Strict blood pressure control is vital to prevent cerebral sequelae. Most units now measure blood pressure using automated oscillometric sphygmomanometers, although some of these devices may underestimate blood pressure. Mean differences of 5 mmHg (systolic) and 15 mmHg (diastolic, K4) have been reported for the Dynamap device, with individual observations showing discrepancies of up to 30 mmHg compared with standard mercury devices. Thus, if automated pressure measuring devices are being used as a guide to therapy, values should be validated against a standard mercury sphygmomanometer.
There is a loss of autoregulatory control within the cerebral circulation above a mean arterial pressure of 150 mmHg. Thus, to allow a safety margin, treatment of blood pressure should be commenced below this level. Blood pressure management should be guided by the following principles: keep mean arterial pressure below 125 mmHg or diastolic blood pressure below 110 mm Hg, avoid rapid precipitous decrements in blood pressure, and confirm blood pressure reduction by standard mercury sphygmomanometry.
Several agents are available for the acute treatment of severe hypertension. No evidence exists that any drug is superior; therefore the choice of drug therapy should depend on clinical experience and availability.
Hydralazine (5 mg intravenously every 15-20 min) is the most widely used parenteral antihypertensive drug in pregnancy. It is a vasodilator which acts directly on the arterioles. It has the advantage that it increases cardiac output, and thus may improve placental and renal blood flow. Vasodilatation with hydralazine has been associated with fetal distress. This can be prevented by prior infusion of 400 to 500 ml of colloid ( PatersoDIBE0W^ll®t.„§l 1994). The pharmacokinetics of hydralazine
(maximal effect 15-20 min, duration of action 6-8 h) suggest that the drug is best given by intermittent intravenous bolus injections rather than by continuous infusion.
Guidelines for the use of hydralazine are shown in Fig 1. A single bolus of 5 mg reduces mean arterial pressure by a mean of 12 mmHg (95 per cent confidence limits, 10-14 mmHg). This effect is increased by up to two further boluses, although there is a tendency to tachyphylaxis. A sustained fall in mean arterial pressure to values below 125 mmHg can be achieved in 89 per cent of women by using up to three boluses of hydralazine (P.aters0D.:BE0.W.D.llle.ílla/: 1994). Side-effects include tachycardia, flushing, nasal congestion, headache, tremors, and nausea. Tachycardia may warrant treatment with a b-adrenergic blocking agent. If repeated bolus hydralazine therapy fails to reduce mean arterial pressure below 125 mmHg, labetalol or nifedipine may be used.
Labetalol (20 mg intravenously every 15-20 min, increasing to 80 mg) is a combined a r and a2-adrenergic blocking agent with some b-blocking activity. It causes arteriolar vasodilatation without significant tachycardia. It may exert beneficial effects on fetal lung maturation, and appears not to have any deleterious effects on uteroplacental blood flow at the above doses. However, higher doses have been associated with increasing fetal compromise, as suggested by a deterioration in umbilical artery Doppler waveform indices.
Nifedipine (10 mg orally) acts primarily by inhibiting extracellular calcium influx into cells through slow calcium channels, leading to vasodilatation and decreased total peripheral resistance. It can be administered orally or sublingually, although the latter route may lead to precipitous falls in blood pressure with consequent fetal distress.
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