Supraventricular tachycardia in pregnancy

K. Robins* and G. Lyons

Department of Obstetric Anaesthesia, St James’ University Hospital, Beckett Street, Leeds LS9 7TF, UK

*Corresponding author. E-mail: kayrobins14@hotmail.com

Accepted for publication: August 13, 2003


    Abstract
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 Abstract
 Introduction
 Case reports
 Discussion
 References
 
We present four cases of supraventricular tachycardia in pregnancy of varied aetiology. Risk factors for the development of supraventricular tachycardia and options for obstetric anaesthetic management, during pregnancy, labour, and at Caesarean section are discussed. We recommend the use of adenosine as first line therapy.

Br J Anaesth 2004; 92: 140–3

Keywords: anaesthesia, obstetric; complications, supraventricular tachycardia; heart, arrhythmia


    Introduction
 Top
 Abstract
 Introduction
 Case reports
 Discussion
 References
 
In women of reproductive age, the commonest arrhythmia is paroxysmal supraventricular tachycardia (SVT). SVT in pregnancy is defined as any tachyarrhythmia with a heart rate greater than 120 beats min–1,1 requiring atrial or atrioventricular junctional tissue for its initiation and maintenance. The term paroxysmal describes an arrhythmia that begins and ends abruptly.

Atrioventricular nodal re-entry and Wolf-Parkinson-White syndrome account for the majority of SVT in this population, with an incidence of 1.2 per 1000 people. Over half these patients are symptomatic.2 Symptoms of shortness of breath, palpitations, dizziness, presyncope, and syncope frequently occur during normal pregnancy. The presence of SVT is likely to cause an exacerbation or new onset of these symptoms and in particular, the patient feels unwell. The diagnosis is confirmed by ECG.

Pregnancy has been identified as a risk factor for paroxysmal SVT.3 An increase in mainly atrial or ventricular premature beats has been reported to occur.4 The increase in frequency of arrhythmias and in symptoms during pregnancy may be a result of the associated haemodynamic, hormonal, autonomic, and emotional changes. An expanded circulating volume may increase myocardial irritability and a faster sinus heart rate may alter tissue excitability, initiating a re-entry circuit. It has been postulated that oestrogens may heighten cardiac excitability as they have this effect on uterine muscle.5 6 Furthermore, oestrogens sensitize the myocardium to catecholamines by increasing the number of alpha-adrenergic receptors.7 Peripartum oxytocic, tocolytic and anaesthetic drugs have also been suggested as triggers for inducing SVT.

We present four cases of maternal SVT, three of whom underwent Caesarean section. Our case series allows the broad range of this disorder and its impact on management to be appreciated.


    Case reports
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 Abstract
 Introduction
 Case reports
 Discussion
 References
 
Case 1
A 29-yr-old physiotherapist, with a BMI of 29 (height 1.62 m and weight full term 76 kg), gave a history of paroxysmal SVT from the age of 14 yr. She experienced an increase in frequency of symptoms during her first pregnancy. Her pre-pregnant symptoms consisted of palpitations every 2 months, lasting around 5 min but occasionally up to 20 min, and terminated by breath holding. More serious symptoms such as syncope, dizziness, dyspnoea, or chest pains did not occur. Full investigations revealed no cause for these episodes, which were never demonstrated by electrocardiography.

Other past medical history included removal of a cystic haemangioma from her posterior fossa 5 yr before her pregnancy. This was a benign lesion, which was removed uneventfully, and MRI scans have shown no recurrence. Phaeochromocytoma may be associated with this tumour and catecholamine levels were investigated to exclude this as a cause for the arrhythmias.

During pregnancy, these episodes increased in frequency but remained the same, consisting of palpitations lasting 5 min and terminated by breath holding. Again no serious symptoms occurred. One of the longer episodes was documented on ECG at the accident and emergency department revealing SVT at a rate of 188 beats min–1.

At 40 weeks gestation, signs of proteinuric hypertension were noted at an antenatal clinic visit. Because of concerns that induction of labour may exacerbate her cardiac problems, it was decided to deliver her by Caesarean section later that day.

Caesarean section took place under a combined spinal epidural anaesthetic, uneventfully delivering a healthy male infant. Spinal related hypotension was prevented with an infusion of ephedrine 30 mg and phenylephrine 400 µg in 500 ml of normal saline, which was commenced immediately after the spinal injection. Syntocinon 5 u were administered slowly after delivery without problem. No further episodes of SVT occurred either intraoperatively or in the immediate postoperative period and she was discharged home 3 days later.

Case 2
A 27-yr-old with a BMI of 37 (height 1.65 m and weight 101 kg), presented in her fifth pregnancy with a history of three normal vaginal deliveries and one spontaneous miscarriage at 12 weeks. The pregnancy had been uneventful except for an episode of abdominal discomfort and ‘tightening’ at 26 weeks, which settled with simple analgesics. She was to undergo an elective Caesarean section at 39 weeks gestation for a breech presentation.

A combined spinal epidural was performed. An epidural test dose of lidocaine 1 mg kg–1 excluded intravascular placement of the catheter. Adequate anaesthesia was accomplished with the spinal and the operation commenced uneventfully.

Ephedrine 30 mg in 500 ml normal saline was given to prevent post spinal hypotension and a further bolus of 6 mg was administered. Shortly after the further bolus, a run of SVT was noted on the ECG and she complained of feeling ‘light-headed’. Carotid sinus massage was initiated which terminated the event and normal sinus rhythm was restored. Arterial pressure had decreased to 80/50 mm Hg and a bolus of phenylephrine 100 µg was administered.

Delivery of a healthy baby occurred shortly afterwards. A 5-u bolus of syntocinon was given without adverse effect. Boluses of alfentanil were required for pain after delivery, but otherwise the operation continued uneventfully.

There were no further episodes of SVT or symptoms postoperatively and she was unable to recall any previous symptoms either before or during pregnancy. She was discharged 3 days after delivery without cardiac follow-up.

Case 3
A 31-yr-old, with a BMI of 40 (height 1.58 m and weight, full term 100 kg), presented in her third pregnancy. She gave a history of pelvic inflammatory disease and had had two previous normal vaginal deliveries. During this pregnancy she had had intermittent hypertension without proteinuria, which settled spontaneously. At 28 weeks gestation she was admitted to hospital with possible spontaneous rupture of membranes. Her heart rate was noted to be 152 beats min–1 and irregular but she was asymptomatic. She was discharged home after ruptured membranes were excluded and an ultrasound scan showed no problems with the baby.

Spontaneous onset of labour occurred at 38 weeks and 2 days gestation. She complained of feeling dizzy and felt generally unwell. Her heart rate was noted to be 160 beats min–1 and a 12 lead ECG showed the presence of a SVT. Arterial pressure was stable and the SVT settled slowly. A Caesarean section was decided to be the best course of action because of uncertainty about maternal health and concern for the fetus.

A combined spinal epidural, using 2.5 ml heavy bupivacaine 0.5% and diamorphine 0.4 mg, was performed and a healthy baby was delivered uneventfully. Hypotension was treated initially with phenylephrine20 µg boluses and then with an infusion. Syntocinon 5 u were given after delivery and an infusion of 40 u in 500 ml normal saline commenced. This infusion was stopped because of worsening hypotension. Sinus rhythm was maintained throughout the perioperative period and the phenylephrine infusion was weaned postoperatively.

A cardiac echo was performed but no abnormalities were found.

On questioning, she gave a history of episodes of feeling generally unwell and occasional dizziness, which had commenced in this last pregnancy. The episodes occurred every few weeks and had settled spontaneously after 20 min to 1 h.

Case 4
A 33-yr-old with a BMI of 23.5 (height 1.79 m and weight 75 kg at term) and a history of mitral valve prolapse with typical paroxysmal SVT since the age of 13 yr, presented in her second pregnancy. She took verapamil as needed for her SVT episodes. Her first pregnancy had been uneventful; she had a spontaneous vaginal delivery with an epidural for pain relief.

At 37 weeks gestation during her second pregnancy she was admitted with a flu-like illness and feeling very unwell. Her heart rate was over 240 beats min–1, which reduced to 190 beats min–1 with carotid sinus massage. Arterial pressure remained stable and a 12 lead ECG revealed SVT. Adenosine 6 mg was given in divided doses with no effect. A further 6 mg bolus given rapidly reverted her back into sinus rhythm.

She was discharged and returned at 40 weeks in labour, which developed spontaneously. An epidural was sited uneventfully and she delivered vaginally. Syntometrine (ergometrine 0.5 µg and syntocinon 5 u) was administered post-delivery intramuscularly with no adverse effects.


    Discussion
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 Abstract
 Introduction
 Case reports
 Discussion
 References
 
Our incidence of symptomatic SVT during pregnancy is 1 in 8000, with four cases and 31 000 deliveries over 8 yr. This seems low compared with the quoted incidence,2 which may reflect a large number of asymptomatic patients. However, 1 in 8000 is a sufficiently common occurrence to present to most anaesthetists during their working lives.

Pregnancy may predispose to and exacerbate symptoms of paroxysmal SVT. Several case reports8 and a retrospective study of 60 patients with documented SVT3 showed pregnancy to be associated with both an increased risk, and an exacerbation of symptoms.

Clearly, both mother and fetus are at risk when SVT occurs during pregnancy. There are no maternal deaths as a result of arrhythmia reported in the Confidential Enquiries into Maternal Deaths (CEMD), but two deaths9 10 may have been associated with them. There is minimal information on morbidity associated with SVT in pregnancy. Many case histories suggest a favourable outcome for mother and baby after an uncomplicated SVT. However, emergency Caesarean section is often a consequence, increasing maternal risk and if pre-term, increasing fetal risk. This is demonstrated in our third case, when an SVT arose de-novo, giving concerns about a possible cardiac event having caused the arrhythmia, and, given the uncertainty, Caesarean section was felt the safest course of action for the fetus. A cardiac lesion may predispose to SVT as with our patient with mitral valve prolapse (Case 4). This was our most severe case of SVT requiring pharmacological treatment to terminate the event.

Drug use during labour or at Caesarean section may also precipitate SVT. Tocolytics11 and oxytocics have been implicated. Our patients received oxytocics uneventfully. Care with the use of syntocinon was highlighted in the most recent CEMD.12 Recommendations are that it should only be given as a bolus of 5 u maximum and administered slowly, or as an infusion, especially in the presence of cardiovascular compromise.13

Sympathomimetics are also potential initiators of tachycardias. Ephedrine, which is popular for treating hypotension associated with regional anaesthesia, is the most likely cause of our third case. A study into the use of a combination of phenylephrine and ephedrine to treat hypotension after spinal anaesthesia for Caesarean section has shown it to be more effective. The combination is associated with less tachycardia, less nausea and improved venous and arterial umbilical pH.14 The combination abolishes the increase in heart rate by ephedrine and the decrease in heart rate by phenylephrine, and is a good choice particularly in susceptible individuals.

The reduced atrial filling caused by regional anaesthesia has been implicated in increasing arrhythmogenicity.15 A fluid pre-load not only helps to prevent a reduction in atrial filling, but also reduces sympathomimetic requirements which may trigger SVT.16 Phenylephrine may be a useful drug if hypotension occurs after regional anaesthesia; it increases vagal tone by indirectly stimulating baroreceptor reflexes and therefore reduces SVT occurrence. The use of phenylephrine to terminate an SVT occurring at induction of anaesthesia, in a patient with Wolf-Parkinson-White syndrome has been described.17 Avoidance of aortocaval compression by using a left tilt is also important to maintain atrial filling.

Treatment of SVT in pregnancy may also affect the fetus. For this reason, pharmacological treatment is best reserved for those with haemodynamic changes, severe symptoms or sustained arrhythmias. Non-pharmacological treatment including vagal manoeuvres such as carotid massage, Valsalva manoeuvre and facial ice immersion are well tolerated and aid in diagnosis.

Adenosine, a naturally occurring purine nucleotide, transiently depresses sinus node activity and slows atrioventricular conduction, and is effective in terminating SVT. It is rapidly metabolized with an elimination half-life of less than 10 s, making it ideally suitable for use in pregnancy. Numerous case reports,18 and a retrospective study,19 suggest that adenosine is safe and effective. One of our cases was treated with adenosine that only became effective after a second more rapid bolus was administered, highlighting the need to give a 6–12 mg dose rapidly. Although an increase in intravascular volume occurs in pregnancy, the concentration of adenosine deaminase, the enzyme responsible for degradation, declines, and so doses of 6–12 mg should be adequate. Although there are no serious complications reported with the use of adenosine during pregnancy, one report of a transient fetal bradycardia20 suggests that placental transfer can occur. Monitoring of fetal heart rate during administration of adenosine is advised.

If adenosine fails, other antiarrhythmics may be indicated and the risk of their use should be weighed against the risk of continuing SVT. Beta-blockers have been used extensively in pregnancy, to treat maternal hypertension and cardiac problems, and are generally well tolerated.21 They are the agents of choice in Wolf-Parkinson-White syndrome, where AV nodal blocking drugs may lead to acceleration of conduction through the accessory pathway and the arrhythmia being sustained. Verapamil, a calcium channel-blocking agent, is as effective as adenosine in converting an SVT to sinus rhythm.22 Peripheral vasodilation and negative inotropy are unwanted side-effects. There are reports of its safe use in pregnancy for treatment of SVT.23 Digoxin has been used in all stages of gestation for maternal and fetal indications without causing harm.24 Amiodarone is perhaps best avoided because of its potential teratogenic effects and reports of fetal toxicity, but again there are reports of its safe use during pregnancy.25

Synchronized electrical cardioversion may become necessary for SVT resistant to pharmacological therapy, particularly if hypotension develops. Direct current electrical shock has been used at all stages in pregnancy without significant complication.26 The amount of current reaching the fetus is thought to be negligible. However, transient fetal dysrhythmia has been described,27 and monitoring of fetal heart rate during maternal cardioversion is advisable. Implantable devices have been successfully used during pregnancy for malignant tachyarrhythmias.28 Both temporary and permanent endocardial pacing has been used in pregnancy, although mainly in the treatment of bradyarrhythmias.29

To summarize, SVT occurring during pregnancy, labour or at Caesarean section is not uncommon. Avoidance of certain drugs and treatment of any precipitating factors, in particular hypotension caused by regional anaesthesia using a fluid preload and phenylephrine, are appropriate. Adeno sine is the first line treatment. Our cases highlight the necessity of keeping antiarrhythmic drugs readily available on the labour ward.


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 Abstract
 Introduction
 Case reports
 Discussion
 References
 
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