Single-FiO2 lung modelling with machine learning: a computer simulation incorporating volumetric capnography.

We investigated whether machine learning (ML) analysis of ICU monitoring data incorporating volumetric capnography measurements of mean alveolar PCO2 can partition venous admixture (VenAd) into its shunt and low V/Q components without manipulating the inspired oxygen fraction (FiO2). From a 21-compartment ventilation / perfusion (V/Q) model of pulmonary blood flow we generated blood gas and mean alveolar PCO2 data in simulated scenarios with shunt values from 7.3% to 36.5% and a range of FiO2 settings, indirect calorimetry and cardiac output measurements and acid- base and hemoglobin oxygen affinity conditions. A 'deep learning' ML application, trained and validated solely on single FiO2 bedside monitoring data from 14,736 scenarios, then recovered shunt values in 500 test scenarios with true shunt values 'held back'. ML shunt estimates versus true values (n = 500) produced a linear regression model with slope = 0.987, intercept = -0.001 and R2 = 0.999. Kernel density estimate and error plots confirmed close agreement. With corresponding VenAd values calculated from the same bedside data, low V/Q flow can be reported as VenAd-shunt. ML analysis of blood gas, indirect calorimetry, volumetric capnography and cardiac output measurements can quantify pulmonary oxygenation deficits as percentage shunt flow (V/Q = 0) versus percentage low V/Q flow (V/Q > 0). High fidelity reports are possible from analysis of data collected solely at the operating FiO2.

Pulmonary gas exchange evaluated by machine learning: a computer simulation.

Using computer simulation we investigated whether machine learning (ML) analysis of selected ICU monitoring data can quantify pulmonary gas exchange in multi-compartment format. A 21 compartment ventilation/perfusion (V/Q) model of pulmonary blood flow processed 34,551 combinations of cardiac output, hemoglobin concentration, standard P50, base excess, VO2 and VCO2 plus three model-defining parameters: shunt, log SD and mean V/Q. From these inputs the model produced paired arterial blood gases, first with the inspired O2 fraction (FiO2) adjusted to arterial saturation (SaO2) = 0.90, and second with FiO2 increased by 0.1. 'Stacked regressor' ML ensembles were trained/validated on 90% of this dataset. The remainder with shunt, log SD, and mean 'held back' formed the test-set. 'Two-Point' ML estimates of shunt, log SD and mean utilized data from both FiO2 settings. 'Single-Point' estimates used only data from SaO2 = 0.90. From 3454 test gas exchange scenarios, two-point shunt, log SD and mean estimates produced linear regression models versus true values with slopes ~ 1.00, intercepts ~ 0.00 and R2 ~ 1.00. Kernel density and Bland-Altman plots confirmed close agreement. Single-point estimates were less accurate: R2 = 0.77-0.89, slope = 0.991-0.993, intercept = 0.009-0.334. ML applications using blood gas, indirect calorimetry, and cardiac output data can quantify pulmonary gas exchange in terms describing a 20 compartment V/Q model of pulmonary blood flow. High fidelity reports require data from two FiO2 settings.

Intrapulmonary shunting is a key contributor to hypoxia in COVID-19: An update on the pathophysiology.

BACKGROUND: The pathophysiology of COVID-19 remains poorly understood. We aimed to estimate the contribution of intrapulmonary shunting and ventilation-to-perfusion (VA/Q) mismatch using a mathematical model to construct oxygen-haemoglobin dissociation curves (ODCs). METHODS: ODCs were constructed using transcutaneous pulse oximetry at two different fractions of inspired oxygen (FiO2). 199 patients were included from two large district general hospitals in the South East of England from 1st to 14th January 2021. The study was supported by the National Institute of Health Research (NIHR) Clinical Research Network. RESULTS: Overall mortality was 29%. Mean age was 68.2 years (SEM 1·2) with 46% female. Median shunt on admission was 17% (IQR 8-24.5); VA/Q was 0.61 (IQR 0.52-0.73). Shunt was 37.5% higher in deaths (median 22%, IQR 9-29) compared to survivors (16%, 8-21; p = 0.0088) and was a predictor of mortality (OR 1.04; 95% CI 1.01-1.07). Admission oxygen saturations were more strongly predictive of mortality (OR 0.91, 95% CI 0.87-0.96). There was no difference in VA/Q mismatch between deaths (0.60; IQR 0.50-0.73) and survivors (0.61; IQR 0.52-0.73; p = 0.63) and it was not predictive of mortality (OR 0.68; 95% CI 0.18-2.52; p = 0.55). Shunt negatively correlated with admission oxygen saturation (R -0.533; p<0.0001) whereas VA/Q was not (R 0.1137; p = 0.12). INTERPRETATION: Shunt, not VA/Q mismatch, was associated with worsening hypoxia, though calculating shunt was not of prognostic value. This study adds to our understanding of the pathophysiology of hypoxaemia in COVID-19. Our inexpensive and reliable technique may provide further insights into the pathophysiology of hypoxia in other respiratory diseases.

Identifying putative ventilation-perfusion distributions in COVID-19 pneumonia.

Busana et al. (doi.org/10.1152/japplphysiol.00871.2020) published 5 patients with COVID-19 in whom the fraction of non-aerated lung tissue had been quantified by computed tomography. They assumed that shunt flow fraction was proportional to the non-aerated lung fraction, and, by randomly generating 106 different bimodal distributions for the ventilation-perfusion ([Formula: see text]) ratios in the lung, specified as sets of paired values {[Formula: see text]}, sought to identify as solutions those that generated the observed arterial partial pressures of CO2 and O2 (PaCO2 and PaO2). Our study sought to develop a direct method of calculation to replace the approach of randomly generating different distributions, and so provide more accurate solutions that were within the measurement error of the blood-gas data. For the one patient in whom Busana et al. did not find solutions, we demonstrated that the assumed shunt flow fraction led to a non-shunt blood flow that was too low to support the required gas exchange. For the other four patients, we found precise solutions (prediction error < 1x10-3 mmHg for both PaCO2 and PaO2), with distributions qualitatively similar to those of Busana et al. These distributions were extremely wide and unlikely to be physically realisable, because they predict the maintenance of very large concentration gradients in regions of the lung where convection is slow. We consider that these wide distributions arise because the assumed value for shunt flow is too low in these patients, and we discuss possible reasons why the assumption relating to shunt flow fraction may break down in COVID-19 pneumonia.

Fisiología respiratoria: relación ventilación/perfusión / Respiratory fisiology: ventilation/perfusion relationship

Las alteraciones de la relación entre la ventilación y el flujo sanguíneo (V/Q) en diversas regiones del pulmón alteran el aporte de oxígeno (O2) y remoción del dióxido de carbono (CO2) al organismo. Fisiológicamente existen diferencias regionales en la relación V/Q. Determinadas patologías pueden alterar esta relación, produciendo tres escenarios distintos: Cortocircuito (Shunt), Alteración V/Q y aumento del espacio muerto. Para evaluar estos escenarios y realizar una aproximación diagnostica son de utilidad el estudio de los gases arteriales y venosos, la diferencia alveolo arterial y la respuesta al suministrar O2

Alterations in the ventilation perfusion relationship (V/Q) in various lung regions alter the supply of oxygen (O2) and the removal of carbon dioxide (CO2) in the body. Physiologically, there are regional differences in the V/Q ratio. Certain pathologies can alter this relationship, producing three different scenarios: Shunt, V/Q mismach and dead space increased. To evaluate these scenarios and carry out a diagnostic approach, it is useful to study arterial and venous gasometry, the alveolar arterial difference and the response to oxygen supplying.

Effect of Global Ventilation to Perfusion Ratio, for Normal Lungs, on Desflurane and Sevoflurane Elimination Kinetics.

BACKGROUND: Kinetics of the uptake of inhaled anesthetics have been well studied, but the kinetics of elimination might be of more practical importance. The objective of the authors' study was to assess the effect of the overall ventilation/perfusion ratio (VA/Q), for normal lungs, on elimination kinetics of desflurane and sevoflurane. METHODS: The authors developed a mathematical model of inhaled anesthetic elimination that explicitly relates the terminal washout time constant to the global lung VA/Q ratio. Assumptions and results of the model were tested with experimental data from a recent study, where desflurane and sevoflurane elimination were observed for three different VA/Q conditions: normal, low, and high. RESULTS: The mathematical model predicts that the global VA/Q ratio, for normal lungs, modifies the time constant for tissue anesthetic washout throughout the entire elimination. For all three VA/Q conditions, the ratio of arterial to mixed venous anesthetic partial pressure Part/Pmv reached a constant value after 5 min of elimination, as predicted by the retention equation. The time constant corrected for incomplete lung clearance was a better predictor of late-stage kinetics than the intrinsic tissue time constant. CONCLUSIONS: In addition to the well-known role of the lungs in the early phases of inhaled anesthetic washout, the lungs play a long-overlooked role in modulating the kinetics of tissue washout during the later stages of inhaled anesthetic elimination. The VA/Q ratio influences the kinetics of desflurane and sevoflurane elimination throughout the entire elimination, with more pronounced slowing of tissue washout at lower VA/Q ratios.

Arterial and Mixed Venous Kinetics of Desflurane and Sevoflurane, Administered Simultaneously, at Three Different Global Ventilation to Perfusion Ratios in Piglets with Normal Lungs.

BACKGROUND: Previous studies have established the role of various tissue compartments in the kinetics of inhaled anesthetic uptake and elimination. The role of normal lungs in inhaled anesthetic kinetics is less understood. In juvenile pigs with normal lungs, the authors measured desflurane and sevoflurane washin and washout kinetics at three different ratios of alveolar minute ventilation to cardiac output value. The main hypothesis was that the ventilation/perfusion ratio (VA/Q) of normal lungs influences the kinetics of inhaled anesthetics. METHODS: Seven healthy pigs were anesthetized with intravenous anesthetics and mechanically ventilated. Each animal was studied under three different VA/Q conditions: normal, low, and high. For each VA/Q condition, desflurane and sevoflurane were administered at a constant, subanesthetic inspired partial pressure (0.15 volume% for sevoflurane and 0.5 volume% for desflurane) for 45 min. Pulmonary arterial and systemic arterial blood samples were collected at eight time points during uptake, and then at these same times during elimination, for measurement of desflurane and sevoflurane partial pressures. The authors also assessed the effect of VA/Q on paired differences in arterial and mixed venous partial pressures. RESULTS: For desflurane washin, the scaled arterial partial pressure differences between 5 and 0 min were 0.70 ± 0.10, 0.93 ± 0.08, and 0.82 ± 0.07 for the low, normal, and high VA/Q conditions (means, 95% CI). Equivalent measurements for sevoflurane were 0.55 ± 0.06, 0.77 ± 0.04, and 0.75 ± 0.08. For desflurane washout, the scaled arterial partial pressure differences between 0 and 5 min were 0.76 ± 0.04, 0.88 ± 0.02, and 0.92 ± 0.01 for the low, normal, and high VA/Q conditions. Equivalent measurements for sevoflurane were 0.79 ± 0.05, 0.85 ± 0.03, and 0.90 ± 0.03. CONCLUSIONS: Kinetics of inhaled anesthetic washin and washout are substantially altered by changes in the global VA/Q ratio for normal lungs.

The evolution of the ventilatory ratio is a prognostic factor in mechanically ventilated COVID-19 ARDS patients.

BACKGROUND: Mortality due to COVID-19 is high, especially in patients requiring mechanical ventilation. The purpose of the study is to investigate associations between mortality and variables measured during the first three days of mechanical ventilation in patients with COVID-19 intubated at ICU admission. METHODS: Multicenter, observational, cohort study includes consecutive patients with COVID-19 admitted to 44 Spanish ICUs between February 25 and July 31, 2020, who required intubation at ICU admission and mechanical ventilation for more than three days. We collected demographic and clinical data prior to admission; information about clinical evolution at days 1 and 3 of mechanical ventilation; and outcomes. RESULTS: Of the 2,095 patients with COVID-19 admitted to the ICU, 1,118 (53.3%) were intubated at day 1 and remained under mechanical ventilation at day three. From days 1 to 3, PaO2/FiO2 increased from 115.6 [80.0-171.2] to 180.0 [135.4-227.9] mmHg and the ventilatory ratio from 1.73 [1.33-2.25] to 1.96 [1.61-2.40]. In-hospital mortality was 38.7%. A higher increase between ICU admission and day 3 in the ventilatory ratio (OR 1.04 [CI 1.01-1.07], p = 0.030) and creatinine levels (OR 1.05 [CI 1.01-1.09], p = 0.005) and a lower increase in platelet counts (OR 0.96 [CI 0.93-1.00], p = 0.037) were independently associated with a higher risk of death. No association between mortality and the PaO2/FiO2 variation was observed (OR 0.99 [CI 0.95 to 1.02], p = 0.47). CONCLUSIONS: Higher ventilatory ratio and its increase at day 3 is associated with mortality in patients with COVID-19 receiving mechanical ventilation at ICU admission. No association was found in the PaO2/FiO2 variation.

Hypoxic pulmonary vasoconstriction as a regulator of alveolar-capillary oxygen flux: A computational model of ventilation-perfusion matching.

The relationship between regional variabilities in airflow (ventilation) and blood flow (perfusion) is a critical determinant of gas exchange efficiency in the lungs. Hypoxic pulmonary vasoconstriction is understood to be the primary active regulator of ventilation-perfusion matching, where upstream arterioles constrict to direct blood flow away from areas that have low oxygen supply. However, it is not understood how the integrated action of hypoxic pulmonary vasoconstriction affects oxygen transport at the system level. In this study we develop, and make functional predictions with a multi-scale multi-physics model of ventilation-perfusion matching governed by the mechanism of hypoxic pulmonary vasoconstriction. Our model consists of (a) morphometrically realistic 2D pulmonary vascular networks to the level of large arterioles and venules; (b) a tileable lumped-parameter model of vascular fluid and wall mechanics that accounts for the influence of alveolar pressure; (c) oxygen transport accounting for oxygen bound to hemoglobin and dissolved in plasma; and (d) a novel empirical model of hypoxic pulmonary vasoconstriction. Our model simulations predict that under the artificial test condition of a uniform ventilation distribution (1) hypoxic pulmonary vasoconstriction matches perfusion to ventilation; (2) hypoxic pulmonary vasoconstriction homogenizes regional alveolar-capillary oxygen flux; and (3) hypoxic pulmonary vasoconstriction increases whole-lobe oxygen uptake by improving ventilation-perfusion matching.

The impact of ventilation-perfusion inequality in COVID-19: a computational model.

COVID-19 infection may lead to acute respiratory distress syndrome (CARDS) where severe gas exchange derangements may be associated, at least in the early stages, only with minor pulmonary infiltrates. This may suggest that the shunt associated to the gasless lung parenchyma is not sufficient to explain CARDS hypoxemia. We designed an algorithm (VentriQlar), based on the same conceptual grounds described by J.B. West in 1969. We set 498 ventilation-perfusion (VA/Q) compartments and, after calculating their blood composition (PO2, PCO2, and pH), we randomly chose 106 combinations of five parameters controlling a bimodal distribution of blood flow. The solutions were accepted if the predicted PaO2 and PaCO2 were within 10% of the patient's values. We assumed that the shunt fraction equaled the fraction of non-aerated lung tissue at the CT quantitative analysis. Five critically-ill patients later deceased were studied. The PaO2/FiO2 was 91.1 ± 18.6 mmHg and PaCO2 69.0 ± 16.1 mmHg. Cardiac output was 9.58 ± 0.99 L/min. The fraction of non-aerated tissue was 0.33 ± 0.06. The model showed that a large fraction of the blood flow was likely distributed in regions with very low VA/Q (Qmean = 0.06 ± 0.02) and a smaller fraction in regions with moderately high VA/Q. Overall LogSD, Q was 1.66 ± 0.14, suggestive of high VA/Q inequality. Our data suggest that shunt alone cannot completely account for the observed hypoxemia and a significant VA/Q inequality must be present in COVID-19. The high cardiac output and the extensive microthrombosis later found in the autopsy further support the hypothesis of a pathological perfusion of non/poorly ventilated lung tissue.NEW & NOTEWORTHY Hypothesizing that the non-aerated lung fraction as evaluated by the quantitative analysis of the lung computed tomography (CT) equals shunt (VA/Q = 0), we used a computational approach to estimate the magnitude of the ventilation-perfusion inequality in severe COVID-19. The results show that a severe hyperperfusion of poorly ventilated lung region is likely the cause of the observed hypoxemia. The extensive microthrombosis or abnormal vasodilation of the pulmonary circulation may represent the pathophysiological mechanism of such VA/Q distribution.

Analysis of different image-registration algorithms for Fourier decomposition MRI in functional lung imaging.

BACKGROUND: Motion correction is mandatory for the functional Fourier decomposition magnetic resonance imaging (FD-MRI) of the lungs. Therefore, it is important to evaluate the quality of various image-registration algorithms for pulmonary FD-MRI and to determine their impact on FD-MRI outcome. PURPOSE: To evaluate different image-registration algorithms for FD-MRI in functional lung imaging. MATERIAL AND METHODS: Fifteen healthy volunteers were examined in a 1.5-T whole-body MR scanner (Magnetom Avanto, Siemens AG) with a non-contrast enhanced 2D TrueFISP pulse sequence in coronal view and free-breathing (acquisition time 45 s, 250 images). Three image-registration algorithms were used to compensate the spatial variation of the lungs (fMRLung 3.0, ANTs, and Elastix). Quality control for image registration was performed by edge detection (ED), quotient image criterion (QI), and dice similarity coefficient (DSC). Ventilation, perfusion, and a ventilation/perfusion quotient (V/Q) were calculated using the three registered datasets. RESULTS: Average computing times for the three image-registration algorithms were 1.0 ± 1.6 min, 38.0 ± 13.5 min, and 354 ± 78 min for fMRLung, ANTs, and Elastix, respectively. No significant difference in the quality of motion correction provided by different image-registration algorithms occurred. Significant differences were observed between fMRLung- and Elastix-based perfusion values ​​of the left lung as well as fMRLung- and ANTs-based V/Q quotient of the right and the entire lung (P < 0.05). Other ventilation and perfusion values were not significantly different. CONCLUSION: The mandatory motion correction for functional FD-MRI of the lung can be achieved through different image-registration algorithms with consistent quality. However, a significantly difference in computing time between the image-registration algorithms still requires an optimization.

Semi-automated Analysis of Ventilation-Perfusion Single-Photon Emission Tomography in the Diagnosis of Pulmonary Embolism - Does it add extra value?

AIM: Diagnosis of pulmonary embolism using V/P-SPECT may include the application of advanced image-processing techniques to identify V/P-mismatches. Aim of this study was to evaluate the benefit in clinical decision making in the diagnosis of pulmonary embolism.by whether adding to conventional reading a software that automatically calculates and visualizes the ventilation/perfusion-quotient pixel by pixel. METHODS: 63 consecutive patients with a clinical suspicion of PE who underwent V/P-SPECT were included in this retrospective study. Images were randomly ordered both for standard as well as for software-assisted reading using V/P-quotients. Studies were read independently by 2 experienced and 2 inexperienced raters. Diagnostic performance and observer agreement of all readers and both reading methods were determined. RESULTS: Expert observers consistently achieved a high diagnostic accuracy both in conventional as well as in software-assisted reporting (sensitivity: 0.94 vs. 0.94, specificity: 0.96 vs. 0.97, LR+: 17.32 vs. 28.86, LR- stayed constant at 0.06). For inexperienced readers, diagnostic performance improved: sensitivity raised from 0.74 to 0.85 and specificity from 0.86 to 0.95, LR+ raised from 5.20 to 15.69, LR- decreased from 0.31 to 0.16. Inter-rater reliability (Fleiss' κ) improved from 0.63 to 0.86 by using V/P quotient. CONCLUSION: Benefit from a software-tool that calculates V/P-ratio automatically is only small when used by experienced physicians If inexperienced readers use the software, the diagnostic accuracy increases. Images generated by automated calculation of V/P-mismatches are easy to read and their use might help to standardize and objectify interpretation of V/P-SPECT in the diagnosis of PE.

Modeling lung perfusion abnormalities to explain early COVID-19 hypoxemia.

Early stages of the novel coronavirus disease (COVID-19) are associated with silent hypoxia and poor oxygenation despite relatively minor parenchymal involvement. Although speculated that such paradoxical findings may be explained by impaired hypoxic pulmonary vasoconstriction in infected lung regions, no studies have determined whether such extreme degrees of perfusion redistribution are physiologically plausible, and increasing attention is directed towards thrombotic microembolism as the underlying cause of hypoxemia. Herein, a mathematical model demonstrates that the large amount of pulmonary venous admixture observed in patients with early COVID-19 can be reasonably explained by a combination of pulmonary embolism, ventilation-perfusion mismatching in the noninjured lung, and normal perfusion of the relatively small fraction of injured lung. Although underlying perfusion heterogeneity exacerbates existing shunt and ventilation-perfusion mismatch in the model, the reported hypoxemia severity in early COVID-19 patients is not replicated without either extensive perfusion defects, severe ventilation-perfusion mismatch, or hyperperfusion of nonoxygenated regions.

Changes in shunt, ventilation/perfusion mismatch, and lung aeration with PEEP in patients with ARDS: a prospective single-arm interventional study.

BACKGROUND: Several studies have found only a weak to moderate correlation between oxygenation and lung aeration in response to changes in PEEP. This study aimed to investigate the association between changes in shunt, low and high ventilation/perfusion (V/Q) mismatch, and computed tomography-measured lung aeration following an increase in PEEP in patients with ARDS. METHODS: In this preliminary study, 12 ARDS patients were subjected to recruitment maneuvers followed by setting PEEP at 5 and then either 15 or 20 cmH2O. Lung aeration was measured by computed tomography. Values of pulmonary shunt and low and high V/Q mismatch were calculated by a model-based method from measurements of oxygenation, ventilation, and metabolism taken at different inspired oxygen levels and an arterial blood gas sample. RESULTS: Increasing PEEP resulted in reduced values of pulmonary shunt and the percentage of non-aerated tissue, and an increased percentage of normally aerated tissue (p < 0.05). Changes in shunt and normally aerated tissue were significantly correlated (r = - 0.665, p = 0.018). Three distinct responses to increase in PEEP were observed in values of shunt and V/Q mismatch: a beneficial response in seven patients, where shunt decreased without increasing high V/Q; a detrimental response in four patients where both shunt and high V/Q increased; and a detrimental response in a patient with reduced shunt but increased high V/Q mismatch. Non-aerated tissue decreased with increased PEEP in all patients, and hyperinflated tissue increased only in patients with a detrimental response in shunt and V/Q mismatch. CONCLUSIONS: The results show that improved lung aeration following an increase in PEEP is not always consistent with reduced shunt and V/Q mismatch. Poorly matched redistribution of ventilation and perfusion, between dependent and non-dependent regions of the lung, may explain why patients showed detrimental changes in shunt and V/Q mismatch on increase in PEEP, despite improved aeration. TRIAL REGISTRATION: ClinicalTrails.gov, NCT04067154. Retrospectively registered on August 26, 2019.

Intra-pulmonary arteriovenous anastomoses and pulmonary gas exchange: evaluation by microspheres, contrast echocardiography and inert gas elimination.

KEY POINTS: Imaging techniques such as contrast echocardiography suggest that anatomical intra-pulmonary arteriovenous anastomoses (IPAVAs) are present at rest and are recruited to a greater extent in conditions such as exercise. IPAVAs have the potential to act as a shunt, although gas exchange methods have not demonstrated significant shunt in the normal lung. To evaluate this discrepancy, we compared anatomical shunt with 25-µm microspheres to contrast echocardiography, and gas exchange shunt measured by the multiple inert gas elimination technique (MIGET). Intra-pulmonary shunt measured by 25-µm microspheres was not significantly different from gas exchange shunt determined by MIGET, suggesting that MIGET does not underestimate the gas exchange consequences of anatomical shunt. A positive agitated saline contrast echocardiography score was associated with anatomical shunt measured by microspheres. Agitated saline contrast echocardiography had high sensitivity but low specificity to detect a ≥1% anatomical shunt, frequently detecting small shunts inconsequential for gas exchange. ABSTRACT: The echocardiographic visualization of transpulmonary agitated saline microbubbles suggests that anatomical intra-pulmonary arteriovenous anastomoses are recruited during exercise, in hypoxia, and when cardiac output is increased pharmacologically. However, the multiple inert gas elimination technique (MIGET) shows insignificant right-to-left gas exchange shunt in normal humans and canines. To evaluate this discrepancy, we measured anatomical shunt with 25-µm microspheres and compared the results to contrast echocardiography and MIGET-determined gas exchange shunt in nine anaesthetized, ventilated canines. Data were acquired under the following conditions: (1) at baseline, (2) 2 µg kg-1  min-1 i.v. dopamine, (3) 10 µg kg-1  min-1 i.v. dobutamine, and (4) following creation of an intra-atrial shunt (in four animals). Right to left anatomical shunt was quantified by the number of 25-µm microspheres recovered in systemic arterial blood. Ventilation-perfusion mismatch and gas exchange shunt were quantified by MIGET and cardiac output by direct Fick. Left ventricular contrast scores were assessed by agitated saline bubble counts, and separately by appearance of 25-µm microspheres. Across all conditions, anatomical shunt measured by 25-µm microspheres was not different from gas exchange shunt measured by MIGET (microspheres: 2.3 ± 7.4%; MIGET: 2.6 ± 6.1%, P = 0.64). Saline contrast bubble score was associated with microsphere shunt (ρ = 0.60, P < 0.001). Agitated saline contrast score had high sensitivity (100%) to detect a ≥1% shunt, but low specificity (22-48%). Gas exchange shunt by MIGET does not underestimate anatomical shunt measured using 25-µm microspheres. Contrast echocardiography is extremely sensitive, but not specific, often detecting small anatomical shunts which are inconsequential for gas exchange.

Heavy upright exercise increases ventilation-perfusion mismatch in the basal lung: indirect evidence for interstitial pulmonary edema.

Ventilation-perfusion (V̇a/Q̇) mismatch during exercise may result from interstitial pulmonary edema if increased pulmonary vascular pressure causes fluid efflux into the interstitium. If present, the increased fluid may compress small airways or blood vessels, disrupting V̇a/Q̇ matching, but this is unproven. We hypothesized that V̇a/Q̇ mismatch would be greatest in basal lung following heavy upright exercise, consistent with hydrostatic forces favoring edema accumulation in the gravitationally dependent lung. We applied new tools to reanalyze previously published magnetic resonance imaging data to determine regional V̇a/Q̇ mismatch following 45 min of heavy upright exercise in six athletes (V̇o2max = 61 ± 7 mL·kg-1·min-1). In the supine posture, regional alveolar ventilation and local perfusion were quantified from specific ventilation imaging, proton density, and arterial spin labeling data in a single sagittal slice of the right lung before exercise (PRE), 15 min after exercise (POST), and in recovery 60 min after exercise (REC). Indices of V̇a/Q̇ mismatch [second moments (log scale) of ventilation (LogSDV) and perfusion (LogSDQ) vs. V̇a/Q̇ distributions] were calculated for apical, middle, and basal lung thirds, which represent gravitationally nondependent, middle, and dependent regions, respectively, during upright exercise. LogSDV increased after exercise only in the basal lung (PRE 0.46 ± 0.06, POST 0.57 ± 0.14, REC 0.55 ±0.14, P = 0.01). Similarly, LogSDQ increased only in the basal lung (PRE 0.40 ± 0.06, POST 0.51 ± 0.10, REC 0.44 ± 0.09, P = 0.04). Increased V̇a/Q̇ mismatch in the basal lung after exercise is potentially consistent with interstitial pulmonary edema accumulating in gravitationally dependent lung during exercise.NEW & NOTEWORTHY We reanalyzed previously published MRI data with new tools and found increased ventilation-perfusion mismatch only in the basal lung of athletes following 45 min of cycling exercise. This is consistent with the development of interstitial edema in the gravitationally dependent lung during heavy exercise.

Índice de perfusión en una reanimación con riesgo biológico, como medida de mala tolerancia fisiológica / Perfusion index in a resuscitation with biological risk, as a measure of poor physiological tolerance

Introducción: Realizar de una forma adecuada una reanimación cardiopulmonar precisa unos conocimientos técnicos y unas mínimas condiciones físicas. Realizar esta reanimación un equipo de protección individual frente a riesgos biológicos nivel D colocado aumenta el sobresfuerzo al que se ven sometidos los reanimadores.El objetivo de este estudio es comprobar la existencia de un patrón de mala tolerancia fisiológica al uso de los equipos de protección nivel D, categoría 4-5-6B para la actuación en incidentes con riesgo biológico objetivado mediante la medición del índice de perfusión antes y después de una reanimación simulada.Material y métodos: Se ha realizado un estudio cuasiexperimental no controlado sobre 96 voluntarios elegidos mediante un muestreo aleatorio estratificado por sexo, nivel de formación y categoría profesional, estudiantes de Medicina y Enfermería y profesionales Médicos y Enfermeros. Se realizó una toma del índice de perfusión antes de realizar la reanimación y otra después de la reanimación simulada.Resultados: Un 15% de los voluntarios presentaron un índice de perfusión posterior más bajo al basal, lo que se traduce en una situación de vasoconstricción periférica después de la realización del ejercicio físico que supuso el caso clínico, cuando lo esperable era una vasodilatación para aumentar la perfusión.Conclusiones: Extrapolando estos datos, podemos concluir que, en la muestra de estudio que nos ocupa, los voluntarios que presentan menos índice de perfusión al finalizar que al comenzar no toleran bien el esfuerzo que supone el caso clínico

Introduction: Perform a cardiopulmonary resuscitation requires technical knowledge and minimal physical conditions. Perform this resuscitation a team of individual protection against biological risks level D placed increases the overexertion that encourage rescuers are subjected.The objective of this study is to prove the existence of a pattern of poor physiological tolerance to the use of personal protective equipment level D, category 4-5-6B for action in incidents with biological risk objectified by measuring the perfusion index before and after a simulated resuscitation.Material and methods: We have performed a quasiexperimental not controlled on 96 volunteers chosen through a random sampling, stratified by sex, level of education and professional category, medical and nursing students and professionals doctors and nurses.A decision of the perfusion index before performing the resuscitation and other simulated after resuscitation.Results: A 15% of the volunteers presented a perfusion index lower back to baseline, which translates into a situation of peripheral vasoconstriction after the completion of the physical exercise that involved the clinical case, when expected was a vasodilatation to Increase perfusion.Conclussion: Extrapolating these data, we can conclude that, in the sample for the study, the volunteers who have less perfusion index at the end of that at the beginning do not tolerate well the effort involved in the case

Effect of net gas volume changes on alveolar and arterial gas partial pressures in the presence of ventilation-perfusion mismatch.

The second gas effect (SGE) occurs when nitrous oxide enhances the uptake of volatile anesthetics administered simultaneously. Recent work shows that the SGE is greater in blood than in the gas phase, that this is due to ventilation-perfusion mismatch, that as mismatch increases, the SGE increases in blood but is diminished in the gas phase, and that these effects persist well into the period of nitrous oxide maintenance anesthesia. These modifications of the SGE are most pronounced with the low soluble agents in current use. We investigate further the effect of net gas volume loss during nitrous oxide uptake on low concentrations of other gases present using partial pressure-solubility diagrams. The steady-state equations of gas exchange were solved assuming a log-normal distribution of ventilation-perfusion ratios using Lebesgue-Stieltjes integration. It was shown that under these conditions the classical partial pressure-solubility diagram must be modified, that for currently used volatile anesthetic agents the alveolar-arterial partial pressure difference is less than that predicted in the past, and that the alveolar-arterial partial pressure difference may even be reversed during uptake in the case of highly insoluble gases such as sulfur hexafluoride. Comparing this with the situation described previously for nitrogen in steady-state air breathing, we show that for nitrogen, the direction of the alveolar-arterial gradient is opposite to the direction of net gas volume movement. Although gas uptake with ventilation-perfusion inequality exceeding that when matching is optimal is shown to be possible, it is less likely than alveolar-arterial partial pressure reversal. NEW & NOTEWORTHY Net uptake of gases administered with nitrous oxide may proceed against an alveolar-arterial partial pressure gradient. The alveolar-arterial gradient for nitrogen in the steady-state breathing air depends not only on the existence of a distribution of ventilation-perfusion ratios in the lung but also on the presence of a net change in gas volume and is opposite in direction to the direction of net gas volume uptake.

Revisiting atelectasis in lung units with low ventilation/perfusion ratios.

Patients on high inspired O2 concentrations are at risk of atelectasis, a problem that has been quantitatively assessed using analysis of ratio of ventilation to perfusion (V̇a/Q̇) equations. This approach ignores the potential of the elastic properties of the lung to support gas exchange through "apneic" oxygenation in units with no tidal ventilation, and is based on an error in the conservation of mass equations. To fill this gap, we correct the error and compare the pressure drops associated with apneic gas exchange with the pressure differences that can be supported by lung recoil. We analyze a worst case scenario: a small test unit in the Weibel model A tree structure with zero tidal ventilation, 100% inspired O2, the rest of the lung being normally ventilated tidally. We first computed the gas flux to the (unventilated) test unit and estimated the associated pressure drops. We then computed the difference in local gas pressure relative to the surrounding lung that would cause the unit to collapse. We compared these two, and finally computed the degree of airway narrowing that would effect change from the stable (apneic gas exchange) regime to the unstable regime leading to collapse. We find that except under extreme conditions of loss of airway caliber exceeding roughly 90%, lung recoil is sufficient to maintain oxygenation through convective transport alone. We further argue that the fundamental V̇a/Q̇ equations are invalid in these circumstances, and that the issue of atelectasis in low V̇a/Q̇ will require modifications to account for this additional mode of gas exchange. NEW & NOTEWORTHY Breathing high concentrations of oxygen increases the likelihood of atelectasis because of oxygen absorption, which is thought to be inevitable in regions with relatively low ventilation/perfusion ratios. However, airspaces of the lung resist collapse because of the forces of interdependence, and can, with low or even zero active tidal ventilation, draw in an inspiratory flow of oxygen sufficient to replace the oxygen consumed, thus preventing collapse of airspaces served by all but the most narrowed airways.

Defectos de perfusión en el mapa de iodo pulmonar: causas y semiología / Perfusion defects in pulmonary perfusion iodine maps: causes and semiology

Objetivo: Describir la utilidad de la tomografía computarizada con energía dual (TCED) en la obtención de mapas de perfusión pulmonar para aportar información morfológica y funcional en el tromboembolismo pulmonar (TEP). Revisar la semiología de los defectos de perfusión debidos a TEP y diferenciarlos de los defectos no debidos a TEP que son alteraciones que quedan fuera del rango utilizado en el mapa de iodo y están causados por otras enfermedades del parénquima pulmonar o por artefactos. Conclusión: La angiografía por TC de las arterias pulmonares es la técnica de elección en el diagnóstico de TEP. Las nuevas TC con energía dual son útiles para detectar defectos de perfusión secundarios a obstrucción completa o parcial de las arterias pulmonares, y tiene su mayor utilidad en la detección de TEP en ramas subsegmentarias

Objective: to describe the usefulness of dual-energy CT for obtaining pulmonary perfusion maps to provide morphological and functional information in patients with pulmonary embolisms. To review the semiology of perfusion defects due to pulmonary embolism so they can be differentiated from perfusion defects due to other causes: alterations outside the range used in the iodine map caused by other diseases of the lung parenchyma or artifacts. Conclusion: CT angiography of the pulmonary arteries is the technique of choice for the diagnosis of pulmonary embolisms. New dual-energy CT scanners are useful for detecting perfusion defects secondary to complete or partial obstruction of pulmonary arteries and is most useful for detecting pulmonary embolisms in subsegmental branches