HIGH BLOOD PRESSURE DURING PREGNANCY
High blood pressure complicates almost 10 percent of all pregnancies, multiple fetuses. Causes of hypertension in pregnancy are multiple, and many current and previously used classification systems are elaborate and confusing, due in part to difficulty in making an etiological diagnosis by clinical criteria alone. The consensus group recommends the schema proposed by the American College of Obstetrics and Gynecologists in 1972, which has been in wide use for some time, is practical and concise, and considers hypertension associated with gestation in only four categories: 1. chronic hypertension (of whatever cause, but mainly essential in nature); 11. preeclampsia; III. preeclampsia superimposed upon chronic hypertension; and IV. transient hypertension.
Preeclampsia (pure or superimposed) represents the greatest danger for the fetus and is associated with life-threatening maternal syndromes, while transient hypertension is a fairly benign disorder characterized by mild to moderate elevations of blood pressure late in pregnancy which return to normal postpartum. Essential hypertension, too, is usually well tolerated if elevations remain (with or without therapy) below diastolic levels of 100 mm Hg (phase V), but complications such as midtrimester loss, growth retardation, and abruption may occur more frequently. Because the preeclamptic syndromes and essential hypertension comprise over three-quarters of the hypertensive disorders in pregnancy, this document focuses on the presentation, pathophysiology, and management of these diseases.
Preeclampsia, a disease peculiar to pregnancy, mainly in nulliparas, presents primarily after gestational week 20, most frequently near term. Signs helpful in its diagnosis are presence of proteinuria, edema (especially if of recent and rapid onset), and any of the following: hemoconcentration, hypoalbuminemia, hepatic function and/or coagulation abnormalities, and increased urate levels. The predictive value of raised serum iron, low antithrombin 111, and hypocalciuria are under investigation.
A major pathophysiological feature of this disease is a marked increase in peripheral resistance. This vasospasm is due, in part, to exaggerated vascular responsiveness to circulating angiotensin 11 and catecholamines (and possibly an imbalance between thromboxane and prostacyclin production). Prior to intervention, cardiac output is often decreased, pulmonary capillary wedge pressure is normal or low, and intravascular volume is below that of normal pregnant women. Renal hemodynamics also decrease due, in part, to a characteristic morphological lesion in the glomerulus, and there may be increased vascular permeability leading to albumin loss from the intravascular space. Uteroplacental perfusion is often compromised, which may lead to fetal growth retardation.
Preeclampsia can lead to two life-threatening complications. The first is a rapidly developing syndrome characterized by microangiopathic hemolytic anemia and marked signs of liver dysfunction as well as coagulation changes. This variant, termed HELLP (hemolysis elevated liver enzymes low platelet count), constitutes an emergency requiring prompt pregnancy termination. The second complication is progression of preeclampsia to a convulsive phase termed eclampsia, at one time the major cause of cerebral bleeding and maternal mortality in this disorder. Pending or frank eclampsia also requires immediate termination of gestation.
Therapy for preeclampsia when gestation is advanced is delivery. Severe intrapartum hypertension is controlled with intravenous hydralazine, which is successful in most instances. Favorable results have been recorded with parenteral diazoxide, labetalol, and clonidine as well as oral nifedipine. Nitroprusside should be avoided unless maternal jeopardy is extreme. Magnesium sulfate remains the drug of choice to prevent or treat eclamptic convulsions.
Women with essential hypertension often experience reductions in blood pressure during the first two trimesters; failure for this to occur is an unfavorable prognostic sign. When pharmacological intervention is required, alpha methyldopa, because of its long history of safe use and a trial including a 7-year followup of the neonate, remains the drug of choice to treat chronic hypertension in pregnancy. Data relevant to beta blocking agents and combined beta and alpha adrenergic receptor antagonists demonstrate their usefulness with little or no evidence of fetal jeopardy. Thiazide diuretics, which have been used safely in normotensive gravidas, may be used in hypertensive pregnant women especially those who are salt sensitive. Preliminary information concerning calcium channel antagonists is also encouraging, but angiotensin converting enzyme inhibitors are contraindicated in pregnant women.
Finally, like all pregnant women, those with hypertension should refrain from alcohol and tobacco. The roles of calcium supplementation and low-dose aspirin (which decreases thromboxane synthesis while sparing prostacyclin production) to prevent preeclampsia and/or chronic and transient hypertension are under investigation.
SOURCE: National Institute of Health, National Heart, Lung and Blood Institute, NIH Publication No. 91-3029
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