The left ventricle in well newborns versus those with perinatal asphyxia, haemodynamically significant ductus arteriosus or fetal growth restriction.

Hemodynamic changes accompanying the initial breaths at the time of birth are especially important for a smooth transition of fetal to neonatal circulation. Understanding the normal transitional physiology and the clinical impact of adverse adaptation is important for delineating pathology so as to guide physiologically relevant therapies. Disorders such as severe perinatal asphyxia, hemodynamically significant patent ductus arteriosus (and its surgical ligation) and utero-placental insufficiency underlying fetal growth restriction, can adversely affect left ventricular (LV) function. The left ventricle is the predominant chamber involved in systemic perfusion during postnatal life. Cardiac output is closely linked to afterload; the latter is determined by arterial properties such as stiffness and compliance. This article outlines normal transition in term and preterm infants. It also highlights the adverse impact of three not uncommon neonatal disorders on LV function. Perinatal asphyxia leads to a reduced LV output, superior vena cava and coronary artery blood flow and an increase in the troponin level. Multiple haemodynamic changes are observed in the premature infant with a large patent ductus arteriosus. They need careful analysis to determine when ligation should proceed. Ligation itself generally results in a dramatic increase in afterload which may lead to a reduction in LV contractility and the need for ionotropic support. Fetal growth restricted infants have a higher systolic pressure, a somewhat hypertrophied heart arising from an increased arterial wall thickness/stiffness and systemic peripheral resistance. Point of care ultrasound (POCUS) helps differentiate normal transition and that resulting from neonatal disorders. It may be increasingly utilized in guiding management.