The airway occlusion pressure (P0.1) to monitor respiratory drive during mechanical ventilation: increasing awareness of a not-so-new problem

2018 ◽  
Vol 44 (9) ◽  
pp. 1532-1535 ◽  
Author(s):  
Irene Telias ◽  
Felipe Damiani ◽  
Laurent Brochard
CHEST Journal ◽  
1988 ◽  
Vol 93 (3) ◽  
pp. 571-576 ◽  
Author(s):  
Catherine S.H. Sassoon ◽  
C. Kees Mahutte ◽  
Teresita T. Te ◽  
Daniel H. Simmons ◽  
Richard W. Light

2020 ◽  
Vol 1 (1) ◽  
pp. 8-13
Author(s):  
Natsumi Hamahata ◽  
Ryota Sato ◽  
Kimiyo Yamasaki ◽  
Sophie Pereira ◽  
Ehab Daoud

Background: Quantification of the patient’s respiratory effort during mechanical ventilation is very important, and calculating the actual muscle pressure (Pmus) during mechanical ventilation is a cumbersome task and usually requires an esophageal balloon manometry. Airway occlusion pressure at 100 milliseconds (P0.1) can easily be obtained non-invasively. There has been no study investigating the association between Pmus and P0.1. Therefore, we aimed to investigate whether P0.1 correlates to Pmus and can be used to estimate actual Pmus Materials and Methods: A bench study using lung simulator (ASL 5000) to simulate an active breathing patient with Pmus from 1 to 30 cmH2O by increments of 1 was conducted. Twenty active breaths were measured in each Pmus. The clinical scenario was constructed as a normal lung with a fixed setting of compliances of 60 mL/cmH2O and resistances of 10 cmH2O/l/sec. All experiments were conducted using the pressure support ventilation mode (PSV) on a Hamilton-G5 ventilator (Hamilton Medical AG, Switzerland), Puritan Bennett 840TM (Covidien-Nellcor, CA) and Avea (CareFusion, CA). Main results: There was significant correlation between P 0.1 and Pmus (correlation coefficient = - 0.992, 95% CI: - 0.995 to -0.988, P-value<0.001). The equation was calculated as follows: Pmus = -2.99 x (P0.1) + 0.53 Conclusion: Estimation of Pmus using P 0.1 as a substitute is feasible, available, and reliable. Estimation of Pmus has multiple implications, especially in weaning of mechanical ventilation, adjusting ventilator support, and calculating respiratory mechanics during invasive mechanical ventilation. Keywords: P 0.1, Inspiratory occlusion pressure, WOB, Esophageal balloon, mechanical ventilators, respiratory failure Keywords: P 0.1, P mus, Inspiratory occlusion pressure, WOB, Esophageal balloon, mechanical ventilators, respiratory failure


2020 ◽  
Vol 201 (9) ◽  
pp. 1086-1098 ◽  
Author(s):  
Irene Telias ◽  
Detajin Junhasavasdikul ◽  
Nuttapol Rittayamai ◽  
Lise Piquilloud ◽  
Lu Chen ◽  
...  

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.


2020 ◽  
Vol 201 (9) ◽  
pp. 1027-1028
Author(s):  
Catherine S. Sassoon ◽  
Magdy Younes

CHEST Journal ◽  
1987 ◽  
Vol 91 (4) ◽  
pp. 496-499 ◽  
Author(s):  
A. Bruce Montgomery ◽  
Rolf H.O. Holle ◽  
Sara R. Neagley ◽  
David J. Pierson ◽  
Robert B. Schoene

Sign in / Sign up

Export Citation Format

Share Document