DP09: NO "PDA" WITHOUT "PA": PERIPARTUM MANAGEMENT OF A PARTURIENT WITH PATENT DUCTUS ARTERIOSUS AND SEVERE PULMONARY HYPERTENSION
Maia C Young, MD; Dominick Morrow, MD; Hiram Acevedo Bonilla, MD
University of Florida College of Medicine Jacksonville
BACKGROUND: Patent ductus arteriosus (PDA), defined as a fetal shunt from the lungs to the aorta which remains open after 72-96 hours of life,1,2 is present in 0.05% of term neonates, up to 60% of preterm neonates, and as many as 80% of newborns under 1kg.2 Unrepaired PDAs can be asymptomatic or clinically significant depending on the severity of left-to-right intracardiac shunting, which is a result of the ratio of pulmonary vascular resistance (PVR) to systemic vascular resistance (SVR). A low ratio leads to more shunting, increased pulmonary blood flow, and increased left heart blood volume leading to pulmonary edema, pulmonary hypertension (pHTN), heart failure, and renal failure among other sequelae.3 In the pregnant patient, circulating blood volume and cardiac output typically increase while SVR is expected to decrease,4 potentially worsening pulmonary congestion in patients with pre-existing PDA.
CASE: We present the case of a 32-year-old G3P1102 woman from Central America with an intrauterine pregnancy at 37w4d gestational age and known medical history of PDA. She was evaluated in the outpatient cardiology clinic where she was normotensive with sinus tachycardia. However, cardiac auscultation revealed a loud, holosystolic murmur with S4 gallop for which urgent TTE was performed.
TTE showed low-normal LV systolic function with EF 50-55%, mild RV enlargement, PA pressure 99mmHg, RSVP >100mg and main PA diameter of 4.6cm with prominent forward flow, suggestive of severe pHTN. Thus, direct admission the following day to the cardiac care unit was planned to optimize her labor and delivery.
Prior to the onset of labor, an arterial line was placed for precise BP monitoring. The patient became hypotensive to 96/60 mmHg requiring 500ml boluses of LR and initiation of a norepinephrine drip at 4-10 mcg/min at the recommendation of cardiac anesthesiology and critical care anesthesiology colleagues, with vasopressin and epinephrine as additional agents if necessary. Phenylephrine was avoided due to the risk of increasing PVR.
A 0.0625% bupivacaine epidural was administered instead of the standard 0.125% in order to prevent further hemodynamic shifts and reduce the need for additional vasoconstrictors. Although initiated at 8 ml/hr, the epidural rate was decreased to 6 ml/hr due to the patient’s hypotension.
About 26 hours after admission and 7.5 hours after the first stage of labor, the patient gave birth to a healthy baby via vacuum-assisted vaginal delivery.
CONCLUSION: Pregnancy is a state of high flow via increased cardiac output and low resistance via systemic vasodilation. The prevalence of unrepaired PDA in the adult population may be higher than one may think. Assistance in the second stage of labor can reduce maternal effort via Valsalva and prevent an increase in pulmonary blood flow. Even in pregnant patients with PDA who appear clinically indistinguishable from their counterparts with normal cardiac physiology, a cardiology workup is warranted to optimize labor and delivery. For the parturient with pHTN secondary to a large PDA, an interdisciplinary approach is crucial to enhancing outcomes for both mother and baby.