Review
Hyperkalemia Revisited
Walter A. Parham, MD
Ali A. Mehdirad, MD, FACC
Kurt M. Biermann, BS
Carey S. Fredman, MD, FACC
Key words: Albuterol;
calcium; electrocardiog-
raphy; electrophysiology;
glucose; hemodialysis;
hyperkalemia; insulin; ion
exchange resins; potassium
toxicity; sodium bicarbonate
From: Divisions of
Cardiology (Drs. Fredman,
Mehdirad, Parham; and Mr.
Biermann) and Critical Care
Medicine (Dr. Parham),
Department of Internal
Medicine, St. Louis
University School of
Medicine and St. Johns
Mercy Medical Center,
St. Louis, Missouri 63110
Address for reprints:
Walter A. Parham, MD,
St. Louis University School
of Medicine, Department
of Internal Medicine,
Division of Cardiology,
3635 Vista Ave., FDT 13,
St. Louis, MO 63110
E-mail:
waparham1@hotmail.com
2006 by the Texas Heart
Institute, Houston
40 Hyperkalemia Revisited
Hyperkalemia is a common clinical condition that can induce deadly cardiac arrhythmias.
Electrocardiographic manifestations of hyperkalemia vary from the classic sine-wave
rhythm, which occurs in severe hyperkalemia, to nonspecific repolarization abnormali-
ties seen with mild elevations of serum potassium. We present a case of hyperkalemia,
initially diagnosed as ventricular tachycardia, to demonstrate how difficult hyperkalemia
can be to diagnose. An in-depth review of hyperkalemia is presented, examining the
electrophysiologic and electrocardiographic changes that occur as serum potassium lev-
els increase. The treatment for hyperkalemia is then discussed, with an emphasis on the
mechanisms by which each intervention lowers serum potassium levels. An extensive
literature review has been performed to present a comprehensive review of the causes
and treatment of hyperkalemia. (Tex Heart Inst J 2006;33:40-7)
yperkalemia is a common clinical condition that can induce deadly cardiac
H arrhythmias. Electrocardiographic manifestations of hyperkalemia vary
from the classic sine-wave rhythm, which occurs in severe hyperkalemia,
to nonspecific repolarization abnormalities seen with mild elevations of serum
potassium. Herein, we describe the clinical electrocardiographic abnormalities as-
sociated with hyperkalemia and present an in-depth review of the literature regard-
ing its treatment.
Case Report
A 69-year-old woman with end-stage renal disease experienced the sudden onset of
crampy abdominal pain and emesis several hours after a routine hemodialysis treat-
ment. Severe fatigue and dysphoria followed, which prompted her to summon
emergency medical personnel for assistance. She was taken to the local emergency
department, where she continued to have severe fatigue but denied chest pain, pal-
pitations, dyspnea, pre-syncopal symptoms, fever, or additional gastrointestinal
discomfort. The patients medications at the time of admission included omepra-
zole, glipizide, labetalol, doxepin, quinine, phenergan, lactulose, aspirin, and seve-
lamer. Her medical history included long-standing diabetes mellitus, hypertension,
and end-stage renal disease that had necessitated dialysis for the past 4 years.
Physical examination of the patient in the emergency department revealed a
woman with ashen skin who was in moderate distress. Her blood pressure was
141/87 mmHg with a pulse of 100 beats/min. She was breathing 32 times/min
with an oxygen saturation of 97% on 3 liters of oxygen via nasal cannula. On car-
diovascular examination, heart sounds were inaudible. Her lung fields were clear
to auscultation bilaterally, and results of the abdominal examination were normal.
The extremities were without cyanosis or edema. Neurologically, she was alert and
oriented, with diminished deep tendon reflexes.
Results of multiple 12-lead electrocardiograms revealed a wide QRS complex
rhythm with a rate of 70 to 100 beats/min and a QRS duration of 238 msec, which
led to a diagnosis of ventricular tachycardia (Fig. 1). The patient was subsequently
treated with a lidocaine bolus and infusion. Because her arrhythmia continued un-
abated, we initiated a procainamide infusion and discontinued the lidocaine. One
hour after admission, the patients serum potassium level was found to be at 10.0
mEq/L. The procainamide infusion was discontinued; and calcium, insulin, glu-
cose, and bicarbonate were given intravenously. She then underwent emergent dial-
ysis and her potassium level gradually returned to normal.
After dialysis, her electrocardiographic results returned to baseline, with a QRS
duration of 95 msec (compared with 238 msec at presentation; see Fig. 2), and her
cardiac enzymes were found to be within normal limits. A transthoracic echocar-
diogram revealed normal left ventricular systolic function, and she was discharged
Volume 33, Number 1, 2006

Fig. 1 Admission electrocardiogram.
Fig. 2 Electrocardiogram after the correction of hyperkalemia.
from the hospital in stable condition with no further
arrhythmias. The cause of her hyperkalemia was never
ascertained; however, it was postulated that there might
have been an inappropriate potassium concentration in
her dialysis fluid.
Discussion
Extracellular potassium concentration is normally
maintained between 4.0 and 4.5 mEq/L by a complex
interplay of potassium excretion and consumption.
Ninety-five percent of total body potassium is intra-
cellular; only 2% is extracellular. A 70-kg man, for
instance, has about 3,920 mEq of potassium in the
intracellular space but only 59 mEq in the extracellu-
lar space.1 Given that the total daily intake of potas-
sium from a normal diet can be up to 200 mEq, one
can see how precisely and quickly the body must be
able to respond to any given potassium load in order
to prevent severe hyperkalemia.
Total body potassium levels are regulated mostly by
the kidneys, with only 5% to 10% of ingested potassi-
um excreted in the feces.1 Renal excretion of potas-
sium is determined by the rate of potassium filtration
across the glomerular basement membrane and by the
rate of its secretion and resorption in the distal tubules
of the nephron. When increased intake of potassium
Texas Heart Institute Journal
overwhelms the ability of the kidneys to excrete po-
tassium, or when a decrease in renal function occurs,
hyperkalemia may result. Because there are often no
clinical signs or symptoms to suggest hyperkalemia,
clinicians must frequently rely on clinical information
(that is, a history of renal failure or the ingestion of
medications known to cause hyperkalemia), laborato-
ry data, and electrocardiographic changes to make the
diagnosis.
Hyperkalemia is a common cause of the cardiac ar-
rhythmias seen in clinical practice. The challenge in
managing hyperkalemia comes from the fact that it
can be difficult, if not impossible, to identify the con-
dition solely on the basis of electrocardiographic infor-
mation. Patients who present with hyperkalemia may
have a normal electrocardiogram or have changes that
are so subtle that physicians frequently have difficul-
ty attributing these changes to increased potassium
levels. In a study performed at the University of Pitts-
burgh Medical Center, only 46% of patients with po-
tassium levels greater than 6.0 mEq/L had electro-
cardiographic changes, and only 55% of patients with
potassium levels greater than 6.8 mEq/L had changes
consistent with hyperkalemia.2 In fact, there have been
several reports in the literature of patients who had
potassium levels greater than 7.5 mEq/L with no elec-
trocardiographic manifestations of hyperkalemia.3 - 5
Even when there is evidence of hyperkalemia on a pa-
tients electrocardiogram, physicians often miss the
diagnosis. Wrenn and colleagues6 designed a study to
determine the ability of physicians to predict the pres-
ence of hyperkalemia solely on the basis of their pa-
tients electrocardiograms. The physicians in this study
were able to predict hyperkalemia with a sensitivity of
35% to 43% and a specificity of 85% to 86%. This
small study further emphasizes how difficult hyper-
kalemia can be to diagnose. Nevertheless, hyperka-
lemia can manifest with classic electrocardiographic
changes that suggest its presence.
Effects of Hyperkalemia on
Impulse Production and Propagation
Potassium and sodium concentrations in the intracel-
lular and extracellular compartments play a vital role
in the electrophysiologic function of the myocardium.
Concentration gradients are established across the
myocyte membrane secondary to very high intracel-
lular potassium concentrations and a relative paucity
of potassium ions in the extracellular space. The op-
posite is true of sodium ions, which are abundant ex-
tracellularly and relatively few intracellularly. These
concentration gradients are maintained by sodium-
potassium adenosine triphosphatase (Na-K ATPase)
pumps on the cellular wall, which actively pump sodi-
um out of the myocyte and potassium inward. These
concentration gradients establish an electrical poten-
Hyperkalemia Revisited 41
tial across the cell membrane, leading to a resting
membrane potential of 90mV. The potassium gradi-
ent across the cellular membrane is the most impor-
tant factor in establishing this membrane potential;
therefore, any changes in extracellular potassium con-
centration may have profound effects upon myocyte
electrophysiologic function.7 For instance, as potassi-
um levels increase in the extracellular space, the mag-
nitude of the concentration gradient for potassium
across the myocyte diminishes, thus decreasing the
resting membrane potential (that is, 90 mV to 80
mV; see Fig. 3).
Phase 0 of the action potential occurs when voltage-
gated sodium channels open and sodium enters the
myocyte down its electrochemical gradient (Fig. 3).
The rate of rise of phase 0 of the action potential (Vmax)
is directly proportional to the value of the resting
membrane potential at the onset of phase 0.7-9 This is
because the membrane potential at the onset of depo-
larization determines the number of sodium channels
activated during depolarization, which in turn deter-
mines the magnitude of the inward sodium current
and the Vmax of the action potential. As illustrated in
Figure 4, Vmax is greatest when the resting membrane
potential at the onset of the action potential is approx-
imately 75 mV, and does not increase as the mem-
brane potential becomes more negative. Conversely,
as the resting membrane potential becomes less neg-
ative (that is, 70 mV), as in the setting of hyper-
kalemia (Fig. 3), the percentage of available sodium
channels decreases. This decrease leads to a decre-
ment in the inward sodium current and a concurrent
decrease in the Vmax; therefore, as the resting mem-
brane potential becomes less negative in hyperkale-
mia, Vmax decreases. This decrease in Vmax causes a slow-
ing of impulse conduction through the myocardium
Fig. 3 Illustration of a normal action potential (solid line) and
the action potential as seen in the setting of hyperkalemia
(interrupted line). The phases of the action potential are
labeled on the normal action potential. Note the decrease in
both the resting membrane potential and the rate of phase 0
of the action potential (Vmax) seen in hyperkalemia. Phase 2 and
3 of the action potential have a greater slope in the setting of
hyperkalemia compared with the normal action potential.
42 Hyperkalemia Revisited
Fig. 4 Curve relating Vmax to the resting membrane potential
at the onset of action potential. As the membrane potential
becomes less negative, as in the setting of hyperkalemia, the
Vmax decreases, leading to a depression of conduction through
the myocardium.
and a prolongation of membrane depolarization; as a
result, the QRS duration is prolonged.
As previously discussed, increasing the extracellular
potassium concentration results in a decrease in the
resting membrane potential (that is, from 90 mV to
80 mV). In turn, the threshold potential decreases
(that is, from 75 mV to 70 mV); this 5-mV de-
crease, however, is less than the decrease in resting po-
tential. Therefore, the difference between the resting
and threshold potentials decreases to approximately
10 mV (as opposed to 15 mV in a physiologic milieu).
As potassium levels increase further, the resting mem-
brane potential continues to become less negative,
and thus progressively decreases Vmax. The changes in
threshold potential now parallel the changes in resting
potential, and the difference between the two reaches
a constant value of approximately 15 mV. The de-
crease in Vmax levels causes a slowing of myocardial
conduction, manifested by progressive prolongation
of the P wave, PR interval, and QRS complex. In
summary, the early effect of mild hyperkalemia on
myocyte function is to increase myocyte excitability
by shifting the resting membrane potential to a less
negative value and thus closer to threshold potential;
but as potassium levels continue to rise, myocyte de-
pression occurs and Vmax continues to decrease.
Hyperkalemia also has profound effects upon phase
2 and phase 3 of the action potential. After the rapid
influx of sodium across the cell membrane in phase 0,
potassium ions leave the cell along its electrochemical
gradient, which is reflected in phase 1 of the action
potential. As the membrane potential reaches 40 to
45 mV during phase 0, calcium channels are stim-
ulated, allowing calcium to enter the myocyte. The
Volume 33, Number 1, 2006
maximum conductance of these channels occurs ap-
proximately 50 msec after the initiation of phase 0
and is reflected in phase 2 of the action potential.7
During phase 2, potassium efflux and calcium in-
flux offset one another so that the electrical charge
across the cell membrane remains the same, and the
so-called plateau phase of the action potential is cre-
ated (Fig. 3). During phase 3, the calcium channels
close, while the potassium channels continue to con-
duct potassium out of the cell; in this way, the elec-
tronegative membrane potential is restored.7 One of
the potassium currents (Ikr), located on the myocyte
cell membrane, is mostly responsible for the potas-
sium efflux seen during phases 2 and 3 of the cardiac
action potential.10 For reasons that are not well under-
stood, these Ikr currents are sensitive to extracellular
potassium levels, and as the potassium levels increase
in the extracellular space, potassium conductance
through these currents is increased so that more potas-
sium leaves the myocyte in any given time period.10
This leads to an increase in the slope of phases 2 and 3
of the action potential in patients with hyperkalemia
and therefore, to a shortening of the repolarization
time. This is thought to be the mechanism responsible
for some of the early electrocardiographic manifesta-
tions of hyperkalemia, such as ST-T segment depres-
sion, peaked T waves, and Q-T interval shortening.11,12
Surface Electrocardiogram
Manifestations of Hyperkalemia
In experimental models, there is a very orderly pro-
gression of electrocardiographic changes induced by
hyperkalemia.13,14 The earliest electrocardiographic
manifestation of hyperkalemia is the appearance of
narrow-based, peaked T waves. These T waves are of
relatively short duration, approximately 150 to 250
msec, which helps distinguish them from the broad-
based T waves typically seen in patients with myocar-
dial infarction or intracerebral accidents.7 Peaked T
waves are usually seen at potassium concentrations
greater than 5.5 mEq/L and are best seen in leads II,
III, and V2 through V4, but are present in only 22% of
patients with hyperkalemia.8,11,15 It may be that in-
creased myocyte excitability, shortening of the myo-
cyte action potential, and an increase in the slope of
phase 2 and 3 of the action potential account for the
T wave peaking seen in mild hyperkalemia.11
As serum potassium levels increase to greater than
6.5 mEq/L, the rate of phase 0 of the action potential
decreases, leading to a longer action potential and, in
turn, a widened QRS complex and prolonged PR in-
terval. Electrophysiologically, this appears as delayed
intraventricular and atrioventricular conduction.7,11 As
the intraventricular conduction delay worsens, the
QRS complex may take on the appearance of a left or
right bundle branch block configuration. A clue that
Texas Heart Institute Journal
these electrocardiographic changes are due to hyper-
kalemia, and not to bundle branch disease, is that in
hyperkalemia the conduction delay persists through-
out the QRS complex and not just in the initial or
terminal portions, as seen in left and right bundle
branch block, respectively.11,16 As potassium levels
reach 8 to 9 mEq/L, sinoatrial (SA) node activity may
stimulate the ventricles without evidence of atrial
activity, producing a sinoventricular rhythm. This
occurs because the SA node is less susceptible to the
effects of hyperkalemia and can continue to stimulate
the ventricles without evidence of atrial electrical ac-
tivity.11,17 The electrocardiographic manifestations of
continued SA node function in the absence of atrial
activity may be very similar to those of ventricular
tachycardia, given the absence of P waves and a wid-
ened QRS complex (Fig 1).
As the hyperkalemia worsens and the potassium lev-
els reach 10 mEq/L, sinoatrial conduction no longer
occurs, and passive junctional pacemakers take over
the electrical stimulation of the myocardium (acceler-
ated junctional rhythm).11,12,18 If hyperkalemia contin-
ues unabated, the QRS complex continues to widen
and eventually blends with the T wave, producing the
classic sine-wave electrocardiogram. Once this occurs,
ventricular fibrillation and asystole are imminent.
In addition to the previously mentioned arrhyth-
mias, many other electrocardiographic abnormalities
have been associated with hyperkalemia. In patients
with acutely elevated serum potassium levels, a pseu-
domyocardial infarction pattern has been reported to
appear as massive ST-T segment elevation develops
secondary to derangements in myocyte repolariza-
tion.19-23 Early stages of hyperkalemia may manifest
with only shortening of the PR and QT interval.8
Sinus tachycardia and bradycardia, idioventricular
rhythm, and 1st-, 2nd-, and 3rd-degree heart block
have all been described on the presenting electrocar-
diograms of patients with hyperkalemia.7 Given the
vast array of electrocardiographic manifestations of
hyperkalemia, the difficulty in consistently identify-
ing hyperkalemia on the basis of electrocardiographic
abnormalities, and the fact that the electrocardiogram
during hyperkalemia may progress from normal to
that of ventricular tachycardia and asystole precipi-
tously, physicians need to consider this diagnosis in
patients at risk.8
Causes of Hyperkalemia
Numerous causes of hyperkalemia are seen in clinical
practice. The most common are renal disease and the
ingestion of medications that predispose the patient
to hyperkalemia.2 Medications known to cause hyper-
kalemia include angiotensin-converting enzyme in-
hibitors, angiotensin-receptor blockers, penicillin G,
trimethoprim, spironolactone, succinylcholine, alter-
Hyperkalemia Revisited 43
native medicines, and heparin, to name just a few.24-30
In their study in a university setting, Acker and col-
leagues2 reported that 75% of all patients with severe
hyperkalemia had renal failure, and 67% were taking
a drug that predisposed them to hyperkalemia. Other
less common causes of hyperkalemia include massive
crushing injury with resultant muscle damage, large
burns, high-volume blood transfusions, human im-
munodeficiency virus infection, and tumor lysis syn-
drome.8,31-35 In many patients, the cause of hyperka-
lemia is multifactorial and never clearly defined.
Treatment of Hyperkalemia
Although hyperkalemia is one of the deadliest electro-
lyte abnormalities, it is also one of the most treatable.
As previously discussed, the diagnosis of hyperkalemia
can be difficult if one relies solely on electrocardio-
graphic criteria. Frequently, physicians must initiate
treatment for hyperkalemia on the basis of a patients
clinical scenario (such as a cardiac arrest occurring in a
chronic dialysis patient). More commonly, however,
the patient is treated when laboratory data become
available. Most authorities recommend treatment for
hyperkalemia when electrocardiographic changes are
present or when serum potassium levels are greater
than 6.5 mEq/L, regardless of the electrocardiogram.36,37
The treatment for hyperkalemia can be thought of in
3 distinct steps. First, antagonize the effects of hyper-
kalemia at the cellular level (membrane stabilization).
Second, decrease serum potassium levels by promoting
the influx of potassium into cells throughout the body.
Third, remove potassium from the body.
Membrane Stabilization. The initial treatment of
hyperkalemia should be the infusion of calcium. Cal-
cium antagonizes the effects of hyperkalemia at the
cellular level through 3 major mechanisms. First, in
the setting of hyperkalemia, the resting membrane po-
tential is shifted to a less negative value, that is, from
90 mV to 80 mV, which in turn moves the resting
membrane potential closer to the normal threshold
potential of 75 mV, resulting in increased myocyte
excitability. When calcium is given, the threshold po-
tential shifts to a less negative value (that is, from 75
mV to 65 mV), so that the initial difference between
the resting and threshold potentials of 15 mV can be
restored.38 For example, if a myocyte has a normal
resting membrane potential of 90 mV and a normal
threshold potential of 75 mV, then 15 mV of depo-
larization is required before reaching the threshold
potential. In the setting of hyperkalemia, the resting
membrane potential may change to a new level (that
is, 80 mV), so that now only 5 mV of depolarization
must occur before reaching the threshold potential of
75 mV. When calcium is given, the threshold poten-
tial becomes less negative (that is, it changes from 75
mV to 65 mV). Thus the difference between the hy-
44 Hyperkalemia Revisited
perkalemia-induced resting membrane potential of
80 mV and the calcium-induced threshold potential
of 65 is now back to 15 mV, and myocyte excitabili-
ty can return to normal.
Second, it has been shown in animal studies that in-
creasing levels of calcium shift the curve relating Vmax to
the resting membrane potential at the onset of action
potential upward and to the right (Fig. 5).9 Therefore,
at any given level of resting membrane potential, up to
approximately 75 mV, the Vmax is increased when high
calcium concentrations are present.39 This serves to re-
turn myocyte excitability back to normal in the setting
of hyperkalemia, where myocyte depolarization is de-
creased secondary to decreased rates of Vmax.
Finally, in cells with calcium-dependent action po-
tentials, such as SA and atrioventricular nodal cells,
and in cells in which the sodium current is depressed,
an increase in extracellular calcium concentration will
increase the magnitude of the calcium inward current
and the Vmax by increasing the electrochemical gra-
dient across the myocyte. This would be expected to
speed impulse propagation in such tissues, reversing
the myocyte depression seen with severe hyperkale-
mia.40
The effects of intravenous calcium occur within 1 to
3 minutes but last for only 30 to 60 minutes. There-
fore, further, more definitive treatment is needed to
lower serum potassium levels. Calcium gluconate is the
preferred preparation of intravenous calcium. The
dose should be 10 mL of a 10% calcium gluconate
solution infused over 2 to 3 minutes. Calcium chlo-
ride may also be used but provides about 3 times the
amount of calcium per 10-mL dose, so the dose needs
to be attenuated accordingly to avoid potential calci-
um toxicity.36 Because hypercalcemia can potentiate
Fig. 5 Curve relating Vmax to the resting membrane potential
under conditions of hyperkalemia (solid line) and in the setting
of increased calcium concentration (interrupted line). For any
given resting membrane potential, up to approximately 75
mV, increasing calcium levels lead to an increase in Vmax.
Volume 33, Number 1, 2006
digitalis toxicity, calcium should be used in patients
taking digitalis only if there is loss of P waves or a
widened QRS complex.8 In this situation, calcium glu-
conate should be diluted in 100 mL of D5W (dextrose
[5%] in water) and infused over 30 minutes.
Promotion of Potassium Influx into Cells. After the
administration of calcium, the next goal of treatment
is to shift potassium intracellularly. This is most fre-
quently done by giving insulin. Insulin stimulates the
Na-K ATPase pump, which moves potassium intra-
cellularly in exchange for sodium in a 2:3 ratio; this ef-
fect is independent of insulins effect on glucose.41 Ten
units of intravenous insulin is typically given, followed
by close monitoring of serum blood sugar. Fifty mL of
50% dextrose is frequently co-administered with insu-
lin in normoglycemic patients to prevent hypoglyce-
mia. If a patient is already hyperglycemic, supplemental
glucose is not needed. The effect of the insulin is seen
within 10 to 20 minutes of administration and can be
expected to decrease potassium levels by 0.6 to 1.0
mEq/L.36,42,43
Growing evidence suggests that there may be a role
for albuterol in the treatment of patients with severe
hyperkalemia. Catecholamines activate Na-K ATPase
pumps through 2 receptor stimulation in a manner
that is additive to the effect of insulin.36,44 In a study
by Montoliu and coworkers,41 0.5 mg of intravenous
albuterol was given to patients with hyperkalemia,
leading to a 1-mEq/L decrease in serum potassium
levels with minimal adverse effects.41 Because there are
no approved intravenous forms of agonists available
in the United States, studies have been performed to
determine whether nebulized agonists would have a
similar effect on serum potassium levels. One such
study found that albuterol, when given in very high
doses (1020 mg vs the normal 0.5 mg), decreased po-
tassium levels by 0.62 to 0.98 mEq/L.45 The onset of
action for inhaled albuterol was immediate and lasted
for 1 to 2 hours. Although in these studies the effects
varied among individuals, 2 agonist administration
was found to be safe and was associated with a signifi-
cant decrease in serum potassium levels. Therefore, 2
agonist therapy should be considered as an adjunctive
treatment for patients with severe hyperkalemia.
Sodium bicarbonate infusion can shift potassium
from the extracellular to intracellular space by in-
creasing blood pH. However, routine bicarbonate
therapy for the treatment of hyperkalemia is contro-
versial.36,46-49 In a study by Blumberg and associates,50
12 dialysis patients with potassium levels of 5.25 to
8.15 mEq/L received 390 mmol of intravenous so-
dium bicarbonate over a 6-hour period. No change
in potassium levels was seen until 4 hours after drug
administration, when a decrease of 0.7 mEq/L was
noted; at 6 hours, however, the decrease in potassi-
um level was only 0.35 mEq/L.50 Due to the lack of
Texas Heart Institute Journal
a quick or sustained decrement in potassium levels,
physicians should reserve the use of intravenous sodi-
um bicarbonate for situations wherein severe acidemia
is present or there is another indication for its admin-
istration (such as phenobarbital or tricyclic antide-
pressant overdose).
Potassium Removal from the Body. The final task in
treating patients with severe hyperkalemia is to re-
move potassium from the patients body. The quick-
est, most efficient way to do this is through the use of
hemodialysis.42 In 1970, Morgan and colleagues51 re-
ported the removal of 48 mEq/L of potassium using a
Kiil dialyzer over a 10-hour period; others confirmed
these findings.52,53 Because of the time, expense, and
invasive nature of hemodialysis therapy, it is rarely
used as a 1st-line treatment for hyperkalemia unless a
patient is already on dialysis and has life-threatening
hyperkalemia. For most patients, treatment with an
exchange resin such as sodium polystyrene sulfonate
is more appropriate.
Ion exchange resins can be administered orally or
rectally and work by exchanging gut cations, most im-
portantly potassium, for sodium ions that are released
from the resin. Most studies have found exchange
resins to decrease serum potassium levels by about 1
mEq/L over a 24-hour period.54 It should be empha-
sized that the extended time required for exchange
resins to work exclude their use in the emergent treat-
ment of hyperkalemia. Exchange resins can cause
significant constipation and are typically given in com-
bination with a laxative such as sorbitol. Not only does
a laxative prevent constipation, but it also promotes the
elimination of potassium from the gut once it binds to
the resin. Although generally safe, the combination of a
resin and sorbitol has been reported to cause intestinal
necrosis, and as such should be used cautiously and
only when necessary.36,55,56
Conclusion
As our case presentation illustrates, hyperkalemia can
be very challenging to diagnose. Patients with severe
hyperkalemia frequently have normal electrocardio-
grams or electrocardiographic abnormalities that are
difficult to attribute to hyperkalemia. The diagnosis
of hyperkalemia must be considered in any patient
with clinical risk factors that would predispose them
to its development. Most commonly, patients with
hyperkalemia have underlying renal dysfunction or
are taking a medication known to increase serum po-
tassium concentrations. The treatment of hyperka-
lemia must be swift and appropriate to prevent the
development of fatal cardiac arrhythmias. If a patient
has electrocardiographic evidence of hyperkalemia, or
the potassium level is greater than 6.5 mEq/L, the 1st
drug to be administered should be calcium, because
Hyperkalemia Revisited 45
of its rapid onset of action and ability to stabilize
myocyte electrical activity. Insulin, with or without
glucose, and 2 agonists should then be quickly ad-
ministered to decrease extracellular potassium levels.
Exchange resins and hemodialysis are then used, in
the appropriate clinical settings, to decrease systemic
potassium levels. Sodium bicarbonate therapy has lit-
tle use in the routine treatment of hyperkalemia un-
less severe metabolic acidosis is present. Finally, and as
a matter of course, physicians should perform a thor-
ough search to identify the cause of the hyperkalemia
in their patient in order to prevent a recurrence.
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