Preeclampsia is a multisystem pregnancy disease defined as new onset hypertension with proteinuria, organ dysfunction, or both after 20 weeks gestation. It can affect the brain, the kidneys, the liver, the hematological system, the lungs, and the placenta. Preeclampsia can be classified as antenatal, early antenatal if it occurs before 34 weeks gestation, late antenatal if it occurs at 34 weeks or later, and postnatal. Preeclampsia is believed to be caused by poor placental implantation and immunological involvement which cause vascular inflammation and endothelial dysfunction. Preterm birth and intrauterine growth restriction are among the most common perinatal outcomes of preeclampsia. It can also cause stillbirth. There are two different phenotypes of preeclampsia: preeclampsia with fetal growth restriction and preeclampsia without fetal growth restriction. Preeclampsia with fetal growth restriction is characterized by low cardiac output and high peripheral vascular resistance, whereas preeclampsia without fetal growth restriction is characterized by high cardiac output and low peripheral vascular resistance. Acetylsalicylic acid is the only evidence-based preventive drug treatment for preeclampsia. Should preeclampsia occur at 37 weeks gestation or later, initiating birth is the only suitable therapy. Preeclampsia management protocols suggest antihypertensive drug therapy to reduce blood pressure. The hypothesis of two phenotypes of preeclampsia offers personalized therapy approach possibilities depending on the cardiac parameters of the mother.