Education in Heart
Management of arrythmias during pregnancy
1
Cardiology, Toronto General
Hospital, Toronto, Ontario,
Canada
2
Toronto General Hospital,
Toronto, Ontario, Canada
Correspondence to
Dr Danna A Spears, Toronto
General Hospital, Toronto, ON
M5G 2C4, Canada;
​danna.​spears@​uhn.​ca
© Author(s) (or their
employer(s)) 2023. No
commercial re-­use. See rights
and permissions. Published
by BMJ.
To cite: Albertini L,
Spears DA. Heart Epub ahead
of print: [please include Day
Month Year]. doi:10.1136/
heartjnl-2023-322746
Lisa Albertini ‍ ‍,1 Danna A Spears ‍ ‍2
INTRODUCTION
A sensation of abnormal or irregular heart beating
is a very common symptom in pregnancy. This is
often secondary to sinus tachycardia, sinus brady-
cardia and sinus arrhythmia, or isolated premature
atrial or ventricular arrhythmias (VAs). The overall
incidence of arrhythmia documented in pregnancy
is reported to be in the range of 0.03%–0.5% of
pregnancies,1 making this one of the most common
cardiac complications of pregnancy, in women with
and without structural heart disease.2–4 The inci-
dence of arrhythmia in pregnancy is increasing, a
rise attributable to the increase in the proportion
of women with structural heart disease achieving
successful pregnancies in the last decade.5
Clinical evaluation of the symptomatic pregnant
patient begins with a careful history, detailing the
timing of onset of symptoms, frequency and poten-
tial exacerbating factors. A careful family history,
probing for a history of unexplained sudden death,
heart failure, cardiac transplant or pacemaker or
defibrillator implantation may give clues to poten-
tially high-­risk inherited arrhythmia conditions.
A personal history of syncope or presyncope in
association with arrhythmia symptoms is also an
important indication for more comprehensive
evaluation.
The initial step in evaluation of gestational
arrhythmia symptoms is to obtain a 12-­lead ECG.
Features such as ventricular pre-­ excitation in
the form of a delta wave, pathological Q waves
suggesting prior myocardial infarction, bundle
branch block, hypertrophy, QTc prolongation or T
wave inversion are important observations. These
findings suggest underlying cardiac pathology and
should prompt further evaluation. Ambulatory ECG
monitoring (Holter monitoring) is an important
tool for documenting intermittent arrhythmia, and
also for establishing symptom-­rhythm correlation.
In selected cases, exercise stress testing can be used
to evaluate exertional symptoms. When a high-­risk
arrhythmia is suspected on the basis of syncope, an
implantable loop recorder may be considered.6
Review of the ECG obtained during tachycardia
can offer a great deal of information regarding
the mechanism of arrhythmia. Important features
to note include QRS width (<120 ms considered
‘narrow complex’), whether the rhythm is regular,
consistency of QRS morphology and the relation-
ship between atrial and ventricular activity. The
differential diagnosis of a wide complex tachy-
cardia includes a supraventricular arrhythmia
with pre-­ excitation (figure 1) over an accessory
pathway (AP), conduction delay or block in right
or left bundle branch or ventricular tachycardia
(VT). Conduction with aberrancy may be related to
conduction delay at shorter cycle lengths, or a fixed
conduction deficit.
Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746
Learning objectives
⇒ To review the potential arrhythmia
complications during pregnancy and
puerperium in women with and without known
cardiovascular disease.
⇒ To recognise arrhythmia conditions associated
with a high risk of pregnancy-­related cardiac
complications for which intervention before
considering pregnancy is appropriate.
⇒ To be aware of important medication
contraindications during pregnancy and
lactation, as they pertain to arrhythmia
management and anticoagulation.
Supraventricular arrhythmia: no structural heart
disease
Supraventricular tachycardia (SVT) is defined as
an atrially driven narrow complex rhythm with a
resulting heart rate exceeding 100/min. SVT is a
broad term for arrhythmias which include atrial
tachycardia (AT), atrial flutter, junctional tachy-
cardia, atrioventricular nodal re-­ entrant tachy-
cardia (AVNRT) and atrioventricular re-­ entrant
tachycardia (AVRT) in the presence of an AP.
SVT may complicate up to 0.5% of pregnancies.1
This arrhythmia may be a longstanding arrhythmia
exacerbated by pregnancy, but nearly half of these
gestational presentations will be the first presen-
tation. SVT complicating pregnancy is associated
with an 8% adverse neonatal or fetal event rate,
including premature birth, small for gestational age
(SGA), respiratory distress syndrome (RDS).3 7
Inappropriate sinus tachycardia
When sinus rate exceeds 100/min at rest, with
elevated average daily heart rate exceeding 90/
min, a diagnosis of inappropriate sinus tachycardia
(IST) may be considered. This is a generally benign
condition that may be indistinguishable from the
normal heart rate changes expected in pregnancy,
given that the average sinus rate rises steadily with
each trimester, to a peak in the third trimester. It
is critical to exclude secondary causes of sinus
tachycardia such as anaemia, infection, pulmonary
embolism, thyrotoxicosis and substance abuse or
withdrawal. The diagnosis of IST should be made
only after excluding a diagnosis of AT. When P
wave axis and morphology are identical to that in
normal sinus rhythm, with some suppression of
tachycardia during sleep, IST should be suspected.
Most cases can be managed conservatively, with
reassurance and supportive measures such as
avoiding caffeine and other stimulants.8 Attempts
at controlling heart rate with beta-­ blocker treat-
ment is often not effective and may be limited by
  1
 Education in Heart
Figure 1 Pre-­excited atrial fibrillation. Note the irregular rhythm, and non-­uniform QRS morphology with evidence of a delta wave (indicated by
arrow).
the adverse effects of beta-­blockade. Ivabradine is
commonly used outside of pregnancy to treat IST.
This drug targets the HCN4 channel responsible for
the cardiac ‘funny’ current (If), and has shown tera-
togenicity when used in pregnancy.9
Atrial tachycardia
AT has a generally regular rate, with organised atrial
activity that can be focal or re-­ entrant (figure 2).
The ECG will show P waves representing atrial
activity, with an isoelectric segment discriminating
this from atrial flutter. AT is rare in pregnancy, but it
is an important entity to recognise, given the risk of
tachycardia-­induced cardiomyopathy. Compromise of
left ventricular function may occur in incessant focal
AT, when the arrhythmia is present for >90% of a
monitoring period or when the average daily heart rate
over a 24-­hour period exceeds ~100 beats per minute.
Tachycardia-­induced cardiomyopathy may complicate
up to 10% of cases of poorly controlled AT.10
AV nodal re-entrant tachycardia and AV re-
entrant tachycardia
AVNRT and AVRT occur with equal frequency in the
pregnant population. AVNRT and AVRT typically
have abrupt onset and offset. They may have their first
presentation in pregnancy, but women with AVRT are
more likely to have had this diagnosis prior to preg-
nancy. AVNRT is mediated by the presence of a slow
AV nodal pathway, which is present from birth. The
ECG is characterised by atrial activity in the form of
a retrograde P wave which may be obscured by the
QRS complex on the ECG, or inscribed shortly after,
creating a ‘pseudo-­R’ wave’ in lead V1, or ‘pseudo-­S
wave’ in the inferior leads. AVRT is mediated via an AP
which is conducting tissue that bypasses the AV node,
also present from birth. When antegrade conduction is
present, PR interval shortening and a delta wave may
be seen on the surface ECG, indicating ventricular
Figure 2 Atrial tachycardia (A) versus normal sinus rhythm (B) in the same patient during pregnancy. Note the clear change in P wave morphology
and axis during tachycardia.
2 Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746
pre-­excitation. A proportion of APs are capable only
of retrograde conduction, showing no evidence of pre-­
excitation on the surface ECG. Ebstein’s anomaly is
a congenital condition with the potential for multiple
AP and related arrhythmias, conferring a higher risk of
adverse cardiac outcomes in pregnancy.
Management of SVT
When making management decisions in the preg-
nant patient, the potential adverse effects of medical
therapy and the risk of poorly controlled arrhythmia
should be considered. There are established guide-
lines for SVT management which apply in pregnant
patient.8 Acute management (figure 3) of a regular,
narrow complex tachycardia includes an attempt
at a Valsalva manoeuvre, which is the most effective
of the vagal manoeuvres, terminating tachycardia in
>40% of patients when manoeuvre is performed
seated, followed by rapid adoption of the supine
position with the legs elevated.11 Recognition of
caval compression in the supine position after ~20
weeks of gestation has led to further modification of
this manoeuvre by the addition of 45 degrees of left
pelvic tilt.12 Adenosine, when administered via rapid
intravenous push in doses of 6–24 mg is effective at
terminating maternal SVT.1 13 Adenosine is safe to use
during pregnancy.1 13 Other options for management
of acute, regular SVT of calcium channel blocking
drugs verapamil or diltiazem, which may terminate
SVT in 64%–98% of patients.14 These agents should
be avoided in the setting of ventricular dysfunction
and the ECG should be reviewed carefully to rule out
ventricular pre-­excitation or VT, as this may result in
haemodynamic instability or, in the setting of AVRT,
ventricular fibrillation.15
SVT management decisions should take into
consideration the severity of arrhythmia symp-
toms, and the frequency of episodes. In many cases,
conservative management and reassurance may

Figure 3 Flow chart for management of narrow complex tachycardia in the absence of severe structural heart disease in pregnancy. IV, intravenous.
be appropriate. Beta-­blockade or calcium channel
blockade may reduce the frequency and severity of
SVT, for women with frequent or severe symptoms
without ventricular pre-­excitation.15 If higher doses
of AV nodal blocking agents are needed, the addi-
tion of digoxin may be useful to further suppress
arrhythmia.8 Second-­ line therapy includes class I
antiarrhythmic agents, such as propafenone and
flecainide.14 Sotalol is a beta-­blocker that is also
considered a class III antiarrhythmic agent. Sotalol
is also effective in management of SVT,15 however
QT prolongation and proarrhythmia potential
precludes its routine use as a first-­line agent. Cath-
eter ablation is an option (class IIb) for treatment
of refractory arrhythmias in pregnancy, as long as
efforts are made to reduce radiation exposure, or to
avoid fluoroscopy completely.
The first goal of treatment for AT is AV nodal
blockade for control of ventricular rate during
episodes. Antiarrhythmic therapy with flecainide or
propafenone may be used if this is not achievable, with
concomitant use of an AV nodal blocking agent,15 16
whereas sotalol can be used alone, given its intrinsic
AV nodal blocking properties. Electric cardioversion
may not be effective without premedication with an
antiarrhythmic agent, particularly when managing an
automatic focal AT, as AT is likely to resume.
Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746
Education in Heart
Considering the published society guidelines
for SVT management, and pharmacological strat-
egies detailed here, note must be made regarding
the use of drugs which are to be avoided during
pregnancy. Atenolol is to be avoided in preg-
nancy, given the established risk of intrauterine
growth restriction, and other beta-­ blockers
should be used. The use of diltiazem in pregnant
animal models has been associated with signifi-
cant teratogenicity, with no major apparent tera-
togenic risk in human pregnancy.8 17
Atrial flutter and atrial fibrillation
Atrial fibrillation (AF) is a disorganised, irregular
atrial arrhythmia that may be associated with rapid
ventricular response. AF flutter (AFl) is a re-­ en-
trant atrial arrhythmia where the ECG is remark-
able for the appearance of flutter waves that have
been compared with a ‘sawtooth’ pattern. These
arrhythmias are typically seen in women who
have underlying structural heart disease.1 7 Both
atrial arrhythmias are associated with an increased
adverse neonatal or fetal event rate depending on
the arrhythmia burden. Adverse events are seen in
35% of women whose arrhythmia is paroxysmal,
whereas the event rate is as high as 50% in women
when AF/AFl is persistent.7
3
Education in Heart
In the absence of structural heart disease, the risk
of embolic events is low. Systemic anticoagulation
is not always required in this circumstance, but it
is important to be aware that left atrial thrombus
has been reported.18 Stroke risk-­ scoring systems
(CHADS2 or CHA2DS2VASC score) have been
validated for use in the non-­pregnant population
with AF/AFl, but these have not been studied for
risk prediction in pregnancy.8 The risk factors that
have been identified for increased risk of embolism
include a history of advanced age, congestive heart
failure, hypertension, established vascular disease,
diabetes and prior cardioembolic events. When
anticoagulation is indicated, the choice of antico-
agulant will be dictated by the stage of pregnancy
and underlying cardiac disease.8 Direct anticoagu-
lants have not been studied for use in pregnancy,
and, at this time, these agents should not be used
in pregnancy.
In the absence of structural heart disease or
thromboembolic risk factors, or if the acute
onset of AF/AFl results in haemodynamic insta-
bility, immediate cardioversion should be under-
taken (figure 4).8 Sustained AF/AFl of unknown
or >48 hours duration carries a risk of throm-
boembolism, 19 and cardioversion should be
undertaken only after at least 3 weeks of antico-
agulation prior to cardioversion. Alternatively, a
precardioversion trans-­o esophageal echocardio-
gram can be performed to exclude intracardiac
thrombus. 8 After cardioversion, anticoagulation
should be considered for at least 4 weeks unless
another indication for anticoagulation mandates
more prolonged therapy.
Control of ventricular rate response in AF is
accomplished with the use of AV nodal blocking
drugs. First-­line therapy includes beta-­ blockade.
Digoxin may be added to improve rate control and
limit the total dose of beta-­blocker given. The dose
of digoxin should be titrated to achieve control
of resting ventricular rate, rather than targeting
serum levels. Circulating digoxin-­ like fragments
can falsely elevate measured levels.20 A second-­line
choice for AV nodal blockade is the calcium-­channel
blocker verapamil. Pharmacological cardioversion
is a second-­line option if attempts at ventricular
rate control fail, or if AV nodal blocking agents
are contraindicated.8 The benefit of atrial rhythm
control compared with control of ventricular rate
in pregnancy has not been well studied.
Supraventricular arrhythmia: structural heart
disease
Up to 15% of pregnancies in women with structural
heart disease will be complicated by supraventric-
ular arrhythmias requiring treatment. In this setting,
haemodynamic assessment is critical.21 Risk factors
for SVT include a pre-­ existing arrhythmia diag-
nosis, mitral valve disease, the use of a beta-­blocker
prior to pregnancy and other left-­sided structural
lesions. Atrial arrhythmias in this population of
women are associated with increased gestational
morbidity and mortality.7 Chronic atrial dilatation
4 Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746
and atrial myopathic changes occurring in response
to underlying structural disease, as well as scar
formation from prior surgical intervention, create
the substrate for intra-­atrial re-­entry. It is important
to maintain a high level of suspicion for intra-­atrial
re-­entry in the pregnant patient with adult congen-
ital heart disease with concurrent tachycardia.
Management of SVT: structural heart disease
Management of gestational SVT in this population is
guided by the underlying cardiac lesion, the symptom-
atic and haemodynamic impact of the arrhythmia as
well as the need for thromboprophylaxis. Haemody-
namic compromise and placental hypoperfusion may
be the consequence of poorly controlled tachycardia,
and sinus rhythm should be restored with cardiover-
sion. If a pacemaker or defibrillator is present, atrial
overdrive pacing for arrhythmia termination may be
considered.22 Haemodynamic instability mandates
immediate cardioversion regardless of underlying
cardiac disease, anticoagulation status or availability of
fetal monitoring.8
A large proportion of patients with structural heart
disease may present with intracardiac thrombus.
Women with a prior intracardiac repair, cyanosis,
Fontan circulation or systemic right ventricle are at
elevated risk for thromboembolism, and systemic anti-
coagulation should be considered if atrial arrhythmias
are documented.23 Those with a mechanical valve will
have a pre-­existing indication for chronic anticoagula-
tion irrespective of atrial arrhythmia.
In women with complex structural heart disease,
the preferred strategy is restoration of sinus rhythm to
maintain AV synchrony, to optimise haemodynamics.8
First-­line treatment is beta-­blockade, with the added
benefit of controlling potential VA in high-­risk patients.
Cardioversion can be undertaken immediately for
IART or AF of <48 hours duration in women without
complex structural heart disease. This is followed by
anticoagulation for at least 4 weeks. Conversely, a TEE
to exclude intracardiac thrombus should be completed
prior to cardioversion in the pregnant patient with
moderate or complex structural heart disease.22
IART or AF of >48 hours duration should be
managed with a minimum of 3 weeks of anticoag-
ulation prior to cardioversion unless thrombus can
be excluded by TEE.22 Anticoagulation should be
considered for at least 4 weeks after cardioversion
in all women, unless another indication for antico-
agulation mandates more prolonged therapy.
Appropriate choice of anticoagulant will vary
according to stage of pregnancy, to minimise the risk
of embryopathy as well as both fetal and maternal
bleeding complications. Warfarin dosing >5 mg/
day is associated with a higher risk of embryop-
athy, miscarriage and stillbirth. Women requiring
warfarin >5 mg/day should be transitioned to low
molecular weight heparin (LMWH) or unfraction-
ated heparin (UFH) from 6 weeks gestation. Women
requiring lower doses of warfarin may continue
with warfarin therapy until 36 weeks gestation, at
which time LMWH or UFH should be initiated to
reduce the risk of maternal and fetal haemorrhage.

Figure 4 Flow chart for management of atrial fibrillation/flutter or IART in pregnancy. DC, direct current.
When LMWH is used, close monitoring of anti-­Xa
levels is recommended. It is important to note that
LMWH dose should be held for 24 hours prior to
regional anaesthesia delivery.8
An alternative to direct current cardioversion
is administration of an antiarrhythmic to restore
normal rhythm. This should be undertaken with
an awareness of the recognising the potential for
both bradycardia and pro-­ arrhythmia. Class IA
and IC antiarrhythmic drugs should not be used
in the setting of abnormal function of the systemic
ventricle or coronary artery disease.22 Sotalol, with
the risk of negative inotropy, should not be used
in women with significant systemic ventricular
dysfunction.
Flecainide or propafenone may be used as first-­
line agents for chronic rhythm control in women
with simple structural lesions.22 Sotalol has been
used for arrhythmia management in CHD,24
however, meta-­ analyses suggest an association
with increased all-­cause mortality.22 In the setting
of moderate-­ to-­
severe structural heart disease,
antiarrhythmic therapy should be tailored to the
underlying cardiac substrate in consultation with
an electrophysiologist with experience in managing
this patient population.8
Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746
Education in Heart
Ventricular arrhythmias
Gestational VA may include asymptomatic isolated
premature ventricular complexes (PVC), non-­
sustained VT or sustained VA resulting in syncope or
sudden cardiac death. Sustained VAs are rare, seen
in <0.01% of pregnancies.1 Women with structural
heart disease are more likely to develop VA during
pregnancy, and arrhythmia recurrence during preg-
nancy is seen in 27% of women with a prior history
of VA. Preterm delivery is the most common compli-
cation of this gestational arrhythmia.7 A diagnosis
of peripartum cardiomyopathy must be undertaken
when VA is seen in the last 6 weeks of pregnancy or
early postpartum period.
The standard evaluation of a woman with docu-
mented VA includes ECG, cardiac imaging and
rhythm monitoring. The 12-­lead ECG should be
examined for QT prolongation and other abnor-
malities of repolarisation such as T wave inversion,
hypertrophy or conduction delay. The finding of
structural heart disease, particularly dysfunction
of the systemic ventricle, is the primary prognostic
indicator in the setting of maternal VA.7
Ventricular arrhythmias: no structural heart disease
Idiopathic VAs are defined by the absence of under-
lying congenital lesions, structural abnormalities
or primary inherited arrhythmia conditions. The
mechanism of these arrhythmias is predominantly
5
Education in Heart
cyclic AMP-­mediated delayed afterdepolarisation.25
These arrhythmias may be worsened by either
physical or emotional stress. The course is typically
benign, although life-­threatening arrhythmias have
been reported.26 27 Fascicular VT is a verapamil-­
sensitive VA, and is the most common of the idio-
pathic left ventricular VAs28 with a characteristic
ECG showing narrow right bundle branch block
morphology and superior axis.
Ventricular arrhythmias: structural heart disease
The mechanism of arrhythmia and associated risk
of adverse events, including cardiac arrest, is influ-
enced by the nature of the underlying condition.
Arrhythmia complications are particularly common
in peripartum cardiomyopathy (PPCM), seen in
18.7%, with one study reporting cardiac arrest in
2.2%.29 The inherited cardiomyopathies, hyper-
trophic cardiomyopathy and arrhythmogenic right
ventricular cardiomyopathy (ARVC) are associ-
ated with frequent adverse arrhythmia outcomes,
particularly in women with New York Heart Asso-
ciation class <2 or heart failure symptoms prior
to pregnancy.7 Fortunately, the incidence of gesta-
tional VA is not increased in women with ARVC
already managed with beta-­blockade, in whom RV
structural changes or exacerbation of arrhythmia is
rare.30 Women with severe RV dysfunction at base-
line are at highest risk of complications.31
The complexity of the underlying cardiac lesion,
the history of anatomic repair and age at which
repair was completed will influence the risk of
gestational VA. Women with complex CHD,
including Fontan circulation, D-­transposition of the
great arteries, L-­transposition of the great arteries,
double outlet right ventricle, tetralogy of Fallot,
Ebstein’s anomaly, aortic coarctation and aortic
stenosis, are at highest risk of gestational VA.22
Acute VA management
The initial treatment for a haemodynamically stable
patient with regular, monomorphic, wide complex
rhythm is intravenous adenosine or beta-­ blocker
(figure 5). Verapamil may be used specifically to
terminate fascicular VT.8 Any VA with haemody-
namic instability should be treated with immediate
cardioversion/defibrillation. Intravenous procain-
amide can be used to terminate haemodynamically
stable wide complex tachycardia. Pre-­excited AF,
seen in patients with an AP, is a unique arrhythmia
characterised by rapid, irregular wide complex
tachycardia with an irregular QRS appearance,
and should be managed with immediate cardio-
version or intravenous procainamide.8 Gestational
arrhythmia exacerbations in the setting of inherited
arrhythmia conditions, such as long QT syndrome
or Brugada syndrome are uncommon, but should
be managed by a team with experience in this area
of electrophysiology if they occur.
6 Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746
Chronic management of ventricular arrhythmias:
no structural heart disease
When there is no underlying structural heart
disease, the goal of therapy is to control symp-
toms, and to minimise arrhythmia burden. A high
burden of ventricular ectopy (20%–24%) may
result in ventricular dysfunction, and suppres-
sion of arrhythmia, if LV function is declining, is
critical.32 33 First-­line therapy for VA prophylaxis
is beta-­blockade.8 The exception is idiopathic
fascicular VT, which typically responds well to
verapamil.34 In cases where the use of beta-­blocker
is not effective, or treatment is poorly tolerated,
verapamil is an alternative first-­line agent. Second-­
line agents, in the absence of structural heart disease
include the class IC antiarrhythmics flecainide or
propafenone.34
Chronic management of ventricular arrhythmias:
structural heart disease
The most important aspect of VA management is to
address the underlying cardiac disease with respect
to optimising haemodynamics.34 When gestational
VAs occur in women with structural heart disease,
beta-­blockers are effective and safe for VA manage-
ment. Sotalol may be useful for treating arrhyth-
mias in women with coronary artery disease, but
its use should be avoided in the setting of heart
failure or significant renal impairment.34 figure 6 If
VA is refractory to medical therapy, catheter abla-
tion may be offered. There is growing experience
with catheter ablation in pregnancy, particularly
using a non-­fluoroscopic approach. If implantable
cardioverter-­defibrillator implantation is indicated,
it should not be delayed by pregnancy.
Cardioversion in pregnancy
Direct current cardioversion is recommended for
any arrhythmia with signs of haemodynamic insta-
bility.8 This is both safe and effective during preg-
nancy. In women with more severe cardiac lesions,
postcardioversion fetal distress has been reported.
For this reason, if possible, monitoring of the fetus
during or immediately after cardioversion should
be considered. In addition, if gestation has reached
the age of neonatal viability, cardioversion should
be supported by an obstetrics team if emergency
caesarean section is required. The placement of
the defibrillator pads is as per standard protocol,
but pads should not be placed on breast tissue.
The energy recommendation for cardioversion
and defibrillation in the non-­ pregnant adult are
unchanged in pregnancy.35
Telemetry rhythm monitoring in labour and
delivery
Cardiac telemetry is indicated in women who are at
risk for sudden, haemodynamically unstable, or life-­
threatening arrhythmia. Fortunately, intrapartum
arrhythmias are extremely uncommon, even for
women who might be considered higher risk, with
a history of cardiac arrest, VA or pre-­excited tachy-
cardia. Although idiopathic PVCs are generally felt

Figure 5 Flow chart for management of wide complex tachycardia in pregnancy. AF, atrial fibrillation; ICD, implantable cardioverter-­defibrillator; IV,
intravenous; LQTS, long QT syndrome.
to be benign, women with a PVC burden exceeding
10% have been shown to have a higher risk of
cardiac complications,36 and consideration should
be given to periodic rhythm monitoring and cardiac
telemetry during labour in this group.
SUMMARY
Symptoms of palpitations are very common in
pregnancy. The frequency of documented gesta-
tional arrhythmia is increasing, likely due to the
successful treatment of women with structural
heart disease to achieve reproductive age. Manage-
ment planning should take into consideration the
frequency of symptoms, the haemodynamic impact
of arrhythmia and the presence of underlying
structural heart disease. High-­risk features include
a history of syncope, severe structural disease or
low ejection fraction. In most cases, arrhythmia
can be managed through pregnancy without
catheter ablation, however, options for zero-­
fluoroscopic ablation exist at specialised centres.
Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746
Education in Heart
Contributors Both authors listed have contributed equally to the
generation of this manuscript.
Funding The authors have not declared a specific grant for this
research from any funding agency in the public, commercial or
not-­for-­profit sectors.
Competing interests None declared.
Patient consent for publication Not applicable.
Ethics approval Not applicable.
Provenance and peer review Commissioned; externally peer
reviewed.
Author note References which include a * are considered to be
key references.
Supplemental material This content has been supplied by
the author(s). It has not been vetted by BMJ Publishing Group
Limited (BMJ) and may not have been peer-­reviewed. Any opinions
or recommendations discussed are solely those of the author(s)
and are not endorsed by BMJ. BMJ disclaims all liability and
responsibility arising from any reliance placed on the content.
Where the content includes any translated material, BMJ does not
warrant the accuracy and reliability of the translations (including but
not limited to local regulations, clinical guidelines, terminology, drug
names and drug dosages), and is not responsible for any error and/
or omissions arising from translation and adaptation or otherwise.
ORCID iDs
Lisa Albertini http://orcid.org/0000-0002-7200-1606
7
 Education in Heart
Figure 6 Safety of anti-­arrhythmia medications and anticoagulants in pregnancy. AAD, anti-­arrhythmic drug; BB, beta-­blocker; FDA, Food and Drug
Administration.
Danna A Spears http://orcid.org/0000-0002-2513-1627
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*8 Joglar JA, Kapa S, Saarel EV, et al. 2023 HRS expert consensus
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Key messages
⇒ Arrhythmia is one of the most common cardiovascular complications of
pregnancy, in women with and without structural heart disease.
⇒ Clinical evaluation of the symptomatic pregnant patient begins with a
careful history, detailing the timing of onset of symptoms, frequency and
potential exacerbating factors.
⇒ A careful family history, probing for a history of unexplained sudden death,
heart failure, cardiac transplant or pacemaker or defibrillator implantation
may give clues to potentially high-­risk inherited arrhythmia conditions.
⇒ Management decisions in the pregnant patient are guided by considering
the potential adverse effects of medical therapy versus the risk of poorly
controlled or symptomatic arrhythmia.
⇒ In most cases, the established guidelines for supraventricular tachycardia
(SVT) management apply in pregnant patient.
⇒ The plan for managing SVT for the duration of pregnancy should take into
consideration the frequency of episodes and their haemodynamic impact.
⇒ In many cases, conservative management and reassurance may be
appropriate.
⇒ The thromboembolic risk in atrial fibrillation (AF)/AF flutter in the absence
of structural heart disease is low in the pregnant patient and systemic
anticoagulation is not always required.
⇒ The choice of anticoagulant depends on the stage of pregnancy and
underlying cardiac disease.
⇒ Women with structural heart disease are more likely to develop ventricular
arrhythmia (VA) during pregnancy.
⇒ Adverse cardiovascular outcomes are more common in women with poor
functional class (New York Heart Association class <2) or heart failure
symptoms prior to pregnancy.
⇒ Direct current cardioversion is safe and effective during pregnancy and
recommended for any arrhythmia with signs of haemodynamic instability.
⇒ Intrapartum cardiac telemetry is employed to identify arrhythmia which may
result in significant haemodynamic compromise or death if not immediately
recognised.
⇒ A history of non-­sustained or sustained ventricular arrhythmia, cardiac arrest
or pre-­excited atrial fibrillation should prompt referral to a centre capable of
intrapartum telemetry monitoring.
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10 Albertini L, Spears DA. Heart 2023;0:1–10. doi:10.1136/heartjnl-2023-322746