dc.creatorOspina-Tascón, G. A.
dc.creatorHernández P., Glenn
dc.creatorBruhn, Alejandro
dc.creatorBautista Rincón, Diego F.
dc.creatorMadriñán, H. J.
dc.creatorValencia, J. D.
dc.creatorBermúdez, W. F.
dc.creatorQuiñones, Edgardo
dc.creatorCalderón-Tapia, Luis E.
dc.creatorDe Backer, D.
dc.date.accessioned2020-04-01T15:29:29Z
dc.date.available2020-04-01T15:29:29Z
dc.date.created2020-04-01T15:29:29Z
dc.date.issued2020
dc.identifierAnnals of Intensive Care. 2020 Mar 24;10(1):35
dc.identifier10.1186/s13613-020-00651-1
dc.identifierhttps://doi.org/10.1186/s13613-020-00651-1
dc.identifierhttps://repositorio.uc.cl/handle/11534/28646
dc.description.abstractAbstract Background Ventilation/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. Methods Forty-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 ($$V_{{{\text{CO}}_{2} }}$$VCO2) and CO2 exhaled fraction ($$F_{{{\text{ECO}}_{2} }}$$FECO2) 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. Results Percentage 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). Conclusion Increased 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.
dc.languageen
dc.rightsThe Author(s)
dc.rightsacceso abierto
dc.subjectAcute respiratory distress syndrome
dc.subjectDead-space ventilation
dc.subjectVD/VT
dc.subjectVentilation/perfusion mismatch
dc.subjectMicrocirculation
dc.subjectMicrocirculatory blood fow
dc.titleMicrocirculatory dysfunction and dead-space ventilation in early ARDS: a hypothesis-generating observational study.
dc.typeartículo


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