scholarly journals P1‐79: Diaphragm dysfunction developed after COVID‐19 infection without pneumonia

Respirology ◽  
2021 ◽  
Vol 26 (S3) ◽  
pp. 106-106
Keyword(s):  
Diaphragm Dysfunction

Ventilator Weaning

2018 ◽  
Author(s):  
Brian Brajcich ◽  
Ann Hwalek ◽  
Joseph Posluszny
Keyword(s):  
Respiratory Mechanics ◽  
Spontaneous Breathing Trial ◽  
Clinical Status ◽  
Ventilator Weaning ◽  
Evidence Based ◽  
Airway Patency ◽  
Diaphragm Dysfunction ◽  
Complex Process ◽  
Abcde Bundle ◽  
Based Medicine

Ventilator weaning/liberation is a complex process that requires focus on a patient’s respiratory mechanics, strength, awareness, airway patency, and secretions while also keeping in mind a patient’s overall clinical status and critical illness. The recommendations in the chapter are based on evidence-based medicine when available. When no clear data can definitively guide patient management, clinical guidelines and accepted practices are described.  Our hope is that the reader finds this chapter as a reliable and safe way to approach ventilator liberation. This review contains 4 figures, 6 tables and 77 references Key Words: ABCDE bundle, diaphragm dysfunction, negative inspiratory force, reintubation, RSBI, sedation, spontaneous breathing trial, tracheostomy, ventilator liberation, ventilator weaning

scholarly journals Ventilator-induced diaphragm dysfunction in critical illness

2018 ◽  
Vol 243 (17-18) ◽  
pp. 1331-1339 ◽  
Author(s):  
Yung-Yang Liu ◽  
Li-Fu Li
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Muscle Atrophy ◽  
Structural Damage ◽  
Molecular Mechanisms ◽  
Substantial Reduction ◽  
Mechanical Stretch ◽  
Janus Kinase ◽  
Diaphragm Muscle ◽  
Diaphragm Dysfunction

Mechanical ventilation is an essential intervention for intensive care unit patients with acute lung injury. However, the use of controlled mechanical ventilation in both animal and human models causes ventilator-induced diaphragm dysfunction, wherein a substantial reduction in diaphragmatic force-generating capacity occurs, along with structural injury and atrophy of diaphragm muscle fibers. Although diaphragm dysfunction, noted in most mechanically ventilated patients, is correlated with poor clinical outcome, the specific pathophysiology underlying ventilator-induced diaphragm dysfunction requires further elucidation. Numerous factors may underlie this condition in humans as well as animals, such as increased oxidative stress, calcium-activated calpain and caspase-3, the ubiquitin–proteasome system, autophagy–lysosomal pathway, and proapoptotic proteins. All these alter protein synthesis and degradation, thus resulting in muscle atrophy and impaired contractility and compromising oxidative phosphorylation and upregulating glycolysis associated with impaired mitochondrial function. Furthermore, infection combined with mechanical stretch may induce multisystem organ failure and render the diaphragm more sensitive to ventilator-induced diaphragm dysfunction. Herein, several major cellular mechanisms associated with autophagy, apoptosis, and mitochondrial biogenesis—including toll-like receptor 4, nuclear factor-κB, Src, class O of forkhead box, signal transducer and activator of transcription 3, and Janus kinase—are reviewed. In addition, we discuss the potential therapeutic strategies used to ameliorate ventilator-induced diaphragm dysfunction and thus prevent delay in the management of patients under prolonged duration of mechanical ventilation. Impact statement Mechanical ventilation (MV) is life-saving for patients with acute respiratory failure but also causes difficult liberation of patients from ventilator due to rapid decrease of diaphragm muscle endurance and strength, which is termed ventilator-induced diaphragmatic damage (VIDD). Numerous studies have revealed that VIDD could increase extubation failure, ICU stay, ICU mortality, and healthcare expenditures. However, the mechanisms of VIDD, potentially involving a multistep process including muscle atrophy, oxidative loads, structural damage, and muscle fiber remodeling, are not fully elucidated. Further research is necessary to unravel mechanistic framework for understanding the molecular mechanisms underlying VIDD, especially mitochondrial dysfunction and increased mitochondrial oxidative stress, and develop better MV strategies, rehabilitative programs, and pharmacologic agents to translate this knowledge into clinical benefits.

scholarly journals Attenuation of ventilation-induced diaphragm dysfunction through toll-like receptor 4 and nuclear factor-κB in a murine endotoxemia model

2018 ◽  
Vol 98 (9) ◽  
pp. 1170-1183 ◽  
Author(s):  
Li-Fu Li ◽  
Yung-Yang Liu ◽  
Ning-Hung Chen ◽  
Yen-Huey Chen ◽  
Chung-Chi Huang ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Diaphragm Dysfunction ◽  
Endotoxemia Model

scholarly journals Comparative Efficacy of Angiotensin II Type 1 Receptor Blockers Against Ventilator‐Induced Diaphragm Dysfunction in Rats

2020 ◽  
Author(s):  
Stephanie E. Hall ◽  
Bumsoo Ahn ◽  
Ashley J. Smuder ◽  
Aaron B. Morton ◽  
J. Matthew Hinkley ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Comparative Efficacy ◽  
Diaphragm Dysfunction ◽  
Receptor Blockers

Assessment of diaphragm dysfunction during cardiac rehabilitation after heart surgery: the role of ultrasound imaging

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
F Maranta ◽  
V Rizza ◽  
I Cartella ◽  
S Pellegrino ◽  
A Bonaccorso ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Functional Recovery ◽  
Heart Surgery ◽  
Respiratory Cycle ◽  
Invasive Technique ◽  
Valve Repair ◽  
Combined Surgery ◽  
Diaphragm Dysfunction ◽  
Diaphragm Function ◽  
The Right

Abstract Background Diaphragm dysfunction is a frequent and underdiagnosed complication of cardiac surgery. It can cause dyspnoea, decreased exercise performance and, in more severe cases, respiratory failure. Ultrasonography (US) is a valuable, non-invasive technique for the assessment of diaphragm function. Only few trials have been conducted using US to evaluate diaphragm functional recovery after cardiovascular rehabilitation (CR). Purpose The aim of the study was to assess with US the incidence of diaphragm dysfunction after heart surgery and to define the impact of an inpatient CR programme on diaphragm functional recovery. Methods We performed a single-centre prospective cohort study, enrolling 185 patients hospitalized in our CR unit: 99 patients underwent mitral valve repair or replacement, 28 tricuspid valve repair or replacement, 53 aortic valve replacement, 30 coronary artery bypass grafting, 59 combined surgery and 14 other surgical procedures. Diaphragm US was performed at admission and after 10 rehabilitative sessions. We assess the following parameters on quiet breathing: excursion, time of inspiration, time of a respiratory cycle and contraction velocity (slope) in M-mode on the right anterior subcostal projections and thickening fraction (TF) in B-mode on the right intercostal projections. TF was defined as [(thickness at end inspiration–thickness at end expiration)/thickness at end expiration]. Results The median excursion at admission was 1.6 cm. Patients with excursion <2 cm (lower limit for the general population) were considered with diaphragm dysfunction. Following cardiac surgery, the incidence of diaphragm dysfunction was 70.8%. Patients with excursion <2 cm at admission gained an important benefit from CR, with a significant improvement in TF (p<0.001), excursion (p<0.001), time of inspiration (p<0.001), time of a respiratory cycle (p<0.001) and slope (p<0.001). Conversely, in patients with excursion ≥2 cm there was no significant improvement in slope (p=0.539) and excursion (p=0.179). At the final assessment, diaphragm function recovered in 50.5% of the patients, whilst 49.5% had a failure of recovery (excursion relative change between admission and discharge <33%). The multivariate analysis identified combined surgery (OR 3.08; 95% CI 1.59–5.99, p=0.001) and post-surgical pneumothorax (OR 3.05; 95% CI 1.23–7.55, p=0.036) as independent predictors of failure of diaphragm function recovery. Conclusions US might be a valuable tool for initial and follow-up assessment of patients after cardiac surgery. CR has been shown to be an effective strategy to improve diaphragm parameters in patients with post-surgical dysfunction. Patients undergoing combined surgery or developing post-surgical pneumothorax might benefit from a personalised rehabilitation programme to improve diaphragm function. Funding Acknowledgement Type of funding source: None

scholarly journals Magnesium sulfate ameliorates sepsis-induced diaphragm dysfunction in rats via inhibiting HMGB1/TLR4/NF-κB pathway

Neuroreport ◽  
2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Jihong Jiang ◽  
Qi Chen ◽  
Xia Chen ◽  
Jinbao Li ◽  
Shitong Li ◽  
...  
Keyword(s):  
Magnesium Sulfate ◽  
Diaphragm Dysfunction

scholarly journals Interactions between Cytosolic Phospholipase A2 Activation and Mitochondrial Reactive Oxygen Species Production in the Development of Ventilator-Induced Diaphragm Dysfunction

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Xian-Long Zhou ◽  
Xiao-Jun Wei ◽  
Shao-Ping Li ◽  
Rui-Ning Liu ◽  
Ming-Xia Yu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Phospholipase A2 ◽  
Cytosolic Phospholipase A2 ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Diaphragm Dysfunction ◽  
Cytosolic Phospholipase ◽  
Mitochondrial Ros ◽  
Cpla2 Activation

Cytosolic phospholipase A2 (cPLA2) has been reported to be critical for infection-induced mitochondrial reactive oxygen species (ROS) production and diaphragm dysfunction (DD). In the present study, we aim to investigate whether cPLA2 was involved in ventilator-induced diaphragm dysfunction (VIDD). Our results showed that mechanical ventilation (MV) induced cPLA2 activation in the diaphragm with excessive mitochondrial ROS generation and muscle weakness. Specific inhibition of cPLA2 with CDIBA resulted in decreased mitochondrial ROS levels and improved diaphragm forces. In addition, mitochondria-targeted antioxidant MitoTEMPO attenuated ventilator-induced mitochondrial oxidative stress and downregulated cPLA2 activation in vivo. Both CDIBA and MitoTEMPO were able to attenuate protein degradation, muscle atrophy, and weakness following prolonged MV. Furthermore, laser Doppler imaging showed that MV decreased diaphragm tissue perfusion and induced subsequent hypoxia. An in vitro study also demonstrated a positive association between cPLA2 activation and mitochondrial ROS generation in C2C12 cells cultured under hypoxic condition. Collectively, our study showed that cPLA2 activation positively interacts with mitochondrial ROS generation in the development of VIDD, and ventilator-induced diaphragm hypoxia serves as a possible contributor to this positive feedback loop.

Diaphragm Dysfunction In Experimental Pulmonary Arterial Hypertension

2010 ◽  
Author(s):  
Frances S. de Man ◽  
M. L. Handoko ◽  
Hieronymus W.H. van Hees ◽  
Ingrid Schalij ◽  
Pieter E. Postmus ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Diaphragm Dysfunction ◽  
Pulmonary Arterial
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