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Zang M, Zeng C, Lagier D, Leng N, Grogg K, Motta-Ribeiro G, Laine AF, Winkler T, Melo MFV. Effects of Lung Expansion on Global and Regional Pulmonary Blood Volume in a Sheep Model of Acute Lung Injury. Anesthesiology 2025; 142:1071-1084. [PMID: 39946655 PMCID: PMC12074886 DOI: 10.1097/aln.0000000000005412] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 05/14/2025]
Abstract
BACKGROUND Pulmonary capillary blood volume is a major determinant of lung gas transport efficiency and also potentially related to ventilator-induced lung injury. However, knowledge on how lung expansion influences pulmonary blood volume in injured lungs is scant. The hypothesis was that lung expansion produced by positive end-expiratory pressure (PEEP) modulates the global and regional spatial distribution of pulmonary blood volume. METHODS In a lung injury model exposed to distinct lung expansion within clinical range (PEEP of 5 to 20 cm H 2 O), this study aimed to determine whole-lung and regional blood volume, their dynamic changes, and association with gas volume changes. Seven healthy sheep were subjected to 3 h of low-lung volume mechanical ventilation at a PEEP of 0 cm H 2 O and systemic endotoxemia. PEEP values of 5 (low), 20 (high), and 12 (intermediate) cm H 2 O were applied to produce distinct lung expansion. Respiratory-gated positron emission tomography with 11 C-labeled carbon monoxide and four-dimensional computed tomography were obtained to quantify blood volume and aeration. RESULTS Transpulmonary pressures were lowest at a PEEP of 12 cm H 2 O. Changes in whole-lung blood volume correlated with gas volume changes between PEEP of 5 and 12 cm H 2 O at end expiration ( P < 0.001) and end inspiration ( P < 0.001) but not between 12 and 20 cm H 2 O. Tissue-normalized blood volume ( ) was heterogeneously distributed, with mean values in nondependent regions ( = 0.116 ± 0.055) approximately seven times smaller than those in mid-dependent regions ( = 0.832 ± 0.132). A positive end-expiratory pressure of 12 cm H 2 O resulted in the most homogeneous distribution, with the largest means in mid-dependent regions and inspiratory 10th percentile, a measure of lowest values, throughout the lung. increased with inspiration at PEEP of 5 and 12 cm H 2 O but decreased with a PEEP of 20 cm H 2 O in mid-nondependent regions. CONCLUSIONS During low-volume mechanical ventilation and systemic endotoxemia, lung blood volume is markedly heterogeneously distributed, and modulated by PEEP. Nondependent regions are susceptible to low blood volume and capillary closure. Recruitment of pulmonary vascular blood volume with gas volume is nonlinear, limited at an intermediate PEEP, indicating its advantage to spatial distribution of blood volume.
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Affiliation(s)
- Mingyang Zang
- Department of Biomedical Engineering, Columbia University, New York, New York, USA
| | - Congli Zeng
- Department of Anesthesiology, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York, USA
| | - David Lagier
- Experimental Interventional Imaging Laboratory (LIIE), European Center for Research in Medical Imaging (CERIMED), Aix Marseille University, Marseille, France
| | - Nan Leng
- Department of Anesthesiology, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York, USA
| | - Kira Grogg
- Department of Radiology, Massachusetts General Hospital, Boston, Massachusetts, USA
| | - Gabriel Motta-Ribeiro
- Biomedical Engineering Program, Alberto Luiz Coimbra Institute for Graduate Studies and Research in Engineering, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
| | - Andrew F. Laine
- Department of Biomedical Engineering, Columbia University, New York, New York, USA
| | - Tilo Winkler
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
| | - Marcos F. Vidal Melo
- Department of Anesthesiology, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York, USA
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Joelsson JP, Karason S. Ventilator-induced lung injury in rat models: are they all equal in the race? Lab Anim Res 2025; 41:14. [PMID: 40390135 PMCID: PMC12090643 DOI: 10.1186/s42826-025-00240-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/16/2024] [Revised: 02/10/2025] [Accepted: 02/14/2025] [Indexed: 05/21/2025] Open
Abstract
Risk of ventilator-induced lung injury (VILI) is an inevitable and precarious accompaniment of ventilator treatment in critically ill patients worldwide. It can both instigate and aggravate acute respiratory distress syndrome (ARDS) where the only prevention or treatment so far has been empirical approach of what is considered to be lung protective ventilator settings in an attempt to shield the lung tissues against the mechanical stress that unavoidably follows ventilator treatment. The weakened state of the patients limits clinical drug research and pushes for drug discovery in animal models. Mice and rats are often the choice of small animal model, representing about 95% of all laboratory animal studies, as their physiology can mimic that which is found in humans. Mice have been a more popular choice for ventilator studies but due to technical issues, there is some advantage gained in using rats as they are substantially larger. Inducing VILI and ARDS in these models can prove challenging and often the acute nature of the injury used to produce similar tissue damage as in humans does not necessarily fully reflect clinical reality. The aim of this review was to analyse and summarize methods of recent publications in the field, describing what approaches have been utilized to simulate these conditions, possibly identifying a common track enabling comparison of results between studies. However, the study shows a high variety of methods employed by researchers causing comparisons of results difficult and perhaps implying that a more standardized approach should be used.
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Affiliation(s)
| | - Sigurbergur Karason
- University of Iceland, Reykjavik, Iceland
- Landspitali-University Hospital, Reykjavik, Iceland
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3
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Liu X, Li Y, Gu Y, Wang F, Tian B, Liu W, Ye Q. A modified rat model of 8 minutes asphyxial cardiac arrest and cardiopulmonary resuscitation. PLoS One 2025; 20:e0322473. [PMID: 40299857 PMCID: PMC12040107 DOI: 10.1371/journal.pone.0322473] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/11/2024] [Accepted: 03/21/2025] [Indexed: 05/01/2025] Open
Abstract
The animal model of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) serves as a crucial tool for investigating the pathophysiology and treatment strategies associated with cardiac arrest, however, standardized procedures for such models remain insufficiently established. We aimed to modify and specify the existing rat model of asphyxial CA and CPR while providing an analysis of long-term outcomes.A total of 46 rats were allocated into two groups,sham and CA group.In CA group, cardiac arrest was induced through 8 minutes of hypoxia prior to the administration of CPR. In sham group, only tracheal intubation and vascular catheterization were conducted under isoflurane anesthesia. Key parameters along with arterial blood gas results during modeling were meticulously recorded. After a 2-week postoperative observation period, the survival rate of rats and neurobehavioral changes on days 1, 3, 7, and 14 following resuscitation were assessed. Two weeks later, a pathological examination of brain tissue was conducted to evaluate neuronal damage. Results indicated that the average duration of cardiac arrest in CA group was 292.9 ± 12.5 seconds, with a return of spontaneous circulation rate of 78.95% and a survival rate at day 14 reaching 32%. After a duration of 2 weeks, the neurobehavioral scores of the surviving rats returned to their initial baseline levels; however, pathological examination revealed evidence of neuronal damage. In conclusion, we present a refined protocol for establishing a stable rat model of asphyxial CA and CPR, which may assist researchers in this field in enhancing the success rate of modeling.
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Affiliation(s)
- Xin Liu
- Department of Anesthesiology, People’s Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University,Yinchuan, Ningxia Hui Autonomous Region, China
| | - Yan Li
- Department of Anesthesiology, People’s Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University,Yinchuan, Ningxia Hui Autonomous Region, China
| | - Yinghua Gu
- Department of Anesthesiology, People’s Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University,Yinchuan, Ningxia Hui Autonomous Region, China
| | - Fa Wang
- Department of Anesthesiology, People’s Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University,Yinchuan, Ningxia Hui Autonomous Region, China
| | - Biyun Tian
- Department of Anesthesiology, People’s Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University,Yinchuan, Ningxia Hui Autonomous Region, China
| | - Wenxun Liu
- Department of Anesthesiology, People’s Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University,Yinchuan, Ningxia Hui Autonomous Region, China
| | - Qingshan Ye
- Department of Anesthesiology, People’s Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University,Yinchuan, Ningxia Hui Autonomous Region, China
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Deshwal H, Elkhapery A, Ramanathan R, Nair D, Singh I, Sinha A, Vashisht R, Mukherjee V. Patient-Self Inflicted Lung Injury (P-SILI): An Insight into the Pathophysiology of Lung Injury and Management. J Clin Med 2025; 14:1632. [PMID: 40095610 PMCID: PMC11900086 DOI: 10.3390/jcm14051632] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/14/2025] [Revised: 02/19/2025] [Accepted: 02/26/2025] [Indexed: 03/19/2025] Open
Abstract
Acute respiratory distress syndrome (ARDS) is a heterogeneous group of disease entities that are associated with acute hypoxic respiratory failure and significant morbidity and mortality. With a better understanding and phenotyping of lung injury, novel pathophysiologic mechanisms demonstrate the impact of a patient's excessive spontaneous breathing effort on perpetuating lung injury. Patient self-inflicted lung injury (P-SILI) is a recently identified phenomenon that delves into the impact of spontaneous breathing on respiratory mechanics in patients with lung injury. While the studies are hypothesis-generating and have been demonstrated in animal and human studies, further clinical trials are needed to identify its impact on ARDS management. The purpose of this review article is to highlight the physiologic mechanisms of P-SILI, novel tools and methods to detect P-SILI, and to review the current literature on non-invasive and invasive respiratory management in patients with ARDS.
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Affiliation(s)
- Himanshu Deshwal
- Division of Pulmonary, Sleep and Critical Care Medicine, Department of Medicine, School of Medicine, West Virginia University, Morgantown, WV 26506, USA
| | - Ahmed Elkhapery
- Department of Medicine, Rochester General Hospital, Rochester, NY 14621, USA
| | - Rudra Ramanathan
- Division of Pulmonary, Sleep and Critical Care Medicine, School of Medicine, New York University Grossman, New York, NY 10016, USA
| | - Deepak Nair
- Department of Medicine, Sinai Hospital of Baltimore, Baltimore, MD 21215, USA
| | - Isha Singh
- Department of Medicine, School of Medicine, West Virginia University, Morgantown, WV 26506, USA
| | - Ankur Sinha
- Section of Interventional Pulmonology, Division of Pulmonary, Allergy and Critical Care Medicine, School of Medicine, Stanford University, Stanford, CA 94305, USA
| | - Rishik Vashisht
- Division of Pulmonary and Critical Care Medicine, Macon and Joan Brock Virginia Health Sciences at Old Dominion University, Norfolk, VA 23508, USA
| | - Vikramjit Mukherjee
- Division of Pulmonary, Sleep and Critical Care Medicine, School of Medicine/Bellevue Hospital, New York University Grossman, New York, NY 10016, USA;
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Zhou D, Lv Y, Wang C, Li D. The modified effect of mechanical ventilation setting on relationship between fluid balance and hospital mortality for sepsis patients: a retrospective study. BMC Anesthesiol 2025; 25:91. [PMID: 39979809 PMCID: PMC11841162 DOI: 10.1186/s12871-025-02954-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/01/2024] [Accepted: 02/06/2025] [Indexed: 02/22/2025] Open
Abstract
BACKGROUND Fluid supplement may be affected by ventilatory management due to physiological interaction between heart and lung. The aim of the present study was to explore the effects of ventilator strategies on the relationship of fluid balance and hospital mortality for sepsis patients. METHODS This was a retrospective cohort study included sepsis patients with invasive mechanical ventilation (MV) over 24 h from Medical Information Mart for Intensive Care (MIMIC) IV database. The accumulative fluid balance increased by 6 h intervals were calculated as fluid intake minus fluid output. The modes (assisted or controlled) and levels (high or low) of positive end-expiratory pressure (PEEP) of MV every 6 h were recorded. The modification effect for modes and levels of PEEP on the relationship of fluid balance and hospital mortality were tested by multivariable regression models, respectively. RESULTS A total of 4466 sepsis patients with invasive MV were included, of which hospital mortality was 26.5%. Fluid balance seemed to have U-shape relationship with hospital mortality. The majority of patients used controlled ventilation at the beginning, and switched to assisted ventilation gradually; however, the PEEP level did not change a lot during the first 24 h. The relationship between fluid balance and hospital mortality was not modified by the ventilator mode; while the PEEP level may modify the relationship. CONCLUSIONS For sepsis patients admitted to ICU with invasive MV, the PEEP level, but not the mode of MV, appeared to modify the relationship of fluid balance and hospital mortality. The setting of mechanical ventilation may be an important consideration for fluid therapy.
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Affiliation(s)
- Dawei Zhou
- Department of Critical Care Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
| | - Yi Lv
- Department of Critical Care Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, China
| | - Chao Wang
- Department of Critical Care Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, China
| | - Dan Li
- Department of Critical Care Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, China
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Francovich JE, Katira BH, Jonkman AH. Electrical impedance tomography to set positive end-expiratory pressure. Curr Opin Crit Care 2025; 31:00075198-990000000-00250. [PMID: 39976222 PMCID: PMC12052045 DOI: 10.1097/mcc.0000000000001255] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/21/2025]
Abstract
PURPOSE OF REVIEW To summarize the rationale and concepts for positive end-expiratory pressure (PEEP) setting with electrical impedance tomography (EIT) and the effects of EIT-based PEEP setting on cardiopulmonary function. RECENT FINDINGS EIT allows patient-specific and regional assessment of PEEP effects on recruitability and overdistension, including its impact on ventilation-perfusion (V̇/Q) mismatch. The overdistension and collapse (OD-CL) method is the most used EIT-based approach for PEEP setting. In the RECRUIT study of 108 COVID-19 ARDS patients, the PEEP level corresponding to the OD-CL crossing point showed low overdistension and collapse (below 10% and 5%, respectively) regardless of recruitability. In a porcine model of acute respiratory distress syndrome (ARDS), it was shown that at this crossing point, respiratory mechanics (compliance, ΔP) were consistent, with adequate preload, lower right ventricular afterload, normal cardiac output, and sufficient gas exchange. A recent meta-analysis found that EIT based PEEP setting improved lung mechanics and potentially outcomes in ARDS patients. EIT thus provides critical insights beyond respiratory mechanics and oxygenation for individualized PEEP optimization. EIT-based methods for PEEP setting during assisted ventilation have also been proposed. SUMMARY EIT is a valuable technique to guide individualized PEEP setting utilizing cardiopulmonary information that is not captured by respiratory mechanics and oxygenation response alone.
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Affiliation(s)
| | - Bhushan H. Katira
- Department of Pediatrics, Washington University in St. Louis, School of Medicine, St. Louis, Missouri, USA
| | - Annemijn H. Jonkman
- Department of Adult Intensive Care, Erasmus Medical Center, Rotterdam, The Netherlands
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Manji A, Wang L, Pape CM, McCaig LA, Troitskaya A, Batnyam O, McDonald LJ, Appleton CT, Veldhuizen RA, Gill SE. Effect of aging on pulmonary cellular responses during mechanical ventilation. JCI Insight 2025; 10:e185834. [PMID: 39946196 PMCID: PMC11949020 DOI: 10.1172/jci.insight.185834] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/13/2024] [Accepted: 01/28/2025] [Indexed: 03/25/2025] Open
Abstract
Acute respiratory distress syndrome (ARDS) results in substantial morbidity and mortality, especially in elderly people. Mechanical ventilation, a common supportive treatment for ARDS, is necessary for maintaining gas exchange but can also propagate injury. We hypothesized that aging leads to alterations in surfactant function, inflammatory signaling, and microvascular permeability within the lung during mechanical ventilation. Young and aged male mice were mechanically ventilated, and surfactant function, inflammation, and vascular permeability were assessed. Additionally, single-cell RNA-Seq was used to delineate cell-specific transcriptional changes. The results showed that, in aged mice, surfactant dysfunction and vascular permeability were significantly augmented, while inflammation was less pronounced. Differential gene expression and pathway analyses revealed that alveolar macrophages in aged mice showed a blunted inflammatory response, while aged endothelial cells exhibited altered cell-cell junction formation. In vitro functional analysis revealed that aged endothelial cells had an impaired ability to form a barrier. These results highlight the complex interplay between aging and mechanical ventilation, including an age-related predisposition to endothelial barrier dysfunction, due to altered cell-cell junction formation, and decreased inflammation, potentially due to immune exhaustion. It is concluded that age-related vascular changes may underlie the increased susceptibility to injury during mechanical ventilation in elderly patients.
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Affiliation(s)
- Aminmohamed Manji
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
- Department of Physiology and Pharmacology
| | - Lefeng Wang
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
- Department of Medicine, and
| | - Cynthia M. Pape
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
- Department of Medicine, and
| | - Lynda A. McCaig
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
- Department of Medicine, and
| | - Alexandra Troitskaya
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
- Department of Physiology and Pharmacology
| | - Onon Batnyam
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
| | - Leah J.J. McDonald
- Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada
| | | | - Ruud A.W. Veldhuizen
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
- Department of Physiology and Pharmacology
- Department of Medicine, and
| | - Sean E. Gill
- Centre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada
- Department of Physiology and Pharmacology
- Department of Medicine, and
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Zhang X, Ye X, Xie Y, Yang Z, Spanos M, Guo Z, Jin Y, Li G, Lei Z, Schiffelers RM, Sluijter JPG, Wang H, Chen H, Xiao J. GEV Sod2 Powder: A Modified Product Based on Biovesicles Functioned in Air Pollution PM2.5-Induced Cardiopulmonary Injury. RESEARCH (WASHINGTON, D.C.) 2025; 8:0609. [PMID: 39949511 PMCID: PMC11822167 DOI: 10.34133/research.0609] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Received: 12/16/2024] [Revised: 01/16/2025] [Accepted: 01/20/2025] [Indexed: 02/16/2025]
Abstract
The prevention of air pollution-related cardiopulmonary disorders has been largely overlooked despite its important burden. Extracellular vesicles (EVs) have shown great potential as carriers for drug delivery. However, the efficiency and effect of EVs derived from different sources on ambient fine particulate matter (PM2.5)-induced cardiopulmonary injury remain unknown. Using PM2.5-exposed cellular and mouse models, we investigated the prevention of air pollution-related cardiopulmonary injury via an innovative strategy based on EV delivery. By using a "2-step" method that combines bibliometric and bioinformatic analysis, we identified superoxide dismutase 2 (Sod2) as a potential target for PM2.5-induced injury. Sod2-overexpressing plasmid was constructed and loaded into human plasma-, bovine milk-, and fresh grape-derived EVs, ultimately obtaining modified nanoparticles including PEV Sod2 , MEV Sod2 , and GEV Sod2 , respectively. GEV Sod2 , especially its lyophilized GEV Sod2 powder, exhibited superior protection against PM2.5-induced cardiopulmonary injury as compared to PEV Sod2 and MEV Sod2 . High-sensitivity structured illumination microscopy imaging and immunoblotting showed that GEV Sod2 powder treatment altered lysosome positioning by reducing Rab-7 expression. Our findings support the use of fruit-derived EVs as a preferred candidate for nucleic acid delivery and disease treatment, which may facilitate the translation of treatments for cardiopulmonary injuries.
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Affiliation(s)
- Xiao Zhang
- />School of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
- Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science,
Shanghai University, Shanghai 200444, China
- Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Medicine,
Shanghai University, Shanghai 200444, China
| | - Xuan Ye
- />School of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
| | - Yuling Xie
- Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science,
Shanghai University, Shanghai 200444, China
- Department of Cardiovascular Surgery,
Fujian Medical University Union Hospital, Fuzhou 350001, China
- Fujian Provincial Center for Cardiovascular Medicine, Fuzhou 350001, China
| | - Zijiang Yang
- Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science,
Shanghai University, Shanghai 200444, China
- Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Medicine,
Shanghai University, Shanghai 200444, China
| | - Michail Spanos
- Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
| | - Zilin Guo
- Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science,
Shanghai University, Shanghai 200444, China
- Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Medicine,
Shanghai University, Shanghai 200444, China
| | - YuXin Jin
- QianWeiChang College,
Shanghai University, Shanghai 200444, China
| | - Guoping Li
- Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
| | - Zhiyong Lei
- CDL Research,
University Medical Center Utrecht, Utrecht, The Netherlands
- Department of Cardiology, Laboratory of Experimental Cardiology,
University Medical Center Utrecht, Utrecht, The Netherlands
- UMC Utrecht Regenerative Medicine Center, Circulatory Health Research Center, University Medical Center,
Utrecht University, Utrecht, The Netherlands
| | | | - Joost P. G. Sluijter
- Department of Cardiology, Laboratory of Experimental Cardiology,
University Medical Center Utrecht, Utrecht, The Netherlands
- UMC Utrecht Regenerative Medicine Center, Circulatory Health Research Center, University Medical Center,
Utrecht University, Utrecht, The Netherlands
| | - Hongyun Wang
- Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science,
Shanghai University, Shanghai 200444, China
- Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Medicine,
Shanghai University, Shanghai 200444, China
| | - Huihua Chen
- />School of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
| | - Junjie Xiao
- Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science,
Shanghai University, Shanghai 200444, China
- Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Medicine,
Shanghai University, Shanghai 200444, China
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Zakynthinos GE, Tsolaki V, Mantzarlis K, Xanthopoulos A, Oikonomou E, Kalogeras K, Siasos G, Vavuranakis M, Makris D, Zakynthinos E. Navigating Heart-Lung Interactions in Mechanical Ventilation: Pathophysiology, Diagnosis, and Advanced Management Strategies in Acute Respiratory Distress Syndrome and Beyond. J Clin Med 2024; 13:7788. [PMID: 39768712 PMCID: PMC11728210 DOI: 10.3390/jcm13247788] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/11/2024] [Revised: 12/13/2024] [Accepted: 12/17/2024] [Indexed: 01/16/2025] Open
Abstract
Patients in critical condition who require mechanical ventilation experience intricate interactions between their respiratory and cardiovascular systems. These complex interactions are crucial for clinicians to understand as they can significantly influence therapeutic decisions and patient outcomes. A deep understanding of heart-lung interactions is essential, particularly under the stress of mechanical ventilation, where the right ventricle plays a pivotal role and often becomes a primary concern. Positive pressure ventilation, commonly used in mechanical ventilation, impacts right and left ventricular pre- and afterload as well as ventricular interplay. The right ventricle is especially susceptible to these changes, and its function can be critically affected, leading to complications such as right heart failure. Clinicians must be adept at recognizing and managing these interactions to optimize patient care. This perspective will analyze this matter comprehensively, covering the pathophysiology of these interactions, the monitoring of heart-lung dynamics using the latest methods (including ECHO), and management and treatment strategies for related conditions. In particular, the analysis will delve into the efficacy and limitations of various treatment modalities, including pharmaceutical interventions, nuanced ventilator management strategies, and advanced devices such as extracorporeal membrane oxygenation (ECMO). Each approach will be examined for its impact on optimizing right ventricular function, mitigating complications, and ultimately improving patient outcomes in the context of mechanical ventilation.
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Affiliation(s)
- George E. Zakynthinos
- 3rd Department of Cardiology, “Sotiria” Chest Diseases Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece; (G.E.Z.); (E.O.); (K.K.); (G.S.); (M.V.)
| | - Vasiliki Tsolaki
- Critical Care Department, University Hospital of Larissa, Faculty of Medicine, University of Thessaly, Mezourlo, 41335 Larissa, Greece; (V.T.); (K.M.); (D.M.)
| | - Kostantinos Mantzarlis
- Critical Care Department, University Hospital of Larissa, Faculty of Medicine, University of Thessaly, Mezourlo, 41335 Larissa, Greece; (V.T.); (K.M.); (D.M.)
| | - Andrew Xanthopoulos
- Department of Cardiology, University Hospital of Larissa, Faculty of Medicine, University of Thessaly, 41110 Larissa, Greece;
| | - Evangelos Oikonomou
- 3rd Department of Cardiology, “Sotiria” Chest Diseases Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece; (G.E.Z.); (E.O.); (K.K.); (G.S.); (M.V.)
| | - Konstantinos Kalogeras
- 3rd Department of Cardiology, “Sotiria” Chest Diseases Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece; (G.E.Z.); (E.O.); (K.K.); (G.S.); (M.V.)
| | - Gerasimos Siasos
- 3rd Department of Cardiology, “Sotiria” Chest Diseases Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece; (G.E.Z.); (E.O.); (K.K.); (G.S.); (M.V.)
- Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
| | - Manolis Vavuranakis
- 3rd Department of Cardiology, “Sotiria” Chest Diseases Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece; (G.E.Z.); (E.O.); (K.K.); (G.S.); (M.V.)
| | - Demosthenes Makris
- Critical Care Department, University Hospital of Larissa, Faculty of Medicine, University of Thessaly, Mezourlo, 41335 Larissa, Greece; (V.T.); (K.M.); (D.M.)
| | - Epaminondas Zakynthinos
- Critical Care Department, University Hospital of Larissa, Faculty of Medicine, University of Thessaly, Mezourlo, 41335 Larissa, Greece; (V.T.); (K.M.); (D.M.)
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10
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Katira BH, Brochard LJ. Fluids Matter in Lung Injury but Not Where We Thought. Am J Respir Crit Care Med 2024; 211:301-303. [PMID: 39642349 PMCID: PMC11936132 DOI: 10.1164/rccm.202412-2354ed] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/02/2024] [Accepted: 12/04/2024] [Indexed: 12/08/2024] Open
Affiliation(s)
- Bhushan H Katira
- Washington University in St Louis School of Medicine, Paediatric Critical Care Medicine, St Louis, Missouri, United States
| | - Laurent J Brochard
- St Michael's Hospital in Toronto, Li Ka Shing Knowledge Institute, Keenan Research Centre, Toronto, Canada
- University of Toronto, Interdepartmental Division of Critical Care Medicine, Toronto, Ontario, Canada;
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11
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Yuan S, Chen X, Mi L, Chi Y, Huang H, Liu B, Yue C, Zhao Z, Su L, Long Y, Akin Ş, Ince C, He H. Effect of fluid and driving pressure on cyclical "on-off" flow of pulmonary microcirculation during mechanical ventilation. Intensive Care Med Exp 2024; 12:112. [PMID: 39630324 PMCID: PMC11618265 DOI: 10.1186/s40635-024-00689-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/28/2024] [Accepted: 10/23/2024] [Indexed: 12/08/2024] Open
Abstract
OBJECTIVES This study aimed to identify the cyclical "on-off" flow of pulmonary microcirculation during inspiration and expiration by sidestream dark field imaging (SDF) technology in vivo and investigate the effects of volume status and driving pressure on cyclical "on-off" flow of microcirculation. METHODS 24 ARDS-modeled rabbits were randomly divided into high-driving pressure group (HDP group) and low-driving pressure group (LDP group). Lung microcirculation measurements were performed using the SDF microscope at two timepoints (T1 CVP 2-4 mmHg, T2 CVP 8-10 mmHg). From T1 to T2, 10 ml/kg saline was infused to increase CVP. The cyclical "on-off" pulmonary microcirculation was quantitatively assessed by the change of microcirculation between expiration and inspiration. RESULTS Proportion of perfused vessels (PPV), microvascular flow index (MFI), perfused vessel density (PVD), and total vessel density (TVD) at expiration were significantly higher than inspiration in the HDP group. The HDP group has a higher ΔPPV and ΔPVD. After fluid loading, ΔPPV and ΔMFI decreased. TNF-α, IL-6, Ang-2, and vWF levels in the HDP group were higher. The HDP group also has a higher lung wet-weight/body weight ratio, lung wet-to-dry weight ratio, and more severe damage of pulmonary capillaries than the LDP group. CONCLUSIONS The difference in alveolar perfused microcirculation between inspiration and expiration defined as cyclical "on-off flow" can be detected. High driving pressure can enhance the cyclical "on-off" flow, and fluid loading can relieve it. High driving pressure can potentially cause injury to pulmonary capillaries due to the phenomenon of "on-off" flow, thereby exacerbating ARDS.
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Affiliation(s)
- Siyi Yuan
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China
| | - Xiangyu Chen
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China
| | - Liangyu Mi
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China
| | - Yi Chi
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China
| | - Haoping Huang
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China
| | - Bo Liu
- Department of Critical Care Medicine, Affiliated Hospital of Jining Medical University, Jining, China
| | - Chaofu Yue
- Deparment of Intensive Care Unit, Qu Jing NO.1 Hospital, Qu Jing, Yun Nan, China
| | - Zeming Zhao
- Jiamusi Central Hospital, Jiamusi, Heilongjiang Province, China
| | - Longxiang Su
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China
| | - Yun Long
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China.
| | - Şakir Akin
- Department of Intensive Care, Erasmus MC University Hospital, Rotterdam, Netherlands
- Department of Intensive Care, Haga Teaching Hospital, The Hague, The Netherlands
| | - Can Ince
- Department of Intensive Care, Erasmus MC University Hospital, Rotterdam, Netherlands
| | - Huaiwu He
- Department of Critical Care Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, 1 Shuaifuyuan, Beijing, China.
- Department of Intensive Care, Erasmus MC University Hospital, Rotterdam, Netherlands.
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12
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Castellví-Font A, Goligher EC, Dianti J. Lung and Diaphragm Protection During Mechanical Ventilation in Patients with Acute Respiratory Distress Syndrome. Clin Chest Med 2024; 45:863-875. [PMID: 39443003 DOI: 10.1016/j.ccm.2024.08.007] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/25/2024]
Abstract
Patients with acute respiratory distress syndrome often require mechanical ventilation to maintain adequate gas exchange and to reduce the workload of the respiratory muscles. Although lifesaving, positive pressure mechanical ventilation can potentially injure the lungs and diaphragm, further worsening patient outcomes. While the effect of mechanical ventilation on the risk of developing lung injury is widely appreciated, its potentially deleterious effects on the diaphragm have only recently come to be considered by the broader intensive care unit community. Importantly, both ventilator-induced lung injury and ventilator-induced diaphragm dysfunction are associated with worse patient-centered outcomes.
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Affiliation(s)
- Andrea Castellví-Font
- Critical Care Department, Hospital del Mar de Barcelona, Critical Illness Research Group (GREPAC), Hospital del Mar Research Institute (IMIM), Passeig Marítim de la Barceloneta 25-29, Ciutat Vella, 08003, Barcelona, Spain; Interdepartmental Division of Critical Care Medicine, University of Toronto, 27 King's College Circle, Toronto, Ontario M5S 1A1, Canada; Division of Respirology, Department of Medicine, University Health Network, Toronto, Canada
| | - Ewan C Goligher
- Interdepartmental Division of Critical Care Medicine, University of Toronto, 27 King's College Circle, Toronto, Ontario M5S 1A1, Canada; Division of Respirology, Department of Medicine, University Health Network, Toronto, Canada; University Health Network/Sinai Health System, University of Toronto, 27 King's College Circle, Toronto, Ontario M5S 1A1, Canada; Toronto General Hospital Research Institute, 200 Elizabeth Street, Toronto, Ontario M5G 2C4, Canada; Department of Physiology, University of Toronto, 27 King's College Circle, Toronto, Ontario M5S 1A1, Canada.
| | - Jose Dianti
- Critical Care Medicine Department, Centro de Educación Médica e Investigaciones Clínicas "Norberto Quirno" (CEMIC), Av. E. Galván 4102, Ciudad de Buenos Aires, Argentina
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13
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Xia T, Pan Z, Wan H, Li Y, Mao G, Zhao J, Zhang F, Pan S. Mechanisms of mechanical stimulation in the development of respiratory system diseases. Am J Physiol Lung Cell Mol Physiol 2024; 327:L724-L739. [PMID: 39316681 DOI: 10.1152/ajplung.00122.2024] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/09/2024] [Revised: 09/06/2024] [Accepted: 09/11/2024] [Indexed: 09/26/2024] Open
Abstract
During respiration, mechanical stress can initiate biological responses that impact the respiratory system. Mechanical stress plays a crucial role in the development of the respiratory system. However, pathological mechanical stress can impact the onset and progression of respiratory diseases by influencing the extracellular matrix and cell transduction processes. In this article, we explore the mechanisms by which mechanical forces communicate with and influence cells. We outline the basic knowledge of respiratory mechanics, elucidating the important role of mechanical stimulation in influencing respiratory system development and differentiation from a microscopic perspective. We also explore the potential mechanisms of mechanical transduction in the pathogenesis and development of respiratory diseases such as asthma, lung injury, pulmonary fibrosis, and lung cancer. Finally, we look forward to new research directions in cellular mechanotransduction, aiming to provide fresh insights for future therapeutic research on respiratory diseases.
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Affiliation(s)
- Tian Xia
- Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
- Institute of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
| | - Ziyin Pan
- Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University, Shanghai, People's Republic of China
| | - Haoxin Wan
- Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
- Institute of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
| | - Yongsen Li
- Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
- Institute of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
| | - Guocai Mao
- Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
- Institute of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
| | - Jun Zhao
- Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
- Institute of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
| | - Fangbiao Zhang
- Department of Cardiothoracic Surgery, Lishui Municipal Central Hospital, Lishui, People's Republic of China
| | - Shu Pan
- Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
- Institute of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China
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14
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Zochios V, Yusuff H, Antonini MV. Prone Positioning and Right Ventricular Protection During Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. ASAIO J 2024; 70:e119-e122. [PMID: 38941486 DOI: 10.1097/mat.0000000000002261] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/30/2024] Open
Affiliation(s)
- Vasileios Zochios
- From the University Hospitals of Leicester National Health Service Trust, Glenfield Hospital Extracorporeal Membrane Oxygenation Unit, Leicester, United Kingdom
- Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom
| | - Hakeem Yusuff
- From the University Hospitals of Leicester National Health Service Trust, Glenfield Hospital Extracorporeal Membrane Oxygenation Unit, Leicester, United Kingdom
- Department of Respiratory Sciences, University of Leicester, Leicester, United Kingdom
- National Institute for Health and Care Research (NIHR) Leicester Biomedical Research Unit, Glenfield Hospital, Leicester, United Kingdom
| | - Marta Velia Antonini
- Intensive Care Unit, Bufalini Hospital, AUSL della Romagna, Cesena, Italy
- Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy
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15
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Marongiu I, Slobod D, Leali M, Spinelli E, Mauri T. Clinical and Experimental Evidence for Patient Self-Inflicted Lung Injury (P-SILI) and Bedside Monitoring. J Clin Med 2024; 13:4018. [PMID: 39064059 PMCID: PMC11278124 DOI: 10.3390/jcm13144018] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/17/2024] [Revised: 07/01/2024] [Accepted: 07/07/2024] [Indexed: 07/28/2024] Open
Abstract
Patient self-inflicted lung injury (P-SILI) is a major challenge for the ICU physician: although spontaneous breathing is associated with physiological benefits, in patients with acute respiratory distress syndrome (ARDS), the risk of uncontrolled inspiratory effort leading to additional injury needs to be assessed to avoid delayed intubation and increased mortality. In the present review, we analyze the available clinical and experimental evidence supporting the existence of lung injury caused by uncontrolled high inspiratory effort, we discuss the pathophysiological mechanisms by which increased effort causes P-SILI, and, finally, we consider the measurements and interpretation of bedside physiological measures of increased drive that should alert the clinician. The data presented in this review could help to recognize injurious respiratory patterns that may trigger P-SILI and to prevent it.
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Affiliation(s)
- Ines Marongiu
- Department of Anesthesia, Critical Care and Emergency, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; (I.M.)
| | - Douglas Slobod
- Department of Critical Care Medicine, McGill University, Montreal, QC H4A 3J1, Canada
| | - Marco Leali
- Department of Pathophysiology and Transplantation, University of Milan, 20122 Milan, Italy
| | - Elena Spinelli
- Department of Anesthesia, Critical Care and Emergency, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; (I.M.)
| | - Tommaso Mauri
- Department of Anesthesia, Critical Care and Emergency, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; (I.M.)
- Department of Pathophysiology and Transplantation, University of Milan, 20122 Milan, Italy
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16
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Xingzheng L, Weiguang G, Quanqiu Y, Huifen Z, Zijun Z, Qiming Z, Suhua Y, Fu Z, Zhigang J. The impact of positive end-expiratory pressure on right ventricular function in patients with moderate-to-severe ARDS: a prospective paired-design study. Front Med (Lausanne) 2024; 11:1424090. [PMID: 39015782 PMCID: PMC11250698 DOI: 10.3389/fmed.2024.1424090] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/27/2024] [Accepted: 06/14/2024] [Indexed: 07/18/2024] Open
Abstract
Objective To determine the effects of varying positive end-expiratory pressures (PEEPs) on right ventricular function, hemodynamics, oxygenation, and the incidence of acute cor pulmonale (ACP) in patients with moderate-to-severe acute respiratory distress syndrome (ARDS). Methods This prospective paired-design study involved patients with moderate-to-severe ARDS in the ICU. Participants received lung-protective ventilation and hemodynamic monitoring. During the study, mechanical ventilation was administered with PEEPs of 5 cmH2O, 10 cmH2O, and 15 cmH2O, while maintaining an end-inspiratory plateau pressure ≤ 30 cmH2O. Various assessments, including transthoracic echocardiography, cardiac output measurement, and blood gas analysis, were conducted at baseline and after 1 h of ventilation at each PEEP. Subsequently, variations in ventilation oxygenation, echocardiographic parameters, and hemodynamic indicators under different PEEPs were analyzed to explore the potential effects of PEEP on right ventricular function and hemodynamics, as well as the incidence of ACP. Results A total of 317 ARDS patients were screened. Among them, 104 met the diagnostic criteria for moderate-to-severe ARDS, and 52 completed the study. The baseline PEEP of these 52 participants, acquired before commencement, was 11.5 ± 1.7 cmH2O, and the incidence of ACP was 25.0% (13/52). Intensive care unit mortality, overall hospital mortality, and 28-day mortality rates were 19.2% (10/52), 21.2% (11/52), and 32.7% (17/52), respectively. During the study, ACP incidences at PEEPs of 5 cmH2O, 10 cmH2O, and 15 cmH2O were 17.3% (9/52), 21.2% (11/52), and 38.5% (20/52), respectively. Meanwhile, the PaO2/FiO2 ratio improved with increasing PEEP, reaching 162.0 (140.9, 174.0), 171.0 (144.0, 182.0), and 176.5 (151.0, 196) mmHg at PEEPs of 5 cmH2O, 10 cmH2O, and 15 cmH2O, respectively. In addition, higher PEEPs were associated with a slight increase in PaCO2, showing statistically significant differences compared to moderate and low PEEPs. Compared to a PEEP of 5 cmH2O or 10 cmH2O, right ventricular function exhibited substantial changes at 15 cmH2O PEEP, manifested as increased pulmonary artery systolic pressure, enlarged right ventricular end-diastolic area, and decreased tricuspid annular plane systolic excursion, all with significant differences. Conversely, variations in left ventricular end-diastolic area and ejection fraction were not statistically significant. In terms of hemodynamics, increasing PEEP resulted in a decline in cardiac index (CI), with statistically significant differences between different PEEPs. Specifically, compared to the value at a PEEP of 5 cmH2O, the CI at a PEEP of 15 cmH2O decreased by 14.3% (2.63 [2.20, 2.95] vs. 3.07 [2.69, 3.67], p < 0.001). The decline in the stroke volume index with PEEP was more obvious (22.1 [18.4, 27.1] vs. 27.0 [24.2, 33.0], p < 0.001), reaching 18.1%. Additionally, both end-diastolic volume index and extravascular lung water index decreased significantly with increasing PEEP, while the pulmonary vascular permeability index remained unaffected. Conclusion Different PEEPs can affect the incidence of ACP in patients with moderate-to-severe ARDS. High PEEP improves oxygenation and reduces extravascular lung water without significantly affecting the pulmonary vascular permeability index and left ventricular systolic function. Nevertheless, it can cause right ventricular dilation, as well as substantial declines in right ventricular systolic function and CI, thereby causing ACP.
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Affiliation(s)
- Luo Xingzheng
- Department of Critical Care Medicine, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Gu Weiguang
- Department of Critical Care Medicine, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Ye Quanqiu
- Department of Critical Care Medicine, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Zhou Huifen
- Department of Critical Care Medicine, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Zheng Zijun
- Department of Critical Care Medicine, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Zou Qiming
- Department of Critical Care Medicine, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Yuan Suhua
- Department of Medical Records, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Zhang Fu
- Department of Ultrasound, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
| | - Jian Zhigang
- Department of Critical Care Medicine, Xiaolan People’s Hospital of Zhongshan, Zhongshan, Guangdong, China
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17
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Cruces P, Retamal J, Damián A, Lago G, Blasina F, Oviedo V, Medina T, Pérez A, Vaamonde L, Dapueto R, González-Dambrauskas S, Serra A, Monteverde-Fernandez N, Namías M, Martínez J, Hurtado DE. A machine-learning regional clustering approach to understand ventilator-induced lung injury: a proof-of-concept experimental study. Intensive Care Med Exp 2024; 12:60. [PMID: 38954052 PMCID: PMC11220131 DOI: 10.1186/s40635-024-00641-8] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/17/2024] [Accepted: 06/17/2024] [Indexed: 07/04/2024] Open
Abstract
BACKGROUND The spatiotemporal progression and patterns of tissue deformation in ventilator-induced lung injury (VILI) remain understudied. Our aim was to identify lung clusters based on their regional mechanical behavior over space and time in lungs subjected to VILI using machine-learning techniques. RESULTS Ten anesthetized pigs (27 ± 2 kg) were studied. Eight subjects were analyzed. End-inspiratory and end-expiratory lung computed tomography scans were performed at the beginning and after 12 h of one-hit VILI model. Regional image-based biomechanical analysis was used to determine end-expiratory aeration, tidal recruitment, and volumetric strain for both early and late stages. Clustering analysis was performed using principal component analysis and K-Means algorithms. We identified three different clusters of lung tissue: Stable, Recruitable Unstable, and Non-Recruitable Unstable. End-expiratory aeration, tidal recruitment, and volumetric strain were significantly different between clusters at early stage. At late stage, we found a step loss of end-expiratory aeration among clusters, lowest in Stable, followed by Unstable Recruitable, and highest in the Unstable Non-Recruitable cluster. Volumetric strain remaining unchanged in the Stable cluster, with slight increases in the Recruitable cluster, and strong reduction in the Unstable Non-Recruitable cluster. CONCLUSIONS VILI is a regional and dynamic phenomenon. Using unbiased machine-learning techniques we can identify the coexistence of three functional lung tissue compartments with different spatiotemporal regional biomechanical behavior.
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Affiliation(s)
- Pablo Cruces
- Facultad de Ciencias de la Vida, Universidad Andres Bello, Santiago, Chile
- Unidad de Paciente Crítico Pediátrico, Hospital El Carmen Dr. Luis Valentín Ferrada, Santiago, Chile
| | - Jaime Retamal
- Departamento de Medicina Intensiva, Pontificia Universidad Católica de Chile, Santiago, Chile.
| | - Andrés Damián
- Centro Uruguayo de Imagenología Molecular (CUDIM), Montevideo, Uruguay
- Unidad Académica de Medicina Nuclear e Imagenología Molecular, Hospital de Clínicas, Universidad de la República, Montevideo, Uruguay
| | - Graciela Lago
- Centro Uruguayo de Imagenología Molecular (CUDIM), Montevideo, Uruguay
- Academia Nacional de Medicina, Montevideo, Uruguay
| | - Fernanda Blasina
- Unidad Académica de Neonatología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
| | - Vanessa Oviedo
- Departamento de Medicina Intensiva, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Tania Medina
- Unidad de Paciente Crítico Pediátrico, Hospital El Carmen Dr. Luis Valentín Ferrada, Santiago, Chile
| | - Agustín Pérez
- Department of Structural and Geotechnical Engineering, School of Engineering, Pontificia Universidad Católica de Chile, Santiago, Chile
- Institute for Biological and Medical Engineering, Schools of Engineering, Medicine and Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Lucía Vaamonde
- Departamento de Pediatría y Unidad de Cuidados Intensivos de Niños del Centro Hospitalario Pereira Rossell, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
| | - Rosina Dapueto
- Centro Uruguayo de Imagenología Molecular (CUDIM), Montevideo, Uruguay
| | - Sebastian González-Dambrauskas
- Departamento de Pediatría y Unidad de Cuidados Intensivos de Niños del Centro Hospitalario Pereira Rossell, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
- Red Colaborativa Pediátrica de Latinoamérica (LARed Network), Montevideo, Uruguay
| | - Alberto Serra
- Red Colaborativa Pediátrica de Latinoamérica (LARed Network), Montevideo, Uruguay
- Centro Asistencial del Sindicato Médico del Uruguay (CASMU), Montevideo, Uruguay
| | - Nicolas Monteverde-Fernandez
- Red Colaborativa Pediátrica de Latinoamérica (LARed Network), Montevideo, Uruguay
- Cuidados Intensivos Pediátricos y Neonatales (CINP), Medica Uruguaya, Montevideo, Uruguay
| | - Mauro Namías
- Fundación Centro Diagnóstico Nuclear, Buenos Aires, Argentina
| | - Javier Martínez
- Red Colaborativa Pediátrica de Latinoamérica (LARed Network), Montevideo, Uruguay
- Hospital Central de las Fuerzas Armadas (HCFFAA), Montevideo, Uruguay
| | - Daniel E Hurtado
- Department of Structural and Geotechnical Engineering, School of Engineering, Pontificia Universidad Católica de Chile, Santiago, Chile
- Institute for Biological and Medical Engineering, Schools of Engineering, Medicine and Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile
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Joseph A, Petit M, Vieillard-Baron A. Hemodynamic effects of positive end-expiratory pressure. Curr Opin Crit Care 2024; 30:10-19. [PMID: 38085886 DOI: 10.1097/mcc.0000000000001124] [Citation(s) in RCA: 6] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/03/2024]
Abstract
PURPOSE OF REVIEW Positive end-expiratory pressure (PEEP) is required in the Berlin definition of acute respiratory distress syndrome and is a cornerstone of its treatment. Application of PEEP increases airway pressure and modifies pleural and transpulmonary pressures according to respiratory mechanics, resulting in blood volume alteration into the pulmonary circulation. This can in turn affect right ventricular preload, afterload and function. At the opposite, PEEP may improve left ventricular function, providing no deleterious effect occurs on the right ventricle. RECENT FINDINGS This review examines the impact of PEEP on cardiac function with regards to heart-lung interactions, and describes its consequences on organs perfusion and function, including the kidney, gut, liver and the brain. PEEP in itself is not beneficious nor detrimental on end-organ hemodynamics, but its hemodynamic effects vary according to both respiratory mechanics and association with other hemodynamic variables such as central venous or mean arterial pressure. There are parallels in the means of preventing deleterious impact of PEEP on the lungs, heart, kidney, liver and central nervous system. SUMMARY The quest for optimal PEEP settings has been a prominent goal in ARDS research for the last decades. Intensive care physician must maintain a high degree of vigilance towards hemodynamic effects of PEEP on cardiac function and end-organs circulation.
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Affiliation(s)
- Adrien Joseph
- Medical Intensive Care Unit, Ambroise Paré Hospital, Assistance Publique-Hôpitaux de Paris, Boulogne-Billancourt
| | - Matthieu Petit
- Medical Intensive Care Unit, Ambroise Paré Hospital, Assistance Publique-Hôpitaux de Paris, Boulogne-Billancourt
- Inserm, CESP, Paris-Saclay University, Université de Versailles Saint-Quentin-en-Yvelines, Villejuif, France
| | - Antoine Vieillard-Baron
- Medical Intensive Care Unit, Ambroise Paré Hospital, Assistance Publique-Hôpitaux de Paris, Boulogne-Billancourt
- Inserm, CESP, Paris-Saclay University, Université de Versailles Saint-Quentin-en-Yvelines, Villejuif, France
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19
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Silva PL, Scharffenberg M, Rocco PRM. Understanding the mechanisms of ventilator-induced lung injury using animal models. Intensive Care Med Exp 2023; 11:82. [PMID: 38010595 PMCID: PMC10682329 DOI: 10.1186/s40635-023-00569-5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/19/2023] [Accepted: 11/17/2023] [Indexed: 11/29/2023] Open
Abstract
Mechanical ventilation is a life-saving therapy in several clinical situations, promoting gas exchange and providing rest to the respiratory muscles. However, mechanical ventilation may cause hemodynamic instability and pulmonary structural damage, which is known as ventilator-induced lung injury (VILI). The four main injury mechanisms associated with VILI are as follows: barotrauma/volutrauma caused by overstretching the lung tissues; atelectrauma, caused by repeated opening and closing of the alveoli resulting in shear stress; and biotrauma, the resulting biological response to tissue damage, which leads to lung and multi-organ failure. This narrative review elucidates the mechanisms underlying the pathogenesis, progression, and resolution of VILI and discusses the strategies that can mitigate VILI. Different static variables (peak, plateau, and driving pressures, positive end-expiratory pressure, and tidal volume) and dynamic variables (respiratory rate, airflow amplitude, and inspiratory time fraction) can contribute to VILI. Moreover, the potential for lung injury depends on tissue vulnerability, mechanical power (energy applied per unit of time), and the duration of that exposure. According to the current evidence based on models of acute respiratory distress syndrome and VILI, the following strategies are proposed to provide lung protection: keep the lungs partially collapsed (SaO2 > 88%), avoid opening and closing of collapsed alveoli, and gently ventilate aerated regions while keeping collapsed and consolidated areas at rest. Additional mechanisms, such as subject-ventilator asynchrony, cumulative power, and intensity, as well as the damaging threshold (stress-strain level at which tidal damage is initiated), are under experimental investigation and may enhance the understanding of VILI.
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Affiliation(s)
- Pedro Leme Silva
- Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil
| | - Martin Scharffenberg
- Department of Anesthesiology and Intensive Care Medicine, Pulmonary Engineering Group, University Hospital Carl Gustav Carus at Technische Universität Dresden, Dresden, Germany
| | - Patricia Rieken Macedo Rocco
- Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
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20
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Webb L, Burton L, Manchikalapati A, Prabhakaran P, Loberger JM, Richter RP. Cardiac dysfunction in severe pediatric acute respiratory distress syndrome: the right ventricle in search of the right therapy. Front Med (Lausanne) 2023; 10:1216538. [PMID: 37654664 PMCID: PMC10466806 DOI: 10.3389/fmed.2023.1216538] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/04/2023] [Accepted: 07/21/2023] [Indexed: 09/02/2023] Open
Abstract
Severe acute respiratory distress syndrome in children, or PARDS, carries a high risk of morbidity and mortality that is not fully explained by PARDS severity alone. Right ventricular (RV) dysfunction can be an insidious and often under-recognized complication of severe PARDS that may contribute to its untoward outcomes. Indeed, recent evidence suggest significantly worse outcomes in children who develop RV failure in their course of PARDS. However, in this narrative review, we highlight the dearth of evidence regarding the incidence of and risk factors for PARDS-associated RV dysfunction. While we wish to draw attention to the absence of available evidence that would inform recommendations around surveillance and treatment of RV dysfunction during severe PARDS, we leverage available evidence to glean insights into potentially helpful surveillance strategies and therapeutic approaches.
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Affiliation(s)
- Lece Webb
- Division of Pediatric Critical Care Medicine, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, United States
| | - Luke Burton
- Division of Pediatric Critical Care Medicine, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, United States
| | - Ananya Manchikalapati
- Division of Pediatric Critical Care, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, United States
| | - Priya Prabhakaran
- Division of Pediatric Critical Care Medicine, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, United States
| | - Jeremy M. Loberger
- Division of Pediatric Critical Care Medicine, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, United States
| | - Robert P. Richter
- Division of Pediatric Critical Care Medicine, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, United States
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21
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Motta-Ribeiro GC, Winkler T, Costa ELV, de Prost N, Tucci MR, Vidal Melo MF. Worsening of lung perfusion to tissue density distributions during early acute lung injury. J Appl Physiol (1985) 2023; 135:239-250. [PMID: 37289955 PMCID: PMC10393328 DOI: 10.1152/japplphysiol.00028.2023] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/17/2023] [Revised: 05/12/2023] [Accepted: 06/05/2023] [Indexed: 06/10/2023] Open
Abstract
Lung perfusion magnitude and distribution are essential for oxygenation and, potentially, lung inflammation and protection during acute respiratory distress syndrome (ARDS). Yet, perfusion patterns and their relationship to inflammation are unknown pre-ARDS. We aimed to assess perfusion/density ratios and spatial perfusion-density distributions and associate these to lung inflammation, during early lung injury in large animals at different physiological conditions caused by different systemic inflammation and positive end-expiratory pressure (PEEP) levels. Sheep were protectively ventilated (16-24 h) and imaged for lung density, pulmonary capillary perfusion (13Nitrogen-saline), and inflammation (18F-fluorodeoxyglucose) using positron emission and computed tomography. We studied four conditions: permissive atelectasis (PEEP = 0 cmH2O); and ARDSNet low-stretch PEEP-setting strategy with supine moderate or mild endotoxemia, and prone mild endotoxemia. Perfusion/density heterogeneity increased pre-ARDS in all groups. Perfusion redistribution to density depended on ventilation strategy and endotoxemia level, producing more atelectasis in mild than moderate endotoxemia (P = 0.010) with the oxygenation-based PEEP-setting strategy. The spatial distribution of 18F-fluorodeoxyglucose uptake was related to local Q/D (P < 0.001 for Q/D group interaction). Moderate endotoxemia yielded markedly low/zero perfusion in normal-low density lung, with 13Nitrogen-saline perfusion indicating nondependent capillary obliteration. Prone animals' perfusion was remarkably homogeneously distributed with density. Lung perfusion redistributes heterogeneously to density during pre-ARDS protective ventilation in animals. This is associated with increased inflammation, nondependent capillary obliteration, and lung derecruitment susceptibility depending on endotoxemia level and ventilation strategy.NEW & NOTEWORTHY Perfusion redistribution does not follow lung density redistribution in the first 16-24 h of systemic endotoxemia and protective tidal volume mechanical ventilation. The same oxygenation-based positive end-expiratory pressure (PEEP)-setting strategy can lead at different endotoxemia levels to different perfusion redistributions, PEEP values, and lung aerations, worsening lung biomechanical conditions. During early acute lung injury, regional perfusion-to-tissue density ratio is associated with increased neutrophilic inflammation, and susceptibility to nondependent capillary occlusion and lung derecruitment, potentially marking and/or driving lung injury.
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Affiliation(s)
- Gabriel C Motta-Ribeiro
- Biomedical Engineering Program, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
| | - Tilo Winkler
- Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States
| | - Eduardo L V Costa
- Divisão de Pneumologia, Faculdade de Medicina, Instituto do Coração (Incor), Hospital das Clínicas, Universidade de São Paulo, São Paulo, Brazil
- Instituto de Ensino e Pesquisa do Hospital Sírio Libanês, São Paulo, Brazil
| | - Nicolas de Prost
- Hôpitaux Universitaires Henri Mondor and Université Paris Est Créteil and INSERM - Unité U955, Créteil, France
| | - Mauro R Tucci
- Divisão de Pneumologia, Faculdade de Medicina, Instituto do Coração (Incor), Hospital das Clínicas, Universidade de São Paulo, São Paulo, Brazil
| | - Marcos F Vidal Melo
- Department of Anesthesiology, Columbia University Irving Medical Center, New York, New York, United States
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22
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Spinelli E, Scaramuzzo G, Slobod D, Mauri T. Understanding cardiopulmonary interactions through esophageal pressure monitoring. Front Physiol 2023; 14:1221829. [PMID: 37538376 PMCID: PMC10394627 DOI: 10.3389/fphys.2023.1221829] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/13/2023] [Accepted: 07/07/2023] [Indexed: 08/05/2023] Open
Abstract
Esophageal pressure is the closest estimate of pleural pressure. Changes in esophageal pressure reflect changes in intrathoracic pressure and affect transpulmonary pressure, both of which have multiple effects on right and left ventricular performance. During passive breathing, increasing esophageal pressure is associated with lower venous return and higher right ventricular afterload and lower left ventricular afterload and oxygen consumption. In spontaneously breathing patients, negative pleural pressure swings increase venous return, while right heart afterload increases as in passive conditions; for the left ventricle, end-diastolic pressure is increased potentially favoring lung edema. Esophageal pressure monitoring represents a simple bedside method to estimate changes in pleural pressure and can advance our understanding of the cardiovascular performance of critically ill patients undergoing passive or assisted ventilation and guide physiologically personalized treatments.
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Affiliation(s)
- Elena Spinelli
- Department of Anesthesia, Critical Care and Emergency, IRCCS (Institute for Treatment and Research) Ca’ Granda Maggiore Policlinico Hospital Foundation, Milan, Italy
| | - Gaetano Scaramuzzo
- Department of Translational Medicine, University of Ferrara, Ferrara, Italy
| | - Douglas Slobod
- Department of Critical Care Medicine, McGill University, Montreal, QC, Canada
| | - Tommaso Mauri
- Department of Anesthesia, Critical Care and Emergency, IRCCS (Institute for Treatment and Research) Ca’ Granda Maggiore Policlinico Hospital Foundation, Milan, Italy
- Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy
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23
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Shah N, Katira BH. Role of cardiopulmonary interactions in development of ventilator-induced lung injury-Experimental evidence and clinical Implications. Front Physiol 2023; 14:1228476. [PMID: 37534365 PMCID: PMC10391157 DOI: 10.3389/fphys.2023.1228476] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2023] [Accepted: 07/07/2023] [Indexed: 08/04/2023] Open
Abstract
Ventilator-induced lung injury (VILI) impacts outcomes in ARDS and optimization of ventilatory strategies improves survival. Decades of research has identified various mechanisms of VILI, largely focusing on airspace forces of plateau pressure, tidal volume and driving pressure. Experimental evidence indicates the role of adverse cardiopulmonary interaction during mechanical ventilation, contributing to VILI genesis mostly by modulating pulmonary vascular dynamics. Under passive mechanical ventilation, high transpulmonary pressure increases afterload on right heart while high pleural pressure reduces the RV preload. Together, they can result in swings of pulmonary vascular flow and pressure. Altered vascular flow and pressure result in increased vascular shearing and wall tension, in turn causing direct microvascular injury accompanied with permeability to water, proteins and cells. Moreover, abrupt decreases in airway pressure, may result in sudden overperfusion of the lung and result in similar microvascular injury, especially when the endothelium is stretched or primed at high positive end-expiratory pressure. Microvascular injury is universal in VILI models and presumed in the diagnosis of ARDS; preventing such microvascular injury can reduce VILI and impact outcomes in ARDS. Consequently, developing cardiovascular targets to reduce macro and microvascular stressors in the pulmonary circulation can potentially reduce VILI. This paper reviews the role of cardiopulmonary interaction in VILI genesis.
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24
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Vieillard-Baron A, Boissier F, Pesenti A. Hemodynamic impact of prone position. Let's protect the lung and its circulation to improve prognosis. Intensive Care Med 2023; 49:692-694. [PMID: 36820879 DOI: 10.1007/s00134-023-07001-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/13/2023] [Accepted: 02/05/2023] [Indexed: 02/24/2023]
Affiliation(s)
- Antoine Vieillard-Baron
- Service de Médecine Intensive Réanimation, Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Paré, 92100, Boulogne-Billancourt, France.
- INSERM UMR 1018, Clinical Epidemiology Team, CESP, Université de Paris Saclay, Villejuif, France.
| | - Florence Boissier
- Service de Médecine Intensive Réanimation, Centre Hospitalo-Universitaire de Poitiers, Poitiers, France
- INSERM CIC 1402 (IS-ALIVE Group), Université de Poitiers, Poitiers, France
| | - Antonio Pesenti
- Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
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25
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Morgan S, Aneman A, Nair P. Mechanical ventilation post-bilateral lung transplantation: A scoping review. Acta Anaesthesiol Scand 2023; 67:576-587. [PMID: 36808616 DOI: 10.1111/aas.14219] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/10/2023] [Revised: 01/30/2023] [Accepted: 02/02/2023] [Indexed: 02/22/2023]
Abstract
BACKGROUND Evidence from lung protective ventilation (LPV) in the acute respiratory distress syndrome has commonly been applied to guide periprocedural ventilation in lung transplantation. However, this approach may not adequately consider the distinctive features of respiratory failure and allograft physiology in the lung transplant recipient. This scoping review was conducted to systematically map the research describing ventilation and relevant physiological parameters post-bilateral lung transplantation with the aim to identify any associations with patient outcomes and gaps in the current knowledge base. METHODS To identify relevant publications, comprehensive literature searches of electronic bibliographic databases were conducted with the guidance of an experienced librarian in MEDLINE, EMBASE, SCOPUS and the Cochrane Library. The search strategies were peer-reviewed using the PRESS (Peer Review of Electronic Search Strategies) checklist. The reference lists of all relevant review articles were surveyed. Publications were included in the review if they described relevant ventilation parameters in the immediate post-operative period, published between 2000 and 2022 and involved human subjects undergoing bilateral lung transplantation. Publications were excluded if they included animal models, only single-lung transplant recipients or only patients managed with extracorporeal membrane oxygenation. RESULTS A total of 1212 articles were screened, 27 were subject to full-text review and 11 were included in the analysis. The quality of the included studies was assessed to be poor with no prospective multi-centre randomised controlled trials. The frequency of reported retrospective LPV parameters was as follows: tidal volume (82%), tidal volume indexed to both donor and recipient body weight (27%) and plateau pressure (18%). Data suggest that undersized grafts are at risk of unrecognised higher tidal volume ventilation indexed to donor body weight. The most reported patient-centred outcome was graft dysfunction severity in the first 72 h. CONCLUSION This review has identified a significant knowledge gap that indicates uncertainty regarding the safest ventilation practice in lung transplant recipients. The risk may be greatest in patients with established high-grade primary graft dysfunction and undersized allografts, and these factors may define a sub-group that warrants further investigation.
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Affiliation(s)
- Stephen Morgan
- Intensive Care Medicine, St. Vincent's Hospital, Sydney, New South Wales, Australia
- University of New South Wales, Sydney, New South Wales, Australia
| | - Anders Aneman
- University of New South Wales, Sydney, New South Wales, Australia
- Intensive Care Medicine, Liverpool Hospital, Sydney, New South Wales, Australia
| | - Priya Nair
- Intensive Care Medicine, St. Vincent's Hospital, Sydney, New South Wales, Australia
- University of New South Wales, Sydney, New South Wales, Australia
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26
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García-Hidalgo MC, González J, Benítez ID, Carmona P, Santisteve S, Pérez-Pons M, Moncusí-Moix A, Gort-Paniello C, Rodríguez-Jara F, Molinero M, Belmonte T, Torres G, Labarca G, Nova-Lamperti E, Caballero J, Bermejo-Martin JF, Ceccato A, Fernández-Barat L, Ferrer R, Garcia-Gasulla D, Menéndez R, Motos A, Peñuelas O, Riera J, Torres A, Barbé F, de Gonzalo-Calvo D. Identification of circulating microRNA profiles associated with pulmonary function and radiologic features in survivors of SARS-CoV-2-induced ARDS. Emerg Microbes Infect 2022; 11:1537-1549. [PMID: 35603455 PMCID: PMC9176679 DOI: 10.1080/22221751.2022.2081615] [Citation(s) in RCA: 16] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
There is a limited understanding of the pathophysiology of postacute pulmonary sequelae in severe COVID-19. The aim of current study was to define the circulating microRNA (miRNA) profiles associated with pulmonary function and radiologic features in survivors of SARS-CoV-2-induced ARDS. The study included patients who developed ARDS secondary to SARS-CoV-2 infection (n = 167) and a group of infected patients who did not develop ARDS (n = 33). Patients were evaluated 3 months after hospital discharge. The follow-up included a complete pulmonary evaluation and chest computed tomography. Plasma miRNA profiling was performed using RT-qPCR. Random forest was used to construct miRNA signatures associated with lung diffusing capacity for carbon monoxide (DLCO) and total severity score (TSS). Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses were conducted. DLCO < 80% predicted was observed in 81.8% of the patients. TSS showed a median [P25;P75] of 5 [2;8]. The miRNA model associated with DLCO comprised miR-17-5p, miR-27a-3p, miR-126-3p, miR-146a-5p and miR-495-3p. Concerning radiologic features, a miRNA signature composed by miR-9-5p, miR-21-5p, miR-24-3p and miR-221-3p correlated with TSS values. These associations were not observed in the non-ARDS group. KEGG pathway and GO enrichment analyses provided evidence of molecular mechanisms related not only to profibrotic or anti-inflammatory states but also to cell death, immune response, hypoxia, vascularization, coagulation and viral infection. In conclusion, diffusing capacity and radiological features in survivors from SARS-CoV-2-induced ARDS are associated with specific miRNA profiles. These findings provide novel insights into the possible molecular pathways underlying the pathogenesis of pulmonary sequelae. Trial registration:ClinicalTrials.gov identifier: NCT04457505.. Trial registration:ISRCTN.org identifier: ISRCTN16865246..
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Affiliation(s)
- María C García-Hidalgo
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Jessica González
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Iván D Benítez
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Paola Carmona
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain
| | - Sally Santisteve
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain
| | - Manel Pérez-Pons
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Anna Moncusí-Moix
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Clara Gort-Paniello
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Fátima Rodríguez-Jara
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain
| | - Marta Molinero
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Thalia Belmonte
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Gerard Torres
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Gonzalo Labarca
- Molecular and Translational Immunology Laboratory, Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepcion, Concepcion, Chile.,Internal Medicine Unit, Complejo Asistencial Dr. Víctor Ríos Ruiz, Los Ángeles, Chile
| | - Estefania Nova-Lamperti
- Molecular and Translational Immunology Laboratory, Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepcion, Concepcion, Chile
| | - Jesús Caballero
- Grup de Recerca Medicina Intensiva, Intensive Care Department Hospital Universitari Arnau de Vilanova, IRBLleida, Lleida, Spain
| | - Jesús F Bermejo-Martin
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Hospital Universitario Río Hortega de Valladolid, Valladolid, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Salamanca, Spain
| | - Adrián Ceccato
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - Laia Fernández-Barat
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Servei de Pneumologia, Hospital Clinic, Universitat de Barcelona; IDIBAPS, Barcelona, Spain
| | - Ricard Ferrer
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Intensive Care Department, Vall d'Hebron Hospital Universitari. SODIR Research Group, Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain
| | | | - Rosario Menéndez
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Pulmonology Service, University and Polytechnic Hospital La Fe, Valencia, Spain
| | - Ana Motos
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Servei de Pneumologia, Hospital Clinic, Universitat de Barcelona; IDIBAPS, Barcelona, Spain
| | - Oscar Peñuelas
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Hospital Universitario de Getafe, Madrid, Spain
| | - Jordi Riera
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Intensive Care Department, Vall d'Hebron Hospital Universitari. SODIR Research Group, Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain
| | - Antoni Torres
- CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain.,Pneumology Department, Clinic Institute of Thorax (ICT), Hospital Clinic of Barcelona - Insitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) - ICREA, University of Barcelona (UB), Barcelona, Spain
| | - Ferran Barbé
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
| | - David de Gonzalo-Calvo
- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain.,CIBER of Respiratory Diseases (CIBERES), Institute of Health Carlos III, Madrid, Spain
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- Translational Research in Respiratory Medicine, University Hospital Arnau de Vilanova and Santa Maria, IRBLleida, Lleida, Spain
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27
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Bachmann MC, Cruces P, Díaz F, Oviedo V, Goich M, Fuenzalida J, Damiani LF, Basoalto R, Jalil Y, Carpio D, Hamidi Vadeghani N, Cornejo R, Rovegno M, Bugedo G, Bruhn A, Retamal J. Spontaneous breathing promotes lung injury in an experimental model of alveolar collapse. Sci Rep 2022; 12:12648. [PMID: 35879511 PMCID: PMC9310356 DOI: 10.1038/s41598-022-16446-2] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/21/2022] [Accepted: 07/11/2022] [Indexed: 11/30/2022] Open
Abstract
Vigorous spontaneous breathing has emerged as a promotor of lung damage in acute lung injury, an entity known as “patient self-inflicted lung injury”. Mechanical ventilation may prevent this second injury by decreasing intrathoracic pressure swings and improving regional air distribution. Therefore, we aimed to determine the effects of spontaneous breathing during the early stage of acute respiratory failure on lung injury and determine whether early and late controlled mechanical ventilation may avoid or revert these harmful effects. A model of partial surfactant depletion and lung collapse was induced in eighteen intubated pigs of 32 ±4 kg. Then, animals were randomized to (1) SB‐group: spontaneous breathing with very low levels of pressure support for the whole experiment (eight hours), (2) Early MV-group: controlled mechanical ventilation for eight hours, or (3) Late MV-group: first half of the experiment on spontaneous breathing (four hours) and the second half on controlled mechanical ventilation (four hours). Respiratory, hemodynamic, and electric impedance tomography data were collected. After the protocol, animals were euthanized, and lungs were extracted for histologic tissue analysis and cytokines quantification. SB-group presented larger esophageal pressure swings, progressive hypoxemia, lung injury, and more dorsal and inhomogeneous ventilation compared to the early MV-group. In the late MV-group switch to controlled mechanical ventilation improved the lung inhomogeneity and esophageal pressure swings but failed to prevent hypoxemia and lung injury. In a lung collapse model, spontaneous breathing is associated to large esophageal pressure swings and lung inhomogeneity, resulting in progressive hypoxemia and lung injury. Mechanical ventilation prevents these mechanisms of patient self-inflicted lung injury if applied early, before spontaneous breathing occurs, but not when applied late.
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Affiliation(s)
- María Consuelo Bachmann
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Pablo Cruces
- Escuela de Medicina Veterinaria, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile.,Unidad de Paciente Crítico Pediátrico, Hospital El Carmen de Maipú, Santiago, Chile
| | - Franco Díaz
- Unidad de Paciente Crítico Pediátrico, Hospital El Carmen de Maipú, Santiago, Chile.,Escuela de Postgrado, Universidad Finis Terrae, Santiago, Chile
| | - Vanessa Oviedo
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Mariela Goich
- Escuela de Medicina Veterinaria, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile
| | - José Fuenzalida
- Escuela de Medicina Veterinaria, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago, Chile
| | - Luis Felipe Damiani
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.,Departamento de Ciencias de La Salud, Carrera de Kinesiología, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Roque Basoalto
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Yorschua Jalil
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.,Departamento de Ciencias de La Salud, Carrera de Kinesiología, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - David Carpio
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Niki Hamidi Vadeghani
- Institute for Biological and Medical Engineering, Schools of Engineering, Medicine and Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Rodrigo Cornejo
- Unidad de Pacientes Críticos, Departamento de Medicina, Hospital Clínico Universidad de Chile, Santiago, Chile
| | - Maximiliano Rovegno
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Guillermo Bugedo
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Alejandro Bruhn
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
| | - Jaime Retamal
- Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.
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28
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Zochios V, Brodie D, Shekar K, Schultz MJ, Parhar KKS. Invasive mechanical ventilation in patients with acute respiratory distress syndrome receiving extracorporeal support: a narrative review of strategies to mitigate lung injury. Anaesthesia 2022; 77:1137-1151. [PMID: 35864561 DOI: 10.1111/anae.15806] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 06/21/2022] [Indexed: 11/28/2022]
Abstract
Veno-venous extracorporeal membrane oxygenation is indicated in patients with acute respiratory distress syndrome and severely impaired gas exchange despite evidence-based lung protective ventilation, prone positioning and other parts of the standard algorithm for treating such patients. Extracorporeal support can facilitate ultra-lung-protective ventilation, meaning even lower volumes and pressures than standard lung-protective ventilation, by directly removing carbon dioxide in patients needing injurious ventilator settings to maintain sufficient gas exchange. Injurious ventilation results in ventilator-induced lung injury, which is one of the main determinants of mortality in acute respiratory distress syndrome. Marked reductions in the intensity of ventilation to the lowest tolerable levels under extracorporeal support may be achieved and could thereby potentially mitigate ventilator-induced lung injury and theoretically patient self-inflicted lung injury in spontaneously breathing patients with high respiratory drive. However, the benefits of this strategy may be counterbalanced by the use of continuous deep sedation and even neuromuscular blocking drugs, which may impair physical rehabilitation and impact long-term outcomes. There are currently a lack of large-scale prospective data to inform optimal invasive ventilation practices and how to best apply a holistic approach to patients receiving veno-venous extracorporeal membrane oxygenation, while minimising ventilator-induced and patient self-inflicted lung injury. We aimed to review the literature relating to invasive ventilation strategies in patients with acute respiratory distress syndrome receiving extracorporeal support and discuss personalised ventilation approaches and the potential role of adjunctive therapies in facilitating lung protection.
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Affiliation(s)
- V Zochios
- Department of Cardiothoracic Critical Care Medicine and ECMO, Glenfield Hospital, University Hospitals of Leicester National Health Service Trust, Leicester, UK.,Department of Cardiovascular Sciences, University of Leicester, UK
| | - D Brodie
- Columbia University College of Physicians and Surgeons, New York, NY, USA.,Centre for Acute Respiratory Failure, New York-Presbyterian Hospital, New York, NY, USA
| | - K Shekar
- Adult Intensive Care Services and Critical Care Research Group, The Prince Charles Hospital, Brisbane, QLD, Australia.,Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia.,Faculty of Medicine, University of Queensland, Brisbane and Bond University, Goldcoast, QLD, Australia
| | - M J Schultz
- Department of Intensive Care, Amsterdam University Medical Centres, Amsterdam, the Netherlands.,Mahidol-Oxford Tropical Medicine Research Unit, Mahidol University, Bangkok, Thailand.,Nuffield Department of Medicine, Oxford University, Oxford, UK.,Department of Medical Affairs, Hamilton Medical AG, Bonaduz, Switzerland
| | - K K S Parhar
- Department of Critical Care Medicine, University of Calgary and Alberta Health Services, Calgary, AB, Canada
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Millington SJ, Cardinal P, Brochard L. Setting and Titrating Positive End-Expiratory Pressure. Chest 2022; 161:1566-1575. [DOI: 10.1016/j.chest.2022.01.052] [Citation(s) in RCA: 18] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/02/2021] [Revised: 01/12/2022] [Accepted: 01/28/2022] [Indexed: 12/16/2022] Open
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30
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Slobod D, Assanangkornchai N, Alhazza M, Mettasittigorn P, Magder S. Right Ventricular Loading by Lung Inflation During Controlled Mechanical Ventilation. Am J Respir Crit Care Med 2022; 205:1311-1319. [PMID: 35213296 DOI: 10.1164/rccm.202111-2483oc] [Citation(s) in RCA: 25] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
RATIONALE The inspiratory rise in transpulmonary pressure during mechanical ventilation increases right ventricular (RV) afterload. One mechanism is that when alveolar pressure (Palv) exceeds left atrial pressure, West zone 1 or 2 (non-zone 3) conditions develop and Palv becomes the downstream pressure opposing RV ejection. The tidal volume (VT) at which this impact on the RV becomes hemodynamically evident is not well established. OBJECTIVES To determine the magnitude of RV afterload and prevalence of significant non-zone 3 conditions during inspiration across the range of VT currently prescribed in clinical practice. METHODS In post-operative passively ventilated cardiac surgery patients, we measured right atrial, RV, pulmonary artery, pulmonary artery occlusion (Ppao), plateau (Pplat), and esophageal (Peso) pressures during short periods of controlled ventilation with VT increments ranging between 2-12 ml/kg PBW. The inspiratory increase in RV afterload was evaluated hemodynamically and echocardiographically. The prevalence of non-zone 3 conditions was determined using 2 definitions based on changes in Peso, Ppao and Pplat. RESULTS Fifty-one patients were studied. There was a linear relationship between VT, driving pressure and transpulmonary pressure and the inspiratory increase in the RV isovolumetric contraction pressure. Echocardiographically, increasing VT was associated with a greater inspiratory increase in markers of afterload and a decrease in stroke volume. Non-zone 3 conditions were present in >50% of subjects at a VT ≥ 6 ml/kg PBW. CONCLUSIONS In the range of VT currently prescribed, RV afterload increases with increasing VT. A mechanical ventilation strategy that limits VT and driving pressure is cardio-protective.
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Affiliation(s)
| | - Nawaporn Assanangkornchai
- McGill University, Montreal, Quebec, Canada.,Prince of Songkla University, 26686, Hat Yai, Songkhla, Thailand
| | - Manal Alhazza
- Guelph General Hospital, 60386, Guelph, Ontario, Canada
| | - Pattra Mettasittigorn
- Thammasat University Hospital, 176056, Anesthesiology, Khlong Nueng, Pathum Thani, Thailand
| | - Sheldon Magder
- Royal Victoria Hospital, 55980, Montreal, Quebec, Canada;
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Better intraoperative cardiopulmonary stability and similar postoperative results of spontaneous ventilation combined with intubation than non-intubated thoracic surgery. Gan To Kagaku Ryoho 2022; 70:559-565. [PMID: 34985733 DOI: 10.1007/s11748-021-01768-1] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/13/2021] [Accepted: 12/23/2021] [Indexed: 11/04/2022]
Abstract
OBJECTIVES Non-intubated spontaneous ventilation video-assisted thoracic surgery lobectomy is a well-known procedure, but there are doubts regarding its safety. To solve this problem, we developed a safe procedure for spontaneous ventilation thoracic surgery (spontaneous ventilation with intubation). This study analyzed the intraoperative parameters and postoperative results of spontaneous ventilation with intubation. METHODS Between March 11, 2020 and March 26, 2021, 38 spontaneous ventilation with intubation video-assisted thoracic surgery lobectomies were performed. We chose the first 38 non-intubated spontaneous ventilation video-assisted thoracic surgery lobectomy cases with a laryngeal mask performed in 2017 for comparison. RESULTS There were no significant differences between the non-intubated spontaneous ventilation and spontaneous ventilation with intubation groups in postoperative surgical results (surgical time: 98,7 vs. 88,1 min (p = 0.067); drainage time: 3.5 vs. 2.7 days (p = 0.194); prolonged air leak 15.7% vs. 10.5% (p = 0.5); conversion rate to relaxation: 5.2% vs. 13.1% (p = 0.237); failure of the spontaneous ventilation rate: 10.5% vs. 13.1% (p = 0.724); and morbidity: 21% vs. 13.1% (p = 0.364)) and oncological outcomes. Significantly lower lowest systolic and diastolic blood pressure (systolic, 83.1 vs 132.3 mmHg, p = 0.001; diastolic 47.8 vs. 73.4 mmHg, p = 0.0001), lowest oxygen saturation (90.3% vs 94.9%, p = 0.026), and higher maximum pCO2 level (62.5 vs 54.8 kPa, p = 0.009) were found in the non-intubated spontaneous ventilation group than in the spontaneous ventilation with intubation group. CONCLUSIONS Spontaneous ventilation with intubation is a more physiological procedure than non-intubated spontaneous ventilation in terms of intraoperative blood pressure stability and gas exchange. The surgical results were similar in the two groups.
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Lai Y, Huang Y. Mechanisms of Mechanical Force Induced Pulmonary Vascular Endothelial Hyperpermeability. Front Physiol 2021; 12:714064. [PMID: 34671268 PMCID: PMC8521004 DOI: 10.3389/fphys.2021.714064] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2021] [Accepted: 08/30/2021] [Indexed: 12/27/2022] Open
Abstract
Mechanical ventilation is a supportive therapy for patients with acute respiratory distress syndrome (ARDS). However, it also inevitably produces or aggravates the original lung injury with pathophysiological changes of pulmonary edema caused by increased permeability of alveolar capillaries which composed of microvascular endothelium, alveolar epithelium, and basement membrane. Vascular endothelium forms a semi-selective barrier to regulate body fluid balance. Mechanical ventilation in critically ill patients produces a mechanical force on lung vascular endothelium when the endothelial barrier was destructed. This review aims to provide a comprehensive overview of molecular and signaling mechanisms underlying the endothelial barrier permeability in ventilator-induced lung jury (VILI).
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Affiliation(s)
- Yan Lai
- State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.,Department of Critical Care Medicine, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
| | - Yongbo Huang
- State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.,Department of Critical Care Medicine, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
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33
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Fan ML, Tong HQ, Sun T, Zhang HW, Han J, Cheng SY, Lu SF, Han X, Zhang Q, Sun WX, Chen JD, Chen XH. Animal model of coronary microembolization under transthoracic echocardiographic guidance in rats. Biochem Biophys Res Commun 2021; 568:174-179. [PMID: 34246051 DOI: 10.1016/j.bbrc.2021.05.045] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/15/2021] [Accepted: 05/14/2021] [Indexed: 11/20/2022]
Abstract
The aim of the study was to develop a model of coronary microembolization (CME) in rats at a lower cost. We developed a novel rat model without thoracotomy and ventilation under the guidance of echocardiography. Rats were sacrificed at 3 h, 24 h and 1 month postoperatively in both the Echo-CME and Open-chest CME groups for the comparison of the modeling accuracy, mortality, cardiopulmonary circulation, pleural adhesion and ventilation-induced lung injury (VILI). Results showed that the coronary microthrombus formed at 3 h and reached its peak at 24 h postoperatively, which included platelet aggregation and fibrin web. The Echo-group increases success rates, decreased mortality, postoperative complications including pleural adhesion, cardiopulmonary dysfunction and VILI postoperatively than the Open-chest group at 1month postoperatively. The ejection fraction of the CME group decreased to 50% and obvious cardiac fibrosis formed at 3 months postoperatively. Our unique surgical method provided a platform to study molecular mechanisms and potential new pathways for CME treatment.
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Affiliation(s)
- Man-Lu Fan
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Hua-Qin Tong
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Tong Sun
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Hao-Wen Zhang
- School of Health Preservation and Rehabilitation, Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, 210023, China
| | - Jie Han
- Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Song-Yi Cheng
- Department of Cardiology, Nanjing Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210001, China
| | - Sheng-Feng Lu
- Acupuncture and Tuina College, Nanjing University of Chinese Medicine, Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210023, China
| | - Xuan Han
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China
| | - Qian Zhang
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China
| | - Wei-Xin Sun
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Jian-Dong Chen
- Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China.
| | - Xiao-Hu Chen
- Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China.
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Battaglini D, Robba C, Ball L, Silva PL, Cruz FF, Pelosi P, Rocco PRM. Noninvasive respiratory support and patient self-inflicted lung injury in COVID-19: a narrative review. Br J Anaesth 2021; 127:353-364. [PMID: 34217468 PMCID: PMC8173496 DOI: 10.1016/j.bja.2021.05.024] [Citation(s) in RCA: 73] [Impact Index Per Article: 18.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/09/2021] [Revised: 04/17/2021] [Accepted: 05/16/2021] [Indexed: 12/20/2022] Open
Abstract
COVID-19 pneumonia is associated with hypoxaemic respiratory failure, ranging from mild to severe. Because of the worldwide shortage of ICU beds, a relatively high number of patients with respiratory failure are receiving prolonged noninvasive respiratory support, even when their clinical status would have required invasive mechanical ventilation. There are few experimental and clinical data reporting that vigorous breathing effort during spontaneous ventilation can worsen lung injury and cause a phenomenon that has been termed patient self-inflicted lung injury (P-SILI). The aim of this narrative review is to provide an overview of P-SILI pathophysiology and the role of noninvasive respiratory support in COVID-19 pneumonia. Respiratory mechanics, vascular compromise, viscoelastic properties, lung inhomogeneity, work of breathing, and oesophageal pressure swings are discussed. The concept of P-SILI has been widely investigated in recent years, but controversies persist regarding its mechanisms. To minimise the risk of P-SILI, intensivists should better understand its underlying pathophysiology to optimise the type of noninvasive respiratory support provided to patients with COVID-19 pneumonia, and decide on the optimal timing of intubation for these patients.
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Affiliation(s)
- Denise Battaglini
- Anesthesia and Intensive Care, San Martino Policlinico Hospital, IRCCS for Oncology and Neuroscience, Genoa, Italy; Department of Medicine, University of Barcelona, Barcelona, Spain
| | - Chiara Robba
- Anesthesia and Intensive Care, San Martino Policlinico Hospital, IRCCS for Oncology and Neuroscience, Genoa, Italy; Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy
| | - Lorenzo Ball
- Anesthesia and Intensive Care, San Martino Policlinico Hospital, IRCCS for Oncology and Neuroscience, Genoa, Italy; Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy
| | - Pedro L Silva
- Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; COVID-19 Virus Network, Ministry of Science, Technology, and Innovation, Brasilia, Brazil
| | - Fernanda F Cruz
- Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; COVID-19 Virus Network, Ministry of Science, Technology, and Innovation, Brasilia, Brazil
| | - Paolo Pelosi
- Anesthesia and Intensive Care, San Martino Policlinico Hospital, IRCCS for Oncology and Neuroscience, Genoa, Italy; Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy
| | - Patricia R M Rocco
- Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; COVID-19 Virus Network, Ministry of Science, Technology, and Innovation, Brasilia, Brazil.
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35
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See KC. Acute cor pulmonale in patients with acute respiratory distress syndrome: A comprehensive review. World J Crit Care Med 2021; 10:35-42. [PMID: 33728264 PMCID: PMC7941786 DOI: 10.5492/wjccm.v10.i2.35] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/06/2020] [Revised: 01/01/2021] [Accepted: 01/28/2021] [Indexed: 02/06/2023] Open
Abstract
Acute respiratory distress syndrome (ARDS)-related acute cor pulmonale (ACP) is found in 8%-50% of all patients with ARDS, and is associated with adverse hemodynamic and survival outcomes. ARDS-related ACP is an echocardiographic diagnosis marked by combined right ventricular dilatation and septal dyskinesia, which connote simultaneous diastolic (volume) and systolic (pressure) overload respectively. Risk factors include pneumonia, hypercapnia, hypoxemia, high airway pressures and concomitant pulmonary disease. Current evidence suggests that ARDS-related ACP is amenable to multimodal treatments including ventilator adjustment (aiming for arterial partial pressure of carbon dioxide < 60 mmHg, plateau pressure < 27 cmH2O, driving pressure < 17 cmH2O), prone positioning, fluid balance optimization and pharmacotherapy. Further research is required to elucidate the optimal frequency and duration of routine bedside echocardiography screening for ARDS-related ACP, to more clearly delineate the diagnostic role of transthoracic echocardiography relative to transesophageal echocardiography, and to validate current and novel therapies.
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Affiliation(s)
- Kay Choong See
- Department of Medicine, National University Hospital, Singapore 119228, Singapore
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36
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Magliocca A, Rezoagli E, Zani D, Manfredi M, De Giorgio D, Olivari D, Fumagalli F, Langer T, Avalli L, Grasselli G, Latini R, Pesenti A, Bellani G, Ristagno G. Cardiopulmonary Resuscitation-associated Lung Edema (CRALE). A Translational Study. Am J Respir Crit Care Med 2021; 203:447-457. [PMID: 32897758 DOI: 10.1164/rccm.201912-2454oc] [Citation(s) in RCA: 27] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023] Open
Abstract
Rationale: Cardiopulmonary resuscitation is the cornerstone of cardiac arrest (CA) treatment. However, lung injuries associated with it have been reported.Objectives: To assess 1) the presence and characteristics of lung abnormalities induced by cardiopulmonary resuscitation and 2) the role of mechanical and manual chest compression (CC) in its development.Methods: This translational study included 1) a porcine model of CA and cardiopulmonary resuscitation (n = 12) and 2) a multicenter cohort of patients with out-of-hospital CA undergoing mechanical or manual CC (n = 52). Lung computed tomography performed after resuscitation was assessed qualitatively and quantitatively along with respiratory mechanics and gas exchanges.Measurements and Main Results: The lung weight in the mechanical CC group was higher compared with the manual CC group in the experimental (431 ± 127 vs. 273 ± 66, P = 0.022) and clinical study (1,208 ± 630 vs. 837 ± 306, P = 0.006). The mechanical CC group showed significantly lower oxygenation (P = 0.043) and respiratory system compliance (P < 0.001) compared with the manual CC group in the experimental study. The variation of right atrial pressure was significantly higher in the mechanical compared with the manual CC group (54 ± 11 vs. 31 ± 6 mm Hg, P = 0.001) and significantly correlated with lung weight (r = 0.686, P = 0.026) and respiratory system compliance (r = -0.634, P = 0.027). Incidence of abnormal lung density was higher in patients treated with mechanical compared with manual CC (37% vs. 8%, P = 0.018).Conclusions: This study demonstrated the presence of cardiopulmonary resuscitation-associated lung edema in animals and in patients with out-of-hospital CA, which is more pronounced after mechanical as opposed to manual CC and correlates with higher swings of right atrial pressure during CC.
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Affiliation(s)
- Aurora Magliocca
- Dipartimento di Medicina Cardiovascolare, Istituto di Ricerche Farmacologiche Mario Negri, IRCCS, Milan, Italy.,Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy
| | - Emanuele Rezoagli
- Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy
| | - Davide Zani
- Department of Veterinary Medicine, University of Milan, Lodi, Italy
| | - Martina Manfredi
- Department of Veterinary Medicine, University of Milan, Lodi, Italy
| | - Daria De Giorgio
- Dipartimento di Medicina Cardiovascolare, Istituto di Ricerche Farmacologiche Mario Negri, IRCCS, Milan, Italy
| | - Davide Olivari
- Dipartimento di Medicina Cardiovascolare, Istituto di Ricerche Farmacologiche Mario Negri, IRCCS, Milan, Italy
| | - Francesca Fumagalli
- Dipartimento di Medicina Cardiovascolare, Istituto di Ricerche Farmacologiche Mario Negri, IRCCS, Milan, Italy
| | - Thomas Langer
- Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy
| | - Leonello Avalli
- Department of Emergency and Intensive Care, San Gerardo Hospital, Monza, Italy
| | - Giacomo Grasselli
- Department of Medical Physiopathology and Transplants, University of Milan, Milano, Italy; and.,Dipartimento di Anestesia-Rianimazione e Emergenza Urgenza, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy
| | - Roberto Latini
- Dipartimento di Medicina Cardiovascolare, Istituto di Ricerche Farmacologiche Mario Negri, IRCCS, Milan, Italy
| | - Antonio Pesenti
- Department of Medical Physiopathology and Transplants, University of Milan, Milano, Italy; and.,Dipartimento di Anestesia-Rianimazione e Emergenza Urgenza, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy
| | - Giacomo Bellani
- Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy.,Department of Emergency and Intensive Care, San Gerardo Hospital, Monza, Italy
| | - Giuseppe Ristagno
- Department of Medical Physiopathology and Transplants, University of Milan, Milano, Italy; and.,Dipartimento di Anestesia-Rianimazione e Emergenza Urgenza, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy
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De Santis Santiago R, Teggia Droghi M, Fumagalli J, Marrazzo F, Florio G, Grassi LG, Gomes S, Morais CCA, Ramos OPS, Bottiroli M, Pinciroli R, Imber DA, Bagchi A, Shelton K, Sonny A, Bittner EA, Amato MBP, Kacmarek RM, Berra L. High Pleural Pressure Prevents Alveolar Overdistension and Hemodynamic Collapse in Acute Respiratory Distress Syndrome with Class III Obesity. A Clinical Trial. Am J Respir Crit Care Med 2021; 203:575-584. [PMID: 32876469 PMCID: PMC7924574 DOI: 10.1164/rccm.201909-1687oc] [Citation(s) in RCA: 42] [Impact Index Per Article: 10.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2019] [Accepted: 09/01/2020] [Indexed: 12/16/2022] Open
Abstract
Rationale: Obesity is characterized by elevated pleural pressure (Ppl) and worsening atelectasis during mechanical ventilation in patients with acute respiratory distress syndrome (ARDS).Objectives: To determine the effects of a lung recruitment maneuver (LRM) in the presence of elevated Ppl on hemodynamics, left and right ventricular pressure, and pulmonary vascular resistance. We hypothesized that elevated Ppl protects the cardiovascular system against high airway pressure and prevents lung overdistension.Methods: First, an interventional crossover trial in adult subjects with ARDS and a body mass index ≥ 35 kg/m2 (n = 21) was performed to explore the hemodynamic consequences of the LRM. Second, cardiovascular function was studied during low and high positive end-expiratory pressure (PEEP) in a model of swine with ARDS and high Ppl (n = 9) versus healthy swine with normal Ppl (n = 6).Measurements and Main Results: Subjects with ARDS and obesity (body mass index = 57 ± 12 kg/m2) after LRM required an increase in PEEP of 8 (95% confidence interval [95% CI], 7-10) cm H2O above traditional ARDS Network settings to improve lung function, oxygenation and [Formula: see text]/[Formula: see text] matching, without impairment of hemodynamics or right heart function. ARDS swine with high Ppl demonstrated unchanged transmural left ventricular pressure and systemic blood pressure after the LRM protocol. Pulmonary arterial hypertension decreased (8 [95% CI, 13-4] mm Hg), as did vascular resistance (1.5 [95% CI, 2.2-0.9] Wood units) and transmural right ventricular pressure (10 [95% CI, 15-6] mm Hg) during exhalation. LRM and PEEP decreased pulmonary vascular resistance and normalized the [Formula: see text]/[Formula: see text] ratio.Conclusions: High airway pressure is required to recruit lung atelectasis in patients with ARDS and class III obesity but causes minimal overdistension. In addition, patients with ARDS and class III obesity hemodynamically tolerate LRM with high airway pressure.Clinical trial registered with www.clinicaltrials.gov (NCT02503241).
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Affiliation(s)
- Roberta De Santis Santiago
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Maddalena Teggia Droghi
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Jacopo Fumagalli
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Francesco Marrazzo
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Gaetano Florio
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Luigi G Grassi
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Susimeire Gomes
- Divisao de Pneumologia, Instituto do Coração, Hospital das Clinícas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, São Paulo, Brazil; and
| | - Caio C A Morais
- Divisao de Pneumologia, Instituto do Coração, Hospital das Clinícas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, São Paulo, Brazil; and
| | - Ozires P S Ramos
- Divisao de Pneumologia, Instituto do Coração, Hospital das Clinícas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, São Paulo, Brazil; and
| | - Maurizio Bottiroli
- Department of Anesthesia and Critical Care, Niguarda Hospital and University of Milano-Bicocca, Milan, Italy
| | - Riccardo Pinciroli
- Department of Anesthesia and Critical Care, Niguarda Hospital and University of Milano-Bicocca, Milan, Italy
| | - David A Imber
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Aranya Bagchi
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Kenneth Shelton
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Abraham Sonny
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Edward A Bittner
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Marcelo B P Amato
- Divisao de Pneumologia, Instituto do Coração, Hospital das Clinícas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, São Paulo, Brazil; and
| | - Robert M Kacmarek
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
| | - Lorenzo Berra
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Harvard University, Boston, Massachusetts
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Assessment of Electrical Impedance Tomography to Set Optimal Positive End-Expiratory Pressure for Venoarterial Extracorporeal Membrane Oxygenation-Treated Patients. Crit Care Med 2021; 49:923-933. [PMID: 33595959 DOI: 10.1097/ccm.0000000000004892] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
OBJECTIVES Patients on venoarterial extracorporeal membrane oxygenation have many risk factors for pulmonary complications in addition to their heart failure. Optimal positive end-expiratory pressure is unknown in these patients. The aim was to evaluate the ability of electrical impedance tomography to help the physician to select the optimal positive end-expiratory pressure in venoarterial extracorporeal membrane oxygenation treated and mechanically ventilated patients during a positive end-expiratory pressure trial. DESIGN Observational prospective monocentric. SETTING University hospital. PATIENTS Patients (n = 23) older than 18 years old, on mechanical ventilation and venoarterial extracorporeal membrane oxygenation. INTERVENTIONS A decreasing positive end-expiratory pressure trial (20-5 cm H2O) in increments of 5 cm H2O was performed and monitored by a collection of clinical parameters, ventilatory and ultrasonographic (cardiac and pulmonary) to define an optimal positive end-expiratory pressure according to respiratory criteria (optimal positive end-expiratory pressure selected by physician with respiratory parameters), and then adjusted according to hemodynamic and cardiac tolerances (optimal positive end-expiratory pressure selected by physician with respiratory, hemodynamic, and echocardiographic parameters). At the same time, electrical impedance tomography data (regional distribution of ventilation, compliance, and overdistension collapse) were recorded and analyzed retrospectively to define the optimal positive end-expiratory pressure. MEASUREMENTS AND MAIN RESULTS The median of this optimal positive end-expiratory pressure was 10 cm H2O in our population. Electrical impedance tomography showed that increasing positive end-expiratory pressure promoted overdistention of ventral lung, maximum at positive end-expiratory pressure 20 cm H20 (34% [interquartile range, 24.5-40]). Decreasing positive end-expiratory pressure resulted in collapse of dorsal lung (29% [interquartile range, 21-45.8]). The optimal positive end-expiratory pressure selected by physician with respiratory parameters was not different from the positive end-expiratory pressure chosen by the electrical impedance tomography. However, there is a negative impact of a high level of intrathoracic pressure on hemodynamic and cardiac tolerances. CONCLUSIONS Our results support that electrical impedance tomography appears predictive to define optimal positive end-expiratory pressure on venoarterial extracorporeal membrane oxygenation, aided by echocardiography to optimize hemodynamic assessment and management.
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Isgro G, Yusuff HO, Zochios V. The Right Ventricle in COVID-19 Lung Injury: Proposed Mechanisms, Management, and Research Gaps. J Cardiothorac Vasc Anesth 2021; 35:1568-1572. [PMID: 33546967 PMCID: PMC7810029 DOI: 10.1053/j.jvca.2021.01.014] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/07/2021] [Accepted: 01/08/2021] [Indexed: 12/16/2022]
Affiliation(s)
- Graziella Isgro
- Department of Anesthesia and Intensive Care Medicine, Glenfield Hospital, University Hospitals of Leicester National Health Service Trust, Leicester, UK
| | - Hakeem O Yusuff
- Department of Anesthesia and Intensive Care Medicine, Glenfield Hospital, University Hospitals of Leicester National Health Service Trust, Leicester, UK; University of Leicester, Leicester, UK
| | - Vasileios Zochios
- Department of Critical Care Medicine, University Hospitals Birmingham National Health Service Foundation Trust, Queen Elizabeth Hospital Birmingham, Birmingham, UK; Birmingham Acute Care Research, Institute of Inflammation and Ageing, Centre of Translational Inflammation Research, University of Birmingham, Birmingham, UK
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Vieillard-Baron A, Prigent A, Repessé X, Goudelin M, Prat G, Evrard B, Charron C, Vignon P, Geri G. Right ventricular failure in septic shock: characterization, incidence and impact on fluid responsiveness. CRITICAL CARE : THE OFFICIAL JOURNAL OF THE CRITICAL CARE FORUM 2020; 24:630. [PMID: 33131508 PMCID: PMC7603714 DOI: 10.1186/s13054-020-03345-z] [Citation(s) in RCA: 75] [Impact Index Per Article: 15.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 08/04/2020] [Accepted: 10/14/2020] [Indexed: 11/30/2022]
Abstract
Objective Incidence of right ventricular (RV) failure in septic shock patients is not well known, and tricuspid annular plane systolic excursion (TAPSE) could be of limited value. We report the incidence of RV failure in patients with septic shock, its potential impact on the response to fluids, as well as TAPSE values. Design Ancillary study of the HEMOPRED prospective multicenter study includes patients under mechanical ventilation with circulatory failure. Setting This is a multicenter intensive care unit study Patients Two hundred and eighty-two patients with septic shock were analyzed. Patients were classified in three groups based on central venous pressure (CVP) and RV size (RV/LV end-diastolic area, EDA). In group 1, patients had no RV dilatation (RV/LVEDA < 0.6). In group 2, patients had RV dilatation (RV/LVEDA ≥ 0.6) with a CVP < 8 mmHg (no venous congestion). RV failure was defined in group 3 by RV dilatation and a CVP ≥ 8 mmHg. Pulse pressure variation (PPV) was systematically recorded. Interventions None. Measurements and main results In total, 41% of patients were in group 1, 17% in group 2 and 42% in group 3. A correlation between RV size and CVP was only observed in group 3. Higher RV size was associated with a lower response to passive leg raising for a given PPV. A large overlap of TAPSE values was observed between the 3 groups. 63.5% of patients with RV failure had a normal TAPSE. Conclusions RV failure, defined by critical care echocardiography (RV dilatation) and a surrogate of venous congestion (CVP ≥ 8 mmHg), was frequently observed in septic shock patients and negatively associated with response to a fluid challenge despite significant PPV. TAPSE was unable to discriminate patients with or without RV failure.
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Affiliation(s)
- Antoine Vieillard-Baron
- Intensive Care Unit, Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Pare, Boulogne Billancourt, France. .,Faculty of Medicine Simone Veil, Saint Quentin en Yvelines, France. .,Inserm U1018, Center for Research in Epidemiology and Population Health (CESP), Faculty of Paris Saclay, Villejuif, France.
| | - Amélie Prigent
- Intensive Care Unit, Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Pare, Boulogne Billancourt, France.,Faculty of Medicine Simone Veil, Saint Quentin en Yvelines, France
| | - Xavier Repessé
- Intensive Care Unit, Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Pare, Boulogne Billancourt, France
| | - Marine Goudelin
- Intensive Care Unit, Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Pare, Boulogne Billancourt, France
| | - Gwenaël Prat
- Intensive Care Unit, Brest University Hospital, Brest, France
| | - Bruno Evrard
- Intensive Care Unit, Limoges University Hospital, Limoges, France
| | - Cyril Charron
- Intensive Care Unit, Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Pare, Boulogne Billancourt, France
| | - Philippe Vignon
- Intensive Care Unit, Limoges University Hospital, Limoges, France.,INSERM CIC 1435, Limoges University Hospital, Limoges, France.,Faculty of Medicine, University of Limoges, Limoges, France
| | - Guillaume Geri
- Intensive Care Unit, Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Pare, Boulogne Billancourt, France.,Faculty of Medicine Simone Veil, Saint Quentin en Yvelines, France.,Inserm U1018, Center for Research in Epidemiology and Population Health (CESP), Faculty of Paris Saclay, Villejuif, France
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Veskemaa L, Graw JA, Pickerodt PA, Taher M, Boemke W, González-López A, Francis RCE. Tert-butylhydroquinone augments Nrf2-dependent resilience against oxidative stress and improves survival of ventilator-induced lung injury in mice. Am J Physiol Lung Cell Mol Physiol 2020; 320:L17-L28. [PMID: 33026237 DOI: 10.1152/ajplung.00131.2020] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023] Open
Abstract
Oxidative stress caused by mechanical ventilation contributes to the pathophysiology of ventilator-induced lung injury (VILI). A key mechanism maintaining redox balance is the upregulation of nuclear factor-erythroid-2-related factor 2 (Nrf2)-dependent antioxidant gene expression. We tested whether pretreatment with an Nrf2-antioxidant response element (ARE) pathway activator tert-butylhydroquinone (tBHQ) protects against VILI. Male C57BL/6J mice were pretreated with an intraperitoneal injection of tBHQ (n = 10), an equivalent volume of 3% ethanol (EtOH3%, vehicle, n = 13), or phosphate-buffered saline (controls, n = 10) and were then subjected to high tidal volume (HVT) ventilation for a maximum of 4 h. HVT ventilation severely impaired arterial oxygenation ([Formula: see text] = 49 ± 7 mmHg, means ± SD) and respiratory system compliance, resulting in a 100% mortality among controls. Compared with controls, tBHQ improved arterial oxygenation ([Formula: see text] = 90 ± 41 mmHg) and respiratory system compliance after HVT ventilation. In addition, tBHQ attenuated the HVT ventilation-induced development of lung edema and proinflammatory response, evidenced by lower concentrations of protein and proinflammatory cytokines (IL-1β and TNF-α) in the bronchoalveolar lavage fluid, respectively. Moreover, tBHQ enhanced the pulmonary redox capacity, indicated by enhanced Nrf2-depentent gene expression at baseline and by the highest total glutathione concentration after HVT ventilation among all groups. Overall, tBHQ pretreatment resulted in 60% survival (P < 0.001 vs. controls). Interestingly, compared with controls, EtOH3% reduced the proinflammatory response to HVT ventilation in the lung, resulting in 38.5% survival (P = 0.0054 vs. controls). In this murine model of VILI, tBHQ increases the pulmonary redox capacity by activating the Nrf2-ARE pathway and protects against VILI. These findings support the efficacy of pharmacological Nrf2-ARE pathway activation to increase resilience against oxidative stress during injurious mechanical ventilation.
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Affiliation(s)
- Lilly Veskemaa
- Department of Anesthesiology and Operative Intensive Care Medicine CCM/CVK, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Jan A Graw
- Department of Anesthesiology and Operative Intensive Care Medicine CCM/CVK, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Philipp A Pickerodt
- Department of Anesthesiology and Operative Intensive Care Medicine CCM/CVK, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Mahdi Taher
- Department of Anesthesiology and Operative Intensive Care Medicine CCM/CVK, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Willehad Boemke
- Department of Anesthesiology and Operative Intensive Care Medicine CCM/CVK, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Adrián González-López
- Department of Anesthesiology and Operative Intensive Care Medicine CCM/CVK, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.,CIBER-Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain
| | - Roland C E Francis
- Department of Anesthesiology and Operative Intensive Care Medicine CCM/CVK, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
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Low Stretch Ventilation: Good for the Heart? Anesthesiology 2020; 132:944-946. [PMID: 32265348 DOI: 10.1097/aln.0000000000003244] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
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What have we learned from animal models of ventilator-induced lung injury? Intensive Care Med 2020; 46:2377-2380. [PMID: 32500178 PMCID: PMC7270159 DOI: 10.1007/s00134-020-06143-x] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/29/2020] [Accepted: 05/26/2020] [Indexed: 11/25/2022]
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Ko RE, Lee JG, Kim SY, Kim YT, Choi SM, Kim DH, Cho WH, Park SI, Jo KW, Kim HK, Paik HC, Jeon K. Extracorporeal membrane oxygenation as a bridge to lung transplantation: analysis of Korean organ transplantation registry (KOTRY) data. Respir Res 2020; 21:20. [PMID: 31931798 PMCID: PMC6958687 DOI: 10.1186/s12931-020-1289-2] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/16/2019] [Accepted: 01/08/2020] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND The use of extracorporeal membrane oxygenation (ECMO) as a bridge to lung transplantation has greatly increased. However, data regarding the clinical outcomes of this approach are lacking. The objective of this multicenter prospective observational cohort study was to evaluate lung transplantation outcomes in Korean Organ Transplantation Registry (KOTRY) patients for whom ECMO was used as a bridge to transplantation. METHODS Between March 2015 and December 2017, a total of 112 patients received lung transplantation and were registered in the KOTRY, which is a prospective, multicenter cohort registry. The entire cohort was divided into two groups: the control group (n = 85, 75.9%) and bridge-ECMO group (n = 27, 24.1%). RESULTS There were no significant differences in pre-transplant and intraoperative characteristics except for poorer oxygenation, more ventilator use, and longer operation time in the bridge-ECMO group. The prevalence of primary graft dysfunction at 0, 24, 48, and 72 h after transplantation did not differ between the two groups. Although postoperative hospital stays were longer in the bridge-ECMO group than in the control group, hospital mortality did not differ between the two groups (25.9% vs. 13.3%, P = 0.212). The majority of patients (70.4% of the bridge-ECMO group and 77.6% of the control group) were discharged directly to their homes. Finally, the use of ECMO as a bridge to lung transplantation did not significantly affect overall survival and graft function. CONCLUSIONS Short- and long-term post-transplant outcomes of bridge-ECMO patients were comparable to recipients who did not receive ECMO.
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Affiliation(s)
- Ryoung-Eun Ko
- Department of Critical Care Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
| | - Jin Gu Lee
- Department of Thoracic and Cardiovascular Surgery, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
| | - Song Yee Kim
- Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
| | - Young Tae Kim
- Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Sun Mi Choi
- Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
| | - Do Hyung Kim
- Department of Thoracic and Cardiovascular Surgery, Pusan National University YangSan Hospital, Gyeongsangnam-do, Korea
| | - Woo Hyun Cho
- Department of Pulmonology and Critical Care Medicine, Pusan National University YangSan Hospital, Gyeongsangnam-do, Korea
| | - Seung-Il Park
- Department of Thoracic and Cardiovascular Surgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Kyung-Wook Jo
- Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Hong Kwan Kim
- Department of Thoracic and Cardiovascular Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea
| | - Hyo Chae Paik
- Department of Thoracic and Cardiovascular Surgery, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
| | - Kyeongman Jeon
- Department of Critical Care Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. .,Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul, 06351, Korea.
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In Memoriam: Brian Kavanagh, 1962 to 2019. Anesthesiology 2019. [DOI: 10.1097/aln.0000000000002944] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
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Katira BH, Engelberts D, Otulakowski G, Giesinger RE, Yoshida T, Post M, Kuebler WM, Connelly KA, Kavanagh BP. Abrupt Deflation after Sustained Inflation Causes Lung Injury. Am J Respir Crit Care Med 2019; 198:1165-1176. [PMID: 29902384 DOI: 10.1164/rccm.201801-0178oc] [Citation(s) in RCA: 30] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022] Open
Abstract
RATIONALE Ventilator management in acute respiratory distress syndrome usually focuses on setting parameters, but events occurring at ventilator disconnection are not well understood. OBJECTIVES To determine if abrupt deflation after sustained inflation causes lung injury. METHODS Male Sprague-Dawley rats were ventilated (low Vt, 6 ml/kg) and randomized to control (n = 6; positive end-expiratory pressure [PEEP], 3 cm H2O; 100 min) or intervention (n = 6; PEEP, 3-11 cm H2O over 70 min; abrupt deflation to zero PEEP; ventilation for 30 min). Lung function and injury was assessed, scanning electron microscopy performed, and microvascular leak timed by Evans blue dye (n = 4/group at 0, 2, 5, 10, and 20 min after deflation). Hemodynamic assessment included systemic arterial pressure (n = 6), echocardiography (n = 4), and right (n = 6) and left ventricular pressures (n = 6). MEASUREMENTS AND MAIN RESULTS Abrupt deflation after sustained inflation (vs. control) caused acute lung dysfunction (compliance 0.48 ± 1.0 vs. 0.82 ± 0.2 m/cm H2O, oxygen saturation as measured by pulse oximetry 67 ± 23.5 vs. 91 ± 4.4%; P < 0.05) and injury (wet/dry ratio 6.1 ± 0.6 vs. 4.6 ± 0.4; P < 0.01). Vascular leak was absent before deflation and maximal 5-10 minutes thereafter; injury was predominantly endothelial. At deflation, left ventricular preload, systemic blood pressure, and left ventricular end-diastolic pressure increased precipitously in proportion to the degree of injury. Injury caused later right ventricular failure. Sodium nitroprusside prevented the increase in systemic blood pressure and left ventricular end-diastolic pressure associated with deflation, and prevented injury. Injury did not occur with gradual deflation. CONCLUSIONS Abrupt deflation after sustained inflation can cause acute lung injury. It seems to be mediated by acute left ventricular decompensation (caused by increased left ventricular preload and afterload) that elevates pulmonary microvascular pressure; this directly injures the endothelium and causes edema, which is potentiated by the surge in pulmonary perfusion.
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Affiliation(s)
- Bhushan H Katira
- 1 Translational Medicine, The Research Institute.,2 Department of Critical Care Medicine.,3 Department of Anesthesiology, and.,4 Interdepartmental Division of Critical Care Medicine
| | | | | | - Regan E Giesinger
- 5 Division of Neonatology, Department of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Canada
| | - Takeshi Yoshida
- 1 Translational Medicine, The Research Institute.,2 Department of Critical Care Medicine.,3 Department of Anesthesiology, and.,4 Interdepartmental Division of Critical Care Medicine
| | - Martin Post
- 1 Translational Medicine, The Research Institute
| | - Wolfgang M Kuebler
- 7 Department of Surgery, and.,8 Department of Physiology, University of Toronto, Toronto, Canada.,6 Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, Toronto, Canada; and.,9 Institute of Physiology, Charité-Universitätsmedizin, Berlin, Germany
| | - Kim A Connelly
- 6 Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, Toronto, Canada; and
| | - Brian P Kavanagh
- 1 Translational Medicine, The Research Institute.,2 Department of Critical Care Medicine.,3 Department of Anesthesiology, and.,4 Interdepartmental Division of Critical Care Medicine
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Motta-Ribeiro GC, Hashimoto S, Winkler T, Baron RM, Grogg K, Paula LFSC, Santos A, Zeng C, Hibbert K, Harris RS, Bajwa E, Vidal Melo MF. Deterioration of Regional Lung Strain and Inflammation during Early Lung Injury. Am J Respir Crit Care Med 2019; 198:891-902. [PMID: 29787304 DOI: 10.1164/rccm.201710-2038oc] [Citation(s) in RCA: 56] [Impact Index Per Article: 9.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022] Open
Abstract
RATIONALE The contribution of aeration heterogeneity to lung injury during early mechanical ventilation of uninjured lungs is unknown. OBJECTIVES To test the hypotheses that a strategy consistent with clinical practice does not protect from worsening in lung strains during the first 24 hours of ventilation of initially normal lungs exposed to mild systemic endotoxemia in supine versus prone position, and that local neutrophilic inflammation is associated with local strain and blood volume at global strains below a proposed injurious threshold. METHODS Voxel-level aeration and tidal strain were assessed by computed tomography in sheep ventilated with low Vt and positive end-expiratory pressure while receiving intravenous endotoxin. Regional inflammation and blood volume were estimated from 2-deoxy-2-[(18)F]fluoro-d-glucose (18F-FDG) positron emission tomography. MEASUREMENTS AND MAIN RESULTS Spatial heterogeneity of aeration and strain increased only in supine lungs (P < 0.001), with higher strains and atelectasis than prone at 24 hours. Absolute strains were lower than those considered globally injurious. Strains redistributed to higher aeration areas as lung injury progressed in supine lungs. At 24 hours, tissue-normalized 18F-FDG uptake increased more in atelectatic and moderately high-aeration regions (>70%) than in normally aerated regions (P < 0.01), with differential mechanistically relevant regional gene expression. 18F-FDG phosphorylation rate was associated with strain and blood volume. Imaging findings were confirmed in ventilated patients with sepsis. CONCLUSIONS Mechanical ventilation consistent with clinical practice did not generate excessive regional strain in heterogeneously aerated supine lungs. However, it allowed worsening of spatial strain distribution in these lungs, associated with increased inflammation. Our results support the implementation of early aeration homogenization in normal lungs.
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Affiliation(s)
- Gabriel C Motta-Ribeiro
- 1 Department of Anesthesia, Critical Care and Pain Medicine.,2 Biomedical Engineering Program, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
| | - Soshi Hashimoto
- 1 Department of Anesthesia, Critical Care and Pain Medicine.,3 Department of Anesthesiology and Intensive Care, Kyoto Prefectural University of Medicine, Kyoto, Japan; and
| | - Tilo Winkler
- 1 Department of Anesthesia, Critical Care and Pain Medicine
| | - Rebecca M Baron
- 4 Department of Medicine (Pulmonary and Critical Care), Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
| | | | | | - Arnoldo Santos
- 1 Department of Anesthesia, Critical Care and Pain Medicine.,6 CIBER de Enfermedades Respiratorias, Madrid, Spain
| | - Congli Zeng
- 1 Department of Anesthesia, Critical Care and Pain Medicine
| | - Kathryn Hibbert
- 7 Department of Medicine (Pulmonary and Critical Care), Massachusetts General Hospital, and
| | - Robert S Harris
- 7 Department of Medicine (Pulmonary and Critical Care), Massachusetts General Hospital, and
| | - Ednan Bajwa
- 7 Department of Medicine (Pulmonary and Critical Care), Massachusetts General Hospital, and
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Thille AW, Mauri T, Talmor D. Update in Critical Care Medicine 2017. Am J Respir Crit Care Med 2019; 197:1382-1388. [PMID: 29554433 DOI: 10.1164/rccm.201801-0055up] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Affiliation(s)
- Arnaud W Thille
- 1 Réanimation Médicale, Centre Hospitalier Universitaire de Poitiers, Poitiers, France.,2 INSERM Centre d'Investigation Clinique 1402 ALIVE, Faculté de Médecine et Pharmacie, Université de Poitiers, Poitiers, France
| | - Tommaso Mauri
- 3 Department of Anesthesia, Critical Care and Emergency, Maggiore Policlinico Hospital, University of Milan, Milan, Italy; and
| | - Daniel Talmor
- 4 Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston Massachusetts
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Grune J, Tabuchi A, Kuebler WM. Alveolar dynamics during mechanical ventilation in the healthy and injured lung. Intensive Care Med Exp 2019; 7:34. [PMID: 31346797 PMCID: PMC6658629 DOI: 10.1186/s40635-019-0226-5] [Citation(s) in RCA: 32] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/13/2019] [Accepted: 02/13/2019] [Indexed: 02/12/2023] Open
Abstract
Mechanical ventilation is a life-saving therapy in patients with acute respiratory distress syndrome (ARDS). However, mechanical ventilation itself causes severe co-morbidities in that it can trigger ventilator-associated lung injury (VALI) in humans or ventilator-induced lung injury (VILI) in experimental animal models. Therefore, optimization of ventilation strategies is paramount for the effective therapy of critical care patients. A major problem in the stratification of critical care patients for personalized ventilation settings, but even more so for our overall understanding of VILI, lies in our limited insight into the effects of mechanical ventilation at the actual site of injury, i.e., the alveolar unit. Unfortunately, global lung mechanics provide for a poor surrogate of alveolar dynamics and methods for the in-depth analysis of alveolar dynamics on the level of individual alveoli are sparse and afflicted by important limitations. With alveolar dynamics in the intact lung remaining largely a "black box," our insight into the mechanisms of VALI and VILI and the effectiveness of optimized ventilation strategies is confined to indirect parameters and endpoints of lung injury and mortality.In the present review, we discuss emerging concepts of alveolar dynamics including alveolar expansion/contraction, stability/instability, and opening/collapse. Many of these concepts remain still controversial, in part due to limitations of the different methodologies applied. We therefore preface our review with an overview of existing technologies and approaches for the analysis of alveolar dynamics, highlighting their individual strengths and limitations which may provide for a better appreciation of the sometimes diverging findings and interpretations. Joint efforts combining key technologies in identical models to overcome the limitations inherent to individual methodologies are needed not only to provide conclusive insights into lung physiology and alveolar dynamics, but ultimately to guide critical care patient therapy.
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Affiliation(s)
- Jana Grune
- Institute of Physiology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany
- DZHK (German Centre for Cardiovascular Research), partner site Berlin, 10117 Berlin, Germany
| | - Arata Tabuchi
- Institute of Physiology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany
| | - Wolfgang M. Kuebler
- Institute of Physiology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany
- DZHK (German Centre for Cardiovascular Research), partner site Berlin, 10117 Berlin, Germany
- The Keenan Research Centre for Biomedical Science at St. Michael’s, Toronto, Canada
- Departments of Surgery and Physiology, University of Toronto, Toronto, Canada
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Ingelse SA, Juschten J, Maas MAW, Matute-Bello G, Juffermans NP, van Woensel JBM, Bem RA. Fluid restriction reduces pulmonary edema in a model of acute lung injury in mechanically ventilated rats. PLoS One 2019; 14:e0210172. [PMID: 30653512 PMCID: PMC6336323 DOI: 10.1371/journal.pone.0210172] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/22/2018] [Accepted: 12/18/2018] [Indexed: 02/06/2023] Open
Abstract
Experimental acute lung injury models are often used to increase our knowledge on the acute respiratory distress syndrome (ARDS), however, existing animal models often do not take into account the impact of specific fluid strategies on the development of lung injury. In contrast, the current literature strongly suggests that fluid management strategies have a significant impact on clinical outcome of patients with ARDS. Thus, it is important to characterize the role of fluid management strategies in experimental models of lung injury. In this study we investigated the effect of two different fluid strategies on commonly used outcome variables in a short-term model of acute lung injury, in relation to age. Infant (2–3 weeks) and adult (3–4 months) Wistar rats received intratracheal instillations of lipopolysaccharide and 24 hours later were mechanically ventilated for 6 hours. During mechanical ventilation, rats from both age groups were randomized to either a standard or conservative intravenous fluid strategy. We found that the hemodynamic response in infant and adult rats was similar in both fluid strategies. Lung wet-to-dry ratios were lower in adult, but not in infant rats receiving the conservative fluid strategy as compared to the standard fluid strategy. There were age-related differences in markers of alveolar capillary barrier disruption and alveolar fluid clearance, yet these were unaffected by fluid strategy. Finally, we found significantly higher IL-1β and TNF-α concentrations in the adult rats treated with the conservative as compared to the standard fluid regimen. In conclusion, the choice of fluid strategy in mechanically ventilated rats with experimental LPS-induced acute lung injury has a significant effect on pulmonary extravascular water, an important and well-recognized lung injury marker, and on the local pro-inflammatory cytokine profiles. We advocate the use of a more uniform, conservative, fluid strategy regimen in experimental models of acute lung injury.
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Affiliation(s)
- Sarah A. Ingelse
- Pediatric Intensive Care Unit, Emma Children’s Hospital, Academic Medical Center, Amsterdam, The Netherlands
- Laboratory of Experimental Intensive Care and Anesthesiology (L·E·I·C·A), Academic Medical Center, Amsterdam, The Netherlands
- * E-mail:
| | - Jenny Juschten
- Laboratory of Experimental Intensive Care and Anesthesiology (L·E·I·C·A), Academic Medical Center, Amsterdam, The Netherlands
- Department of Intensive Care, Academic Medical Center, Amsterdam, The Netherlands
- Department of Intensive Care and Research VUmc Intensive Care (REVIVE), VU Medical Center, Amsterdam, The Netherlands
| | - Martinus A. W. Maas
- Laboratory of Experimental Intensive Care and Anesthesiology (L·E·I·C·A), Academic Medical Center, Amsterdam, The Netherlands
| | - Gustavo Matute-Bello
- Center for Lung Biology, Division of Pulmonary, Critical Care and Sleep Medicine, University of Washington, and Medical Research Service, VA Puget Sound Healthcare System, Seattle, WA, United States of America
| | - Nicole P. Juffermans
- Laboratory of Experimental Intensive Care and Anesthesiology (L·E·I·C·A), Academic Medical Center, Amsterdam, The Netherlands
- Department of Intensive Care, Academic Medical Center, Amsterdam, The Netherlands
| | - Job B. M. van Woensel
- Pediatric Intensive Care Unit, Emma Children’s Hospital, Academic Medical Center, Amsterdam, The Netherlands
| | - Reinout A. Bem
- Pediatric Intensive Care Unit, Emma Children’s Hospital, Academic Medical Center, Amsterdam, The Netherlands
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