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. 2020 Mar 24;10(1):35.
doi: 10.1186/s13613-020-00651-1.

Microcirculatory dysfunction and dead-space ventilation in early ARDS: a hypothesis-generating observational study

Gustavo A Ospina-Tascón  1   2 , Diego F Bautista  3 , Humberto J Madriñán  3 , Juan D Valencia  3 , William F Bermúdez  3 , Edgardo Quiñones  3 , Luis Eduardo Calderón-Tapia  3 , Glenn Hernandez  4 , Alejandro Bruhn  4 , Daniel De Backer  5
Affiliations

Microcirculatory dysfunction and dead-space ventilation in early ARDS: a hypothesis-generating observational study

Gustavo A Ospina-Tascón et al. Ann Intensive Care. .

Abstract

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 ([Formula: see text]) and CO2 exhaled fraction ([Formula: see text]) 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.

Keywords: Acute respiratory distress syndrome; Dead-space ventilation; Microcirculation; Microcirculatory blood flow; VD/VT; Ventilation/perfusion mismatch.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Relationships between pulmonary dead-space fraction (VD/VT) and the microcirculatory blood flow at baseline and 24 h after. a Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and the proportion of small vessels perfused at baseline. b Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and the proportion of small vessels perfused 24 h after. c Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and MFI at baseline. d Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and MFI 24 h after. PPV: percentage of small vessels perfused; VD/VT: pulmonary dead-space fraction; HI: heterogeneity index of microcirculatory blood flow; MFI: microcirculatory blood flow index
Fig. 2
Fig. 2
Relationships between pulmonary dead-space fraction (VD/VT) and some respiratory mechanics and oxygen parameters at baseline and 24 h after. a Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and the PaO2/FiO2 ratio at baseline. b Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and the PaO2/FiO2 ratio 24 h after. c Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and PEEP levels at baseline. d Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and PEEP levels 24 h after. e Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and the VT/CRS at baseline. f Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and the VT/CRS 24 h after. g Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and Pmaw at baseline. h Scatter plot depicting the correlation between pulmonary dead-space fraction (VD/VT) and Pmaw 24 h after. PaO2/FiO2 ratio: arterial oxygen partial pressure to oxygen inspiratory fraction; PEEP: positive end-expiratory pressure; VT/CRS: tidal volume-to-respiratory system compliance ratio (i.e., driving pressure); Pmaw: mean pressure of the airway
Fig. 3
Fig. 3
Relationships between dynamic variations in pulmonary dead-space fraction (VD/VT) and microcirculatory blood flow. Scatter plot depicting the correlation between variations in pulmonary dead-space fraction (Δ-VD/VT) vs. percentage of change in small vessels perfused (Δ-PPV) between baseline and 24 h after
See this image and copyright information in PMC

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