Resuscitation with mechanical ventilation: The effects of Chest Compression Synchronized Ventilation (CCSV) or Intermitted Positive Pressure Ventilation (IPPV) on lung injury in a pig model

Resuscitation ◽  
2013 ◽  
Vol 84 ◽  
pp. S15
Author(s):  
Wolfgang Dersch ◽  
Philipp Hoselmann ◽  
Christian Neuhaus ◽  
Ulrich Palm ◽  
Elisabeth Bösl ◽  
...  
2014 ◽  
Vol 120 (4) ◽  
pp. 943-950 ◽  
Author(s):  
Matteo Pecchiari ◽  
Ario Monaco ◽  
Antonia Koutsoukou ◽  
Patrizia Della Valle ◽  
Guendalina Gentile ◽  
...  

Abstract Background: Recent studies in healthy mice and rats have reported that positive pressure ventilation delivered with physiological tidal volumes at normal end-expiratory volume worsens lung mechanics and induces cytokine release, thus suggesting that detrimental effects are due to positive pressure ventilation per se. The aim of this study in healthy animals is to assess whether these adverse outcomes depend on the mode of mechanical ventilation. Methods: Rats were subjected to 4 h of spontaneous, positive pressure, and whole-body or thorax-only negative pressure ventilation (N = 8 per group). In all instances the ventilatory pattern was that of spontaneous breathing. Lung mechanics, cytokines concentration in serum and broncho–alveolar lavage fluid, lung wet-to-dry ratio, and histology were assessed. Values from eight animals euthanized shortly after anesthesia served as control. Results: No evidence of mechanical ventilation–dependent lung injury was found in terms of lung mechanics, histology, or wet-to-dry ratio. Relative to control, cytokine levels and recruitment of polymorphonuclear leucocytes increased slightly, and to the same extent with spontaneous, positive pressure, and whole-body negative pressure ventilation. Thorax-only negative pressure ventilation caused marked chest and lung distortion, reversible increase of lung elastance, and higher polymorphonuclear leucocyte count and cytokine levels. Conclusion: Both positive and negative pressure ventilation performed with tidal volumes and timing of spontaneous, quiet breathing neither elicit an inflammatory response nor cause morpho-functional alterations in normal animals, thus supporting the notion of the presence of a critical volume threshold above which acute lung injury ensues. Distortion of lung parenchyma can induce an inflammatory response, even in the absence of volotrauma.


PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0127759 ◽  
Author(s):  
Clemens Kill ◽  
Monika Galbas ◽  
Christian Neuhaus ◽  
Oliver Hahn ◽  
Pascal Wallot ◽  
...  

Author(s):  
W. Alan Hodson

The improved survival rate of premature infants with respiratory failure is attributable to advances in mechanical ventilation, although an adverse consequence has been an increased incidence of bronchopulmonary dysplasia (BPD) (1;32). Positive pressure ventilation with its attendant “barotrauma” is suspected in the causation of BPD. While many attempts to alter respirator variables, such as pressure and time components, have produced optimal patterns for gas exchange, evidence is lacking to support any one pattern that minimizes the incidence of chronic lung injury. The high incidence of BPD has promoted a search for alternative methods of ventilation that might reduce lung injury through a reduction in peak pressure applied to the lung. Additional motivation has come from the need for oxygenation when mechanical ventilation has failed or pulmonary interstitial emphysema has developed. Less compelling reasons have come from the desire to avoid high swings in thoracic pressure that might adversely affect cardiac output, venous return, and cerebral blood flow.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Shinichiro Ohshimo

AbstractAcute respiratory distress syndrome (ARDS) is a fatal condition with insufficiently clarified etiology. Supportive care for severe hypoxemia remains the mainstay of essential interventions for ARDS. In recent years, adequate ventilation to prevent ventilator-induced lung injury (VILI) and patient self-inflicted lung injury (P-SILI) as well as lung-protective mechanical ventilation has an increasing attention in ARDS.Ventilation-perfusion mismatch may augment severe hypoxemia and inspiratory drive and consequently induce P-SILI. Respiratory drive and effort must also be carefully monitored to prevent P-SILI. Airway occlusion pressure (P0.1) and airway pressure deflection during an end-expiratory airway occlusion (Pocc) could be easy indicators to evaluate the respiratory drive and effort. Patient-ventilator dyssynchrony is a time mismatching between patient’s effort and ventilator drive. Although it is frequently unrecognized, dyssynchrony can be associated with poor clinical outcomes. Dyssynchrony includes trigger asynchrony, cycling asynchrony, and flow delivery mismatch. Ventilator-induced diaphragm dysfunction (VIDD) is a form of iatrogenic injury from inadequate use of mechanical ventilation. Excessive spontaneous breathing can lead to P-SILI, while excessive rest can lead to VIDD. Optimal balance between these two manifestations is probably associated with the etiology and severity of the underlying pulmonary disease.High-flow nasal cannula (HFNC) and non-invasive positive pressure ventilation (NPPV) are non-invasive techniques for supporting hypoxemia. While they are beneficial as respiratory supports in mild ARDS, there can be a risk of delaying needed intubation. Mechanical ventilation and ECMO are applied for more severe ARDS. However, as with HFNC/NPPV, inappropriate assessment of breathing workload potentially has a risk of delaying the timing of shifting from ventilator to ECMO. Various methods of oxygen administration in ARDS are important. However, it is also important to evaluate whether they adequately reduce the breathing workload and help to improve ARDS.


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