Electrical cardioversion during pregnancy: safe or not?
C. H. N. Tromp
A. C. M. Nanne
P. J. M. Pernet
A. C. Bolte
R. Tukkie Department of Cardiology
, Kennemer Gasthuis, Haarlem,
Two pregnant patients with a sustained symptomatic maternal supraventricular arrhythmia are presented. Both patients were treated with direct-current cardioversion. Electrical cardioversion during pregnancy is a rarely applied but highly effective procedure in the treatment of maternal cardiac arrhythmias and is assumed safe for both mother and child. However, once foetal viability is reached, monitoring of the foetal heart rate is advised and facilities for immediate caesarean section should be available.
The occurrence of symptomatic maternal arrhythmias
during pregnancy is a cause for concern for the well-being
of both the mother and the foetus. As in the non-pregnant
population, sustained symptomatic arrhythmias should be
treated. Treatment depends upon the diagnosed or
suspected specific arrhythmia. In case of supraventricular
arrhythmias, electrical cardioversion (ECV) is applied
when physical treatment such as sinus carotid massage or
A 34-year-old woman without a relevant medical or
obstetric history is pregnant of her third child. The course
of the pregnancy is uncomplicated until a gestational age of
21 +1 weeks, when she experiences progressive palpitations
and feelings of agitation. Physical examination reveals an
irregular pulse rate of 160 beats/min. Blood pressure (BP)
is 127/86 mmHg, and there is no peripheral oedema.
Auscultation of heart and lungs is normal. Anaemia and
hyperthyroidism are excluded. The electrocardiogram
(ECG) shows atrial fibrillation with a ventricular rate of
194 beats/min, and slight repolarisation disturbance in leads
II, III, aVF and V3V6. Echocardiography demonstrates no
structural or functional abnormalities of the maternal heart.
Treatment with a -blocker is started to control ventricular
rate. This does not result in conversion to sinus rhythm, and
ECV (50 J) is successfully applied. The foetal condition is
monitored by ultrasound, and no adverse effects are seen.
The patient is discharged the same day without medication.
At a gestational age of 40 + 1 weeks, she gives birth to a
healthy boy of 3620 g. During 24 h of postpartum
observation, no complications are noted. Paediatric evaluation
shows no abnormalities.
The second patient is a 29-year-old primigravida with no
relevant medical history and with antenatal care provided
by a community midwife. At a gestational age of 34 weeks,
she is referred to the hospital with palpitations. Maternal
pulse rate is 160 beats/min, BP 118/79 mmHg, and SpO2
98%. Anaemia and hyperthyroidism are excluded.
Auscultation of heart and lungs reveals no abnormalities, and
oedema of lower extremities is absent. The ECG shows a
small complex tachycardia and a long r-p interval with a
positive p wave in leads I and aVL and a negative p wave
in leads II, III and aVF. Occasionally, 2:1 block is shown to
the ventricle which excluded an atrioventricular re-entry
tachycardia (AVRT); however, atrioventricular nodal
reentry tachycardia (AVNRT) and adenosine-sensitive atrial
tachycardia cannot be ruled out. The diagnosis is most
likely ectopic atrial tachycardia. Since adenosine and
verapamil did not terminate the tachycardia, ECV is
performed. ECV (100, 200 and 360 J) decreases the heart
rate to some extent, but conversion to sinus rhythm does
not occur. For additional rate control, digoxin and
propranolol are given. Echocardiography shows normal systolic LV
function and mild mitral and tricuspid insufficiency, which
can be physiological in the third trimester of pregnancy.
Foetal non-stress test and biophysical profile remain
reactive throughout pharmacological treatment and ECV
procedures. Maternal atrial tachycardia persists with variance
in conduction, resulting in fluctuations of ventricular rate.
Because of her declining clinical condition, echocardiography
is repeated and reveals a decrease in left ventricular function
probably due to tachycardiomyopathy. At a gestational age of
36+6 weeks, the foetal non-stress test shows deceleration of
the foetal heart rate and a caesarean section is performed for
foetal indications. A healthy baby girl of 3095 g is born.
Postpartum drug-refractory symptomatic paroxysmal atrial
tachycardia persists, and 18 months after delivery, a catheter
ablation was performed. A subsequent pregnancy was
Cardiac arrhythmias are frequently diagnosed for the first
time during pregnancy. An important risk factor for
arrhythmias during pregnancy is the presence of organic
heart disease. In most cases, there is no previous history of
heart disease, and fortunately, arrhythmias that occur during
pregnancy are almost always benign and no treatment is
necessary. Sustained symptomatic arrhythmia, however,
requires treatment. The incidence of maternal arrhythmias
is 1.2 per 1000 pregnant women, of which 50% is
asymptomatic. The incidence increases in the third trimester.
During pregnancy, impressive haemodynamic,
neurocardiogenic and autonomic changes occur, and it is supposed
that the hyperdynamic circulation and the increased sensitivity
of adrenergic receptors play a provocative role [1, 3, 5, 9].
Symptoms are dyspnoea, palpitations, dizziness and (pre)
syncope [3, 5]. Most common arrhythmias in pregnancy are
AVNRT, AVRT, atrial tachycardia and atrial fibrillation
. Atrial flutter and atrial fibrillation are often
associated with hyperthyroidism.
Diagnosis can be hampered by the fact that symptoms of
shortness of breath, palpitations, dizziness and presyncope
frequently occur during normal pregnancy and increase
with gestational age . The presence of an arrhythmia is
likely to cause an increase or even a new onset of these
symptoms. As a result, the patient feels unwell. Clinical
assessment and ECG investigation are mandatory for an
accurate diagnosis of the arrhythmia . Echocardiography is
essential to exclude structural and functional heart disease.
Treatment of supraventricular tachycardias in pregnancy
is the same as for the non-pregnant population. Initial
treatment consists of stimulation of the vagus nerve by
means of carotid massage or Valsalva manoeuvres.
Firstline pharmacological treatment in case of failure of physical
procedures is with adenosine. Second choice is verapamil
but only after the first trimester of pregnancy and only in
acute circumstances [46, 9]. A low dose of -blockers can
be effective treatment for supraventricular extrasystoles or
tachycardia. When drugs fail or in case of life-threatening
symptoms as shock of pulmonary oedema, ECV is
indicated [26, 9, 10].
We searched the English literature from 1965 and found
44 case reports that describe the use of ECV during
pregnancy. There is considerable variation in specific
arrhythmias for which ECV is applied and required energy
varied from 50 to 400 J. Successful ECV after one or more
attempts is reported in 41 pregnant women (93.2%). ECV
in the non-pregnant population is reported to be successful
in 4292% [11, 12]. ECV success depends on the type and
length of the arrhythmia, cardioversion method, voltage and
type of energy. In three cases, a normal sinus rhythm is
acquired only after additional drug treatment . Two
maternal deaths are reported shortly after cardioversion
[16, 17]. In both cases, maternal death is attributed to the
severity of underlying heart disease and no relation with
cardioversion has been assumed.
There are limited data on perinatal outcome: 22 cases do
not report pregnancy outcome , and 13 cases report
an uncomplicated continuation of pregnancy resulting in
term vaginal deliveries [2, 3, 1315, 17, 2124]. Three
cases of a spontaneous preterm delivery are reported [8, 21,
25]. However, as in two cases where the delivery is 4 to
8 weeks after cardioversion, a direct relation with ECV is
unlikely [8, 21]. In two cases, foetal distress directly after
the cardioversion is noted, necessitating an immediate
caesarean section at 37 and 28 weeks of gestational age,
respectively [10, 26]. Both women are known with
underlying cardiac disease. Both neonates are born healthy.
The first case shows a notably hypertonic uterus, while the
current used was only 50 J. It was hypothesised that the
hypertonic uterus resulted in foetal bradycardia, which
could be a direct consequence of the cardioversion. Caution
should be applied since the hyperaemic uterine muscle as
well as the amnion fluid are excellent conductors of
electricity [10, 27]. However, the uterus is usually not
involved in the ECV trajectory, and only a minimum amount
of current reaches the uterus. It is supposed that there is little
effect on the foetal heart because of the high fibrillation
threshold of a small heart [1, 8, 10, 20, 28, 29]. Possible
explanations are placement of the pads over the apex beneath
the left breast and/or the relatively large third trimester uterus.
These cases underline the importance of carrying out the
procedure with facilities available for foetal monitoring and
emergency caesarean section .
Provided that a multidisciplinary approach, continuous
foetal heart rate monitoring and the possibility to perform
a caesarean section are applied, it can be concluded that
cardioversion is a safe and effective treatment for maternal
tachycardia in pregnancy.
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