Zusammenfassung
Das akute Lungenversagen des Erwachsenen (ARDS) ist gekennzeichnet durch eine generalisierte pulmonale Entzündungsreaktion mit einem nicht-kardiogen ausgelöstem Lungenödem, einer pulmonalen Hypertonie und einer ausgeprägten Zunahme des intrapulmonalen Shunts mit konsekutiver Hypoxämie [1, 43]. Die Mortalität dieses Syndroms ist auch heute noch höher als 50% [8, 37, 38]. Mögliche pathogenetische Mechanismen, die unter anderem für die schlechten Behandlungsergebnisse eine Rolle spielen können, sind sowohl die pulmonale Hypertonie als auch die zur Aufrechterhaltung normaler Blutgase notwendige aggressive Beatmungsstrategie. Die pulmonale Hypertonie bewirkt einerseits einen Anstieg des mikrovaskulären Filtrationsdruckes [7], der das alveolo-interstitielle Lungenödem verstärkt [15], und andererseits wird durch den pulmonalen Hypertonus ein Rechtsherzversagen begünstigt [36, 39]. Systemisch infundierte Vasodilatatoren senken zwar den pulmonal-arteriellen Druck (PAP), doch auf Grund der diffusen Wirkung auf das Gefäßbett im großen und kleinen Kreislauf sind sie nur eingeschränkt einsetzbar: Im Systemkreislauf verursacht die auftretende Dilatation eine arterielle Hypotonie mit möglichen negativen Folgen für die Durchblutung unterschiedlichster Organe.
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Rossaint, R., Lewandowski, K., Falke, K. (1993). NO in der Therapie des ARDS. In: Kleinberger, G., Lenz, K., Ritz, R., Schuster, HP., Simbruner, G., Slany, J. (eds) Beatmung. Intensivmedizinisches Seminar, vol 5. Springer, Vienna. https://doi.org/10.1007/978-3-7091-7543-9_7
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