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Pulmonary vasodilators in the anesthetic management of a parturient with severe pulmonary hypertension for forceps-assisted vaginal delivery
Abstract Number: T-73
Abstract Type: Case Report/Case Series
Pulmonary hypertension (PHTN) in pregnancy is associated with significant maternal morbidity and mortality. While no consensus statement regarding mode of delivery exists, cesarean section under general anesthesia (GA) is often performed to avoid cardiopulmonary failure during vaginal delivery, but this carries significant maternal risk(1). Vaginal delivery has been reported less frequently but may offer a safer alternative in the presence of vasodilator-responsive PHTN(2,3).
A 35 year-old G1P0 woman with idiopathic PHTN and a history of syncope related to AVNRT presented to our service for multidisciplinary delivery planning in the late 3rd trimester. Prior cardiac MRI identified no intracardiac defects and right heart catheterization demonstrated pulmonary artery systolic pressure (PASP) of 75 mmHg, cardiac output of 3.1 L/min, and wedge pressure of 5 mmHg. One week prior to planned induction, inhaled iloprost and tadalafil 40 mg/day were initiated. Two days later, she was admitted to the cardiac ICU in active labor at 3 cm cervical dilation. A pulmonary artery catheter was placed and a treprostinil infusion was started at 3 ng/kg/min which decreased her PASP to 36 mmHg. After 12 hours of labor with a patient-controlled epidural analgesia infusion of 0.0625% bupivacaine and fentanyl 2 µg/mL, she developed early preeclampsia and was taken to the cardiac O.R. for vaginal delivery. Inhaled nitric oxide at 20 ppm was started in the O.R. and treprostinil increased. Epidural lidocaine (200 mg) was given for supplemental analgesia and the patient delivered a healthy infant with forceps assistance. Postoperatively she was anticoagulated with a heparin drip and received diltiazem and magnesium for preeclampsia. She was discharged home on hospital day 10 on a combination of atenolol, nifedipine, tadalafil, warfarin, and treprostinil at 18 ng/kg/min with return to her baseline PASP of 45 mmHg. Both mother and baby were well 1 month postpartum.
Aggressive titration of vasodilator therapies and PASP monitoring allowed us to optimize the patient’s cardiopulmonary function and offer the best opportunity for vaginal delivery while avoiding the risks of GA. Additionally, using the TeamSTEPPS-based multidisciplinary team briefing model allowed us to quickly and safely execute our care plan when she presented unexpectedly. Continued development of novel pulmonary vasodilator therapies may increasingly permit safe vaginal delivery closer to term, especially in the presence of drug-responsive disease. We also speculate that vasodilator and prostanoid-based therapies for PHTN might have contributed to initiation of her labor given the known roles of nitric oxide and prostaglandins in this process. Future studies may be warranted to investigate this.
1. Bedard D, et al. Euro Heart J 2009 Feb;30(3):256-65.
2. Smedstad KG, et al. Can J Anaesth 1994 Jun;41(6):502-12.
3. Smith JS, et al. Lung 2012 Apr;190(2):155-160.