Direct current cardioversion during pregnancy should be performed with facilities available for fetal monitoring and emergency caesarean section
*Correspondence: Dr E. J. Barnes, 169C Woodstock Road, Oxford, OX2 7NA, UK.
Direct current cardioversion is reported as being a safe procedure during pregnancy1,2. However, the importance of carrying out fetal monitoring with an obstetrician at hand is illustrated by a woman treated in the third trimester of pregnancy, where direct current cardioversion resulted in an emergency caesarean section.
A 24 year old woman attended the casualty department complaining of palpitations and heavy central chest pain that had begun 1 hour earlier. She was 28 weeks pregnant.
At nine months of age she had received a Mustard operation for transposition of the great arteries (after intra-atrial repair, systemic venous blood is routed to the left ventricle and pulmonary artery. Pulmonary venous blood reaches the systemic circulation via the right ventricle). During childhood she had recurrent episodes of supraventricular tachycardia, which had responded to carotid sinus massage. A pacemaker was inserted at 13 years of age to treat nocturnal bradycardia. At 22 years of age, she delivered her first child spontaneously at term without complications.
There had been no problems previously during her current pregnancy. A fetal cardiac ultrasound scan at 25 weeks of gestation was normal. She was not taking any medication.
On examination she was centrally cyanosed. Her pulse rate was 200 beats per minute and her blood pressure was 100/50 mmHg. Her heart sounds were normal and she had no signs of cardiac failure. A 12-lead electrocardiogram confirmed a supraventricular tachycardia, with lateral ST depression and T wave inversion. A cardiogram showed a fetal heart rate of 160 beats per minute, with no abnormal features.
Carotid sinus massage and the Valsalva manoeuvre failed to terminate the tachycardia. She was treated with intravenous adenosine 3, 6 and 12 mg. With a dose of 12 mg adenosine, she converted to sinus rhythm and the blood pressure remained at 100/50 mmHg. Within minutes, the supraventricular tachycardia returned and she was treated with verapamil 5 mg intravenously. Again, sinus rhythm was restored. The fetal heart rate was monitored throughout. The woman was admitted to the ward for observation.
Two hours later, the supraventricular tachycardia recurred, the heart rate being 185 beats per minute. Adenosine and verapamil failed to terminate the tachycardia. Her blood pressure was 110/60 mmHg. The woman was turned to the left lateral position to maximise her venous return. She was treated with 240 mg sotalol and a loading dose of 500 μg of digoxin orally in an attempt to control the ventricular rate. Thirty minutes later, she developed increasing chest pain. Her blood pressure decreased to 60/40 mmHg, with a persisting heart rate of 200 beats per minute. She was transferred urgently to the operating theatre for direct current cardioversion under general anaesthesia.
The fetal heart rate was monitored constantly. A synchronised shock of 50 J was delivered and the maternal heart rhythm was converted immediately to sinus rhythm, at a rate of 90 beats per minute. Her blood pressure increased to 110/80 mmHg.
Before the cardioversion, the fetal heart rate was 130 beats per minute. Immediately after cardioversion, the fetal heart rate decreased to 80 beats per minute. The bradycardia was sustained over the following 5 minutes, and the fetal heart rate then decreased further. The heart also was noted to be dyskinetic. Emergency caesarean section was performed. At caesarean section the uterus was tightly contracted.
A female infant was delivered. The baby gave a weak cry at delivery but had irregular, weak respiration. She was intubated and ventilated with 1 PPV for approximately 1 minute. She was bradycardic at delivery but after 1 minute the heart rate was 10 bpm. Apgar scores were 7 and at 5 minutes were 10. She was transferred to the neonatal unit.
Following caesarean section, the mother remained in sinus rhythm, and her infant made a full recovery.
Paroxysmal supraventricular tachycardia is relatively common in the third trimester and is thought to be related to the haemodynamic changes occurring during this time1. Supraventricular tachycardia in a patient with an ectopic focus or with underlying organic heart disease may be particularly resistant to treatment.
Current evidence suggests that if a maternal arrhythmia is serious and refractory to other treatments, then synchronised direct current cardioversion is the treatment of choice, and is safe in pregnancy1,2. However, the number of reported cases of direct current cardioversion in pregnancy is small. In 1981, Ueland et al.2 summarised 15 previously reported cases. Thirteen women were successfully treated by cardioversion with energies from 50 to 300 J. In one case, there was loss of fetal heart rate variability in a 37-week fetus for 36 minutes, resulting in an emergency caesarean section. There was one maternal and fetal death, which occurred shortly after an attempted cardioversion in a moribund patient suffering from atrial fibrillation and congestive heart failure. The fetal death was thought to be unrelated to the direct current cardioversion.
Since 1981, we have found a further four case reports where direct current cardioversion was used without detrimental effects on the fetus3–6, and a recent article from Mexico reports 20 cases of direct current cardioversion during pregnancy7. All these pregnancies progressed to term.
Should we attribute the fetal distress in this case directly to the direct current cardioversion? Electric shocks from various household appliances are associated with a fetal mortality as high as 75%8. Usually, in these cases, electricity is conducted from hand to foot and includes the uterus directly in its path. Amniotic fluid and uterine muscle are excellent conductors of electricity. Direct current cardioversion would not usually include the uterus in its path but it is possible that it may do so, particularly where the uterus is very large in the third trimester, or when the cardioversion pads are placed over the apex beneath the left breast and extending below the ribs. The tightly contracted uterus found at caesarean section in this case supports this theory and may have led to fetal distress with bradycardia.
Might the contracted uterus and fetal distress be attributed to the sotalol? Beta-blockers may have an oxytocic action9, which is dose dependent, and the sotalol may have caused a sustained uterine contraction coincidental with the direct current cardioversion. Beta-blockers cross the placenta and may cause fetal bradycardia and neonatal respiratory depression10; however, these effects are usually sustained, as the half-life of beta-blockers in the neonate is prolonged11. In this case the fetal bradycardia and respiratory depression resolved within minutes of delivery. It seems unlikely that the sotalol could account for these effects.
Might the digoxin be responsible for the sustained uterine contraction? Weaver and Pearson12 noticed that spontaneous labour occurred one week earlier and lasted half as long in 22 women taking digoxin, compared with 64 women who were not, concluding that digoxin was responsible for uterine stimulation. However, Norris13 attempted to induce labour by administering digoxin, 0.5 mg per day for two weeks, to 128 women in a placebo-controlled, double-blind trial. He found no difference in the time of onset or duration of labour. It seems highly unlikely then that one 500-μg dose of digoxin in the case we report would account for sustained uterine contraction and subsequent fetal distress.
We conclude that direct current cardioversion led directly to a sustained uterine contraction, causing fetal distress, necessitating emergency caesarean section. This case demonstrates the importance of carrying out the procedure with facilities available for fetal monitoring and emergency caesarean section.