Abstract
BackgroundVentilation/perfusion inequalities impair gas exchange in acute respiratory distress syndrome (ARDS). Although increased dead-space ventilation (VD/VT) has been described in ARDS, its mechanism is not clearly understood. We sought to evaluate the relationships between dynamic variations in VD/VT and extra-pulmonary microcirculatory blood flow detected at sublingual mucosa hypothesizing that an altered microcirculation, which is a generalized phenomenon during severe inflammatory conditions, could influence ventilation/perfusion mismatching manifested by increases in VD/VT fraction during early stages of ARDS.MethodsForty-two consecutive patients with early moderate and severe ARDS were included. PEEP was set targeting the best respiratory-system compliance after a PEEP-decremental recruitment maneuver. After 60 min of stabilization, hemodynamics and respiratory mechanics were recorded and blood gases collected. VD/VT was calculated from the CO2 production (V_{{{text{CO}}_{2} }}) and CO2 exhaled fraction (F_{{{text{ECO}}_{2} }}) measurements by volumetric capnography. Sublingual microcirculatory images were simultaneously acquired using a sidestream dark-field device for an ulterior blinded semi-quantitative analysis. All measurements were repeated 24 h after.ResultsPercentage of small vessels perfused (PPV) and microcirculatory flow index (MFI) were inverse and significantly related to VD/VT at baseline (Spearman’s rho = − 0.76 and − 0.63, p < 0.001; R2 = 0.63, and 0.48, p < 0.001, respectively) and 24 h after (Spearman’s rho = − 0.71, and − 0.65; p < 0.001; R2 = 0.66 and 0.60, p < 0.001, respectively). Other respiratory, macro-hemodynamic and oxygenation parameters did not correlate with VD/VT. Variations in PPV between baseline and 24 h were inverse and significantly related to simultaneous changes in VD/VT (Spearman’s rho = − 0.66, p < 0.001; R2 = 0.67, p < 0.001).ConclusionIncreased heterogeneity of microcirculatory blood flow evaluated at sublingual mucosa seems to be related to increases in VD/VT, while respiratory mechanics and oxygenation parameters do not. Whether there is a cause–effect relationship between microcirculatory dysfunction and dead-space ventilation in ARDS should be addressed in future research.
Highlights
Ventilation/perfusion inequalities impair gas exchange in acute respiratory distress syndrome (ARDS)
To avoid the selection of cases with transitory hypoxemia simulating ARDS, patients were enrolled only after successfully completing a two-step selection process [16, 17]: (a) first, patients mechanically ventilated through an endotracheal tube with a Positive end-expiratory pressure (PEEP) ≥ 5 and FiO2 ≥ 0.5 for at least 12 h and meeting the moderate and severe ARDS criteria according to Berlin Consensus definitions [1] were declared potentially eligible; (b) potential candidates were subjected to a FiO2 trial at 1.0 while maintaining PEEP ≥ 10 for at least 30 min, after which, new arterial blood gases were collected
Similar findings were observed between Dead-space ventila‐ tion fraction (VD/Tidal volume (VT)) and the microcirculatory flow index at baseline (Spearman rho = − 0.63, p < 0.001; R2 = 0.48, p < 0.001) and 24 h after (Spearman rho = − 0.65, p < 0.001; R2 = 0.60, p < 0.001) (Fig. 1c, d)
Summary
Ventilation/perfusion inequalities impair gas exchange in acute respiratory distress syndrome (ARDS). Intensive Care (2020) 10:35 epithelial permeability, with subsequent loss of aerated lung tissue and increased lung stiffness [1] These alterations lead to imbalances between ventilation and perfusion relationships, which result in hypoxemia and impaired carbon dioxide clearance. It has been considered that pulmonary perfusion in ARDS occurs in non-ventilated (VA/Q < 0.005) or poorly ventilated (0.005 < VA/Q < 0.1) lung units, which, in turn, results in vasoconstriction of perfusing arterioles [5] Such VA/Q mismatch in some lung regions in which perfusion largely exceeds ventilation, account for hypoxemia, which is the clinical hallmark of ARDS [1, 6, 7]. Increased dead-space ventilation has been described in patients subjected to protective ventilation strategies with low plateau pressures [9, 10], which suggest that mechanisms different to alveolar overdistention should be implied
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
