Faculty Opinions recommendation of Mechanical ventilation guided by esophageal pressure in acute lung injury.

Author(s):  
Ivor Douglas
2000 ◽  
Vol 92 (2) ◽  
pp. 550-550
Author(s):  
Craig G. Hartford ◽  
Johan M. van Schalkwyk ◽  
Geoffrey G. Rogers ◽  
Martin J. Turner

Background Dynamic intraesophageal pressure (Pes) is used to estimate intrapleural pressure (Ppl) to calculate lung compliance and resistance. This study investigated the nonhuman primate Ppl-Pes tissue barrier frequency response and the dynamic response requirements of Pes manometers. Methods In healthy monkeys and monkeys with acute lung injury undergoing ventilation, simultaneous Ppl and Pes were measured directly to determine the Ppl-Pes tissue barrier amplitude frequency response, using the swept-sine wave technique. The bandwidths of physiologic Pes waveforms acquired during conventional mechanical ventilation were calculated using digital low-pass signal filtering. Results The Ppl-Pes tissue barrier is amplitude-uniform within the bandwidth of conventional Pes waveforms in healthy and acute lung injury lungs, and does not significantly attenuate Ppl-Pes signal transmission between 1 and 40 Hz. At Pes frequencies higher than conventional clinical regions of interest the Ppl-Pes barrier resonates significantly, is pressure amplitude dependent at low-pressure offsets, and is significantly altered by acute lung injury. Allowing for 5% or less Pes waveform error, the maximum Pes bandwidths during conventional ventilation were 1.9 Hz and 3.4 Hz for physiologic and extreme-case waveforms in healthy lungs and 4.6 Hz and 8.5 Hz during acute lung injury. Conclusions In monkeys, the Ppl-Pes tissue barrier has a frequency response suitable for Ppl estimation during low-frequency mechanical ventilation, and Pes manometers should have a minimum uniform frequency response up to 8.5 Hz. However, the Ppl-Pes tissue barrier adversely affects the accurate estimation of dynamic Ppl at high frequencies, with varied airway pressure amplitudes and offsets, such as the Ppl encountered during high-frequency oscillatory ventilation.


2008 ◽  
Vol 359 (20) ◽  
pp. 2095-2104 ◽  
Author(s):  
Daniel Talmor ◽  
Todd Sarge ◽  
Atul Malhotra ◽  
Carl R. O'Donnell ◽  
Ray Ritz ◽  
...  

2003 ◽  
Vol 94 (3) ◽  
pp. 975-982 ◽  
Author(s):  
Timothy C. Bailey ◽  
Erica L. Martin ◽  
Lin Zhao ◽  
Ruud A. W. Veldhuizen

Mechanical ventilation is a necessary intervention for patients with acute lung injury. However, mechanical ventilation can propagate acute lung injury and increase systemic inflammation. The exposure to >21% oxygen is often associated with mechanical ventilation yet has not been examined within the context of lung stretch. We hypothesized that mice exposed to >90% oxygen will be more susceptible to the deleterious effects of high stretch mechanical ventilation. C57B1/6 mice were randomized into 48-h exposure of 21 or >90% oxygen; mice were then killed, and isolated lungs were randomized into a nonstretch or an ex vivo, high-stretch mechanical ventilation group. Lungs were assessed for compliance and lavaged for surfactant analysis, and cytokine measurements or lungs were homogenized for surfactant-associated protein analysis. Mice exposed to >90% oxygen + stretch had significantly lower compliance, altered pulmonary surfactant, and increased inflammatory cytokines compared with all other groups. Our conclusion is that 48 h of >90% oxygen and high-stretch mechanical ventilation deleteriously affect lung function to a greater degree than stretch alone.


Author(s):  
Iris Duroi ◽  
Frederik Van Durme ◽  
Tony Bruyns ◽  
Sofie Louage ◽  
Alex Heyse

Severe COVID-19 may predispose to both venous and arterial thrombosis. We describe a patient with acute ischaemic stroke while suffering from COVID-19 and respiratory failure, necessitating mechanical ventilation. Deep sedation may delay diagnosis.


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