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 These data guide the management of preeclampsia, because efforts should be directed to BP control rather than injudicious volume resuscitation.

Hyperuricemia in preeclampsia occurs at least in part because of decreased renal excretion of uric acid. However, the development of hyperuricemia frequently predates increases in serum blood urea nitrogen and creatinine, suggesting that other mechanisms are involved as well. Hyperuricemia has been used as a marker of severity of preeclampsia, and it is a risk factor for fetal mortality.²⁴

Clinical Presentation of Preeclampsia

Severity of illness is defined as mild, moderate, or severe depending on the presenting signs and symptoms and associated comorbidities. Because of the multisystem nature of the process, preeclampsia may manifest with a wide spectrum of organ-specific abnormalities in addition to the general findings of edema, hypertension, and proteinuria. Because the pathologic abnormalities associated with preeclampsia are not necessarily secondary to hypertension, the severity of preeclampsia does not always correlate with the degree of BP elevation.¹⁵ BP elevations are classified as mild, moderate, or severe. Hypertension in preeclampsia may result from increases in systemic vascular resistance and cardiac output.

In mild preeclampsia, SBP is 130 to 140 mm Hg and DBP is 80 to 95 mm Hg. Peripheral edema is minimal, and there are no associated visual or cerebral symptoms. In moderately severe preeclampsia, the SBP may increase to as high as 150 to 160 mm Hg, and the DBP can be as high as 110 mm Hg. An increase in SBP of 25 mm Hg or more and an increase in DBP of 15 mm Hg or more suggests the presence of moderate to severe preeclampsia. Peripheral edema, hyperreflexia, and visual symptoms are present with moderately severe preeclampsia. In severe forms of preeclampsia, the SBP is greater than 160 mm Hg, and the DBP is 110 mm Hg or greater. In severe preeclampsia, there are signs of multiple organ system involvement. Pulmonary, cardiac, renal, and neurologic disturbances may be present. Severe renal involvement in preeclampsia leads to glomeruloendotheliosis, which manifests as marked proteinuria (excretion of greater than 5 g protein daily). Oliguria (urine output less than 500 mL/day) is also common, and the serum creatinine concentration is usually greater than 1.6 mg/dL. Acute renal failure is relatively rare, although clinical evidence of renal involvement in preeclampsia significantly increases perinatal mortality.²⁵ Hepatic involvement is manifested by epigastric or right upper quadrant pain with elevated circulating levels of bilirubin and transaminases. Severe preeclampsia itself is the commonest cause of hepatic tenderness and liver dysfunction in pregnancy.²⁶ Severe hepatic pathology can result in subcapsular hematomas and lacerations that may require surgical intervention. Neurologic changes may include persistent headaches, visual disturbances, focal neurologic deficits, and severe hyperreflexia with or without clonus. Computed tomography of the brain may show cerebral edema, especially in the occipital region.

Severe preeclampsia associated with central nervous system irritability, manifesting as generalized tonic-clonic seizures not caused by other cerebral pathology, is defined as eclampsia.²⁷ Eclampsia can occur without significant hypertension or proteinuria. Cardiovascular and respiratory changes can manifest as pulmonary edema, resulting from iatrogenic fluid overload, acute systolic left ventricular failure, or diastolic left ventricular dysfunction secondary to chronic essential hypertension. Pulmonary edema may also result from increased capillary permeability or from a decrease in colloid osmotic pressure that occurs to some extent during normal pregnancy but can be accentuated by preeclampsia.²⁸ Hematologic disturbances consist of thrombocytopenia, disseminated intravascular coagulation, and hemolysis.

It is unknown whether preeclampsia leads to persistent chronic hypertension after delivery, although it seems that this is unlikely. Nevertheless, an episode of preeclampsia may identify a subgroup of women with increased risk for eventual development of essential hypertension at a later time. In a recent study, women with preeclampsia had an increased risk of cardiovascular disease death later in life, independent of other measured risk factors.²⁹ These findings reinforced previously reported recommendations that a history of preeclampsia should be used to target women at risk for cardiovascular disease. Debate continues as to whether the presence of preeclampsia or the duration of the disease process may be responsible for influencing factors that later lead to the development of essential hypertension. Women who develop preeclampsia superimposed on previously undiagnosed essential hypertension or underlying renal disease are predisposed to the later development of essential hypertension.

Other Causes of Hypertension in Pregnancy

Some of the less common causes of hypertension are listed in Box 159-1.

Primary aldosteronism in pregnant women has been reported but is uncommon. The treatment of hypertension in these patients is directed toward medical management during the pregnancy and postpartum operative intervention if an adenoma is present.

Renal artery stenosis can be associated with preeclampsia. Medical therapy with antihypertensive agents is recommended. Although ideal therapy for these patients would include angiotensin-converting enzyme (ACE) inhibitors, these agents are contraindicated during pregnancy, and other alternatives must be employed.³⁰

Coarctation of the aorta is a rare cause of hypertension. It may be previously undiagnosed and then initially diagnosed during a patient’s first pregnancy. It can be associated with preeclampsia. The greatest risk to these patients is aortic rupture due to cystic medial necrosis of the aortic wall. This risk is amplified because the normal physiologic changes of pregnancy place further stresses on the abnormal aorta. Increases in BP, cardiac output, and the strain of labor with contractions can increase this risk. Aggressive medical management with antihypertensive medications, including β-adrenergic blockers, improves outcome in these high-risk patients.

Pheochromocytoma is a rare cause of hypertension, but patients have a poor outcome if the tumor is not diagnosed and treated. These patients can present with nausea, vomiting, profuse diaphoresis, severe headache, generalized weakness, palpitations, and seizures. The immediate causes of sudden death are secondary to pulmonary edema, cerebral hemorrhage, and cardiovascular collapse. Because of the risk of significant morbidity and mortality to both mother and fetus, it was previously recommended that immediate surgical intervention be carried out during pregnancy. Currently, most experts advocate medical therapy with α- and β-adrenergic blockade during pregnancy and tumor removal after delivery.

General Treatment Principles

The benefits of a well-balanced low-salt diet and exercise have been shown to decrease the incidence and severity of hypertension. Bennett conducted a retrospective analysis of women who had prior bariatric surgery before becoming pregnant. These patients had lower rates of hypertensive disorders in subsequent pregnancies.³¹ Previously, some experts were concerned that aggressive management of hypertension in pregnancy might be detrimental, perhaps because hypertension improved uterine blood flow. These concerns appear to be unfounded, because later studies showed that uterine blood flow either increases or shows no change after hypertension is controlled. Nevertheless, caution must be exercised to ensure that treatment of hypertension during pregnancy does not induce hypotension, which adversely affects maternal hemodynamics and compromises fetal well-being. There is significant correlation between maternal BP control and fetal morbidity, and evidence now suggests that antihypertensive treatment for severe hypertension results in improved perinatal outcome. The development of mild hypertension or preeclampsia at or near term is associated with minimal maternal and neonatal complications. However, the onset of severe gestational hypertension and/or severe preeclampsia early in gestation is associated with significant maternal and perinatal complications.³² General recommendations for management and monitoring of hypertension in pregnant patients include stabilization and treatment of acute changes in BP. Specific goal-directed therapy is indicated for various organ system abnormalities that may be present, particularly in those patients with moderate to severe preeclampsia. If proteinuria is not present and there is no suspicion of preeclampsia, conservative management on an outpatient basis is usually adequate. Immediate hospitalization with bed rest is recommended for patients presenting with proteinuria if there is a high index of suspicion for the diagnosis of preeclampsia.

Antihypertensive Drug Therapy

There is now an extensive pharmaceutical armamentarium available for the treatment of hypertension in pregnancy. In 1979, the U.S. Food and Drug Administration (FDA) established categories for all drugs with potential and real adverse effects on the fetus.³³ Although helpful to the clinician, these categories most often do not reflect current scientific knowledge regarding specific teratogenic effects of the drugs.³⁴

The FDA categories are listed in Table 159-1. Most antihypertensive drugs used during pregnancy are classified as category C. Thiazide diuretics, prazosin, and α-methyldopa are designated as category A; metoprolol is a category B agent. Because most antihypertensive drugs are used later in pregnancy, the potential teratogenic effects of these drugs are usually not of concern. However, if treatment is initiated for patients with preexisting essential hypertension or early onset gestational hypertension, teratogenic effects must be considered when choosing antihypertensive drugs. It may be necessary to change antihypertensive therapy early in pregnancy, if the patient is taking drugs that could increase the risks of fetal abnormalities.

TABLE 159-1 FDA Categories of Fetal Drug Toxicities

FDA, U.S. Food and Drug Administration.

The goal of hypertensive therapy in pregnancy is prevention of maternal complications such as intracerebral hemorrhage, stroke, and decompensated heart failure. There are no convincing data to determine the optimal BP goal with drug therapy. There is disagreement concerning the proper normal values for BP during pregnancy, but most agree that acute treatment is mandated (1) if the SBP is greater than 160 mm Hg or the DBP is 110 mm Hg or greater or (2) if the SBP is more than 30 mm Hg greater than the baseline value or the DBP is more than 15 mm Hg greater than baseline. If acute and urgent drug therapy management is required, some patients may need to be hospitalized, depending on their compliance with drug therapy and the urgency of lowering the BP based on concomitant organ system involvement. For patients presenting with SBP 140 mm Hg or higher and DBP 90 mm Hg or higher, urgent drug therapy should be implemented if there is concurrent evidence of symptoms, underlying essential hypertension, or end-organ involvement. If the patient presents after the 24th gestational week and fetal viability is ascertained, both cardiac and fetal telemetry may be required. For patients presenting with SBP less than 140 mm Hg and DBP less than 90 mm Hg and no evidence of significant proteinuria, management and treatment can be provided on an outpatient basis, with frequent office visits and close maternal and fetal assessments. If the hypertension is refractory to standard therapy, hypertension worsens despite adequate drug therapy, or the suspicion of preeclampsia arises, then immediate hospitalization is recommended.

Conservative drug therapy is advocated for moderately severe preeclampsia, but the treatment of choice for severe preeclampsia and associated end-organ involvement is immediate delivery of the fetus. Delay in delivery for patients with severe preeclampsia and end-organ involvement can result in serious maternal and fetal complications. If the fetus is of mature gestational age, factors influencing the decision to deliver are dependent on progression of the disease process, assessment of fetal lung maturity, and status of the cervix. Conservative management of preeclamptic patients at a gestational age less than 24 weeks is associated with serious maternal complications, and termination of the pregnancy should be considered. For patients at 28 to 32 weeks of gestation, conservative management with vigilant monitoring and assessment should be performed in a hospital setting. There is not enough evidence from the limited trials performed to recommend either early delivery or expectant care for women with severe preeclampsia before 34 weeks of pregnancy.³⁵

During pregnancy, the clinician must decide when to use antihypertensive medications and what level of BP to target. The choice of antihypertensive agents is more limited in pregnancy, since not all available antihypertensive drugs have been adequately evaluated in pregnant women, and some agents are contraindicated.³⁶ A first-line drug still used today in the pregnant patient, although less commonly in the general populace, is oral α-methyldopa, a central α₂-adrenergic agonist. Historically this has been a first-line drug of choice for many obstetricians over the years, and there has been little evidence to convince them otherwise. The starting dose is 250 mg orally 2 to 3 times a day for the first 48 hours of treatment. Dosing can be increased every 2 days until the desired BP level is achieved. The maximum daily dose is 4 g. β-Adrenergic blocker therapy with oral labetalol, a combined α- and β-adrenergic antagonist, has become popular as a single-agent antihypertensive. The recommended initial dose is 100 mg orally twice daily. The dose can be increased as indicated, either semiweekly or weekly. The maintenance dose is usually 200 to 400 mg administered twice daily. The benefits of β-adrenergic blockade make this an attractive drug for parturients with underlying chronic essential hypertension and possible cardiac and vascular involvement. Diuretics also may be used, although care must be exercised to prevent excessive fluid losses, which can exacerbate the decrease in blood volume associated with preeclampsia. As mentioned previously, ACE inhibitors and angiotensin II receptor antagonists should be avoided intrapartum because these agents can increase perinatal morbidity and mortality.

For acute and emergent drug therapy for severe hypertension, intravenous (IV) antihypertensive drugs should be used; IV infusions are particularly attractive because they provide rapid control of BP and can be titrated easily. Intravenous hydralazine, a direct arteriolar vasodilator, remains the standard for many obstetricians, although other drugs may be preferable since hydralazine may decrease BP precipitously.³⁷ Excessive lowering of BP is a particular problem when hydralazine is administered to preeclamptic patients with contracted blood volume. If hydralazine is used, it should be given as 5- to 10-mg IV boluses every 15 to 30 minutes until BP is controlled. Onset of the hypotensive effect is 10 to 20 minutes, and duration of action is about 8 hours. Infusions of hydralazine are difficult to titrate and may be associated with increased incidence of fetal distress.

Intravenous labetalol, a nonselective β- and α-adrenergic receptor blocker, is also commonly used for the acute management of hypertension. Labetalol rapidly decreases BP but not at the expense of uteroplacental blood flow. Labetalol crosses the placenta but rarely causes significant neonatal bradycardia. An initial IV bolus of 10 or 20 mg should be given, followed by boluses of 40 to 80 mg at 10- to 15-minute intervals as needed to control hypertension. Labetalol also can be given by continuous IV infusion; the usual dose is 1 to 4 mg/min. Contraindications to the use of labetalol are the same as those for other β-adrenergic antagonists, notably heart block and acute asthma.

Sodium nitroprusside is a potent arterial and venous vasodilator that quickly decreases the BP. Rapid titration with a continuous IV infusion can be instituted starting at a dose of 0.25 to 0.5 µg/kg/min and adjusted every few minutes and titrated to effect. Invasive arterial monitoring is often recommended in conjunction with its use. As with all potent vasodilators, care must be taken when using sodium nitroprusside, because patients with volume depletion may be particularly sensitive to its effects. Despite a paucity of data, concern regarding the risks of fetal cyanide toxicity prompts some practitioners to avoid using this drug in pregnant patients. Careful attention to dosing and duration of use should minimize the risk of toxicity.

Other less frequently used agents include IV nitroglycerin, oral clonidine, and β-adrenergic blockers other than labetalol. Intravenous nitroglycerin is easily titrated and is especially attractive for the management of patients with pulmonary edema. However, its antihypertensive potency is somewhat limited. Oral clonidine, a centrally acting α₂-adrenergic agonist, is an effective antihypertensive drug, but concerns about the risk of rebound hypertension after cessation limit its use.

There remains considerable debate concerning the use of β-adrenergic blockers in pregnancy because of the potential risks of fetal bradycardia and a decrease in perfusion to the uteroplacental bed. Beta-blockers have been used during pregnancy without evidence of teratogenic effects. Although there is limited experience, they are considered as indicated in pregnant women with hypertension, mitral stenosis with pulmonary hypertension, coarctation of the aorta, ischemic heart disease, supraventricular and ventricular arrhythmias, and can be continued during delivery.^2,38,39 Esmolol has been used widely for heart rate control in pregnancy, but its efficacy is limited as an antihypertensive agent.

Antihypertensive drugs commonly used during pregnancy are listed in Table 159-2.

TABLE 159-2 Antihypertensive Drugs Commonly Used in Pregnancy

Management of Hypertension During Labor and Delivery

Management of hypertension during labor and delivery is directed toward avoiding acute and maternal complications. Antihypertensive drug therapy with judicious use of IV fluids is of paramount importance to avoid unnecessary complications. Postpartum monitoring is advocated for high-risk, chronically hypertensive patients. Hypertension associated with preeclampsia usually resolves spontaneously within a few weeks after delivery. These patients are at risk for development of acute complications such as hypertensive encephalopathy, pulmonary edema, and acute renal failure. The choice of antihypertensive medications or the doses used may have to be adjusted after delivery. Minute amounts of all antihypertensive agents are found in breast milk. Although limited data are available, adverse perinatal effects have not been observed with the more commonly used drugs such as α-methyldopa, hydralazine, and the various α-adrenergic blockers.

Key Points