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DR. Hodgson is Chief Resident Yale University School of Medicine, New Haven, Conn.
DR. NORWITZ is Associate Professor, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Conn.
While most ob/gyns can recite a long list of risk factors for this lethal complication, mounting evidence suggests that maternal hypotension should be taken into account as well.
Clinicians don't appreciate stillbirth as much as they should. Would it surprise you to learn, for instance, that antepartum stillbirths-defined as fetal demise after 20 weeks' gestation and before delivery-account for more perinatal deaths than either complications of prematurity or sudden infant death syndrome?1,2 And despite intensive efforts, about half of all stillbirths remain unexplained.3-5 While hypertensive disorders are well-known causes of adverse pregnancy outcome, including stillbirth, we'd like to consider the far more provocative question: Does low blood pressure increase the risk of this complication?
The perinatal mortality rate in the United States has decreased by 75% since 1950, due primarily to a drop in neonatal mortality. Although fetal deaths also decreased during that time, stillbirths continue to contribute disproportionately to perinatal mortality. In 1998, for example, the neonatal mortality rate in the US was 4.8 per 1,000 births, while the comparable fetal mortality rate was 6.7 per 1,000 births.6
What causes stillbirth?
Physiologic adaptations occur in the maternal cardiovascular system in response to the demands of pregnancy. In healthy normotensive women, blood pressure fluctuates significantly and in predictable ways throughout pregnancy. It falls in early pregnancy and is usually 10 mm Hg below baseline in the second trimester, declining to a mean of 105/60 mm Hg.19-21 The fall in blood pressure is due primarily to a reduction in systemic vascular resistance. Both low resistance in the uteroplacental circulation and systemic vasodilatation contribute to the decline in vascular resistance. We don't fully understand the factors responsible for this vasodilatation but they include decreased vascular responsiveness to the pressor effects of angiotensin II and norepinephrine, increased release of endothelial prostacyclin, enhanced nitric oxide production, and a direct effect of estrogen, progesterone, prolactin, and related hormones.
Blood pressure reaches a nadir around 20 to 28 weeks and returns to baseline at term.22-24 Keep in mind, however, that blood pressure measurements are subject to change depending on the technique and instrument used and positioning of the patient.24-26 For the sake of consistency and standardization, measurements in pregnancy should always be taken from the brachial artery at the level of the heart with the patient in the sitting position at rest for at least 5 minutes using an appropriate-sized manual cuff and listening for the 5th Korotkoff's sound (disappearance, not muffling) to designate diastolic pressure.23,27,28
Blood pressure abnormalities and adverse pregnancy outcomes
A sustained elevation in blood pressure of ≥ 140 mm Hg systolic, ≥90 mm Hg diastolic, or both should be regarded as abnormal at any stage of pregnancy, and may represent chronic hypertension, preeclampsia, or gestational non-proteinuric hypertension.26,29 On the other hand, conventional wisdom suggests that low blood pressure in pregnancy is reassuring, despite the fact that the data supporting this view are limited. In fact, several studies suggest that low blood pressure in the third trimester increases the threat of both stillbirth and growth restriction.17,18,30-32