Oxytocin during Caesarean section

I read with interest the paper (Mora et al. Anaesthesia 2001; 56: 1051–8) investigating the incidence of myocardial ischaemia in normal patients undergoing elective Caesarean section. The authors interrogated a number of possible triggers (hypotension, tachycardia and ephedrine) without establishing a connection, yet did not comment on the relationship (if any) between the ECG changes and the administration of intravenous oxytocin, a drug that is not only known to be associated with arrhythmias and tachycardias, but is actually used in come cardiac catheter labs to 'unmask' variant angina! The recommended dose in the British National Formulary is 5␣IU given after Caesarean delivery; the dose given to all patients in the study was double this, with 'more available at the request of the surgeon'. From personal experience, I have seen many healthy young women respond with a tachycardia and, on occasion, ST segment depression. In one fit 19-year-old, after intravenous oxytocin was given slowly as recommended, there was severe ST segment depression on the ECG, responding partially to glyceryl trinitrate and 100% O2, but with segmental 'stunning' on echocardiography later that day and a rise in troponin. Thankfully, she made an eventual full recovery. That was the last time I used an intravenous bolus of oxytocin and now use only intravenous infusions. There has been no complaint from the obstetricians, nor have I seen the same cardiac repercussions! I would respectfully suggest that at least some of the ECG changes and ischaemia may have been due to a simple factor – the over-generous use of intravenous oxytocin. Many thanks for the opportunity to reply to the issues raised by Dr Spence. The dose of oxytocin used during our study was not only the same as that routinely used in our institution, but also mirrored the dose used in the study performed by Trotter et al. – with whom we were making comparisons [1]. Although further doses of oxytocin were available, in the form of a slow intravenous infusion, for the treatment of persistent uterine atony, no patient in the study required it. In another comparison study, Palmer et al. used oxytocin by infusion, in keeping with the practice suggested by Dr Spence, and still documented a 47.3% incidence of ECG abnormalities in their patients [2]. Unfortunately, Mathew et al. and Zakowski et al. did not comment on oxytocin use in their studies [3, 4]. In the discussion section of our paper, we commented on the possible causes of the ECG changes noted. We excluded triggers such as hypotension, tachycardia and ephedrine use. Sudden hypervolaemia in the presence of sympathetic block has been noted to lead to increased myocardial workload and oxygen demand [5]. The resultant increased left ventricular end-diastolic pressure arising from maternal auto transfusion following umbilical cord clamping coupled with the high incidence of venous air embolism may have been responsible for the peroperative ECG changes [6, 7]. We noted that oxytocic agents could also have played a role. Whatever the aetiology of peroperative ECG changes, oxytocin is unlikely to have been responsible for the significant incidence of postoperative ECG changes noted in our study. We respectfully suggest that although oxytocin may have a role in the peroperative electrocardiographic changes noted during Caesarean section, it is likely to be one of many co-existing variables. ECG changes have been documented whether it is given as a slow bolus dose or as an infusion. It appears that the haemodynamic stresses and complications of Caesarean section can produce a situation where myocardial oxygen demands outstrip supply leading to ischaemia in a minority of cases, albeit without permanent damage. Again, further to our findings, we would urge caution and careful monitoring in patients with pre-existing cardiac disease undergoing Caesarean section. C. Moran J. GardinerRotunda Hospital, Dublin, Ireland