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Re-Examining Permissive Hypercapnia in ARDS Barnes, Tavish; Zochios, Vasileios; Parhar, Ken

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Re-Examining Permissive Hypercapnia in ARDS Barnes, Tavish; Zochios, Vasileios; Parhar, Ken University of Birmingham Re-examining Permissive Hypercapnia in ARDS Barnes, Tavish; Zochios, Vasileios; Parhar, Ken DOI: 10.1016/j.chest.2017.11.010 License: Creative Commons: Attribution-NonCommercial-NoDerivs (CC BY-NC-ND) Document Version Peer reviewed version Citation for published version (Harvard): Barnes, T, Zochios, V & Parhar, K 2017, 'Re-examining Permissive Hypercapnia in ARDS: A Narrative review', Chest. https://doi.org/10.1016/j.chest.2017.11.010 Link to publication on Research at Birmingham portal General rights Unless a licence is specified above, all rights (including copyright and moral rights) in this document are retained by the authors and/or the copyright holders. The express permission of the copyright holder must be obtained for any use of this material other than for purposes permitted by law. •Users may freely distribute the URL that is used to identify this publication. •Users may download and/or print one copy of the publication from the University of Birmingham research portal for the purpose of private study or non-commercial research. •User may use extracts from the document in line with the concept of ‘fair dealing’ under the Copyright, Designs and Patents Act 1988 (?) •Users may not further distribute the material nor use it for the purposes of commercial gain. Where a licence is displayed above, please note the terms and conditions of the licence govern your use of this document. When citing, please reference the published version. Take down policy While the University of Birmingham exercises care and attention in making items available there are rare occasions when an item has been uploaded in error or has been deemed to be commercially or otherwise sensitive. If you believe that this is the case for this document, please contact [email protected] providing details and we will remove access to the work immediately and investigate. Download date: 28. Sep. 2021 Accepted Manuscript Re-examining permissive hypercapnia in ARDS: A narrative review Tavish Barnes, MD, Vasileios Zochios, MD, Ken Parhar, MD PII: S0012-3692(17)33115-X DOI: 10.1016/j.chest.2017.11.010 Reference: CHEST 1438 To appear in: CHEST Received Date: 5 July 2017 Revised Date: 20 October 2017 Accepted Date: 13 November 2017 Please cite this article as: Barnes T, Zochios V, Parhar K, Re-examining permissive hypercapnia in ARDS: A narrative review, CHEST (2017), doi: 10.1016/j.chest.2017.11.010. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT Word Count - Abstract: 110 Word Count – Body: 3987 Re-examining permissive hypercapnia in ARDS: A narrative review Tavish Barnes MD 1, Vasileios Zochios MD 2, Ken Parhar MD 1 1) Department of Critical Care Medicine, University of Calgary, Calgary, Canada 2) Department of Critical Care Medicine, University Hospitals Birmingham NHS Foundation Trust, Queen Elizabeth Hospital, College of Medical and Dental Sciences, University of Birmingham, Birmingham, England Corresponding author : Dr Ken Kuljit Singh Parhar Department of Critical Care Medicine. University of Calgary ICU Administration - Ground Floor - McCaig Tower Foothills Medical Center 3134 Hospital Drive NW Calgary, Alberta T2N 5A1 [email protected] Co-Author Email Addresses: Tavish Barnes MD : [email protected] MANUSCRIPT Vasileios Zochios MD : [email protected] .uk Disclosures : The authors (TB, VZ, KP) declare no conflicts of interest. Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. ACCEPTED ACCEPTED MANUSCRIPT Abbreviations Abbreviation Definition ABG Arterial Blood Gas ACP Acute Cor Pulmonale ALI Acute Lung Injury ARDS Acute Respiratory Distress Syndrome CI Confidence Interval CO 2 Carbon Dioxide CVP Central Venous Pressure Ees:Ea Ratio of elastance of right ventricle to elastance of pulmonary artery system ECLS Extra Corporeal Life Support HA Hypercapnic Acidosis HR Heart Rate IL-8 Interleukin 8 LPV Lung Protective Ventilation mPAP Mean Pulmonary Arterial Pressure MV Mechanical Ventilation NF-κB Nuclear factor kappa-light-chain-enhancer of activated B cells OR Odds Ratio PA Pulmonary Artery PaCO 2 Partial Pressure of arterial MANUSCRIPTCarbon Dioxide PaO 2 Partial Pressure of arterial Oxygen PBW Predicted Body Weight PEEP Positive End Expiratory Pressure Ppao Pulmonary artery Occlusion Pressure Pplat Plateau Pressure PVR Pulmonary Vascular Resistance RV Right Ventricle RVEDA/LVEDA Ratio of Right Ventricular End Diastolic Area to Left Ventricular End Diastolic Area RVEF Right Ventricular Ejection Fraction RVSWI Right Ventricular Stroke Work Index SVR Systemic Vascular Resistance TEE Trans Esophageal Echocardiography TTE Trans Thoracic Echocardiography VILI Ventilator Induced Lung Injury ACCEPTED 2 ACCEPTED MANUSCRIPT Abstract Lung protective ventilation has become the cornerstone of management in patients with ARDS. A subset of patients are unable to tolerate lung protective ventilation without significant carbon dioxide elevation. In these patients permissive hypercapnia is used. Although thought to be benign, it is becoming increasingly evident that elevated carbon dioxide levels have significant physiological effects. In this narrative review, we highlight clinically relevant end organ effects in both animal models and clinical studies. We also explore the association between elevated carbon dioxide, acute cor pulmonale and ICU mortality. We conclude with a brief review of alternative therapies for CO2 management currently under investigation in patients with moderate to severe ARDS. MANUSCRIPT ACCEPTED 3 ACCEPTED MANUSCRIPT Keywords: Permissive hypercapnia Mechanical Ventilation Acute respiratory distress syndrome Acute cor pulmonale Right ventricular dysfunction MANUSCRIPT ACCEPTED 4 ACCEPTED MANUSCRIPT 1. Introduction An improved understanding of the pathophysiology and clinical management of acute respiratory distress syndrome (ARDS) has led to lung protective ventilation (LPV) becoming a cornerstone of management. Early strategies of mechanical ventilation in ARDS were tailored to achieve tidal volume ventilation of 10-15 ml/kg predicted body weight (PBW) 1. High pressure, high tidal volume ventilation strategies were utilized to overcome densely consolidated, poorly compliant lung regions in an effort to achieve 2,3 adequate arterial oxygenation and normal carbon dioxide (CO 2) levels . This notion was disproven when the landmark ARMA trial by the ARDS Network demonstrated significant mortality benefit, (22% reduction) with pressure and volume limited LPV (6ml/kg vs 12 ml/kg PBW) 1. LPV may improve outcomes through several mechanisms including: decreased stretch and sheer forces applied to the alveolar wall (volutrauma and barotrauma), less cyclic recruitment-derecruitmMANUSCRIPTent of atelectatic areas of lung (atelectrauma) and attenuation of systemic cytokine response (biotrauma) 4. Unfortunately, mortality in severe ARDS remains high – upwards of 40% 5. A consequence of low tidal volume ventilation is a reduced ability to clear CO 2 due to reduced minute ventilation. A subset of patients cannot tolerate LPV without significant PaCO 2 elevation. In these patients, a higher respiratory rate to increase minute ventilation and lower PaCO 2 or permissive hypercapnia to facilitate low tidal volume ventilation, are used. Although initially thought to be benign or even protective, it is becoming increasingly evident that elevated CO 2 levels have significant physiological effects that mayACCEPTED in fact be deleterious. This review will outline both the physiological and clinical sequelae of permissive hypercapnia in ARDS. 2. Effects of hypercapnic acidosis in animal models 5 ACCEPTED MANUSCRIPT 2.1 Cytokine Response Normal CO 2 arterial tension is generally within the range of 35– 45 mmHg. Classification of hypercapnia is variably defined but will be referred to in this review as mild, moderate and severe according to ranges of 46-50 mmHg, 50-75 mmHg and greater than 75 mmHg, respectively6. At the molecular level, hypercapnic acidosis inhibits production of pro-inflammatory cytokines and has been shown to attenuate inflammation related to ventilator induced lung injury (VILI) by inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and interleukin 8 (IL-8) 7,8. Hypercapnic acidosis reduces oxidative reactions in the endotoxin-injured rat lung model 9. Hypercapnic acidosis has also been associated with less severe VILI in isolated perfused rabbit lungs ex vivo 10 and in vivo 11 . It has been suggested by several groups that therapeutic hypercapnia might provide benefitMANUSCRIPT in ARDS 12-14 and while decreasing host oxidative injury via hypercapnic acidosis would be of benefit in many cases, it may be deleterious when the etiology of ARDS is pulmonary infection and free radicals generated may play a role in facilitating bacterial injury and death 15 . At the cellular level, hypercapnia alone lowers release of IL-8 from lipopolysaccharide-stimulated neutrophils 16 while hypercapnic acidemia attenuates lung neutrophil recruitment and function.
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