Barotrauma and Mechanical Ventilation Publications (937)
Barotrauma and Mechanical Ventilation Publications
Our primary objective was to determine the effects of recruitment manoeuvres on mortality in adults with acute respiratory distress syndrome.Our secondary objective was to determine, in the same population, the effects of recruitment manoeuvres on oxygenation and adverse events (e.g. rate of barotrauma).
For this updated review, we searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (OVID), Embase (OVID), the Cumulative Index to Nursing and Allied Health Literature (CINAHL, EBSCO), Latin American and Caribbean Health Sciences (LILACS) and the International Standard Randomized Controlled Trial Number (ISRCTN) registry from inception to August 2016.
We included randomized controlled trials (RCTs) of adults who were mechanically ventilated that compared recruitment manoeuvres versus standard care for patients given a diagnosis of ARDS.
Two review authors independently assessed trial quality and extracted data. We contacted study authors for additional information.
Ten trials met the inclusion criteria for this review (n = 1658 participants). We found five trials to be at low risk of bias and five to be at moderate risk of bias. Six of the trials included recruitment manoeuvres as part of an open lung ventilation strategy that was different from control ventilation in aspects other than the recruitment manoeuvre (such as mode of ventilation, higher positive end-expiratory pressure (PEEP) titration and lower tidal volume or plateau pressure). Six studies reported mortality outcomes. Pooled data from five trials (1370 participants) showed a reduction in intensive care unit (ICU) mortality (risk ratio (RR) 0.83, 95% confidence interval (CI) 0.72 to 0.97, P = 0.02, low-quality evidence), pooled data from five trials (1450 participants) showed no difference in 28-day mortality (RR 0.86, 95% CI 0.74 to 1.01, P = 0.06, low-quality evidence) and pooled data from four trials (1313 participants) showed no difference in in-hospital mortality (RR 0.88, 95% CI 0.77 to 1.01, P = 0.07, low-quality evidence). Data revealed no differences in risk of barotrauma (RR 1.09, 95% CI 0.78 to 1.53, P = 0.60, seven studies, 1508 participants, moderate-quality evidence).
We identified significant clinical heterogeneity in the 10 included trials. Results are based upon the findings of several (five) trials that included an "open lung ventilation strategy", whereby the intervention group differed from the control group in aspects other than the recruitment manoeuvre (including co-interventions such as higher PEEP, different modes of ventilation and higher plateau pressure), making interpretation of the results difficult. A ventilation strategy that included recruitment manoeuvres in participants with ARDS reduced intensive care unit mortality without increasing the risk of barotrauma but had no effect on 28-day and hospital mortality. We downgraded the quality of the evidence to low, as most of the included trials provided co-interventions as part of an open lung ventilation strategy, and this might have influenced results of the outcome.
High frequency jet ventilation allows adequate oxygenation and carbon dioxide removal even in cases of tracheal stenosis up to frequencies of around 150 min(-1); however, in an in vivo animal model, high frequency jet ventilation along with normal frequency jet ventilation (superimposed high frequency jet ventilation) has been shown to improve oxygenation by increasing lung volume and carbon dioxide removal by increasing tidal volume across a large spectrum of frequencies without increasing barotrauma. General anesthesia with a continuous, intravenous, short-acting agent is safe and effective during rigid bronchoscopy procedures.
Deep sedation plus muscle relaxants may be required to treat PVD or to reduce oxygen consumption and carbon dioxide production. Although minimization and protocolization of sedation in the intensive care unit improves costs and outcomes, it is important to consider goals on an individual basis.
Several interventions are available to protect against VILI. However, most patients at risk of lung injury do not develop VILI. VILI occurs most readily in patients with concomitant physiologic insults. VILI prevention strategies must balance risk of lung injury with untoward side effects from the preventive effort, and may be most effective when targeted to subsets of patients at increased risk.
We re-explored these routes in rat models of hypoxemia.
Hypoxemia was induced in spontaneously breathing, anesthetized rats by breathing a hypoxic gas mix (FiO2 0.1). Pilot studies infusing pure O2 gas caused early death, likely due to pulmonary embolism. Instead, rats (n = 6/group) were given intravenous O2 via a continuous infusion of pre-oxygenated Hartmann's solution (10 ml/kg/h) for 3 h with normal Ringer's lactate used in control animals. In separate experiments (n = 8/group), bowel intraluminal oxygenation was assessed with pure O2 administered through a cannula placed into the jejunal lumen at a dose of a 15 ml/kg bolus followed by a continuous infusion of 50 ml/kg/h; no treatment was given to controls. Echocardiography, arterial blood gas analysis, mean arterial pressure, muscle and liver tPO2, muscle microvascular perfused vessel density, and urine output were measured.
Administration of oxygenated Hartmann's solution (PO2 of solution at end-experiment = 87.5 ± 1.7 kPa) was safe but did not increase either systemic or tissue oxygenation. Similarly, the administration of bowel O2 was safe but did not improve neither systemic nor liver oxygenation.
In this rat model of hypoxemia, the intravenous infusion of gaseous O2 was unfeasible as it induced early mortality. Although safe, both intravenous infusion of oxygenated Hartmann's solution and bowel O2 administration were unable to improve arterial or tissue oxygenation.
4%) developed pneumothorax, and these were compared with those patients who did not. The most common tool for diagnosis used was chest X-ray followed by a clinical examination.
Case notes of 1298 patients admitted in PICU over 1-year study.
Patients with pneumothorax had higher mortality rate (P < 0.001), longer length of stay (P < 0.001), higher need for mechanical ventilation (MV) (P < 0.001), and were of younger age (P < 0.001), lower body weight (P < 0.001), higher pediatric index of mortality 2 score on admission (P < 0.001), higher pediatric logistic organ dysfunction score (P < 0.001), compared to their counterpart. Iatrogenic pneumothorax (IP) represented 95% of episodes of pneumothorax. The most common causes of IP were barotrauma secondary to MV, central vein catheter insertion, and other (69.6%, 13.2%, and 17.2%, respectively). Compared to ventilated patients without pneumothorax, ventilated patients who developed pneumothorax had a longer duration of MV care (P < 0.001) and higher nonconventional and high-frequency oscillatory ventilation settings (P < 0.001).
This study demonstrated that pneumothorax is common in Alexandria University PICU patients, especially in those on MV and emphasized the importance of the strict application of protective lung strategies among ventilated patients to minimize the risk of pneumothorax.
A meta-analysis of randomized controlled trials was performed using the Cochrane Review Methods.
Six studies (259 participants) were included. The PaO2/FiO2 ratio in PCV was higher than in VCV [weighted mean difference (WMD) = 11.04 mmHg, 95 % confidence interval (CI) = 0.30 to 21.77, P = 0.04, I(2) = 3 %] and peak inspiratory pressure was significantly lower in PCV (WMD = -4.91 cm H2O, 95 % CI = -7.30 to -2.53, P < 0.0001, I (2) = 91 %). No differences in PaCO2, tidal volume, heart rate and blood pressure were observed. There were also no differences incompliance, plateau and mean airway pressure.
Our meta-analysis provided the evidence of improved oxygenation in PCV. However, it is difficult to draw any definitive conclusions due to the fact that the duration of ventilation in the studies reviewed was insufficient to reveal clinically relevant benefits or disadvantages of PCV. Significantly lower peak inspiratory pressure is the advantage of PCV.
Several databases of published and unpublished literature were searched systematically for studies describing TTJV in human subjects. Complications were categorized as device failure, barotrauma (including subcutaneous emphysema), and miscellaneous. Device failure was defined by the inability to place and/or use the TTJV device, not patient survival.
Forty-four studies (428 procedures) met the inclusion criteria. Four studies included both emergency and elective procedures. Thirty studies described 132 emergency TTJV procedures; 90 were CICO emergencies. Eighteen studies described 296 elective TTJV procedures. Device failure occurred in 42% of CICO emergency vs 0% of non-CICO emergency (P<0.001) and 0.3% of elective procedures (P<0.001). Barotrauma occurred in 32% of CICO emergency vs 7% of non-CICO emergency (P<0.001) and 8% of elective procedures (P<0.001). The total number of procedures with any complication was 51% of CICO emergency vs 7% of non-CICO emergency (P<0.001) and 8% of elective procedures (P<0.001). Several reports described TTJV-related subcutaneous emphysema hampering subsequent attempts at surgical airway or tracheal intubation.
TTJV is associated with a high risk of device failure and barotrauma in the CICO emergency. Guidelines and recommendations supporting the use of TTJV in CICO should be reconsidered.
Although the specific etiology of process is unknown, the muscle presents oxidative stress and mitochondrial changes. These cause changes in protein turnover, resulting in atrophy and impaired contractility, and leading to impaired functionality. The term 'ventilator-induced diaphragm dysfunction' was first coined by Vassilakopoulos et al. in 2004, and this phenomenon, along with injury cause by over-distention of the lung and barotrauma, represents a challenge in the daily life of ventilated patients. Diaphragmatic dysfunction affects prognosis by delaying extubation, prolonging hospital stay, and impairing the quality of life of these patients in the years following hospital discharge. Ultrasound, a non-invasive technique that is readily available in most ICUs, could be used to diagnose this condition promptly, thus preventing delays in starting rehabilitation and positively influencing prognosis in these patients.
We are lacking a comprehensive understanding of mechanotransduction processes in the healthy lung and know little about the interactions between simultaneously activated stretch-, HO-, and cytokine-induced signaling cascades in ARDS. Nevertheless, as we are unraveling these mechanisms we are gathering increasing evidence for the importance of stretch-activated ion channels (SACs) in the activation of lung-resident and inflammatory cells. In addition to the discovery of new SAC families in the lung, e.g., two-pore domain potassium channels, we are increasingly assigning mechanosensing properties to already known Na(+), Ca(2+), K(+), and Cl(-) channels. Better insights into the mechanotransduction mechanisms of SACs will improve our understanding of the pathways leading to ventilator-induced lung injury and lead to much needed novel therapeutic approaches against ARDS by specifically targeting SACs. This review 1) summarizes the reasons why the time has come to seriously consider SACs as new therapeutic targets against ARDS, 2) critically analyzes the physiological and experimental factors that currently limit our knowledge about SACs, and 3) outlines the most important questions future research studies need to address.