Dataset Information

Repeated endo-tracheal tube disconnection generates pulmonary edema in a model of volume overload: an experimental study.

ABSTRACT:

Background

An abrupt lung deflation in rodents results in lung injury through vascular mechanisms. Ventilator disconnections during endo-tracheal suctioning in humans often cause cardio-respiratory instability. Whether repeated disconnections or lung deflations cause lung injury or oedema is not known and was tested here in a porcine large animal model.

Methods

Yorkshire pigs (~ 12 weeks) were studied in three series. First, we compared PEEP abruptly deflated from 26 cmH₂O or from PEEP 5 cmH₂O to zero. Second, pigs were randomly crossed over to receive rapid versus gradual PEEP removal from 20 cmH₂O. Third, pigs with relative volume overload, were ventilated with PEEP 15 cmH₂O and randomized to repeated ETT disconnections (15 s every 15 min) or no disconnection for 3 h. Hemodynamics, pulmonary variables were monitored, and lung histology and bronchoalveolar lavage studied.

Results

As compared to PEEP 5 cmH₂O, abrupt deflation from PEEP 26 cmH₂O increased PVR, lowered oxygenation, and increased lung wet-to-dry ratio. From PEEP 20 cmH₂O, gradual versus abrupt deflation mitigated the changes in oxygenation and vascular resistance. From PEEP 15, repeated disconnections in presence of fluid loading led to reduced compliance, lower oxygenation, higher pulmonary artery pressure, higher lung wet-to-dry ratio, higher lung injury score and increased oedema on morphometry, compared to no disconnects.

Conclusion

Single abrupt deflation from high PEEP, and repeated short deflations from moderate PEEP cause pulmonary oedema, impaired oxygenation, and increased PVR, in this large animal model, thus replicating our previous finding from rodents. Rapid deflation may thus be a clinically relevant cause of impaired lung function, which may be attenuated by gradual pressure release.

SUBMITTER: Katira BH

PROVIDER: S-EPMC8857825 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Repeated endo-tracheal tube disconnection generates pulmonary edema in a model of volume overload: an experimental study.

Katira Bhushan H BH Engelberts Doreen D Bouch Sheena S Fliss Jordan J Bastia Luca L Osada Kohei K Connelly Kim A KA Amato Marcelo B P MBP Ferguson Niall D ND Kuebler Wolfgang M WM Kavanagh Brian P BP Brochard Laurent J LJ Post Martin M

Critical care (London, England) 20220218 1

<h4>Background</h4>An abrupt lung deflation in rodents results in lung injury through vascular mechanisms. Ventilator disconnections during endo-tracheal suctioning in humans often cause cardio-respiratory instability. Whether repeated disconnections or lung deflations cause lung injury or oedema is not known and was tested here in a porcine large animal model.<h4>Methods</h4>Yorkshire pigs (~ 12 weeks) were studied in three series. First, we compared PEEP abruptly deflated from 26 cmH<sub>2</su ...[more]

PMID: 35180891

Similar Datasets

Project description:BackgroundTracheostomy tube capping is a commonly used test to determine if the tracheostomy tube can be removed. The success of the capping trial depends on the patient's ability to maintain sufficient spontaneous breathing with an occluded tracheostomy tube. The impact of an occluded tracheotomy tube on airway resistance is currently unknown. The aim of this study was to investigate tracheal pressure during capping or stoma button insertion and potential determinants concerning cuff.MethodsEight cuffed and uncuffed tracheostomy tubes and three stoma buttons of various manufacturers and sizes were inserted into the trachea model. Cuffs were completely deflated or contained atmospheric pressure. The trachea was ventilated bidirectional with a respirator in volume-controlled mode and volume flows 15-60 L/min. Tracheal pressure drop during inspiration as a parameter of pressure required to move gas through the airway was measured.ResultsTracheal pressure drops occurred linearly or irregularly during capping trials to a maximum of 4.2 kPa at flow rates of 60 L/min for atmospheric pressure cuffs. In tracheostomy tubes with completely deflated cuffs, pressure drop in the trachea reaches a maximum of 3.4 kPa at a flow rate of 60 L/min. For tracheostomy tubes with cuff smaller inner or outer diameters do not regularly result in lower tracheal pressure drop. The pressure drop varies between different tracheostomy tubes depending on the manufacturer. In cuffed tracheostomy tubes, we observed three phenomena: sail-like positioning, folding over, and tightening of the cuff during flow. The maximum tracheal pressure drop during stoma button insertion reaches 0.014 kPa.ConclusionsThe cuff is a central element for the pressure drop in the airway and thus airway resistance during spontaneous translaryngeal breathing with a capped TT. Complete deflation reduces the pressure drop in the trachea. Due to deformation of the cuff, measured pressures are irregular as the volume flow is increased. Incomplete deflated cuffs and material characteristics of tracheostomy tubes and cuffs in addition to anatomical and clinical variables may cause unsuccessful capping trials due to increased airway resistance. All stoma buttons showed that pressure drop and thus airway resistance due to stoma buttons has no clinical relevance.

Project description:Mechanisms that contribute to myocardial fibrosis, particularly in response to left ventricular pressure overload (LVPO), remain poorly defined. To test the hypothesis that a myocardial-specific profile of secreted factors is produced in response to PO, levels of 44 factors implicated in immune cell recruitment and function were assessed in a murine model of cardiac hypertrophy and compared with levels produced in a model of pulmonary fibrosis (PF). Mice subjected to PO were assessed at 1 and 4 wk. Protein from plasma, LV, lungs, and kidneys were analyzed by specific protein array analysis in parallel with protein from mice subjected to silica-instilled PF. Of the 44 factors assessed, 13 proteins were elevated in 1-wk PO myocardium, whereas 18 proteins were found increased in fibrotic lung. Eight of those increased in 1-wk LVPO were not found to be increased in fibrotic lungs (CCL-11, CCL-12, CCL-17, CCL-19, CCL-21, CCL-22, IL-16, and VEGF). Additionally, six factors were increased in plasma of 1-wk LVPO in the absence of increases in myocardial levels. In contrast, in mice with PF, no factors were found increased in plasma that were not elevated in lung tissue. Of those factors increased at 1 wk, only TIMP-1 remained elevated at 4 wk of LVPO. Immunohistochemistry of myocardial vasculature at 1 and 4 wk revealed similar amounts of total vasculature; however, evidence of activated endothelium was observed at 1 wk and, to a lesser extent, at 4 wk LVPO. In conclusion, PO myocardium generated a unique signature of cytokine expression versus that of fibrotic lung.NEW & NOTEWORTHY Myocardial fibrosis and the resultant increases in myocardial stiffness represent pivotal consequences of chronic pressure overload (PO). In this study, cytokine profiles produced in a murine model of cardiac fibrosis induced by PO were compared with those produced in response to silica-induced lung fibrosis. A unique profile of cardiac tissue-specific and plasma-derived factors generated in response to PO are reported.

Project description:IntroductionLeakage of orogastric secretions past the cuff of a tracheal tube is a contributory factor in ventilator-associated pneumonia. Current bench test methods specified in the International Standard for Anaesthetic and Respiratory Equipment (EN ISO 5361:2023) to test cuff leakage involve using a glass or plastic rigid cylinder model of the trachea. There is a need for more realistic models to inform cuff leakage.MethodsWe used human computerised tomography data and additive manufacturing (3D printing), combined with casting techniques to fabricate a bio-inspired synthetic tracheal model with analogous tissue characteristics. We conducted cuff leakage tests according to EN ISO 5361:2023 and compared results for high-volume low-pressure polyvinyl chloride and polyurethane cuffs between the rigid cylinder trachea with our bio-inspired model.ResultsThe tracheal model demonstrated close agreement with published tracheal tissue hardness for cartilaginous and membranous soft tissues. For high-volume low-pressure polyvinyl chloride cuffs the leakage rate was >50% lower in the bio-inspired tracheal model compared with the rigid cylinder model (151 [8] vs 261 [11] ml h-1). For high-volume low-pressure polyurethane cuffs, much lower leakage rates were observed than polyvinyl chloride cuffs in both models with leakage rates higher for the bio-inspired trachea model (0.1 [0.2] vs 0 [0] ml h-1).ConclusionA reproducible tracheal model that incorporates the mechanical properties of the human trachea can be manufactured from segmented CT images and additive manufactured moulds, providing a useful tool to inform future cuff development, leakage testing for industrial applications, and clinical decision-making. There are differences between cuff leakage rates between the bio-inspired model and the rigid cylinder recommended in EN ISO 5361:2023. The bio-inspired model could lead to more accurate and realistic cuff leakage rate testing which would support manufacturers in refining their designs. Clinicians would then be able to choose better tracheal tubes based on the outcomes of this testing.

Dataset Information

Repeated endo-tracheal tube disconnection generates pulmonary edema in a model of volume overload: an experimental study.

Background

Methods

Results

Conclusion

Publications

Repeated endo-tracheal tube disconnection generates pulmonary edema in a model of volume overload: an experimental study.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets