Maternal cardiovascular deterioration in severe pre-eclampsia is due to a combination of factors in the setting of severe trophoblastic ischaemia and the outpouring of maternal cathecolamines, leading to increased left ventricular afterload and increasing ventricular volumes, resulting in increased left ventricular stroke work and demand myocardial ischaemia. This is the substrate for ventricular arrhythmias. Foetal cardiac dysfunction is most likely on the basis of the increased afterload, consequent upon widespread vasoconstriction, due to angiogenic imbalances. In this integrated model, chronic trophoblastic ischaemia is the central role player by releasing vasoactive substances that induce haemodynamic alterations in the maternofoetal complex, augmented and modified by 'latent' maternal cardiovascular dysfunction and increased maternal cathecolamine secretion on the one hand, and altered foetal signalling mechanisms on the other, all three components of the materno-placental-foetal complex being in constant interaction with each other. This unified hypothesis may explain the development of both maternal and foetal morbidity and/or mortality on a unitary basis in severe, complicated preeclampsia.