THỞ MÁY CHO BỆNH NHÂN NONARDS

CHƯƠNG TRÌNH ĐÀO TẠO Y KHOA LIÊN TỤC THỞ MÁY CHO BỆNH NHÂN NON-ARDS Trình bày: BSCK1 Nguyễn Lý Minh Duy TP HCM, ngày 17 tháng 12 năm 2019 TỔNG QUAN • 1543 Vesalius, concept of mechanical ventilation • 1774 Joseph Priestly and Willhelm Scheele independently discovered oxygen mouth to mouth resuscitation by Tossach DISCOVERIES SERIES ATS DISCOVERIESATS SERIES ventilation is a life-sustaining Mechanical ventilation is a Mechanical life-sustaining the treatment of patients with therapy for the treatment oftherapy patientsforwith acute respiratory failure It isacute a veryrespiratory common failure It is a very common modality in intensive care units, and indeed modality in intensive care units, and indeed the the advent the advent of its use heralded dawnofofits use heralded the dawn of care units Interest in modern intensive care units.modern Interestintensive in mechanical ventilation has mechanical increased ventilation has increased markedly from both a research and a clinical markedly from both a research and a clinical perspective over the past 15perspective years sinceover the the past 15 years since the publication publication of a milestone article in theof a milestone article in the New England New England Journal of Medicine by the Journal of Medicine by the investigators that highlighted the ARDSNet investigators thatARDSNet highlighted the importance of a lung-protective ventilation importance of a lung-protective ventilation strategy (1) strategy (1) Although recognition of theAlthough recognition of the importance importance of lung protection appears toofbelung protection appears to be relatively new, there are fascinating accounts relatively new, there are fascinating accounts dating dating back hundreds of years thatback link hundreds of years that link ventilation ventilation to the development of lung to the development of lung injury In this injury In this article, I provide a very brief,article, I provide a very brief, relatively personal perspective of the history relatively personal perspective of the history of mechanical of mechanical ventilation, with an emphasisventilation, with an emphasis Figure (Left) Woodcut of theFigure only known firsthand likeness Andreas (reprinted (Left) Woodcut of theofonly knownVesalius firsthand likeness of Andreas Vesalius (reprinted on ventilator-induced lung on injury (VILI) ventilator-induced lung injury (VILI) from Reference 48) (Right) Frontispiece of De Humani Corporis Fabricaof(reprinted fromCorporis Fabrica (reprinted from from Reference 48) (Right) Frontispiece De Humani I focus on historical aspectsI of bothon historical focus aspects 49) of both Reference Reference 49) TỔNG QUAN 1900s-1950: Negative ventilation • 1864: Alfred Jones first body enclosing device • 1929: Drinker and Shaw The first iron lung ATS DISCOVERIES SERIES Figure Pneumatic chamber: Patented by Wilhelm Schwake in Germany in 1926 (51) Schwake was concerned with precise matching of the ventilator and the patient’s breathing pattern Reprinted from Reference 13 understanding of ventilator-induced diaphragmatic dysfunction (19) Many of these improvements have clearly led to much better ventilators and discussed a previous publication by William Tossach Tossach had helped resuscitate a coalminer who was apneic and pulseless “Tossach had applied his mouth close to the patient’s and by blowing strongly, holding the nostrils at the same time, raised his chest fully by his breath The surgeon felt 6–7 quick beats of the heart In one hour the patient began to come to himself, within four hours, he walked home, and in as many days returned to his work” (11) Later on in the Discussion Fothergill writes “It has been suggested to me by some that a pair of bellows might possibly be applied with more advantage in these cases, than the blast of a man’s mouth; but if any person can be got to try the charitable experiment by blowing, it would seem preferable to the other [because] the lungs of one man may bear, without injury, as great a force as those of another man can exert; which by the bellows cannot always be determined” (11) Fothergill clearly understood the possibility of injury caused by ventilation and in many ways can be viewed as the father of VILI, with his incredibly insightful conclusions 270 years ago In 1829, d’Etioles demonstrated that using bellows for ventilation could cause pneumothoraces, leading to death This study was widely interpreted as suggesting that the lungs of a patient who was pulseless could not tolerate positive pressure ventilation This likely set the field back many years Indeed, in 1837 the Royal Humane Society removed the use of bellows as well as mouth-to-mouth resuscitation from its list of recommended treatments (20) Mechanical ventilation was originally introduced in patients with normal lung function, essentially to replace the neuromuscular pump (e.g., comatose TỔNG QUAN 1950 to the present • Bjorn Ibsen & Lassen : positive airway pressure ”hand bagged” mortality of polio patients 87 % to 40 % • Revolution of ventilator: flow delivery exhalation valves, microprocessors, triggering, flow delivery, and the development of new modes of ventilation • Barach & Ashbaugh: positive end-expiratory pressure (PEEP) TỔNG QUAN BAROTRAUMA VOLUTRAUMA “Air leaks” Volume not PIP Injurious Mediators and Mechanotransduction Systemic inflammation Role for PMNs 00 90 19 80 19 70 19 19 Early ICUs Genomics/ Proteomics Diffuse lung injury 60 Ventilation and surfactant B E D S I D E BIOTRAUMA 20 B E N C H ATS DISCOVERIES SERIE “Baby lung” of ARDS Respirator lung Surfactant trials YIE LD positive negative vent trials Large positive vent trial Yield normal blood gas to low V strategy gure Timeline highlighting a number of basic science (top) and clinical (bottom) observations that have had an impact on our current understan TỔNG QUAN TỔNG QUAN • Thơng khí học cứu mạng (?) Gây tổn hại • ARDS – Thơng khí giảm Vt tăng PEEP/ ARDS – High Driving Pressure VILI • Non – ARDS ? – Low Vt – High PEEP – Low Driving Pressure LOW TIDAL VOLUME PROS Tác giả Thiết kế So sánh Kết cục Lee 1990 RCT 103 BN 12 vs ml/kg Vt thấp biến chứng hơ hấp, thời gian thở máy ngắn Gajic O 2005 RCT 3261 BN 10 vs ml/kg Nguy ARDS tăng gấp lần Determann 2010 RCT 150 BN 10 vs ml/kg Vt thấp bị ARDS Serpa Neto 2015 Cohort 2184 BN >10 vs 8ml/kg Tăng tỷ lệ tử vong OR12 1,66 (1,15 - 2,38) OR24 1,51 ( 1,08 - 2,11) CARING FOR THE CRITICALLY ILL PATIENT LOW TIDAL VOLUME CARING FOR THE CRITICALLY ILL PATIENT Association Between Association Between Use of Lung-Protective Ventilation With Low Ventilation With Lower Tidal Volumes PROTECTIVE VENTILATION AND LOWERand TIDALClinical VOLUMES Outcom and Clinical Outcomes Among Patients Without Acute Respir Acute Respiratory Distress Syndrome A Meta-analysis , Without 0.10Table Demographic, Ventilation, and Laboratory Characteristics of the Patients at the Final A Meta-analysis mL/kg Ary Serpa Neto, MD, MSc Follow-up Visit Se´rgio Oliveira Cardoso, MD the de- Neto, MD, MSc Ary Serpa Context Lung-protective mechanical ventilation withMean the use of(SD) lower tidal volumes has been found to improve outcomes of patients with acute respiratory distress syn- Jose´ Antoˆnio Manetta, MD Se ´ rgio OliveiraĐIỂM Cardoso, MD DÂN ĐẶC SỐ convendrome (ARDS) It has been suggested that use of lower tidal volumes also benefits Victor Galva˜o Moura Pereira, MD Jose´ Antoˆnio Manetta, MD Conventional patients who not have ARDS Protective nlyVictor ranDaniel Crepaldi Espo´sito, MD Galva˜o Moura Pereira, MD P Ventilation Objective To determine whetherVentilation use of lower tidal volumes is associated with imManoela de Oliveira Prado proved outcomes of patients receiving Crepaldi Espo´sito, MD asDaniel 0.26 Value (n ventilation = 1416)who not have ARDS.(n = 1406) Pasqualucci, MD Data Sources MEDLINE, CINAHL, Web of Science, and Cochrane Central Register Manoela de Oliveira Prado Pasqualucci, MDAge, y Maria Cecı´lia Toledo 59.97 (7.92) 60.22 (7.36) 93 of Controlled Trials up to August 2012 Maria Cecı´lia Toledo Weight, kg Damasceno, MD, PhD Tidal Marcus J Schultz, MD,volume, PhD M Damasceno, MD, PhD Study Selection Eligible studies evaluated use of lower vs higher tidal volumes in pa72.71 (12.34) 72.13 (12.16) 93 tients without ARDS at onset of mechanical ventilation and reported lung injury devel- Marcus J Schultz, MD, PhD a mortality, pulmonary6.45 infection, atelectasis, and biochemical10.60 alterations (1.09) (1.14) Ͻ.001 mL/kgopment, IBW overall M ECHANICAL VENTILATION Data Extraction Three reviewers extracted data on study characteristics, methods, is a life-saving in pa- ECHANICAL 6.40 by (2.39) 3.41 (2.79) 01 strategy PEEP, cm H2O a and outcomes Disagreement was resolved VENTILATION consensus in patients with acute a life-saving strategy Data Synthesis Twenty articles (2822 participants) using respiratory failure pressure, cm H2O a 16.63 (2.58)were included Meta-analysis 21.35 (3.61) 006 Howtilation isinPlateau patients with acute a fixed-effects model showed a decrease in lung injury development (risk ratio [RR], 0.33; ever, unequivocal evidence suggests respiratory failure.rate, How- 95% CI, 0.23 to 0.47; I , 0%; number needed to treat [NNT], 11), and mortality Respiratory 18.02 (4.14) 13.20(RR, (4.43) 01 has the 9; NNT, that mechanical ventilation ever, unequivocal evidence suggests 0.64; 95% CI, 0.46 to 0.89; I , 0%; NNT, 23) in patients receiving ventilation with lower a breaths/min potential to aggravate and precipitate that inmechanical ventilation has the tidal volumes The results of lung injury development were similar when stratified by nary In acute respiratory dislung injury a,b of study (randomized vs nonrandomized) the type and were significant only in9.13 randompotential to aggravate and precipitateL/min 8.46 (2.90) (2.70) 72and in a Minute-volume, tress syndrome (ARDS), nition) lung injury In acute respiratory dis- ized trials for pulmonary infection and only in nonrandomized trials for mortality Metamilder form of ARDS formerly showed, in protective ventilation groups, a lower Pa(ARDS), O2/FIO2 aand in a analysis using a random-effects model 304.41 (65.74) 312.97 (68.13) 51 known tress syndrome incidence of pulmonary infection (RR, 0.45; 95% CI, 0.22 to 0.92; I , 32%; NNT, 26), as acute lung injury (ALI), mechanie group milder form of ARDS formerly known stay (6.91 [2.36] vs 8.87 [2.93] days, respectively; PaCO(ALI), Hg a lower mean (SD) hospital length of41.05 (3.79) 37.90 (4.19) cal ventilation can cause.003 ventilator2, mm mechanias acute lung injury wer V standardized mean difference [SMD], 0.51; 95% CI, 0.20 to 0.82; I , 75%), higher mean associated lung injury VentilatorT a cal ventilationpH can cause ventilator- (SD) PaCO levels (41.05 [3.79] vs 37.90 [4.19] mm Hg, respectively; SMD, −0.51; 95% (0.03) 7.40 (0.03) associated lung injury is.11 a frequent CI,associated 0.22 lung injury Ventilator- CI, −0.70 to −0.32; I , 54%), and lower7.37 mean (SD) pH values (7.37 [0.03] vs 7.40 [0.04], complication in critically ill patients Abbreviations: F IO , fraction of inspired oxygen; IBW, ideal body weight; PEEP, positive end-expiratory pressure injury is a frequent respectively; SMD, 1.16; 95% CI, 0.31 to 2.02; I , 96%) but similar mean (SD) ratios of 2;associated 95% lungina Atcritically O to fraction of inspired oxygen (304.40 [65.7] vs 312.97 [68.13], respectively; SMD, receiving mechanical ventilation, and the final visit complication ill follow-up patients Pa 2 1 2 2 2 b 2 Context Lu has been foun drome (ARDS patients who Objective T proved outco Data Source of Controlled Study Selec tients without opment, over Data Extrac and outcome Data Synthe a fixed-effects 95% CI, 0.23 0.64; 95% CI, tidal volumes the type of stu ized trials for p analysis using incidence of p lower mean (S standardized m (SD) PaCO2 lev CI, −0.70 to − respectively; S PaO2 to fractio 0.11; 95% CI did not influe CARING FOR THE CRITICALLY ILL PATIENT CARING FOR THE CRITICALLY ILL PATIENT LOW TIDAL VOLUME Association Between Association Between Use of Lung-Protective Ventilation With Low Ventilation With Lower Tidal Volumes and Clinical Outcom and Clinical Outcomes Among Patients Without Acute Respir Without Acute Respiratory Distress Syndrome A Meta-analysis A Meta-analysis Ary Serpa Neto, MD, MSc Se´rgio Oliveira Cardoso, MD Jose´ Antoˆnio Manetta, MD Victor Galva˜o Moura Pereira, MD Daniel Crepaldi Espo´sito, MD Manoela de Oliveira Prado Pasqualucci, MD Maria Cecı´lia Toledo Damasceno, MD, PhD Marcus J Schultz, MD, PhD KẾT CỤC Ary Serpa Neto, MD, MSc Se´rgio Oliveira Cardoso, MD Context Lung-protective mechanical ventilation with the use of lower tidal volumes has been found to improve outcomes of patients with acute respiratory distress syn- Jose´ Antoˆnio Manetta, MD drome (ARDS) It has been suggested that use of lower tidal volumes also benefits Victor Galva˜o Moura Pereira, MD patients who not have ARDS Daniel Crepaldi Espo´sito, MD Objective To determine whether use of lower tidal volumes is associated with imManoela de Oliveira Prado proved outcomes of patients receiving ventilation who not have ARDS Pasqualucci, MD Data Sources MEDLINE, CINAHL, Web of Science, and Cochrane Central Register Maria Cecı´lia Toledo of Controlled Trials up to August 2012 Damasceno, MD, PhD Study Selection Eligible studies evaluated use of lower vs higher tidal volumes in patients without ARDS at onset of mechanical ventilation and reported lung injury devel- Marcus J Schultz, MD, PhD • 47/1113 Low Vt vs 38/1090 High Vt tổn thương phổi RR = 0,33 (0,23 – 0,41) NNT = 11 • Tỷ lệ tử vong nhóm bệnh nhân Low Vt giảm RR = is a life-saving strategy in patients with acute is a life-saving strategy(0,46 – 0,89) NNT = 23 0,64 respiratory failure Howin patients with acute ever, unequivocal evidence suggests respiratory failure Howthat mechanical ventilation has the ever, unequivocal•evidence suggests Tần suất viêm phổi xẹp phổi nhóm Vt giảm potentialLow to aggravate and precipitate that mechanical ventilation has the lung injury In acute respiratory dispotential to aggravate and precipitate tress syndrome (ARDS), and in a RR = 0,45 (0,22 – 0,92 ) NNT = 26 lung injury In acute respiratory dismilder form of ARDS formerly known M ECHANICAL VENTILATION tress syndrome (ARDS), and in a milder form of ARDS formerly known as acute lung injury (ALI),2 mechanical ventilation can cause ventilatorassociated lung injury Ventilatorassociated lung injury is a frequent complication in critically ill patients opment, overall mortality, pulmonary infection, atelectasis, and biochemical alterations Data Extraction Three reviewers extracted data on study characteristics, methods, and outcomes Disagreement was resolved by consensus M ECHANICAL VENTILATION Data Synthesis Twenty articles (2822 participants) were included Meta-analysis using a fixed-effects model showed a decrease in lung injury development (risk ratio [RR], 0.33; 95% CI, 0.23 to 0.47; I2, 0%; number needed to treat [NNT], 11), and mortality (RR, 0.64; 95% CI, 0.46 to 0.89; I2, 0%; NNT, 23) in patients receiving ventilation with lower tidal volumes The results of lung injury development were similar when stratified by the type of study (randomized vs nonrandomized) and were significant only in randomized trials for pulmonary infection and only in nonrandomized trials for mortality Metaanalysis using a random-effects model showed, in protective ventilation groups, a lower incidence of pulmonary infection (RR, 0.45; 95% CI, 0.22 to 0.92; I2, 32%; NNT, 26), as acute lung injury (ALI),2 mechanilower mean (SD) hospital length of stay (6.91 [2.36] vs 8.87 [2.93] days, respectively; cal ventilation can cause ventilatorstandardized mean difference [SMD], 0.51; 95% CI, 0.20 to 0.82; I2, 75%), higher mean associated lung injury Ventilator(SD) PaCO2 levels (41.05 [3.79] vs 37.90 [4.19] mm Hg, respectively; SMD, −0.51; 95% associated lung injury is a frequent CI, −0.70 to −0.32; I2, 54%), and lower mean (SD) pH values (7.37 [0.03] vs 7.40 [0.04], respectively; SMD, 1.16; 95% CI, 0.31 to 2.02; I , 96%) but similar mean (SD) ratios of complication in critically ill patients PaO2 to fraction of inspired oxygen (304.40 [65.7] vs 312.97 [68.13], respectively; SMD, receiving mechanical ventilation, and Context Lu has been foun drome (ARDS patients who Objective T proved outco Data Source of Controlled Study Selec tients without opment, over Data Extrac and outcome Data Synthe a fixed-effects 95% CI, 0.23 0.64; 95% CI, tidal volumes the type of stu ized trials for p analysis using incidence of p lower mean (S standardized m (SD) PaCO2 lev CI, −0.70 to − respectively; S PaO2 to fractio 0.11; 95% CI did not influe anuscript Lung-protective ventilation initiated in the emergency department (LOV-ED): a quasi-experimental, before-after trial Brian M Fuller, MD, MSCI, Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA Nicholas M Mohr, MD, MS, • 1192Departments BN trước can thiệp of Emergency Medicine and Anesthesiology, Division of Critical Care, Roy J and Lucille A Carver College of Medicine, University of Iowa, 200 Hawkins Drive, 1008 RCP, Iowa • 513 City, BNIAsau can thiệp 52242, USA – – – – Author Manuscript Author Manuscript Ian T Ferguson, MPH, al School of Medicine Fuller and etMedical Science, University College Dublin, Dublin 4, Ireland Vt thấp bảo vệ phổi Anne M Drewry, MD, MSCI, PEEP tránhofxẹp phổi Department Anesthesiology, Division of Critical Care Medicine, Washington University School of Medicine St Louis, St Louis, MO 63110, USA Tránh tăng inoxy mức Đầu cao Christopher Palmer, MD, Brian T Wessman, MD, Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington Figure Distribution of emergency department tidal volume University School of Medicine in St Louis, Louis, in MO 63110, USA There was St an increase lung-protective ventilation in the ED associated with the Author Manuscript Author Manuscript Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA intervention (47.8% to 96.2%) Enyo Ablordeppey, MD, MPH, ED: emergency department; PBW: predicted body weight Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA anuscript Lung-protective ventilation Table initiated in the emergency Ventilator variables in the emergency department department (LOV-ED): a quasi-experimental, before-after trial * Group Intervention Group (n= Odds Ratio or Between-Group Brian M Fuller, MD, MSCI, Pre-intervention (n= 1,192) 513) Difference (95% CI) Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington Tidal volume, mL University School of Medicine in St Louis, St Louis, MO 63110, USA Median (IQR) 500 (500–550) 420 (370–470) Author Manuscript Ian T Ferguson, MPH, Mean (SD) 515.7 (71.6) 422.0 (71.5) −93.7 (−99.5 to −87.8) School of Medicine and Medical Science, University College Dublin, Dublin 4, Ireland Tidal volume, mL/kg PBW Nicholas M Mohr, MD, MS, 8.1 (7.3–9.1) 6.3 (6.0–6.7) Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Roy J and Mean (SD) 8.3 (1.5) (0.8) (−1.9 to −1.7) Lucille A Carver College of Medicine, University of Iowa,6.4200 Hawkins Drive,−1.8 1008 RCP, Iowa PEEP City, IA 52242, USA Median (IQR) Median (IQR) Anne (5–5) (5–8) M Drewry, MD, MSCI, Mean Department (SD) 5.4 (1.5)of Critical Care Medicine, 6.5 (2.5) (0.9 to 1.3) School of Anesthesiology, Division Washington1.1 University of Medicine in St Louis, St Louis, MO 63110, USA Respiratory rate Median (IQR) Christopher Author Manuscript 14 (12–16) 20 (20–24) Palmer, MD, of Emergency Medicine and Anesthesiology, of Critical Care, Washington Mean Departments (SD) 15.3 (3.5) 20.9 Division (3.8) 5.6 (5.3 to 5.9) University School of Medicine in St Louis, St Louis, MO 63110, USA FiO2 Brian Median (IQR) T Wessman, MD, 80 (50–100) 40 (40–60) of Emergency Medicine and Anesthesiology, Division of Critical Care, Mean Departments (SD) 75.0 (25.9) 53.4 (21.7) −21.6 (−23.5Washington to −19.8) University School of Medicine in St Louis, St Louis, MO 63110, USA Head-of-bed elevation, n (%) 989 (39.4) 704 (92.6) 19.4 (14.6–25.7) Enyo Ablordeppey, MD, MPH, Lung protective ventilation, of n (%) 1202 (47.8) 731 (96.2) (21.8–64.7) Departments Emergency Medicine and Anesthesiology, Division of Critical 37.6 Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA Manuscript Lung-protective ventilation initiated in the emergency Table Table department (LOV-ED): a quasi-experimental, before-after trial Results of outcome analyses Brian M Fuller, MD, MSCI, Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA Author Manuscript After Matching Matching Before Ian T Ferguson, MPH, School of Medicine and Medical Science, University College Dublin, Dublin 4, Ireland Nicholas M Mohr, MD, Pre-intervention MS, *OR OR or Between-Group InterventionGroup Group Intervention or or Between-Group aOR Between-Group Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Roy J and Difference (95% CI) Group(n= (n=1,192) 490) (n= 513) 490) Group (n= Difference Difference(95% (95%CI) CI) Lucille A Carver College of Medicine, University of Iowa, 200 Hawkins Drive, 1008 RCP, Iowa City, IA 52242, USA Pr Gr 0.48 (0.33–0.69) 71 (14.5) 36 (7.4) (7.4) 0.47(0.33–0.69) (0.31–0.71) Primary composite (14.3) 38 0.48 Anne M Drewry, MD, MSCI,171 0.37 (0.23–0.58) 53Division (10.8) 20Washington (4.1) University School 0.37 0.35(0.23–0.58) (0.21–0.60) outcome, n (%) 130 (10.9) 22 (4.3) Department of Anesthesiology, of Critical Care Medicine, of Medicine in St Louis, St Louis, 63110, USA •ARDS 86 (7.2) 23 0.60 0.60 (0.38–0.97) 37 MO (7.6) 23 (4.5) (4.7) 0.60(0.38–0.97) (0.35–1.03) •VACs Christopher Palmer, MD, Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA Author Manuscript Ventilator-free days 2.17 (1.06 to 3.29) 16.0 14.7 (11.4) (11.7) 18.2 18.4 (10.5) (10.4) 2.17 3.69(1.06 (2.30toto3.29) 5.07) Brian T Wessman, MD, Departments of Emergency Medicine and Anesthesiology, Division of Critical Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA Hospital-free 0.87 (−0.09 todays 1.84) 10.8 (9.6) 9.4 (9.5) 11.6 11.7 (9.2) (9.2) 0.87 2.38(−0.09 (1.21toto1.84) 3.55) Enyo Ablordeppey, MD, MPH, ICU-free days 15.0 15.8 0.77 0.77 (−0.30 toDepartments 1.83) of Emergency Medicine 13.6 (10.8) (11.1) 16.0(10.0) (9.9) 2.36(−0.30 (1.04toto1.83) 3.68) and Anesthesiology, Division of Critical Care, Washington University School of Medicine in St Louis, St Louis, MO 63110, USA Mortality, n (%) 0.65 (0.51–0.83) Jacob Keeperman, MD, 338 167 (28.4) (34.1) 105 (20.5) 96 (19.6) 0.65 0.47(0.51–0.83) (0.35–0.63) Correspondence M Fuller primaryand outcome pulmonary outcome that combines the event rate for ARDS and VACs ateThe for ARDS VACs.wasto: aBriancomposite Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication As a service to our Author Manusc customers we are providing this early version of the manuscript The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain OR:distress odds ratio; CI: confidence interval; aOR: adjusted odds ratio; acute respiratory distress syndrome; VAC: ventilat ratory syndrome; VAC: ventilator-associated condition; ICU:ARDS: intensive care unit Meetings: Partial data from the implementation phase of this work was presented at the American Thoracic Society Conference on May 17, 2016 in San Francisco, California The results of the study will be presented as an oral abstract presentation (Star Research Presentation) on January 22, 2017 in Honolulu, Hawaii for the Society of Critical Care Medicine 46th annual congress * From logistic regression modeling (categorical data) and generalized estimating equations negative binomial regression (con ations negative binomial regression (continuous data) Summary Conflict of Interest Statement: All authors declare that no conflicts of interest exist SAU NGƯNG TIM • Ấn tim hiệu chấn thương phổi ? thời gian thở máy, nằm viện, tỷ lệ tử vong • Hội chứng sau ngưng tim – – – – Tổn thương não RL CN tim Thiếu máu, tổn thương tái tưới máu Stress oxy hố, RL đơng máu, phản ứng viêm Suy đa quan • Nguy cao ARDS Thơng khí ? SAU NGƯNG TIM Ventilator Management and Respiratory Care After Cardiac Arrest cine ] Ventilation, Infection, and Injury Oxygenation, 57 58 59 60 61 62 63 64 65 66 Q2 Nicholas J Johnson, MD; David J Carlbom, MD; and David F Gaieski, MD 67 68 69 Return of spontaneous circulation after cardiac arrest results in a systemic inflammatory state called the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagulopathy, neuronal injury, and organ dysfunction Perturbations in oxygenation and ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated nt and Respiratory with poor outcome Further, patients who experience cardiac arrest are at risk for a number of 70 71 72 73 74 75 other pulmonary complications Up to 70% of patients experience early infection after cardiac 76 arrest, and the respiratory tract is the most common source Vigilance for early-onset pneu- 77 ] TIÊU PaO MỤC porary Reviews in Critical Care Medicine Tác giả Thiết kế Primary Outcome Kilgannon 2010 Cohort 6326 BN PaO2 ≥ 300 mmHg, ≤ 60 mmHg tăng tử vong Secondary Outcome lator Management and Respiratory Kilgannon Cohort PaO tương quan PaO tăng 100mmHg After 2011 Cardiac4459 Arrest thuận tử vong, nghịch tăng 24 % nguy tử cục thần kinh ation, Ventilation, Infection,kết and Injury Bellomo 2011 Cohort 12108 Johnson 2016 Cohort 544 vong PaO2 ≥ 300 mmHg tăng tử vong ohnson, MD; David J Carlbom, MD; and David F Gaieski, MD Tăng oxy không ảnh PaO2 ≥ 300 mmHg hưởng kết cục thần thời điểm 12 tăng lệ tử vong Return of spontaneous circulation kinh after cardiac arrest results in atỷsystemic inflammatory state called the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagulopathy, neuronal injury, and organ dysfunction Perturbations in oxygenation and ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated with poor outcome Further, patients who experience cardiac arrest are at risk for a number of other pulmonary complications Up to 70% of patients experience early infection after cardiac arrest, and the respiratory tract is the most common source Vigilance for early-onset pneumonia, as well as aggressive diagnosis and early antimicrobial agent administration are important components of critical care in this population Patients who experience cardiac arrest MỤC] TIÊU PaCO2 porary Reviews in Critical Care Medicine Tác giả Thiết kế Primary Outcome Robert 2013 Cohort 193 BN PaCO2 ≥ 50 mmHg, ≤ 30 mmHg kết cục xấu thần kinh Secondary Outcome lator Management and Respiratory After Schneider Cardiac Cohort Arrest PaCO ≤ 30 mmHg PaCO 2013 16452 tăng tử vong ation, Ventilation, Infection, and Injury Bennett 2013 Cohort 195 Vaahersalo 2014 Cohort 409 PaCO2 không liên quan kết cục thần kinh ohnson, MD; David J Carlbom, MD; and David F Gaieski, MD ≥ 45 mmHg tỷ lệ xuất viện cao PaO2 không liên quan kết cục thần kinh PaCO2 ≥ 45 mmHg PaO2 không liên quan kèm với kết cục thần kết cục thần kinh 12 tháng Return of spontaneous circulation kinh after tốt cardiac arrest results in a systemic inflammatory state called the post-cardiac arrest syndrome, characterized by oxidative stress, coagulHelmershorst Cohort PaCO which ≤ 35 ismmHg opathy, dysfunction 2015 neuronal injury, 5258and organ tăng tử vongPerturbations in oxygenation and ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated with poor outcome Further, patients who experience cardiac arrest are at risk for a number of Tolins 2017 Cohort PaCO2 31 – 49 mmHg kết hợp với kết cục arrest, and the respiratory tract isthần the most kinh common có lợi source Vigilance for early-onset pneuother pulmonary complications Up to 70% of patients experience early infection after cardiac monia, as well as aggressive diagnosis and early antimicrobial agent administration are important components of critical care in this population Patients who experience cardiac arrest ophysiology ARDS and PCAS, Beitler et al8 demonstrated analassociation between low between theofpathophysiology of ARDS and PCAS, Beitler et demonstrated an asso mation, leukocyte activation, activation volumes (defined # mL/kg) and as favorable including inflammation, leukocyte tidalasvolumes (defined # mL porary Reviews in Critical Care Medicine activation, ] tidal activation thways, and altered permeability of neurologicofstatus inneurologic 256 patients whoinexperienced of coagulation pathways, and altered permeability status 256 patients 61 61 alalveolar and epithelial barriers out-of-hospital cardiac arrest The authors found endothelial and epithelial barriers out-of-hospital cardiac also arrest The NGUY CƠ ARDS al Contributors to Lung Injury andtoARDS Cardiac Arrest TABLE ] Potential Contributors LungAfter Injury and ARDS After Cardiac Arrest lator Management and Respiratory After Cardiac Arrest Contributing Factor Aspiration sion Pulmonary contusion Details Details 60 30% have witnessed 30% periarrest have emesis witnessed periarrest emesis 40% experience pulmonary contusion pulmonary after CPR56contusion 40% experience ation, Ventilation, Infection, Known and Injury to affect lungsKnown in other states to disease affect lungs in other disease 57 usion injury Ischemia-reperfusion injury 58,59 d lung injury 90% of patients are mechanically ventilated after arrestvent Ventilator-induced lung injury 90% of patients are mechanically ohnson, MD; David J Carlbom, MD; and David F Gaieski, MD 80,81 Early-onset pneumonia is common Infection Early-onset pneumonia is common80,8 mation/post-cardiac Sepsis-like syndromeSepsis-like with significant pathophysiological Systemic inflammation/post-cardiac syndrome with significant p 27,61 27,61 me overlap with ARDS arrest syndrome with ARDS Return of spontaneous circulation after cardiac arrest resultsoverlap in a systemic inflammatory state called the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagulyCPR resuscitation ¼ cardiopulmonary resuscitation opathy, neuronal injury, and organ dysfunction Perturbations in oxygenation and ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated with poor outcome Further, patients who experience cardiac arrest are at risk for a number of views in Critical CareReviews Medicinein Critical Care Medicine - # - C H E S T - 1-7# Contemporary other pulmonary complications Up to 70% of patients experience early infection after cardiac [ [ arrest, and the respiratory tract is the most common source Vigilance for early-onset pneu- REV 5.5.0 DTD Š CHEST1440_proof ŠCHEST1440_proof 18 December 2017 Š pm Š EO: CHEST-17-2042 REV 5.5.0 DTD Š Š 8:33 18 December 2017 Š 8:33 pm Š EO: CHES monia, as well as aggressive diagnosis and early antimicrobial agent administration are important components of critical care in this population Patients who experience cardiac arrest ] THƠNG KHÍ porary Reviews in Critical Care Medicine • Một vài nghiên cứu: LowRespiratory Vt cải thiện tiên lượng Nonlator Management and ARDS After Cardiac Arrest • Sutherasan ation, Ventilation, (2015) Infection,812 andbệnh Injurynhân ngưng tim / 12 năm ohnson, MD; David J Carlbom, MD; and David F Gaieski, MD ü Xu hướng Vt 8,9 ml/Kg ü PEEP tăng 3,5 6,5 cm H2O Return of spontaneous circulation after cardiac arrest results in a systemic inflammatory state • Beitler 256syndrome, bệnhwhich nhân ngưngbytim ngoại viện called the(2017): post-cardiac arrest is characterized oxidative stress, coagulinjury, and organ Perturbations in oxygenation ü opathy, Vt ≤neuronal 8ml/kg cải dysfunction thiện kết cục thần kinhand ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated with poor outcome Further, patients who experience cardiac arrest are at risk for a number of other pulmonary complications Up to 70% of patients experience early infection after cardiac arrest, and the respiratory tract is the most common source Vigilance for early-onset pneumonia, as well as aggressive diagnosis and early antimicrobial agent administration are important components of critical care in this population Patients who experience cardiac arrest [ Contemporary Reviews in Critical Care Medicine 56 SAU NGƯNG TIM ] Q1 57 58 59 60 Ventilator Management and Respiratory Care After Cardiac Arrest 61 62 63 64 Oxygenation, Ventilation, Infection, and Injury 10 11 65 66 881 12 TABLE 4] Recommendations for Ventilator Parameters Nicholas J Johnson, MD; David J Carlbom, MD; and David F Gaieski, MD in CriticalQ2 Care Medicine ] 13 and Goals After Cardiac Arrest 882 14 Q15 15 883 16 884 17 18 885 19 involving a 67univ 68 56 service57that69inclu 70 Return of spontaneous circulation after cardiac arrest results in a systemic inflammatory state Parameter/Goal Recommendation that low 58 tidal 71 vo called the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagul72 opathy, neuronal injury, and organ dysfunction Perturbations in oxygenation and medical ventilation59 transpo PaO2 70-100 mm Hg 73 may exacerbate secondary injury after cardiac arrest and have been shown to be associated60 74 influenced subse SpO2 92%-97% with poor outcome Further, patients who experience cardiac arrest are at risk for a number of 75 61 other pulmonary complications Up to 70% of patients experience early infection after cardiac highlighting76 the PaCO2 40-50 mm Hg arrest, and the respiratory tract is the most common source Vigilance for early-onset pneu-62 77 subsequent in-h monia, as well as aggressive diagnosis and early antimicrobial agent administration are63 78 Tidal volume Management and Respiratory Cardiac Arrest 20 886 21 887 22 23 888 24 889 25 ARDS important components of critical care in this population Patients who experience cardiac arrest 64 4-8 mL/kg of predicted are at risk for the development of ARDS Risk factors include aspiration, pulmonary contusions (from chest compressions), systemic and reperfusion injury Early evidence65 bodyinflammation, weight105 ntilation, Infection, and Injury 890 26 27 79 80 81 Conclusions suggests that they may benefit from ventilation with low tidal volumes Meticulous attention66 82 83 No ARDS 6-8assessment mL/kg and of predicted 891 to mechanical ventilation, early optimization of respiratory gas exchange, 67 29 84 Meticulous atten avid Gaieski, MD at potential andF.therapies targeted pulmonary complications may improve outcomes after body weight 892J Carlbom, MD; and David 28 ( ): - 68 respiratory param 86 PEEP $ cm H2O 893 69 32 87 Q6 KEY WORDS: cardiac arrest; cardiopulmonary resuscitation; critical care; mechanical ventilation outcomes after c Higher if ARDS, significant 33 88 894 70 turn of spontaneous circulation after cardiac arrest results in a systemic 34 89 atelectasis, highinflammatory BMI, and state and CO 712 tension 895 appropriate neuroprognostication, and More than 500,000 patients experience 35 the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagul90 led stable hemodynamics 3-9 72 meticulous respiratory care cardiac arrest in the United States each year 36 91 896 neuronal injury, and organ dysfunction Perturbations in oxygenation and ventilation neurologic statu athy, 30 31 37 cardiac arrest Survival with a favorable neurologic outcome CHEST 2017; - - - - Abnormal arterial tensions of oxygen and 85 92 CTSN – TĂNG ÁP LỰC NỘI SỌ • Tăng thơng khí co mạch giảm lượng máu lên não giảm áp lực nội sọ • PaCO2 < 35 > 45 mmHg / 20 phút đầu = 14 x nguy tử vong • High Vt/CTSN nặng tăng nguy ARDS • Tăng Vt mục tiêu tăng thơng khíà có lợi ? • Tăng tần số MVà điều chỉnh PaCO2 RÀO CẢN • Khơng nhận bệnh nhân có nguy ARDS • Khơng tính cân nặng lý tưởng: LOV-ED • Lo ngại sử dụng an thần: ARMA trial /ARDS, Serpa Neto / non-ARDS • Lo ngại toan hơ hấp: tăng áp lực nội sọ KẾT LUẬN • Thơng khí Vt thấp bệnh nhân khơng ARDS giảm nguy ARDS, giảm thời gian nằm viện, tử vong • Bệnh nhân nguy ARDS: Vt – ml/kg predicted body weight, PEEP ≥ cmH2O • Theo dõi nhận diện ARDS Vt ml/kg PBW • Thơng khí Vt thấp áp dụng cấp cứu 2019 Annual Update in Intensive Care and Emergency Medicine 2019 Edited by Jean-Louis Vincent TÀI LIỆU THAM KHẢO 1.Annual Update in Intensive Care and Emergency Medicine 2019 tr47 – 59 Simonis, F.D., Schultz, M and Artigas, A., Towards Safer Ventilation in Critically ill Patients without ARDS Neto, A.S., Cardoso, S.O (2012) Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory distress syndrome: a metaanalysis Jama, 308(16), pp.1651-1659 4.Simonis, F.D., Neto, A.S., Binnekade, J.M., Braber, A., Bruin, K.C., Determann, R.M., Goekoop, G.J., Heidt, J., Horn, J., Innemee, G and De Jonge, E., 2018 Effect of a low vs intermediate tidal volume strategy on ventilator-free days in intensive care unit patients without ARDS: a randomized clinical trial Jama, 320(18), pp.1872-1880 Neto, A.S., Rabello Filho, R., Cherpanath, T., Determann, R., Dongelmans, D.A., Paulus, F., Tuinman, P.R., Pelosi, P., de Abreu, M.G., Schultz, M.J and PROVE Network Investigators, 2016 5.Associations between positive end-expiratory pressure and outcome of patients without ARDS at onset of ventilation: a systematic review and meta-analysis of randomized controlled trials Annals of intensive care, 6(1), p.109 Neto, A.S and Jaber, S., 2016 What’s new in mechanical ventilation in patients without ARDS: lessons from the ARDS literature Intensive care medicine, 42(5), pp.787-789 Sahetya, S.K., Mallow, C., Sevransky, J.E., Martin, G.S., Girard, T.D., Brower, R.G and Checkley, W., 2019 Association between hospital mortality and inspiratory airway pressures in mechanically ventilated patients without acute respiratory distress syndrome: a prospective cohort study Critical Care, 23(1), p.367 Fuller, B.M., Ferguson, I.T., Mohr, N.M., Drewry, A.M., Palmer, C., Wessman, B.T., Ablordeppey, E., Keeperman, J., Stephens, R.J., Briscoe, C.C and Kolomiets, A.A., 2017 Lung-protective ventilation initiated in the emergency department (LOV-ED): a quasi-experimental, before-after trial Annals of emergency medicine, 70(3), pp.406-418 9.Johnson, N.J., Carlbom, D.J and Gaieski, D.F., 2018 Ventilator management and respiratory care after cardiac arrest: oxygenation, ventilation, infection, and injury Chest, 153(6), pp.1466-1477 10 Slutsky, A.S., 2015 History of mechanical ventilation From Vesalius to ventilator-induced lung injury American journal of respiratory and critical care medicine, 191(10), pp.1106-1115 CHÂN THÀNH CẢM ƠN SỰ LẮNG NGHE CỦA QUÝ ANH,CHỊ 37 ... quản cấp cứu 6,8 – % ARDS 14 – 27,5 % • Huyền thoại “500ml” • 10% bệnh nhân thở máy non-ARDS điều chỉnh máy thở • 42 % bệnh nhân nhận thông số chuyển ICU • 28 % khơng đổi 24 • Stolze cs: sử dụng... máu động mạch,TNF alpha, IL1, IL6, IL8a, IL 12 / thơng khí • Kallet 2001,2006: Bất đồng bệnh nhân – máy thở, nguy xẹp phổi • Lipshutz AK and Gropper (2013): Yếu thuốc dãn LOW TIDAL VOLUME Nghiên... toan hơ hấp: tăng áp lực nội sọ KẾT LUẬN • Thơng khí Vt thấp bệnh nhân không ARDS giảm nguy ARDS, giảm thời gian nằm viện, tử vong • Bệnh nhân nguy ARDS: Vt – ml/kg predicted body weight, PEEP ≥