Cardiac Arrhythmias During Pregnancy A Clinical Approach

Fetal and Maternal Medicine Review 2011; 22:2 123–143
C Cambridge University Press 2011

doi:10.1017/S0965539511000076
CARDIAC ARRHYTHMIAS DURING PREGNANCY: A

CLINICAL APPROACH
1 1 1,2
ZACHARY LAKSMAN, LOUISE HARRIS AND CANDICE K SILVERSIDES
1
University of Toronto, Division of Cardiology, University Health Network, Toronto, Canada. 2 University of
Toronto, Obstetric Medicine Program, Mount Sinai Hospital and University Health Network, Toronto, Canada
INTRODUCTION
Physiologic changes in maternal haemodynamics, hormones and autonomic

properties contribute to arrhythmias in pregnancy. While arrhythmias most
commonly occur in pregnant women with structural heart disease or those with
a history of cardiac arrhythmias, they can also occur de novo in women with no
documented cardiac disease.
Arrhythmias are classified as tachycardias and bradycardias and while both occur
in pregnant women, tachycardias are more common. Of the tachyarrhythmias,
supraventricular tachycardias (SVT) are the most common.
The approach to diagnosis of arrhythmias in pregnant women is similar to
the approach used in the non-pregnant patient. Once the diagnosis is established,
treatment strategies need to be tailored to the individual factoring in the type of
arrhythmia, the underlying cardiac condition of the woman, the physiologic changes
of pregnancy including changes in drug metabolism, and the potential adverse effects
of medication on the developing fetus during pregnancy and lactation. This review will
provide an overview of the most common arrhythmias presenting during pregnancy.
PHYSIOLOGIC CHANGES DURING PREGNANCY
During pregnancy there are a number of physiologic changes that may impact
the mechanisms of arrhythmogenesis. An increase in maternal intravascular and
extravascular fluid volumes augments preload and increases atrial and ventricular
size1–4 . The resultant myocardial stretch may contribute to arrhythmogenesis
by mechanisms such as stretch-activated ion channel mediated membrane
depolarization, shortening of the refractory period, slowing of conduction, and spatial
Candice K. Silversides, MD, Toronto General Hospital, 585 University Avenue, 5N-521, Toronto, Ontario
M5G 2N2, Canada. E-mail candice.silversides@uhn.on.ca
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124 Zachary Laksman, Louise Harris and Candice K Silversides
dispersion of refractoriness and conduction5–8 . The hormonal and autonomic changes

of pregnancy may have an effect on arrhythmogenesis in pregnancy. An increase in
adrenergic responsiveness during pregnancy has been documented and is thought to
be related to effects on the regulation of adrenergic receptors9–12 . In the non-pregnant
state, for example, idiopathic ventricular tachycardia (VT) originating at the right
ventricular outflow tract occurs more frequently in women than men, and hormonal
variation that occurs during premenstrual, perimenopausal, and pregnancy periods
may contribute to VT initiation in women with this form of VT13 . Progesterone has
also been implicated in the genesis of pregnancy related idiopathic VT14 .
Physiologic changes also impact antiarrhythmic drug dosing during pregnancy.
Changes in absorption, volume of distribution, and protein binding and excretion
(hepatic and renal) will affect drug kinetics and need to be considered when prescribing
drugs during pregnancy.
CLINICAL APPROACH TO ARRHYTHMIAS
All women who present with arrhythmias should undergo a detailed history, physical
exam, electrocardiogram, and a transthoracic echocardiogram.
A detailed history should be recorded outlining the onset (sudden vs. gradual),
duration, and frequency of symptoms. Women should be asked about the rate of the
arrhythmia (tachycardia vs. bradycardia) and the rhythm (regular or irregular rhythm).
Symptoms related to arrhythmias include palpitations, shortness of breath, presyn-
cope, syncope, and chest pain. In some instances, arrhythmias can lead to heart failure,
myocardial ischaemia, or transient ischaemia or stroke. Not all important arrhythmias
are associated with symptoms, and some arrhythmias can be detected incidentally at
the time of the electrocardiogram (ECG) or Holter monitoring. When pregnant women
with arrhythmia-related symptoms were evaluated with 24-hour Holter monitoring,
only 10% of symptomatic episodes were associated with documented arrhythmias.15
Women with a previous history of arrhythmias, with structural heart disease, and with
a family history of sudden death (i.e. women with hypertrophic cardiomyopathy) are
at increased risk of tachyarrhythmia in pregnancy.16,17
Palpitations are the most common symptom in pregnancy. In the majority of
women, palpitations are benign. It is important to identify characteristics of high-
risk patients who may require more extensive diagnostic testing and management of
their condition. The description of the palpitations can provide helpful information18 .
Palpitations associated with dizziness, presyncope or syncope are suggestive of
haemodynamic instability and warrant further investigation. Reported identification
of a regular rapid pounding in the neck or visible neck pulsations associated with the
sensation of palpitations is suggestive of atrioventricular nodal reentrant tachycardia.
The physical examination should include blood pressure and heart rate
measurements, a complete cardiac exam, and a screen for systemic disease. Stable
vital signs during a tachycardia are not helpful in distinguishing SVT from VT. Signs
of AV dissociation (physical exam findings of VT) include irregular cannon A waves
Cardiac arrhythmias during pregnancy: a clinical approach 125
in the jugular venous pulse, representing intermittent right atrial contraction against
a closed tricuspid valve, and variability in the loudness of the first heart sound.
Non-invasive testing should include an ECG and a transthoracic echocardiogram
to rule out structural heart disease. The 12-lead ECG may change during pregnancy
owing to the change of position of the heart in the thorax19 . These changes can
include a small Q wave and inverted T wave in lead III, and more rarely, a
shift of the QRS axis, rightward more commonly than leftward20 . Non-specific
changes in the ST segments and T waves can also occur21,22 . The ECG can provide
useful information and may identify cardiac disorders such as Wolff-Parkinson-
White syndrome, long QT syndrome, short QT syndrome, Brugada syndrome,
arrhythmogenic right ventricular cardiomyopathy (ARVC), electrolyte imbalances,
and evidence of underlying structural heart diseases (conduction abnormalities,
previous myocardial infarction or possible cardiomyopathy). Further testing with a
24-hour Holter monitor may be useful to document symptom-rhythm correlation and
the burden of arrhythmia. Ambulatory ECG monitoring can be helpful in women with
VT to further define risk or monitor the effect of therapy. Event recorders to document
symptoms can be worn continuously or applied at the time of symptoms. These are
useful for prolonged monitoring (weeks to months) in patients who have intermittent
and infrequent symptoms.
A transthoracic echocardiogram should be performed in all women with
arrhythmias. Transthoracic echocardiograms help identify structural heart disease
and are safe during pregnancy. Cardiac MRI may be indicated in some cases
and is of particular value in women suspected of having arrhythmogenic RV
cardiomyopathy/dysplasia23 .
Tilt table testing is used to diagnosis neurocardiogenic syncope, which can occur
during pregnancy and in the immediate postpartum period. It is rarely required in preg-
nancy, but can be safely performed in pregnant women with undiagnosed syncope24 .
Other cardiac investigations including exercise stress testing, T wave alternans,
signal averaged ECG and electrophysiology studies may sometimes be considered.
These tests should be ordered after consultation with a cardiologist and/or cardiac
electrophysiologist.
Baseline bloodwork should be done to exclude anaemia, thyrotoxicosis, electrolyte
imbalance, and assess renal function. Specifically, screening for hypopotassemia
and hypomagnesemia should be performed as they may contribute to abnormal
repolarization or potentiate the arrhythmogenic effects of catecholamines or
antiarrhythmic agents25 . Magnesium sulfate toxicity can present with changes in
PR, QRS, and QT intervals as well as AV nodal conduction block at magnesium levels
of 2–2.5 mmol/L. Empirical calcium may be lifesaving in these situations26 .
ELECTROCARDIOGRAPHIC APPROACH TO ARRHYTHMIAS
The ECG approach to diagnosing tachycardia is shown in Figure 1. The initial step
in this algorithm is to obtain a 12-lead ECG of the arrhythmia and determine if the
Hemodynamically stable
tachycardia
Narrow QRS complex Wide QRS complex
Very rarely, VT can present with

a narrow QRS Regular Irregular
SVT
SVT VT
Atrial fibrillation or
Irregularly atrial flutter with
Regular Irregular variable block
Rhythm Rhythm AND aberrancy or
preexcitation
SVT with SVT with
aberrancy preexcitation
Atrial
fibrillation
Sinus Atrial Junctional

tachycardia tachycardia Atrial flutter AVNRT AVRT
tachycardia
Figure 1 Electrocardiographic diagnostic algorithm for tachycardias.

Abbreviations: VT, ventricular tachycardia; SVT, supraventricular tachycardia; AVRNT, atrioventricular nodal
reciprocating tachycardia; AVRT, atrioventricular reciprocating tachycardia.
tachycardia is narrow (QRS duration < 120 msec) or wide (QRS duration ≥120 msec)
complex.
Stratification of the narrow complex tachycardia is based on the rhythm (regular
or irregular). When uncertain of the underlying atrial rhythm, vagal maneuvers
or adenosine can slow the AV node allowing for identification of the underlying
atrial rhythm27 . Figure 2 depicts the various forms of supraventricular tachycardias.
(Figure 2)
The differential of a wide complex tachycardia includes VT, SVT with aberrant
conduction, SVT with preexcitation, SVT in a pacemaker dependent patient, and
ECG artifact. ECG findings consistent with VT include specific QRS morphologies
and signs of AV dissociation such as fusion or capture beats28 (Figure 1). Unfortunately,
AV dissociation is only clearly discernable in 30% of VT. In emergent circumstances,
a wide complex tachycardia should be treated as VT until proven otherwise.
THERAPY FOR ARRHYTHMIAS
Antiarrhythmic medications are classified according to the Vaughan Williams

classification (Class I-V, see Table 1). Data on drug safety and efficacy during
pregnancy is limited. While this review will provide an overview of some common
antiarrhythmic medications, detailed information pertaining to drug safety during
pregnancy is available elsewhere.
Figure 2 Mechanisms of supraventricular tachycardia27 .
ATRIAL AND VENTRICULAR ECTOPIC BEATS
Atrial premature beats (APBs) and ventricular premature beats (VPBs) are the most
frequent arrhythmia (∼ 50% of pregnancies) detected in pregnant women and usually
dissipate in the postpartum period.
The evaluation of ectopic beats during pregnancy includes a complete history and
physical exam. If ectopy was documented on a continuous monitor, correlation should
be sought for the symptoms that prompted the investigation. VPBs are more common
in women with structural heart disease including congenital heart disease29 , valvular
heart disease, mitral valve prolapse30 , hypertension, left ventricular hypertrophy31 ,
and dilated cardiomyopathy32 . Women should be advised to avoid potential precipitant
factors such as smoking, coffee intake, alcohol intake, or other stimulants33 .
Table 1 Antiarrhythmic Drugs
Vaughan-Williams Class Potential Adverse FDA Use during
128
Drug Mechanism of Action Effects in Pregnancy category∗47,86,109 Breast Feeding110
Zachary Laksman, Louise Harris and Candice K Silversides

Adenosine Class V No reported teratogenicity. C Compatible
Purine nucleoside No increased fetal risk.
Amiodarone Class III Side effects may include neonatal D Not recommended.
Prolongs action potential and hypothyroidism, hyperthyroidism, Unknown effect on nursing
refractory period of Pukinje prolonged QT, bradycardia, small for infant but may be of concern
cells and ventricular myocytes. gestational age, prematurity,
neurodevelopmental problems.
Beta blockers Class II No reported teratogenicity. C† Compatible†

Metoprolol B-adrenergic receptors May impair fetal growth. Newborns
exposed near the time of delivery are at
risk of bradycardia and hypoglycemia.
Propranolol
Digoxin Class V No reported teratogenicity. C Compatible
Cardiac Glycoside
Diltiazem Class IV C Compatible
Calcium channel blocker No adverse events in humans. Animal
studies have documented tocolytic
properties and skeletal abnormalities at
supratherapeutic doses.
Disopyramide Class IA No reported teratogenicity. C Compatible
Na-channel blockade Limited experience and evidence regarding
oxytocic properties and therefore
generally reserved for refractory cases.
Flecainide Class IC Developmental toxicity in animals with C Compatible
Na-channel blockade limited information regarding early
exposure in human pregnancy.
Lidocaine Class IB No reported teratogenicity. B Compatible
Na-channel blockade Experience with use as anaesthetic shows
it to be relatively safe when used with
careful drug monitoring. Requires dose
adjustment in women with hepatic
dysfunction. Potential for fetal
bradycardia
Table 1 Continued
Vaughan-Williams Class Potential Adverse FDA Use during

Drug Mechanism of Action Effects in Pregnancy category∗47,86,109 Breast Feeding110
Procainamide Class IA No reported teratogenicity. C Compatible. However, the

Na-channel blockade Antinuclear antibodies and lupus like long-term effects of
syndrome with chronic therapy. exposure are not known.
Propafenone Class IC No reported teratogenicity; however, no C Compatible
Na-channel blockade reported experience of use in early
pregnancy. Potential for fetal bradycardia
Quinidine Class IA No reported teratogenicity. C Compatible
Na-channel blockade Adverse reactions reported at
supratherapeutic doses including
oxytocic effects and preterm labour.
Cardiac arrhythmias during pregnancy: a clinical approach

Sotalol Class III No reported teratogenicity. B Compatible
Nonselecgive B-adrenergic There has not been associated fetal growth
antagonist with Class III restriction, however, newborns exposed
electrophysiology properties near the time of delivery may be
susceptible to similar risks as beta
blockers (described above).
Verapamil Class IV No reported teratogenicity. C Compatible
Calcium channel blocker No increased fetal risk.
∗
Category A: Controlled studies show no risk – Controlled studies in women fail to demonstrate a risk to the fetus in the 1st trimester (and there is
no evidence of a risk in later trimesters), and the possibility of fetal harm appears remote; Category B: No evidence of risk in humans - Either animal
reproduction studies have not demonstrated a fetal risk but there are no controlled studies in pregnant women or animal-reproduction studies have shown
an adverse effect (other than a decrease in fertility) that was not confirmed in controlled studies in women in the 1st trimester (and there is no evidence of
a risk in later trimesters); Category C: Risk cannot be ruled out – Either studies in animals have revealed adverse effects on the fetus (teratogenic or
embryocidal or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the
potential benefit justifies the potential risk to the fetus; Category D: Positive evidence of risk – There is positive evidence of human fetal risk, but the
benefits from use in pregnant women may be acceptable despite the risk (e.g., if the drug is needed in a life-threatening situation or for a serious disease for
which safer drugs cannot be used or are ineffective); Category X: Contraindicated in pregnancy – Studies in animals or human beings have demonstrated
fetal abnormalities or there is evidence of fetal risk based on human experience or both, and the risk of the use of the drug in pregnant women clearly
outweighs any possible benefit.
†
Atenolol has a FDA category D classification and has been associated with significant effects on some nursing infants (should be given to nursing mothers
129
with caution).
In most cases no therapy is required for etopic beats in the asymptomatic

woman. Pregnant women with symptomatic ectopy should be reassured of their
generally benign nature. If ectopic activity continues and is associated with intolerable
symptoms, treatment with cardioselective beta blockers such as metoprolol may be
effective.
TACHYCARDIAS
Paroxysmal supraventricular rachycardia
Paroxysmal supraventricular tachycardia (PSVT) usually presents as a narrow

complex tachycardia (less than 120 ms); however, it can also manifest as a wide
complex tachycardia. When diagnostic certainty is lacking, wide complex tachycardia
should be managed as ventricular tachycardia until an alternative diagnosis can
be confirmed. PSVT is the most common sustained arrhythmia detected during
pregnancy. In one single-center study, the prevalence of PSVT has been estimated
to be 24 per 100,000 hospital admissions in pregnant women34 . The differential
diagnosis of supraventricular tachycardia relates to its underlying mechanism and
includes atrioventricular nodal reciprocating tachycardia (AVNRT), atrioventricular
reciprocating tachycardia (AVRT), atrial tachycardia, and junctional tachycardia
(Figure 1).
Atrioventricular nodal reciprocating tachycardia (AVNRT) is the most common
PSVT in women of childbearing age, followed by AVRT35 . AVRT occurs when an
accessory pathway connecting the atria and the ventricle is present and forms the
substrate for a reciprocating circuit. These two types of PSVT may be difficult to
distinguish from the surface ECG during tachycardia. Accessory pathways can also
act as bystanders in other types of tachycardias, such as AT, atrial flutter, and atrial
fibrillation in that they may be involved in, but not critical to the tachycardia’s
circuit.26 Pregnancy may increase the risk of first onset of PSVT35,36 or result in an
increase in the frequency or severity of a previously diagnosed PSVT36 .
PSVT is usually well tolerated in women without structural heart disease37 .
However, women with structurally abnormal hearts may not be able to tolerate the
haemodynamic consequences of a tachyarrhythmia. If haemodynamic compromise is
evident, direct-current (DC) cardioversion should be performed. Cardioversion with
up to 300J has been used safely in pregnancy38 . Although there is not thought to be
significant current transfer to the fetus, and electrical cardioversion does not result
in compromise of blood flow to the fetus, the fetus should be monitored before and
immediately after administration for signs of distress39–41 . There are case reports
of direct current cardioversion leading to sustained uterine contraction and fetal
arrhythmias42 . In the third trimester, some physicians prefer to perform electrical
cardioversion under general anesthesia and intubation considering the more difficult
airway and increased risk of gastric aspiration during pregnancy.
In cases when the woman is haemodynamically stable, acute episodes of SVT may
be terminated by transiently blocking AV nodal conduction. Vagal manoeuvers are
usually attempted first including the Valsalva manoeuver and carotid sinus massage
and positioning the patient in left lateral decubitus position. If vagal manoeuvers
fail, intravenous adenosine (6 to 12 mg) is an appropriate choice in pregnancy,
terminating approximately 90% of PSVT43 . Adenosine is a purine nucleoside that
depresses AV nodal conduction and sinus node automaticity. Higher doses may be
required, with the safe administration of 24 mg having been reported with no effect
on the monitored fetal heart rate39 . Adenosine can also be a useful diagnostic tool to
differentiate between different types of PSVT (Figure 2). Because of the very short half
life of adenosine (<10 seconds), maternal side effects of bradycardia and dyspnoea are
typically transient and of no clinical consequence44 . Care should be taken when using
adenosine in women with severe reactive airway disease. Recommended second-line
drugs are intravenous beta-adrenergic blockers such as propranolol and metoprolol
(28). The experience with intravenous calcium channel blockers such as verapamil
and diltiazem is more limited; however, there have been reports of successful use
of verapamil in the treatment of maternal PSVT45,46 . Caution should be exercised
when using verapamil because the longer half-life (∼5 hours) can cause significant
hypotension, especially when given as a rapid intravenous bolus injection44 .
Suppression, prevention and rate control of SVT can be accomplished with
atrioventricular (AV) nodal blocking agents. Digoxin has been used most extensively
and is considered safe in pregnancy and during lactation47 . There are however case
reports of infant death and miscarriage related to maternal digitalis toxicity48,49 . There
is little data on the efficacy of AV nodal blocking agents in terms of their efficacy in
prophylactic use50 . Beta blockers such as metoprolol are often used, but the fetal
risk of beta blockers needs to be discussed with the mother, specifically the risk
of fetal growth retardation. Metoprolol is a selective beta 1 adrenergic antagonist.
Both nonselective and selective beta blockers readily cross the placenta. Prospective
clinical studies have shown the incidence of fetal growth retardation associated with
propranolol use to be approximately 4%51 . Neonatal hypoglycemia has also been
reported and infant blood glucose should be monitored for 24 to 48h post delivery52 .
Higher doses may be required in pregnancy because of increased metabolism and
clearance of metoprolol during pregnancy53,54 .
Other antiarrhythmic agents are sometimes required for use as suppressive therapy
in highly selected patients with significant symptomatic SVT. Quinidine has been
used in pregnant women, but its availability may be limited. Use of procainamide to
treat maternal SVTs has been limited, in part because of the relatively high incidence
of antinuclear antibodies and the lupus like syndrome, and because it is only available
in intravenous form47 . There is limited experience on the use of dysopyramide in
pregnancy. It has oxytocic properties and should be reserved for highly selected
patients55 . Flecainide in addition to a beta blocker has been used safely in pregnant
women for the treatment of fetal SVTs, and can also be used to treat maternal SVT47,56 .
However, Class IC agents may be proarrhythmic in women with structurally abnormal
hearts and therefore are contraindicated in these patients. Sotalol can be used during
pregnancy57 . Sotalol can lengthen the QT interval and predispose to torsade de pointes.
If sotalol is required, monitoring for QTc prolongation is important. Amiodarone, is a
class D drug.
For women with symptomatic PSVT, consideration of radiofrequency catheter
ablation of the accessory pathway or the slow pathway before pregnancy may be
appropriate. Generally, radiofrequency catheter ablation during pregnancy is not
performed because of the procedural radiation exposure. In very rare cases of
refractory PSVT during pregnancy, ablation may be considered, preferably in the
second trimester28 .
Focal Atrial Tachycardia
Focal atrial tachycardia (AT) is relatively rare during pregnancy. AT is characterized

by regular atrial activation that does not require the sinus node or the AV node for
initiation or maintenance of the arrhythmia. AT typically manifests as atrial rates
of 100 to 250 bpm28 . Short salvos of non-sustained AT are frequently found on
electrocardiographic monitoring and are rarely symptomatic. AT may be found in
women with structurally normal hearts, but is also associated with underlying heart
disease, and repaired congenital heart disease58–61 . The arrhythmia usually dissipates
after delivery, suggesting that pregnancy is related to its underlying pathophysiology.
AT is typically not an inherently dangerous rhythm, but if incessant and fast, can
precipitate angina or heart failure, degenerate into atrial fibrillation, and can lead to
tachycardia cardiomypathy.
As in the nonpregnant state, AT can be refractory to DC cardioversion. Furthermore,
because AT can be caused by enhanced automaticity, as well as focal or micro-
reentrant patterns, vagal manoeuvers and AV nodal blocking agents will usually not
terminate the arrhythmia58,59 . For these reasons, the goal of therapy is to obtain
rate control with AV nodal blocking agents (digoxin, beta blockers, calcium channel
blockers). Antiarrhythmic agents can be considered in refractory cases, although the
arrhythmia responds poorly to Class IA antiarrhythmic drugs. A Class III agent such
as sotalol, can be considered62,63 , but risks and benefits of the medications need to be
considered.
Atrial fibrillation and atrial flutter
Atrial flutter manifests as an organized atrial rhythm with a rate typically between
250 and 350 bpm. The term encompasses a variety of macro-reentry circuit based
tachycardias, the classic type (typical flutter) being dependent upon the cavotricuspid
isthmus for propagation of the arrhythmia28 .
Atrial fibrillation is also a supraventricular tachyarrhythmia, but is characterized by
uncoordinated atrial activation and an irregular ventricular response. On the surface
ECG, P waves are replaced by rapid oscillations or fibrillatory waves that vary in
amplitude, shape and timing64 . The ventricular response to atrial fibrillation depends
on the properties of the AV node, the level of vagal and sympathetic tone, the presence
of accessory pathways, and the action of drugs65 .
Atrial fibrillation and atrial flutter in pregnancy often occur in women with
structural heart disease such as mitral stenosis66 , hypertrophic cardiomyopathy67 ,
peripartum cardiomypathy68 , congenital heart disease69 , or in women with metabolic
abnormalities such as hyperthyroidism70 . Less commonly, atrial fibrillation and
flutter occur in women with structurally normal hearts (“lone atrial fibrillation”).
When women present with these arrhythmias during pregnancy, provoking factors
such as hyperthyroidism or alcohol abuse should be addressed. Atrial fibrillaton and
flutter are associated with an increased risk of thromboembolic complications.
The underlying cardiac diagnosis, the duration of the arrhythmia, the ventricular
rate and the haemodynamic status of the patient all need to be incorporated into
decision making when treating atrial fibrillation or flutter.
The immediate management of atrial fibrillation or flutter causing haemodynamic
instability requires DC cardioversion64 . Atrial fibrillation with rapid ventricular rates
in women with preexcitation is also best treated with DC cardioversion. For women
who are haemodynamically stable, quinidine or procainamide can be considered for
pharmacologic conversion. Amiodarone has also been used, but is typically avoided
because of the potential adverse fetal effects71,72 .
Alternatively, a rate control strategy can be employed using digoxin, a beta
blocker or a nondihydropiridine calcium channel blocker. In women with known
or suspected preexcitation, AV nodal blocking agents are contra-indicated because
they can facilitate antegrade conduction over the accessory pathway and potentially
lead to ventricular fibrillation in the setting of rapidly conducted atrial fibrillation.
In these women, Class IA (eg, quinidine, procainamide) and Class IC (eg, flecainide)
antiarrhythmic drugs are the most effective at blocking conduction in the accessory
pathway and preventing recurrences of tachycardia. Anticoagulation to prevent
thromboembolic complications in pregnant women with atrial fibrillation and
atrial flutter has not been systematically studied and, when used, the choice of
anticoagulants needs to be tailored to the individual. Women with non-valvular atrial
fibrillation and a low CHADS2 score may be candidates for aspirin therapy alone64 .
In women at higher risk for thromboembolic complications, the use of low molecular
weight heparin, unfractionated heparin, or warfarin may be required. The risks and
benefits of anticoagulation need to be considered. Prior to pregnancy, definitive
treatment of atrial flutter, and sometimes atrial fibrillation, can be accomplished
with radiofrequency catheter ablation73 .
Ventricular tachycardia
Ventricular tachycardia (VT) is not commonly identified during pregnancy and when
identified it is an indicator of risk even in the absence of structural heart disease74 .
Ventricular tachycardia encompasses both sustained and nonsustained forms, both
exhibiting AV dissociation and rates greater than 100 beats per minute. Sustained
tachycardia has a duration of at least 30 seconds, or is associated with haemodynamic

compromise. While a differential diagnosis is available for wide complex tachycardia,
a wide complex tachycardia should always be treated as ventricular tachycardia
until absolutely excluded. Ventricular tachycardia can be further classified into
monomorphic or polymorphic forms, the former being defined as having a uniform
and stable QRS morphology.
While monomorphic ventricular tachycardia can occur in the absence of
structural heart disease, monomorphic ventricular tachycardia in pregnant women
is often associated with structural heart disease including congenital heart disease,
hypertrophic cardiomyopathy, dilated cardiomyopathy, aortic stenosis, coronary
artery disease, and arrhythmogenic RV cardiomyopathy/dysplasia. Polymorphic VT
in the absence of structural heart disease may occur in women with either an
acquired or inherited form of prolonged QT interval, and in women with a normal
QT interval who have catecholiminergic polymorphic VT. Electrolyte imbalances, in
particular hypomagnesemia, hypoxia, anaemia, hypotension, hypertensive crises and
heart failure can precipitate VT. Underlying thyrotoxicosis should also be ruled out
as well as ingestion or toxicity of drugs including cocaine and digitalis75,76 .
The risk of VT during pregnancy is increased in women with structural heart disease
and a history of previous VT77 . Newly diagnosed VT should be thoroughly investigated
and this includes a complete cardiac exam, drug history, ECG, echocardiogram and
blood investigations78,79 . For women with new onset VT in the postpartum period,
peripartum cardiomyopathy should be excluded80 .
Women without identifiable structural heart disease can develop VT; this is
known as idiopathic VT13,78 . Idiopathic VT most commonly arises from the right
or left ventricular outflow tract. Idiopathic left VT is an unusual type of VT that
occurs in women without apparent structural heart disease and can be identified
by its morphologic pattern of right bundle branch block with left axis deviation.
It is important to differentiate idiopathic VT from other known causes of VT
because of its more benign course, excellent prognosis, and implications for drug
and ablation therapy81,82 . Idiopathic VT in pregnant women is similarly felt to be
benign. Its reported responsiveness to beta blocker therapies suggests that it may
be associated with depressed parasympathetic tone and that it is catecholamine
sensitive13,78 .
The management of an acute episode of VT in pregnancy is similar to that in
nonpregnant women. Pregnant women with haemodynamically unstable VT should
be electrically cardioverted. Although there is a small perceived risk of inducing fetal
arrhythmias, cardioversion and defibrillation on the external chest are considered safe
at all stages of pregnancy83–85 . There is very low to no risk of electric arcing to fetal
monitors, although it is reasonable to remove them during cardiac arrest26 . Reversible
causes should be sought out and corrected. Advanced cardiac life support management
of cardiac arrest in pregnancy is available26 . While the guidelines highlight maternal
modifications, it should be noted that the ACLS protocol is the same, and ACLS
drugs should be given in typical sequence and doses. Pharmacologic cardioversion
can be considered in haemodynamically stable patients with sustained ventricular
tachycardia. In pregnant women with sustained monomorphic VT, intravenous
lidocaine is recommended23 . Lidocaine appears to have few adverse fetal effects even
early in pregnancy despite placental crossing86 . Intravenous amiodarone can also be
considered.
Drug therapy for recurrent VT targeted at prophylaxis, suppression, or reducing
the risk of sudden cardiac death should be reserved for clinical scenarios where the
benefit outweighs the harm. The selection of an antiarrhythmic agent for management
of ventricular arrhythmias in pregnancy requires consideration of the aetiology and
pathophysiology of the arrhythmia, its associated conditions, and the risk inherent in
the therapy.
Idiopathic VT
This VT responds well to verapamil for both termination and for prophylaxis87,88 . It
can also be suppressed by beta blockade78 . Sotalol can be considered as second line
therapy in patient with idiopathic VT and normal renal function if beta blockade is
ineffective23 .
Congenital long QT syndrome
Beta blockade has been shown to be protective, specifically postpartum. In these

women, the risk of cardiac arrest is higher in the postpartum period compared with
before or during pregnancy. Pregnancy itself has not been shown to be associated with
an increased risk of cardiac events89 . The relative tachycardia seen during pregnancy
may shorten the QT interval and thus decrease the risk of life threatening arrhythmias.
Beta blockers are recommended throughout pregnancy and in the postpartum period
in women with LQTS23 . These women should also be monitored on telemetry during
labour and delivery as the QTc may prolong90 . Any episode of syncope in patients
with LQTS is an ominous sign in pregnancy and may be a sentinel warning before
sudden cardiac arrest91,92 .
In other forms of VT during pregnancy, beta blockers, quinidine and procainamide
have been used. Flecainide has been used in women with structurally normal hearts
without adverse fetal outcome93–95 . Amiodarone is a Class D drug, but may need to
be considered in rare instances. In pregnant women, the potential adverse side effects
of antiarrhythmic therapy needs to be carefully considered, and these drugs need to
be used with caution.
Women at high risk for sudden death may require an implantable cardioverter
defibrillator (ICD) for primary or secondary prevention of sudden cardiac death.
Successful pregnancy in women with ICDs has been reported96 .
BRADYCARDIA
Sinus bradycardia
Sinus bradycardia is a rhythm in which fewer than 60 impulses arise from the
sinoatrial (SA) node per minute. Sinus bradycardia is not common during the
antepartum period as there is normally a physiologic increase in heart rate of 10 to

20 beats/min above baseline. However, mild sinus bradycardia may occur transiently
after normal delivery, and may persist for a few days in the postpartum period37 . In
the absence of structural heart disease, sinus bradycardia is seldom associated with
symptoms and requires no intervention.
First and second degree AV block
First degree AV block is diagnosed when the PR interval on the surface ECG is
more than 200 milliseconds following a normally timed P wave. The P waves are
all conducted with a constant PR interval. Second degree AV block is used to define
intermittent failure of AV conduction. Type 1 second degree AV block (Wenckebach
or Mobitz type I block) manifests as progressive prolongation of the PR interval before
a nonconducted atrial impulse. The PR interval immediately after the nonconducted
P wave returns to baseline before subsequent prolongation. Type 2 second-degree
(Mobitz type II) AV block has a constant PR interval in all conducted P waves with
intermittent nonconducted atrial impulses97 .
There is no specific association between first and second-degree heart block and
pregnancy. First-degree atrioventricular block can be seen in women with structural
heart disease such as rheumatic or congenital heart disease37 . The site of AV delay is
usually located above the bundle of His and rarely progresses to advanced heart block.
Second-degree AV block is sometimes seen in pregnancy. Mobitz type I
(Wenckebach) AV block is more commonly encountered and generally has a benign
outcome98 . Mobitz type II AV block, with block usually below the AV node, may
precede a Stokes-Adams attack and complete heart block. A permanent pacemaker is
often required for treatment.
Complete heart block
As discussed above, AV block is defined as an interruption or delay in the transmission

of an impulse from the atria to the ventricles. Complete heart block, or third degree
AV node block, results in complete electrical and mechanical AV dissociation and is
manifest on the ECG when supraventricular impulses are faster than, and independent
from, the QRS complexes.
Complete heart block (CHB) may be congenital or acquired. The prevalence of new
onset of CHB during pregnancy is unknown, however, 30 percent of cases of congenital
complete heart block remain undiscovered until adulthood, and may present for the
first time during pregnancy99 . In general, newly acquired and congenital CHB are
rarely first detected during pregnancy and are usually associated with prior cardiac
surgeries, congenital heart disease, acute myocardial infarction, cardiomyopathy, drug
intoxication, or metabolic disturbances37,41,100 . Most women with CHB present before

pregnancy and will often have a permanent pacemaker implanted.
Pregnancy in women with a permanent pacemaker is usually uneventful101,102 . In
women with a pacemaker who undergo caesarean delivery, the interference generated
by monopolar surgical diathermy/electrocautery can be sufficient to temporarily
inhibit pacemaker output, or may give rise to a temporary increase in pacing rate.
Therefore, during a caesarean delivery, the pacemaker should be programmed to avoid
inappropriate inhibition or high rate pacing.
In the absence of concomitant intraventricular conduction delay, asymptomatic
women with newly diagnosed CHB can be managed without a pacemaker during
pregnancy102 . Labour is felt to be a high-risk period for women with CHB as the
Valsalva maneuver during delivery can be associated with a vasovagal reaction
resulting in slowing of the heart rate and potentially syncope. Despite the theoretical
risk of bradycardias, temporary transvenous pacemakers also have risks and risks and
benefits needs to be considered. In one small case series of asymptomatic women
with CHB, temporary pacemakers were inserted, but no significant change in heart
rate was detected before, during or after delivery103 .
The indications for permanent pacing during pregnancy are similar to those in the
general population104 . Although rare, women with CHB who develop symptoms of
syncope or presyncope may need to have a pacemaker implanted during pregnancy.
Radiation exposure due to the use of fluoroscopy during pacemaker implantation
is the most frequent concern for pregnant women and physicians. Precautions
can be used to minimize radiation exposure including shielding of the mothers
abdomen, limiting fluoroscopy exposure time, beam size and imaging area105 . During
fluoroscopy for pacemaker implantation, the uterus is positioned outside the field
of view, and therefore the fetus is exposed to internal and external scattered
radiation only. If necessary, pacemaker implantation can also be safely performed
under transesophageal, or a combination of electrocardiographic and transthoracic
echocardiogram guidance106–108 .
CONCLUSION
Arrhythmias can occur during pregnancy and, in general, the approach to diagnosis
and management of arrhythmias in the pregnant woman is similar to that in
the nonpregnant woman. When arrhythmia therapy is warranted, the benefits of
antiarrhythmic therapy for the mother need to be weighed against any adverse effects
of antiarrhythmic drugs on the developing fetus. Data on drug safety and efficacy
during pregnancy is limited.
ACKNOWLEDGEMENTS
The authors wish to thank Ms. Angela Kennie for her assistance with Figure 1.
SUPPORT
This work was supported by operating grants from the Heart and Stroke Foundation
of Ontario and the Canadian Institutes of Health Research. The University of Toronto
Pregnancy and Heart Disease Program acknowledges a generous donation from
Mrs. Josephine Rogers.
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Fetal and Maternal Medicine Review 2011; 22:2 123–143

C Cambridge University Press 2011

CARDIAC ARRHYTHMIAS DURING PREGNANCY: A

Physiologic changes in maternal haemodynamics, hormones and autonomic

PHYSIOLOGIC CHANGES DURING PREGNANCY

dispersion of refractoriness and conduction5–8 . The hormonal and autonomic changes

CLINICAL APPROACH TO ARRHYTHMIAS

ELECTROCARDIOGRAPHIC APPROACH TO ARRHYTHMIAS

Narrow QRS complex Wide QRS complex

Very rarely, VT can present with

Sinus Atrial Junctional

Figure 1 Electrocardiographic diagnostic algorithm for tachycardias.

THERAPY FOR ARRHYTHMIAS

Antiarrhythmic medications are classified according to the Vaughan Williams

Figure 2 Mechanisms of supraventricular tachycardia27 .

ATRIAL AND VENTRICULAR ECTOPIC BEATS

Table 1 Antiarrhythmic Drugs

Vaughan-Williams Class Potential Adverse FDA Use during

Zachary Laksman, Louise Harris and Candice K Silversides

Beta blockers Class II No reported teratogenicity. C† Compatible†

Vaughan-Williams Class Potential Adverse FDA Use during

Procainamide Class IA No reported teratogenicity. C Compatible. However, the

Cardiac arrhythmias during pregnancy: a clinical approach

In most cases no therapy is required for etopic beats in the asymptomatic

Paroxysmal supraventricular rachycardia

Paroxysmal supraventricular tachycardia (PSVT) usually presents as a narrow

Focal Atrial Tachycardia

Focal atrial tachycardia (AT) is relatively rare during pregnancy. AT is characterized

Atrial fibrillation and atrial flutter

tachycardia has a duration of at least 30 seconds, or is associated with haemodynamic

Congenital long QT syndrome

Beta blockade has been shown to be protective, specifically postpartum. In these

antepartum period as there is normally a physiologic increase in heart rate of 10 to

First and second degree AV block

Complete heart block

As discussed above, AV block is defined as an interruption or delay in the transmission

intoxication, or metabolic disturbances37,41,100 . Most women with CHB present before

19 Nihoyannopoulos P. Cardiovascular examination in pregnancy and the approach to diagnosis of cardiac

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