Neurocirculatory Asthenia

Birth is a major turning point in the life of the newborn, as it moves from intrauterine life to extrauterine life. This sudden transition forces the newborn to adapt quickly. Oxygenation, which was only provided by the placenta during uterine life, will have to be provided by the lungs, which will open when the newborn cries for the first time. This phenomenon will change the way blood reaches the lungs and will require the newborn's heart to work harder. In addition, the cardiac workload will also increase due to the clamping of the umbilical cord, which will force the heart to pump through more resistant blood vessels.
This transition, generally well tolerated in newborns at term, can be much more complicated in premature newborns, particularly in extremely low gestational age newborns (e.g. ELGAN, born before 28 weeks of amenorrhoea). There are several causes of this difficult adaptation on the cardiovascular system: poor heart function, difficulty in revascularizing lungs due to the physiological characteristics of premature newborns (high pulmonary vascular resistance, persistence of the ductus arteriosus), and a tone of the blood vessel muscles that is probably immature. In addition, respiratory failure is often associated with pulmonary immaturity.
The consequences of a difficult adaptation to extrauterine life, combined with cardiovascular failure, will be poor organ perfusion, whose brain. Moreover, ELGANs have immature regulation of their brain vascularisation. Variations in the vascularisation of the brain (in the event of cardiovascular failure) may be responsible for irreversible lesions with intraventricular hemorrhage. Ultimately, these bleedings carry a high risk of mortality or severe disability in premature infants.
Several hypotheses have been put forward as to the causes of this poor adaptation to extrauterine life, but there are few recommendations on adapted medical management. Cardiac ultrasound and the use of drugs to support the heart and blood vessels have been suggested. However, a large number of ELGANs will develop complications that investigators cannot predict or intervene in time. In addition, studies on the drugs used have not been carried out on ELGANs, which limits the conclusions investigators can draw.
These factors encourage us to improve our fundamental knowledge of the cardiovascular system in the ELGANs. The aim is to identify the most effective clinical tools and treatments for assessing and treating neonatal cardiovascular failure at an early stage, before complications appear. Investigators aim to compare the architecture and composition of the heart, blood vessels, and blood of fetuses under 28 weeks of amenorrhea gestation with those of fetuses over or equal to 34 weeks of amenorrhea gestation.
For this research, investigators need tissues (heart muscle, blood, and vessels) from fetuses of different ages. These tissues are usually already taken during the foetopathology examination to try to provide a medical explanation of the medical abortion. There will be no change to the foetopathology examination carried out on the foetus, with the exception that some of the tissue taken will have additional analyses carried out in our INSERM laboratory attached to the Montpellier University Hospital.
Population resulting from medical abortion is motivated by the ethical impossibility of taking such invasive samples from live newborns. The non-use of animals is justified by the difficulty of extrapolating results to humans. The indication for abortion and its performance will be carried out by current practice. Participants will be offered and explained the study during the pre abortion visit.
This research does not alter the patient's care. No additional examination or consultation is required. No personal benefit is expected from the study, but it will enable us to gain a better understanding of ELGAN's hemodynamics and to consider future clinical studies.

Modern intensive care units (ICUs) are increasingly adopting newer modes of mechanical ventilation such as adaptive pressure control (APC) modes but there are limited data available regarding risks and benefits of newer modes versus traditional ventilation modes. APC can inadvertently deliver high tidal volumes, which maybe harmful. High tidal volumes may be unrecognized by the provider, due to the complexities of ventilator algorithms and patient interactions. The objective of this aim is to identify risk factors for excess tidal volumes in patients on adaptive pressure control.

Intracranial hemorrhage is a condition characterized by high mortality rates and suboptimal functional outcomes. It precipitates both direct brain injury and subsequent secondary injuries, including delayed cerebral ischemia, brain edema, and hydrocephalus. Complications such as cardiac injury may also arise, categorizing them within the cerebrocardiac syndrome (CCS). The clinical spectrum of CCS encompasses acute myocardial injury, acute coronary syndrome, left ventricular systolic and diastolic dysfunction, cardiac arrhythmias, and sudden cardiac death, all of which are associated with increased mortality and deterioration in patient status. The precise pathophysiological mechanisms underlying both cerebral and cardiac injuries remain enigmatic, and the implications for diagnosis and therapeutic strategies are yet to be fully explored.
In this study, we propose to enroll patients with intracranial hemorrhage who will undergo conventional treatment and comprehensive multidisciplinary evaluations. Our observational research is grounded in a multimodal omics and imaging approach, aimed at investigating both local and systemic injuries subsequent to intracranial hemorrhage. This comprehensive strategy is intended to facilitate precise diagnosis, risk stratification, and clinical decision-making, while also shedding light on the pathophysiological mechanisms involved.
The primary objectives of this research are to address the following key questions:
* [Question 1] What are the pathophysiological mechanisms underlying cardiac injury in patients with intracranial hemorrhage?
* [Question 2] What are the pathophysiological mechanisms responsible for early and delayed brain injuries following intracranial hemorrhage?"