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 general consensus that the degree of increase in systolic (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 a SBP greater than 160 mm Hg is advocated because of the increase in maternal complications with this degree of hypertension.⁶

Sustained (rather than transient) increases in BP are the key risk factor; accordingly, BP should be measured on at least two separate occasions. 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 give falsely 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 blood pressure cuffs are accurate during pregnancy but may underestimate blood pressure 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 increases by 30% to 40% in the second trimester, peaking at about the 24th week of gestation. The increase in cardiac output during the first two trimesters of pregnancy is primarily caused by increased maternal blood volume. 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 due to the so-called autotransfusion effect (see Chapter 158).

Systemic vascular resistance and consequently BP decrease 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 normal pregnancy, vascular resistance is determined by a proper balance of the effects of vasoconstricting factors 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 159-1). The most common hypertensive states are gestational hypertension without the presence of proteinuria, essential chronic hypertension, and preeclampsia (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 mother and fetus. Severe maternal hypertension during pregnancy is associated with placental abruption and intrauterine growth retardation.⁷

Preeclampsia is defined as primarily diastolic hypertension that occurs transiently during the pregnancy, usually manifesting after the 20th gestational week, and resolves within 1 to 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 non–pregnancy-related causes of hypertension such as renal artery stenosis, polycystic kidneys, glomerular or interstitial renal disease, pheochromocytoma, coarctation of the aorta, primary aldosteronism, Cushing’s 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 extremes of BP 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, such as 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 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.⁸

Pathology of Preeclampsia

Preeclampsia is a pregnancy-related multisystem disease process that usually occurs after the 32nd week of gestation. Systemic hypertension and significant proteinuria (0.3 g or greater in a 24-hour urine collection) are invariably present. Clinical onset is usually characterized by rapid weight gain associated with generalized edema, followed by onset of hypertension or proteinuria or both. The incidence of preeclampsia in the United States is 5% to 7%. The highest frequency occurs in young primigravidas, and the second highest incidence is in older multiparous women, a group that has a higher maternal mortality rate than the young primigravidas. The incidence is higher in patients with preexisting hypertension or renal vascular disease, and the symptoms may present earlier than the 32nd gestational week in these patients. Diastolic hypertension is most often seen in association with preeclampsia. It is less common to record SBP values greater than 160 mm Hg. If the SBP is greater than 200 mm Hg, the clinician should consider the possibility of underlying essential hypertension, which may be superimposed on the preeclamptic state. Because preeclampsia is a multisystem disease process, it may imitate or mask other pathologic conditions, and a thorough investigation to rule out other coexisting pathologies should be carried out.⁹ Familial prevalence of preeclampsia has been reported.^10,11 In some cases, preeclampsia manifests 1 to 7 days after delivery.^12,13 Most commonly, if preeclampsia is present in the postpartum period, it manifests as the HELLP syndrome, a severe variant of the preeclamptic spectrum of diseases.¹⁴ This syndrome always includes some, if not all, of the following features: microangiopathic hemolytic anemia (H), elevated liver enzymes (EL), and low platelets (LP). The syndrome can develop without substantial BP changes or with no significant changes compared with BP readings taken during the pregnancy.

A significant elevation of the BP in the second trimester is associated with an increased risk of preeclampsia later in the pregnancy.¹⁵ One-third of pregnant women with mean arterial pressures greater than 90 mm Hg in the second trimester develop preeclampsia later during pregnancy. Only 2% of women with mean arterial pressures less than 90 mm Hg develop preeclampsia. Relatively mild hypertension early in pregnancy, which might be ignored in nonpregnant patients, should not be overlooked or dismissed in the parturient. As many as 25% of all pregnant women have slightly elevated BPs in the last month of pregnancy, but the incidence of preeclampsia is also highest during this period. Accordingly, clinicians must remain vigilant when faced with new-onset hypertension and look for other signs and symptoms that might suggest the presence of the preeclamptic syndrome.

The exact pathogenesis of preeclampsia is still unknown, although it is believed to be related to endothelial cell injury and dysfunction that occurs in most maternal organs as a result of toxic substances released from a poorly perfused placenta. Genetic and immunologic factors also have been implicated in the pathogenesis of preeclampsia.^16,17 The generalized vasospasm that occurs in preeclampsia is responsible for many of the organ-specific signs and symptoms seen in this multisystem disease. Widespread vasospasm is associated with increased circulating levels of vasoconstrictors, increased sensitivity to angiotensin II, and decreased levels of vasodilators. An imbalance in circulating angiogenic factors is emerging as a prominent mechanism that mediates endothelial dysfunction and the clinical signs and symptoms of preeclampsia.¹⁸ There is an imbalance in the ratio of prostacyclin to thromboxane production that contributes to the pathogenesis of preeclampsia, although preeclampsia is not simply a state of prostacyclin deficiency. This idea has prompted studies of low-dose aspirin to prevent development of preeclampsia. Duley et al. reviewed 59 trials involving 37,560 women that examined the use of antiplatelet agents in preeclampsia. Antiplatelet agents including low-dose aspirin showed moderate benefits when used for prevention of preeclampsia and its consequences, decreasing preterm births, fetal and neonatal deaths, and small-for-gestational age babies. However, they recommended that further information would be required to assess which women are most likely to benefit, when treatment is best started, and at what dose.¹⁹ The maternal organs most affected in preeclampsia are the kidneys, brain, liver, and hematologic system. Despite a lack of understanding of the exact pathogenesis of preeclampsia, significant improvements in identification of the disease, monitoring, and management of these complex cases has improved perinatal and maternal morbidity and mortality. If vasospasm affects the uteroplacental bed, the incidence of intrauterine growth retardation, stillbirths, and neonatal deaths increases.²⁰

Peripheral edema is a common symptom and complaint of pregnant women that cannot be ignored, because it may herald the onset of preeclampsia. The majority of women with preeclampsia present with generalized edema, and significant weight gain is the first symptom. However, since peripheral edema is a ubiquitous symptom during pregnancy, it is no longer considered a hallmark trait of preeclampsia. Preeclampsia is often manifested initially by peripheral edema that is usually accompanied by a gradual increase in BP. Sodium retention is partly responsible for edema formation and hypertension. In normal pregnancy, the glomerular filtration rate increases by as much as 50%. There is a concomitant increase in sodium reabsorption by the renal tubules and a 60% to 80% increase in renal blood flow. Renal blood flow increases because of the increase in cardiac output and a decrease in renal vascular resistance. In preeclampsia, sodium retention is caused by a decrease in the glomerular filtration rate, possibly resulting from vasospasm of the renal vasculature, commonly seen in preeclampsia. Renin and aldosterone secretion decrease in patients with preeclampsia, probably as a result of extracellular volume expansion and associated edema. The exact cause of the decreased activity of these factors is unknown, but it may be related to decreased renal prostaglandin synthesis, increased systemic BP, or expansion of extracellular volume. In spite of the decreased levels of renin and aldosterone, sensitivity to angiotensin II is increased, a factor that may play a role in the pathogenesis of hypertension in preeclampsia.²¹ Vascular maladaptation with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms. Although sodium retention occurs in preeclampsia, blood volume actually can be diminished compared with that in normotensive pregnant patients.²² Plasma volume contracts as extracellular fluid is preferentially shifted from the vascular space to the interstitium. However, the decrease in plasma volume does not indicate volume depletion in patients with preeclampsia. In contrast to hypovolemic patients, cardiac output is increased and central venous and pulmonary capillary wedge pressures are normal to high in patients with preeclampsia.²³