We describe the placement of a left ventricular assist device (LVAD) in a pig with spontaneously occurring atrial septal defect (ASD) (incidental finding) that created a right-left cardiac shunt, with subsequent severe hypoxaemia. Early diagnosis was critical in order to prevent end-organ damage due to hypoxaemia. Adequate monitoring alerted us to the deterioration in oxygenation, haemodynamics and cerebral oxygen metabolism. This forced us to change the level of assistance provided by the pump, and thus dramatically correct this impairment. Necropsy revealed an ostium secundum ASD. In conclusion, if hypoxaemia presents after implementation of an LVAD, the presence of a right-left shunt must be ruled out. The first step must be a judicious reduction in assist device flow to minimize intracardiac shunting. Subsequently, atrial septal closure of the defect should be considered. We report an experimental model of severe hypoxaemia after placement of an LVAD as part of a larger research project.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1258/la.2011.011067 | DOI Listing |
Front Mol Biosci
January 2025
Research Department, Children's Cancer Hospital Egypt, Cairo, Egypt.
Introduction: COVID-19 severity and high in-hospital mortality are often associated with severe hypoxemia, hyperlactatemia, and acidosis, yet the key players driving this association remain unclear. It is generally assumed that organ damage causes toxic acidosis, but since neutrophil numbers in severe COVID-19 can exceed 80% of the total circulating leukocytes, we asked if metabolic acidosis mediated by the glycolytic neutrophils is associated with lung damage and impaired oxygen delivery in critically ill patients.
Methods: Based on prospective mortality outcome, critically ill COVID-19 patients were divided into ICU- survivors and ICU-non-survivors.
Int J Dev Neurosci
February 2025
Department of Digestive and Nutrition, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe neurological injury during infancy, often resulting in long-term cognitive deficits. This study aimed to investigate the neuroprotective effects of Edaravone (EDA), a free radical scavenger, and elucidate the potential role of brain-derived neurotrophic factor (BDNF) in mediating these effects in neonatal HIE rats. Using the Rice-Vannucci model, HIE was induced in neonatal rats, followed by immediate administration of EDA after the hypoxic-ischemic insult.
View Article and Find Full Text PDFCurr Opin Pediatr
December 2024
Division of Neonatology, Montreal Children's Hospital, McGill University Health Center, Montreal, Quebec, Canada.
Purpose Of Review: This review outlines the prevalence and complications of apneas and intermittent hypoxemic events in preterm infants, examines current monitoring limitations in neonatal ICUs (NICUs), and explores emerging technologies addressing these challenges.
Recent Findings: New evidence from the Prematurity-Related Ventilatory Control (Pre-Vent) study, which analyzed cardiorespiratory data from 717 extremely preterm infants, exposes the varying frequency, duration, and severity of apneas, intermittent hypoxemia, bradycardias, and periodic breathing during hospitalization, and highlights the negative impact of intermittent hypoxemia on pulmonary outcomes at discharge. Although traditional monitoring methods cannot differentiate between apnea types and quantify their burden, recent advancements in sensor technologies and data integration hold promise for improving real-time detection and evaluation of apneas in the NICU.
Unlabelled: The rapid growth that occurs during larval development requires a dramatic rewiring of central carbon metabolism to support biosynthesis. Larvae achieve this metabolic state, in part, by coordinately up-regulating the expression of genes involved in carbohydrate metabolism. The resulting metabolic program exhibits hallmark characteristics of aerobic glycolysis and establishes a physiological state that supports growth.
View Article and Find Full Text PDFBone fracture ruptures blood vessels and disrupts the bone marrow, the site of new red blood cell production (erythropoiesis). Current dogma holds that bone fracture causes severe hypoxia at the fracture site, due to vascular rupture, and that this hypoxia must be overcome for regeneration. Here, we show that the early fracture site is not hypoxic, but instead exhibits high oxygen tension (> 55 mmHg, or 8%), similar to the red blood cell reservoir, the spleen.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!