You are on page 1of 30



Heart disease in pregnancy is one of cause of non-obstetric maternal mortality that

quite important.The incidence of heart disease in pregnancy varies between 0,4-4,1%. In
2005-2006 the incidence of heart disease in pregnancy in Indonesia approximately
1,2%. In fact, the incidence was greater in Indonesia, because our recording system or
medical records were not going well.
Some changes in the cardiovascular or hematological systems during pregnancy
causing difficulties for diagnosis of heart disease and can aggravate the heart disease
itself, especially in the intrapartum period. Intrapartum and postpartum periods was
critical period where most deaths occurred in this period.
Patients with heart disease need a pre-conception counseling about the risk of
disease that deteriorate if the patient is pregnant, so require special management during
pregnancy and classified as high-risk pregnancy. And during pregnancy, patient need a
multidisciplinary approach management by obstetrician, cardiologists, anesthesiologists
and neonatologists.


A. Changes In Cardiovascular System During Pregnancy
Some changes in the cardiovascular system occur during pregnancy, where the
blood volume and cardiac output increased in the first trimester and reaches the peak at
20-24 weeks gestation until term. Patients with previous heart problems, decompensation
may occur at the peak of this changes 1.
Plasma volume reaches a maximum of 40% above baseline at 24 weeks gestation.
Almost the same, cardiac output (CO) reaches 30% to 50% above baseline, reaching a
peak at the end of the second trimester and plateau until delivery. In the early pregnancy,
the increased CO related to the increased stroke volume (SV), whereas at the end of
pregnancy, the heart rate becomes the main factor for the increased CO. Heart rate began
to increased at the age of 20 weeks and continued to increased until 32 weeks'
gestation. This is persist until 2-5 days after delivery1,2.
The increased CO occurs because of three factors: 1). Increased preload due to
increased blood volume, 2).Afterload reduction due to a decreased in systemic vascular
resistance, 3).The increased in maternal heart rate 10-15 beats/min 1.Stroke volume
increased during the first and second trimesters, but decreased when the third trimester
due to compression of the inferior vena cava by the uterus.Blood pressure decreased
about 10 mmHg below baseline at the end of the second trimester due to active
vasodilation through the action of local mediators such as prostacyclin and nitric oxide, as
well as a decreased in systemic vascular resistance due to the addition of new blood
vessels in the uterus and placenta1,2,3.
Uterine contractions, position (tilt left vs supine), pain, anxiety bleeding, and
uterine involution cause significant hemodynamic changes during inpartu and
postpartum.Increased CO up to 15% at the beginning of inpartu, 25% at the first stage,
and 50% during the straining effort.Each contraction makes SV increased, with a resultant
increased CO 50%.Blood loss during labor about 300 ml up to 400 ml when vaginal
delivery and 500 ml up to 800 ml when the cesarean section may affect the hemodynamic
Immediately after birth, cardiac filling pressure increased due to the decompression
of the inferior vena cava and the return of blood from the uterus into the systemic
circulation.It reached 80% increased in CO in the early postpartum due to autotranfusion
associated with uterine involution and resorption of oedema of the legs.It also causes a

Pregnancy also initiate a change of hemostasis, that is an increased in the
concentration of coagulation factors, fibrinogen, and platelet adhesion and reduced
fibrinolysis that cause hypercoagulability and an increased risk of thromboembolic
events. In addition, the resistance of the return of venous blood flow by enlarging uterus
increases the risk of thromboembolism.

Parameter Gestation Inpartu & Post

Hemodynamic Normal Labor Labor
Blood volume

Heartbeat 10-15 beats /

Cardiac output 30%-50%
additional 50%
above baseline
Blood pressure
10 mmHg

Stroke volume (300-500

Systemic vascular resistance 20%

Blood volume increased 50%
Peripheral vascular resistance decreased 20%
Blood pressure:
- decreased systolic 5-10 mmHg
- decreased diastolic 10-15 mmHg
- blood pressure return after 24 weeks until term
CVP remained (10 cmH2O)
Increased heart rate 10-15 beats/min
Cardiac output increased by 30-50% (increased from 5-10 weeks gestation and
reached the peak at 20-24 weeks)
Right ventricular ejection fraction increased
Blood tends hypercoagulable
ECG changes
- left axis deviation of 15 degrees

- low voltage QRS
- T wave inversion in lead III
- Q waves in leads III and AVF
- Atrial and ventricular premature beats
Changes in chest X-ray
- The hearts position more horizontal
- A little pleural effusion in early postpartum
Cardiac output increased by 20-30% during inpartu
Each contraction causes 300-500 ml of blood flow from the uterus into the systemic
Increased blood pressure 10-20 mmHg for each contraction
Supine position decreasedthe cardiac output by 30%
Oxygen consumption increased by 100%
Cardiac output increased by 10-20% in the early postpartum period
Stroke volume increased
Reflex bradycardia
These changes persist 1-2 weeks after delivery

B. Classification of Heart Disease

Determining the function of the heart is important for pregnant patients with heart
disease. Functional status for patients with heart disease are generally grouped according
to the classification system of the New York Heart Association (NYHA) 1, as follows:
1. Class I; patients with heart disease but without any limitation of physical activity.
Ordinary physical activity does not cause fatigue, palpitation, dyspnoea or angina
2. Class II; patients with heart disease with slight limitation of physical
activity. Would feel better with rest. Regular physical activity cause fatigue,
palpitation, dyspnoea or angina pain.
3. Class III; Patients with heart disease with a limitation of physical
activity. Comfortable at rest. Minimal physical activity causes fatigue, palpitation,
dyspnoea or angina pain.

4. Class IV; Patients with heart disease that characterized by an inability to perform
all physical activity. Symptoms of cardiac insufficiency may occur at rest.If physical
activity is done, the discomfort more increased.


Arrhythmias in pregnancy are common and may cause concern for the wellbeing of
both the mother and the fetus. For some mothers the arrhythmias may be a recurrence of a
previously diagnosed arrhythmia or the first presentation in a woman with known
structural heartdisease. In most cases, however, there is no previous history of heart
disease, and the new occurrence of a cardiac problem can generate considerable anxiety.
The majority of arrhythmias that occur during pregnancy are benign, and simply
troublesome; hence, advice about appropriate actions during symptomatic episodes,
together with reassurance, is usually all that is required. In the remaining minority of
cases, judicious use of antiarrhythmic drugs will lead to a safe and successful outcome for
both mother and baby3,. In women with known structural heart disease, however,
arrhythmia is one of the five independent predictors of having a cardiac event during the
pregnancy and should therefore be treated seriously
Although the prevalence of heart disease is limited only 0,5 to 1,0 percent of
pregnant women, but the important thing is, is it possible for maternal morbidity and
mortality, as well as causing a significant effect on the fetus 4,5.


The prevalence of arrhythmia in pregnancy is not known with certainty.The most
common hapenned is atrial ectopy and ventricular ectopy that approximately 50-60% of
pregnant women4.Moreover recent studies reported the occurrence of supraventricular
tachycardia during pregnancy between 1,5 to 3,0 percent in women with heart disease 4,6,7.
Copeland and Stern reported that in healthy pregnant women can occur second-degree AV
block type I (Weckenbach) and also can be found the condition of total AV block.

The mechanism of arrhythmia during pregnancy is not known with certainty, there
is suspect that arrhythmogenic factors in pregnancy cause arrhythmia. Factors that can
trigger arrhythmia during pregnancy and delivery, including cardiac electrophysiological
effects directly from hormones, changes in autonomic tone, hemodynamic disorders
during pregnancy, hypokalemia in pregnancy, and underlying heart disease 4,5.
Treatment of arrhythmia during pregnancy should consider the side effects of the
drugs to the mother or fetus3. Antiarrhythmic therapy should not cause complications in
pregnancy, safe, and well tolerated by the fetus. So, its requires knowledge of the
physiological changes in the cardiovascular system during pregnancy, symptoms and

signs resembling heart disease in normal pregnancy, and time to start anti-arrhythmia
drug in pregnant women, considering many antiarrhythmic drugs that can potentially
have adverse effects both on maternal and fetal due to antiarrhythmic drugs always pass
the placenta barrier.


Pathogenesis of arrhythmia in pregnancy still unclear, but several hypotheses
explain the occurrence of arrhythmia during pregnancy because of changes in
hemodynamic, hormonal, autonomic and emotional 1,2,4,5.
Physiological or hemodynamic changes that occur during pregnancy is started in
early first trimester of pregnancy 5-8 weeks, reaching a peak in the second trimester, and
maintained until the end of pregnancy1,2,4,5. Major cardiocirculation changes that occur
during pregnancy including an increased in blood volume, cardiac output and decreased
peripheral resistance.Increased blood volume is about 1600 ml in pregnancy.Blood
volume began to increased at 7 weeks of pregnancy and the peak at 32 weeks 4,5. The
composition of whole blood was changed, red blood cells increased by 20% and plasma
volume increased by 45% to 50% 4,5. Plasma is a part of the blood that experienced the
greatest improvement.Uterine contractions can lead 300 ml of blood to flow back into the
central circulation. Theblood flow to the uterus in late pregnancy increased more than 50
times compared to non-pregnant state. Cardiac output increased by 50%.It is caused by an
increase in heart rate of 20% and an increased in stroke volume in order to fulfill the
requirement of oxygen.And reduction of peripheral resistance also happened, due to
reduction of systemic resistance by 25%4,5. At 20 weeks of gestation, there is a decreasing
in blood pressure due to relaxation of smooth muscle of veins that are affected by the
hormone progesterone in response to the decreasing of peripheral resistance.
The increased blood volume during pregnancy will lead to an increased in end-
diastolic volume of the left ventricle, this situation can lead to irritability of the heart
muscle.Increased heart rate as a result of an increasing cardiac output during pregnancy
will affect the refractory period and conduction velocity that which in turn will lead to
Hormonal changes that occur during pregnancy holds a very important role in the
development of arrhythmia.Estrogen increased exitability and the frequency of the
potential action in the sensitive tissue.Besides that, estrogen will also increase the amount
of alpha adrenergic receptors and increases the sensitivity of adrenergic receptorson the

tissue.As a result of changes in the autonomic nerves, it willeffect on the refractory period
and conduction velocity of the reentrant circuit.
Emotional psychological changes that occur during pregnancy will cause a lot of
stress or anxiety.Fear or anxiety will activate the pituitary-adrenal pathway and stimulates
the sympathetic nervous system which could potentially causearrhythmia.Additionally,
arrhythmia may be an early sign of heart problems during pregnancy, that is peripartum


There are three main principles for the diagnosis of arrhythmia in pregnancy, the
first, proper diagnosis in order to provide appropriate treatment or therapy, the second,
must be ensured are there any structural disorder of the heart that associated with
arrhythmia, and the last one is to get rid of a systemic disorder that can lead to
arrhythmia, eg abnormalities of thyroid function, electrolyte imbalance, arrhythmogenic
effects of drugs, alcohol, coffee and cigarettes, hemorrhage, pulmonary embolism,
infection and inflammation4,5. Palpitations, dizziness and syncope is a symptom that often
occurs in pregnant women, but it is rarely a symptom of heart arrhythmia. If arrhythmia
occurs, it can affect hemodynamics.The decreased in blood pressure that associated with
arrhythmias may cause fetal bradycardia and requires immediate treatment.
A thorough history and examination of the patient is paramount. It should be
remembered that in the third trimester,patients may become more symptomatic with
activity and thus even minor arrhythmias may present with associated symptoms such as
breathlessness or chest pain. Palpitations are the most common symptom and while
syncope or pre-syncope may reflect a cardiac cause, it may also result from the
physiological drop in blood pressure because of peripheral vasodilatation that is maximal
in the second trimester. A thorough family history concentrating particularly on any
sudden premature or unexplained deaths that may identify a genetic propensity to life
threatening arrhythmias is also important. Identifying the presence of structural heart
disease increases the likelihood of arrhythmias and these are more likely to be significant.
Conditions such as mitral stenosis may present for the first time during pregnancy,
particularly as pregnancy is often the first time a woman is examined by a healthcare
professional since childhood. Women with congenital heart disease, particularly those
having undergone surgery, are particularly vulnerable to arrhythmias, which may be
haemodynamically compromising and warrant special consideration. Patients who had

atrial surgery, such as a Mustard procedure for transposition or a Fontan procedure, are
particularly vulnerable to atrial flutter, as are those with any cause of right ventricular
impairment. Patients who have undergone surgical correction of tetralogy of Fallot may
experience atrial flutter or ventricular tachycardia arising from the right ventricular
outflow tract, particularly if the correction was incomplete and there is a residual
haemodynamic abnormality.
While the resting electrocardiogram (ECG) is usually unaltered in pregnancy
apart from a physiological increase in heart rate, changes may occur. The electrical axis
can be displaced slightly due to cardiac rotation resulting from the gravid uterus, but
tends to remain within the normal range. The increase in heart rate can be associated with
shortened PR, QRS and QT intervals. Other more obvious changes should be regarded as
abnormal and investigated4,5.
ECG (Electrocardiography) at rest is one important tool for the diagnosis of
arrhythmia.Interpretation of electrocardiographic abnormalities in pregnant women must
be good, and should consider the normal physiological changes that occur in pregnancy.
There is an increased in heart rate while rest approximately 10 times per minute during
pregnancy because of there is increased in plasma volume and cardiac output during
pregnancy.This may lead to a decreased in the PR interval, QRS, and QT, but generally
there is no change in the amplitude of the P wave, QRS complex and the T wave. Shifting
of electrical axis can be occured, more often to the left, because the rotation of the heart
due to an enlarged uterus 5. Atrial ectopy and ventricular ectopy are common in pregnant
women. Can also arise pathological Q waves and T inversion in inferior lead.
Ideally, a 12 lead ECG should be recorded during symptoms, although this is rarely
achieved. Because of their spatial pattern, paroxysmal arrhythmias are the most difficult
to diagnose. They can be short lived and the majority have no pattern, so attempting
capture with a routine 24 h Holter monitor is often fruitless 4. Detecting the arrhythmia
predominantly depends upon its frequency. If it occurs on a daily basis then a 24 h or 48 h
Holter may be sufficient. It is crucial for the woman to keep an accurate diary so any
symptoms can be related to any abnormality on the Holter 4. Asymptomatic arrhythmias
should not be treated unless felt to be life threatening. Episodes which are less frequent or
which have evaded detection are best documented using a patient activated event
recorder. It is important that the woman continues with her normal activity while wearing

the device and keeps a diary of her symptoms, which can be related to the recorded
rhythm. Finally, implantable loop recorders are increasingly being used, particularly in
patients with unexplained syncope. There is no experience of these devices in pregnancy;
however, there are no theoretical contraindications to their use.
Arrhythmia during pregnancy may show symptoms such as sinus tachycardia,
atrial ectopy, ventricular ectopy, supraventricular tachycardia, atrial fibrillation, sinus
bradycardia and atrioventricular block4,5.
In 1965, Mendelson was the first person who reported the incidence of
supraventricular tachycardia during pregnancy. Tawam et al found that there was
increased in the risk of new onset (34%) or exacerbation (29%) of supraventricular
tachycardia during pregnancy4,5. Supraventricular tachycardia may indicate the
hemodynamic disorders depend on the presence or absence of heart structural
abnormalities.Physical and psychological stress is a stimulus that triggers
supraventricular tachycardia in the majority of pregnant women without structural heart
Antiarrhythmic drugs
The decision to treat a woman depends upon the frequency, duration and tolerability of
the arrhythmia. It is a balance between the benefit of arrhythmia reduction or termination
and the maternal and fetal side effects of any drug treatment. The greatest risk to the fetus
is during organogenesis and this is complete by the end of the first trimester. The smallest
recommended dose should be used initially and be accompanied by regular monitoring of
maternal and fetal clinical condition. Various drugs have been used to terminate fetal
arrhythmias, providing useful safety data. However, the literature is limited to single or
small case series. These include digoxin, adenosine, amiodarone, flecainide,
procainamide, propranolol, propafenone, quinidine, sotalol and verapamil 4,5,8,9.
The majority of drugs available, however, only have class C evidence for use in
pregnancy8,9. Therapeutic levels of drugs may also be difficult to maintain in the pregnant
woman as pregnancy tends to decrease the concentration of drugs because
of an increased volume of distribution and increased drug metabolism. This may explain
why women previously stable on therapy have breakthrough arrhythmias during
Historically, there has been concern regarding the effect of b-blockers and intrauterine
growth restriction (IUGR). This effect seems to be limited to atenolol and when used

either at the time of conception and/or during the first trimester. It was not seen with other
antihypertensives used in the first trimester, or when atenolol was taken in the second or
third trimester only4,8,9. Therefore, where benefit exceeds riskfor example, arrhythmias,
mitral stenosis, Marfan syndrome, thyrotoxicosisb-blockers should not be withheld.
DC cardioversion
DC cardioversion is safe in all stages of pregnancy; because the amount of current
reaching the fetus is small, it is only associated with a small risk of inducing fetal
arrhythmias4,5. There have been reports of the need for emergency caesarean section
because of fetal arrhythmia, particularly in women who are compromised; hence the fetus
should be carefully monitored before and throughout the procedure 4,5.


Pathological bradycardia in pregnant women is rare. Some women who have
physiological bradycardia may, in the second trimester, feel symptomatic as their blood
pressure drops due to a reduction in systemic resistance; however, treatment is rarely
required. Rarely, symptomatic bradycardia has been attributed to supine hypotensive
syndrome of pregnancy4, which is a result of compression of the inferior vena cava by the
gravid uterus and responds to maternal changing of position 4. Congenital heart block is
rare and does not usually pose a problem during the pregnancy. There is conflicting
advice about whether to advise temporary pacing for delivery. Proponents state concern
that the Valsalva manoeuvre associated with delivery increases the chance of worsening
bradycardia and syncope, and pacing also allows for an adequate heart rate response for
the increased cardiovascular stress. The alternative view is that,from experience, patients
rarely use the device that has been inserted. Spinal anaesthesia for caesarean section,
however,can be associated with a higher incidence of all grades of bradycardia (up to

Paroxysmal supraventricular tachycardia
The three common types of SVT are as follows 4,5: (1) AV nodal reentrant tachycardia:
This is the most common type and involves a reentrant circuit utilizing the AV node
andperinodal atrial tissue. This arrhythmia can be treated with antiarrhythmic drugs or AV

nodal blocking drugs (such as adenosine, beta-blockers, calcium channel blockers or
(2) Tachycardias using overt or concealed accessory pathways including WPW syndrome:
In most cases the reentrant impulse travels from the atria via the normal conduction
system to the ventricles and then returns to the atria via an accessory pathway. Rarely the
impulse travels in the reverse direction. This arrhythmia can be treated with
antiarrhythmic drugs or AV nodal blocking drugs. In WPW syndrome the accessory
pathway can conduct anterogradely and retrogradely. The abnormal accessory pathway
may conduct at dangerously fast rates occasionally inducing ventricular fibrillation and
sudden death
(3) Atrial tachycardia: This tachycardia is caused by reentry or an automatic focus
entirely within the atria. The AV node is not part of the reentrant circuit so drugs that
delay AV conduction may slow the ventricular rate but do not terminate the tachycardia.
Termination of the arrhythmia requires the use of an antiarrhythmic drug or electrical
Treatment of the acute episode of SVT 4,58,9
It is uncommon for brief episodes of supraventricular arrhythmia to cause significant
compromise to mother or fetus in the absence of structural cardiac disease. Vagal
manoeuvres should be tried initially. If vagal manuvers are ineffective, adenosine is the
agent of choice. Given in sufficient dosage (624 mg), adenosine will always terminate
SVT with the exception of atrial tachycardia. Adenosine will not terminate most atrial
tachycardias but will temporarily increase the degree of AV block. If the tachycardia
resumes soon after termination, a longer acting agent such as intravenous verapamil or
beta-blocker may be used with caution to avoid hypotension. If the patient is
haemodynamically unstable, she should be electrically cardioverted. Persistent atrial
tachycardia should be electrically cardioverted. Fetal monitoring is essential during
cardioversion or in the setting of maternal haemodynamic instability and is also advisable
during adenosine administration .

AV nodal reentrant tachycardia. A 24-year-old woman presented with frequent
palpitations and sustained SVT during the 32nd week of pregnancy. The acute attack was
terminated with intravenous adenosine (18 mg). Symptoms improved but were not
eliminated with metoprolol. She underwent successful radiofrequency ablation 8 weeks

Prevention of recurrent SVT

Recurrent, brief episodes of SVT can be managed with simple reassurance. More
troublesome SVT is managed with medication. AV nodal-blocking drugsbeta-blockers,
verapamil or digoxinare reasonable choices but beta-blockers have the best safety record
(with the exception of atenolol ); however, these drugs will not prevent atrial tachycardia..
If the patient has atrial tachycardia or SVT resistant to AV nodal-blocking drugs,
flecainide can be considered. If a woman is poorly responsive to medical therapy or
thought to be at a high risk of malignant arrhythmia associated with WPW syndrome,
radiofrequency ablation should be considered during pregnancy.

Suggested management of SVT in pregnancy10.

SVT supraventricular tachycardia; DC direct current

Atrial fibrillation and atrial flutter

AF and flutter (AFl) are relatively rare in pregnancy in the absence of structural heart
disease. These arrhythmias can be problematic for two main reasons. Firstly, the
increased heart rate and loss of effective atrial contraction may cause cardiac failure. The
second important consideration is the increased risk of thromboembolism. The loss of
effective atrial contraction and the physiological prothrombotic state of pregnancy
combine to increase the risk of thrombus formation in the left atrial appendage. If
required, beta-blockers, digoxin or verapamil are preferred for heart rate control during
AF or AFl. In the event of new onset AF/AFl or haemodynamic instability, cardioversion
(either electrical or pharmacological) should be undertaken torestore normal rhythm.
Sotalol is probably the antiarrhythmic of choice but amiodarone and flecainide are
second-lineoptions4,10. In the setting of underlying cardiac disease the issue of
anticoagulation can be complex and needs to be decided on an individual basis. With
respect to the choice of anticoagulant,in brief, warfarin can be used in the second and
early third trimester and heparin (unfractionated or low molecular weight) is
recommended at other times4,10. If the heart is structurally normal and there is no history
of thromboembolic events or thrombophilia, anticoagulation is not usually indicated.

Atrial premature beats

Atrial premature beats (APB) in pregnant woman with structurally normal hearts are
benign. Atrial premature beats become more frequent during pregnancy or may develop
for the first time and many patients are worried about it. Patient education and
reassurance are the first level of intervention of this benign condition. Exacerbating
factors, such as chemical stimulants should be identified and eliminated. Drug therapy is
not needed in the vast majority of pregnant women. In patients who remain highly
symptomatic, treatment with selective -adrenergic receptor-blocking agents should be
considered.The few randomized studies of their use in pregnancy have yielded conflicting
results regarding their effectiveness and safety. -Blocking agents readily cross the
placenta and could, in large doses, cause a relative fetal bradycardia. Preferred drug for
treatment of APBs is a 1-selective agent (metoprolol) 4,10. In contrast, 2-blocking agents
are associated in some cases with reduced utero-placental perfusion and/or fetal growth

retardation and should not be given.

Ventricular tachycardia
The majority of women who present with new onset VT in pregnancy have a structurally
normal heart (idiopathic VT). The most common type of idiopathic VT arises from the
right ventricular outflow tract and has a distinctive ECG appearance (left bundle branch
block morphology with inferior axis.. It is often precipitated by sympathetic stimulation
and may respond to beta-blockade. Data from non-pregnant patients with idiopathic VT
suggest that the long-term prognosis is excellent. however, prolonged episodes could
potentially result in hypotension and fetal hypoxia so adequate treatment is essential. If
beta-blockade is not successful, class IC or III drugs may be used or radiofrequency
ablation may be necessary. The second most common type of idiopathic VT arises in the
left ventricle and is termed fascicular VT or idiopathic left ventricular VT. This VT
alsohas a distinctive ECG appearance (right bundle branch block morphology with
superior axis10,12,13. This VT is often mistaken for SVT because the QRS duration during
tachycardia may be relatively narrow. The tachycardia may respond to verapamil or beta-
Treatment of the acute episode of VT
Patients with haemodynamic compromise should be electrically cardioverted
immediately. In uncompromised patients intravenous lignocaine or sotalol can be used.
There is little evidence that intravenous amiodarone is useful in terminating 10
an attack of VT.
Prevention of the recurrent VT
VT associated with structural cardiac disease is potentially malignant. Most patients with
VT in this setting should undergo defibrillator implantation. Antiarrhythmic drug therapy
can be used in patients with idiopathic VT in the absence of structural heart disease. Beta-
blockers are the firstline therapy. If beta-blockers are ineffective or not tolerated calcium
channel blockers (for idiopathic left ventricular VT), sotalol or flecainide can be
considered but the severity and frequency of episodes must be weighed against adverse
drug effects. Idiopathic VT can be cured with catheter ablation with a very high success
rate (.90%). The choice of pharmacologic therapy in the setting of a structurally abnormal
heart is more complex as some antiarrhythmic medication may worsen the situation 10.12,13.

Idiopathic right ventricular VT. A 31-year-old woman presented with new onset
intermittent, frequent episodes of broad complex tachycardia during the 24th week of
pregnancy. The tachycardia had the ECG appearance of VT arising in the right ventricular
outflow tract. The arrhythmia settled with oral metoprolol. She remained
haemodynamically stable throughout. She had only occasional brief episodes after the
commencement of regular metoprolol. Successful radiofrequency ablation was
undertaken 8 weeks post delivery10

Suggested management of VT in pregnancy. AA antiarrhythmic; VT ventricular
tachycardia; DC direct current10

Long QT syndrome
Hereditary long QT syndrome (LQTS) is caused by an abnormality of genes coding for
cardiac ion channels. Patients with this condition show a prolonged corrected QT interval
on the ECG during sinus rhythm. LQTS may cause torsades de pointes, a potentially fatal
form of polymorphic VT. The mainstay of treatment is beta-blockade but patients with
recurrent arrhythmia despite beta-blockade should be considered for defibrillator
Implantation4. It is possible that the increased heart rate and subsequent shortening of the
QT interval that occur during pregnancy may be protective as several series have
demonstrated that dangerous cardiac arrhythmias and sudden death occur rarely in the
LQTS group until after delivery. The postpartum period is a time of increased risk.
Treatment withbeta-blockers has been associated with decreased chance of postpartum
arrhythmia, especially in those with the LQT2 genetic mutation, and hence should be
continued throughout pregnancy and postpartum in women already taking that
medication. Data have also suggested that babies from mothers with LQTS requiring
urgent caesarean section for fetal distress are extremely likely to be carriers of the genetic
condition. LQTS has also been linked to sudden infant death syndrome;therefore, routine
screening of the progeny of mothers with this condition is imperative. Drugs that
potentially prolong the QT interval should be avoided. During an episode of torsades de
pointes intravenous magnesium and temporary overdrive pacing may stabilize the

Idiopathic left ventricular VT. A 27-year-old woman presented with frequent, distressing
palpitationsduring the 28th week of pregnancy. She remained haemodynamically stable
throughout. The acute attack was initially thought to be SVT but was unresponsive to
adenosine. She was reviewed by a cardiologist who diagnosed idiopathic left ventricular
VT. The arrhythmia was terminated with intravenous lignocaine. Further episodes were
prevented with oral verapamil. She underwent successful radiofrequency ablation 12
weeks postpartum10

A 12-lead-ECG of a patient with wide-QRS complex tachycardia from a 28-year-old

pregnant woman (31 week ofgestation). The tracing shows a right bundle branch
block like morphology with a triphasic appearance in V1, but an R/S ratio of less
than 1 in V6 and a northwest QRS axis, typical for a ventricular tachycardia. There
is one-to-one ventriculoatrial conduction during the tachycardia. The p waves are
negative in leads II and III

12-lead- ECG of a 34-year-old pregnant woman with a fast polymorphic ventricular
tachycardia (25 week of gestation)10

Ventricular fibrillation and ventricular flutter

Life-threatening ventricular fibrillation (VF) or ventricular flutter (VFlut) can occur in
any stage of pregnancy and is associated with a high risk of sudden cardiac death. In
patients with VF or VFlut, DC defibrillation is the method of choice (100-360 J). Prompt
cardiopulmonary resuscitation and early defibrillation by either DC-countershock or an
automated external defibrillator (AED) significantly improve the likelihood of successful
resuscitation from VF. For long-term therapy, the implantable cardioverter defibrillator is
an excellent approach to terminate ventricular tachyarrhythmias and to prevent sudden
death. There are a few reports on ICD therapy during pregnancy, and these studies clearly
show that ICD implantation did not negatively influence pregnancy, delivery or fetal

Ventricular premature beats

Ventricular premature beats (VPB) in pregnant woman with structurally normal hearts are
benign and therapy is usually not necessary. Patient education and reassurance are the
first level of interventions of this benign condition. Exacerbating factors, such as
chemical stimulants should be identified and eliminated. In patients who remain highly
symptomatic after all steps have been taken, treatment with selective -adrenergic

receptor-blocking agents is indicated. The few randomized studies of their use in
pregnancy have yielded conflicting results regarding their effectiveness and safety. -
Blocking agents readily cross the placenta and could, in large doses, cause a relative fetal
bradycardia11. Preferred drugs for treatment of VPBs are 1- selective agents like
metoprolol. In contrast, 2-blocking agentshas been associated in some cases with
reduced uteroplacentalperfusion and/or fetal growth retardation, and hence shouldnot be
chosen for treating VPBs. There is no indication for treatment with class III
antiarrhythmic drugs due to their side effects and risk for proarrhythmia 10,12.


Arrhythmias that cause prolonged maternal hypotension and threaten placental perfusion
require urgent treatment. However, treatment may also be required to prevent symptoms
such as syncope, dyspnoea or distressing palpitations. The decision to use a particular
therapy must take into account the risks of that therapy to mother and child. Although
randomized data in the setting of maternal arrhythmias do not exist, experience suggests
that many antiarrhythmic drugs appear to be relatively safe in pregnancy . The lowest
therapeutic dose should be used. If possible, the introduction of drugs during the first
trimester should be avoided and,where relevant, drug levels and medication-related ECG
changes must be monitored closely.
If a woman is planning pregnancy and suffers from recurrent bouts of tachyarrhythmia,
radiofrequency ablation prior to conception should be considered.

Pharmacokinetics during pregnancy
There are multiple reasons why maintaining therapeutic drug levels in pregnant women
can be challenging. The volume of distribution rises and that can increase the necessary
loading dose to reach adequate serum concentrations. There is reduced protein binding
due to a reduction in plasma proteins. These changes in combination are important
because even though the serum concentration on testing can appear low, the active free
fraction of the drug is unchanged or elevated. Gastrointestinal absorption of drugs may be
affected by alterations in gastric acidity and motility. The glomerular filtration rate
increases, augmenting the excretion of renally cleared drugs, and liver enzymes are also
variably induced that can affect hepatically excreted substances.

Adenosine is first-line therapy for the termination of SVT. It is an endogenous purine
nucleoside and is highly effective at modulating conduction through the AV node. It can
cause flushing and dyspnoea but these side-effects are short-lived. It should be avoided in
women with severe asthma as it may cause bronchospasm. The extremely short half-life
is advantageous with respect to side-effects and unlike calcium channel blockers and
beta-blockers it does not cause hypotension, an important factor in the acute management
of SVT. It is generally agreed that adenosine does not cross the placenta in significant
amounts to cause fetal bradycardia, although there is one report in the literature of a
transient drop in heart rate without any significant consequences. Adenosine is not
known to be teratogenic. It is advisable to monitor fetal heart rate during
Digoxin is a cardiac glycoside that exerts its antiarrhythmic activity via inhibition of the
sodium/potassium ATPase. The AV nodal tissue is particularly sensitive and responds
with slowed conduction. A vagotonic effect may also be important. It has been used to
control the rate of supraventricular and atrial tachyarrhythmias in the mother and fetus for
decades.Maternal toxicity can cause fetal death Digoxin crosses the placenta and
maternal levels to some extent reflect those of the fetus. The various physiological
changes of pregnancy alter the pharmacokinetics of digoxin variably and regular
monitoring of serum levels is essential; however, in the third trimester they can appear
spuriously high due to digoxin-like substances that interfere with the radioassay10,11.

Class IA antiarrhythmic agents: quinidine,procainamide and disopyramide

These drugs predominantly block sodium channels and also potassium channels. They
have been used to treat broad and narrow complex tachycardia in pregnancy but are not
commonly used in Australia. These agents prolong the action potential duration,
refractory period and QT interval, and consequently can predispose to torsades de pointes
so monitoring of the QT interval is crucial 10,11. They do not appear to be teratogenic.
Quinidine has been used safely in pregnancy for many years to treat fetal and maternal
tachyarrhythmias although other agents have largely superseded it. It is excreted in breast
milk, but is probably safe in breastfeeding. Disopyramide has a limited role in pregnancy
as it may precipitate premature labour. Prolonged use of procainamide can cause a lupus-
like syndrome and this drug is no longer available in Australia 10,11.

Class IB lignocaine and mexiletine
Class IB drugs shorten the action potential duration and effective refractory period
particularly in ventricular muscle. Lignocaine is only available in intravenous form and
can be used in the acute management of VT. It does cross the placenta, but is not thought
to be teratogenic at clinically relevant doses. Neonatal toxicity is theoretically possible
although at least one report was probably the result of inadvertent scalp injection during
anaesthetic administration for episiotomy. Acidosis resulting from fetal distress increases
the potential for toxicity. Lignocaine levels should be monitored carefully. This agent
secreted in small amounts in the breast milk, but the dose is insufficient
to be harmful. Mexiletine is an oral agent structurally similar to lignocaine. Experience of
use in pregnancy is limited; however, there are no reports of teratogenicity or long-term
adverse effects to the fetus 10,11. Although it is excreted in breast milk and breast-feeding is
discouraged, levels are unlikely to be harmful to the infant.
Class IC flecainide
Class IC drugs are potent sodium-channel blockers and cause marked slowing of
conduction. Flecainide is the only drug of this class in use in Australia. Unfortunately it
can be pro-arrhythmic in the setting of structural heart disease. It crosses the placenta and
is sometimes used to treat fetal tachycardia. Rarely fetal cardiotoxicity can occur48 and
levels should be monitored carefully. It does not appear to be teratogenic. It is excreted in
breast milk but the effect on the infant is not clear. It is not infrequently used in patients
who are not pregnant with lone AF as an antiarrhythmic; however, given the lack of
experience with this drug in pregnancy other agents may be more suitable in gravid
women. Flecainide may be useful as chronic therapy in women with WPW syndrome 10,11.

Class II agents: beta-blockers

Beta-blockers are useful for rate control in atrial arrhythmias as well as suppressing some
supraventricular and VTs via theiranti-sympathetic actions. Beta-blockers, particularly
atenolol, taken at the time of conception or during the first trimester, may be associated
with intrauterine growth restriction(IUGR)10,11. Other questionable effects on the fetus
include bradycardia and neonatal hypoglycaemia. These agents are safe and highly
effective treatment for many tachyarrhythmias and the benefits often far outweigh the
risks. Our agent of choice is metoprolol, largely because it is less protein bound and

therefore less likely to be transferred to breast milk. Data are lacking to support a
particular beta-blocker in the treatment of arrhythmias during pregnancy.

Class III agents: sotalol and amiodarone10,11

Class III agents block potassium channels and prolong myocardial repolarization. This
manifests as QT prolongation on the ECG. These drugs may cause an acquired LQTS and
dangerousventricular arrhythmias.Sotalol has been used in the treatment of fetal and
maternal tachyarrhythmia because it readily crosses the placenta. It can also cause fetal
bradycardia. Sotalol may be teratogenic, although data are inconclusive. Given these
ambiguities it is not a first choice antiarrhythmic; however in some difficultcases its use
is warranted and complications are rare. Close fetal monitoring is essential. Sotalol is
readily excreted in breast milk and some data have suggested that the infant may ingest
up to 20% of the maternal dose, although breastfeeding is consideredsafe if the child is
regularly assessed for the signs of toxicity. Amiodarone does not cross the placenta
readily but fetal serum levels may still be up to a quarter of the mothers. It has a long
half-life and contains significant amounts of iodine that contributeto a long list of well-
known side-effects. It can cause maternal andfetal hyper- or hypothyroidism,
bradycardia,QT prolongationand IUGR. There is a possible increased risk of learning
difficultiesand teratogenicitywith the drug but evidence is scant. If possible amiodarone
should be avoided in pregnancy, especially during the first trimester. Unfortunately in
some patients amiodarone succeeds where other therapy has not and in those potentially
life-threatening situations it may be necessary to use this agent. Amiodarone is secreted in
breast milk in amounts so large that the child may effectively be on a low adult
maintenance dose and breast feeding should be discouraged.

Class IV agents: calcium channel blockers

Verapamil and diltiazem are the commonly used calcium channel blockers with cardiac
activity. Cardiac effects include negative inotropy and slowed conduction through the AV
Node10,11. Data from animal studies suggest that diltiazem may be teratogenic but this has
not been confirmed in humans. A recent prospective cohort study of 299 pregnant women
did not show an increase in birth defects or fetal loss. Babies exposed to calcium channel
blockers had lower birth weightsbut this may have been due to maternal
factors.Verapamil and diltiazem are excreted in breast milk although no major adverse

events have been reported. Verapamil when used intravenously can cause maternal
hypotension and should be used cautiously. It does cross the placenta to some degree and
can potentially cause fetal bradycardia although reports are rare.We could find no data to
support the widely held view that diltiazem does not cross the placenta. Reassuringly,
reports of fetal bradycardia do not exist but experience is limited.


Women with implantable cardiac defibrillators (ICD) should not be discouraged from
falling pregnant unless they have underlying structural heart disease that would be
considered a contraindication. Data have shown that pregnancy does not increase the risk
of major ICD-related complications, nor does it appear to increase the rate of discharges
from the device.ICD discharge does not appear to affect fetal outcome 4,10. After a shock
has been administered the fetus should be checked largely because of the possibility of
fetal hypotension associated with the arrhythmia. ICDs can be implanted during


Direct current cardioversion is well tolerated in all stages of pregnancy and should be
performed if clinically indicated.There is a theoretical risk of inducing ventricular
fibrillation in the fetus; however, there are no data to support this. Thereis one report in
the literature of fetal distress following maternalcardioversion, albeit in the setting of
maternal hypotensionfrom tachyarrhythmia, requiring urgent caesarean section 10. If
possible, obstetric and paediatric staff should be close at hand and fetal heart rate should
be monitored.


If an arrhythmia is poorly controlled and the patient is planning pregnancy, it is wise to
consider radiofrequency catheter ablation prior to conception. Elective
electrophysiological testing and radiofrequency ablation procedures are contraindicated in
pregnancy because of potential radiation exposure to the developing fetus. Ablation may
be warranted in cases where the tachyarrhythmia is not well controlled on medication
placing the mother and fetus at risk of prolonged episodes of hypotension or even more ]
sinister consequences10. Where possible the procedure should be performed after the first

Studies in patients whowere not pregnant have shown that the potential radiation dose to
a developing embryo or fetus during an ablation procedure would be small, resulting in a
minimal increase in risk for childhood cancers, genetic abnormalities or serious birth
defects. Although there are many case reports in the literature regarding radiofrequency
ablation in pregnancy without any negative outcome, the largest series reports only three
cases. Fluoroscopy time should be kept to a minimum. Using venous access routes other
than the femoral vessels and ensuring the maternal bladder is empty are other ways to
minimize the radiation dose. Lead aprons do not seem to be usefulin reducing exposure
significantly as scatter from the thorax of the mother is the major radiation source to the
fetus Theuse of electroanatomical mapping systems.

In the event of cardiac arrest in pregnancy general standard guidelines for
cardiopulmonary resuscitation and advanced life support should be followed with a few
alterations. The gravid uterus pressing on the inferior vena cava and abdominal aorta can
compromise venous return and cardiac output, in turn impeding the effectiveness of chest
compression. Tilting the patient partly toward the left lateral position by using a
rolledtowel or even the lap of a kneeling attending resuscitator can help alleviate this
problem. If this technique is employed it is imperative that the back and shoulders are
stabilized to enable adequate forceful chest compressions. Alternatively the uterus can be
pulled to the side. Cricoid pressure should be applied during positive pressure ventilation
because of the increased risk of regurgitation and aspiration in pregnant women and chest
compressions should be a little higher than usual to allow for the elevation of the
hemidiaphragm and abdominal contents. Paediatric and obstetric staff should be on hand
as soon as possible and when available the fetal heart rate should be monitored.
Emergency caesarean section should be considered if the pregnancy has progressed to the
stage that the fetus could be viable but the complexities of this issue are beyond the scope
of this article. The American Heart Associations most recent cardiopulmonary
resuscitation guidelines provide an excellent outline of the topic.


A variety of maternal and fetal arrhythmias can occur during pregnancy, for
which antiarrhythmic drug therapy may be indicated. Although no drug is completely
safe, most are well tolerated and can be given with relatively low risk. Drug therapy
should be avoided during the first trimester of pregnancy if possible and drugs with the
longest record of safety should be used as first line therapy. Conservative therapies should
be used when appropriate. Several therapeutic options exist for most arrhythmias in the
mother and fetus. The use of an implantable cardioverter defibrillator is an option for
women of childbearing potential with life-threatening ventricular arrhythmia


1. Himpunan Kedokteran Fetomaternal Perkumpulan Obstetri dan Ginekologi

Indonesia, 2007. Tata Laksana Kehamilan Pada Penyakit Jantung. Hal 1-12
2. Himpunan Kedokteran Fetomaternal Perkumpulan Obstetri dan Ginekologi
Indonesia, 2012. Panduan Penatalaksanaan Kasus Obstetri. Kehamilan
Dengan Penyakit Jantung (IV), 50-75.
3. Abbas AE, Steven J. Lester, Heidi Connolly, 2005. Pregnancy and the
cardiovascular system. International Journal of Cardiology 98, 179 189
4. Adamson DL, Nelson-Piercy C (2007). Managing Palpitations and
Arrhythmias during Pregnancy. Heart 93, 1630-1636
5. Elkayam U (2001). Pregnancy and Cardiovascular Disease in Heart Disease,
6th edition. Ediion : Braunwald E, W.B. Saunders Company, USA, 65 : 1790-
6. Ferrero S, Colombo BM, Ragni N (2004) Maternal Arrhytmias during
Pregnancy. Archive Gynecology Obstetric 269, 244-253
7. Folley MR (2006). Maternal Cardiovascular and Haemodynamic Adaptation
to Pregnancy. Uptodate
8. Girling JC (2004). Physiology in Pregnancy. Anaesthesia and Intensive Care
Medicine, 215-218
9. Julie Arafeh RN, MSN, Yasser Y. El-Sayed, MD (2004). Cardiac Disease in
Pregnancy. Neo Reviews vol.5 No.6 June 2004, e232-e235
10. Oakley C, MD, Warnes CA, MD (2007). Heart Disease In Pregnancy.
Blackwell Publishing. British Medical Journal Books
11. Podrid PJ, MD (2006). Management of Arrhythmias in Pregnancy. Uptodate
12. Ramesh M. Gowda, Ijaz A. Khan, Nirav J. Mehta, Balendu . Vasavada,
Terrence J. Sacci (2003). Cardiac arrhythmias in pregnancy: clinical and
therapeutic consideratios. International Journal of Cardiology 88, 129-133
13. Richard L. Page, MD, Dallas, Tex (1995). Treatment of Arrhythmias during
Pregnancy. American Heart Journal 130, 871-6
14. Roger Small (2006). Anti-arrhythmic drugs. Anaesthesia and Intensive Care
Medicine 7, 294-297
15. Tan HL, Lie KI (2001). Treatment of Tachyarrhythmias during Pregnancy
and Lactation, Eur Heart Journal 22, 458464
16. Theodore Chow, MD, Joseph Galvin, MRCPI, Brian McGovern, MD (1998).
Antiarrhythmic Drug Therapy in Pregnancy and Lactation. Am J Cardiol 82,
17. Thorne AS (2004). Pregnancy and Heart Disease. Heart 90, 450456
18. Vardas PE (2008). Arrhythmias in Pregnancy. University Hospital

ofHeraklion Crete, Greece
19. Williams H (2005). Arrhytmias: the option for treatment.
HospitalPharmacyst. Vol 12 : 57-60
20. Iriyama, takayuki et all. Management of patient with arrythmogenic right
ventrikuler cardiomyopathy during pregnancy. 2012
21. Joachim Trappe, Flans. Emergency therapy of maternal and fetal arrhythmias
during pregnancy. 2010
22. Cordina, Rachael, Mc Guire, Mark. Maternal Cardiac Arrhythmias during
pregnancy and lactation. 2009