this influx increases potassium excretion.
A recent study of over 33,000 patients demonstrated
that 13% of patients taking low-to-moderate doses of
diuretics had hypokalemia.8
While any medication or substance that affects
renal function can induce hypokalemia, there are
several that the emergency clinician should be par-
ticularly aware of. Antibiotics (such as penicillin or
penicillin derivatives) increase sodium activity and,
thus, potassium excretion.9 Antineoplastic medica-
tions can cause acute and chronic renal insufficiency,
resulting in potassium wasting and a wide spectrum
of associated electrolyte disturbances. Cisplatin, an
antineoplastic agent used to treat solid tumors, is
known to cause hypokalemia, hypomagnesemia,
hypercalciuria, and metabolic acidosis through the
mutation of the thiazide-sensitive Na-Cl cotrans-
porter gene in the distal convoluted tubule.10
Genetic disorders are another important cause
of hypokalemia secondary to abnormal renal losses.
Bartter syndrome is classified as a dysfunction of the
sodium reabsorption in the ascending limb of the
loop of Henle that causes a hypokalemic metabolic
Table 2. Common Causes Of Hypokalemia
Inadequate Intake
Eating disorders
Alcoholism
Renal Loss
Diuretics
Increased mineralocorticoid activity
Hypomagnesemia
Genetic
Gastrointestinal Loss
Vomiting
Diarrhea
Increased output from an ostomy
Nasogastric drainage
3 Copyright 2016 EB Medicine. All rights reserved.
acidosis with renal salt wasting. Gitelman syndrome
also causes hypokalemia, but through a defect in the
distal convoluted tubule.
Gastrointestinal Loss
Gastrointestinal loss is another common cause of
potassium loss, accounting for about 15% of potas-
sium that is excreted via stool. Normal excretion
from stool is a fraction of normal total loss, at about
10 mEq daily.7 In pathologically induced states (such
as in diarrhea and vomiting), this loss occurs at an
accelerated rate. After a prolonged period of diar-
rhea and vomiting, dehydration further induces
hypokalemia, either through secondary hyperal-
dosteronism or an alkalosis-related increase in the
filtered bicarbonate load. This increased load of
bicarbonate exceeds the reabsorptive capacity of the
proximal tubule and allows increased distal nephron
potassium excretion.
Sweat Loss
Sweat accounts for 5% of total daily loss of potas-
sium, and contains a potassium concentration of
5 to 8 mmol/L.11
Etiologies Of Hyperkalemia
Hyperkalemia is classified as mild, moderate, or
severe, depending on the serum potassium level.12
(See Table 1, page 3.) In the general population,
hyperkalemia has been found in 2.6% to 3.2% of pa-
tients studied, but in patients with chronic kidney
disease, its occurrence is between 7.7% and 73%.13-
15
A retrospective chart review of almost 250,000
patients with chronic kidney disease found that a
single episode of hyperkalemia increased the risk of
mortality within 1 day of the event being found.16
Based upon this risk, the emergency clinician
should prioritize diagnostic testing, intervene at an
early stage of the patients workup, and maintain a
low threshold for admission.
Pseudohyperkalemia
Approximately 70% of clinical decisions are based
upon laboratory values, with potassium being one
of the 10 most tested analytes in the United States.17
Although laboratory errors can occur during the
analysis of a substance, the majority of errors occur
before the sample is analyzed. Pseudohyperkalemia
or factitious hyperkalemia is a false elevation in
the serum potassium levels. Mechanical factors are
some of the most common causes of pseudohyper-
kalemia. A tourniquet applied for periods greater
than 1 minute causes an altered water balance that
results in hemoconcentration and hemolysis of cells.
Patients should be discouraged from fist clenching
during the collection phase due to a local release
of potassium from the forearm muscle. In a quality
Copyright 2016 EB Medicine. All rights reserved. 4
improvement study of almost 245,000 patients, there
was a reduction of serum potassium levels by up to
26% after the cessation of fist clenching.18 In another
study, after implementation of proper phlebotomy
techniques, there was a reduction of unexplained
hyperkalemia by 13%.19 (See Table 3.) Other me-
chanical factors that can cause pseudohyperkalemia
include vigorous mixing, transport in pneumatic
tubes or unpadded canisters, traumatic phlebotomy,
and inappropriate needle diameter.
Mechanical factors are the most common causes
of pseudohyperkalemia, but patient factors can also
influence potassium levels. Patient fear can result
in hyperventilation, with an associated hyperkale-
mic response. Familial pseudohyperkalemia is an
autosomal dominant disorder that causes leakage of
potassium across the cell membrane when blood is
stored at room temperature.20 Both leukocytosis and
thrombocytosis have been linked to pseudohyper-
kalemia as well, though the exact mechanism is not
clearly understood at this time.
When pseudohyperkalemia is encountered, it
may be important to redraw the specimen. However,
new data from a study of 45 patients with suspected
pseudohyperkalemia show a negative predictive value
of 100% for hyperkalemia when there is a glomerular
filtration rate (GFR) > 60 mL/min/1.73 m2 and a nor-
mal electrocardiogram (ECG).21 Though larger studies
are needed to validate practice, we do not recommend
redrawing specimens in patients who have a normal
ECG and renal function and who do not have extenu-
ating circumstances, such as being on multiple medica-
tions known to increase potassium.
Impaired Excretion Of Potassium
Renal excretion of potassium is dependent upon
the rate of flow in the distal nephron, aldosterone,
and the secretory pathways of potassium. Hyper-
kalemia occurs when one or more of these systems
are impaired. Patients with renal failure, however,
can maintain near-normal potassium levels unless
their GFR decreases to < 15 mL/min/1.73 m2.
Table 3. Proper Phlebotomy Techniques To
Reduce Pseudohyperkalemia
Use the proper gauge of needle based upon the patients age
Decrease tourniquet time
Do not allow the patient to clench fist
Draw the sample swiftly and gently
Remove the tourniquet before withdrawing the needle from the
patient
Do not aggressively agitate the sample after collection
Pack the samples safely for transport
Adapted from WHO guidelines on Drawing Blood: Best Practices in
Phlebotomy. Geneva World Health Organization; 2010.
Reprints: www.ebmedicine.net/empissues
Medication-Induced Hyperkalemia Penicillin G contains 0.33 mmol of sodium and 1.7
Adverse drug reactions are common, with an esti- mmol of potassium per 1 million units.25 The admin-
mated 50 adverse drug reactions occurring for every istration of penicillin has also been linked to cardiac
1000 patient-years in the elderly.22 In hospitalized arrest secondary to hyperkalemia after the rapid
patients, medications were reported as the primary infusion of the medication.26
cause for hyperkalemia, with a rate of 35% to 75% of
all cases, often the result of impaired potassium ex- Medications That Affect Aldosterone Secretion
cretion.23 Medications that induce hyperkalemia are Angiotensin-converting enzyme (ACE) inhibitors
potassium-containing agents, drugs that affect aldo- block angiotensin II synthesis, which effectively
sterone secretion, drugs that cause tubular resistance decreases aldosterone secretion and impairs renal
to the action of aldosterone, and drugs that cause potassium secretion by reducing the GFR. Angioten-
transmembrane shifting of potassium. (See Table 4.) sin II receptor blockers (ARBs) competitively bind to
angiotensin II receptors, decreasing adrenal synthe-
Potassium-Containing Agents sis of aldosterone. These 2 medications contribute to
Hyperkalemia caused by potassium supplementa- 10% to 38% of all admissions secondary to hyperka-
tion is fairly rare in persons with normally function- lemia.27 In the outpatient setting, ACE inhibitors and
ing kidneys secondary to potassium adaptation. ARBs contribute to up to 10% of all hyperkalemia
Blood transfusions have the potential to cause hy- cases and account for as much as 6% of all hyperka-
perkalemia, and even cardiac arrest, in some cases. lemia in enrolled clinical trials.27
The supernatant of packed red blood cells contains Nonsteroidal anti-inflammatory drugs (NSAIDs)
60 mEq/L of potassium, and when it is stored, there indirectly inhibit the synthesis of aldosterone by
is a decrease in ATP synthesis that causes potassium inhibiting the production of renal prostaglandin.
to leak out of the cells.24 A prospective study of 125 Concurrent hyperkalemia was first related to indo-
patients demonstrated that when blood is stored for methacin in 1985.28 Since then, several other studies
more than 12 days, there is a more pronounced rise have attempted to correlate NSAID use with hyper-
in potassium in the recipient as compared to patients kalemia. Originally, COX-2 inhibitors were thought
who receive blood that is less than 12 days old.24 to cause more instances of hyperkalemia as com-
Penicillin is another medication that contains pared to nonselective NSAIDs, but new literature
potassium that may be unknown to the clinician. fails to demonstrate this.29,30
Hyperkalemia has also been described in pa-
tients who are being treated with heparin doses of
5000 units daily. The hyperkalemia from heparin is
Table 4. Medications That Can Cause related to not only inhibition of adrenal aldosterone
Hyperkalemia production in the zona glomerulosa, but also the
Medication Mechanism Causing final enzymatic step in aldosterone production.
Hyperkalemia
Packed red blood cells Potassium infusion Medications That Cause Tubular Resistance To The
Penicillin G Potassium infusion Action Of Aldosterone
Beta blockers Decrease beta 2-driven potas-
Trimethoprim, an antibiotic similar to the potassi-
sium uptake um-sparing diuretic amiloride, competitively inhib-
Succinylcholine Depolarizes cell membranes
its luminal sodium transport channels, causing a
reduction in negative luminal charge and decreased
Digoxin Decreases Na+/K+-ATPase
potassium secretion. Patients who take both high-
activity
dose and low-dose antimicrobial therapies are at
Spironolactone Aldosterone antagonism
risk for developing hyperkalemia and renal failure,
ACE inhibitors, ARBs Decrease aldosterone synthesis,
especially with concurrent use of an ACE inhibitor.31
renal blood flow, and glomeru-
When used in conjunction with spironolactone, there
lar filtration rate
is a 12-fold increase in the risk of hyperkalemia and
Nonsteroidal anti-inflammatory Decrease renin release, renal
a 2-fold increase in the risk of sudden cardiac death
drugs blood flow, and glomerular
as compared to amoxicillin.32-34
filtration rate
Heparin Decreases aldosterone syn-
Medications That Cause Transmembrane Shifting Of
thesis
Potassium
Trimethoprim Blocks luminal sodium channels
Nonselective beta blockers can cause hyperkalemia
Pentamidine Blocks luminal sodium channels by 2 separate pathways. Catecholamine-stimulated
renin release is inhibited by beta blockade and
Abbreviations: ACE, angiotensin-converting enzyme; ARBs, an-
causes a decrease in the amount of aldosterone
giotensin II receptor blockers; Na+/K+-ATPase, sodium-potassium
synthesis. To a greater extent, however, beta blockers
adenosine triphosphatase.
decrease the function of Na+/K+-ATPase by decreas-

November 2016 www.ebmedicine.net 5 Copyright 2016 EB Medicine. All rights reserved.

ing the amount of cyclic adenosine monophosphate
(cAMP) in the cells.
Differential Diagnosis
Both hypokalemia and hyperkalemia can present
with vague complaints, making the differential di-
agnosis expansive. Hypokalemia and hyperkalemia
should both be considered in the differential for any
patient presenting with generalized fatigue, weak-
ness, or even paralysis, along with other important
diagnoses including diabetic emergencies, myocar-
dial infarction, renal failure, viral illnesses, cere-
brovascular accidents, seizures, spinal shock, and
myasthenic crisis.
Prehospital Care
A potassium-related emergency is generally not
known by the prehospital provider, so management
defaults to stabilization and rapid transport. An
exception is the patient with known end-stage renal
disease, in which case hyperkalemia should be sus-
pected and transport to an emergency department
(ED) with access to onsite dialysis prioritized.
Intravenous access and cardiac monitoring
should be obtained in patients with a suspected po-
tassium derangement. An ECG should be obtained
in order to assess for signs of hyperkalemia or hy-
pokalemia. If signs of hyperkalemia or hypokalemia
are present, medical direction should be obtained
and Advanced Cardiac Life Support (ACLS) proto-
cols followed.
Emergency Department Evaluation
History
Hypokalemia can present with generalized weak-
ness, palpitations, or, rarely, paralysis.35 Data from a
review of 43,805 patients have shown that patients
with severe hypokalemia typically present with
weakness and myalgias.35 Hyperkalemia can also
present as generalized weakness, ascending paraly-
sis, palpitations, and paresthesias. More importantly,
the emergency clinician should ask questions tar-
geted at the underlying cause that may have led to a
potassium derangement, including history of kidney
failure, gastrointestinal complaints, and thyroid dis-
orders. A review of the patients medications should
be performed to determine whether any drug
interactions can be implicated. Previous records and
laboratory values should also be reviewed to assess
for a pattern of potassium derangement.
Physical Examination
Much like the vagueness that may be obtained dur-
ing a history, the same is true for the physical exami-
Copyright 2016 EB Medicine. All rights reserved. 6
nation of a patient with a potassium derangement.
The general appearance of the patient could vary
from a benign examination to a patient in extremis.
Vital signs will typically be within normal limits.
Intravascular volume status should be assessed in all
patients to determine perfusion status. Cardiovascu-
lar examination may reveal bradycardia or pauses.
Abdominal examination may reveal hypoactive
bowel sounds. An in-depth neurologic evaluation
should be conducted, which may reveal generalized
weakness or decreased deep tendon reflexes. Lastly,
the patient should be examined for the presence of
an arteriovenous fistula.
Diagnostic Studies
The majority of patients who experience a derange-
ment in potassium can be identified by a thorough
history, but in certain cases, the diagnosis may not
seem apparent. An ECG should be obtained imme-
diately if an electrolyte disorder is suspected, and
all patients should have a complete blood count and
basic metabolic profile.
When the cause of hypokalemia is not apparent
after a thorough history and physical examination, a
diagnostic approach aimed at testing for the regula-
tion of potassium excretion and the assessment of
the patients acid/base status should be completed.
A random urine potassium-to-creatinine ratio can
be obtained to better aid the emergency clinician in
diagnosing the cause of hypokalemia. When hypo-
kalemia is caused by transcellular potassium shift-
ing, gastrointestinal loss, or use of diuretics, the urine
potassium-to-creatinine ratio is usually < 13 mEq/g
creatinine. If the ratio is higher than this, renal potas-
sium wasting is a consideration. In a prospective study
of 43 patients, the potassium-to-creatinine ratio method
was able to correctly diagnosis patients with either
hypokalemic periodic paralysis versus a renal potas-
sium wasting disease.36 After the determination of a
patients urinary potassium excretion, a blood gas level
may be helpful for interpreting the results. (See Table
5, page 7.)
For the hyperkalemic patient, a decrease in
distal sodium delivery, mineralocorticoid deficiency,
or abnormal cortical collecting tubule function may
lead to the electrolyte abnormality. To determine the
cause of the hyperkalemia, the emergency clinician
should obtain urine sodium, potassium, and osmo-
lality as well as a serum osmolality. If the urine sodi-
um is > 25 mEq/L, then the transtubular potassium
gradient (TTKG) can be used to aid in determining
whether the hyperkalemia is due to a mineralocor-
ticoid deficiency. However, if the urine sodium con-
centration is < 25 mEq/L, the hyperkalemia should
be assumed to be as a result of a decrease in distal
flow, such as from acute kidney injury.
Reprints: www.ebmedicine.net/empissues
TTKG = [Potassiumurine/(Urineosmolality/Serumosmolality)]
/Potassiumserum
When the TTKG is < 6, the hyperkalemia is
most likely due to impaired aldosterone bioactivity
in the distal nephron, but when the TTKG > 6, the
hyperkalemia is most likely caused by potassium
overload or cellular shifting of potassium. If the
TTKG is < 6, the patient should be administered
0.05 mg of 9--fludrocortisone and have the TTKG
repeated in 4 hours. An increase in the TTKG to > 6
would suggest an aldosterone deficiency.
Electrocardiogram Findings In Hypokalemia
As serum potassium levels decline, the transmem-
brane gradient is decreased, causing prolongation
of the phase 3 repolarization and an increase in the
relative refractory periods of cardiac myocytes. The
ECG findings associated with hypokalemia can be
broken down into repolarization changes and con-
duction abnormalities.
The earliest repolarization changes seen in pa-
tients with hypokalemia are a decrease in the T-wave
amplitude, PR-interval prolongation, ST depression,
T-wave inversions, and eventual U-wave formation.
A U wave has been described as a positive deflec-
tion after the T wave that is best seen in the precor-
dial leads of V2 and V3. Patients with hypokalemia
also have an increased refractory period, an overall
increase in the action potential, and are therefore
at risk for cardiac dysrhythmias. Although there is
no threshold of QT prolongation at which torsades
de pointes is certain to occur, once the QT interval
becomes longer than 500 milliseconds, the risk of
torsades de pointes increases 2- to 3-fold.
In the Framingham Heart Study, potassium
levels were inversely related to the occurrence of
premature ventricular complexes (PVCs), and a
decrease of 0.48 mEq/L of potassium was associated
with a 27% greater chance of having PVCs.37 A more
recent retrospective review with 671 patients found
that even mild hypokalemia (mean 3.42, range 2.7-
3.6 mmol/L) increases the risk of PVCs and death.38
Not only have ectopic ventricular beats been noted
to occur in patients with hypokalemia, but also
abnormal atrial rhythms. Recently, atrial fibrillation
Table 5. Typical Causes Of Hypokalemia In Conjunction With Laboratory Testing
Cause of Hypokalemia Acidosis
Lower gastrointestinal losses
Diabetic ketoacidosis
Renal tubular acidosis
Surreptitious vomiting (bulimia)
Diuretic use
Vomiting
Gitelman or Bartter syndrome
November 2016 www.ebmedicine.net
has also been linked to hypokalemia. The Rotterdam
study showed that patients with hypokalemia (de-
fined as < 3.5 mEq/L) were more likely to develop
atrial fibrillation compared to patients with normo-
kalemia, after adjustment for potential confounders,
including serum magnesium concentrations.39
Electrocardiogram Findings In Hyperkalemia
Increased extracellular potassium causes an increase
in transmembrane permeability and influx of potas-
sium into the cells. With this influx of potassium,
there is a decrease in the magnitude of the resting
potential, a decrease in the velocity of phase 0 of the
action potential, and delayed conduction between the
myocytes. The effects of these changes are dependent
upon the tissue affected, with atrial myocardium be-
ing the most sensitive and the specialized tissue (SA
node and HIS bundle) being the least sensitive.
Based upon theory and experimental settings,
there is a correlation between potassium levels and
ECG changes. (See Figure 1, page 8.) As potassium
increases to 6.5 to 7.5 mEq/L, prolongation of the
QRS segment, loss of the P wave, and ectopic beats
can be seen. (See Figure 2, page 8.) When serum po-
tassium reaches a level > 7.5 mEq/L, the QRS pattern
may become a sine wave. (See Figure 3, page 9.)
However, numerous studies have shown that
an ECG alone is not sensitive for diagnosing hy-
perkalemia. A retrospective review demonstrated
that only 55% of patients with a potassium level
6.8 mEq/L had signs of hyperkalemia.40 Al-
though highly inaccurate, an ECG may be the only
tool that an emergency clinician can use to make a
rapid diagnosis. However, the lack of proficiency
by some physicians to recognize ECG findings
suggestive of hyperkalemia is concerning. In one
study, residents in cardiology missed the find-
ings of hyperkalemia in 81% of cases.41 In another
study, attending physicians who practiced emer-
gency medicine had a sensitivity of only 0.62 for
diagnosing moderate to severe hyperkalemia.42
Treatment Of Hypokalemia
The mainstay of treatment for hypokalemia is to
prevent life-threatening arrhythmias and address the
Alkalosis Potassium Wasting No Potassium Wasting
7 Copyright 2016 EB Medicine. All rights reserved.
underlying etiology. The management of hypokale-
mia begins with an in-depth review of the patients
medical record to assess for medications that may
cause potassium wasting, and a thorough history
to assess for any etiology that may cause hypokale-
mia. If medications are implicated as the reason for
hypokalemia, the need for the medication should be
reassessed and it should be discontinued, if possible.
Alternate treatment modalities, such as changing
a patient from a potassium-wasting diuretic for
hypertension to an ACE inhibitor or an ARB, should
be explored.
When serum potassium decreases by 0.3 mEq/L,
there is a 100 mEq/L reduction in total body potas-
sium. For patients with borderline or low-normal
potassium concentrations (3.5-4.0 mEq/L) an in-

Figure 1. Electrocardiogram With Peaked T Waves And PR Depression In Hyperkalemia

Image courtesy of Rob Cooney, MD.

Figure 2. Electrocardiogram With A Widened QRS In Hyperkalemia

Image courtesy of Rob Cooney, MD.

Copyright 2016 EB Medicine. All rights reserved. 8 Reprints: www.ebmedicine.net/empissues

crease in dietary potassium should be encouraged.43
In patients with hypertension, recent myocardial
infarction, or congestive heart failure, treatment with
potassium supplementation should be considered to
keep the serum potassium level at least 4.5 mEq/L.44
For patients with hypertension, Whelton et al found
that potassium replacement was associated with a
significant decrease in both systolic and diastolic
blood pressure.45
In asymptomatic patients with mild to moderate
hypokalemia, oral replacement therapy is recom-
mended. Potassium bicarbonate is preferred in the
patient with hypokalemia and metabolic acidosis,
while potassium phosphate is recommended in
patients with hypokalemia and hypophosphatemia.
Potassium chloride is the preferred method of potas-
sium replacement in all other patients.43 Patients
should be treated with 60 to 80 mEq per day, but
they may require up to 150 mEq per day if continued
potassium loss occurs.
In patients with severe hypokalemia or ECG
changes, an intravenous method of potassium
replacement should be initiated. However, close
cardiac monitoring must be used in order to moni-
tor for any arrhythmia that may develop. Consen-
sus guidelines recommend intravenous potassium
chloride at a rate of 10 to 20 mEq/h as safe.46 Rates
> 20 mEq/h are highly irritating to peripheral veins,
and a central vein should be used. A replacement of
20 mEq of intravenous potassium would raise serum
potassium by 0.2 mEq. After stabilization of the pa-
tient, oral potassium should be administered.
Approximately 50% of patients with hypokale-
mia also have concomitant magnesium deficiency,
and routine magnesium replacement should be
considered for patients with hypokalemia. A routine
serum magnesium level may not adequately reflect
the bodys total store of magnesium. Approximately
99% of the bodys total store of magnesium lies
intracellularly within the bones and muscles and
only 0.6% is ionized in the extracellular space. Thus,
a normal serum magnesium may grossly underesti-
mate a true body deficit of magnesium.
In symptomatic or severe hypomagnesemia
(< 0.5 mmol/L), intravenous magnesium sulfate
Figure 3. Electrocardiogram In Hyperkalemia Depicting A Sine Wave
Image courtesy of Rob Cooney, MD.
November 2016 www.ebmedicine.net
should be initiated at 0.5 g/h.47 Some patients may
require maintenance therapy, which can be achieved
with oral supplementation of magnesium oxide
(400 mg 2 or 3 times daily) or magnesium gluconate
(500 mg 2 or 3 times daily).47
Treatment Of Hyperkalemia
Patients with suspected or known hyperkalemia
need intravenous access, cardiac monitoring, and
fluid resuscitation. Treatment should be initiated
based upon the patients symptomatology, ECG
findings, and laboratory values. However, the abso-
lute potassium value for treatment should be seen as
arbitrary, and used in conjunction with the emergen-
cy clinicians clinical judgment. The overall goal for
the treatment of hyperkalemia should be to stabilize
the cardiac membrane to prevent life-threatening
dysrhythmias, to shift potassium from the extracel-
lular space into the cell, to enhance elimination, and
to treat the underlying cause of hyperkalemia. A Co-
chrane review of the literature from 2005, updated
in 2009, does not make specific recommendations for
the level to begin treatment, but does note that beta
agonists, insulin and glucose, and dialysis are all
acceptable means of treatment for acute hyperkale-
mia.48 (See Table 6, page 12.)
For patients who have received treatment for
hyperkalemia and who are boarding in the emer-
gency department for a prolonged period of time,
the emergency physician should continue to treat
the underlying cause for the patients hyperkalemia.
The emergency clinician should also be aware of the
rebound effects of potassium once the initial treat-
ment medications dissipate and should be cognizant
that repeat dosing may be needed.
Membrane Stabilization
Calcium directly stabilizes the cardiac membrane by
reducing the threshold potential of cardiac myocytes
and should be given to any patient with concern
for hyperkalemia with a wide QRS. Calcium recre-
ates the electrical gradient, but does not decrease
the amount of serum potassium. A Cochrane review
9 Copyright 2016 EB Medicine. All rights reserved.
 Clinical
Clinical Pathway ForPathway For Management
Emergency Of Hypokalemia
Department Management Of Multiple
Shocks In The Emergency Department

Patient presents with

suspected hypokalemia

Check serum potassium

Perform emergent ECG

Serum potassium 3.0 to 3.4 mEq/L Cardiac dysrhythmia Cardiac arrest

No symptoms
Nondiagnostic ECG

Administer potassium chloride orally Administer potassium chloride IV Commence Advanced

Discharge with recommendation 10-20 mEq/h (Class II) Cardiac Life Support
to increase dietary potassium and Administer magnesium sulfate
repeat potassium level (Class II) 1-2 grams IV over 1 h (Class II)
Consider oral magnesium sulfate

Administer potassium chloride

10 mEq IV over 5 min; repeat once
if needed (Class II)
Administer magnesium sulfate 1-2
grams IV push over 2 min (Class II)

Abbreviations: ECG, electrocardiogram; IV, intravenous; K, potassium.

Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I Class II Class III Indeterminate
Always acceptable, safe Safe, acceptable May be acceptable Continuing area of research
Definitely useful Probably useful Possibly useful No recommendations until further
Proven in both efficacy and effectiveness Considered optional or alternative treat- research
Level of Evidence: ments
Level of Evidence: Generally higher levels of evidence Level of Evidence:
One or more large prospective studies Nonrandomized or retrospective studies: Level of Evidence: Evidence not available
are present (with rare exceptions) historic, cohort, or case control studies Generally lower or intermediate levels Higher studies in progress
High-quality meta-analyses Less robust randomized controlled trials of evidence Results inconsistent, contradictory
Study results consistently positive and Results consistently positive Case series, animal studies, Results not compelling
compelling consensus panels
Occasionally positive results

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patients individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2016 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

Copyright 2016 EB Medicine. All rights reserved. 10 Reprints: www.ebmedicine.net/empissues

 Clinical Pathway For Management Of Hyperkalemia
Clinical Pathway For Management Of Hyperkalemia
In The Emergency Department

Patient presents with

suspected hyperkalemia

Check serum potassium

Perform emergent ECG

Mild to moderate hyperkalemia Severe hyperkalemia (serum potas-

(serum potassium 5.5 mEq/L to 7.5 Cardiac arrest
sium > 7.5 mEq/L)
mEq/L) ECG changes (peaked T waves in 2
Patient clinically stable; no ECG leads, absent P waves, broad QRS,
changes sine wave, bradycardia, ventricular
tachycardia)

Administer: Administer: Commence Advanced

IV fluid resuscitation
D50 25 gm IV with regular insulin
5-10 units IV
If serum potassium 6 mEq/L, give
calcium gluconate 1 gram IV
Albuterol 10-20 mg nebulized
Treat the underlying cause (Class I
and II)
IV fluid resuscitation
D50 25 gm IV with regular insulin
5-10 units IV
Calcium chloride 1 gram IV
Albuterol 10-20 mg, nebulized (Class
I and II)
If acidotic, consider sodium bicarbon-
ate 50-100 mEq IV
If end-stage renal disease, com-
mence emergent dialysis
Cardiac Life Support
Administer:
IV fluid resuscitation
Calcium chloride, 1 gram IV
D50 25 gm IV with regular insulin
5-10 units IV (Class I and II)
Sodium bicarbonate 50-100 mEq IV

Abbreviations: D50, dextrose 50%; ECG, electrocardiogram; IV, intravenous.

For Class of Evidence definitions, see page 10.

November 2016 www.ebmedicine.net 11 Copyright 2016 EB Medicine. All rights reserved.

recommends calcium as an adjunct therapy when
cardiac arrhythmias are present in a patient with
hyperkalemia, but no randomized controlled trials
support this recommendation.48
Calcium is available for injection as either cal-
cium gluconate or calcium chloride. A Cochrane re-
view recommends calcium chloride as the preferred
treatment agent in the setting of cardiac arrhythmia
due to a 3-fold difference in the calcium bioavailabil-
ity between the gluconate and chloride solutions.48
The onset of action of calcium occurs in < 3
minutes. The recommended dose is 1 gram (10 mL
of 10% solution) IV, given over 3 to 5 minutes, and it
can be repeated in 5 minutes if there is no change in
the patients ECG. The duration of the action of cal-
cium is 30 to 60 minutes, and during this time, other
interventions to lower the serum potassium should
be undertaken.
Transcellular Shift
The administration of dextrose and insulin stimu-
lates a transcellular shift of potassium extracellularly
to intracellularly. The effect of insulin on potassium
regulation is dose-dependent. Stimulation of the
NA-H antiporter on the cell membrane causes an
activation of the Na+/K+-ATPase channel and allows
the influx of extracellular potassium.
A Cochrane review recommends dextrose and
insulin as a means of treatment for acute hyperkale-
mia.48 An intravenous dose of 25 grams of dextrose
followed by 10 units of regular insulin is the rec-
ommended dosage. The dextrose should be given
before the insulin to avoid accidental iatrogenic
hypoglycemia.49 The onset of action of this treat-
Table 6. Interventions Used In The Treatment Of Hyperkalemia
Medication Dosage Onset
Calcium chloride, 1 gram IV over 5 min < 3 minutes
calcium gluconate
Sodium bicarbonate 50-100 mEq IV 5-10 minutes
Dextrose and insulin 25 grams dextrose and < 15 minutes
5-10 units regular
insulin IV
Albuterol 10-20 mg nebulized over 15-30 minutes
10 min
Sodium polystyrene 15 to 30 grams orally 2-24 hours
sulfonate
Dialysis N/A 1-2 minutes
after starting
treatment
Abbreviation: Na+/K+-ATPase, Sodium-potassium adenosine triphosphatase.
Copyright 2016 EB Medicine. All rights reserved. 12
ment modality is < 15 minutes, with peak onset 30 to
60 minutes following infusion.48 The total duration
of action ranges between 4 and 6 hours, and it can
lower serum potassium 0.6 mEq/L. When combined
with albuterol, a synergistic effect was reported by
Allon and Copkeney, and was found to be superior
to either treatment alone.50
Although a significant reduction in serum
potassium is evident by this treatment, it may be
complicated by hypoglycemia. Two recent studies
have shown that hypoglycemia occurs at differing
rates, but is most pronounced in patients with acute
kidney injury or end-stage renal disease.51,52 In these
retrospective chart reviews, the rate of hypoglycemia
ranged from 8.7% to 13% of patients treated with
this modality.51,52 In these patients, a protocol should
be initiated to monitor serum glucose for several
hours post treatment. A recent study by Chothia et
al demonstrated that a glucose-only bolus causes a
clinically significant decrease in potassium concentra-
tions in hemodialysis patients without the side effect
of hypoglycemia; however, the study contained only
10 patients.53 Further research in this area needs to be
conducted before this can become common practice.
Sodium bicarbonate has been classically taught
as a treatment for acute hyperkalemia. However, lit-
tle data exist on its efficacy as a treatment modality.
In the only randomized trial of sodium bicarbonate
for the treatment of acute hyperkalemia, the authors
found bicarbonate therapy did not lower the serum
concentration of potassium at 60 minutes.54 At this
time, a Cochrane review does not recommend the
routine usage of sodium bicarbonate as a mono-
therapy; however, sodium bicarbonate may be used
as an adjunctive therapy in patients with concurrent
Duration Therapeutic Effect/Comment
30-60 minutes No effect on serum potassium; stabilizes cardiac membrane.
Calcium chloride may cause significant tissue irritation and
necrosis (central line administration recommended).
Calcium gluconate may require 3 times the dosage of
calcium chloride.
2 hours Redistributes serum potassium.
Adjunctive therapy only if patient is acidotic.
4-6 hours Activates the Na+/K+-ATPase pump; no effect on total
body potassium.
Monitor blood glucose closely for up to next 1-3 hours.
2-3 hours Activates the Na+/K+-ATPase pump; no effect on total
body potassium.
Use as adjunctive therapy; caution with patients with
cardiovascular disease.
Variable Removes potassium via the gastrointestinal tract.
Unspecified Removes serum potassium and total body potassium.
Reprints: www.ebmedicine.net/empissues
metabolic acidosis and hyperkalemia.48
Beta-adrenergic receptor agonists induce the
upregulation of Na+/K+-ATPase activity through a
distinct pathway that is separate from that of insulin.
The typical dose needed to achieve this effect is 4
times the normal dose of albuterol that is typically
given in the ED. Serum potassium levels decrease by
0.6 mEq/L after inhalation of 10 mg of albuterol and
1.0 mEq/L after 20 mg is inhaled. With dosing at 20
mg, side effects are common; however, most centers
use 10 mg to 15 mg with no side effects.
Terbutaline, another beta-adrenergic receptor
agonist, has also been shown to lower serum potas-
sium levels. In a prospective trial of 14 patients with
chronic kidney disease on hemodialysis, terbuta-
line given 7 mcg/kg subcutaneously was found to
decrease serum potassium levels by 1.31 mEq/L.55
Given the relatively small number of patients in
the study and unknown absorption rates of subcu-
taneous injections, the authors cannot recommend
terbutaline for the emergent management of hyper-
kalemia at this time, but further research should be
conducted in this area.
Removal Of Potassium
Cation Exchange Resins
Historically, the only United States Food and Drug
Administration (FDA) medication approved to
treat hyperkalemia was the cation exchange resin
sodium polystyrene sulfonate (SPS). In the colon,
SPS exchanges sodium for potassium and binds
0.65 mmol/L of potassium in vivo. However, little
data in todays literature can support its use for the
emergent treatment of hyperkalemia. The landmark
study for SPS, published in 1961, found that there
was very little effect of SPS compared to sorbitol
alone in the treatment of hyperkalemia.56 A 2015
retrospective study of 138 patients found that oral
SPS therapy lowered serum potassium levels by
0.14 mmol/L more than the control group (patients
who did not receive SPS), but the authors ques-
tioned its true clinical significance, despite finding
statistical significance, because SPS failed to lower
potassium below the predetermined minimal clini-
cally important difference of 0.2 mmol/L.57
The onset of action of SPS occurs 2 hours post
ingestion, with the peak onset of action at 6 hours.57
This slow treatment effect provides little relief of
acute hyperkalemia in the acute setting. There is
also a risk associated with the use of SPS. In 2009,
the FDA issued a recommendation that sorbitol not
be added to SPS powder due to its association with
bowel necrosis. However, a recent systematic review
with 58 reported cases showed that SPS with or
without sorbitol was associated with bowel necro-
sis and one-third of these patients eventually died
due to gastrointestinal injury.58 Therefore, cation
exchange resins should not be used as an acute treat-
November 2016 www.ebmedicine.net
ment for hyperkalemia but may be used for sub-
acute treatment in select patient populations.
Although SPS has fallen out of favor, 2 new
cation exchange resins have been developed and are
currently undergoing testing for use in the treatment
of hyperkalemia. Sodium zirconium cyclosilicate
(ZS-9) is a cation exchanger that traps potassium in
the intestine and exchanges it for sodium and hydro-
gen.59 In phase 2 testing, a reduction of 0.92 mEq/L
of potassium was found after administration of ZS-9
in patients with stage 3 chronic kidney disease, as
compared to placebo, at 38 hours.60 In phase 3 testing,
ZS-9 was found to reduce serum potassium levels by
0.5 to 0.7 mmol/L, depending on the time variable
studied.61 The authors noted that after one 10-gram
dose, the mean serum potassium level decreased by
0.4 mmol/L at 1 hour and 0.6 mmol/L at 2 hours.61
The HARMONIZE trial (Effect of Sodium Zirconium
Cyclosilicate on Potassium Lowering for 28 Days
Among Outpatients With Hyperkalemia) also found
a reduction of 1.1 mEq/L of potassium at 48 hours
post ingestion, but a reduction of only 0.2 mEq/L at
1 hour.62 When studied in patients with heart failure
and hyperkalemia, ZS-9 lowered potassium and
maintained normokalemia during the study period of
28 days.63
Patiromer (Veltassa) is a novel cation exchange
resin that binds potassium in exchange for calcium in
the colon.64 In patients with chronic kidney disease
who were receiving renin-angiotensin-aldosterone
system therapy, a reduction of 1.01 mEq/L of potas-
sium was noted at 72 hours post ingestion.64 Other
studies, including PEARL-HF (Prevention of Hyper-
kalemia in Patients with Heart Failure using a novel
polymeric potassium binder, RLY5016),65 and AME-
THYST-DN (Effect of Patiromer on Serum Potassium
Level in Patients With Hyperkalemia and Diabetic
Kidney Disease) 66 have all shown the varying de-
grees of potassium reduction in select populations,
but they have not examined the acute phase. Adverse
reactions, including gastrointestinal symptoms,
hypokalemia, and hypomagnesemia have all been
reported in varying degrees.64,66 Despite these 2 novel
agents and their promise to lower potassium levels,
neither has been studied in the acute phase, and until
further studies elucidate their role in the treatment of
acute hyperkalemia, they cannot be recommended.
Dialysis
Dialysis is the only other form of definitive potas-
sium removal and should be considered in patients
with severe hyperkalemia or patients with moder-
ate hyperkalemia and end-stage renal disease. Two
studies have shown that the usage of low-potassium
or potassium-free dialysate is both safe and effec-
tive in lowering the serum potassium level, and, by
increasing the blood flow during dialysis, a greater
effect on potassium lowering is also noted.67,68
Although dialysis removes 1 mmol/L of se-
13 Copyright 2016 EB Medicine. All rights reserved.
rum potassium in the first hour and 2 mmol/L by
3 hours, a rebound of serum potassium can be seen
post dialysis. The magnitude of postdialysis serum
potassium rebound is proportional to the predialysis
serum potassium level, with 35% of the reduction
equated by 1 hour post treatment.68
Special Considerations
Rapid Sequence Intubation
Although controversial, many physicians are
concerned with succinylcholine-induced hyperka-
lemia. Succinylcholine results in skeletal muscle cell
depolarization, causing an intracellular potassium
efflux and subsequent neuromuscular blockade.
Recent literature found that this efflux results in
a mean potassium increase of 0.4 mEq/L, usually
occurring a few minutes after administering suc-
cinylcholine.69 Often, this increase is transient and
without clinical impact, but cases have described
sudden death following the administration of suc-
cinylcholine. Patients with upper or lower motor
neuron defects, prolonged chemical denervation,
direct muscle trauma (crush injury), thermal trauma,
disuse atrophy, and severe infection have all been
linked to an increased risk of hyperkalemia follow-
ing rapid sequence intubation with succinylcholine.
If there is a high clinical suspicion of hyperkalemia
either by history or from an ECG suggesting associ-
ated changes, alternative paralytics should be used
for rapid sequence intubation.
Genetic Disorders
Bartter syndrome, Gitelman syndrome, and Liddle
syndrome are all genetic disorders that can present
with hypokalemia early in life. Bartter syndrome is
caused by a dysfunction of sodium reabsorption in
the ascending limb of the loop of Henle. This causes
renal salt loss and a hypokalemic metabolic alkalo-
sis. Gitelman syndrome is caused by defects in the
distal convoluted tubule. In Gitelman syndrome,
patients present during adolescence with muscle
cramps and weakness and are found to have hypo-
magnesemia, hypokalemia, and metabolic alkalosis
on routine laboratory testing. Liddle syndrome is an
autosomal dominantly inherited disease that pres-
ents with hypertension and hypokalemia at a young
age, secondary to a decrease in renin activity and
aldosterone secretion. Acute management should be
aimed at correction of potassium based upon symp-
tomatology and serum values.
Myocardial Infarction
In patients with myocardial infarction, both hypoka-
lemia and hyperkalemia have been associated with
increased mortality. In a retrospective study of 468
patients, patients with hypokalemia were 4 times
more likely to have a malignant ventricular arrhyth-
Copyright 2016 EB Medicine. All rights reserved. 14
mia when compared to normokalemic patients who
had also suffered a myocardial infarction.70 Accord-
ing to Grodzinsky et al, patients with hyperkalemia
on admission for acute myocardial infarction also
had an increase in mortality. In this retrospective
review of 38,689 patients with acute myocardial
infarction, inhospital mortality exceeded 15% once
potassium was > 5.5 mEq/L, regardless of whether
or not the patient was dialysis dependent.71 Based
upon these studies, the emergency clinician should
aggressively treat patients with hypokalemia and
hyperkalemia in the setting of acute myocardial
infarction.
Digoxin Toxicity
The foxglove plant, Digitalis purpurea, was first
used by Sir William Withering in 1785 to treat heart
failure. The usage of digoxin has continued since
this time for heart failure treatment, but it has also
been associated with significant mortality. Digoxin is
considered a cardiac glycoside that reversibly inhib-
its the Na+/K+-ATPase pump, causing an increase in
intracellular sodium and a decrease in intracellular
potassium, leading to an increase in potassium in
the serum. In an acute toxicity, mortality correlates
with the degree of hyperkalemia. The first study
to correlate hyperkalemia with mortality during
digoxin toxicity noted that no patients with a potas-
sium level > 5.5 mEq/L survived, but patients with a
potassium level < 5 mEq/L survived.72 Due to these
findings, it has been accepted that patients with a
serum potassium level > 5 mEq/L should receive
digoxin-specific antibody fragments.
Although hyperkalemia is a major concern for the
emergency clinician when faced with digitalis toxic-
ity, the clinician should also be aware of the effects of
hypokalemia in association with the usage of digoxin.
In patients with hypokalemia, digoxin toxicity may
occur at normal serum concentration levels because
both potassium and digoxin competitively bind to
the Na+/K+-ATPase pump. In patients with hypo-
kalemia and digoxin toxicity, potassium should be
repleted cautiously, to selectively inhibit the binding
of digoxin to the Na+/K+-ATPase pump. All patients
receiving digoxin-specific antibody fragments should
have their potassium monitored closely due to the
rapid fluctuations in potassium that may occur, and
they should be admitted to a monitored bed.
Periodic Paralysis
Hypokalemic Periodic Paralysis
Hypokalemic periodic paralysis (HPP) is the most
common form of periodic paralysis, with an inci-
dence of 1 in 100,000.73 HPP is 4 times more common
in men than women, and in the majority of cases, it
is caused by a mutation in the gene that codes for
the alpha1-subunit of the dihydropyridine-sensitive
calcium channel in skeletal muscle. At this time, the
Reprints: www.ebmedicine.net/empissues
exact cause of potassium transport that leads to HPP
is unknown. Attacks occur in late childhood and are
provoked by stress, vigorous activity, or a high-car-
bohydrate meal.
During an attack, the patient may experience
hyporeflexia, generalized weakness that is more
profound in the proximal muscles as compared to
the distal, in the legs as compared to the arms, and
with preserved respiratory status. Cardiac dys-
rhythmias are uncommon during an attack despite
showing classic signs of hypokalemia on an ECG
tracing. Diagnosis is typically made by a family
history of similar episodes, but if presenting for the
first time, a complete workup for hypokalemia and
thyroid disorders should be initiated. Treatment
during an acute attack should commence only after
confirmation of hypokalemia. If the patient is able
to tolerate oral potassium replacement, 2 protocols
have been used. The first protocol recommends 30
mEq of potassium chloride every 30 minutes until
normalization of serum potassium. This method,
however, may overshoot the amount of potassium
needed and cause hyperkalemia.74 A second, more
conservative protocol recommends 10 mEq of
potassium chloride every hour until normalization
of the serum potassium.75 All patients with HPP
should be admitted to a monitored bed until serum
potassium levels normalize.
Hyperkalemic Periodic Paralysis
Hyperkalemic periodic paralysis (PP) is another
uncommon channelopathy that the emergency clini-
cian may face. PP is caused by SCN4A mutation that
causes sodium channels on skeletal muscle cells to
close slowly and undergo mytonia that eventually
leads to paralysis. During paralysis, potassium is
released from the cells into the extracellular matrix.
Attacks typically occur in the first decade of life and
may present as single-limb weakness. Episodes of
PP are typically more common than those associated
with HPP, but they last a shorter duration. Acute
attacks will usually not warrant treatment unless
cardiac dysrhythmias are present.
Andersen Syndrome
Andersen syndrome is characterized by the triad
of periodic paralysis, ventricular arrhythmias, and
dysmorphic body features in association with a pro-
longed QT interval. Typically manifesting in the first
or second decade of life, potassium levels may be
low, normal, or high during an attack. The majority
of cases are related to a mutation in the gene encod-
ing Kir2.1. Acute treatment should not be initiated
until laboratory values are obtained, due the varied
potassium levels during an attack. If treatment is ini-
tiated prior to laboratory values being obtained, the
emergency clinician should tailor treatment modali-
ties based upon the patient's ECG.
November 2016 www.ebmedicine.net
Controversies And Cutting Edge
The major controversy in the management of potas-
sium disorders lies in the usage of SPS for the treat-
ment of emergent hyperkalemia. SPS was designed
when dialysis was still in its infancy and physi-
cians had few options for treatment. The original
study conducted by Scherr et al was the first to use
a binding substance in an attempt to lower serum
potassium.56 In the study, 32 patients with renal
failure were enrolled to receive SPS and a low-cal-
orie diet. At the conclusion of the study, 30 patients
had a decrease or no increase in serum potassium
and 23 patients had a mean fall of potassium of at
least 0.4 mEq/L.56
Several confounding factors were present in the
study and perhaps overlooked by the FDA. Only 7
of the 32 patients from the study were truly hyper-
kalemic (potassium > 5 mEq/L), and 22% of the
enrolled participants were given other medications
that can also lower potassium (insulin and bicar-
bonate) at the same time.56 Oliguric patients (23)
were treated differently from patients with chronic
renal failure by receiving 20% dextrose and a high-
calorie diet, which can increase carbohydrate load
and may have increased natural insulin driving
potassium into the cells. Furthermore, no control
group was used in the study.56
The second study on SPS was also fraught with
errors. Flinn et al conducted a study where pa-
tients received SPS and sorbitol and a second group
received sorbitol alone.76 Both study groups were
provided a diet without potassium, and serum levels
were checked on day 0 and day 5. The SPS/sorbi-
tol group had a decrease of 1.4 mEq/L, while the
sorbitol-alone group had a decrease of 1.7 mEq/L.76
Based upon this study, it was found that sorbitol
alone can decrease potassium at a greater rate than
SPS/sorbitol; however, SPS alone was approved for
the management of hyperkalemia.
Neither the Scherr et al study nor the Flinn et al
study are relevant to the emergent management of
hyperkalemia in the ED. The primary endpoint of
the Scherr et al study was to determine the lowering
effects of SPS on potassium at 24 hours while the
Flinn study used 5 days as its time frame.56,76
Although SPS may not be warranted for the
treatment of emergent hyperkalemia in the modern
world, several circumstances exist where SPS is
indicated. During austere conditions of natural or
man-made disasters in which dialysis may not be
readily available, SPS can be used to treat hyperkale-
mia in the interim, as well as extending inter-dialysis
intervals for patients with end-stage renal disease.
Another instance in which SPS may be beneficial is
when there is a prolonged time to dialysis in pa-
tients who present to the ED. These patients should
undergo transcellular shifting of potassium, and, in
15 Copyright 2016 EB Medicine. All rights reserved.
 Risk Management Pitfalls For Potassium Emergencies
In The Emergency Department
1. Sure, the patient had hypokalemia, and I was
treating it with intravenous potassium, but I
didnt think she needed a monitor.
All patients receiving potassium via the
intravenous route should be on a cardiac
monitor both during and after infusion to assess
for dysrhythmias.
2. That end-stage renal disease patient is always
here with moderate hyperkalemia. I gave him
a dose of sodium polystyrene sulfate and sent
him to dialysis.
Emergent dialysis is the treatment of choice
for patients who are dialysis-dependent with
hyperkalemia. The binding resins have not been
proven to rapidly lower potassium levels in the
acute setting.
3. Although the patients potassium was
7.1 mEq/L, she had a normal ECG.
The ECG is unreliable in predicting which
patients with hyperkalemia will rapidly
decompensate and it should not be the sole
factor in initiating treatment.
4. The laboratory results were clearly due to
hemolysis, so I didnt treat the hyperkalemia.
Although new data have shown that not all
laboratory tests need to be redrawn, particularly
in patients with normal renal function and a
normal ECG, the clinical picture should guide
care. If you suspect renal failure with associated
hyperkalemia, then the patient should be treated
appropriately and tests redrawn.
5. The patients potassium was the low end of
normal after his myocardial infarction, and his
cardiac arrest was most likely secondary to his
underlying heart condition.
Hypokalemia has been associated with
ventricular fibrillation in myocardial infarction
patients and a serum potassium of at least 4.5
mEq/L should be maintained.
Copyright 2016 EB Medicine. All rights reserved. 16
6. The patient had moderate hyperkalemia with
ECG changes. I gave a dose of calcium and
admitted him to the internist. I cant believe he
coded when he got to the floor.
Calcium is a membrane stabilizer and is
cardioprotective for patients with hyperkalemia.
However, it does not lower the total serum
potassium, and other interventions must be
employed.
7. Sure, the child had some fatigue, but he
looked well. I sent him back to his pediatrician
for a further workup.
Genetic renal disorders of childhood can present
with vague complaints and warrant testing in
the ED, if suspected.
8. The patients potassium was 2.4 mEq/L, but
she was asymptomatic. I sent her home with
a prescription for oral potassium replacement
and a repeat basic metabolic panel in a week.
Severe hypokalemia warrants intravenous
potassium replacement and admission
for further stabilization, due to the risk of
arrhythmia.
9. I treated the patients hyperkalemia with
insulin and dextrose and sent him to the floor. I
am not sure why he was unresponsive when he
got there.
Patients treated with insulin and dextrose for
hyperkalemia should be placed on a glucose
monitoring protocol for several hours.
10. I gave the patient one of the new potassium-
binding resins for her hyperkalemia and sent
her home for follow-up with her primary care
physician.
Both sodium zirconium cyclosilicate and
patiromer have not been studied in the acute
management of hyperkalemia. The only proven
acute management strategy for potassium
removal is dialysis.
Reprints: www.ebmedicine.net/empissues
conjunction with nephrology, a decision should be
made whether potassium-binding agents may be of
use. More important, though, is that the emergency
clinician should understand the underlying etiol-
ogy for hyperkalemia and address it so that rebound
hyperkalemia does not occur.
Disposition
The etiology for a patients potassium derangement
should be identified and treated before a final dispo-
sition is made. Patients with mild hypokalemia and
without any ECG changes can be safely discharged
home with follow-up potassium testing to be com-
pleted within 1 week. They should be instructed to
increase their dietary potassium and to return to the
ED for any concerning symptoms. However, patients
with moderate or severe hypokalemia with or with-
out QT prolongation require admission to a moni-
tored bed for intravenous potassium replacement.
Patients with mild hyperkalemia can be safely
discharged if the underlying cause for their hyperka-
lemia is treated in the ED and a repeat serum potas-
sium level is within normal limits. Patients with per-
sistent hyperkalemia should be admitted, due to the
relatively high risk of mortality associated with this
electrolyte imbalance. Emergent treatment should be
aimed at transcellularly shifting potassium from the
extracellular fluid to the intracellular space, while
long-term management should be aimed at treating
the underlying cause of hyperkalemia. For patients
with end-stage renal disease and hyperkalemia,
emergent dialysis should be the emergency clini-
cians primary option for treatment.
Time- And Cost-Effective Strategies
It may not be necessary to repeat the serum po-
tassium blood draw if it is hemolyzed.
Risk Management Caveat: This practice has been
reported in the literature only once and is not
common practice. Khodorkovsky reported that,
if the serum potassium specimen is hemolyzed
but the patient has a normal ECG and a GFR >
60, then the negative predictive value for true
hyperkalemia was 100%.21 If laboratory tests
are to be repeated, it may be cheaper to check a
serum potassium only instead of another basic
metabolic panel.
If hyperkalemia is suspected, treatment should
begin without laboratory confirmation.
Risk Management Caveat: Based upon the history
and physical examination and a simple rhythm
strip, hyperkalemia can be inferred. Treatment
can begin with membrane stabilization until lab-
oratory tests confirm hyperkalemia. However,
one must be cognizant of other medications that
the patient may be taking, especially digoxin.
November 2016 www.ebmedicine.net
Knowing which medications can cause hypoka-
lemia and hyperkalemia may decrease undue
hospital admissions.
Knowing how certain medications interact with
others may decrease the amount of hypokalemia
and hyperkalemia.
Summary
Potassium disorders can be life-threatening, and
emergent management skills are necessary to pre-
vent deterioration. A heightened sense of awareness
for these disorders is needed due to the vagueness
of the symptomatology that a patient may present
with, and a stepwise, evidence-based approach to
the treatment of both hypokalemia and hyperka-
lemia is crucial. In all cases, the underlying cause
for either hypokalemia or hyperkalemia should be
identified and aggressively treated. For patients with
asymptomatic hypokalemia and a normal ECG, oral
replacement with potassium chloride is the treat-
ment of choice, but for patients with an abnormal
ECG or who are symptomatic, intravenous potassi-
um chloride and magnesium sulfate are indicated. In
a patient with mild hyperkalemia, interventions to
shift potassium transcellularly are indicated, while
in patients with moderate to severe hyperkalemia,
calcium for membrane stabilization is recommend-
ed. Potassium-binding agents are not recommended
for acute management in that they have relative
variability in their onset times; however, they may
have a role in the subacute phase of care, especially
in patients who do not have immediate access to
dialysis.
Case Conclusions
In the first case, you explained to the admitting physician
that treatment with IV fluids of the elderly patient with
weakness from diarrhea was currently underway, which
was targeting the underlying cause of dehydration. You al-
ready gave the patient calcium chloride 1 gram IV, dextrose
50% 25 grams IV plus regular insulin 10 units IV, and
nebulized albuterol 20 mg. You explained that the current
best-practice evidence supports emergent dialysis and does
not support the routine use of SPS because it may unneces-
sarily expose the patient to the risk of bowel necrosis.
For the young patient with diarrhea and vomiting,
outpatient management was inappropriate, given that the
patient had ECG changes associated with hypokalemia. You
began treatment with 20 mEq of potassium chloride IV,
40 mEq of potassium chloride orally, and started empiri-
cally with 2 grams IV magnesium sulfate. You discussed
with the internist your concern that her serum magnesium
levels could be unreliable due to only a small percentage
of ionized magnesium being found in the serum. Together,
you decided that taking the patient to an observation unit
was the best disposition location in this case.
17 Copyright 2016 EB Medicine. All rights reserved.
 For the dialysis-dependent patient with dyspnea
and weakness, you did a quick MEDLINE search and
learned that although both sodium zirconium cyclosilicate
and patiromer have shown promise as potassium-binding
agents, they have not been studied in acute hyperkalemia,
and the only definitive means of potassium removal is
through dialysis. You shared this with the renal consul-
tant, who agreed to admit him for dialysis.
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ficacy and safety of RLY5016, a polymeric potassium binder,
in a double blind placebo controlled study in patients with
chronic heart failure (the PEARL-HF) trial. Eur Heart J.
2011;32(7):820-828. (Prospective study; 105 patients)
66. Bakris GL, Pitt B, Weir MR, et al. Effect of patiromer on
serum potassium level in patients with hyperkalemia and
diabetic kidney disease: the AMETHYST-DN randomized
clinical trial. JAMA. 2015;314(2):151-160. (Prospective study;
306 patients)
67. Gutzeiller JP, Schneditz D, Huber AR, et al. Increasing blood
flow increases K+/V (urea) and potassium removal but fails
to improve phosphate removal. Clin Neph. 2003;59(2):103-
136. (Prospective crossover study; 13 patients)
68. Zehnder C, Gutzwiller JP, Huber AR, et al. Low potassium
19 Copyright 2016 EB Medicine. All rights reserved.
 and glucose free dialysis maintains urea but removes potas- 2. Which of the following medications does NOT
sium. Neph Dial Transplant. 2001;16(1):78-84. (Prospective cause hyperkalemia?
study; 12 patients)
69. Blaine A, Ract C, Leblanc P, et al. The limits of succinylcho-
a. Heparin
line for critically ill patients. Anesth Analg. 2012;115(4):873- b. Angiotensin-converting enzyme inhibitors
879. (Prospective observational study; 153 patients) c. Angiotensin receptor blockers
70. Su J, Fu X, Ma Y, et al. Additional predictive value of d. Cisplatin
serum potassium to thrombosis in myocardial infarction
risk score for early malignant ventricular arrhythmias in
patients with acute myocardial infarction. Am J Emerg Med.
3. Through which mechanism does trimethoprim
2012;30(7):1089-1094. (Retrospective study; 468 patients) cause hyperkalemia?
71. Grodzinsky A, Goyal A, Gosch K et al. Prevalence and a. It is a potassium-containing agent
prognosis of hyperkalemia in patients with acute myocardial b. It affects aldosterone secretion
infarction. Am J Med. 2016;129(8):858-865. (Retrospective c. It causes tubular resistance to the action of
study; 38,689 patients)
72. Bismuth C, Gaultier M, Conso F, et al. Hyperkalemia in acute
aldosterone
digitalis poisoning: prognostic significance and therapeutic d. It causes transmembrane shifting of
implications. Clin Toxicol. 1973;6(2):153-162. potassium
73. Fontaine B. Periodic paralysis. Adv Genet. 2008;63:3-23.
(Review) 4. Typically, what is the earliest ECG finding in
74. Venance SL,Cannon SC, Fialho D, et al. The primary periodic
paralyses: diagnosis, pathogenesis and treatment. Brain.
hyperkalemia?
2006;129(Pt 1):8-17. (Review) a. Peaked T waves
75. Lin SH, Lin YF, Chen DT, et al. Laboratory tests to determine b. Prolongation of the PR interval
the cause of hypokalemia and paralysis. Arch Intern Med. c. QRS widening
2004;164(14):1561-1566. (Prospective study; 43 patients) d. Sine wave formation
76. Flinn RB, Merrill JP, Welzant WR. Treatment of the oliguric
patient with a new sodium exchange resin and sorbitol; a
preliminary report. NEJM. 1961 Jan 19;264:111-115. (Prospec- 5. Post myocardial infarction, what level should
tive study; 16 patients) the clinician aim for the patients serum potas-
sium to be?
CME Questions a. 3.2 mEq/L
b. 3.6 mEq/L
c. 3.8 mEq/L
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serum?
a. Dialysis
b. Insulin and dextrose
c. Sodium bicarbonate
d. Albuterol

1. Which body systems allow for the most excre- 8. In which of the following situations should
tion of potassium? succinylcholine NOT be used for rapid se-
a. Renal and gastrointestinal quence intubation?
b. Gastrointestinal and integumentary a. Motor vehicle crash
c. Renal and integumentary b. Asthma
d. Pulmonary and renal c. Guillain-Barr syndrome
d. Myocardial infarction

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 Physician CME Information

Introducing Date of Original Release: November 1, 2016. Date of most recent review: October 10, 2016.
Termination date: November 1, 2019.
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Emergency Medicine Practice.... Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement.
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