[Circulatory and respiratory problems in preeclampsia]

Abstract

The hemodynamic and cardiovascular changes seen during PE vary according to the natural history of the disease, its severity and eventual therapeutic measures taken. In the early stages of pregnancy, patients who will eventually develop PE, present with a blood pressure which even though within normal limits, is higher than in other women. Similarly, their cardiac output is higher with a normal or decreased peripheral vascular resistance. As soon as the clinical signs of the disease appear, the hemodynamic picture usually shifts toward that of a high peripheral resistance with low cardiac output. Sometimes however, a clinically hyperkinetic circulation may be demonstrated. In PE patients, cardiac preload pressures are usually normal even though the circulatory volumes are lower by 600 to 800 ml when compared to those found in normal pregnancy. The cardiac function is however usually preserved during PE. PE induces an exaggerated capillary permeability. This results in the worsening of the airway edema which may render the intubation very difficult. The increased capillary permeability contributes, among other factors, to the heightened risk of acute pulmonary edema. It is not justified to administer an anti-hypertensive treatment to PE women presenting with only moderate hypertension. An anti-hypertensive treatment must only be initiated whenever the hypertension is severe (i.e. SBP> or =160 mmHg and/or DBP> or =110 mmHg) in order to reduce the risk of maternal complications. In the absence of objective comparative data assessing anti-hypertensive agents for the PE patient, the choice of therapy relies predominantly on the practitioners' own experience. Systematic circulatory volume expansion has not been proven to improve the maternal nor the neonatal prognosis. Such treatment is to be reserved solely for situations in which correcting a hypo-volemia is absolutely necessary. The treatment of acute pulmonary edema in a PE patient is symptomatic and includes the administration of vasodilating agents and of diuretics. A benefit in setting-up an invasive monitoring of the pulmonary artery occlusive pressure has not been demonstrated. The sonographic surveillance of the hemodynamic state can however be useful in these circumstances.