Dysfunction of respiratory muscles in critically ill patients on the intensive care unit

David Berger, Stefan Bloechlinger, Stephan von Haehling, Wolfram Doehner, Jukka Takala, Werner J Z'Graggen, Joerg C Schefold, David Berger, Stefan Bloechlinger, Stephan von Haehling, Wolfram Doehner, Jukka Takala, Werner J Z'Graggen, Joerg C Schefold

Abstract

Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed 'ventilator-induced diaphragmatic dysfunction' (VIDD) and should be distinguished from peripheral muscular weakness as observed in 'ICU-acquired weakness (ICU-AW)'. Interestingly, VIDD and ICU-AW may often be observed in critically ill patients with, e.g. severe sepsis or septic shock, and recent data demonstrate that the pathophysiology of these conditions may overlap. VIDD may mainly be characterized on a histopathological level as disuse muscular atrophy, and data demonstrate increased proteolysis and decreased protein synthesis as important underlying pathomechanisms. However, atrophy alone does not explain the observed loss of muscular force. When, e.g. isolated muscle strips are examined and force is normalized for cross-sectional fibre area, the loss is disproportionally larger than would be expected by atrophy alone. Nevertheless, although the exact molecular pathways for the induction of proteolytic systems remain incompletely understood, data now suggest that VIDD may also be triggered by mechanisms including decreased diaphragmatic blood flow or increased oxidative stress. Here we provide a concise review on the available literature on respiratory muscle weakness and VIDD in the critically ill. Potential underlying pathomechanisms will be discussed before the background of current diagnostic options. Furthermore, we will elucidate and speculate on potential novel future therapeutic avenues.

Keywords: Cachexia; Diaphragm; ICU‐acquired weakness; Mechanical ventilation; Sepsis; VIDD; Weakness; weaning failure.

Figures

Figure 1
Figure 1
Assessment of diaphragmatic motion (motion mode, phased array 3.5–5 Mhz transducer). Sub‐costal position (mid‐clavicular line, angle of >70° in supine subjects) with visualization of the posterior diaphragmatic third. The diaphragmatic dome should be hit perpendicularly. Liver/spleen may be used as sound windows for right/left hemi‐diaphragm. Diaphragmatic dome excursion at rest should be ≥1 cm (lower limit of normal in healthy controls).101, 108 Inspiratory diaphragmatic position (solid line), expiratory position (dotted line), and excursion (arrow) are indicated.
Figure 2
Figure 2
Assessment of (A) expiratory and (B) inspiratory diaphragmatic thickness (brightness mode, linear array high frequency transducer of >10 Mhz, zone of apposition: mid‐axillary line). Note in‐ and expiratory variation (limits of normal may vary).102, 108 The thickening fraction [i.e. (inspiratory–expiratory diameter) / expiratory diameter] can be assessed.143 Maximum diameters are measured between diaphragmatic pleural line (*) and peritoneal line (#). Central diaphragmatic tendon (c). Liver (L), Lungs (P) are indicated.

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Source: PubMed

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