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12 EMN

October 2009

InFocus

Electrocardiograms You Need


to Know: Hyperkalemia

By James R. Roberts, MD

cases demonstrated a rather marked decrease in serum potassium levels following treatment. In one case the
potassium level went from 8.1 mEq/L
to 6.6 mEq/L following calcium, insulin,
bicarbonate, and Kayexalate therapy.
Additional cases demonstrated more
severe EKG findings that exemplified
the classic sine wave morphology. In all
cases, the clinicians appeared clairvoyant enough to institute empiric therapy
against hyperkalemia based on EKG
findings alone. Bravo to these brave and
gusty souls.

Author Credentials and


Financial Disclosure: James
R. Roberts, MD, is the Chairman of the Department of Emergency
Medicine and the Director of the Division of Toxicology at Mercy Health
Systems, and a Professor of Emergency Medicine and Toxicology at the
Drexel University College of Medicine,
both in Philadelphia.
All faculty and staff in a position to
control the content of this CME activity
have disclosed that they have no financial relationships with, or financial interests in, any commercial companies
pertaining to this educational activity.

Comment: Not all clinicians are as as-

Learning Objectives: After reading this


article, the physician should be able to:
1. Discuss the EKG findings of hyperkalemia.
2. Summarize the progression of EKG
findings based on serum potassium
levels.
3. Identify those patients requiring empiric therapy for hyperkalemia.

Release Date: October 2009


ome EKG findings foretell significant morbidity and even mortality,
and some subtle yet serious results
escape even seasoned cardiologists. Like
QTC prolongation and Brugada and
Wellens syndromes, discussed in previous columns, hyperkalemia is an EKG
standout.

Electrocardiographic
Manifestations of Hyperkalemia
Mattu A, et al
Am J Emerg Med
2000;18(6):721
This erudite paper with spectacular EKG tracings by practicing emergency medicine EKG aficionados and
experts is a concise review of the multiple EKG manifestations of hyperkalemia. Because hyperkalemia is a
life-threatening acute emergency and
a frequent denizen of the ED, it is imperative to be cognizant of the classic
EKG findings of this metabolic abnormality. Hyperkalemia usually occurs
in dialysis patients, but may be seen
in DKA, adrenal insufficiency, acute
digoxin poisoning, severe dehydration
with renal insufficiency, and prescribed
drugs that cause hyperkalemia. Medication-wise, especially consider spironolactone, NSAIDs, Bactrim, and ACE
inhibitors.

This dialysis graft, coupled with an easy-to-ignore complaint of weakness, are


a setup for hyperkalemia. A hallway monitor strip is a poor way to diagnose
hyperkalemia, but a wide QRS should get your attention. Readily obtaining
venous blood in a dialysis patient can be a gargantuan task that can delay lab
results even further.

The medical school adage of hyperkalemia is that the EKG manifests


tall, sharply peaked T waves in the
precordial leads, perhaps a common
and omnipresent finding, albeit one
with minimal sensitivity (about 40%)
and far from perfect specificity
(about 85%). The classic EKG portending imminent cardiac arrest demonstrates a severely wide QRS complex,
and a sine wave appearance, harbingers of a soon-to-occur cardiac catastrophe (asystole or VF). The majority
of patients also demonstrate bradycardia. More subtle changes include
prolonged PR interval and absent P
waves.
The authors augment their discussion with a review of five case histories
with accompanying EKGs. It would be
instructive to pull the original article
because the tracings are quite illustrative. The first case is a classic presentation. A dialysis patient missed
two appointments, and presented with
malaise and myalgias. Vital signs were
normal, and the physical examination
was non-revealing. An EKG demonstrated prominent peak T waves (V1 to
V3) and minimal widening of the QRS.
This patient was empirically treated
for hyperkalemia, and the serum
potassium level was 8.4 mEq/L. The
pharmacologic intervention was also
standard, including 20 ml of 10% calcium gluconate, 2 amps of sodium bicarbonate, 10 units of IV regular insulin
with 1 amp of D50, and 50 grams of

oral Kayexalate. EKG amelioration was


seen within a few minutes of empiric
intervention.
Other cases were similar, and included patients with known renal insufficiency who presented with malaise
and diffuse weakness as the garden-variety clinical manifestations of their hyperkalemia. EKGs demonstrated absent
P waves, irregular rhythms, peaked T
waves, and a widened QRS complex. All

tute as these, and many of us will look


at the EKGs associated with a potassium level in the 6-7 mEq/L range, and
dismiss the tracing as minimally abnormal or delay a decision pending laboratory confirmation. As it turns out, the
next article confirms that it is rare to
treat hyperkalemia based on EKG findings alone, even in the academic ivory
towers of Boston. If one does not have
bedside or point-of-care blood testing,
the serum potassium can take one to
three hours to return, and invariably
the most important specimen is hemolyzed, creating spurious results. Of
interest, the clinical manifestations of
hyperkalemia are similar to those of
hypokalemia. Hyperkalemic patients
usually complain of weakness and
muscle aches, symptoms that should
not be ignored when evaluating the ubiquitous hallway patient with a dialysis

The peaked T waves on this EKG are striking, best described as too sharp to
sit on. But the vicissitudes and vagaries of the T wave, especially on a monitor
strip, make the EKG diagnosis of hyperkalemia tenuous at lower serum levels.
This EKG is not predictive of life-threatening hyperkalemia so one can wait for
lab confirmation, perhaps with a call to the lab tech to move things along. Of
course, bedside testing solves a whole passel of lab turnaround foibles.

October 2009 EMN 13

InFocus
graft in his arm. Patients with hypertension, diabetes, renal failure, and a
slew of other medical problems have
many reasons to be weak, tired, and
achy, but hyperkalemia is one condition that should be high on ones
radar, even when the patient proffers
yet another weak and dizzy complaint
list.
The EKG manifestations of hyperkalemia generally parallel the serum
potassium level. Characteristic EKG
findings are promulgated in every textbook, but in my experience, a plethora
of nonspecific changes can be seen, so
dont be locked into an intense analysis
of any given pattern. I have found that
bradycardia is common, but have not
seen that emphasized. The accompanying figure provides a general overview
of potassium levels and EKG abnormalities, although there is obviously some
overlap. Potassium levels above 8.0
mEq/L generally call for immediate
action, as do the EKG abnormalities
associated with such levels, often marshalling the troops absent a critical
value call from the tardy lab. One may
be forced to treat empirically, based on
EKG evidence alone, especially in code
situations. Expect to be wrong on many
such clinical calls.
Last months column depicted a classic EKG of severe TCA overdose, with
squiggles surprisingly similar to hyperkalemia. My only pearl here is that although the QRS can be wide in TCA
overdose and hyperkalemia, its significant tachycardia and the terminal R
wave in AVR that distinctly herald TCA
toxicity. Fortunately, bicarbonate helps
both conditions.
Effects of Presentation and
Electrocardiogram on Time to
Treatment of Hyperkalemia
Freeman K, et al
Acad Emerg Med
2008;15(3):239
This is a fascinating article from
some prestigious New England university hospitals that essentially describes
standard of care for EKG-based empiric

The bottom line is that the EKG did


not spur early or empiric treatment of
hyperkalemia in this study. Essentially,
no EKG finding prompted early therapy. The potassium levels were actually modest (6.3-7.1 mEq/L) however,
so it is not certain that more ominous
cardiograms would have been met
with similar clinical indifference or
clinician ennui.

Comment: This is indeed a discourag-

This EKG, obviously demonstrating a slow, wide bizarre QRS pattern with an
almost sine wave appearance, is a harbinger of imminent cardiac arrest. The
potassium level is likely well over 8 mEq/L. It calls for an astute clinician who
has the chutzpah to treat empirically with the entire drug regimen aimed at
rapidly decreasing serum potassium levels and stabilizing cardiac depolarization.

treatment of hyperkalemia in the ED,


and provides insight into the expected
turnaround time for laboratory analysis.
The authors attempted to determine
whether EKG features were associated
with a difference in time to treatment
for patients ultimately determined to
have hyperkalemia (level above 6
mEq/L). Excluded subjects were those
who had a give-away chief complaint
of hyperkalemia or needs dialysis,
and those who had a cardiac arrest.
The median potassium level was only
6.5 mEq/L (6.3-7.1). More than a third
of the patients were taking ACE inhibitors, drugs well known to cause
hyperkalemia.
Of the 168 patients treated for hyperkalemia, 12 (12%) were treated
within 30 minutes of triage, and 26
(16%) were treated empirically before
the lab reported the potassium values.
About a third of the EKGs demonstrated abnormalities of the T wave, although many were nonspecific. Only 35
percent were considered textbook tracings. In retrospect, only half of the
cases had an EKG abnormality consistent with hyperkalemia. Importantly,

none of the EKG abnormalities


prompted early treatment. Two cases
of cardiac arrest may have been secondary to hyperkalemia, despite standard therapy.
In this study, the median time from
ED arrival to treatment for hyperkalemia was an amazingly long 117
minutes (range: 59-196). Even when
the laboratory results were available,
it required an additional 67 minutes
(range: 49-82) to initiate treatment.
So-called critical values from the lab
required a mean of 42 minutes (range:
20-95) to receive specific therapy. In
this study the most common presenting complaints were dyspnea (20%),
weakness (19%) or altered mental status (8%). Despite having knowledge
of the potential for hyperkalemia and
having the EKG prior to serum potassium level, even rapid sleuthing of the
EKG did not appear to shorten the
time from ED arrival to specific antipotassium intervention. The authors
speculate that this may be due to
the nonspecific abnormalities seen
in many EKGs in the presence of
hyperkalemia.

EKG Changes Associated with Increasing


Potassium Levels
Typical ECG Appearance
Serum Potassium

Mild: 5.5-6.5 mEq/L

Moderate: 6.5-8.0 mEq/L

Severe: >8.0 mEq/L

Possible ECG Abnormalities

Peaked T waves,
prolonged PR segment

Loss of P wave, prolonged


QRS complex, ST-segment
elevation, ectopic beats and
escape rhythms

Progressive widening of
QRS complex, sine
wave, ventricular
fibrillation, asystole,
axis deviations, bundle
branch blocks, fascicular
blocks

ing report from a university hospital. I


thought my ED had a slug-like mentality when it came to hyperkalemia. The
level of hyperkalemia was probably
not life-threatening in the majority of
cases, and therefore the EKG was not
as provocative or attention-grabbing as
the tracing seen when potassium levels
are well above 8.0 mEq/L, and the patient is circling the drain leading to cardiac arrest. This article actually sets
the standard of care as a rather modest
one, particularly with regard to recognition and treatment of hyperkalemia
in the ED in comparison with the EKG.
It appears that the clinicians from
Boston did not believe that empiric
treatment for hyperkalemia should be
based solely on nonspecific EKG findings. I agree, but would hasten to add
that a sine wave should garner an empiric intervention. While waiting for
lab confirmation is a reasonable approach in the nonacute circumstance,
a widened QRS or sine wave prognosticates a poor outcome, and should
obviously get ones full pharmacologic
attention. Unless I am missing something, this article is the poster child
for point-of-care blood testing in the
ED.
Management of Severe
Hyperkalemia
Weisberg LS
Crit Care Med
2008;36(12):3246
This is a literature-based summary of
hyperkalemia management, termed a potentially lethal electrolyte abnormality by
these authors. A serum potassium level of
6.5 mEq/L or specific EKG abnormalities
were considered emergency action points
for treatment. The standard regimen to
antagonize the effects of potassium on
cardiac depolarization is a threefold approach: redistributing potassium into the
cell (bicarbonate and insulin/glucose), enhancing potassium elimination (dialysis
or Kayexalate), and stabilizing cardiac
cell membranes (calcium infusion). The
treatment of severe hyperkalemia is medical student dogma, and it should be
familiar to all emergency physicians.
The authors nicely detail the science
behind calcium, insulin, bicarbonate,
beta-agonist, and Kayexalate therapies.
As a summary, calcium is the preferred
Continued on next page

14 EMN

October 2009

InFocus

HYPERKALEMIA
Continued from previous page
emergency bullet for cardiac conduction issues; insulin is best for translocating potassium back into the cell;
Kayexalate has debatable efficacy and
is slow; and dialysis is the most reliable tool for removing potassium from
the body. Beta-agonists are iffy, and bicarbonate is minimally helpful. The
empiric treatment of hyperkalemia
generally can be supported under the
proper scenario, and such innocuous
interventions dont usually wreak
havoc even if ones diagnosis is off the
mark. But merely finding weakness
and an abnormal EKG can result in
rather serious consequences if the patient happens to have the rare case of
hypokalemic paralysis. The only downside of the treatment of most patients
with standard hyperkalemia regimens
is hypokalemia. Hyperglycemia, hyperosmolality, and hypercalcemia are of
little clinical consequence. These authors note that a benefit of nebulized

The EKG generally parallels the serum potassium levels.

albuterol (such as 20 mg inhaled over


10 minutes) is seen in only about 60
percent of patients, with the most common side effect being tachycardia.

Comment: I learned the general treatment protocol for severe hyperkalemia, the quintessential shotgun
approach, as an intern. One aims to
push potassium back into the cell, extract it from the serum, and keep the
heart beating and contracting. There
are little data in the literature that any
specific regimen causes any specific
or quantitative result. Some question
any real value of sodium bicarbonate.
When one decides to treat hyperkalemia in the ED, a cornucopia of
therapies is simultaneously initiated.
Most interventions have few down-

sides, and are well worth the potential risks given the lethal potential for
severe untreated hyperkalemia. Importantly, all ED interventions, even
calcium, last only a few hours.
The usual ultimate treatment is hemodialysis, a necessity in the patient
with end-stage renal disease. I personally have minimal regard for nebulized
albuterol. About 40 percent experience
no benefit, and the subset likely to improve is enigmatic so far. It doesnt
seem to produce clinically significant
hypokalemia in the asthmatic patient.
In fact, we never even check potassium
under such circumstances. Albuterol
can make one very tremulous given the
fourfold dose for hyperkalemia vs.
asthma.
The Holy Grail for life-threatening

hyperkalemia is intravenous calcium.


Calcium gluconate can be given via a
peripheral vein as long as one is careful not to allow extravasation. Calcium
chloride always burns, and while it
can be given through a dialysis
catheter (Quinton), the best choice is
a central line. Occasionally I have
given calcium chloride via a large peripheral vein, but stand at the bedside
to make sure that it does not extravasate. Calcium chloride in the subcutaneous tissue is usually associated
with some degree of tissue slough or
necrosis, and there is no antidote.
When it has to be done, it has to be
done. Some clinicians prefer to use
calcium gluconate under all circumstances calling for calcium supplementation, not a bad fail-safe mantra.
Kim (Nephron 1996;72[3]:476) studied
the effect of simultaneously administered
insulin/glucose and bicarbonate for treating hyperkalemia. This synergic effect is
commonly sought, but efficacy is poorly
quantified. For patients with end-stage
renal disease, the treatment regimen consisted of 2 amps of bicarbonate, 1 amp of

In Brief
Improving Medication
Compliance
There is no proven way to ensure patients follow medication directions for
extended periods of time, according to a
new report in the Cochrane Database of
Systematic Reviews.
Researchers led by R. Brian Haynes,
MD, PhD, of McMaster University, updated a 2005 review summarizing randomized control trials of interventions to
help patients follow prescriptions.
They found that four of 10 interventions reported in nine trials showed an
effect on adherence and at least one
clinical outcome for short-term treatments, which lasted one to three weeks.
In those short-term trials, the researchers found one intervention that
significantly improved patient adherence but did not enhance clinical outcome. Some effective approaches
included counseling and providing
written instructions.
For long-term treatments, 36 of 81
interventions reported in 69 trials were
associated with improvements in adherence, but only 25 interventions led to
improvement in at least one treatment
outcome. Some approaches with limited
success included sending reminders to patients and following up with phone calls.

First TB Cases May Predict


Outbreak
The first two cases of tuberculosis in a
region may provide clues on the poten-

tial for an outbreak, according to the


July 1 American Journal of Respiratory
and Critical Care Medicine.
Researchers from the KNCV Tuberculosis Foundation in the Hague,
Netherlands, led by Sandra Kik, MSc,
analyzed data from the Netherlands
Tuberculosis Register and the National
Institute of Public Health from more
than 18,200 patients with reported TB
between 1993 and 2004. They discounted cases that were not cultureconfirmed, could not be exactly
matched between the two databases,
or were duplicates. Remaining cases
were divided into 622 cluster episodes,
with 1,756 individual cases, 54 of
which were large clusters (five or more
cases).
They found that if the first two patients were diagnosed within three
months of each other, lived in urban
areas, and if one or both were of subSaharan African nationality, there was
a 56 percent chance that the two
cases will lead to a large outbreak of
TB. If the patients exhibit none of
those characteristics, the odds are just
one percent.

Rapid Response
Teams Ineffective
Rapid response teams in hospitals do
not result in a reduced rate of cardiopulmonary arrests or deaths, according to
the December 3 issue of JAMA.
Researchers led by Paul S. Chan,
MD, of the University of Missouri,
Kansas City, examined the association

between a rapid response team intervention and long-term challenges in


hospital-wide cardiopulmonary arrests
and mortality rates. The study included
adult inpatients admitted between January 2004 and August 2007 at a 404bed tertiary care academic hospital.
Rapid response team education and
program rollout occurred from Sept. 1
to Dec. 31, 2005. A total of 24,193 patient admissions were evaluated prior to
the intervention and 24,978 after.
The researchers found there were
376 rapid response team activations after intervention implementation. The
most common reasons for activation
were altered neurological status, tachycardia exceeding 130 beats per minute,
tachypnea exceeding 30 breaths per
minute, and hypotension assessed as
blood pressure lower than 90 mmHg.
Case fatality rates after cardiopulmonary arrest were similar prior to
and after the rapid response team
intervention (77.9% vs. 76.1%). Hospital-wide mortality rates did not
meaningfully change after the intervention: 3.22 prior to intervention vs.
3.09 after intervention, per 100
admissions. Secondary analyses revealed few instances of rapid response team undertreatment or
underuse that may have affected the
mortality findings.

EPs: Resuscitation
Practices Lacking
An overwhelming majority of emergency physicians say resuscitation prac-

tices in the United States are not very


effective, according to a recent ACEP
survey.
The college conducted the State of
Resuscitation survey in September, releasing the results in November. A total
of 1056 online questionnaires were
completed by ACEP members in selected sections. The survey was administered by Saperstein Associates, an
independent opinion research company, and was sponsored by ZOLL Medical Corporation.
The survey found almost all EPs
(94%) believe a patient in sudden cardiac arrest is more likely to survive if a
CPR-trained bystander administers
CPR before professional rescuers arrive. More than half said the length of
time between patient collapse and
first responder arrival is an important
factor in determining the success of
resuscitation efforts. Other factors
viewed as having a positive impact included faster patient-to-doctor times
(77%), data collection and sharing
(73%), automated technologies (66%),
and real-time feedback on compressions (65%).
More than half the respondents said
poor survival rates from sudden cardiac
arrest is related to the aging population,
while one-quarter said obesity has contributed most to poor survival rates.
Though EPs said bystander CPR would
improve survival, efforts to teach laypersons are scattered and often nonexistent, and respondents want civic leaders
to be more engaged in the issue.

October 2009 EMN 15

InFocus
D50, and 50 units of regular insulin, either
alone or combined therapy. The bicarbonate alone had little effect on serum
potassium. The glucose/insulin therapy
had a modest benefit, but a combination
of the two lowered serum potassium
from 6.2 to 5.2 mEq/L at 60 minutes.
Plasma osmolality was not an issue, and
there was no hypoglycemia. Bottom line:
Bicarbonate is of minimal importance,
but it seems synergistic with insulin and
may have other benefits on the milieu of
renal failure.
Allon et al (Ann Intern Med 1989;
110[6]:426) studied the effect of nebulized albuterol for acute hyperkalemia
in hemodialysis patients. This was a
randomized prospective double blind
placebo controlled trial studying either
10 or 20 mg of nebulized albuterol. The
beta-agonist lowered serum potassium
levels by approximately 0.6 to 0.9
mEq/L, with a higher dose providing the
greater effect. The hypokalemic effect
was noted within one to two hours, and
there were no adverse cardiovascular
effects. Notably, some patients had no
significant response, but the reason for
this was not known. This report was
one of the first articles to postulate a
potassium-lowering effect of nebulized
albuterol, an intervention that seems to
have gained popularity in the ED. Inhaled beta-agonist may be a good alternative when IV access is not readily
available.
The American Heart Association
recommends immediate therapy for
serum potassium levels greater than 6
mEq/L, but this is hardly a lethal potassium level, or one that cannot await laboratory confirmation. Exactly when
potassium levels become life-threatening is unknown, but treating any level
over the AHA recommendations is
reasonable. An exception to the usual
therapeutic cocktail may be severe dehydration where saline alone will quickly
lower potassium levels that are raised
secondary to pre-renal azotemia.
In these days of the omnipresent sixto infinity-hour ED waits for dialysis or
admission, the return of hyperkalemia
is not an uncommon issue for the EP
who may have moved on to other patients, content that the inpatient team
has taken control. No ED intervention
lasts more than a few hours so the clinician must be vigilant to provide continuing care after the initial bevy of
medications saved the day. I prefer to
check the potassium in about an hour to

gloat over my success, and again two to


three hours later if the patient is still in
the ED. An endocrinologist friend of
mine offered the following regimen for
continuous calcium gluconate, the most
useful immediate cardioprotective in-

tervention for severe hyperkalemia:


Add 6 ampoules of calcium gluconate to
a liter of normal saline, and infuse 1
ml/kg per hour of this concoction. Calcium levels will not get excessively
high, and continued myocardial self-

stabilization will occur. The fluid load


is minimal. In a dialysis patient, I would
continue this for about three to four
hours, augmented with frequent call to
the dialysis center for the more definitive intervention.

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October 2009
Questions:
1. Tall peaked T waves on the EKG are nearly 100% sensitive and specific for hyperkalemia.
True False
2. A slow, wide QRS pattern resembling a sine wave indicates impending cardiac arrest from hyperkalemia.
True False
3. It is extremely dangerous to empirically administer medication therapy for hyperkalemia without confirming the
serum potassium level.
True False
4. Nebulized albuterol is contraindicated in the presence of hyperkalemia.
True False
5. Once hyperkalemia has been treated in the ED, a repeat evaluation of potassium levels and additional therapy for
the next 24 hours is not required.
True False
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