Effect of labetalol infusion on uterine and fetal hemodynamics and fetal cardiac function

Jouppila, Pentti; Räsänen, Juha

doi:10.1016/0028-2243(93)90022-5

Cited by 13 publications

(6 citation statements)

References 18 publications

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“…Although we did not measure the plasma and urinary concentrations of labetalol, we believe that the features of adrenergic blockade may implicate labetalol as a possible causative factor in the pericardial effusions and myocardial hypertrophy noted in our infants. Although short term labetalol infusion does not impair cardiac function and peripheral vascular resistance,8 prolonged α and β adrenergic blockade might have been responsible for the myocardial hypertrophy in our infants. The resolution of the ventricular hypertrophy in case 1 over the first 6 weeks after birth supports this hypothesis.…”

Section: Discussionmentioning

confidence: 60%

Adverse neonatal effects of maternal labetalol treatment

Crooks

Deshpande

Hall

et al. 1998

Archives of Disease in Childhood - Fetal and Neonatal Edition

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Section: Discussionmentioning

confidence: 60%

Adverse neonatal effects of maternal labetalol treatment

Crooks

Deshpande

Hall

et al. 1998

Archives of Disease in Childhood - Fetal and Neonatal Edition

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“…Length of exposure needed to obtain effects. The effect of atenolol did not appear until 30 min after exposure [21,22]. Exposures of labetalol and pindolol for 15-20 min were without effects.…”

Section: Certainty Of Evidence: Highmentioning

confidence: 84%

“…Relevant effects. In adults with hypertension, atenolol decreases the heart rate, cardiac contractility and cardiac output [21], whereas pindolol and labetalol decrease peripheral vascular resistance with minor effects on cardiac output [21,22]. Length of exposure needed to obtain effects.…”

Section: Certainty Of Evidence: Highmentioning

confidence: 99%

Drug exposure during pregnancy and fetal cardiac function – a systematic review

Kolding

Eken

Uldbjerg

2020

Journal of Perinatal Medicine

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Background:The aim of this systematic review was to describe the effects of drug exposure during pregnancy on fetal cardiac function. Methods: We searched MEDLINE, Embase, Cochrane and SCOPUS for studies assessing fetal cardiac function in drug-exposed human pregnancies. Risk of bias was assessed by the Risk Of Bias In Non-randomized Studies of Interventions (ROBIN-I) tool. Results: We included 32 studies on eight different drug groups. They included 51 outcome variables, which were all based on ultrasound techniques primarily assessing systolic function: pulsed wave Doppler, tissue Doppler imaging (TDI), and B-and M-mode. Overall, the risk of bias was moderate. β 2 agonists increased the systolic velocity in the ductus arteriosus and the fetal heart rate. β-blockers caused unchanged or decreased systolic velocity of the pulmonary trunk. Corticosteroids increased the velocity in the ductus arteriosus. Furthermore, in growth-restricted fetuses with an increased myocardial performance index (MPI′) on the right side, corticosteroids normalized this variable. Nonsteroidal anti-inflammatory drugs (NSAIDs), but not acetylsalicylic acid, increased the flow velocities in the ductus arteriosus, decreased the shortening fraction and increased the end-diastolic ventricular diameters. Metformin and insulin normalized the diastolic strain and global longitudinal strain in diabetic pregnancies. Highly active antiretroviral therapy (HAART) exposure increased the E/A ratio on the right side, prolonged the isovolumic relaxation time (IRT) and ejection time, shortened the isovolumic contraction time (ICT), and decreased left myocardial systolic peak velocities. Chemotherapy did not cause detectable changes. Conclusion: Six of the eight drug groups caused detectable changes in fetal cardiac function. However, the evidence was hampered by only a few studies for some drugs.

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“…6,7 Neither labetalol nor pindolol seems to adversely affect uterine or placental hemodynamics. [8][9][10][11][12][13] Both labetalol and pindolol rapidly cross the placenta. 14,15 Studies in human pregnancies suggest that, under resting conditions, their impacts on placental circulation or fetal heart rate and cardiovascular hemodynamics are minimal.…”

Section: Introductionmentioning

confidence: 99%

“…14,15 Studies in human pregnancies suggest that, under resting conditions, their impacts on placental circulation or fetal heart rate and cardiovascular hemodynamics are minimal. [8][9][10][11][12][13] However, it is not known whether labetalol and pindolol might interfere with fetal stress responses.…”

Section: Introductionmentioning

confidence: 99%

Placental and Fetal Hemodynamics After Labetalol or Pindolol in a Sheep Model of Increased Placental Vascular Resistance and Maternal Hypertension

et al. 2009

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We investigated the effects of labetalol and pindolol on uterine, placental, and fetal hemodynamics following norepinephrine-induced maternal hypertension in a sheep model of increased placental vascular resistance. Also, we examined fetal and placental hemodynamic responses to acute hypoxemia after antihypertensive medication. Norepinephrine increased maternal heart rate (HR), mean arterial pressure (MAP) and uterine vascular resistance (R(UtA)), and decreased uterine volume blood flow (Q(UtA)). Both labetalol and pindolol decreased maternal HR, MAP, and R(UtA), but did not restore Q(UtA). Fetal MAP was unaffected while fetal HR and placental volume blood flow (Q(UA)) decreased and placental vascular resistance increased. During hypoxemia, which was induced by decreasing maternal inspiratory oxygen fraction, all these parameters remained unchanged in the labetalol group while fetal HR increased and Q(UA) further decreased in the pindolol group. We conclude that labetalol and pindolol may compromise uterine and placental hemodynamics. Hypoxemic stress provokes divergent hemodynamic responses in fetuses exposed to these differently acting adrenoceptor antagonists.

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Effect of labetalol infusion on uterine and fetal hemodynamics and fetal cardiac function

Cited by 13 publications

References 18 publications

Adverse neonatal effects of maternal labetalol treatment

Adverse neonatal effects of maternal labetalol treatment

Drug exposure during pregnancy and fetal cardiac function – a systematic review

Placental and Fetal Hemodynamics After Labetalol or Pindolol in a Sheep Model of Increased Placental Vascular Resistance and Maternal Hypertension

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