A comprehensive review of hypertension in pregnancy

Abstract

Hypertension is the most common medical disorder encountered during pregnancy. Hypertensive disorders are one of the major causes of pregnancy-related maternal deaths in the United States. We will present a comprehensive update of the literature pertinent to hypertension in pregnancy. The paper begins by defining and classifying hypertensive disorders in pregnancy. The normal vascular and renal physiological changes which occur during pregnancy are detailed. We will summarize the intriguing aspects of pathophysiology of preeclampsia, emphasizing on recent advances in this field. The existing diagnostic tools and the tests which have been proposed for screening preeclampsia are comprehensively described. We also highlight the short- and long-term implications of preeclampsia. Finally, we review the current management guidelines, goals of treatment and describe the potential risks and benefits associated with various antihypertensive drug classes. Preeclampsia still remains an enigma, and the present management focuses on monitoring and treatment of its manifestations. We are hopeful that this in depth critique will stimulate the blossoming research in the field and assist practitioners to identify women at risk and more effectively treat affected individuals.

Figure 1

Relative changes in renal hemodynamics during normal human pregnancy. Dramatic changes occur in systemic hemodynamics during physiologic pregnancy. In uncomplicated pregnancy, mean arterial pressure drops, reaching its nadir between the 16th and 20th weeks of gestation. After the 20th week, mean arterial blood pressure slowly returns to close to pre-pregnancy levels at about 40-week gestation. Changes in systemic blood pressure are paralleled by a change in cardiac output which increases dramatically. The apex is reached between the 16th and 20th weeks of gestation. Plasma volume increases substantially as well but lags behinds the increased cardiac output. MAP: mean arterial pressure. CO: cardiac output.

Figure 2

The amount of angiotensin required to raise blood pressure by 20 mm Hg. This figure demonstrates two important findings obtained from serial observations in primiparas. Women undergoing physiologic pregnancy (■) become resistant to the pressor effect of infused angiotensin II by 14 weeks of gestation. They require significantly higher dose of angiotensin II to increase blood pressure by 20 mm of Hg. In contrast, women destined to develop preeclampsia (♦) regain their sensitivity to angiotensin II between 22–26 weeks of gestation, well before any other clinical manifestations of preeclampsia are appreciated [7].

Figure 3

Changes in renal function during pregnancy. Kidney function also dramatically increases during pregnancy. The rapid developing rise in renal blood flow and glomerular filtration rate were documented in careful studies undertaken in humans. These increments average between 40 and 50%. Dr. Davison and his associates found that these improvements in renal hemodynamics occurred even prior to the changes in cardiac output and plasma volume. GFR: glomerular filtration rate. ERPF: effective renal plasma flow [8].