Ventilator-induced diaphragm dysfunction is thought to be multifactorial in origin, but basically occurs by lack-of-use atrophy. This 1985 paper provides a mechanism, namely, reduced diaphragm perfusion (experimentally induced septic shock in MV dogs) [1]. In contrast, perfusion increased in spontaneously breathing animals.

Do you agree this has been overlooked in VIDD? Also, what potential modalities do you think could prevent diaphragm hypoperfusion in the ICU? For instance, Supinsky (1989) catheterized the phrenic arteries in dogs and was able to reverse diaphragm fatigue by increasing phrenic blood flow. Could this be done in ICU patients?

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[1] Hussain SN, Roussos C. Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs. J Appl Physiol (1985). 1985 Dec;59(6):1802-8. doi: 10.1152/jappl.1985.59.6.1802. PMID: 4077788.

[2] Supinski G, DiMarco A, Ketai L, Hussein F, Altose M. Reversibility of diaphragm fatigue by mechanical hyperperfusion. Am Rev Respir Dis. 1988 Sep;138(3):604-9. doi: 10.1164/ajrccm/138.3.604. PMID: 2974261.