Assist–Control Mechanical Ventilation Attenuates Ventilator-induced Diaphragmatic Dysfunction

2004 ◽  
Vol 170 (6) ◽  
pp. 626-632 ◽  
Author(s):  
Catherine S. H. Sassoon ◽  
Ercheng Zhu ◽  
Vincent J. Caiozzo
Keyword(s):  
Mechanical Ventilation ◽  
Control Mechanical Ventilation ◽  
Diaphragmatic Dysfunction

scholarly journals Transcriptome profiling of the diaphragm in a controlled mechanical ventilation model reveals key genes involved in ventilator-induced diaphragmatic dysfunction

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ruining Liu ◽  
Gang Li ◽  
Haoli Ma ◽  
Xianlong Zhou ◽  
Pengcheng Wang ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Signaling Pathway ◽  
Wistar Rats ◽  
Cholesterol Metabolism ◽  
Expression Profiles ◽  
Receptor Interaction ◽  
Pathophysiological Mechanism ◽  
Rna Seq ◽  
Diaphragmatic Dysfunction ◽  
Controlled Mechanical Ventilation

Abstract Background Ventilator-induced diaphragmatic dysfunction (VIDD) is associated with weaning difficulties, intensive care unit hospitalization (ICU), infant mortality, and poor long-term clinical outcomes. The expression patterns of long noncoding RNAs (lncRNAs) and mRNAs in the diaphragm in a rat controlled mechanical ventilation (CMV) model, however, remain to be investigated. Results The diaphragms of five male Wistar rats in a CMV group and five control Wistar rats were used to explore lncRNA and mRNA expression profiles by RNA-sequencing (RNA-seq). Muscle force measurements and immunofluorescence (IF) staining were used to verify the successful establishment of the CMV model. A total of 906 differentially expressed (DE) lncRNAs and 2,139 DE mRNAs were found in the CMV group. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to determine the biological functions or pathways of these DE mRNAs. Our results revealed that these DE mRNAs were related mainly related to complement and coagulation cascades, the PPAR signaling pathway, cholesterol metabolism, cytokine-cytokine receptor interaction, and the AMPK signaling pathway. Some DE lncRNAs and DE mRNAs determined by RNA-seq were validated by quantitative real-time polymerase chain reaction (qRT-PCR), which exhibited trends similar to those observed by RNA-sEq. Co-expression network analysis indicated that three selected muscle atrophy-related mRNAs (Myog, Trim63, and Fbxo32) were coexpressed with relatively newly discovered DE lncRNAs. Conclusions This study provides a novel perspective on the molecular mechanism of DE lncRNAs and mRNAs in a CMV model, and indicates that the inflammatory signaling pathway and lipid metabolism may play important roles in the pathophysiological mechanism and progression of VIDD.

Apnea after normocapnic mechanical ventilation during NREM sleep

1994 ◽  
Vol 77 (5) ◽  
pp. 2079-2085 ◽  
Author(s):  
A. M. Leevers ◽  
P. M. Simon ◽  
J. A. Dempsey
Keyword(s):  
Mechanical Ventilation ◽  
Nrem Sleep ◽  
Inspiratory Effort ◽  
Control Mechanical Ventilation ◽  
Inhibitory Effects ◽  
Inspiratory Motor ◽  
Ventilator Mode ◽  
Controlled Mechanical Ventilation ◽  
The Subject ◽  
End Tidal

We determined whether normocapnic mechanical ventilation at high tidal volume (VT) and breathing frequency (f) during non-rapid-eye-movement (NREM) sleep would cause apnea. Seven normal sleeping subjects were placed on assist-control mechanical ventilation (i.e., subject initiates inspiration) and VT was gradually increased to 2.1 times eupneic VT (1.17 +/- 0.04 liters). This high VT was maintained for 5 min, the ventilator mode was switched to controlled mechanical ventilation, and f was increased gradually from 9.5 +/- 1.0 (during assist-control mechanical ventilation) to 14.0 +/- 0.7 breaths/min. Normocapnia (end-tidal PCO2 = 44 +/- 1.2 Torr) was maintained throughout the trials. Inspiratory effort was completely inhibited during the period of sustained high VT and f, and apnea occurred immediately after cessation of the passive mechanical ventilation. The duration of the apnea preceding the first inspiratory effort was 20.3 +/- 2.3 s or 7.1 times the eupneic expiratory duration and 5 times the expiratory duration chosen by the subject during assist-control mechanical ventilation. We conclude that inhibition of inspiratory motor output occurs during and after normocapnic mechanical ventilation at high VT and f during NREM sleep. These neuromechanical inhibitory effects may serve to initiate and prolong apnea.

scholarly journals Ventilator induced Diaphragmatic Dysfunction assessed by Ultrasonography and its impact on Weaning outcome

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
H M A Fawzy ◽  
M H M Hassan ◽  
A A M Alkholy
Keyword(s):  
Mechanical Ventilation ◽  
Operating Characteristics ◽  
Diaphragmatic Dysfunction ◽  
Rapid Shallow Breathing Index ◽  
Weaning Failure ◽  
Significant Difference ◽  
Shallow Breathing ◽  
Ventilation Modes ◽  
Weaning Outcome ◽  
Rapid Shallow Breathing

Abstract Background Ventilator induced diaphragmatic dysfunction (VIDD), as a loss of diaphragmatic force generating capacity due to the use of mechanical ventilation. Difficulties in discontinuing ventilatory support are encountered in 20–25% of mechanically ventilated patients, with a staggering 40% of time spent in the intensive care unit being devoted to weaning. M-mode ultrasonography is now an accepted qualitative method of assessing diaphragmatic motion in normal and pathological conditions. In this study, we evaluated whether diaphragmatic excursion (DE) as measured by M-mode sonography can be a predictor of weaning and diagnosis of VIDD. Aim The aim of this study is to determine the presence of ventilator induced diaphragmatic dysfunction (VIDD) diagnosed by M-mode ultrasonography and its impact on weaning outcome. Methodology This study was conducted prospectively in critical care unit in Ain Shams Hospital, a university-affiliated, tertiary referral center in Cairo, Egypt. Study subjects included 78 patients between August 2017 to August 2018. who required mechanical ventilation ≥72hrs. who fulfilled the spontaneous breath trial (SBT) criteria, at the start of a 1-hr SBT, each hemidiaphragm was evaluated M-mode sonography with the patient in the supine position. Rapid shallow Breathing index (RSBI) was simultaneously calculated at the bedside. Ultrasonographic Diaphragmatic Dysfunction (DD) was diagnosed if an Diaphragmatic Excursion (DE) was <10 mm or negative, the latter indicating paradoxical diaphragmatic movement. Results Diaphragmatic Dysfunction (DD) among the eligible 78 patients was 48% (n = 37). DD group had longer weaning time [39,2 (26-56) hrs. vs. 22.3 (30-16) hrs. p = 0.001) in DD vs. NDD group respectively and total ventilation time [140 (130-150) hrs. vs. 130 (120–140) hrs. p > 0.05) in DD vs. NDD group respectively. Weaning failure was (45.8% vs. 30.8%, p=0.01) in DD vs. NDD group respectively. In NDD group Rt. DE, mean 25.4 ±4.1 mm. While Lt. side was 25.3±4.6 mm, 11.25mm and 22mm (45-15) respectively. In DD group Rt. DE, mean 7.6 ±2.02mm, IQR 2.4 mm and median 8.2mm (10-1.9). While Lt. side was 9.2±0.8mm, 4.3mm and 8.9mm (9.8-5.7) respectively. The area under the receiver operating characteristics curve (ROC) of ultrasonographic criteria in predicting weaning failure was near similar to that of rapid shallow breathing index. Hypercapenic acidosis in NDD group might protect them from VIDD Conclusions DD is present in a significant percentage 48% (nearly half) of our medical ICU patients on MV ≥ 72 hrs which largely account for weaning failure. DD was associated with a significant longer weaning time, and ICU stay, with no significant difference in 30 day mortality Recommendations DE by US measurements is a valuable tool and is recommended as an adjunctive weaning index to aid prediction of weaning outcome. Evaluating the role of spontaneous ventilation modes and advanced ventilation modes as PAV and NAVA effects on decreas ing VIDD versus controlled modes.

scholarly journals Phrenic nerve stimulation prevents diaphragm atrophy in patients with respiratory failure on mechanical ventilation

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Michal Soták ◽  
Karel Roubík ◽  
Tomáš Henlín ◽  
Tomáš Tyll
Keyword(s):  
Mechanical Ventilation ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Intervention Group ◽  
Ventilator Weaning ◽  
Control Group ◽  
Phrenic Nerve Stimulation ◽  
Diaphragm Thickness ◽  
Diaphragmatic Dysfunction ◽  
Diaphragm Atrophy

Abstract Background Diaphragm atrophy and dysfunction is a major problem among critically ill patients on mechanical ventilation. Ventilator-induced diaphragmatic dysfunction is thought to play a major role, resulting in a failure of weaning. Stimulation of the phrenic nerves and resulting diaphragm contraction could potentially prevent or treat this atrophy. The subject of this study is to determine the effectiveness of diaphragm stimulation in preventing atrophy by measuring changes in its thickness. Methods A total of 12 patients in the intervention group and 10 patients in the control group were enrolled. Diaphragm thickness was measured by ultrasound in both groups at the beginning of study enrollment (hour 0), after 24 hours, and at study completion (hour 48). The obtained data were then statistically analyzed and both groups were compared. Results The results showed that the baseline diaphragm thickness in the interventional group was (1.98 ± 0.52) mm and after 48 hours of phrenic nerve stimulation increased to (2.20 ± 0.45) mm (p=0.001). The baseline diaphragm thickness of (2.00 ± 0.33) mm decreased in the control group after 48 hours of mechanical ventilation to (1.72 ± 0.20) mm (p<0.001). Conclusions Our study demonstrates that induced contraction of the diaphragm by pacing the phrenic nerve not only reduces the rate of its atrophy during mechanical ventilation but also leads to an increase in its thickness – the main determinant of the muscle strength required for spontaneous ventilation and successful ventilator weaning. Trial registration: The study was registered with ClinicalTrials.gov (18/06/2018, NCT03559933, https://clinicaltrials.gov/ct2/show/NCT03559933).

scholarly journals Avaliação Ecográfica da Disfunção Diafragmática Induzida pelo Ventilador em Idade Pediátrica

2019 ◽  
Vol 32 (7-8) ◽  
pp. 520 ◽  
Author(s):  
Maria Teresa Dionisio ◽  
Armanda Rebelo ◽  
Carla Pinto ◽  
Leonor Carvalho ◽  
José Farela Neves
Keyword(s):  
Mechanical Ventilation ◽  
Pressure Support ◽  
Early Recognition ◽  
Morphological Changes ◽  
Invasive Mechanical Ventilation ◽  
Extubation Failure ◽  
Volume Control ◽  
Invasive Technique ◽  
Thickness Variation ◽  
Diaphragmatic Dysfunction

Introduction: Invasive mechanical ventilation contributes to ventilator-induced diaphragmatic dysfunction, delaying extubation and increasing mortality in adults. Despite the possibility of having a higher impact in paediatrics, this dysfunction is not routinely monitored. Diaphragm ultrasound has been proposed as a safe and non-invasive technique for this purpose. The aim of this study was to describe the evolution of diaphragmatic morphology and functional measurements by ultrasound in ventilated children.Material and Methods: Prospective exploratory study. Children admitted to Paediatric Intensive Care Unit requiring mechanical ventilation > 48 hours were included. The diaphragmatic thickness, excursion and the thickening fraction were assessed by ultrasound.Results: Seventeen cases were included, with a median age of 42 months. Ten were male, seven had comorbidities and three in seventeen had malnutrition at admission. The median time under mechanical ventilation was seven days. The median of the initial and minimum diaphragmatic thickness was 2.3 mm and 1.9 mm, respectively, with a median decrease in thickness of 13% under pressure-regulated volume control. Diaphragmatic atrophy was observed in 14/17 cases. Differences in the median thickness variation were found between patients with sepsis and without (0.70 vs 0.25 mm; p = 0.019). During pressure support ventilation there was a tendency to increase diaphragmatic thickness and excursion. Extubation failure occurred for diaphragmatic thickening fraction ≤ 35%.Discussion: Under pressure-regulated volume control there was a tendency for a decrease in diaphragmatic thickness. In the pre-extubation stage under pressure support, there was a tendency for it to increase. These results suggest that, by titrating ventilation using physiological levels of inspiratory effort, we can reduce the diaphragmatic morphological changes associated with ventilation.Conclusion: The early recognition of diaphragmatic changes may encourage a targeted approach, namely titration of ventilation, in order to reduce ventilator-induced diaphragmatic dysfunction and its clinical repercussions.

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