Hypertensive disorders in pregnancy

Blood pressure measurements in pregnancy

The definition of hypertension during pregnancy has been controversial in the past. Hypertension is now most commonly defined as a blood pressure (BP) greater than 140/90 mm Hg. Recently, there has been a consensus that the degree of increase in systolic blood pressures (SBPs) and diastolic blood pressures (DBPs) may actually be more important than the baseline values. Many authors now agree that significant hypertension in pregnancy is defined by an increase of at least 30 mm Hg in the SBP and an increase in the DBP of at least 15 mm Hg. Treatment of a DBP greater than 110 mm Hg or an SBP greater than 160 mm Hg is advocated because of the increase in maternal complications with this degree of hypertension.

Sustained (rather than transient) increases in BP are the key risk factors; accordingly, BP should be measured on at least two separate occasions at least 4–6 hours apart. BP measurements should be made in a standardized fashion (e.g., with the patient sitting in the same position) at each evaluation. Measurements in the upper arm in the recumbent position may yield false-low values because of aortal and caval compression by the gravid uterus. BP is best recorded with the patient in the sitting position or in the inferior arm in the lateral recumbent position. Many automated BP cuffs are accurate during pregnancy but may underestimate BP measurements in preeclamptic women. Manual BP readings are best suited for this group.

Physiologic changes in pregnancy

Essential to the management of hypertension in pregnancy is an understanding of the normal physiologic changes in cardiac output, vasomotor tone, and systemic BP that occur. During pregnancy, cardiac output can increase by 50% up to the early third trimester. The increase in cardiac output during this time is primarily caused by increased maternal blood volume, with a small increase in maternal heart rate. Cardiac output plateaus for the remainder of the pregnancy until labor. An increase in cardiac output is seen with each uterine contraction. Cardiac output increases again during the immediate postpartum period after delivery of the fetus and the placenta. It is during this period that cardiac output is highest because of the autotransfusion effect (see Chapter 154 ).

Systemic vascular resistance, and consequently BP, decreases during the second trimester. Increased synthesis of vasodilating prostaglandins may play a role in the regulation of BP and uterine blood flow in pregnancy. In a normal pregnancy, vascular resistance is determined by a proper balance of the effects of vasoconstricting and vasodilating factors, including prostaglandins. This balance may be disturbed in hypertensive states, owing to inadequate prostaglandin synthesis. In pregnancy-related hypertensive states, there is a paradoxical increase in the systemic vascular resistance compared with pregnancy without hypertension. It is noteworthy that all patients with newly acquired or preexisting hypertension in pregnancy have a relative decrease in DBP during the second trimester, reflecting a relative decrease in systemic vascular resistance. Indeed, BP normalizes during the second trimester in some patients with preexisting hypertension.

Causes of hypertension in pregnancy

There are multiple causes of hypertension during pregnancy ( Box 132.1 ). The most common hypertensive states are gestational hypertension without the presence of proteinuria, essential chronic hypertension, and preeclampsia (i.e., gestational hypertension with significant proteinuria). This classification is clinically useful to the practitioner, but the risk from systemic hypertension is significant for all three conditions, regardless of the specific cause of high BP. Hypertension during pregnancy is associated with an increased risk of death for both the mother and fetus. Severe maternal hypertension during pregnancy is associated with placental abruption and intrauterine growth retardation.

Preeclampsia is defined as primarily diastolic hypertension that occurs transiently during the pregnancy, usually manifesting after the 20th gestational week, and resolves within 1–2 months after delivery. Women who develop preeclampsia have a high rate of recurrence of hypertension with subsequent pregnancies and often develop chronic hypertension at a later time.

Essential chronic hypertension (i.e., hypertension that was present before the pregnancy, whether diagnosed or undiagnosed) persists in the postpartum period and accounts for approximately one-third of all cases of hypertension during pregnancy. Essential chronic hypertension may manifest during the first 20 weeks of pregnancy. Women who develop hypertension without proteinuria in the last trimester of pregnancy may have essential hypertension, either unmasked or precipitated by the pregnancy. In these cases of de novo presentation of hypertension, care must be exercised to rule out other nonpregnancy-related causes of hypertension, such as renal artery stenosis, polycystic kidneys, glomerular or interstitial renal disease, pheochromocytoma, coarctation of the aorta, primary aldosteronism, Cushing syndrome, hyperthyroidism, and hyperparathyroidism. Previously undiagnosed essential chronic hypertension is a consideration, particularly in older multiparous women. As the age of parturients has increased, the incidence of essential hypertension in pregnant women has also increased. For some patients, the initial diagnosis of hypertension may be made during a routine prenatal visit with an obstetrician. For some patients, this prenatal visit is their first encounter with a physician as an adult. Essential hypertension should be suspected if there is a family history of hypertension, diabetes, or obesity. If there is a suspicion of preexisting essential hypertension, cardiac echocardiography should be performed to evaluate for left ventricular hypertrophy, which would suggest that hypertension has been a problem for an extended period. If BP extremes are avoided with treatment, there is no significant worsening of maternal and perinatal outcomes for pregnant patients with essential hypertension. Complications related to intrapartum hypertension (e.g., placenta previa, placental abruption, and preeclampsia) are less likely with judicious treatment of elevated BP. Patients with essential hypertension have not been shown to have a higher incidence of preeclampsia, particularly if the BP is well controlled. In general, mortality and morbidity are not increased in patients with uncomplicated mild chronic hypertension. However, morbidity and mortality are both increased in those patients with severe uncontrolled hypertension, and this is further complicated by superimposed preeclampsia.