Motivated by a desire to understand pulmonary physiology, scientists have developed physiological lung models of varying complexity. However, pathophysiology and interactions between human lungs and ventilators, e.g., ventilator-induced lung injury (VILI), present challenges for modeling efforts. This is because the real-world pressure and volume signals may be too complex for simple models to capture, and while complex models tend not to be estimable with clinical data, limiting clinical utility. To address this gap, in this manuscript we developed a new damaged-informed lung ventilator (DILV) model. This approach relies on mathematizing ventilator pressure and volume waveforms, including lung physiology, mechanical ventilation, and their interaction. The model begins with nominal waveforms and adds limited, clinically relevant, hypothesis-driven features to the waveform corresponding to pulmonary pathophysiology, patient-ventilator interaction, and ventilator settings. The DILV model parameters uniquely and reliably recapitulate these features while having enough flexibility to reproduce commonly observed variability in clinical (human) and laboratory (mouse) waveform data. We evaluate the proof-in-principle capabilities of our modeling approach by estimating 399 breaths collected for differently damaged lungs for tightly controlled measurements in mice and uncontrolled human intensive care unit data in the absence and presence of ventilator dyssynchrony. The cumulative value of mean squares error for the DILV model is, on average, ā12 times less than the single compartment lung model for all the waveforms considered. Moreover, changes in the estimated parameters correctly correlate with known measures of lung physiology, including lung compliance as a baseline evaluation. Our long-term goal is to use the DILV model for clinical monitoring and research studies by providing high fidelity estimates of lung state and sources of VILI with an end goal of improving management of VILI and acute respiratory distress syndrome.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8517122 | PMC |
http://dx.doi.org/10.3389/fphys.2021.724046 | DOI Listing |
Sci Rep
November 2022
Department of Medical Biology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centres, Meibergdreef 15, 1105AZ, Amsterdam, The Netherlands.
Few experimental model systems are available for the rare congenital heart diseases of double inlet left ventricle (DILV), a subgroup of univentricular hearts, and excessive trabeculation (ET), or noncompaction. Here, we explore the heart of the axolotl salamander (Ambystoma mexicanum, Shaw 1789) as model system of these diseases. Using micro-echocardiography, we assessed the form and function of the heart of the axolotl, an amphibian, and compared this to human DILV (nā=ā3).
View Article and Find Full Text PDFFront Physiol
October 2021
Department of Bioengineering, University of Colorado Denver|Anschutz Medical Campus, Aurora, CO, United States.
Motivated by a desire to understand pulmonary physiology, scientists have developed physiological lung models of varying complexity. However, pathophysiology and interactions between human lungs and ventilators, e.g.
View Article and Find Full Text PDFEur J Cardiothorac Surg
June 2017
Heart Centre for Children, The Children's Hospital at Westmead, Sydney Children's Hospital Network, Westmead, NSW, Australia.
Objectives: In 2 subtypes of functional single ventricle, double inlet left ventricle (DILV) and tricuspid atresia with transposed great arteries (TA-TGA), systemic output passes through an outflow chamber before entering the aorta. Intracardiac obstruction to this pathway causing systemic outflow tract obstruction (SOTO) may be present at birth or develop over time. Long-term survival after Fontan has not been defined.
View Article and Find Full Text PDFDevelopment
November 2006
Division of Pediatric Cardiology, Department of Pediatrics, Vanderbilt Children's Hospital, Nashville, TN 37232, USA.
The transforming growth factorbeta (Tgfbeta) signaling pathway plays crucial roles in many biological processes. To understand the role(s) of Tgfbeta signaling during cardiogenesis in vivo and to overcome the early lethality of Tgfbr2(-/-) embryos, we applied a Cre/loxp system to specifically inactivate Tgfbr2 in either the myocardium or the endothelium of mouse embryos. Our results show that Tgfbr2 in the myocardium is dispensable for cardiogenesis in most embryos.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!