The effects of tidal volume size and driving pressure levels on pulmonary complement activation: an observational study in critically ill patients
Background Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury. Aims and methods This was a single-cent...
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| Veröffentlicht in: | Intensive care medicine experimental Jg. 8; H. Suppl 1; S. 74 - 11 |
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| Sprache: | Englisch |
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18.12.2020
Springer Nature B.V SpringerOpen |
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| Abstract | Background
Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.
Aims and methods
This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (
V
T
) and driving pressure (Δ
P
), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and
V
T
and Δ
P
. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.
Results
Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median
V
T
and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H
2
O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with
V
T
and Δ
P
. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of
V
T
and Δ
P
on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia.
Conclusion
In this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of
V
T
and the level of Δ
P
. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation. |
|---|---|
| AbstractList | Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.
This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (V
) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and V
and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.
Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median V
and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H
O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with V
and ΔP. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of V
and ΔP on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia.
In this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of V
and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation. BackgroundMechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.Aims and methodsThis was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (VT) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and VT and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.ResultsSeventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median VT and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H2O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with VT and ΔP. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of VT and ΔP on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia.ConclusionIn this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of VT and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation. Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.BACKGROUNDMechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (VT) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and VT and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.AIMS AND METHODSThis was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (VT) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and VT and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median VT and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H2O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with VT and ΔP. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of VT and ΔP on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia.RESULTSSeventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median VT and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H2O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with VT and ΔP. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of VT and ΔP on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia.In this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of VT and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation.CONCLUSIONIn this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of VT and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation. Abstract Background Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury. Aims and methods This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (V T) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and V T and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia. Results Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median V T and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H2O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with V T and ΔP. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of V T and ΔP on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia. Conclusion In this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of V T and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation. Background Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury. Aims and methods This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume ( V T ) and driving pressure (Δ P ), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and V T and Δ P . Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia. Results Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median V T and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm H 2 O, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with V T and Δ P . Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of V T and Δ P on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia. Conclusion In this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of V T and the level of Δ P . The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation. |
| ArticleNumber | 74 |
| Author | Horn, Janneke Juffermans, Nicole P. de Beer, Friso M. Schultz, Marcus J. Bos, Lieuwe D. van der Poll, Tom van Mierlo, Gerard Wouters, Diana Zeerleder, Sacha Wieske, Luuk Lagrand, Wim K. |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33336309$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1097/MCC.0000000000000044 10.1097/CCM.0000000000002838 10.1161/01.CIR.96.10.3542 10.1056/NEJMra1208707 10.1016/j.intimp.2011.09.008 10.1016/0022-1759(93)90240-8 10.1007/s00134-014-3318-4 10.1097/00003246-198703000-00001 10.1136/thorax.2003.013888 10.1007/s12013-014-9983-7 10.1056/NEJM200005043421801 10.1097/00003246-199204000-00006 10.1001/jama.2016.0291 10.7326/0003-4819-151-8-200910200-00011 10.1097/CCM.0000000000001189 10.1097/CCM.0b013e3182923712 10.1093/qjmed/86.10.635 10.1186/s40635-019-0237-2 10.1016/j.trstmh.2011.10.010 10.1186/s13613-016-0190-0 10.1056/NEJMsa1410639 10.1186/1471-2466-9-49 10.4103/0366-6999.226840 10.1016/S2213-2600(16)30305-8 10.1152/jappl.1986.60.2.532 10.1007/s12013-013-9675-8 10.1378/chest.101.6.1644 |
| ContentType | Journal Article |
| Contributor | Witteveen, E de Jong, M D van der Sluijs, K F Straat, M Juffermans, N P Schouten, L R Glas, G J van der Poll, T Bos, L D Schultz, M J Huson, M A van Vught, L A Wiewel, M A Horn, J de Beer, F M Claushuis, T A Hoogendijk, A J Wieske, L Lagrand, W K Scicluna, B van Hooijdonk, R T |
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| Keywords | Intensive care Complement activation Driving pressure Bronchoalveolar lavage Complement component 5 Tidal volume Critical care Complement Mechanical ventilation C5a |
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countries (PRoVENT): an international, multicentre, prospective study publication-title: Lancet Respir Med doi: 10.1016/S2213-2600(16)30305-8 – volume: 67 start-page: 911 issue: 6 year: 2016 end-page: 918 ident: CR12 article-title: Complement activation contributes to ventilator-induced lung injury in rats publication-title: J Physiol Pharmacol – volume: 135 start-page: 651 issue: 3 year: 1987 end-page: 658 ident: CR24 article-title: Activation of the complement system in the adult respiratory distress syndrome publication-title: Am Rev Respir Dis – volume: 60 start-page: 532 issue: 2 year: 1986 end-page: 538 ident: CR23 article-title: Estimation of volume of epithelial lining fluid recovered by lavage using urea as marker of dilution publication-title: J Appl Physiol doi: 10.1152/jappl.1986.60.2.532 – volume: 55 start-page: 1705 issue: 12 year: 2010 end-page: 1716 ident: CR22 article-title: Documentation issues for mechanical ventilation in pressure-control modes publication-title: 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American College of Chest Physicians/Society of Critical Care Medicine publication-title: Chest doi: 10.1378/chest.101.6.1644 – volume: 20 start-page: 468 issue: 4 year: 1992 ident: 356_CR26 publication-title: Crit Care Med doi: 10.1097/00003246-199204000-00006 – volume: 86 start-page: 635 issue: 10 year: 1993 ident: 356_CR17 publication-title: Q J Med doi: 10.1093/qjmed/86.10.635 – volume: 41 start-page: 2373 issue: 10 year: 2013 ident: 356_CR16 publication-title: Crit Care Med doi: 10.1097/CCM.0b013e3182923712 – volume: 163 start-page: 67 issue: 1 year: 1993 ident: 356_CR19 publication-title: J Immunol Methods doi: 10.1016/0022-1759(93)90240-8 – volume: 131 start-page: 1225 issue: 10 year: 2018 ident: 356_CR8 publication-title: Chin Med J (Engl) doi: 10.4103/0366-6999.226840 – volume: 101 start-page: 1644 issue: 6 year: 1992 ident: 356_CR14 publication-title: Chest doi: 10.1378/chest.101.6.1644 – volume: 55 start-page: 1705 issue: 12 year: 2010 ident: 356_CR22 publication-title: Respir Care – volume: 135 start-page: 651 issue: 3 year: 1987 ident: 356_CR24 publication-title: Am Rev Respir Dis – volume: 20 start-page: 25 issue: 1 year: 2014 ident: 356_CR2 publication-title: Curr Opin Crit Care. doi: 10.1097/MCC.0000000000000044 – volume: 11 start-page: 2138 issue: 12 year: 2011 ident: 356_CR10 publication-title: Int Immunopharmacol doi: 10.1016/j.intimp.2011.09.008 – volume: 67 start-page: 1421 issue: 3 year: 2013 ident: 356_CR11 publication-title: Cell Biochem Biophys doi: 10.1007/s12013-013-9675-8 – volume: 307 start-page: 2526 issue: 23 year: 2012 ident: 356_CR15 publication-title: JAMA – volume: 59 start-page: 130 issue: 2 year: 2004 ident: 356_CR31 publication-title: Thorax doi: 10.1136/thorax.2003.013888 – volume: 40 start-page: 950 issue: 7 year: 2014 ident: 356_CR4 publication-title: Intensive Care Med doi: 10.1007/s00134-014-3318-4 – volume: 67 start-page: 911 issue: 6 year: 2016 ident: 356_CR12 publication-title: J Physiol Pharmacol – volume: 6 start-page: 89 issue: 1 year: 2016 ident: 356_CR21 publication-title: Ann Intensive Care doi: 10.1186/s13613-016-0190-0 – volume: 342 start-page: 1301 issue: 18 year: 2000 ident: 356_CR20 publication-title: N Engl J Med doi: 10.1056/NEJM200005043421801 – volume: 106 start-page: 90 issue: 2 year: 2012 ident: 356_CR30 publication-title: Trans R Soc Trop Med Hyg doi: 10.1016/j.trstmh.2011.10.010 – volume: 46 start-page: 300 issue: 2 year: 2018 ident: 356_CR7 publication-title: Crit Care Med doi: 10.1097/CCM.0000000000002838 – year: 2014 ident: 356_CR9 publication-title: Cell Biochem Biophys. doi: 10.1007/s12013-014-9983-7 – volume: 60 start-page: 532 issue: 2 year: 1986 ident: 356_CR23 publication-title: J Appl Physiol doi: 10.1152/jappl.1986.60.2.532 – volume: 151 start-page: 566 issue: 8 year: 2009 ident: 356_CR3 publication-title: Ann Intern Med doi: 10.7326/0003-4819-151-8-200910200-00011 – volume: 372 start-page: 747 issue: 8 year: 2015 ident: 356_CR6 publication-title: N Engl J Med doi: 10.1056/NEJMsa1410639 – volume: 369 start-page: 2126 issue: 22 year: 2013 ident: 356_CR1 publication-title: N Engl J Med doi: 10.1056/NEJMra1208707 – volume: 7 start-page: 35 issue: Suppl 1 year: 2019 ident: 356_CR13 publication-title: Intensive Care Med Exp doi: 10.1186/s40635-019-0237-2 – volume: 9 start-page: 49 year: 2009 ident: 356_CR29 publication-title: BMC Pulm Med doi: 10.1186/1471-2466-9-49 – volume: 43 start-page: 2155 issue: 10 year: 2015 ident: 356_CR5 publication-title: Crit Care Med doi: 10.1097/CCM.0000000000001189 – volume: 96 start-page: 3542 issue: 10 year: 1997 ident: 356_CR18 publication-title: Circulation doi: 10.1161/01.CIR.96.10.3542 – volume: 4 start-page: 882 issue: 11 year: 2016 ident: 356_CR28 publication-title: Lancet Respir Med doi: 10.1016/S2213-2600(16)30305-8 – volume: 15 start-page: 189 issue: 3 year: 1987 ident: 356_CR25 publication-title: Crit Care Med doi: 10.1097/00003246-198703000-00001 – volume: 315 start-page: 788 issue: 8 year: 2016 ident: 356_CR27 publication-title: JAMA doi: 10.1001/jama.2016.0291 |
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Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures.... Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The... BackgroundMechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures.... Abstract Background Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high... |
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| SubjectTerms | Bronchoalveolar lavage Critical care Critical Care Medicine Driving pressure Injuries Intensive Intensive care Lungs Mechanical ventilation Medicine Medicine & Public Health Observational studies Pneumonia Respiration Tidal volume Ventilators |
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| Title | The effects of tidal volume size and driving pressure levels on pulmonary complement activation: an observational study in critically ill patients |
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