Severe and resistant hypertension

Hypertension beyond a mean arterial pressure of 140 mmHg is associated with a risk of cerebrovascular hemorrhage. The mean arterial pressure (MAP) exact level at which the blood-brain barrier begins to break down in pre-eclampsia/eclampsia is unclear but we do know that cerebral autoregulation is affected in this condition and that brain overperfusion can occur at lower MAP levels than in non-pre-eclamptic patients (Belfort et al., 1999a, b, 2000, 2001, 2002a). In practice, any blood pressure above 160/110 mmHg is usually regarded as an indication for aggressive antihypertensive therapy. The goal of antihypertensive therapy should be to maintain systemic MAP between 100 and 126 mmHg. Patients admitted to intensive care units and managed with the benefit of invasive hemody-namic monitoring should have vasodilator therapy titrated against both systemic blood pressure and derived parameters such as systemic vascular resistance (SVR). The SVR should be restored to normal levels (1000 and 1200 dyne.seccm~5), providing the MAP remains above 100 mmHg.

Plasma volume expansion is an essential adjunct to antihypertensive therapy. Diminishing peripheral perfusion may result from vasodilator therapy because of an excessive reduction in blood pressure but more commonly occurs because the necessary rise in cardiac output and stroke volume fails to occur. Many severe pre-eclamptic/ eclamptic patients have a contracted intravascular blood volume, incompatible with a dilated vascu-lature. In these women, vasodilatation leads to falling venous return together with low preload and stroke volume. Clinically this may be evident when the pulse rate rises soon after commencing vasodilatation and typically leads to fetal distress and the development of oliguria. These adverse effects can be prevented by prior plasma volume expansion to increase ventricular preload. Plasma volume expansion on its own may have beneficial effects because it reduces vascular resistance, increases cardiac output and oxygen delivery to the peripheral tissues (Belfort et al., 1991). Plasma volume expansion is probably a more important determinant of the efficacy and safety of vasodilators than the specific characteristics of individual drugs themselves.

Plasma volume expansion, however, carries a risk of iatrogenic pulmonary edema. Patients with pre-eclampsia/eclampsia are susceptible to the development of pulmonary edema because left-sided ventricular filling pressures rise sharply in response to plasma volume expansion even when small volumes of fluid are infused (as little as 400-500ml of intravenous fluid). Right-sided filling pressures (central venous pressure) are not similarly affected and do not change rapidly in response to volume expansion. These disparate effects are reflected when monitoring central venous pressure and pulmonary artery pressure measurements. Hemodynamic monitoring based upon the use of central venous pressure lines only may be misleading and is likely to increase the risk of iatrogenic pulmonary edema. Despite these difficulties, volume expansion should precede vasodilatation using small aliquots of fluid (400 ml) and may take place without invasive monitoring if only one or two challenges are to be given. Those requiring greater volumes of fluid intravenously or those in positive fluid balance are less likely to develop pulmonary edema if the clinician has knowledge of the pulmonary capillary wedge pressure.

Hypertension that fails to respond to standard vasodilator therapy has been cited as an indication for invasive hemodynamic monitoring, the purpose of this being to distinguish hypertension due to high cardiac output from that which arises from elevated systemic vascular resistance. Treatment aimed at reducing a high cardiac output may seem counter-intuitive but life-threatening hypertension due to this cause should be treated with drugs such as labetalol rather than the more traditionally used calcium channel blockers and direct-acting vasodilators such as hydralazine or dihydralazine.

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