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We believe that there is little to support the prevailing concept that a true caloric gain of weight during pregnancy predisposes to toxemia. Pre-existing obesity is quite a different problem.

Ernest W. Page, MD1

The incidence of hypertension among adults in the United States has been estimated at between 29% and 31%. Obesity is commonly associated with treatment-resistant hypertension or hypertension that requires 3 or more antihypertensive agents to achieve blood pressure control by established guidelines.2 Among obese individuals, the incidence of hypertension has been reported as high as 50%.3 In the United States, over one-half of reproductive-age women are overweight or obese. More than one-third of these women are obese, with about 8% classified as extremely obese. During pregnancy, these women are expected to be at increased risk for pregnancy complications related to obesity.4 Maternal obesity and morbid obesity have been reported to be strongly associated with elevated blood pressure readings during the 3 trimesters of pregnancy, as well as with an increased risk for gestational hypertensive disorders.5 To further establish the importance of obesity as a risk factor for hypertensive disorders during pregnancy, one study clearly demonstrated that obesity is a dose-dependent variable: Women with a body mass index (BMI) range of 25–30 kg/m2 demonstrated a relative risk (RR) for preeclampsia of 1.88 (with a 95% confidence interval [CI] of 1.34–2.62), while women with BMI greater than 40 kg/m2 had a RR of 7.17 with a CI of 5.06–10.16.6

The objectives of this chapter include a review of the underlying pathophysiology that predisposes obese women to develop hypertensive disorders, particularly during pregnancy. A review of the definitions of hypertensive disorders occurring during pregnancy is undertaken, as well as the management of mild-to-severe hypertensive disease, including life-threatening complications.


Pathophysiology of Hypertension Related to Obesity

The pathophysiology of hypertension in obesity is complex and multifactorial. Prior to the onset of clinically overt hypertension, there is an increase in cardiac output considered to be a response to the increased demand for peripheral tissue oxygen delivery. The clinical normotensive state is maintained by a compensatory reduction in systemic vascular resistance. Among nulliparous women at risk for development of preeclampsia with marked increase in cardiac output with reduction in systemic vascular resistance, one subgroup at increased risk comparable to women with diabetes mellitus were women with overall increased weight of 14 kg compared to controls not at increased risk.7 Over time, an increase in the activation of the renin-angiotensin-aldosterone axis gradually increases systemic vascular resistance, resulting in a rise in blood pressure and the development of clinical hypertension.

Early hypertension among obese individuals is characterized by increased cardiac output and increased systemic vascular resistance.8,9 The process of moving from clinically normotensive to hypertensive ...

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