Each year, approximately 4 million births occur in the United States, and more than 130 million births occur worldwide. A significant proportion of these are complicated by medical disorders. In the past, many medical disorders were contraindications to pregnancy. Advances in obstetrics, neonatology, obstetric anesthesiology, and medicine have increased the expectation that pregnancy will result in a positive outcome for both mother and fetus despite most of these conditions. Successful pregnancy requires important physiologic adaptations, such as a marked increase in cardiac output. Medical problems that interfere with the physiologic adaptations of pregnancy increase the risk for poor pregnancy outcome; conversely, in some instances, pregnancy may adversely impact an underlying medical disorder.
In pregnancy, cardiac output increases by 40%, most of which is due to an increase in stroke volume. Heart rate increases by ~10 beats/min during the third trimester. In the second trimester, systemic vascular resistance decreases and this is associated with a fall in blood pressure. During pregnancy, a blood pressure of 140/90 mmHg is considered to be abnormally elevated and is associated with an increase in perinatal morbidity and mortality. In all pregnant women, the measurement of blood pressure should be performed in the sitting position, because the lateral recumbent position may result in a blood pressure lower than that recorded in the sitting position. The diagnosis of hypertension requires the measurement of two elevated blood pressures, at least 6 h apart. Hypertension during pregnancy is usually caused by preeclampsia, chronic hypertension, gestational hypertension, or renal disease.
Approximately 5–7% of all pregnant women develop preeclampsia, the new onset of hypertension (blood pressure >140/90 mmHg) and proteinuria (>300 mg/24 h) after 20 weeks of gestation. Although the precise pathophysiology of preeclampsia remains unknown, recent studies show excessive placental production of antagonists to both vascular epithelial growth factor (VEGF) (soluble fms-like tyrosine kinase 1 and sflt-1) and transforming growth factor β (TGF-β) (endoglin). These antagonists to VEGF and TGF-β disrupt endothelial and renal glomerular function resulting in edema, hypertension, and proteinuria. The renal histological feature of preeclampsia is glomerular endotheliosis. Glomerular endothelial cells are swollen and encroach on the vascular lumen. Preeclampsia is associated with abnormalities of cerebral circulatory autoregulation, which increase the risk of stroke at near-normal blood pressures. Risk factors for the development of preeclampsia include nulliparity, diabetes mellitus, a history of renal disease or chronic hypertension, a prior history of preeclampsia, extremes of maternal age (>35 years or <15 years), obesity, antiphospholipid antibody syndrome, and multiple gestation.
Severe preeclampsia is the presence of new-onset hypertension and proteinuria accompanied by end organ damage. Features may include marked elevation of blood pressure (>160/110 mmHg), severe proteinuria (>5 g/24 h), or evidence of central nervous system (CNS) dysfunction (headaches, blurred vision, seizures, coma), renal dysfunction (oliguria or creatinine > 1.5 mg/dL), pulmonary edema, hepatocellular injury (ALT > 2-fold the upper limits of normal), hematologic dysfunction (platelet count < 100,000/L or disseminated intravascular coagulation), or placental dysfunction (oligohydramnios or severe intrauterine growth restriction). The HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome is a special subgroup of severe preeclampsia and is a major cause of morbidity and mortality in this disease. The presence of platelet dysfunction and coagulation disorders further increases the risk of stroke.
Preeclampsia resolves within a few weeks after delivery. For pregnant women with preeclampsia prior to 37 weeks gestation, delivery reduces the mothers morbidity but exposes the fetus to the risk of premature birth. The management of preeclampsia is challenging because it requires the clinician to balance the health of the mother and fetus simultaneously. In general, prior to term, women with mild preeclampsia may be managed conservatively with bed rest, close monitoring of blood pressure and renal function, and careful fetal surveillance. For women with severe preeclampsia, delivery is recommended unless the patient is eligible for expectant management in a tertiary hospital setting. Expectant management of severe preeclampsia remote from term affords some benefits for the fetus but significant risks for the mother.
The definitive treatment of preeclampsia is delivery of the fetus and placenta. For women with severe preeclampsia, aggressive management of blood pressures > 160/110 mmHg reduces the risk of cerebrovascular accidents. Intravenous labetalol or hydralazine are the drugs most commonly used to manage preeclampsia, but labetalol is associated with fewer episodes of maternal hypotension. Nifedipine is also commonly used in pregnancy. Elevated arterial pressure should be reduced slowly to avoid hypotension and a decrease in blood flow to the fetus. Angiotensin-converting enzyme (ACE) inhibitors as well as angiotensin-receptor blockers should be avoided in the second and third trimesters of pregnancy because of their adverse effects on fetal development.
Magnesium sulfate is the treatment of choice for the prevention and treatment of eclamptic seizures. Large, randomized clinical trials have demonstrated the superiority of magnesium sulfate over phenytoin and diazepam, and the efficacy of magnesium sulfate in reducing the risk of seizure and, possibly, the risk of maternal death. Magnesium may prevent seizures by interacting with N-methyl-d-aspartate (NMDA) receptors in the CNS. Given the difficulty of predicting eclamptic seizures on the basis of disease severity, once the decision to proceed with delivery is made, most patients carrying a diagnosis of preeclampsia should be treated with magnesium sulfate. Women who have had preeclampsia appear to be at increased risk of cardiovascular and renal disease later in life.
Chronic Essential Hypertension
Pregnancy complicated by chronic essential hypertension is associated with intrauterine growth restriction and increased perinatal mortality. Pregnant women with chronic hypertension are at increased risk for superimposed preeclampsia and abruptio placenta. Women with chronic hypertension should have a thorough prepregnancy evaluation, both to identify remediable causes of hypertension and to ensure that the prescribed antihypertensive agents are not associated with an adverse outcome of pregnancy (e.g., ACE inhibitors, angiotensin-receptor blockers). α-Methyldopa, labetalol, and nifedipine are the most commonly used medications for the treatment of chronic ...