Unexpected outcome (positive or negative) including adverse drug reactions
BMJ Case Rep: first published as 10.1136/bcr-2018-226747 on 13 February 2019. Downloaded from http://casereports.bmj.com/ on 20 February 2019 by guest. Protected by copyright.
1
Cardiology department, St
Vincent’s Hospital, Darlinghurst,
New South Wales, Australia
2
Department of Obstetrics
and Gynaecology, Centenary
Hospital for Women and
Children, Canberra Hospital,
Garran, Australian Capital
Territory, Australia
Correspondence to
Dr Samuel Birch,
​samuel.​birch1@m
​ y.​nd.​edu.​au
Accepted 28 January 2019
© BMJ Publishing Group
Limited 2019. No commercial
re-use. See rights and
permissions. Published by BMJ.
To cite: Birch S, Lu C. BMJ
Case Rep 2019;12:e226747.
doi:10.1136/bcr-2018-
226747
Case report
Ergometrine-induced atrial fibrillation at
caesarean section
Samuel Birch,1 Corrine Lu2
Summary
A 36-year-old woman with a history of one previous
caesarean section presented to the birthing suite
of a regional hospital with spontaneous rupture
of membranes at 39+2/40 weeks. Syntocinon was
administered to initiate uterine contractions in the
absence of labour, as the patient desired vaginal birth.
A caesarean section was subsequently indicated and
ergometrine was administered for uterine atony. The
patient immediately developed atrial fibrillation (AF). AF
is the most common sustained arrhythmia in the general
population, but is rare in the obstetric population.
AF occurring in an intrapartum setting following the
administration of syntocinon and ergometrine, is not
documented in the literature. We suggest the initiation
of paroxysmal AF was precipitated by an abrupt
alteration in autonomic tone caused by administration of
syntocinon followed by ergometrine.
Background
We present the first case in the literature of atrial
fibrillation (AF) occurring in the intrapartum
setting with the administration of syntocinon and
ergometrine. This case is valuable in understanding
the rare complications of use of syntocinon and
ergometrine.
AF is the most common sustained arrhythmia
worldwide with an estimated prevalence of 0.57%
in men and 0.37% in women.1 It is more common
in developed nations with an estimated prevalence
of 3.29% in the UK in 2016.2 3 It primarily affects
those over the age of 55 years.3 4 The prevalence
of AF in this age group in Australia is 5.35%.4 It is
rare in the obstetric population.5 There is a paucity
of information in the literature about AF in preg-
nancy.5 The incidence of arrhythmias in pregnancy
is estimated at 1.2 for every 1000 pregnancies,
with around half of these episodes of arrhythmias
being asymptomatic.6 In a study conducted in the
USA, arrhythmias occurred in 68 of 100 000 preg-
nancy-related hospitalisations.7 AF was the most
common arrhythmia in this study, constituting 21
of the 68 presentations of arrhythmia.7 There is a
substantial health and economic burden associated
with AF, particularly in regard to the associated
increased risk of stroke.4 In the elderly popula-
tion, AF is often related to co-morbidities such
as hypertension, diabetes, heart failure, previous
myocardial infarction, atrial dilatation or mitral
valve disease.3 8 9 By contrast, in the obstetric popu-
lation, the mechanisms underlying AF are reported
Birch S, Lu C. BMJ Case Rep 2019;12:e226747. doi:10.1136/bcr-2018-226747
to include drug toxicity, hyperthyroidism, pulmo-
nary embolism, structural heart defects, re-entrant
pathways and electrolyte derangements.5
Case presentation
A 36-year-old woman gravida 2, para 1 presented to
the birthing suite of a secondary obstetric hospital
at 39+2/40 weeks with spontaneous rupture of
membranes. She had an obstetric history of one
previous pregnancy with successful delivery by
elective caesarean birth 12 years prior, which was
indicated for breech presentation. She was planning
a vaginal birth after caesarean section. Her current
pregnancy was with a new partner, was planned,
was secondary to spontaneous conception, and
had been uncomplicated. The patient had no other
significant medical history and no known medica-
tion allergies. Her body mass index was recorded as
37. Appropriate antenatal care for intended vaginal
birth was provided. Ultrasounds performed during
the pregnancy demonstrated normal morphology
and appropriate growth of the baby.
The patient was admitted for observation in
preparation for a spontaneous labour. The cervix
was closed on speculum examination and minimal
clear liquor continued to drain at 18 hours after
admission. Antibiotic prophylaxis was commenced.
At around 24 hours after membranes had ruptured,
a trial of induction of labour with a syntocinon
infusion was commenced. At 2  hours after the
commencement of syntocinon, an emergency
caesarean section was performed because of fetal
distress on fetal heart monitoring. There was meco-
nium-stained liquor and the cervix had not dilated.
Regional anaesthesia was delivered as a spinal
block with bupivacaine and fentanyl. Cefazolin
2 g IV was administered as antibiotic prophylaxis.
The baby was delivered in good condition. On
second layer closure of the uterus, in the presence
of ongoing uterine atony, treatment to increase
uterine tone was requested. Syntocinon five units
intravenously was already given in divided doses,
and a 40 IU syntoncinon infusion was in progress.
Therefore, 250 IU of ergometrine was adminis-
tered intravenously. Although the usual protocol
of this hospital for ergometrine administration is
equal doses (250 IU) administered intramuscularly
and intravenously, the anaesthetic team decided to
administer only the intravenous dose. The intra-
venous dose was also administered at a rate that
was faster than that recommended by the protocol
of this hospital. Within minutes of this dose, the
patient complained of feeling hot, nauseated and a
1
 Unexpected outcome (positive or negative) including adverse drug reactions

BMJ Case Rep: first published as 10.1136/bcr-2018-226747 on 13 February 2019. Downloaded from http://casereports.bmj.com/ on 20 February 2019 by guest. Protected by copyright.
Figure 1  Anaesthetic observation print-out demonstrating the onset of the atrial fibrillation and related haemodynamics.

sense of high pressure inside her head and body. The nausea was
treated with ondansetron. The patient was noted to have devel-
oped a tachycardia (figure 1); 12-lead ECG confirmed rapid AF
(figure 2). Shortly before the patient developed rapid AF, her
blood pressure had fallen from a peak of 160/100 mm Hg to
120/70 mm  Hg.
The caesarean section was completed. Uterine tone improved
following the administration of the ergometrine. The operative
blood loss was recorded as 450 mL. The patient remained in
rapid AF and was transferred to recovery for monitoring and
further management.
In recovery, two doses of 50  mg esmolol were adminis-
tered intravenously, but no improvement was noted in the
cardiac rhythm. The decision to administer esmolol was made by
the anaesthetic team in an effort to provide symptomatic relief to
2 Birch S, Lu C. BMJ Case Rep 2019;12:e226747. doi:10.1136/bcr-2018-226747
the patient through the use of a rapid onset rate-control agent.
Decisions regarding rhythm control agents were left for the
cardiology team. After administration of esmolol, the patient’s
blood pressure transiently fell to 95/50 mm Hg. Intravenous
fluids were the only treatment administered for the patient’s
hypotension.
Consultation was sought from the medical registrar for cardi-
ology on duty. The heart rate remained 140–170 bpm during
this time.
The cardiology consultant and registrar implemented conser-
vative measures initially. The patient was kept in recovery with
cardiac monitoring in situ. Electrolyte levels were checked
and found to be normal. The 40 IU syntocinon infusion was
completed as per protocol and a prophylactic magnesium dose
was given intravenously. The heart rhythm remained in rapid AF
 Unexpected outcome (positive or negative) including adverse drug reactions

BMJ Case Rep: first published as 10.1136/bcr-2018-226747 on 13 February 2019. Downloaded from http://casereports.bmj.com/ on 20 February 2019 by guest. Protected by copyright.
Figure 2  12-lead ECG shortly after onset of atrial fibrillation during caesarean section.

with a rate >140 bpm. The patient was then transferred to the
coronary care unit.
A bedside cardiac echocardiogram was normal. The decision
was made for treatment with flecainide.
Investigations
Common causes for AF in the intrapartum setting were excluded.
There was no evidence of Wolff-Parkinson-White syndrome on
the ECG and no evidence of thyroid dysfunction on blood tests.
Imaging investigations to exclude pulmonary embolism were not
performed because the patient had normal oxygen saturation
throughout the admission, had no chest pain and had a nega-
tive troponin level. The medications used in regional anaesthesia
are unlikely to have caused paroxysmal AF. The patient had an
adequate potassium level (4.1 mmol/L) at the time of labour and
a normal, but suboptimal, magnesium level (0.72 mmol/L).
Treatment
A total of four doses of flecainide were administered and the
patient reverted to sinus rhythm at 23 hours after caesarean
section, during discussion and planning for Direct Current
cardioversion (figure 3).
Outcome and follow-up
The remainder of her stay was uneventful. Her treatment with
flecainide continued on discharge and was maintained for 6
weeks after discharge.

Figure 3  12-lead ECG post reversion at 23 hours after onset.

Birch S, Lu C. BMJ Case Rep 2019;12:e226747. doi:10.1136/bcr-2018-226747 3
Unexpected outcome (positive or negative) including adverse drug reactions
Patient’s perspective
On the 10th of September 2017 I had been in the labour
ward for nearly 30 hours with tightenings and half ruptured
membranes with minimal progression to labour. The induction
process was started, but unfortunately due to foetal distress
I was rushed to theatres for an emergency caesarean. I was
trialling a vaginal birth after caesarean (VBAC) and was hopeful
for a vaginal delivery so was disappointed but accepting of the
need for the intervention. It seemed like it took a very short
period of time before I heard the cry of a baby and someone held
my daughter up in front of me for a brief second before she was
whisked away to be seen by the paediatric team.
At this point I heard the Doctor ask for a medication and
the anaesthetist stating I may feel a bit horrible after being
administered this. Shortly after I felt extremely nauseous and
started vomiting, I also experienced a headache and a heavy
ache in my left arm that went to my chest. I was taken to
recovery where I was told my heart rate was very high, at that
point I looked at the monitor and it was jumping between
140bpm–175bpm. Coming from a nursing background I kept
looking at the monitor to interpret the readings. The medical
team relayed to me that my heart was in atrial fibrillation (AF)
and I would require a cardiac consult but they were hopeful
it would revert reasonably quickly as AF usually does. Many
interventions were tried but AF remained. I started to feel
extremely nauseous and wasn’t tired but found it extremely
difficult to keep my eyes open. I could feel my heart beat in my
throat and could barely gather energy to speak. My husband said
he came to see me in recovery at one point and said I was so
pale that he thought I was dead. Many different Doctors came
and consulted about what the plan should be. After 5 hours in
recovery I was transferred to the coronary care unit. At this point
it had been 6 hours since delivery and I had seen my baby for a
brief minute but had not held her.
The AF continued while I was in coronary care and did
not revert until the following day, 23 hours post caesarean,
thankfully before I would have had to have a cardioversion. I
spent 17 hours without seeing my baby but remarkably when
the midwife bought her to me, 23 hours post op, I started to
breastfeed her and this was the precise moment my heart
reverted back to sinus rhythm. I often think, and question, if it
was a coincidence that my heart went into AF when my baby
was taken from me and then reverted from AF when I was able
to hold my baby again.
Discussion
Arrhythmias are the most common cardiac condition in preg-
nancy. Although AF is rare in pregnancy, it is the most common
arrhythmia in pregnancy.5 7 10 Pregnancy constitutes a cardiovas-
cular stressor.5 10 Physiological adaptations of pregnancy may
promote arrhythmias by causing increased myocardial stretch,
increased catecholamine release, electrical remodelling and a
higher frequency of atrial and ventricular premature contrac-
tions.10 AF in pregnancy often reverts without requiring specific
treatment.5 In the available case reports, episodes of lone AF in
pregnancy recovered without any long-term complications for
the patients or their infants.5
AF can be precipitated when one or more triggers occur in the
presence of a susceptible substrate.3 These triggers may include
premature atrial contractions (which are more frequent during
pregnancy),3 as well as other atrial arrhythmias. Rapid firing in
4 Birch S, Lu C. BMJ Case Rep 2019;12:e226747. doi:10.1136/bcr-2018-226747
BMJ Case Rep: first published as 10.1136/bcr-2018-226747 on 13 February 2019. Downloaded from http://casereports.bmj.com/ on 20 February 2019 by guest. Protected by copyright.
Learning points
►► Atrial fibrillation (AF) is uncommon in the obstetric
population, but can be caused by drug toxicity,
hyperthyroidism, pulmonary embolism, structural heart
defects, re-entrant pathways and electrolyte derangements.
►► Although ventricular arrhythmias have been reported in the
setting of administration of syntocinon and ergometrine, we
present the first case in the literature of AF occurring in the
intrapartum setting with the administration of syntocinon
and ergometrine.
►► Both ergometrine and oxytocin can cause abrupt changes in
heart rate, vascular tone and autonomic tone.
►► An abrupt alteration of autonomic tone may constitute a
trigger for AF in the obstetric population and syntocinon
administration followed by administration of ergometrine
may be a cause an abrupt alteration of autonomic tone.
►► Ergometrine should be administered via the intramuscular
route to reduce the risk of arrhythmias and should potentially
be avoided in the peripartum setting in future pregnancies
in our patient (a change in the hospital protocol from
equal doses of intravenous and intramuscular ergometrine
to a dose of only intramuscular ergometrine should be
considered).
the pulmonary veins can also trigger AF.10 Once AF starts, it
may be sustained because of focal electrical activity, re-entrant
circuits, or a combination or both.3 11 12
The autonomic nervous system is also important in AF.9 The
occurrence of paroxysmal AF frequently occurs after an increase
in sympathetic tone followed by increased vagal tone.9 Moni-
toring of stellate ganglion nerve activity in animal models indi-
cates that most paroxysmal atrial tachycardia and paroxysmal AF
occur after a combination of sympathetic and vagal discharges.13
Although some arrhythmias have been reported in the setting
of oxytocin or ergometrine administration, AF has not been
previously reported in this setting, to our knowledge. Tachy-
cardia, as a reflex phenomenon precipitated by oxyctocin or
syntocinon, is well known.14 15 Arrhythmias are also a recognised
complication of ergometrine.16 17 A case of ventricular tachy-
cardia during caesarean section precipitated by ergometrine
has previously been described.18 Oxytocin has been reported to
have an antiarrhythmic effect,19 20 but it has also been reported
to prolong the QTc (the corrected QT interval).21 Two cases of
ventricular tachycardia precipitated by oxytocin, in the setting of
known long-QT syndrome, have been described.22
Oxytocin and its synthetic form, syntocinon, act on the
oxytocin receptor.23 The use of syntocinon in the setting of both
induction of labour and the management of uterine tone is an
international standard of practice.24 Oxytocin is thought to be
released when circulating blood volume is high and it promotes
vasodilation, increases secretion of atrial natriuretic peptide,
and is antiarrhythmic.14 15 Oxytocin suppresses premature
ventricular contractions, reduces rates of ventricular arrhyth-
mias and modulates atrial mechanical and electrical activity
in animal models.14 19 Antihypertensive, negatively inotropic
and negatively chronotropic effects of oxytocin have also been
demonstrated.14 15While oxytocin can act to prolong the QTc
in humans, it does not increase action potential duration in
Purkinje fibres in an animal model, nor does it prolong the QTc
in human ventricular myocytes.18 25 These findings suggest that
the QTc prolonging effect of oxytocin in humans is indirect. This
 Unexpected outcome (positive or negative) including adverse drug reactions
indirect effect of oxytocin on the QTc may be a consequence of
the rapid vascular tone changes and sympatho-vagal changes it
induces during labour.21 25
Both oxytocin and ergometrine can have strong autonomic
effects.14 15 26 27 Vasodilation secondary to oxytocin causes a
paradoxical increase in sympathetic tone and reflex tachycardia
in vivo, despite the negative chronotropic effect of oxytocin in
vitro.14 15 Ergometrine can cause bradycardia, increased vagal
tone, or vasospasm.26 27 Vasospasm caused by ergometrine can
manifest as coronary vasospasm with ST segment changes.18 28
In the peripartum setting, early research demonstrated a strong
vagal effect of ergometrine administered via the intravenous
route, where 12 of 100 patients developed sinoatrial node
block.17 Sinoatrial node block can predispose the patient to
escape rhythms, such as AF or junctional rhythm. Other cardiac
side effects of ergometrine include atrioventricular node block,
premature ventricular contractions and ventricular tachy-
cardia.18 26 27
In our patient’s case, the episode of paroxysmal AF was
temporally related to ergometrine administration after synto-
cinon administration. Although there does not appear to be
information in the literature about the arrhythmic potential
of ergometrine depending on the route of administration, the
rapid administration of intravenous ergometrine may have been
contributory to the onset of AF in our patient. Common causes
for AF in the intrapartum setting were excluded. While oxytocin
may cause QTc prolongation, our patient’s QTc was only mildly
deranged (482 msec) on the first ECG obtained during the
admission (shortly after initiation of paroxysmal AF) and was
normal after reversion to sinus rhythm (445 msec). Ergometrine
may cause myocardial ischaemia, but the patient’s ECGs did
not demonstrate any ST changes and the serum high sensitivity
troponin I level was normal.
We suggest that the initiation of paroxysmal AF in this patient
was precipitated by an abrupt alteration in autonomic tone caused
by syntocinon administration followed by rapid administration
of intravenous ergometrine. Syntocinon may have promoted a
drop in vascular tone (as evidenced by a drop in blood pressure)
followed by a sympathetic discharge, possibly via a baroreceptor
and stretch receptor reflex. The subsequent administration of
ergometrine potentially provided a trigger for increased vagal
output. This suggested mechanism concurs with the mechanism
suggested in the literature for other arrhythmias in the setting of
oxytocin and ergometrine administration.18 21 22 25
Contributors  SB primarily contributed to the discussion, referencing and
formatting of the article. CL primarily contributed to the case details and the patient
perspective of the article.
Funding  The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-for-profit sectors.
Competing interests  None declared.
Patient consent  Obtained.
Provenance and peer review  Not commissioned; externally peer reviewed.
Birch S, Lu C. BMJ Case Rep 2019;12:e226747. doi:10.1136/bcr-2018-226747
BMJ Case Rep: first published as 10.1136/bcr-2018-226747 on 13 February 2019. Downloaded from http://casereports.bmj.com/ on 20 February 2019 by guest. Protected by copyright.
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5
Unexpected outcome (positive or negative) including adverse drug reactions

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6 Birch S, Lu C. BMJ Case Rep 2019;12:e226747. doi:10.1136/bcr-2018-226747