lung disease, retinopathy of prematurity, or intraventricular hemorrhage Initial resuscitation using 21% to 30% oxygen is recommended Once saturation monitoring is established, the use of an oxygen blender to titrate delivery to achieve saturations comparable with a term neonate at a similar age following birth is recommended Regulation of Myocardial Performance Architecture of the Myocyte Fetal myocardial tissue consists of 70% noncontractile tissue, compared with 40% in the mature adult heart Histologic studies have shown that the myocytes making up the left ventricular myocardium are aligned circumferentially in the mid wall and longitudinally in the subepicardial and subendocardial layers of the walls.35,36 Studies of isolated myocardial tissue in fetal and adult lambs suggest that fetal myocardium is less compliant Ventricular myocytes change considerably as they transition from fetal to postnatal life The immature sarcomere and contractile apparatus is relatively disorganized Myofibrils are irregular and scattered along the interior of the cell Intrauterine and early postnatal cardiac growth is a combination of both hyperplasia and hypertrophy Exposure of the developing rodent heart to dexamethasone led to cardiac hypertrophy, characterized by myocytes that were longer and wider, with increased volume.37 Biventricular hypertrophy is a recognized complication of exposure of the preterm myocardium to prolonged and high doses of steroids.38 Neonates born to mothers who had received a single antenatal course of steroids had higher systolic blood pressures and increased myocardial thickness, suggesting modified myocardial development.39 The nature of these changes may relate to earlier transition from a phase of hyperplasia to hypertrophy The functional consequence of an enlarged hypertrophic myocardium, with a reduced overall number of myocytes, is unknown Activation of the Myocyte In contrast to adults, immature myocytes lack transverse tubules, are smaller in size, and have a greater ratio of surface area to volume.40 They are more reliant on transsarcolemmal fluxes of calcium for contraction and relaxation.41 The high ratio of surface area to volume, and the subsarcolemmal location of myofibrils, support direct calcium delivery to and from the contractile proteins The sodiumcalcium exchanger is the major conduit for attachment of calcium to, and release from, the contractile elements.42 Control of Myocytic Activation The control mechanisms governing contraction and relaxation in the immature heart are poorly understood but thought to be substantially different from the fully mature heart In the mature heart, graded control of release of calcium is related to so-called L-type activity, which triggers release from the sarcoplasmic reticulum Graded control of release in immature myocytes is thought to be related to factors influencing the activity of the sodium-calcium channel Recently isoproterenol-induced β-adrenergic stimulation of sodium-calcium exchanger was identified in guinea pig ventricular myocytes An improved understanding of factors that govern myocardial contractility and relaxation may facilitate more physiologically appropriate choice of therapeutic interventions in premature infants Performance and Physiology of the Immature Myocardium At physiologic heart rates, the immature myocardium shows a positive relationship, albeit that contractility falls with extreme tachycardia Both the force-rate trajectory and the optimal heart rate reflect myocytic function and global myocardial contractile behavior Developmentally, the immature myocardium has been shown to exhibit a higher basal contractile state and a greater sensitivity to changes in afterload.43,44 The intolerance of the immature myocardium to increased afterload may be attributable to differences in myofibrillar architecture, or immaturity of receptor development or regulation.45 The Frank-Starling law appears less applicable to the immature myocardium.46