Journal of the Academy of Consultation-Liaison Psychiatry 2021:62:501–510

Published by Elsevier Inc. on behalf of Academy of Consultation-Liaison Psychiatry.

Review Article

Assessment of QTc and Risk of Torsades de

Pointes in Ventricular Conduction Delay and
Pacing: A Review of the Literature and Call to
Action

Margo C. Funk, M.D., M.A., Kevin W. Cates, M.D., M.P.H.,

Aishwarya Rajagopalan, D.O., M.H.S., Chadrick E. Lane, M.D., Junyang Lou, M.D., Ph.D.

Background: Assessment of the heart rate–corrected
QT-interval on the 12-lead electrocardiogram when
prescribing medications known to increase the risk of
Torsades de Pointes has become a common part of
consultation-liaison psychiatry practice. Objectives:
Highlighted by a patient who experienced psychiatric
decompensation due to inaccurate interpretation of QTc
prolongation in the setting of a wide QRS complex, we
aimed to describe the approach to QTc interpretation in
patients with ventricular conduction delay. Methods: We
reviewed the current literature on the approach to
assessment of prolonged repolarization in patients with
ventricular conduction delay due to bundle branch block
(BBB) and ventricular pacing. Results: Physicians of
any specialty may perform initial electrocardiogram
interpretation and should be proficient in the definition,
recognition, and understanding of the basic pathophysi-
ology of electrocardiographic abnormalities. We discuss
current approaches to assessment of the QT-interval in
patients with a wide QRS complex due to bundle branch
block and ventricular pacing, including bivariate QTc
modification, univariate QT-interval modifications, and
use of the JT-interval. Conclusions: The QT-interval is
prolonged ipso facto in patients with a wide QRS com-
plex from ventricular conduction delay/ventricular pac-
ing and must be adjusted for QRS duration. Multiple
formulae have been proposed to account for wide QRS
complex in this setting with no single universally
accepted methodology. We suggest the use of either the
Bogossian formula or JT-interval followed by Hodges or
Framingham heart-rate correction to adjust for a wide
QRS complex. It is critical that the C-L psychiatrist be
able to identify a wide QRS complex on the electrocar-
diogram, understand implications for accurate assess-
ment of prolonged depolarization, and apply an
appropriate correction methodology.
(Journal of the Academy of Consultation-Liaison
Psychiatry 2021; 62:501–510)

Key words: cardiovascular disease, Torsades de pointes, QTc prolongation, wide QRS, bundle branch block,
ventricular pacing.

INTRODUCTION
Prolongation of the heart rate–corrected QT-interval
(QTc) on the electrocardiogram (ECG) is a risk factor
for Torsades de Pointes (TdP), a rare but life-
threatening ventricular arrhythmia. Certain medica-
tions, including psychotropic agents, may lead to pro-
longation of the QTc and precipitate TdP.1 The
Received December 1, 2020; accepted January 27, 2021. From the
Harvard Medical School (M.C.F., K.W.C., A.R., J.L.), Boston, MA;
Boston University School of Medicine (C.E.L.), Boston, MA; VA Bos-
ton Healthcare System (M.C.F., K.W.C., A.R., C.K.L.), Brockton, MA;
Division of Cardiovascular Medicine (J.L.), Brigham and Women’s
Hospital, Boston, MA. Send correspondence and reprint requests to
Margo C. Funk, MD, MA, 940 Belmont Street, Psychiatry 116A7,
Brockton, MA 02301; e-mail: margo.funk@va.gov
Published by Elsevier Inc. on behalf of Academy of Con-
sultation-Liaison Psychiatry.

Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021 501

QTc in Ventricular Conduction Delay
assessment of the QTc has become part of daily clinical
practice of the consultation-liaison (C-L) psychiatrist;
however, there are limited data available on the accu-
rate measurement and interpretation of QTc in cases of
wide QRS complex.
We present the case of a patient who experienced
psychiatric decompensation after psychotropic medi-
cations were changed in the setting of “QTc prolonga-
tion” due to a wide QRS complex from ventricular
pacing (VP). We discuss the approach to QTc inter-
pretation in patients with ventricular conduction delay
(VCD) from bundle branch block and VP. We present a
call-to-action for C-L psychiatrists, as experts at the
interface of psychiatry, psychopharmacology, and
complex medical illness, to become comfortable and
proficient with nuances of ECG interpretation that may
directly impact treatment.
CASE PRESENTATION
An 87-year-old male, Mr. A, with a history of un-
specified neurocognitive disorder, major depressive
disorder, coronary artery disease, and chronic diastolic
heart failure, status after implantation of a dual-
chamber pacemaker for history of second degree
(Mobitz type II) heart block, was brought to the
emergency department by police for agitation and
threatening behavior. He was in his usual state of
health and living alone until 6 weeks before presenta-
tion, when he became acutely confused and paranoid.
Medical workup at the time was unremarkable, and he
was admitted to an inpatient geriatric psychiatry unit
where he was diagnosed with vascular dementia and
stabilized on low-dose olanzapine. He was then dis-
charged to a subacute behavioral health rehabilitation
center. On the day of presentation, he was found
looking for a knife and expressing homicidal ideation
toward staff. Collateral from Mr. A’s daughter and the
rehabilitation center revealed he had been paranoid
throughout his stay, believing that people were plotting
to kill him and intermittently refusing food for fear it
was poisoned. The daughter confirmed olanzapine had
been helpful for the paranoia and agitation, but for
unclear reasons, it was not restarted upon initial
transfer to the rehabilitation center. Mr. A was then
readmitted to the medical inpatient unit for further
evaluation.
502 Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021
Vital signs and laboratory tests (for example,
complete blood count, comprehensive metabolic panel
including serum potassium [4.1 mmol/L], serum mag-
nesium [2.0 mg/dL], urinalysis, urine toxicology) were
unremarkable. Head CT was not obtained, and at-
tempts at brain MRI were precluded by the presence
of the pacemaker. The computer-interpreted ECG
(Figure 1A–B) demonstrated normal sinus rhythm at a
rate of 77 beats per minute (bpm) with VP, a wide QRS
complex of 180 ms, QT-interval of 494 ms, and QTc
(Bazett) of 559 ms. Based on “QTc prolongation,”
olanzapine was withheld, and aripiprazole was initiated
to “minimize cardiac risk.” Over the next 7 days, Mr. A
experienced worsening paranoia and agitation, marked
by poor sleep, response to internal stimuli, elopement
attempts, and episodes of extreme fearfulness that were
difficult to redirect, despite scheduled and as-needed
aripiprazole doses.
On hospital day (HD) 7, aripiprazole was dis-
continued, and quetiapine 12.5 mg po qHS was initi-
ated per recommendation of the C-L psychiatry team
who provided reassurance that the “prolonged” QTc
(Bazett), now 552 ms per computerized interpretation,
was due to the wide QRS complex (170 ms) from VP,
rather than prolonged repolarization. Mr. A quickly
responded to quetiapine, which was titrated to a dose of
25 mg po qHS. By HD 13, he was sleeping well with no
evidence of paranoia and no utilization of as-needed
medications for agitation. On HD 14 and over a
weekend, with the psychiatry consultation team having
signed off, a new medicine team came on service, and
the quetiapine was decreased to 12.5 mg again for
concerns of “QTc prolongation” after the ECG
demonstrated a QTc (Bazett) of 559 ms. Mr. A expe-
rienced recurrence of paranoia. The C-L psychiatry
team was reconsulted, provided reassurance, and rec-
ommended to increase the dose back to 25mg po qHS.
Mr. A’s paranoia resolved, and he was eventually dis-
charged home with stable follow-up ECGs.
DISCUSSION
TdP is a well-known cardiovascular event that occurs in
the setting of prolonged ventricular repolarization. The
QT-interval on the 12-lead ECG, when measured,
corrected, and interpreted accurately, is one of the
central tools in the recognition of TdP risk. Medica-
tions that prolong ventricular repolarization do so
 Funk et al.

FIGURE 1. (A) Twelve-lead ECG from the case presentation demonstrating a wide QRS complex from ventricular pacing. (B) A single cycle length
in lead V3 from the same ECG showing the ventricular pacing spike, widened QRS complex, QT-interval, and JT-interval. (C) Normal
comparison ECG showing a narrow QRS complex. Note the consistent JT-interval duration between panel B and C.

B wide C normal
QRS QRS

JT
pacing JT
spike
QT

QT

through direct blockade of the inward rectifier potas-
sium channel (IKr) of the cardiac myocyte, encoded by
the human-ether-a-go-go related gene.2 Most cases of
TdP occur in the context of multiple risk factors,
including the use of more than one QTc-prolonging
medication, female sex, older age, bradycardia, struc-
tural or functional heart disease, personal or family
history of sudden cardiac death, renal/hepatic impair-
ment, and electrolyte disturbance (hypokalemia, hy-
pomagnesemia, and hypocalcemia).1
The QT-interval is HR-dependent and requires
correction (QTc) to ensure consistency across HRs. The
Bazett formula3 has been used in most clinical, regu-
latory, and research settings since the 1920s and is the
default correction method used by most computerized
ECG interpretation software programs. In 2017, the
FDA transitioned from use of the Bazett formula to the
Fridericia formula4 in recognition of the inadequacy of
the Bazett formula, which overestimates the QTc at fast
HR and underestimates at low HR.5 The American
College of Cardiology (ACC), American Heart Asso-
ciation (AHA), and Heart Rhythm Society (HRS)
recommend the use of linear regression formulae such
as Hodges6 and Framingham7 for HR correction.8
Most online and app-based QTc calculators now
include options for selection of the aforementioned QTc
formulae.
While computerized ECG interpretation is the
standard of care in most clinical settings, it is known to
be unreliable in measuring and correcting the QT-
interval, especially in cases of increased heart rate
and/or prolonged QRS duration.9,10 Furthermore, as
illustrated in our case, clinicians relying on the QTc for
medical decision-making must independently assess
each component of the QTc equation and be aware of
the effect of QRS duration, heart rate, and correction
method on the QTc. If taken at “face value,” the
computer-interpreted ECG may lead to erroneous

Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021 503

QTc in Ventricular Conduction Delay
medical decisions that could negatively impact patient
care. A survey of internists and psychiatrists, when
asked to measure the QT-interval and correctly identify
factors associated with QTc-prolongation, demon-
strated a substantial lack of knowledge about the QT-
interval among both specialties.11 An international
study of 902 physicians found that greater than 50% of
cardiologists and 60% of noncardiologists (including
internal medicine, neurology, pediatrics, emergency
medicine, critical care, gastroenterology, and others)
could not correctly calculate, and commonly over-
estimated, the QTc in healthy subjects.12 Hence, it is
paramount that C-L psychiatrists recognize and close
this widespread practice gap.
The ACC and AHA recognize that physicians of
any specialty may provide initial ECG interpretation in
the absence of a cardiologist overread. When such in-
terpretations contribute to clinical decision-making,
physicians should have an adequate knowledge base
to “define, recognize, and understand the basic patho-
physiology of certain electrocardiographic abnormal-
ities.”13 The American Psychiatric Association, with
the endorsement of the ACC, recently published a set of
clinical considerations advising that psychiatrists
should be proficient in ECG interpretation, especially
as related to measurement and heart rate correction of
the QT-interval.1 Although not explicitly defined, pro-
ficient interpretation of the QT-interval includes accu-
rate identification of ECG elements, measurement of
relevant intervals, and thoughtful use of recommended
heart rate correction formulae, with the ultimate goal of
making appropriate and timely clinical decisions.
Assessment of the QT-Interval With Wide QRS
Complex
Assessment of the QT-interval in the context of a wide
QRS complex from VCD or VP is a common challenge
in electrocardiography.8 The QT-interval is composed of
a period of depolarization (QRS complex) and repolar-
ization (the JT-interval) (Figure 2A). Ventricular depo-
larization originates at the atrioventricular node and
spreads rapidly through the Bundle of His, right and left
(divided into anterior and posterior fascicles) bundle
branches, and Purkinje fibers. This sequence of electrical
activity forms the QRS complex on the ECG, typically
over a period of 80–100 ms (“narrow” QRS; Figure 1C).
Injury to or degeneration of these structures may lead to
slower, cell-to-cell conduction of depolarization and
504 Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021
widening of the QRS complex (Figure 2B–C). VCD is
defined by a QRS complex $110 ms and includes
nonspecific intraventricular conduction delay (QRS
110–119 ms) and left or right bundle branch block
(QRS $ 120 ms).14–16 VP, either by stimulation of the
right ventricle (RV pacing) or both ventricles (biven-
tricular pacing), predominantly depolarizes the ventric-
ular myocardium via cell-to-cell activation, which
predictably widens the QRS complex (Figure 2D).
QT-interval prolongation in VCD and VP is
thought to represent a heterogenous group of patients,
including those with delayed repolarization phases of the
myocardial action potential (“true” QT-interval pro-
longation) and those with normal action potential
repolarization where the QT-interval is prolonged purely
because of QRS widening.8,17 For the purposes of TdP
risk assessment, it is reasonable to consider the presence
of VCD or VP as evidence of structural or functional
heart disease; however, this should be considered sepa-
rately from the interpretation of the QTc, which should
always include a correction for the wide QRS complex.
There is no standardized method for measurement
of the QT-interval in the setting of VCD and VP.18 The
most recent consensus statement on standardization
and interpretation of the ECG by the AHA, ACC, and
HRS recommends adjustment for both QRS duration
as well as heart rate, or the use of an alternative in-
terval, such as the JT.8 Several wide QRS complex
correction methods for the QT- and JT-intervals are
described in detail in the following paragraphs and
presented in Table 1.
QT-Interval Correction Methods for Wide QRS
Complex
A variety of methods to correct the QT-interval for a
wide QRS complex have been studied and validated
(Table 1). A common method used in historical clinical
practice is to subtract a correction factor of 50 ms from
the QTc (Bazett) if the QRS complex is widened
because of VCD or VP. Not surprisingly, this method
fails to accurately compensate for the effect of VP on
the QTc at various heart rates.19 Notably, there are no
studies validating subtraction of 50 ms from the QT-
interval before heart rate correction (i.e., QTc(modi-
fied) = (QT-50)/RR1/2). Another approach, sometimes
known as the “Simple Method,” uses manufacturer’s
monitoring recommendations for in-hospital loading of
the antiarrhythmic drug dofetilide. Using the Simple
 Funk et al.

FIGURE 2. Cardiac Conduction System with ECG Correlates. Active and inactive conduction system components are shown in yellow and grey,
respectively. Depolarization and repolarization are shown in magenta and aqua, respectively. (A) Normal cardiac conduction. (B)
Ventricular depolarization in right bundle branch block (RBBB) demonstrating rapid conduction through the left bundle branch and
anterior/posterior fascicles followed by slower cell-to-cell conduction into the right ventricle. (C) Ventricular depolarization in left bundle
branch block (LBBB) demonstrating rapid conduction through the right bundle branch followed by slower cell-to-cell conduction into the
left ventricle. (D) Ventricular depolarization in the setting of ventricular pacing demonstrating slow cell-to-cell conduction throughout
the ventricles originating with the pacemaker lead in the right ventricle.

A
Normal Cardiac Conduction

Bundle of His LBB Left anterior

fascicle
SA node

Internodal
pathways

AV node

RBB
Left posterior
fascicle

P QRS JT

B C D
RBBB LBBB Ventricular Pacing

Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021 505

QTc in Ventricular Conduction Delay
Method, patients with a wide QRS complex are
considered at risk if the QTc . 500 ms.20
Over the last 3 decades, numerous groups have
derived various correction methods to rigorously cor-
rect the QT-interval for heart rate and prolonged QRS
duration. The largest study to date, by Rautaharju
et al.,21 which compared ECGs from 11,739 subjects
with normal ventricular conduction to those of 1251
subjects with VCD, suggests adjusting the QT-interval
as a linear function using the RR interval and QRS
duration as covariates without additional heart rate
correction (Rautaharju formula). A related linear for-
mula (Rautaharju-JTc) was derived for JT-interval
correction. These formulae effectively removed heart
rate dependence of the QT/JT intervals but are incon-
venient for routine use in the clinical setting because of
their complexity.
The Bogossian formula is a recently derived and
simple methodology, which has been widely validated
in patients with new-onset and chronic LBBB, as well
as right and left VP.22–26 The wide QRS is reduced by a
factor of 0.485 (simplified to 0.50*QRS) and subtracted
from the QT interval. The “modified” QT (QTm) is
then subjected to traditional heart rate correction
formulae. A recent prospective study of patients with
induced right bundle branch block from transient left
VP showed that the use of the Bogossian formula fol-
lowed by QTc correction with the Hodges linear
correction was more reliable than Bogossian in com-
bination with Bazett or Fridericia.26
Several smaller studies that have derived addi-
tional adjustment formulae for VCD/VP are described
in Table 1; however, given the small sample sizes in
narrowly defined patient populations, these methods
will require additional validation to be generalizable.
The “Fixed QRS” method was validated in a study of
48 patients who developed new-onset LBBB after
transcatheter aortic valve replacement.27 Wang et al.
validated a new formula in a sample of 22 subjects
with intermittent LBBB.28 A study of subjects with
right VP by Tang et al.29 validated the use of a
modification of a novel cubic regression spline QTc
method introduced by Rabkin et al.43 Finally, a recent
algorithm by Guidicessi et al.30 recommends a varia-
tion of the fixed QRS method whereby the difference
of QRS-100 is subtracted from the QT-interval. A
further variation of this method [QTm = QT – (QRS-
120)] appears to be used in the Mayo Clinic Online
QTc Calculator44 and is the only known online or app-
506 Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021
based calculator that corrects QTc for a wide QRS
complex. While the availability of this calculator is an
important advancement and provides a conservative
estimate for a modified QT-interval, limitations
include the use of the Bazett formula as the primary
heart rate correction and lack of validation studies for
either formula.
JT-Interval and Alternative Correction Methods for
Wide QRS Complex
An alternative method to adjust the QT-interval in pa-
tients with a wide QRS complex is to use the JT-interval,
which effectively excludes the QRS complex from eval-
uation (i.e., QT = QRS 1 JT). A study of 8025 partic-
ipants of the Third Health and Nutrition Examination
Survey examining all-cause mortality across different
levels of QRS duration demonstrated that the uncor-
rected JT-interval was more predictive of mortality than
the uncorrected QT-interval in patients with QRS
duration . 120 ms.45 Heart rate correction methods
for the JT-interval (JTc) are identical to those for the
QT-interval (QTc), except the bivariate Rautaharju-JTc
correction, and have been studied in a number of clinical
settings.27,31–33 The Bazett, Hodges, Fridericia, Fra-
mingham, Karjalainan-Nomogram,41 and Rautaharju-
JTc formulae were extensively compared by Chiladakis
et al., who recommended the use of Hodges, Framing-
ham, or Karjalainan-Nomogram methods for correction
of the JT-interval.39 The normal range of JTc has been
established to be 355 ms for males and 372 ms for fe-
males.27 An additional JT method, the JT prolongation
index, uses a simple heart rate correction factor to
convert the “normal” JT interval to 100 and designates
an upper limit of 112; however, this method has not been
widely validated.34
A final non–QT-interval method to assess prolon-
gation of repolarization measures the duration from the
peak to the end of the downward slope of the T-wave
(Tpeak-Tend or Tp-Te).35 The Tp-Te is associated with
increased odds of sudden cardiac death and has been
suggested as an alternative to the QTc/JTc in cases of
widened QRS.46 The Tp-Te corresponds to transmural
dispersion of repolarization of the ventricular myocar-
dium, a period during which differential rates of repo-
larization among the different types of myocardial cells
may lend to vulnerability to early afterdepolarizations,
a common trigger for TdP.47 There is no consensus on
the value at which Tp-Te is considered prolonged, with
validation studies ranging from .74 to .113ms
 Funk et al.

TABLE 1. Correction Methods to Estimate Repolarization Abnormality in the Setting of Wide-QRS from Ventricular Conduction Delay and
Ventricular Pacing
Name Formula/Method Validation studies* Requires HR
correction
QT-interval correction methods
Minus 50 Method QTcm = QTc – 50ms Chakravarty et al., 201519 Yes
“Simple Method”20 QTc abnormal when .500ms in setting of VCD n/a Yes
Rautaharju QTc = QT – 155*(RR – 1) – 0.93*(QRS – 139) 1 k Rautaharju et al., 200421 No
k = -22 ms (man); -34 ms (woman)
Bogossian QTm = QT – 0.485*QRS Bogossian et al., 201422 Yes
QTm = QT – 0.50*QRS (simplified) Bogossian et al., 201723
Frommeyer et al., 201724
Weipert et al., 201825
Erkapic et al., 202026
Fixed QRS QTcm = QTc – (QRS – ideal QRS) Yankelson et al., 201827 Yes
ideal QRS = 95 ms (man); 88 ms (woman)
Wang QTm = QT – (0.86*QRS – 71) Wang et al., 201728 Yes
Tang QTcm(Spline) = QTc(Spline)*0.86 Tang et al., 201929 Yes
Giudicessi30 QTm = QT – (QRS – 100) n/a Yes
JT-interval correction methods
JTc JTc = QTc – QRS or JT = QT – QRS Crow et al., 200331 Yes
JTc prolonged if .355 ms (man); .372 ms (woman) Rautaharju et al., 200421
Tsai et al., 201432
Tabatabaei et al., 201633
Yankelson et al., 201827
Rautaharju - JTc JTc = JT 2 155 3 (60/HR 2 1) 1 k Rautaharju et al., 200421 No
k = 34 ms (man); 22 ms (woman)
JT Index JTI = JT (HR 1 100)/518 Zhou et al., 199234 No
prolonged if . 112
Other correction method
Tp-Te Tp – Te = T-wave peak – T-wave end Yan and Antzelevitch, 199835 No
variable upper limits of normal from .74 ms to .113 ms Lubinski et al., 200036
Topilski et al., 200737
Haarmark et al., 200938
Heart rate correction
formulae QTc/JTc
Bazett QTc (JTc) = QT(JT)/RR1/2 Bazett, 19203 n/a
Fridericia QTc (JTc) = QT(JT)/RR1/3 Fridericia, 19204 n/a
Framingham QTc (JTc) = QT(JT) 1 0.154 (1-RR) Sagie et al., 19927 n/a
Chilidakis et al., 201239
Chilidakis et al., 201340
Hodges QTc (JTc) = QT(JT) 1 1.75 (HR 2 60) Hodges et al., 19836 n/a
Chilidakis et al., 201239
Erkapic et al., 202026
Karjalainen-Nomogram QTc (JTc) = QT 1 correction number Karjalainen et al., 199441 n/a
correction number is heart-rate dependent Chilidakis et al., 201239
Chilidakis et al., 201340
Chan-Nomogram QT is plotted on graph as function of HR Chan et al., 200742 n/a

HR = heart rate (bpm); n/a = not applicable; QTcm = QTc modified for wide QRS complex; QTm = QT-interval modified for wide QRS
complex; RR = R-R interval (seconds); VCD = ventricular conduction delay.
* Validation studies include original study if based on a validation data set and subsequent positive validation studies in subjects with wide
QRS.

depending on the type of cardiac pathology.36–38 While CONCLUSIONS

Tp-Te may provide adjunctive risk stratification, it
should not be used as a stand-alone marker of TdP C-L psychiatrists often make expert recommendations
risk.48 about the use of psychotropic medications in patients

Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021 507

QTc in Ventricular Conduction Delay

FIGURE 3. Algorithm for QTc/JTc Adjustment for Wide QRS from Ventricular Conduction Delay or Ventricular Pacing.

STEP 1: Obtain ECG Measurements (QT, QRS, RR/HR)

QRS complex ≥ 110ms?

YES NO

STEP 2: Select Wide QRS STEP 3: Select Heart Rate

Correc on Method Correc on Method
QTc and JTc
Upper Limits of Normal
BOGOSSIAN SIMPLIFIED HODGES
QTm = QT – 0.5*QRS QTc = QTm + 1.75 (HR – 60)
QTc
men 450 ms
JT INTERVAL FRAMINGHAM
women 460 ms
JT = QT – QRS QTc = QTm + 0.154 (1 – RR)

JTc
QTm = QT modified for wide QRS JTc: subs tute JT for QTm
men 355 ms
women 372 ms
OR
STEP 2: Bivariate Wide QRS + Heart Rate Correc on

RAUTAHARJU FORMULA
QTc = QT – 155*(RR – 1) – 0.93*(QRS – 139) + k
k = -22ms, man; -34ms, woman

with complicated medical issues, including cardiac
disease. It is imperative that C-L psychiatrists can
accurately identify and measure ECG components
including the QT-interval, JT-interval, and QRS com-
plex. Furthermore, C-L psychiatrists must understand
the pathophysiologic implications of a wide QRS
complex on the QT-interval and apply appropriate
correction methods. For patients with a wide QRS
complex from VCD or VP, we propose an easy-to-use
algorithm for QTc/JTc adjustment (Figure 3). We
recommend the use of either the simplified Bogossian
formula or the JTc (both of which are easy to use and
widely validated across different populations) to assess
prolongation of repolarization followed by use of the
Hodges or Framingham linear regression heart rate
correction formulae which are most reliable in patients
with VCD/VP.26,33,41 Practice cases demonstrating use
of these methods are included in the Appendix. The
bivariate Rautaharju QTc formula may also be used;
however, its complexity makes it inconvenient for
clinical practice. Looking back to our case, application
of the simplified Bogossian and JTc corrections to the

508 Journal of the Academy of Consultation-Liaison Psychiatry 62:5, September/October 2021


ECGs on HDs 1, 7, and 14 resulted in QTcm(H)/
JTc(H) of 405 ms/320 ms, 388 ms/303 ms, and 409 ms/
320 ms, respectively, confirming that with appropriate
correction for the wide QRS, both QTc and JTc values
were well within the normal range and did not support
the decision to switch nor reduce the patient’s anti-
psychotic medication.
As the expert at the interface of psychopharma-
cology and complex medical illness, the C-L psychi-
atrist must be aware of the knowledge gap about the
QT-interval across medical specialties, serve as liaison
to provide nuanced education about the QTc and
ECG as it relates to prescription of psychotropic
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needlessly result in psychiatric decompensation or
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Disclosure: The authors report no proprietary or
commercial interest in any product mentioned or concept
discussed in this article. Drs. M. C. F., K. W. C., and A.
R. are employed by the US Department of Veterans
Affairs; the opinions expressed in this article belong to
the authors and do not reflect those of the US Depart-
ment of Veterans Affairs.
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