Audrey Hébert

Neonatal hemodynamics is an evolving field of newborn medicine focused on providing comprehensive physiological‐based approaches for the assessment and management of cardio‐pulmonary disorders in the critically ill neonate and infant. Training in neonatal hemodynamics requires a structured approach to echocardiography to ensure expertise in assessing cardiovascular function in critically ill neonates. This educational framework outlines a systematic approach to echocardiography laboratory training for Neonatal Hemodynamics trainees with a focus on competency in image acquisition, interpretation, and integration of findings into neonatal physiology. Training emphasizes hands‐on learning, direct supervision, and progressive assessments, with primary exposure to critically ill neonates and select cases in older pediatric patients to broaden diagnostic skills. By incorporating a structured echocardiography laboratory rotation and interdisciplinary collaboration, this framework aims to support the development of expertise in neonatal cardiovascular assessment.

Postnatal corticosteroids are frequently administered to extremely preterm infants to support respiratory management, yet their effects on the immature cardiovascular system are complex and underexplored. As the second installment in a series on physiology-informed steroid use, this narrative review focuses on the cardiovascular consequences of systemic corticosteroid therapy in preterm neonates. We examine how corticosteroids influence key aspects of cardiovascular physiology, including ductal closure, systemic and pulmonary vascular resistance, myocardial remodeling, and autonomic regulation. Attention is given to the hemodynamic transition of early postnatal life and how steroid exposure may interact with patency of the ductus arteriosus and vascular development. The potential for corticosteroids to contribute to reactive myocardial hypertrophy, systemic hypertension, and pulmonary hypertension is also reviewed in the context of both short- and long-term outcomes. Emerging diagnostic and monitoring tools are discussed for their potential to guide individualized therapy. These include targeted neonatal echocardiography (TnECHO) to assess cardiac function and structure, electrocardiography (ECG) for rhythm and conduction abnormalities, heart rate variability analysis for autonomic function, and circulating biomarkers to evaluate myocardial stress and inflammation. Together, these tools may inform tailored steroid timing and dosing, especially in the research context, while monitoring for signs of cardiovascular side effects in real time. By synthesizing mechanistic insights with evolving clinical evidence, this review highlights the need for a more nuanced understanding of how corticosteroids affect the developing cardiovascular system. It underscores the importance of integrating cardiovascular monitoring into routine care to optimize therapeutic benefit while minimizing unintended harm. Alongside companion reviews addressing respiratory and growth impacts, this installment contributes to a broader framework for individualized, physiology-driven steroid use in extremely preterm infants.

Chronic pulmonary hypertension (cPH) associated with bronchopulmonary dysplasia (BPD) is a major contributor to morbidity and mortality in extremely preterm infants. Despite improvements in neonatal care, the burden of BPD and its pulmonary vascular complications remains significant. Early detection and standardized management of cPH are essential to improve outcomes. Echocardiography plays a central role in screening and guiding treatment, particularly in high-risk infants requiring respiratory support at or beyond 36 weeks postmenstrual age. The Targeted Neonatal Echocardiography—Quebec (TnECHO-Qc) collaborative has developed a province-wide screening and management algorithm for cPH in preterm infants with BPD. This initiative outlines a stepwise approach to echocardiographic evaluation, including specific criteria for identifying elevated pulmonary arterial pressures, grading severity, and scheduling follow-up based on clinical and imaging findings. Additional management elements encompass biomarker use, respiratory and nutritional optimization, and consideration of airway anomalies, reflux, and aspiration. Pharmacologic therapies, including inhaled nitric oxide and pulmonary vasodilators, are considered for moderate to severe cPH with a pre-capillary component (“pulmonary arterial hypertension”) after stabilization of ventilation and oxygenation, and guided by echocardiography follow-up. This collaborative initiative establishes a standardized, multidisciplinary framework to enable timely recognition and individualized management of chronic pulmonary hypertension (cPH) in preterm infants. The primary goal is to reduce adverse outcomes and support long-term health, with the effectiveness of the framework to be evaluated through longitudinal outcome assessments.

Dopamine has been widely used as a first-line cardiovascular agent in neonatal intensive care units (NICUs) for the management of hypotension and circulatory support. While its effectiveness in increasing blood pressure is established, its potential effects on pulmonary vascular resistance, myocardial function, and overall hemodynamics require further consideration. This review explores the role of dopamine in neonatal hemodynamic management and considers alternative vasoactive agents tailored to specific pathophysiological conditions. A more individualized, physiology-based approach to cardiovascular support in neonates may help optimize treatment strategies.

Pulmonary hemorrhage (PH) is a life-threatening complication predominantly affecting preterm infants, particularly those with very low birth weight (VLBW) and fetal growth restriction (FGR). Typically occurring within the first 72 h of life, PH is characterized by acute respiratory deterioration and significant morbidity and mortality. This review synthesizes current evidence on the multifactorial pathogenesis of PH, highlighting the roles of immature pulmonary vasculature, surfactant-induced hemodynamic shifts, and left ventricular diastolic dysfunction. Key risk factors include respiratory distress syndrome (RDS), hemodynamically significant patent ductus arteriosus (hsPDA), sepsis, coagulopathies, and genetic predispositions. Diagnostic approaches incorporate clinical signs, chest imaging, lung ultrasound, and echocardiography. Management strategies are multifaceted and include ventilatory support—particularly high-frequency oscillatory ventilation (HFOV)—surfactant re-administration, blood product transfusion, and targeted hemostatic agents. Emerging therapies such as recombinant activated factor VII and antifibrinolytics show promise but require further investigation. Preventive measures like antenatal corticosteroids and early indomethacin prophylaxis may reduce incidence, particularly in high-risk populations. Despite advancements in neonatal care, PH remains a major contributor to neonatal mortality and long-term neurodevelopmental impairment. Future research should focus on individualized risk stratification, early diagnostic tools, and optimized treatment protocols to improve outcomes. Multidisciplinary collaboration and innovation are essential to advancing care for this vulnerable population.

Pulmonary hemorrhage (PH) is a life-threatening complication predominantly affecting preterm infants, particularly those with very low birth weight (VLBW) and fetal growth restriction (FGR). Typically occurring within the first 72 hours of life, PH is characterized by acute respiratory deterioration and significant morbidity and mortality. This review synthesizes current evidence on the multifactorial pathogenesis of PH, highlighting the roles of immature pulmonary vasculature, surfactant-induced hemodynamic shifts, and left ventricular diastolic dysfunction. Key risk factors include respiratory distress syndrome (RDS), hemodynamically significant patent ductus arteriosus (hsPDA), sepsis, coagulopathies, and genetic predispositions. Diagnostic approaches incorporate clinical signs, chest imaging, lung ultrasound, and echocardiography. Management strategies are multifaceted and include ventilatory support—particularly high-frequency oscillatory ventilation (HFOV)—surfactant re-administration, blood product transfusion, and targeted hemostatic agents. Emerging therapies such as recombinant activated factor VII and antifibrinolytics show promise but require further investigation. Preventive measures like antenatal corticosteroids and early indomethacin prophylaxis may reduce incidence, particularly in high-risk populations. Despite advancements in neonatal care, PH remains a major contributor to neonatal mortality and long-term neurodevelopmental impairment. Future research should focus on individualized risk stratification, early diagnostic tools, and optimized treatment protocols to improve outcomes. Multidisciplinary collaboration and innovation are essential to advancing care for this vulnerable population.

We read with great interest the article by Patel et al. on "Vasopressin-induced hyponatremia in infants <3 months of age in the neonatal intensive care unit" published in Frontiers in Pediatrics. 1 The authors have contributed valuable insights into the potential side effects, such as hyponatremia, of vasopressin use in neonates. Their findings underscore the importance of careful monitoring when vasopressin is used in neonatal intensive care units.On the contrary, clinicians should be cognizant of balancing these unintended risks and their impact on neonatal outcomes against the overall beneficial and potentially life-saving effects on pulmonary hemodynamics and right heart function.Of note, while the risk of hyponatremia is an important consideration, the end-organ consequences of vasopressin-related hyponatremia remain unknown. It is well recognized, however, that acute and severe hyponatremia may lead to serious complications, including cerebral edema, seizures, worsening of respiratory distress, and potential long-term neurodevelopmental impairments. 2 To better understand the clinical relevance of the observed hyponatremia we pose the following questions. First, are there data to suggest that hyponatremia, as described in this cohort, contributed to any adverse clinical outcomes in the index population? Second, did the presence of hyponatremia necessitate adjustments in clinical care, and if so, how were these addressed by the clinical team? Understanding whether interventions were employed to mitigate hyponatremia and whether these interventions led to improved outcomes would add depth to the discussion of the risks and benefits of vasopressin therapy. Prior studies on the use of vasopressin in newborns with refractory acute pulmonary hypertension provide some insights. For example, Ouellet et al. 3 , reported cases of hyponatremia but without evidence of potentially attributable clinical complications, such as seizures, worsening of intraventricular hemorrhage, and respiratory distress.It is noteworthy that, although not statistically significant, the incidence of hyponatremia was lowest in the last year of the study period. Readers may wonder whether this decrease is related to the learning curve related to vasopressin use, changes in the duration of vasopressin use over time, or adjustments in dosing protocols. Understanding the biologic nature of hyponatremia is an important consideration. At first glance, the nature of hyponatremia may be presumed to relate to decreased urinary output; however, higher doses of vasopressin promote natriuresis. 4 It would have been helpful to explore the relationship between the incidence of hyponatremia and maximal and cumulative dose of vasopressin, sodium intake, and urinary sodium losses. Therefore, it would be of interest to know if corrective measures for hyponatremia, such as fluid restriction or sodium supplementation, were systematically employed. Capolupo et al. described how early vasopressin infusion improved oxygenation in infants with congenital diaphragmatic hernia. In their cohort, resulting hyponatremia was managed in all 18/27 infants (66.7%) with fluid restriction: of them, 16/18 (88.9%) also received a careful supplementation of serum sodium during vasopressin administration. 5 Hyponatremia in this context can result from either salt loss, due to renal sodium wasting, or water retention, often related to vasopressin's antidiuretic effects. 2 Understanding the underlying mechanism is crucial, as management strategies differ; for example, water retention-induced hyponatremia may be managed with fluid restriction, while early and aggressive sodium supplementation is indicated in cases of salt loss. It is plausible that modification to care practices over time, either on an individual care basis or thought introduction of standardized care guidelines, may have impacted the frequency of hyponatremia.In summary, clinicians should be cognizant of the balance between managing side effects and optimizing the desired therapeutic effect which is key in critical care management, particularly in the NICU setting. Vasopressin remains a critical therapeutic agent in neonates, particularly for managing refractory hypotension and pulmonary hypertension; however, evidence remains limited to observational studies and clinical trials are lacking.Nevertheless, the potential benefits of vasopressin may outweigh the risks in some patients; therefore, accepting the possibility of hyponatremia and implementing strategies to mitigate risk may be a necessary sacrifice to achieve cardiovascular stability. We commend the authors for their important contribution to understanding the side effects of vasopressin in neonates, and we hope that these additional considerations can further enrich the discussion surrounding the use of Vasopressin in this population.

Introduction: Patent ductus arteriosus (PDA) is the most common cardiovascular problem that develops in extremely preterm infants and is associated with poor clinical outcomes. Uncertainty exists on whether early pharmacotherapeutic treatment of a clinically symptomatic and echocardiography-confirmed haemodynamically significant PDA in extremely preterm infants improves outcomes. Given the wide variation in the approach to PDA treatment in this gestational age (GA) group, a randomised trial design is essential to address the question. Before embarking on a large RCT in this vulnerable population, it is important to establish the feasibility of such a trial. Methods and analysis: Design: a multi-centre, open-labelled, parallel-designed pilot randomised controlled trial. Participants: preterm infants born Intervention (selective early medical treatment (SMART) strategy): selective early pharmacological treatment of a moderate-severe PDA shunt (identified based on pre-defined clinical signs and routine screening echocardiography) within the first 72 postnatal hours with provision for repeat treatment if moderate-severe shunt persists. Comparison (early conservative management strategy): no treatment of PDA in the first postnatal week. Primary outcomes: (1) proportion of eligible infants recruited during the study period; (2) proportion of randomised infants treated outside of protocol-mandated therapy. Sites and sample size: the study is being conducted in seven neonatal intensive care units across Canada and the USA with a target of 100 randomised infants. Analysis: the primary feasibility outcomes will be expressed as proportions. A pre-planned Bayesian analysis will be conducted for secondary clinical outcomes such as mortality, severe intraventricular haemorrhage, procedural PDA closure and chronic lung disease to aid stakeholders including parent representatives decide on the appropriateness of enrolling this vulnerable population in a larger trial if the feasibility of recruitment in the pilot trial is established. Ethics and dissemination: The study has been approved by the IWK Research Ethics Board (#1027298) and six additional participating sites. On the completion of the study, results will be presented at national and international meetings, published in peer-reviewed journals and incorporated into existing systematic reviews. Trial registration number: NCT05011149 (WHO Trial Registration Data Set in Appendix A). Protocol version: Ver 7.2 (dated July 19, 2023).

Background Premature infants are at risk for developing pulmonary hypertension (PH) in the context of bronchopulmonary dysplasia (BPD). Studies suggest a potential link between prolonged patent ductus arteriosus (PDA) exposure and BPD-PH, though management strategies remain controversial. Methods Retrospective echocardiographic evaluation of newborns p = 0.04). Markers of RV function (TAPSE and RV-FAC) were similar between groups. Conclusion In preterm infants <29 weeks with BPD, conservative PDA treatment policy was not associated with higher rate of pulmonary hypertension diagnosis. Impact The association between PDA-management approaches and the occurrence of BPD-associated pulmonary vascular disease in premature infants has sparsely been described. We found that a conservative policy, regarding the PDA, was not associated with an increase in pulmonary hypertension diagnosis. We identified that, in patients with BPD, echocardiographic metrics of LV performance were lower.

Background Acute pulmonary hypertension (aPH) in newborns can be life threatening and challenging to manage. In newborns with refractory aPH, there is currently limited therapeutic agents. Methods Retrospective single-center cohort study in newborns less than one month old who were treated with vasopressin for a minimum of one hour in the context of refractory aPH in the neonatal and pediatric intensive care units of a tertiary university center between 2016 and 2022. The objective was to evaluate the efficacy and safety of vasopressin in newborns as an adjuvant treatment for refractory aPH. Results Twenty-five patients met inclusion criteria. In patients who received vasopressin, oxygenation index improved from 28.4 to 14.4 (p = 0.004) after twelve hours of continuous infusion. Oxygen requirements (FiO₂) decreased from 0.91 to 0.50 (p = 0.004) and mean arterial pressure increased from 41 to 51 mmHg (p = 0.001). In our cohort, 68% of patients presented an episode of hyponatremia (serum sodium <130 mmol/L). Conclusions The use of vasopressin may be associated with improvement in oxygenation and hemodynamic status of neonatal patients with aPH refractory to initial therapy. Further prospective studies are needed to establish the safety profile of vasopressin in newborns, particularly in preterm infants. Impact Vasopressin may be an effective cardiotropic agent to improve oxygenation and hemodynamic status in newborns with acute pulmonary hypertension. Careful monitoring of serum sodium levels are warranted in newborns who are receiving vasopressin infusion. This provides additional evidence for the consideration of vasopressin in newborns with acute pulmonary hypertension refractory to inhaled nitric oxide.