The impact of preterm adversity on cardiorespiratory function

Abstract

Preterm birth is one of the leading causes of neonatal mortality. Babies that survive early-life stress associated with immaturity have significant prevailing short-and long-term morbidities. Oxygen dysregulation in the first few days and weeks after birth is a primary concern as the cardiorespiratory system slowly adjusts to extrauterine life. Infants exposed to rapid alterations in oxygen tension, including exposures to hypoxia and hyperoxia, have altered redox balance and active immune signalling, leading to altered stress responses that impinge on neurodevelopment and cardiorespiratory homeostasis. In this review, we explore the clinical challenges posed by preterm birth, followed by an examination of the literature on animal models of oxygen dysregulation and immune activation in the context of early-life stress.

Vital sign metrics of VLBW infants in three NICUs: implications for predictive algorithms

“…HR and SpO 2 are affected not only by illness and stress, but also by maturation and by clinical care practices such as mode of respiratory support (15)(16)(17). Different bedside monitor hardware and sensors may also contribute to differences in vital sign measurements across units.…”

Comparative assessment of myocardial function between late premature newborns and term neonates using the 2D speckle tracking method

“…Premature newborns also present several specific pathologies, such as hemodynamically significant PDA, pulmonary conditions which cause hypoxemia, including bronchopulmonary dysplasia. These conditions increase in frequency among the extremely premature infants ( 11 , 12 ). As a result, ventricular filling changes and an increase in afterload occurs, especially for the right ventricle ( 12 ).…”

“…These conditions increase in frequency among the extremely premature infants ( 11 , 12 ). As a result, ventricular filling changes and an increase in afterload occurs, especially for the right ventricle ( 12 ). As we have seeked to establish reference values which are not influenced by prematurity- associated pathology, we excluded from our study premature newborns with sepsis, pulmonary hypertension, bronchopulmonary dysplasia, persistent ductus arteriosus, or other cardiac malformations with hemodynamic impact.…”

Epigenetic silencing by early‐life hypoxic stress programmes respiratory motor control

“…An increased understanding of the complex relationship between DNA methylation and site-specific modifications in respiratory neural control networks will advance our appreciation of the notably deleterious impact of early-life exposures to hypoxic stress on cardiorespiratory control. Additional translational studies of oxygen dysregulation (intermittent hypoxia and hyperoxia) combined with other recognized risk factors, such as infection/inflammation (Hocker et al, 2019;McDonald, Dempsey, & O'Halloran, 2020), are required to characterize fully the portfolio of potential drivers of epigeneticdependent and independent mechanisms of respiratory morbidity across the lifespan. Such translational studies will further shape our understanding of the pivotal role of oxygen dysregulation as a driver of cardiorespiratory malaise, with the potential to inform interventional strategies in the clinical setting.…”