title: Hypertension in pregnancy. Pathophysiology and management.
abstract: Hypertension in pregnancy has implications for both maternal and fetal welfare. Extrapolation from concepts of mechanisms operating in hypertension in general to pregnancy-related hypertension is not justified. In the latter, the major features are a hyper-adrenergic state, plasma volume reduction and an increased systemic resistance. A reduction in uteroplacental perfusion may result from or may activate the mechanisms that elevate blood pressure. Humoral factors (e.g. hormonal attenuation of vascular reactivity) and prostacyclin deficiency may be central to the disordered physiology. Treatment of hypertension in pregnancy should aim at avoiding the vascular damage due to blood pressure elevation but not cause a reduction in uteroplacental perfusion. Unlike earlier antihypertensive regimens using centrally acting sympatholytics, adrenergic neuron blockers or diuretics, regimens using beta-blockers or combinations of beta-blockers with alpha-blockers or vasodilating agents such as hydralazine permit effective blood pressure control, even in severe hypertension, and pregnancy can often proceed until term or until fetal maturity is secured. Adverse effects on the fetus (growth retardation, cardiorespiratory depression, hypoglycaemia, hyperbilirubinaemia) formerly attributed to beta-blockers are more likely related to poorly controlled hypertension. Specific benefits of maternal beta-adrenoceptor blockade are suggested by evidence for prevention of proteinuric deterioration and a decrease in the incidence and severity of respiratory distress in premature infants. Hypertension in pregnancy still presents a formidable therapeutic challenge and requires comprehensive management with close monitoring of fetal welfare. The presence or development of proteinuria in a hypertensive pregnant woman implies a major increase in risk to the fetus and warrants immediate admission to hospital for specialist management.
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002216:Captopril / Q000627:therapeutic use; D003000:Clonidine / Q000627:therapeutic use; D003981:Diazoxide / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005260:Female; D005315:Fetal Diseases / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D006830:Hydralazine / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D006993:Hypnotics and Sedatives / Q000627:therapeutic use; D007741:Labetalol / Q000627:therapeutic use; D008278:Magnesium Sulfate / Q000627:therapeutic use; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000188:drug therapy* / Q000503:physiopathology; D012110:Reserpine / Q000627:therapeutic use; D013565:Sympatholytics / Q000627:therapeutic use; D014149:Tranquilizing Agents / Q000627:therapeutic use
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D002121:Calcium Channel Blockers; D004232:Diuretics; D006993:Hypnotics and Sedatives; D013565:Sympatholytics; D014149:Tranquilizing Agents; D006830:Hydralazine; D008278:Magnesium Sulfate; D012110:Reserpine; D002216:Captopril; D003000:Clonidine; D003981:Diazoxide; D007741:Labetalol