Zusammenfassung

     Das akute Atemnotsyndrom (ARDS) ist ein häufiges intensivmedizinisches Krankheitsbild. Die Pathophysiologie ist geprägt vom eingeschränkten Gasaustausch aufgrund einer Flüssigkeitsüberladung der Alveolen nach epi- und endothelialer Permeabilitätssteigerung und Leukozyten-Transmigration. Es resultieren Hypoxämie, Hyperkapnie sowie deletäre Konsequenzen für Makro- und Mikrozirkulation mit der Gefahr eines Multiorganversagens und hoher Mortalität. Abstract Acute respiratory distress syndrome (ARDS) is a common condition in intensive care medicine. Various intra- and extrapulmonal causes may trigger an epithelial and endothelial permeability increase, which leads to impaired gas exchange due to fluid overload of the alveoli and transmigration of leukocytes. This results in hypoxemia and hypercapnia, as well as deleterious consequences for the macro- and microcirculation with the risk of multi-organ failure and high mortality. This review summarizes ARDS pathophysiology and clinical consequences. Kernaussagen Das ARDS ist ein äußerst heterogenes Syndrom. Verschiedene Entitäten münden in eine ähnliche pathophysiologische Kaskade. Das ARDS ist charakterisiert durch einen eingeschränkten Gasaustausch. Das grundlegende pathophysiologische Problem ist eine Schrankenstörung der alveolokapillären Barriere mit resultierendem alveolärem und interstitiellem Lungenödem. Inflammation, Zerstörung der Mikrozirkulation und beatmungsassoziierte Lungenschädigung unterhalten das Krankheitsbild. Die Entwicklung eines pulmonalarteriellen Hypertonus kann zu einem akuten Cor pulmonale mit deletären Konsequenzen für den Organismus führen. Im COVID-19-induzierten ARDS haben der Mechanismus der Inflammation und die Vaskulopathie mit Endothelopathie und Immunothrombose einen besonderen Stellenwert. Eine Fibrosierung der Lunge kann einer vollständigen Resolution des Krankheitsbildes entgegenstehen. Die Definition von verschiedenen ARDS-Phänotypen erlaubt zunehmend eine individualisiertere Behandlung. Als Beispiel sei Dexamethason beim COVID-19-induzierten ARDS genannt. Schlüsselwörter akutes Atemnotsyndrom - ARDS - akutes Lungenversagen - Gasaustausch - Intensivbehandlung - mechanische Beatmung Keywords mechanical ventilation - acute respiratory distress syndrome - gas exchange - critical illness 08 January 2024 © 2024. Thieme. All rights reserved. Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany Literatur 1 Ranieri VM, Rubenfeld GD, Thompson BT. et al. Acute respiratory distress syndrome: the Berlin definition. JAMA 2012; 307: 2526-2533 DOI: 10.1001/jama.2012.5669. (PMID: 22797452) CrossrefPubMedGoogle Scholar 2 Meyer NJ, Gattinoni L, Calfee CS. Acute respiratory distress syndrome. Lancet 2021; 398: 622-637 DOI: 10.1016/S0140-6736(21)00439-6. (PMID: 34217425) CrossrefPubMedGoogle Scholar 3 Bellani G, Laffey JG, Pham T. et al. Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA 2016; 315: 788-800 DOI: 10.1001/jama.2016.0291. (PMID: 26903337) CrossrefPubMedGoogle Scholar 4 Gottschaldt U, Reske A. Pathophysiologie des Lungenversagens. Anästh Intensivmed 2018; 59: 249-264 PubMedGoogle Scholar 5 Lewis CA, Martin GS. Understanding and managing fluid balance in patients with acute lung injury. Curr Opin Crit Care 2004; 10: 13-17 DOI: 10.1097/00075198-200402000-00003. (PMID: 15166844) CrossrefPubMedGoogle Scholar 6 Bos LDJ, Ware LB. Acute respiratory distress syndrome: causes, pathophysiology, and phenotypes. Lancet 2022; 400: 1145-1156 DOI: 10.1016/S0140-6736(22)01485-4. (PMID: 36070787) CrossrefPubMedGoogle Scholar 7 Juss JK, House D, Amour A. et al. Acute respiratory distress syndrome neutrophils have a distinct phenotype and are resistant to phosphoinositide 3-kinase inhibition. Am J Respir Crit Care Med 2016; 194: 961-973 DOI: 10.1164/rccm.201509-1818OC. (PMID: 27064380) CrossrefPubMedGoogle Scholar 8 Matthay MA, Zemans RL, Zimmerman GA. et al. Acute respiratory distress syndrome. Nat Rev Dis Primers 2019; 5: 18 DOI: 10.1038/s41572-019-0069-0. (PMID: 30872586) CrossrefPubMedGoogle Scholar 9 Thille AW, Esteban A, Fernández-Segoviano P. et al. Comparison of the Berlin definition for acute respiratory distress syndrome with autopsy. Am J Respir Crit Care Med 2013; 187: 761-767 DOI: 10.1164/rccm.201211-1981OC. (PMID: 23370917) CrossrefPubMedGoogle Scholar 10 Aublanc M, Perinel S, Guérin C. Acute respiratory distress syndrome mimics: the role of lung biopsy. Curr Opin Crit Care 2017; 23: 24-29 DOI: 10.1097/MCC.0000000000000373. (PMID: 27906708) CrossrefPubMedGoogle Scholar 11 Calfee CS, Delucchi K, Parsons PE. et al. Subphenotypes in acute respiratory distress syndrome: latent class analysis of data from two randomised controlled trials. Lancet Respir Med 2014; 2: 611-620 DOI: 10.1016/S2213-2600(14)70097-9. (PMID: 24853585) CrossrefPubMedGoogle Scholar 12 Frye M, Dierkes M, Küppers V. et al. Interfering with VE-PTP stabilizes endothelial junctions in vivo via Tie-2 in the absence of VE-cadherin. J Exp Med 2015; 212: 2267-2287 DOI: 10.1084/jem.20150718. (PMID: 26642851) CrossrefPubMedGoogle Scholar 13 Ware LB, Matthay MA. Alveolar fluid clearance is impaired in the majority of patients with acute lung injury and the acute respiratory distress syndrome. Am J Respir Crit Care Med 2001; 163: 1376-1383 DOI: 10.1164/ajrccm.163.6.2004035. (PMID: 11371404) CrossrefPubMedGoogle Scholar 14 Takala J. Hypoxemia due to increased venous admixture: influence of cardiac output on oxygenation. Intensive Care Med 2007; 33: 908-911 DOI: 10.1007/s00134-007-0546-x. (PMID: 17342520) CrossrefPubMedGoogle Scholar 15 Gierhardt M, Pak O, Walmrath D. et al. Impairment of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome. Eur Respir Rev 2021; 30: 210059 DOI: 10.1183/16000617.0059-2021. (PMID: 34526314) CrossrefPubMedGoogle Scholar 16 Swenson KE, Swenson ER. Pathophysiology of acute respiratory distress syndrome and COVID-19 lung injury. Crit Care Clin 2021; 37: 749-776 DOI: 10.1016/j.ccc.2021.05.003. (PMID: 34548132) CrossrefPubMedGoogle Scholar 17 Carrasco Loza R, Villamizar Rodríguez G, Medel Fernández N. Ventilator-induced lung injury (VILI) in acute respiratory distress syndrome (ARDS): volutrauma and molecular effects. Open Respir Med J 2015; 9: 112-119 DOI: 10.2174/1874306401509010112. (PMID: 26312103) CrossrefPubMedGoogle Scholar 18 Deutsche Gesellschaft für Anästhesiologie und Intensivmedizin (DGAI) (Federführende Fachgesellschaft). S3-Leitlinie „Invasive Beatmung und Einsatz extrakorporaler Verfahren bei akuter respiratorischer Insuffizienz“. AWMF-Registernummer 001/021. 2017 (in Überarbeitung) Accessed October 26, 2023 at: https://register.awmf.org/de/leitlinien/detail/001–021 PubMedGoogle Scholar 19 Brower RG, Matthay MA, Morris A. Acute Respiratory Distress Syndrome Network. et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301-1308 DOI: 10.1056/NEJM200005043421801. (PMID: 10793162) CrossrefPubMedGoogle Scholar 20 Levy MM. PEEP in ARDS – how much is enough?. N Engl J Med 2004; 351: 389-391 DOI: 10.1056/NEJMe048103. (PMID: 15269320) CrossrefPubMedGoogle Scholar 21 Brower RG, Lanken PN, MacIntyre N. et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004; 351: 327-336 DOI: 10.1056/NEJMoa032193. (PMID: 15269312) CrossrefPubMedGoogle Scholar 22 Beitler JR, Malhotra A, Thompson BT. Ventilator-induced lung injury. Clin Chest Med 2016; 37: 633-646 DOI: 10.1016/j.ccm.2016.07.004. (PMID: 27842744) CrossrefPubMedGoogle Scholar 23 Parsons PE, Eisner MD, Thompson BT. et al. Lower tidal volume ventilation and plasma cytokine markers of inflammation in patients with acute lung injury. Crit Care Med 2005; 33: 1-6 CrossrefPubMedGoogle Scholar 24 Ranieri VM, Suter PM, Tortorella C. et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. JAMA 1999; 282: 54-61 DOI: 10.1001/jama.282.1.54. (PMID: 10404912) CrossrefPubMedGoogle Scholar 25 Vallabhajosyula S, Shankar A, Vojjini R. et al. Impact of right ventricular dysfunction on short-term and long-term mortality in sepsis: a meta-analysis of 1,373 patients. Chest 2021; 159: 2254-2263 DOI: 10.1016/j.chest.2020.12.016. (PMID: 33359215) CrossrefPubMedGoogle Scholar 26 Morales-Quinteros L, Camprubí-Rimblas M, Bringué J. et al. The role of hypercapnia in acute respiratory failure. Intensive Care Med Exp 2019; 7 (Suppl. 1) 39 DOI: 10.1186/s40635-019-0239-0. (PMID: 31346806) CrossrefPubMedGoogle Scholar 27 Kiely DG, Cargill RI, Lipworth BJ. Effects of hypercapnia on hemodynamic, inotropic, lusitropic, and electrophysiologic indices in humans. Chest 1996; 109: 1215-1221 DOI: 10.1378/chest.109.5.1215. (PMID: 8625670) CrossrefPubMedGoogle Scholar 28 Lai C, Adda I, Teboul JL. et al. Effects of prone positioning on venous return in patients with acute respiratory distress syndrome. Crit Care Med 2021; 49: 781-789 DOI: 10.1097/CCM.0000000000004849. (PMID: 33590997) CrossrefPubMedGoogle Scholar 29 Vieillard-Baron A, Price LC, Matthay MA. Acute cor pulmonale in ARDS. Intensive Care Med 2013; 39: 1836-1838 DOI: 10.1007/s00134-013-3045-2. (PMID: 23907498) CrossrefPubMedGoogle Scholar 30 Iba T, Levy JH, Connors JM. et al. The unique characteristics of COVID-19 coagulopathy. Crit Care 2020; 24: 360 DOI: 10.1186/s13054-020-03077-0. (PMID: 32552865) CrossrefPubMedGoogle Scholar 31 O’Donnell JS, Peyvandi F, Martin-Loeches I. Pulmonary immuno-thrombosis in COVID-19 ARDS pathogenesis. Intensive Care Med 2021; 47: 899-902 DOI: 10.1007/s00134-021-06419-w. (PMID: 34052905) CrossrefPubMedGoogle Scholar 32 Ackermann M, Verleden SE, Kuehnel M. et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19. N Engl J Med 2020; 383: 120-128 DOI: 10.1056/NEJMoa2015432. (PMID: 32437596) CrossrefPubMedGoogle Scholar 33 Conway EM, Mackman N, Warren RQ. et al. Understanding COVID-19-associated coagulopathy. Nat Rev Immunol 2022; 22: 639-649 DOI: 10.1038/s41577-022-00762-9. (PMID: 35931818) CrossrefPubMedGoogle Scholar 34 Gelarden I, Nguyen J, Gao J. et al. Comprehensive evaluation of bronchoalveolar lavage from patients with severe COVID-19 and correlation with clinical outcomes. Hum Pathol 2021; 113: 92-103 DOI: 10.1016/j.humpath.2021.04.010. (PMID: 33905777) CrossrefPubMedGoogle Scholar 35 Notz Q, Schmalzing M, Wedekink F. et al. Pro- and anti-inflammatory responses in severe COVID-19-induced acute respiratory distress syndrome – an observational pilot study. Front Immunol 2020; 11: 581338 DOI: 10.3389/fimmu.2020.581338. (PMID: 33123167) CrossrefPubMedGoogle Scholar 36 Sinha P, Furfaro D, Cummings MJ. et al. Latent class analysis reveals COVID-19-related acute respiratory distress syndrome subgroups with differential responses to corticosteroids. Am J Respir Crit Care Med 2021; 204: 1274-1285 DOI: 10.1164/rccm.202105-1302OC. (PMID: 34543591) CrossrefPubMedGoogle Scholar 37 Constantin JM, Grasso S, Chanques G. et al. Lung morphology predicts response to recruitment maneuver in patients with acute respiratory distress syndrome. Crit Care Med 2010; 38: 1108-1117 DOI: 10.1097/CCM.0b013e3181d451ec. (PMID: 20154600) CrossrefPubMedGoogle Scholar 38 Bajwa EK, Malhotra CK, Thompson BT. et al. Statin therapy as prevention against development of acute respiratory distress syndrome: an observational study. Crit Care Med 2012; 40: 1470-1477 DOI: 10.1097/CCM.0b013e3182416d7a. (PMID: 22430234) CrossrefPubMedGoogle Scholar 39 Stapleton RD, Martin TR, Weiss NS. et al. A phase II randomized placebo-controlled trial of omega-3 fatty acids for the treatment of acute lung injury. Crit Care Med 2011; 39: 1655-1662 DOI: 10.1097/CCM.0b013e318218669d. (PMID: 21423000) CrossrefPubMedGoogle Scholar 40 Supady A, Weber E, Rieder M. et al. Cytokine adsorption in patients with severe COVID-19 pneumonia requiring extracorporeal membrane oxygenation (CYCOV): a single centre, open-label, randomised, controlled trial. Lancet Respir Med 2021; 9: 755-762 DOI: 10.1016/S2213-2600(21)00177-6. (PMID: 34000236) CrossrefPubMedGoogle Scholar

Vorschau