hiazide diuretics are sulfonamides, and these were the first drug group used to successfully treat chronic hypertension (Beyer, 1982). hese agents and loop-acting diuretics such as furosemide are commonly used in nonpregnant hypertensive patients. In the short term, they provide sodium and water diuresis with volume depletion. But with time, there is sodium escape, and volume depletion is partially corrected. Some aspect of lowered peripheral vascular resistance likely contributes to their efectiveness in reducing long-term morbidity (Umans, 2015).
Thiazide drugs may be mildly diabetogenic, and expected volume expansion may be curtailed in pregnant women. Sibai and colleagues (1984) showed that plasma volume expanded only about 20 percent over time in hypertensive pregnant women who continued diuretic therapy compared with a 50-percent expansion in women who discontinued treatment. lthough perinatal outcomes were similar in these women, such concerns have led to practices of withholding diuretics as irst-line therapy for chronic hypertension, particularly after 20 weeks' gestation (Working Group Report, 2000). Even so, in a Cochrane review, Churchill and associates (2007) reported no diferences in perinatal outcomes in 1836 nonhypertensive women randomly assigned to a thiazide diuretic or placebo for primary preeclampsia prevention. Overall, thiazide diuretics are considered safe in pregnancy (Briggs, 2015). But for preeclampsia treatment, they are considered to be inefective (Umans, 2015).
Hydralazine relaxes arterial smooth muscle and has been used parenterally for decades to safely treat severe peripartum hypertension (Chap. 40, p. 739). Oral hydralazine mono therapy for chronic hypertension is not generally used because of its weak antihypertensive efects and resultant tachycardia. It may be an efective adjunct for long-term use with other antihypertensives, especially if there is chronic renal insuiciency. In one study, vasodilator treatment of chronically hypertensive women was associated with a twofold rise in rates of low-birthweight and growth-restricted neonates (S u, 2013).
These drugs inhibit the conversion of angiotensin-I to the potent vasoconstrictor angiotensin-II. They can cause severe fetal malformations when given in the second and third trimesters. These include oligohydramnios, hypocalvaria, and renal dysfunction (Chap. 12, p. 241). Some preliminary studies also suggest teratogenic efects, and because of this, they are not recommended at any time during pregnancy (Briggs, 2015; Podymow, 2011).
Angiotensin-receptor blockers act in a similar manner. But, instead of blocking the production of angiotensin-II, they inhibit binding to its receptor. They are presumed to have the same fetal efects as angiotensin-converting enzyme inhibitors and thus are also contraindicated.
The prognosis for pregnancy outcome with chronic hyperten sion is somewhat dependent on the severity of disease ante dating pregnancy. This may be related to indings that many women with severe hypertension have renal disease-as either cause or efect (Cunningham, 1990; Morgan, 2016a). It fol lows that women whose hypertension is severe enough to require antihypertensive therapy are at inordinately high risk for superimposed preeclampsia.