Acquired Long QT Syndrome: Frequency, Onset, and Risk Factors in

Intensive Care Patients

Teri M. Kozik and Shu-Fen Wung
Crit Care Nurse 2012;32:32-41 doi: 10.4037/ccn2012900
2012 American Association of Critical-Care Nurses
Published online http://www.cconline.org

Personal use only. For copyright permission information:

http://ccn.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT

Subscription Information
http://ccn.aacnjournals.org/subscriptions/

Information for authors

http://ccn.aacnjournals.org/misc/ifora.xhtml

Submit a manuscript
http://www.editorialmanager.com/ccn

Email alerts
http://ccn.aacnjournals.org/subscriptions/etoc.xhtml

Critical Care Nurse is the official peer-reviewed clinical journal of the American
Association of Critical-Care Nurses, published bi-monthly by The InnoVision Group
101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050,
ext. 532. Fax: (949) 362-2049. Copyright 2012 by AACN. All rights reserved.

Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013

 Feature

Acquired Long QT Syndrome:

Frequency, Onset, and Risk
Factors in Intensive Care Patients
Teri M. Kozik, RN, MS, PhD, CNS, CCRN
Shu-Fen Wung, RN, MS, PhD, ACNP

BACKGROUND Acquired long QT syndrome is a reversible condition that can lead Acquired long QT syndrome
to torsades de pointes and sudden cardiac death. (aLQTS) is a reversible channelopa-
OBJECTIVE To determine the frequency, onset, frequency of medications, and risk thy caused by delayed ventricular
factors for the syndrome in intensive care patients. repolarization and characterized by
METHODS In a retrospective chart review of 88 subjects, hourly corrected QT inter- a pathological prolongation of the
vals calculated by using the Bazett formula were collected. Acquired long QT syndrome
QT interval on surface electrocar-
was defined as a corrected QT of 500 milliseconds or longer or an increase in corrected
diograms (ECGs; Figure 1). The syn-
QT of 60 milliseconds or greater from baseline level. Risk factors and medications
drome can be the result of exposure
administered were collected from patients medical records.
RESULTS The syndrome occurred in 46 patients (52%); mean time of onset was to an environmental stressor such
7.4 hours (SD, 9.4) from time of admission. Among the 88 patients, 52 (59%) received as hypothermia or to electrolyte dis-
a known QTc-prolonging medication. Among the 46 with the syndrome, 23 (50%) orders, but most often it is associated
received a known QT-prolonging medication. No other risk factor studied was sig- with pharmacological therapy; the
nificantly predictive of the syndrome. QT interval reverts to normal once
CONCLUSIONS Acquired long QT syndrome occurs in patients not treated with a the stressor is removed.6-8 Prolonga-
known QT-prolonging medication, indicating the importance of frequent QT moni- tion of the QT interval is the most
toring of all intensive care patients. (Critical Care Nurse. 2012;32[5]:32-41) common reason a medication is
withdrawn from the market.9,10
The aLQTS predisposes patients

T
he heart contains 2
types of cells: cells that
generate the electrical
activity (conduction
system) and muscle
cells that contract in response to
the electrical activity. The contrac-
tions, or beats, are coordinated by a
network of specialized, autorhythmic
cells integrated within the contractile
myocytes. The autorhythmic cells
spread their action potentials through-
out the myocardial cells via complex
2012 American Association of Critical-Care Nurses
doi: http://dx.doi.org/10.4037/ccn2012900
ion channels within the cardiac cell to the ventricular arrhythmia torsades
membrane, leading to contraction.1,2
Many currents are involved in the
electrical activity of an action R
potential, or depolarization and
repolarization. Depolarization is
P T
due to an inward flux of positive
ions (sodium and calcium) into the
cells and repolarization to a delayed Q
S
outward flux of potassium ions from
QT
the cells.3 Channelopathies are con- interval
ditions caused by malfunction of
these ion channels or the proteins Figure 1 Points used to measure the
that regulate the channels, leading QT interval in a P-QRS-T complex on
a surface electrocardiogram.
to cardiac electrical disorders.4,5

32 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 www.ccnonline.org

Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013

de pointes, which can lead to ven- and torsades de pointes may be and store the data for up to 72 hours
tricular fibrillation.11,12 Torsades de high in hospitalized patients, espe- in a centralized computer database.
pointes is a wide-complex polymor- cially patients in intensive care units Hourly QT intervals, measured from
phic ventricular tachycardia charac- (ICUs), because of the multiple classes the beginning of the QRS complex
terized as a twisting of the points of QT-prolonging medications pre- to the end of the T wave, were ana-
around the isoelectric line of the ECG. scribed and an increase in other lyzed by using the electronic calipers
Torsades de pointes and ventricular potential risk factors. built into the Spacelabs monitor.
fibrillation can lead to a decreased The objective of this study was The monitor automatically corrected
cardiac output, syncope, and sudden to determine the frequency and onset the QT interval by using the Bazett
cardiac death.13-16 The estimated of aLQTS in an ICU population. Med- formula (QTc=QT interval divided
annual incidence of sudden cardiac ications and risk factors associated by the square root of the RR interval);
death is 1 per 1000 deaths in Western with aLQTS are described. heart rate was determined from the
populations, or approximately 20% preceding R to R interval. QTc inter-
of all deaths.3,17,18 The incidence of Methods vals were measured hourly starting
aLQTS is unknown, but the syndrome The sample in this retrospective immediately upon admission to the
most likely is more unrecognized descriptive study consisted of 100 ICU until discharge from the unit or
than rare.19 According to estimates,20 consecutive ICU patients hospital- up to 72 hours.
3000 to 4000 patients die each year ized during October and November Measurements at baseline, first
of sudden cardiac death caused by of 2009. A total of 12 patients whose abnormal QTc interval, maximum
long QT syndromes, highlighting the QT intervals could not be accurately QTc interval, and final QTc interval
importance of developing strategies analyzed (atrial fibrillation, atrial were obtained for each patient.
for early identification and preven- flutter, bundle branch blocks, or Baseline QTc interval, obtained for
tion of the syndromes. continuous paced rhythms) were all patients, was defined as the QTc
Prevention of adverse outcomes excluded, leaving 88 patients for obtained on ICU admission at hour
due to aLQTS is challenging because analysis. This research was conducted zero. The first long QTc interval was
of the multiple classes of medications in the 20-bed ICU at Saint Marys defined as the first QTc interval of
associated with the syndrome. Regional Medical Center, a 380-bed 500 milliseconds or greater or an
Antipsychotics, antidepressants, community hospital in Reno, Nevada. increase of 60 milliseconds or greater
antibiotics, chemotherapeutic agents, The ICU accepts all types of critical from the baseline. The longest QTc
and antiarrhythmics are some of care patients except trauma patients. interval, obtained for all patients,
the most common classes of offend- Approval from the human subject was defined as the longest QTc inter-
ing medications.14,15 With such a vast protection programs was obtained val obtained during the study moni-
array of medications that can cause before the study began. toring period. The final QTc interval
aLQTS, concurrent use of more than was the last QTc interval measured
1 offending medication is not uncom- Data Collection at time of discharge from the ICU or
mon and increases a patients risk Spacelabs cardiac monitors at 72 hours (end of the study period).
for an adverse event. Studies21 indi- (Spacelabs Healthcare) were used to A list of medications known to
cate that the incidence of aLQTS continuously monitor 2 ECG leads prolong the QT interval was obtained
from the Arizona Center for Educa-
Authors tion and Research.22 Any medication
Teri M. Kozik is a cardiovascular clinical nurse specialist and supervisor of the cardiac from this list that was administered
research department at Saint Josephs Medical Center, Stockton, California. orally or intravenously just before
Shu-Fen Wung is an associate professor at the University of Arizona, College of Nursing, ICU admission (eg, in the emergency
Tucson, Arizona. department, in the surgical suite) or
Corresponding author: Teri M. Kozik, RN, MS, PhD, CCRN, 1800 N. California Street, Stockton, CA 95204 (e-mail: in the ICU was included in the study.
teri.kozik@dignityhealth.org).
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
All medications that may be associ-
Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org. ated with aLQTS but were not

www.ccnonline.org CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 33

Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
included on the list were investi-
gated further.
Data on risk factors known to
be associated with aLQTS were col-
lected from the medical records and
included age, sex, race/ethnicity,
home medications (name, dose,
and route), body mass index, and
comorbid conditions. Comorbid
conditions included hypothermia
(core temperature 34C),
hypokalemia (serum potassium
level <3.5 mmol/L), bradycardia
(heart rate <50/min) with complete
atrioventricular block, heart failure
(any New York Heart Association
classification of new-onset or chronic
heart failure), and acute coronary
syndrome (any ischemic changes
revealed on the ECG along with
troponin levels 0.12 g/L).
Statistical Analysis
Data were entered into an SPSS
database (IBM/SPSS Inc). The per-
centage of patients with aLQTS
among all patients was determined.
In addition, central tendencies (mean,
2 standard deviations, median, mode,
and range) were obtained for patients
baseline, first long, longest, and final
QTc intervals for the groups who did
or did not have aLQTS.
Mean onset for aLQTS was the
interval from the time of ICU admis-
sion to the time of the first prolonged
QTc interval; the hour of the first
prolonged QTc interval was used
according to criteria. Onset for aLQTS
was determined for 2 groups: all
patients who had aLQTS, including
patients admitted to the ICU with
aLQTS, and patients with a normal
baseline QTc interval at the time of
ICU admission in whom aLQTS devel-
oped during the ICU stay. A t test was
used to determine if the length of the
34 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012
Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
Table 1 Central tendencies of measurements of QTc for patients with and
without acquired long QT syndrome (aLQTS)
aLQTS Baseline
Present No. of patients 46
Mean 470
Median 465
Mode 450
Range 380-690
Absent No. of patients 42
Mean 437
Median 440
Mode 450
Range 390-470
prolonged QTc interval differed
between the 2 groups.
The percentage of patients who
received a QT-prolonging medication
was obtained. In addition, frequency
of each medication administered to
all patients was obtained. Differ-
ences in medications received and
in host risk factors between groups
who did and did not have aLQTS
were determined by using 2 analy-
sis. For continuous variables (eg,
age and body mass index), 2-sample
t tests were used to compare differ-
ences between patients who did and
did not have aLQTS. Backward
stepwise logistical regression analysis
was used to estimate the probability
of aLQTS within 72 hours of ICU
admission. A total of 13 predictive
variables were used in the analysis.
These included 8 host risk factors
(age, sex, body mass index, brady-
cardia with complete atrioventricular
block, hypokalemia, hypothermia,
acute coronary syndrome, and
heart failure) and 5 medications
(flurane, ondansetron, levofloxacin,
azithromycin, and amiodarone).
Results
The mean length of the study
period was 43.3 (SD, 24.5) hours.
QTc, ms
First long one Longest one Final
46 46 45
511 535 457
510 530 450
500 500 480
410-620 410-690 350-620
42 41
458 435
460 434
480 430
410-490 380-480
The sample consisted of 47 women
(53%) and 41 men (47%). The mean
age was 63.5 (SD, 14.3) years. More
than one-half of the patients (n=46;
52%) had aLQTS during the study
period. A total of 40 patients (46%)
had aLQTS with a QTc interval of
500 milliseconds or greater upon or
after ICU admission. An additional
6 (7%) had an increase of 60 mil-
liseconds or greater from their base-
line QTc interval. Table 1 details the
central tendencies of the QTc inter-
val measurements of patients who
did and did not have aLQTS.
Among the 46 patients who had
aLQTS, the syndrome was present
at the time of ICU admission in 14
and developed in 32 after admission
(Figure 2). For all patients with
aLQTS, including those admitted
with a prolonged QTc, the mean
onset of QT prolongation was 7.4
hours (SD, 9.4; range, 0-32) after
admission. Of the 32 patients with
a normal baseline QTc at ICU admis-
sion in whom aLQTS developed after
the admission, the mean onset of QT
prolongation was 10.6 hours (SD. 9.5).
Among the 14 patients who had
aLQTS at the time of ICU admission,
4 arrived from the surgical suite, 4
were admitted with acute coronary
www.ccnonline.org
 Discussion
16
14
According to estimates,23,24 clini-
12
cally important cardiac arrhythmias
No. of subjects

10 will develop in approximately 1 in 5

8 ICU patients. The incidence of aLQTS
6 and torsades de pointes may be high
4 in hospitalized patients, especially
2 ICU patients, because of the multi-
0 ple classes of QT-prolonging med-
0 1 2 3 5 7 8 9 10 11 13 16 21 22 23 28 32
ications prescribed and an increase
First long QTc upon and after admission to intensive care unit, h
in the incidence of other potential
Figure 2 Frequency by hour of onset of acquired long QT syndrome. risk factors.21
Our study is the first one in
syndrome, 3 were admitted with and 6 categorical variables (Table 3). which the frequency of aLQTS was
respiratory failure, 2 were admitted No variable differed significantly determined in consecutive ICU
with severe infections and sepsis, between the 2 groups. For instance, patients regardless of medications
and 1 was admitted with hyperten- prolonged QTc intervals (550-690 or risk factors. In studies by Ng and
sive crisis. The final study measure- milliseconds) developed during colleagues, the frequency of aLQTS
ments of QTc intervals indicated treatment of all 3 patients who had in a subset of ICU patients who
aLQTS for 2 patients. Of these, 1 therapeutic hypothermia after car- received a known QTc-prolonging
was still in the ICU at the end of the diac arrest. The frequency of hypo- medication was 46.6%25 and 58.4%.21
study period of 72 hours, and 1, thermia did not differ significantly Other research26-29 on the frequency
admitted with hypertensive crisis, between patients who had aLQTS of aLQTS has focused on patients in
was discharged to the telemetry and patients who did not (12 = 2.8; units other than ICUs.
unit after 12 hours in the ICU. P = .09). Among the 23 patients In a retrospective chart review
Among the 46 patients who had admitted with acute coronary syn- of 861 hospitalized patients in
aLQTS, 50% received a known QTc- drome, 13 (57%) had aLQTS, but France with a diagnosis of ventricular
prolonging medication; therefore, differences between those who had tachycardia, ventricular fibrillation,
aLQTS developed in the other 50% aLQTS and those who did not were or sudden cardiac death, Molokhia
of patients in the absence of a not significant (12 =0.2; P=.64). et al27 estimated that 5% to 7% were
known QTc-prolonging medication. Logistical regression was used to caused by long QT syndromes. In
Among 13 patients who underwent estimate the probability that aLQTS another study26 of 258 consecutive
elective surgery, 8 who returned to would occur within 72 hours of ICU hospitalized patients, the preva-
the ICU had a prolonged QTc inter- admission. A total of 13 predictive lence of aLQTS was 3.5% (QTc >500
val within 2 hours. Further investi- variables were
gation revealed that 6 of the 8 used in the
Table 2 Six medications administered before
patients (75%) in whom aLQTS analysis, includ- development of acquired long QT syndrome (aLQTS)
developed after surgery had ing risk factors,
% of all % of patients
received a flurane, a class of anes- comorbid con- No. of patients with aLQTS
thetic medications known to pro- ditions, and 5 Medication patients (n = 88) (n = 46)
long the QTc interval. Data on the medications. Ondansetron 9 10 20
6 medications frequently adminis- Among these Amiodarone 6 7 13
tered before development of aLQTS variables, only Fluranes 6 7 13
are provided in Table 2. 5 medications Levofloxacin 5 6 11
Risk factors were compared were significant Azithromycin 4 5 9
between patients who did and did predictors of Ciprofloxacin 1 1 2
not have aLQTS for 2 continuous aLQTS (Table 4).

www.ccnonline.org CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 35

Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
 prolonged QTc interval, and 8%
Table 3 Host risk factors between patients with and without acquired long QT had QTc intervals greater than 500
syndrome (aLQTS)a
Patients milliseconds.
With aLQTS Without aLQTS
Variable (n = 46) (n = 42) P Measurements of QT Intervals
Age, mean (SD), y 61.05 (2.31) 65.72 (1.99) .13 The length of the QT interval is
Body mass index,b mean (SD) 29.16 (1.26) 30.54 (1.40) .47 predominately affected by heart
Race .42 rate and can vary from beat to beat.12
White 39 (85) 38 (90) Therefore, the measured QT inter-
Nonwhite 7 (15) 4 (10)
val must be corrected before the
Sex .85
Male 21 (46) 20 (48) value can be useful clinically or for
Female 25 (54) 22 (52) research purposes. Several correc-
Hypothermia 3 (7) 0 (0) .09 tion formulas are available, such as
Hypokalemia 10 (22) 4 (10) .12 the Fridericia formula, the Framing-
Acute coronary syndrome along 13 (28) 10 (24) .64 ham linear regression formula, the
with troponin levels 0.12 g/L Hodges formula, and the Bazett
New onset or history of heart failure 7 (15) 7 (17) .85 formula.30-33 Although validated for
a Unless specified otherwise, all values are number (percentage).
b Body mass index calculated as the weight in kilograms divided by the height in meters squared.
congenital LQTS, the Bazett formula
may lead to false-negative or false-
positive results when used for
milliseconds) to 25.2% (QTc >450 patients who received an ECG. QT patients with medication-induced
milliseconds). In other research, prolongation was defined as greater aLQTS.34,35 In a large study36 of
29
Seftchick et al used a retrospective than 450 milliseconds for men and 14548 healthy men and women, a
chart review to determine the fre- greater than 460 milliseconds for comparison of 3 formulas (Fridericia,
quency of a prolonged QTc interval women. According to these defini- Framingham linear regression, and
in 1558 emergency department tions, 35% of the patients had a Bazett) revealed only minor risk-
stratification
differences. The
Table 4 Logistic regression analysis for estimating the probability that acquired long QT syndrome Bazett formula
would occur within 72 hours of admission to the intensive care unit
continues to be
Model log Change in -2 log
Variable b SE likelihood likelihood P used most often
Hypothermia -15.63 27773.71 -32.48 0.00 >.99
clinically
Heart failure 0.59 0.97 -32.70 0.38 .54
because of its
simplicity.14,37,38
Acute coronary syndrome -0.52 0.61 -34.91 0.73 .39
We used this
Hypokalemia 1.27 1.22 -35.55 1.28 .26
formula
Age 0.03 0.02 -41.35 1.81 .18
because it was
Bradycardia with complete heart block 18.62 8564.45 -36.46 1.82 .18
programmed in
Body mass indexa 0.04 0.03 -40.44 2.05 .15 the Spacelabs
Sex 0.97 0.70 -38.33 2.08 .15 monitoring sys-
Levofloxacin -20.43 14615.57 -43.31 3.92 .048 tem we used.
Azithromycin -20.68 16629.53 -43.31 3.92 .048 Several
Amiodarone -20.70 13694.28 -44.25 5.81 .02 abnormal limits
Flurane anesthetic -21.14 14774.12 -45.17 7.65 .006 for QTc meas-
Ondansetron -21.16 12148.85 -46.95 11.20 .001 urements in
a Body mass index calculated as the weight in kilograms divided by the height in meters squared.
QT and QTc
studies have

36 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 www.ccnonline.org

Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013

been recommended.39 These include
absolute QTc prolongation greater
than 450 milliseconds, greater than
480 milliseconds, or greater than 500
milliseconds and an increase of the
QTc from baseline of more than 30
milliseconds or more than 60 mil-
liseconds. Using lower abnormal
limits increases the false-positive
rate. Because a universal threshold
for medication-induced aLQTS does
not exist, experts agree that a change
of QTc from baseline of more than
30 milliseconds should raise concerns
and that a change of QTc of more
than 60 milliseconds should be espe-
cially alarming.16,39 In addition, most
cases of drug-induced torsades de
pointes occur in patients with QTc
intervals greater than 500 millisec-
onds.10,16,39 Therefore, to minimize
false-positive categorization of aLQTS,
we defined aLQTS as an increase in
the QTc of more than 60 milliseconds
from baseline or an absolute QTc of
500 milliseconds or greater.
Medications and aLQTS
Patients are often admitted to
the ICU from the emergency depart-
ment or operating rooms, where
multiple medications are adminis-
tered, and prolongation of the QTc
interval can occur.40-43 In our study,
the patients with aLQTS often had
the syndrome at the time of ICU
admission (30%), or aLQTS devel-
oped soon after their admission to
the unit (70%); the mean time of onset
was 10.6 hours after ICU admission.
Our sample included 8 patients who
had major surgery and returned to
the ICU from the operating room.
Of these patients, 6 had aLQTS after
receiving a known QTc-prolonging
anesthetic agent. Among patients
who had aLQTS (mean QTc, 508
www.ccnonline.org
Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
milliseconds) at the time of ICU
admission, the mean final study QTc
measurement (456 milliseconds)
was within the normal range, indi-
cating that the LQTS was acquired
rather than congenital.
In our study, 50% of patients
with aLQTS had received a known
QTc-prolonging medication. Logistic
regression showed that only 5 med-
ications (flurane, ondansetron, lev-
ofloxacin, azithromycin, and
amiodarone), and no host risk factors,
were significant predictors of aLQTS.
Ondansetron (Zofran). The most
frequently prescribed medication in
patients with aLQTS in our study
was ondansetron. This medication
is frequently used in hospitalized
patients for nausea and/or vomiting,
especially in emergency departments,
after surgery, and in ICUs. The drug
is known for its potential to prolong
the QT interval; several cases of car-
diac dysrhythmias after its adminis-
tration have been reported.44 In a
prospective double-blind study45 to
determine the effects of ondansetron
on the QT interval, 16 healthy vol-
unteers were randomized to 1 of 4
groups to receive either: droperidol
alone (which also can prolong the
QT interval), ondansetron alone, a
combination of droperidol and
ondansetron, or placebo. The results
indicated that ondansetron signifi-
cantly prolonged the QTc interval
(P=.01). In a single-blind study,44
85 patients with postoperative nau-
sea and vomiting were randomized
to receive either droperidol or
ondansetron. Both antiemetics were
associated with a significantly longer
QTc interval after administration
(P <.001).
In December 2001, the Food
and Drug Administration issued a
CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 37
black-box warning against the use
of droperidol as a first-choice med-
ication for nausea and vomiting
because of the increased risk of QTc
prolongation and the subsequent
incidence of torsades de pointes.46
Ondansetron became the first-choice
medication for nausea and vomiting
despite having the same risks.
Ondansetron is often administered
on medical-surgical units and in
outpatient clinics where cardiac
rhythm is not monitored, indicating
a risk for unidentified aLQTS and
the potential consequence of torsades
de pointes. The results of these stud-
ies and of our study indicate that
clinicians should be diligent in
monitoring QTc intervals in ICUs
when administering ondansetron.
Anesthetics. In our study, the
majority of postoperative patients
(62%) had a prolonged QTc interval
when they returned to the ICU. Fur-
ther analysis indicated that 6 of those
patients (75%) had received a flurane
agent. Clinicians have known for
several decades that flurane can affect
cardiac repolarization, leading to
aLQTS.39-43 Cases most often occur
in older patients with predisposing
risk factors such as electrolyte
abnormalities and/or ischemic
heart disease.47,48 However, in a
recently reported case,49 ventricular
tachycardic arrest developed in a
healthy 35-year-old woman after
QTc prolongation during a simple
septoplasy with general anesthesia.
The woman had no identifiable
risk factors and had a normal pre-
operative QTc interval (346-388
milliseconds). The high frequency
of aLQTS in patients given flurane
indicates the importance of moni-
toring QTc intervals in all postoper-
ative ICU patients.
 Fluoroquinolones. Our results
show that fluoroquinolones are asso-
ciated with the development of
aLQTS. Because of their wide spec-
trum, fluoroquinolones, specifically
levofloxacin (Levaquin), have become
the drugs of choice against many
respiratory, gastrointestinal, and
genitourinary pathogens. Two med-
ications in this class, grepafloxacin
and sparfloxacin, have been with-
drawn from the market because of
adverse cardiac events and deaths.50
Ng et al21 found a high frequency
(58.4%) of aLQTS associated with
the use of levofloxacin in ICU patients.
Falagas et al51 also have reported lev-
ofloxacin-induced aLQTS. In another
study by Ng et al,25 moxifloxacin had
the highest rate of QTc prolongation
(48.1%) among all QTc-prolonging
medications (list not reported).
In all reported cases of torsades
de pointes related to fluoro-
quinolones, patients had at least 1
concomitant risk factor for torsades
de pointes.52 In our study, no patients
experienced torsades de pointes.
However, of the 6 patients who
received a fluoroquinolone and in
whom aLQTS developed, all but 1
(83%) had at least 1 other known
aLQTS risk factor. In 10 patients
who received a fluoroquinolone but
in whom aLQTS did not develop, 5
(50%) had at least 1 risk factor for
the syndrome. These results indicate
the importance of monitoring the
QTc interval in all patients receiving
this class of medications.
Azithromycin. We found a signifi-
cant association between azithromycin
and aLQTS. Macrolide antibiotics
such as azithromycin (Zithromax)
are used frequently in treating upper
and lower respiratory tract infections,
such as pneumonia.53 Case reports54,55
38 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012
Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
of QT prolongation that occurred
when azithromycin was combined
with amiodarone or disopyramide
have also been published.
More recently, azithromycin-
associated aLQTS has occurred in
patients not given any other known
QT-prolonging medications.56 For
example, a 90-year-old woman with
interstitial pneumonia and respira-
tory failure53 was given penicillin
(sulbactam) and azithromycin. Four
hours after receiving azithromycin,
the patient had a pronounced pro-
longed QT interval leading to a loss
of consciousness associated with
torsades de pointes. Her electrolyte
levels were within the normal refer-
ence range. Azithromycin was dis-
continued, and the QT interval
normalized the next day. In a second
case,56 a 55-year-old woman with
methicillin-resistant Staphylococcus
aureus sepsis from an implanted
pacemaker pocket experienced
atypical pneumonia on day 7 of her
hospital stay. Treatment with
azithromycin was started. After the
seventh daily dose of azithromycin,
she had 2 brief episodes of torsades
de pointes. A review of earlier ECGs
showed that QT prolongation had
occurred on the day treatment with
azithromycin was initiated.
Amiodarone. Amiodarone is a
class III antiarrhythmic that prolongs
repolarization homogeneously in
the 3 types of myocardial cells (epi-
cardial, endocardial, and midmy-
ocardial), resulting in prolongation
of the QT interval57 with a decreased
transmural dispersion of repolariza-
tion.58 Although amiodarone alone
is associated with a low risk for tor-
sades de pointes in patients with a
prolonged QT interval, concomitant
use with other QT-prolonging
medications can increase arrhyth-
mias, mortality, and ICU lengths of
stay.59 In our study, amiodarone
was a frequently used medication
associated with aLQTS. A total of 9
patients (10%) received amiodarone,
and aLQTS developed in 6 of the 9.
Of the 6 patients, 5 (83%) were given
at least 1 additional QT-prolonging
medication concomitantly. This
finding indicates that all patients
receiving amiodarone should have
QTc intervals monitored in the ICU.
Numerous medications fre-
quently administered in ICUs can
prolong the QTc interval. The risk
increases when 2 or more such med-
ications are administered concur-
rently.60-62 Among the patients in our
study who had aLQTS, 10 (22%)
received 2 or more QTc-prolonging
medications. Among the patients
who did not have aLQTS, 4 (10%)
received more than 1 QTc-prolonging
medication.
Risk Factors and aLQTS
We found no significant associa-
tion between host risk factors and
aLQTS. Risk factors, such as sex,30,63,64
body mass index,65,66 myocardial
ischemia,67,68 heart failure,69,70
hypothermia,71 and hypokalemia,72,73
have been correlated with prolonged
QT intervals in other studies.
Study Limitations
Because we used a retrospective
study design, control of variables
was not possible. For instance, rec-
ommendations for proper lead mon-
itoring in QT studies74,75 are to choose
the lead from a 12-lead ECG with
the longest QTc interval that has a
T wave with at least 2 mm of ampli-
tude and a well-defined end. In
addition, an important aspect of
www.ccnonline.org
measuring QT intervals is using the
same lead for repeat measurements
to ensure consistency.11 In our study,
nurses in the ICU changed leads
periodically, depending on which
lead provided findings that were the
easiest to interpret and had the least
amount of artifacts. Also, patients
may have left the unit for tests or
procedures and returned under the
care of a different nurse, who might
have changed the monitoring lead.
A retrospective analysis indicated
that 29 patients (33%) had lead
changes during the study period.
The most commonly used lead was
lead II (n=65; 74%).
Histories and demographic
information were obtained from the
medical records. Patients history
and findings on physical examina-
tion dictated by physicians and
admission data forms collected by
nurses were used to record comor-
bid conditions and reasons for
admission. Some patients were in a
comatose state or quite ill when they
were admitted; therefore we do not
know if the information provided by
patients families or friends were
complete or accurate.
The study ICU has a protocol to
assess QTc intervals every 6 hours,
and physicians are notified when
QTc prolongation is detected so
that the offending medication can
be discontinued. This practice may
have influenced the lack of torsades
de pointes in any patients. We did
not collect data on medications that
were discontinued or changed because
To learn more about long QT syndrome,
read Long QT Syndrome by Pelter and
Carey in the American Journal of Critical
Care, 2006;15:437-438. Available at
www.ajcconline.org.
www.ccnonline.org
Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
a patient had aLQTS. Finally, the
study sample size was small, possibly
contributing to a lack of power to
observe significance between associ-
ated risk factors and aLQTS.
Conclusions
We found that aLQTS was pres-
ent in approximately one-half of
ICU patients upon or soon after ICU
admission. A total of 6 frequently
administered medications, but not
host risk factors, were significant
predictors of aLQTS. In addition, in
50% of the patients, aLQTS developed
even though the patients did not
receive a known QTc-prolonging
medication, indicating that other
unknown variables may be associ-
ated with the syndrome.
Our results indicate a need to
assess QTc intervals in all ICU
patients immediately upon admis-
sion, because nearly one-third of
our patients had aLQTS when they
were admitted. Because of the high
frequency of aLQTS after ICU admis-
sion, continuous QTc monitoring is
also advised. If monitoring equip-
ment is not available to calculate
QTc intervals automatically, the
intervals should be assessed every
hour to help detect patients in whom
aLQTS develops shortly after admis-
sion. However, assessing QTc inter-
vals every hour may be difficult;
therefore, further research is needed
to determine a standardized yet fea-
sible and safe assessment interval
that can be used to detect patients
in whom aLQTS develops early.
Current best practice guidelines11,76
recommend monitoring patients
receiving a QT-prolonging medica-
tion before the medication is started
and every 8 to 12 hours for 48 to
72 hours after administration of
CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 39
the drug is started or the dosage is
increased. These current guidelines
for detecting aLQTS may not be
sufficient to identify all ICU patients
in whom aLQTS develops. With
proper monitoring policies that
incorporate a consistent protocol
for measuring QTc intervals,
aLQTS may be reversed by early
detection and prompt discontinua-
tion of culprit agents. Using consis-
tent equipment, methods, and lead
selection must be included in pro-
tocol development to ensure accu-
rate and consistent identification
of a prolonged QTc interval.11 Clini-
cians can detect patients at risk for
aLQTS early by being aware of QT-
prolonging medications frequently
used in the ICU.22 CCN
Now that youve read the article, create or contribute to
an online discussion about this topic using eLetters.
Just visit www.ccnonline.org and click Submit a
response in either the full-text or PDF view of the
article.
Acknowledgments
This research was conducted at Saint Marys
Regional Medical Center, Reno, Nevada.
Financial Disclosures
This study was partially supported by Spacelabs
Healthcare, Nevada Organization Nurse Leaders,
and the National Association of Clinical Nurse
Specialists.
References
1. Calkins H. Principles of electrophysiology.
In: Goldman L, Ausiello D, eds. Cecil Medi-
cine. 23rd ed. Philadelphia, PA: Saunders
Elsevier; 2007:390-393.
2. Schoen FJ. The heart. In: Kumar V, Abbas
AK, Fausto N, eds. Robbins and Cotran
Pathologic Basis of Disease. 7th ed. Philadel-
phia, PA: Saunders Elsevier; 2005:555-618.
3. Abriel H, Schlapfer J, Keller DI, et al.
Molecular and clinical determinants of
drug-induced long QT syndrome: an iatro-
genic channelopathy. Swiss Med Wkly. 2004;
134(47-48):685-694.
4. Prez Riera AR, Ferreira C, Dubner SJ,
Schapachnik E, Soares JD, Francis J. Brief
review of the recently described short QT
syndrome and other cardiac channel-
opathies. Ann Noninvasive Electrocardiol.
2005;10(3):371-377.
5. Priori SG, Napolitano C, Schwartz PJ.
Genetics of cardiac arrhythmias. In: Libby P,
Bonow RO, Mann DL, et al, eds. Braunwalds
Heart Disease: A Textbook of Cardiovascular
 Medicine. 8th ed. Philadelphia, PA: Saunders
Elsevier; 2008:101-109.
6. Lankipalli RS, Zhu T, Guo D, Yan G-X.
Mechanisms underlying arrhythmogenesis
in long QT syndrome. J Electrocardiol. 2005;
38:69-73.
7. Saenen JB, Vrints CJ. Molecular aspects of the
congenital and acquired long QT syndrome:
clinical implications. J Mol Cell Cardiol. 2008;
44:633-646.
8. Dumaine R, Antzelevitch C. Molecular
mechanisms underlying the long QT syn-
drome. Curr Opin Cardiol. 2002;17:36-42.
9. Gussak I, Litwin J, Kleinman R, Grisanti S,
Morganroth J. Drug-induced cardiac toxicity:
emphasizing the role of electrocardiography
in clinical research and drug development.
J Electrocardiol. 2004;37(1):19-24.
10. Roden DM. Drug-induced prolongation of
the QT interval. N Engl J Med. 2004;350(10):
1013-1022.
11. Drew BJ, Ackerman MJ, Funk M, et al;
American Heart Association Acute Cardiac
Care Committee of the Council on Clinical
Cardiology, Council on Cardiovascular
Nursing, American College of Cardiology
Foundation. Prevention of torsades de
pointes in hospital settings: a scientific
statement from the American Heart Associ-
ation and the American College of Cardiol-
ogy Foundation. J Am Coll Cardiol. 2010;
55(9):934-947.
12. Al-Khatib SM, LaPointe NM, Kramer JM,
Califf RM. What clinicians should know
about the QT interval. JAMA. 2003;289:
2120-2127.
13. Hoffman P, Warner B. Are hERG channel
inhibition and QT interval prolongation all
there is in drug-induced torsadogenesis? A
review of emerging trends. J Pharmacol Tox-
icol Methods. 2006;53(2):87-105.
14. Wung SF, Kozik TM. Electrocardiographic
evaluation of cardiovascular status. J Cardio-
vasc Nurs. 2008;23(2):169-174.
15. LaPointe NM, Curtis LH, Chan KA, et al.
Frequency of high-risk use of QT-prolonging
medications. Pharmacoepidemiol Drug Saf.
2006;15(6):361-368.
16. Zareba W. Drug induced QT prolongation.
Cardiol J. 2007;14(6):523-533.
17. Pueyo E, Martinez JP, Laguna P. Cardiac
repolarization analysis using the surface
electrocardiogram. Philos Transact A Math
Phys Eng Sci. 2009;367(1887):213-233.
18. Smith TW, Cain ME. Sudden cardiac death:
epidemiologic and financial worldwide per-
spective. J Interv Card Electrophysiol. 2006;
17(3):199-203.
19. Towbin JA, Vatta M. Molecular biology and
the prolonged QT syndromes. Am J Med.
2001;110:385-398.
20. Chiang C-E. Congenital and acquired long
QT syndrome: current concepts and man-
agement. Cardiol Rev. 2004;12(4):222-234.
21. Ng TMH, Bell AM, Hong C, et al. Pharmacist
monitoring of QTc interval-prolonging
medications in critically ill medical patients:
a pilot study. Ann Pharmacother. 2008;42:
475-482.
22. Arizona CERT: Center for Education and
Research on Therapeutics. QT drug lists by
risk groups. http://www.azcert.org/medical-
pros/drug-lists/drug-lists.cfm. Updated
June 24, 2012. Accessed July 4, 2012.
23. Reinelt P, Karth GD, Geppert A, Heinz G.
Incidence and type of cardiac arrhythmias in
critically ill patients: a single center experience
40 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012
Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
in a medical-cardiological ICU. Intensive
Care Med. 2001;27:1466-1473.
24. Drew BJ, Califf RM, Funk M, et al; American
Heart Association; Councils on Cardiovas-
cular Nursing, Clinical Cardiology, and Car-
diovascular Disease in the Young. Practice
standards for electrocardiographic monitor-
ing in hospital settings: an American Heart
Association scientific statement from the
Councils on Cardiovascular Nursing, Clinical
Cardiology, and Cardiovascular Disease in
the Young: endorsed by the International
Society of Computerized Electrocardiology
and the American Association of Critical-Care
Nurses [published correction appears in
Circulation. 2005;111(3):378]. Circulation.
2004;110(17):2721-2746.
25. Ng TMH, Olsen KM, McCarran MA, Speidel
KM, Miller MA, Levit AV. Pharmacologic
predictors of QTc prolongation in the adult
intensive care unit [abstract]. Crit Care Med.
2004;32:A40.
26. Golzari H, Dawson NV, Speroff T, Thomas C.
Prolonged QTc intervals on admission
electrocardiograms: prevalence and corre-
spondence with admission electrolyte abnor-
malities. Conn Med. 2007;71(7):389-397.
27. Molokhia M, Pathak A, Lapeyre-Mestre M,
Caturla L, Montastruc JL, McKeigue P. Case
ascertainment and estimated incidence of
drug-induced long-QT syndrome: study in
Southwest France. Br J Clin Pharmacol. 2008;
66(3):386-395.
28. Ramos-Ros R, Arrojo-Romero M, Paz-Silva E,
et al. QTc interval in a sample of long-term
schizophrenia inpatients. Schizophr Res.
2010;116(1):35-43.
29. Seftchick MW, Adler PH, Hsieh M, et al.
The prevalence and factors associated with
QTc prolongation among emergency
department patients. Ann Emerg Med. 2009;
54(6):763-768.
30. Bazett HC. An analysis of the time-relations
of electrocardiograms. Heart. 1920;7:353-370.
31. Owens RC. QT prolongation with antimicro-
bial agents. Drugs. 2004;64(10):1091-1124.
32. Tisdale JE, Kovacs R, Mi D, et al. Accuracy
of uncorrected versus corrected QT interval
for prediction of torsade de pointes associ-
ated with intravenous haloperidol. Pharma-
cotherapy. 2007;27(2):175-182.
33. Luo S, Michler K, Johnston P, Macfarlane
PW. A comparison of commonly used QT
correction formulae: the effect of heart rate
on the QTc of normal ECGs. J Electrocardiol.
2004;37(suppl):81-90.
34. Indik JH, Pearson EC, Fried K, Woosley RL.
Bazett and Fridericia QT correction formulas
interfere with measurement of drug-induced
changes in QT interval. Heart Rhythm. 2006;
3(9):1003-1007.
35. Malik M. Problems of heart rate correction
in assessment of drug-induced QT interval
prolongation. J Cardiovasc Electrophysiol. 2001;
12(4):411-420.
36. Dekker JM, Crow RS, Hannan PJ, Schouten
EG, Folsom AR. Heart rate-corrected QT
interval prolongation predicts risk of coro-
nary heart disease in black and white mid-
dle-aged men and women: the ARIC study.
J Am Coll Cardiol. 2004;23:1547-1553.
37. Karjalainen J, Viitasalo M, Manttari M,
Manninen V. Relation between QT intervals
and heart rates from 40-120 beats/min in
rest electrocardiograms of men and a simple
method to adjust QT interval values. J Am
Coll Cardiol. 1994;23(7):1547-1553.
38. Milne JR, Ward DE, Spurrell RA, Camm AJ.
The ventricular paced QT intervalthe
effects of rate and exercise. Pacing Clin Elec-
trophysiol. 1982;5(3):352-358.
39. ICH Expert Working Group. The clinical
evaluation of QT/QTc interval prolongation
and proarrhythmic potential for non-antiar-
rhythmic drugs. ICH Harmonised Tripartite
Guideline E14. http://www.ich.org/fileadmin
/Public_Web_Site/ICH_Products
/Guidelines/Efficacy/E14/E14_Guideline
.pdf. Finalized May 2005. Accessed July 4,
2012.
40. McConachie I, Keaveny JP, Healy TE, Vohra
S, Million L. Effect of anaesthesia on the QT
interval. Br J Anesth. 1989;63:558-560.
41. Michaloudis D, Fraidakis O, Lefaki T, et al.
Anaesthesia and the QT interval in humans:
the effects of isofluane and halothane.
Anaesthesia. 1996;51(3):219-224.
42. Schmeling WT, Warltier DC, McDonald DJ,
Madsen KE, Atlee JL, Kampine JP. Prolonga-
tion of the QT interval by enflurane, isoflu-
rane, and halothane in humans. Anesth Analg.
1991;72:137-144.
43. Yildirim H, Adanir T, Atay A, Katircioglu K,
Savaci S. The effects of sevoflurane, isoflu-
rane and desflurane on QT interval of the
ECG. Eur J Anaesthesiol. 2004;21:566-570.
44. Charbit B, Albaladejo P, Funck-Brentano C,
Legrand M, Samain E, Marty J. Prolongation
of the QTc interval after postoperative nau-
sea and vomiting treatment by droperidol
or ondansetron. Anesthesiology. 2005;102:
1094-1100.
45. Charbit B, Alvarez JC, Dasque E, Abe E,
Demolis JL, Funck-Brentano C. Droperidol
and ondansetron-induced QT interval pro-
longation: a clinical drug interaction study.
Anesthesiology. 2008;109(2):206-212.
46 Habib AS. The use of droperidol before and
after the Food and Drug Administration black
box warning: a survey of the members of
the Society of Ambulatory Anesthesia. J
Clin Anesth. 2008;20(1):35-39.
47. Abe K, Takada K, Yoshiya I. Intraoperative
torsade de pointes ventricular tachycardia
and ventricular fibrillation during sevoflurane
anesthesia. Anesth Analg. 1998;86:701-702.
48. Lustik SJ, Eichelberger JP, Chibber AK,
Bronsther O. Torsade de pointes during
orthoptic liver transplantation. Anesth
Analg. 1998;87:300-303.
49. Dolenska S. Intraoperative cardiac arrest in
acquired long QT syndrome. Br J Anaesth.
2009;102(4):503-505.
50. Simko J, Csilek A, Karaszi J, Lorincz I. Proar-
rhythmic potential of antimicrobial agents.
Infection. 2008;36:194-206.
51. Falagas ME, Rafailidis PI, Rosmarakis ES.
Arrhythmias associated with fluoroquinolone
therapy. Int J Antimicrob Agents. 2007;29:
374-379.
52. Amankwa K, Krishnan SC, Tisdale JE. Tor-
sades de pointes associated with fluoro-
quinolones: importance of concomitant risk
factors. Clin Pharmacol. 2004;75:242-247.
53. Huang B-H, Wu C-H, Hsia C-P, Chen CY.
Azithromycin-induced torsade de pointes.
Pacing Clin Electrophysiol. 2007;30:1579-1582.
54. Samarendra P, Kumari S, Evan SJ, Sacchi TJ,
Navarro V. QT prolongation associated with
azithromycin/amiodarone combination.
Pacing Clin Electrophysiol. 2001;24(10):1572-
1574.
55. Granowitz EV, Tabor KJ, Kirchhoffer JB. Poten-
tially fatal interaction between azithromycin
www.ccnonline.org
 and disopyramide. Pacing Clin Electrophysiol.
2000;23(9):1433-1435.
56. Kezerashvili A, Khattak H, Barsky A, Nazari
R, Fisher JD. Azithromycin as a cause of QT-
interval prolongation and torsade de pointes
in the absence of other known precipitating
factors. J Interv Card Electrophysiol. 2007;18:
243-246.
57. Antzelevitch C. Ionic, molecular, and cellular
bases of QT-interval prolongation and torsade
de pointes. Europace. 2007;9(suppl 4):iv4-iv15.
58. Antzelevitch C. Arrhythmogenic mechanisms
of QT prolonging drugs: is QT prolongation
really the problem? J Electrocardiol. 2004;
37(suppl):15-24.
59. Freeman BD, Dixon DJ, Coopersmith CM,
Zehnbauer BA, Buchman TG. Pharmacoepi-
demiology of QT-interval prolonging drug
administration in critically ill patients. Phar-
macoepidemiol Drug Saf. 2008;17(10):971-981.
60. Moss AJ. The QT interval and torsades de
pointes. Drug Saf. 1999;21(suppl 1):5-10.
61. Curtis LH, Ostegye T, Sendersky V, et al.
Prescription of QT-prolonging drugs in a
cohort of about 5 million outpatients. Am J
Med. 2003;114(2):135-141.
62. DePonti F, Poluzzi E, Montanaro N. QT-
interval prolongation by non-cardiac drugs:
lessons to be learned from recent experience.
Eur J Clin Pharmacol. 2000;56:1-18.
63. Arya A. Gender-related differences in ventric-
ular repolarization: beyond gonadal steroids.
J Cardiovasc Electrophysiol. 2005;16(5):525-527.
www.ccnonline.org
Downloaded from ccn.aacnjournals.org at Mobile User on May 9, 2013
64. Bidoggia H, Maciel JP, Capalozza N, et al.
Sex differences on the electrocardiographic
pattern of cardiac repolarization: possible
role of testosterone. Am Heart J. 2000;140(4):
678-683.
65. Carella MJ, Mantz SL, Rovner DR, et al.
Obesity, adiposity, and lengthening of the QT
interval: improvement after weight loss. Int
J Obes Relat Metab Disord. 1996;20(10):938-942.
66. El-Gamal A, Gallagher D, Nawras A, et al.
Effects of obesity on QT, RR, and QTc inter-
vals. Am J Cardiol. 1995;75(14):956-959.
67. Kawabata M, Hirao K, Takeshi S, et al. Tor-
sades de pointes related to transient marked
QT prolongation following successful emer-
gent percutaneous coronary intervention
for acute coronary syndrome. J Electrocardiol.
2008;41(2):117-122.
68. Sezgin AT, Barutcu I, Ozdemir R, et al.
Effect of slow coronary flow on electrocardio-
graphic parameters reflecting ventricular
heterogeneity. Angiology. 2007;58(3):289-294.
69. Phang SH, White PD. The duration of ven-
tricular systole as measured by the QT inter-
val of the electrocardiogram, with a special
reference to cardiac enlargement with and
without congestive failure. Am Heart J. 1943;
26(1):108-113.
70. Xu X, Rials SJ, Wu Y, et al. Left ventricular
hypertrophy decreases slowly but not rapidly
activating delayed rectifier potassium currents
of epicardial and endocardial myocytes in
rabbits. Circulation. 2001;103(11): 1585-1590.
CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 41
71. Gould L, Gopalaswamy C, Kim BS, Patel C.
The Osborn wave in hypothermia. Angiol-
ogy. 1985;36:125-129.
72. Hanton G, Yvon A, Provost JP, Racaud A,
Doubovetzky M. Quantitative relationship
between plasma potassium levels and QT
interval in beagle dogs. Lab Anim. 2007;41(2):
204-217.
73. Kannankeril PJ, Roden DM. Drug-induced
long QT and torsade de pointes: recent
advances. Curr Opin Cardiol. 2007;22(1):39-43.
74. Lepeschkin E, Surawicz B. The measure-
ment of the Q-T interval of the electrocar-
diogram. Circulation. 1952;6:378-388.
75. Rautaharju PM, Surawicz B, Gettes LS.
AHA/ACCF/HRS recommendations for the
standardization and interpretation of the
electrocardiogram, part IV: the ST segment,
T and U waves, and the QT interval. J Am
Coll Cardiol. 2009;53(11):982-991.
76. Drew BJ, Funk M. Practice standards for ECG
monitoring in hospital settings: executive
summary and guide for implementation. Crit
Care Nurs Clin North Am. 2006;18:157-168.