Ventilator induzierter Zwerchfellschaden: ein Update

 

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Zusammenfassung

Der Ventilator induzierte Zwerchfellschaden (engl. ventilator-induced diaphragmatic dysfunction (VIDD)) scheint kein tierexperimentelles Artefakt zu sein, sondern manifestiert sich ebenfalls bei beatmeten Patienten. Die verfügbare Evidenz legt nahe, dass die VIDD auf dem Boden einer hochregulierten Proteolyse in den Atemmuskeln entsteht. Es mehren sich die Hinweise, dass VIDD nicht einfach Teil eines generellen muskulären Prozesses ist: So unterliegen z. B. weder der Musculus latissimus dorsi noch der Musculus pectoralis major diesen rapiden Abbauvorgängen. Erste humane Studienergebnisse zeigten, dass es bei kontrollierter invasiver Beatmung über einen Zeitraum von lediglich 18 – 69 Stunden zu einer deutlichen Abnahme des Faserquerschnitts der diaphragmalen Myofibrillen kommt. Kürzlich konnte gar gezeigt werden, dass extrem kurze Phasen von nur zwei Stunden kontrollierter invasiver Beatmung ausreichen, um einen beginnenden Schaden hervorzurufen. Erstmals konnte ferner in vivo an humanen Individuen gezeigt werden, dass die VIDD auch klinisch bereits nach einem Tag invasiver Beatmung zu einer erheblichen Einschränkung der Kraftgenerierung des Zwerchfells führt. Diese Einschränkung verlief über einen Beobachtungszeitraum von einer Woche progressiv und kam nicht etwa nach einem initialen Abfall der Zwerchfellkraft zum Stillstand. Für den Kliniker besonders wertvoll scheint die Möglichkeit, mittels einer einfachen sonografischen Methode die Zwerchfellbeweglichkeit abzuschätzen und somit einen möglichen Surrogatparameter der VIDD mit hohem prädiktivem Wert am Patientenbett verfügbar zu haben. Bezüglich der möglichen Therapieoptionen der VIDD muss an erster Stelle deren Prävention durch eine ausreichend hohe diaphragmale Leistung genannt werden – ein unverändert bestehend bleibender Widerspruch zu der Intention, durch die (invasive) Beatmung eine möglichst große Entlastung der Atempumpe zu erzielen.

Abstract

There is rising evidence that ventilator-induced diaphragmatic dysfunction (VIDD) is not just an artifactual finding from animal studies, but actually occurs in humans undergoing invasive mechanical ventilation. Initial research findings in humans have demonstrated that periods of controlled invasive mechanical ventilation lasting just 18 – 69 hours can lead to a marked reduction in diaphragmatic myofibers. More recently, it has been shown that even short periods (e. g. two-hours) of controlled invasive mechanical ventilation are sufficient to initiate VIDD. The evidence available at present suggests that VIDD is most likely based on increased proteolysis of the respiratory muscles. Moreover, VIDD seems not to be part of a general muscle wasting process, as suggested by the fact that e. g. the human latissimus dorsi and the pectoralis major muscles seem not to be subjected to early muscle fiber atrophy when directly compared to the human diaphragm. Novel in vivo data have also revealed that VIDD in humans is associated with a reduction in diaphragmatic force generation after only one day of controlled invasive mechanical ventilation. This impairment was observed to progress further over the one-week investigation period. The introduction of a simple bedside ultrasound measurement of diaphragmatic function is of great importance to the clinician, as it may serve as a surrogate measure for VIDD, with high predictive value. Regarding potential therapeutic interventions against VIDD, the primary aim should be to encourage sufficient diaphragmatic use in susceptible patients so as to avoid VIDD; this approach remains in fundamental contrast to that of reducing respiratory muscle load by (invasive) mechanical ventilation.

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