Mechanical ventilation induces a time‐dependent reduction in microvascular oxygenation and vascular conductance in the diaphragm

Abstract

Prolonged mechanical ventilation (MV) promotes diaphragmatic atrophy and contractile dysfunction, collectively termed ventilator‐induced diaphragmatic dysfunction. A local mismatching of O2 delivery (QO2) to consumption (VO2) within the diaphragm may contribute, in part, to muscle dysfunction and weaning difficulties following MV. We tested the hypotheses that longer durations of MV (i.e., 6 hrs.) will 1) cause a mismatching of QO2‐to‐VO2, evident through a reduction microvascular PO2 (i.e., PO2m); and 2) reduce vascular conductance (VC) compared to acute MV (i.e., 30 min). Diaphragm PO2m and VC were measured in vivo in adult female Sprague‐Dawley rats (n=15). Data was collected during spontaneous breathing (SB) and after acute MV and 6 hr of MV. PO2m in the diaphragm was significantly reduced following the onset of MV (SB: 53±6, acute MV: 37±8 mmHg; P<0.05) and by an additional ~51% after 6 hr (versus acute MV) to 18±5 mmHg (P<0.05). Diaphragm VC was diminished after the onset of MV (SB: 0.36±0.02, acute MV: 0.24±0.02) and reduced further after 6 hr MV (0.08±0.01 ml/min/100 g/mmHg; all P<0.05). The diminished microvascular driving pressure of O2 and VC provides important insight, and a potential contributing mechanism, into the inadequate maintenance of the QO2‐to‐VO2 ratio in the diaphragm with prolonged MV. The mechanisms responsible for the reduced PO2m and VC with MV require further studies. (NIH and FBRP)