Oxytocin-Induced Myocardial Ischemia in a Parturient with Hypertrophic Obstructive Cardiomyopathy

Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant genetic disease with an incidence of 0.1–0.5% in pregnant women.[1] It is characterized by an asymmetric hypertrophy of the septum with mitral systolic anterior motion leading to dynamic left ventricular outflow tract (LVOT) obstruction. Even in asymptomatic patient heart failure is a possibility due to dynamic LVOT obstruction aggravated by surgical stress, increased plasma volume expansion due to pregnancy, and associated anesthetic factors. We would like to report an oxytocin-induced myocardial ischemia (MI) in a pregnant woman diagnosed with HOCM who was posted for emergency Cesarean Section (CS). Her pregnancy was uneventful and incidentally detected to have HOCM with LVOT gradient of 60 mmHg along with moderate mitral regurgitation. She was not on any cardiac medications and had no limitations in ordinary physical activity (NYHA grade I). She was in spontaneous labor and planned for emergency CS due to an inadequate pelvis. Surgical anesthesia was successfully initiated with epidural local anesthetic and she was hemodynamically stable with phenylephrine infusion (20 µg/min). After delivery, oxytocin infusion was started at the rate of 2 IU/hour (0.03 IU/min) and increased to 4 IU/hour due to uterine atony. ST depression was noted in lead II and V5 within a few minutes of the commencement of oxytocin and the patient became agitated and restless with pulmonary edema and severe hypotension resistant to phenylephrine. The airway was secured, noradrenaline infusion (5 µg/min) was initiated for the management of hypotension, and furosemide was administered for pulmonary edema. Since oxytocin-induced MI is the suspected cause of the hemodynamic instability, the oxytocin infusion was discontinued and further uterine tone was maintained with rectal misoprostol. She was shifted to ICU and serial monitoring of cardiac troponin was done. She was hemodynamically stable and extubated after 12 hours and discharged after 5 days. Autotransfusion induced cardiac failure could have also caused such changes; yet the occurrence of symptoms, such as the hemodynamic instability associated with ST changes occurred after initiation of oxytocin. Hence, we consider oxytocin could be the triggering agent, and the hemodynamic instability is due to oxytocin-induced MI. Though there are cases of oxytocin-induced MI in literature, such occurrence in pregnancy associated with HOCM is limited. Oxytocin-induced MI has been reported in healthy women who were administered high doses of up to 10 IU of oxytocin.[2] But in actual clinical practice the dose does not exceed more than 3 IU for bolus administration. In a study using incremental bolus doses of 0.05–0.5 IU oxytocin in cardiac disease patients for CS, no major adverse events were observed except for the occurrence of dyspnea after 0.1 IU of oxytocin in a case of aortic stenosis.[3] Oxytocin is preferably administered as an infusion, especially in patients with cardiac disease, to avoid systemic adverse effects like hypotension and tachycardia. Oxytocin-induced MI is primarily due to the hypotension and tachycardia caused by systemic vasodilation, yet another mechanism postulated is oxytocin-induced coronary artery spasm.[4] In the case of HOCM, where there is diastolic dysfunction and already compromised coronary perfusion, severe myocardial injury occurs, even with minimal doses of oxytocin. We would like to highlight that even in HOCM patients with well-preserved myocardial function (NYHA I), trivial doses of oxytocin can induce MI and cardiac failure. Though the occurrence of MI in HOCM patients is multifactorial, like surgical stress, hypotension, autotransfusion, and uterotonics; strict vigilance, anticipation, and monitoring are required in all these high-risk patients. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.