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

Telias, Irene; Damiani, Felipe; Brochard, Laurent

doi:10.1007/s00134-018-5045-8

Cited by 78 publications

(58 citation statements)

References 16 publications

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“…Due to this variation, it is recommended to use an average of three or four P 0.1 measures for a reliable estimation of respiratory drive. In stable, non-intubated patients with COPD, P 0.1 values between 2.4 and 5 cmH 2 O have been reported [7], and from 3 to 6 cmH 2 O in patients with acute respiratory distress syndrome (ARDS) receiving mechanical ventilation [39]. An optimal upper threshold for P 0.1 was 3.5 cmH 2 O in mechanically ventilated patients; a P 0.1 above this level is associated with increased respiratory muscle effort (i.e., esophageal pressure-time product [PTP] > 200 cmH 2 O•s/min [40]).…”

Section: Reference Valuesmentioning

confidence: 99%

“…Although the P 0.1 is readily available on most modern mechanical ventilators, each ventilator type has a different algorithm to calculate P 0.1 ; some require manual activation of the maneuver, others continuously display an estimated value based on the ventilator trigger phase (i.e., the measured pressure decrease before the ventilator is triggered, extrapolated to 0.1 s), whether or not averaged over a few consecutive breaths. Considering that the trigger phase is often shorter than 0.05 s, P 0.1 is likely to underestimate true respiratory drive, especially in patients with high drive [39]. The accuracy of the different calculation methods remains to be investigated.…”

Section: Limitationsmentioning

confidence: 99%

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Physiology of the Respiratory Drive in ICU Patients: Implications for Diagnosis and Treatment

2020

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Section: Reference Valuesmentioning

confidence: 99%

Section: Limitationsmentioning

confidence: 99%

Physiology of the Respiratory Drive in ICU Patients: Implications for Diagnosis and Treatment

2020

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“…The P 0.1 (airway pressure generated in the first 100 ms of inspiration against an expiratory occlusion) provides a measure of the patient's respiratory drive (Fig. 5) [34]. Whitelaw et al [35] demonstrated that an occlusion does not modify cortical respiratory output until it is prolonged beyond 200 ms. Additionally, during the first 100 ms, respiratory pressure generation is independent of pulmonary mechanics or diaphragm function [35,36].…”

Section: Airway Occlusion Pressurementioning

confidence: 99%

“…Whitelaw et al [35] demonstrated that an occlusion does not modify cortical respiratory output until it is prolonged beyond 200 ms. Additionally, during the first 100 ms, respiratory pressure generation is independent of pulmonary mechanics or diaphragm function [35,36]. Although the reliability of P 0.1 has been confirmed only in small studies, a value between 1.5 and 3.5 cmH 2 O [37,38] seems to be an easy method to guide clinicians to adjust ventilation during assisted mechanical ventilation [34,[39][40][41]. P 0.1 values less than 1.5 cmH 2 O might suggest that respiratory effort is inadequate [42], and values greater than 3.5 cmH 2 O suggest high respiratory drive [37].…”

Section: Airway Occlusion Pressurementioning

confidence: 99%

Monitoring Patient Respiratory Effort During Mechanical Ventilation: Lung and Diaphragm-Protective Ventilation

2020

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This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2020. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2020. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from During spontaneous breathing, vigorous patient respiratory efforts can cause lung injury (P-SILI) through different mechanisms (Fig. 2).Excessive global lung stress. As already discussed, patient respiratory efforts can increase tidal volume and P L above safe limits when respiratory drive is elevated.

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“…Lastly, Rapid Shallow Breathing Index (RSBI) is the product between tidal volume and respiratory rate, and it is used to evaluate weaning readiness [20]. p0.1 [21], the drop in pressure in the first 100 ms of an inspiratory effort against occluded airways and an index of respiratory drive, automatically measured by the mechanical ventilators, was collected together with the other ventilator data during AMV.…”

Section: Study Protocolmentioning

confidence: 99%

Assisted mechanical ventilation promotes recovery of diaphragmatic thickness in critically ill patients: a prospective observational study

et al. 2020

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Background: Diaphragm atrophy and dysfunction are consequences of mechanical ventilation and are determinants of clinical outcomes. We hypothesize that partial preservation of diaphragm function, such as during assisted modes of ventilation, will restore diaphragm thickness. We also aim to correlate the changes in diaphragm thickness and function to outcomes and clinical factors. Methods: This is a prospective, multicentre, observational study. Patients mechanically ventilated for more than 48 h in controlled mode and eventually switched to assisted ventilation were enrolled. Diaphragm ultrasound and clinical data collection were performed every 48 h until discharge or death. A threshold of 10% was used to define thinning during controlled and recovery of thickness during assisted ventilation. Patients were also classified based on the level of diaphragm activity during assisted ventilation. We evaluated the association between changes in diaphragm thickness and activity and clinical outcomes and data, such as ventilation parameters. Results: Sixty-two patients ventilated in controlled mode and then switched to the assisted mode of ventilation were enrolled. Diaphragm thickness significantly decreased during controlled ventilation (1.84 ± 0.44 to 1.49 ± 0.37 mm, p < 0.001) and was partially restored during assisted ventilation (1.49 ± 0.37 to 1.75 ± 0.43 mm, p < 0.001). A diaphragm thinning of more than 10% was associated with longer duration of controlled ventilation (10 [5, 15] versus 5 [4, 8.5] days, p = 0.004) and higher PEEP levels (12.6 ± 4 versus 10.4 ± 4 cmH 2 O, p = 0.034). An increase in diaphragm thickness of more than 10% during assisted ventilation was not associated with any clinical outcome but with lower respiratory rate (16.7 ± 3.2 versus 19.2 ± 4 bpm, p = 0.019) and Rapid Shallow Breathing Index (37 ± 11 versus 44 ± 13, p = 0.029) and with higher Pressure Muscle Index (2 [0.5, 3] versus 0.4 [0, 1.9], p = 0.024). Change in diaphragm thickness was not related to diaphragm function expressed as diaphragm thickening fraction. Conclusion: Mode of ventilation affects diaphragm thickness, and preservation of diaphragmatic contraction, as during assisted modes, can partially reverse the muscle atrophy process. Avoiding a strenuous inspiratory work, as measured by Rapid Shallow Breathing Index and Pressure Muscle Index, may help diaphragm thickness restoration.

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

Cited by 78 publications

References 16 publications

Physiology of the Respiratory Drive in ICU Patients: Implications for Diagnosis and Treatment

Physiology of the Respiratory Drive in ICU Patients: Implications for Diagnosis and Treatment

Monitoring Patient Respiratory Effort During Mechanical Ventilation: Lung and Diaphragm-Protective Ventilation

Assisted mechanical ventilation promotes recovery of diaphragmatic thickness in critically ill patients: a prospective observational study

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