Protective Recommendations for Non-invasive Ventilation During COVID-19 Pandemic: A Bench Evaluation of the Effects of Instrumental Dead Space on Alveolar Ventilation.
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ABSTRACT: Introduction
With the current COVID-19 pandemic, concerns have raised regarding the risk for NIV to promote airborne transmission. In case of hospital admission, continuation of therapy in patients undergoing chronic NIV is necessary and several protective circuit configurations have been recommended to reduce the risk of aerosol dissemination. However, all these configurations increase instrumental dead space. We therefore designed this study to evaluate their effects on the tidal volume (VTE) required to preserve stable end-tidal CO2 partial pressure (PETCO2) with constant respiratory rate.Methods
A bench consisting of a test lung connected to an adult-sized mannequin head was set up. The model was ventilated through usual domiciliary configuration (single limb circuit with facial vented mask) which was used as reference. Then, five different circuit configurations including non-vented facial mask with viral/bacterial filter, modification of leak position, and change from single to double-limb circuit were evaluated. For each configuration, pressure support (PS) was gradually increased to reach reference PETCO2. Resulting VTE was recorded as primary outcome.Results
Reference PETCO2 was 38(0) mmHg, with a PS set at 10 cmH2O, resulting in a VTE of 432(2) mL. Compared to reference, all the configurations evaluated required substantial increase in VTE to preserve alveolar ventilation, ranging from +79(2) to +216(1) mL.Conclusions
Modifications of NIV configurations in the context of COVID-19 pandemic result in substantial increase of instrumental dead space. Re-evaluation of treatment efficiency and settings is crucial whenever protective measures influencing NIV equipment are considered.
SUBMITTER: Delorme M
PROVIDER: S-EPMC8046339 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundThe end-tidal alveolar dead space fraction (AVDSf = [PaCO2-PETCO2]/PaCO2) is a metric used to estimate alveolar dead space. Higher AVDSf on the first day of mechanical ventilation is associated with mortality and fewer ventilator-free days. It is not clear if AVDSf is associated with length of ventilation in survivors, how AVDSf performs for risk stratification beyond the first day of ventilation, or whether AVDSf adds predictive value to oxygenation (oxygenation index [OI]) or severity of illness (Pediatric Risk of Mortality [PRISM III]) markers.MethodsRetrospective single-center observational cohort study of children and young adults receiving invasive mechanical ventilation. In those with arterial or capillary blood gases, AVDSf was calculated at the time of every blood gas for the first week of mechanical ventilation.ResultsThere were 2335 children and young adults (median age 5.8 years [IQR 1.2, 13.2]) enrolled with 8004 analyzed AVDSf values. Higher AVDSf was associated with mortality and longer length of ventilation in survivors throughout the first week of ventilation after controlling for OI and PRISM III. Higher OI was not associated with increased mortality until ≥ 48 h of ventilation after controlling for AVDSf and PRISM III. When using standardized variables, AVDSf effect estimates were generally higher than OI for mortality, whereas OI effect estimates were generally higher than AVDSf for the length of ventilation in survivors. An AVDSf > 0.3 was associated with a higher mortality than an AVDSf < 0.2 within each pediatric acute respiratory distress syndrome severity category. The maximum AVDSf within 12 h of intensive care unit admission demonstrated good risk stratification for mortality (AUC 0.768 [95% CI 0.732, 0.803]). AVDSf did not improve mortality risk stratification when added to PRISM III but did improve mortality risk stratification when added to the gas exchange components of PRISM III (minimum 12-h PaO2 and maximum 12-h PCO2) (p < 0.00001).ConclusionsAVDSf is associated with mortality and length of ventilation in survivors throughout the first week of invasive mechanical ventilation. Some analyses suggest AVDSf may better stratify mortality risk than OI, whereas OI may better stratify risk for prolonged ventilation in survivors than AVDSf.
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Project description:COVID-19 pandemic sets the healthcare system to a shortage of ventilators. We aimed at assessing tidal volume (VT) delivery and air recirculation during expiration when one ventilator is divided into 2 test-lungs. The study was performed in a research laboratory in a medical ICU of a University hospital. An ICU (V500) and a lower-level ventilator (Elisée 350) were attached to two test-lungs (QuickLung) through a dedicated flow-splitter. A 50 mL/cmH2O Compliance (C) and 5 cmH2O/L/s Resistance (R) were set in both A and B test-lungs (A C50R5 / B C50R5, step1), A C50-R20 / B C20-R20 (step 2), A C20-R20 / B C10-R20 (step 3), and A C50-R20 / B C20-R5 (step 4). Each ventilator was set in volume and pressure control mode to deliver 800mL VT. We assessed VT from a pneumotachograph placed immediately before each lung, pendelluft air, and expiratory resistance (circuit and valve). Values are median (1st-3rd quartiles) and compared between ventilators by non-parametric tests. Between Elisée 350 and V500 in volume control VT in A/B test- lungs were 381/387 vs. 412/433 mL in step 1, 501/270 vs. 492/370 mL in step 2, 509/237 vs. 496/332 mL in step 3, and 496/281 vs. 480/329 mL in step 4. In pressure control the corresponding values were 373/336 vs. 430/414 mL, 416/185 vs. 322/234 mL, 193/108 vs. 176/ 92 mL and 422/201 vs. 481/329mL, respectively (P<0.001 between ventilators at each step for each volume). Pendelluft air volume ranged between 0.7 to 37.8 ml and negatively correlated with expiratory resistance in steps 2 and 3. The lower-level ventilator performed closely to the ICU ventilator. In the clinical setting, these findings suggest that, due to dependence of VT to C, pressure control should be preferred to maintain adequate VT at least in one patient when C and/or R changes abruptly and monitoring of VT should be done carefully. Increasing expiratory resistance should reduce pendelluft volume.
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Project description:OBJECTIVES:Physiologic dead space is associated with mortality in acute respiratory distress syndrome, but its measurement is cumbersome. Alveolar dead space fraction relies on the difference between arterial and end-tidal carbon dioxide (alveolar dead space fraction = (PaCO2 - PetCO2) / PaCO2). We aimed to assess the relationship between alveolar dead space fraction and mortality in a cohort of children meeting criteria for acute respiratory distress syndrome (both the Berlin 2012 and the American-European Consensus Conference 1994 acute lung injury) and pediatric acute respiratory distress syndrome (as defined by the Pediatric Acute Lung Injury Consensus Conference in 2015). DESIGN:Secondary analysis of a prospective, observational cohort. SETTING:Tertiary care, university affiliated PICU. PATIENTS:Invasively ventilated children with pediatric acute respiratory distress syndrome. INTERVENTIONS:None. MEASUREMENTS AND MAIN RESULTS:Of the 283 children with pediatric acute respiratory distress syndrome, 266 had available PetCO2. Alveolar dead space fraction was lower in survivors (median 0.13; interquartile range, 0.06-0.23) than nonsurvivors (0.31; 0.19-0.42; p < 0.001) at pediatric acute respiratory distress syndrome onset, but not 24 hours after (survivors 0.12 [0.06-0.18], nonsurvivors 0.14 [0.06-0.25], p = 0.430). Alveolar dead space fraction at pediatric acute respiratory distress syndrome onset discriminated mortality with an area under receiver operating characteristic curve of 0.76 (95% CI, 0.66-0.85; p < 0.001), better than either initial oxygenation index or PaO2/FIO2. In multivariate analysis, alveolar dead space fraction at pediatric acute respiratory distress syndrome onset was independently associated with mortality, after adjustment for severity of illness, immunocompromised status, and organ failures. CONCLUSIONS:Alveolar dead space fraction at pediatric acute respiratory distress syndrome onset discriminates mortality and is independently associated with nonsurvival. Alveolar dead space fraction represents a single, useful, readily obtained clinical biomarker reflective of pulmonary and nonpulmonary variables associated with mortality.
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Project description: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 ([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.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.
| S-EPMC7093634 | biostudies-literature
Project description:Primary hypothesisWe hypothesized that higher alveolar dead space fraction (AVDSf) at pediatric acute respiratory distress syndrome (PARDS) onset would be associated with right ventricular (RV) systolic dysfunction within the first 24 h of PARDS.Study design and methodsWe performed a retrospective single-center cohort study of PARDS patients with clinically obtained echocardiograms within 24 h. Primary exposure was AVDSf at PARDS onset. Primary outcome was RV systolic dysfunction as defined by RV global longitudinal strain (GLS) (>-18%). Secondary outcomes included pulmonary hypertension (PH) and RV systolic dysfunction as defined by other echocardiogram parameters, and measures of oxygenation. Unadjusted and adjusted logistic and linear regression were used to investigate AVDSf associations with outcomes.ResultsNinety-one patients were included: median age 6.2 years, 46% female, and 65% with moderate or severe PARDS. Median AVDSf was 0.2 (interquartile range [IQR] 0.0-0.3), 33% had RV dysfunction, and 21% had PH. Unadjusted and adjusted logistic regression showed no association between AVDSf and RV systolic dysfunction or PH by any echocardiographic measure, but unadjusted and adjusted linear regression did show an association between AVDSf and PaO2 /FiO2 .ConclusionAVDSf at PARDS onset was not associated with RV systolic dysfunction or PH within 24 h but was associated with PaO2 /FiO2 ratio and may be more reflective of pulmonary causes of ventilation-perfusion mismatch. Future investigations should focus on clarifying the clinical utility of AVDSf in relation to existing metrics throughout the course of PARDS.
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Project description:BackgroundObtaining a properly fitting non-invasive ventilation (NIV) mask to treat acute respiratory failure is a major challenge, especially in young children and patients with craniofacial abnormalities. Personalization of NIV masks holds promise to improve pediatric NIV efficiency. As current customization methods are relatively time consuming, this study aimed to test the air leak and surface pressure performance of personalized oronasal face masks using 3D printed soft materials. Personalized masks of three different biocompatible materials (silicone and photopolymer resin) were developed and tested on three head models of young children with abnormal facial features during preclinical bench simulation of pediatric NIV. Air leak percentages and facial surface pressures were measured and compared for each mask.ResultsPersonalized NIV masks could be successfully produced in under 12 h in a semi-automated 3D production process. During NIV simulation, overall air leak performance and applied surface pressures were acceptable, with leak percentages under 30% and average surface pressure values mostly remaining under normal capillary pressure. There was a small advantage of the masks produced with soft photopolymer resin material.ConclusionThis first, proof-of-concept bench study simulating NIV in children with abnormal facial features, showed that it is possible to obtain biocompatible, personalized oronasal masks with acceptable air leak and facial surface pressure performance using a relatively short, and semi-automated production process. Further research into the clinical value and possibilities for application of personalized NIV masks in critically ill children is needed.
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Project description:BackgroundPulmonary alveolar proteinosis (PAP) is a rare disease characterized by progressive accumulation of the alveolar surfactant. Whole lung lavage (WLL) using a high volume of warmed saline remains the standard therapy. However, no established bedside monitoring tool can evaluate the physiological effect of WLL in the perioperative period. Indirect calorimetry, which is generally used to measure resting energy expenditure, can detect carbon dioxide (CO2) production and mixed-expired partial pressure of CO2 breath by breath. In this physiological study, we calculated CO2 elimination per breath (VTCO2,br) and Enghoff's dead space using indirect calorimetry and measured the extravascular lung water index to reveal the effect of WLL.Case presentationWe measured VTCO2,br, Enghoff's dead space, and the extravascular lung water and cardiac indices before and after WLL to assess the reduction in shunt by washing out the surfactant. A total of four WLLs were performed in two PAP patients. The first case involved an Asian 62-year-old man who presented with a 3-month history of dyspnea on exertion. The second case involved an Asian 48-year-old woman with no symptoms. VTCO2,br increased, and the Enghoff's dead space decreased at 12 h following WLL. An increase in the extravascular lung water was detected immediately following WLL, leading to a transient increase in Enghoff's dead space.ConclusionWLL can increase efficient alveolar ventilation by washing out the accumulated surfactant. However, the lavage fluid may be absorbed into the lung tissues immediately after WLL and result in an increase in the extravascular lung water.
| S-EPMC10439532 | biostudies-literature
Project description:This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency medicine 2016. Other selected articles can be found online at http://www.biomedcentral.com/collections/annualupdate2016. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901.
| S-EPMC4791785 | biostudies-literature
Project description:BackgroundWe previously reported that there were no differences between the lung-protective actions of pressure-controlled inverse ratio ventilation and volume control ventilation based on the changes in serum cytokine levels. Dead space represents a ventilation-perfusion mismatch, and can enable us to understand the heterogeneity and elapsed time changes in ventilation-perfusion mismatch.MethodsThis study was a secondary analysis of a randomized controlled trial of patients who underwent robot-assisted laparoscopic radical prostatectomy. The inspiratory to expiratory ratio was adjusted individually by observing the expiratory flow-time wave in the pressure-controlled inverse ratio ventilation group (n = 14) and was set to 1:2 in the volume-control ventilation group (n = 13). Using volumetric capnography, the physiological dead space was divided into three dead space components: airway, alveolar, and shunt dead space. The influence of pressure-controlled inverse ratio ventilation and time factor on the changes in each dead space component rate was analyzed using the Mann-Whitney U test and Wilcoxon's signed rank test.ResultsThe physiological dead space and shunt dead space rate were decreased in the pressure-controlled inverse ratio ventilation group compared with those in the volume control ventilation group (p < 0.001 and p = 0.003, respectively), and both dead space rates increased with time in both groups. The airway dead space rate increased with time, but the difference between the groups was not significant. There were no significant changes in the alveolar dead space rate.ConclusionsPressure-controlled inverse ratio ventilation reduced the physiological dead space rate, suggesting an improvement in the total ventilation/perfusion mismatch due to improved inflation of the alveoli affected by heterogeneous expansion disorder without hyperinflation of the normal alveoli. However, the shunt dead space rate increased with time, suggesting that atelectasis developed with time in both groups.
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Project description:Patients with congenital heart disease (CHD) that have surgical repair with cardiopulmonary bypass (CPB) reflect a unique population with multiple pulmonary and systemic factors that may contribute to increased alveolar dead space and low cardiac output syndrome. This study aimed to assess and compare changes in the alveolar dead space fraction (AVDSf) in the immediate postoperative period with outcomes in children with CHD who underwent repair on CPB. A single-center retrospective review study of critically ill children with CHD, younger than 18 years of age admitted to the Pediatric Intensive Care Unit (PICU) after undergoing surgical repair on CPB and received invasive mechanical ventilation for at least 24 h. One hundred and two patients were included in the study. Over the first 24 h, mean AVDSf was significantly higher in patients who had longer hospital length of stay (LOS) (> 21 days) p = 0.02, and longer duration of invasive mechanical ventilation (DMV) (> 170 h) p = 0.01. Cross-sectional analyses at 23-24 h revealed that AVDSf > 0.25 predicts mortality and DMV (p = 0.03 and P = 0.02 respectively); however, it did not predict prolonged hospital LOS. For every 0.1 increase in the AVDSf, the odds of mortality, DMV, and hospital LOS increased by 4.9 [95% CI = 1.45-16.60, p = 0.002], 2.06 [95% CI = 1.14-3.71, p = 0.01], and 1.43[95% CI = 0.84-2.45, p = 0.184], respectively. The area under the ROC curve at 23-24 h for AVDSf was 0.868 to predict mortality as an outcome. AVDSf > 0.25 at 23-24 h postoperatively was an independent predictor of mortality with sensitivity and specificity of 83% and 80%, respectively and was superior to other commonly used surrogates of cardiac output. In the immediate postoperative period of pediatric patients with CHD, high AVDSf is associated with longer hospital length of stay and duration of invasive mechanical ventilation. Increased AVDSf values at 23-24 h postoperatively is associated with mortality in patients with CHD exposed to CPB.
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