Does labetalol predispose to pulmonary edema in severe pregnancy-induced hypertensive disease?

Abstract

We investigated whether use of labetalol, a beta adrenoreceptor blocking antihypertensive agent commonly employed as an alternative to hydralazine, is independently associated with pulmonary edema in women with severe preeclampsia. We retrospectively evaluated women with severe preeclampsia who were given labetalol by intravenous bolus for MAP >120 mm Hg. Outcome variables included: achieving MAP < 120 mm Hg with < 300 mg of labetalol, incidence of adverse effects of the drug, including pulmonary edema, hypotension, and maternal bradycardia. Total intravenous fluid intake exceeding output (+delta I/O) and presence or absence of preeclamptic liver involvement were noted. Statistical analysis included unpaired t-tests and Fisher's exact test. Fifty-one women were studied, 7 (13.7%) of whom developed pulmonary edema. Demographic and pregnancy characteristics were not different between patients who did or did not develop pulmonary edema. No patient had detectable underlying heart disease. Patients with or without pulmonary edema did not differ as regards entry MAP (130 ± 14 vs. 129 ± 18 mm Hg), total dose of labetalol (209 ± 83 vs. 193 ± 39 mg/24 hours), incidence of bradycardia or hypotension (0/7 vs. 8/44), or presence of hepatic involvement (1/7 vs. 9/44). However, there was a significant difference in degree of positive fluid balance. Patients developing pulmonary edema had a net gain of 1,466 ± 429 mL of fluid in the 24 hours in which they received labetalol than those who did not (659 ± 1152 mL, P =. 003). Initial central hemodynamic monitoring data revealed no impairment of cardiac performance (mean cardiac output 7.7 ± 1.8 L/min, cardiac index 4.0 ± 0.8 L/min/m2, left ventricular stroke work index 73 ± 9 g.m.m-2) despite high pulmonary capillary wedge pressures (22 ± 4 mm Hg). We conclude that the incidence of pulmonary edema in patients with severe preeclampsia who are treated with labetalol appears to be a result of an increase in third space fluid accumulation as a manifestation of the severity of their disease, not a direct effect of the drug on cardiac performance.