Ventilation-perfusion Mismatch Research Articles

Doppler demonstration of ventilation-perfusion mismatching due to intrapulmonary shunting.

Doppler demonstration of ventilation-perfusion mismatching due to intrapulmonary shunting.

Changes in Ventilation–Perfusion Mismatch Associated With Inhaled Nitric Oxide in a Patient with Pneumonia That Met Criteria for Acute Respiratory Distress Syndrome

Changes in Ventilation–Perfusion Mismatch Associated With Inhaled Nitric Oxide in a Patient with Pneumonia That Met Criteria for Acute Respiratory Distress Syndrome

Abstract 12146: Acute Nitroglycerin Treatment Improves Exercise Hemodynamics, but Not Ventilation-Perfusion Matching in Patients With Heart Failure With Preserved Ejection Fraction

Introduction: Heart failure with preserved ejection fraction (HFpEF) patients exhibit a marked rise in PCWP during exercise, which may contribute to ventilation-perfusion (V/Q) mismatch and manifest as an increase in alveolar dead space (alveolar V D ) and alveolar-arterial PO 2 difference (AaPO 2 ). Nitrates reduce PCWP during exercise in HFpEF, but whether nitrates also reduce V/Q mismatch during exercise is unknown. Hypothesis: The increase in PCWP and V/Q mismatch during exercise would be attenuated with acute nitroglycerin (NTG) treatment compared with placebo in HFpEF patients. Methods: 13 patients performed a 6min cycling test at 20W and an incremental cycling test (with right-heart and arterial catheterization) with placebo and NTG treatment. The physiologic dead space to tidal volume (V D /V T ) was calculated using the Enghoff modification of the Bohr equation. Alveolar V D was calculated as: V D /V T x V T - anatomic dead space (anatomic V D , estimated as 2mL/kg lean body mass). AaPO 2 was calculated using the alveolar gas equation. Data were analyzed using a 2-way ANOVA. Results: PCWP decreased with NTG at 20W (placebo: 21.1±6.2 vs. NTG: 16.5±6.1mmHg, p=0.02) and peak exercise (placebo: 33.7±7.1 vs. NTG: 26.2±5.6mmHg, p<0.01). However, alveolar V D did not differ between treatments at rest (placebo: 0.11±0.07 vs. NTG:0.12±0.06L/breath, p=0.91), 20W (placebo: 0.22±0.09 vs. NTG: 0.24±0.10L/breath, p=0.62), or peak exercise (placebo: 0.34±0.14 vs. NTG:0.36±0.16L/breath, p=0.83). Nor did AaPO 2 differ between treatments at rest (placebo: 17.6±4.3 vs. NTG: 18.3±5.7mmHg, p=0.76), 20W (placebo: 22.0±6.9 vs. NTG: 22.1±8.1mmHg, p=0.99), or peak exercise (placebo: 25.1±9.1 vs. NTG: 27.8±9.9mmHg, p=0.41). No significant exercise-by-treatment interaction was detected for V D /V T (p=0.80). Conclusions: This study showed that NTG attenuated the increase in PCWP, but had no effect on the increase in alveolar V D or AaPO 2 during exercise. These findings suggest that the exercise-induced increase in V/Q mismatch may not be exclusively related to abnormal exercise hemodynamics. Further study is required to determine the clinical consequences and the mechanism(s) responsible for the progressive increase in V/Q mismatch during exercise in HFpEF patients.

Cyanosis in a Previously Well Child.

Cyanosis in a Previously Well Child.

Novel Pharmacomechanical Thrombolysis for Treating Intermediate-Risk Acute Pulmonary Embolism: The Bashir Endovascular Catheter.

Novel Pharmacomechanical Thrombolysis for Treating Intermediate-Risk Acute Pulmonary Embolism: The Bashir Endovascular Catheter.

Ideal alveolar gas defined by modal gas exchange in ventilation-perfusion distributions.

Under the three-compartment model of ventilation-perfusion ([Formula: see text]) scatter, Bohr-Enghoff calculation of alveolar deadspace fraction (VDA/VA) uses arterial CO2 partial pressure measurement as an approximation of "ideal" alveolar CO2 (ideal [Formula: see text]). However, this simplistic model suffers from several inconsistencies. Modeling of realistic physiological distributions of [Formula: see text] and [Formula: see text] instead suggests an alternative concept of "ideal" alveolar gas at the [Formula: see text] ratio where uptake or elimination rate of a gas is maximal. For alveolar-capillary partial pressure, this "modal" point equals the mean of expired alveolar and arterial partial pressures, regardless of [Formula: see text] scatter severity or overall [Formula: see text]. For example, modal ideal [Formula: see text] can be estimated from the following equation: [Formula: see text]Using a multicompartment computer model of log-normal distributions of [Formula: see text] and [Formula: see text], agreement of this estimate with the modal ideal [Formula: see text] located at the [Formula: see text] ratio of maximal compartmental [Formula: see text] was assessed across a wide range of severity of [Formula: see text] scatter and overall [Formula: see text] ratio. Agreement of VDA/VA for CO2 from the Bohr equation using modal ideal PCO2, with that using the estimated value was also assessed. Estimated modal ideal [Formula: see text] agreed closely with modal ideal [Formula: see text], intraclass correlation (ICC) > 99.9%. There was no significant difference between VDA/VA using either value for ideal [Formula: see text]. Modal ideal [Formula: see text] reflects a physiologically realistic concept of ideal alveolar gas where there is maximal gas exchange effectiveness in a physiological distribution of [Formula: see text], which is generalizable to any inert gas and is practical to estimate from arterial and end-expired CO2 partial pressures.NEW & NOTEWORTHY The three-compartment model of lung ventilation-perfusion mismatch postulates definitive alveolar deadspace and "ideal gas" lung compartments, but these are, in fact, widely different for gases of different blood solubility. Physiologically realistic distributions of ventilation, perfusion, and gas exchange instead suggest an individual "ideal" ventilation-perfusion ratio for every gas, where its alveolar-capillary uptake or elimination rate is maximal (modal). For carbon dioxide, this "ideal" partial pressure is the mean of the arterial and end-tidal partial pressures.

Changes in dead space components during pressure-controlled inverse ratio ventilation: A secondary analysis of a randomized trial.

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.

INHALED PULMONARY VASODILATOR TREATMENT FOR COVID-19: A SYSTEMATIC REVIEW AND META-ANALYSIS

TOPIC: Chest Infections TYPE: Original Investigations PURPOSE: Coronavirus disease 2019 (COVID-19) has become a leading cause of mortality globally. Inhaled pulmonary vasodilators, epoprostenol (iEPO) and nitric oxide (iNO), are used as adjunctive therapies for the treatment of refractory hypoxemia in patients with acute respiratory distress syndrome (ARDS). Hypoxemia in COVID-19 patients is mainly caused by ventilation-perfusion mismatch, which might be improved by inhaled pulmonary vasodilators. However, the effects of inhaled pulmonary vasodilator therapy on the clinical outcomes of COVID-19 remain unclear. Therefore, we conducted this meta-analysis to evaluate the impact of pulmonary vasodilators, iNO and iEPO, on the oxygenation parameters in COVID-19 patients with refractory hypoxemia. METHODS: We performed a comprehensive literature search using PubMed, Embase, and Cochrane Library databases from inception through April 24, 2021, to include all published studies. All statistical analyses were performed using the Review Manager software (RevMan 5.3). The weighted mean difference (MD) with corresponding 95% confidence intervals (CI) were calculated using the random-effects model. A P-value <0.05 was considered statistically significant. The primary outcome measure was the change in oxygenation parameter (PaO2/FiO2) pre and post pulmonary vasodilators. RESULTS: A total of seven studies (three and four studies for iEPO and iNO, respectively) involving 211 patients with COVID-19 (140 patients in iEPO group and 71 in iNO) were included. Overall, pulmonary vasodilators showed significant improvement in oxygenation: PaO2/FiO2 (MD: 12.48, 95% CI: 4.51, 20.44, P = 0.002, I2 = 0%). On subgroup analysis, iEPO showed significant improvement in oxygenation: PaO2/FiO2 (MD: 13.39, 95% CI: 2.84, 23.94, P = 0.01, I2 = 0%), however, iNO showed no improvement in oxygenation: PaO2/FiO2 (MD: 12.80, 95% CI: -4.82, 30.42, P = 0.15, I2 = 47%). CONCLUSIONS: Our meta-analysis showed that inhaled epoprostenol improved oxygenation in COVID-19 patients. However, inhaled nitric oxide therapy was not associated with improvement in oxygenation. Major limitation being lack of control arm and adjustment for confounders. Clinical trials are needed to determine the effect of inhaled pulmonary vasodilators on oxygenation parameters and clinical outcomes of COVID-19 patients. CLINICAL IMPLICATIONS: Inhaled pulmonary vasodilators may play a role as rescue therapy in COVID-19 patients with refractory hypoxemia. DISCLOSURES: No relevant relationships by Ziad Abuhelwa, source=Web Response No relevant relationships by Ragheb Assaly, source=Web Response No relevant relationships by Hazem Ayesh, source=Web Response No relevant relationships by Azizullah Beran Beran, source=Web Response No relevant relationships by Sami Ghazaleh, source=Web Response No relevant relationships by Dana Ghazaleh, source=Web Response No relevant relationships by Mohammed Mhanna, source=Web Response No relevant relationships by Asmaa Mhanna, source=Web Response No relevant relationships by Rami Musallam, source=Web Response No relevant relationships by Omar Sajdeya, source=Web Response No relevant relationships by Omar Srour, source=Web Response

COMMON VARIABLE IMMUNODEFICIENCY WITH GROUP 1 PULMONARY HYPERTENSION TREATED WITH INHALED PROSTACYCLINS

TOPIC: Pulmonary Vascular Disease TYPE: Fellow Case Reports INTRODUCTION: Common Variable Immunodeficiency (CVID) is a disorder that is occasionally complicated by a rare form of interstitial lung disease: granulomatous lymphocytic interstitial lung disease (GLILD). Progression of GLILD may result in Group 3 pulmonary hypertension (PH). Group 1 PH is rare in CVID. We present a patient with CVID with group 1 PH treated with inhaled prostacyclin. CASE PRESENTATION: A 39-year-old woman with medical history of CVID treated with long-term intravenous immunoglobulin (IVIg) therapy, immune mediated thrombocytopenia (ITP) and chronic respiratory failure on 2 liters of supplemental oxygen presented with acute right ventricular (RV) failure and for evaluation of heart and lung transplant. She had worsening dyspnea. She was treated for pneumonia with sepsis. Computed Tomography Angiography (CTA) chest showed pulmonary artery dilation, septal thickening, bilateral reticulation and mild bilateral lower lobe traction bronchiectasis, with scattered pulmonary nodules. This was suggestive of GLILD. Echocardiogram showed a left ventricular ejection fraction of 60%, pulmonary arterial pressure of 78 mmHg, with trivial pericardial effusion and severe RV dysfunction. Right heart catheterization demonstrated, in mmHg, right atrial pressure of 2, mean pulmonary arterial pressure of 42, pulmonary capillary wedge pressure of 2, cardiac output and index of 2.83 and 1.71 respectively with pulmonary vascular resistance of 14 wood units, consistent with severe PAH. Pulmonary function tests showed severe restrictive disease. The degree of PVR elevation was higher than what was expected in the setting of diffuse parenchymal lung disease, suggesting a vasculopathic component beyond that attributable to group 3 disease. There was concern of potentially worsening ventilation perfusion (VQ) mismatch if treated with pulmonary vasodilators. The patient was deemed a poor transplant candidate due to ITP and was started on inhaled Treprostinil, and discharged home on tapering dose of steroids and supplemental oxygen. She was seen in PH clinic where she is was showing improved New York Heart Association functional class and was tolerating inhaled treprostinil with no worsening in hypoxia. DISCUSSION: CVID is a severe immunodeficiency that is caused by failure of antibody production. GLILD is the usual primary pulmonary parenchymal disease associated with CVID. Progression of GLILD can be further complicated by the development of PH which is usually classified as Group 3. Until recently, these patients did poorly. CONCLUSIONS: Group 3 PH is not treated with pulmonary vasodilator therapy. Our patient did well on inhaled prostacyclin, in the setting of parenchymal lung disease. This is attributed to a pulmonary vascular phenotype, similar to those with PAH. Treatment of Group 1 PH in this setting with inhaled prostacyclin could represent a novel frontier in the treatment of pulmonary vascular phenotype. REFERENCE #1: Huston J, Johnson J, Hemnes A, Pugh M. Evidence of pulmonary arterial hypertension in two patients with common variable immunodeficiency. Pulm Circ. 2020 May 1;10(2):2045894020922792. doi: 10.1177/2045894020922792. PMID: 32426112; PMCID: PMC7218961. REFERENCE #2: P501 Pulmonary hypertension rates in common variable immunodeficiency J. Farmer M, Ong S, Barmettler, J. WalterDOI:https://doi.org/10.1016/j.anai.2017.09.067 REFERENCE #3: Pulmonary hypertension in interstitial lung diseaseJ. Behr, J. H. RyuEuropean Respiratory Journal Jun 2008, 31 (6) 1357-1367; DOI: 10.1183/09031936.00171307 DISCLOSURES: No relevant relationships by ALAA ABU SAYF, source=Web Response No relevant relationships by Sara Hegab, source=Web Response Speaker/Speaker's Bureau relationship with Bayer Please note: 11/20/20-4/2021 Added 04/29/2021 by Reem Ismail, source=Web Response, value=Consulting fee No relevant relationships by Rajaninder Sharma, source=Web Response

The Role of Alveolar Edema in COVID-19.

The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threatening hypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation-perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (conservative fluid management, exogenous surfactant replacements and ethanol–oxygen vapor therapy hypothetically) may be greatly helpful for reducing the occurrences of severe cases. Given that late mechanical ventilation may cause mucus (edema fluid) to be blown deep into the small airways, oxygen therapy should be given at the early stages. The optimal time and blood oxygen saturation (SpO2) threshold for oxygen therapy are also discussed.

The effect of acute ventilation-perfusion mismatch on respiratory heat exchange in a porcine model.

BackgroundRespiratory heat exchange is an important physiological process occurring in the upper and lower respiratory tract and is usually completed when inspired gases reach the alveoli. Animal and human studies demonstrated that heat exchange can be modulated by altering pulmonary ventilation and perfusion. The purpose of this study was to examine the effect of acute ventilation-perfusion (V/Q) mismatch on respiratory heat exchange. In clinical practice, monitoring respiratory heat exchange might offer the possibility of real-time tracking of acute V/Q-mismatch.MethodsIn 11 anesthetized, mechanically ventilated pigs, V/Q-mismatch was established by means of four interventions: single lung ventilation, high cardiac output, occlusion of the left pulmonary artery and repeated whole-lung lavage. V/Q-distributions were determined by the multiple inert gas elimination technique (MIGET). Respiratory heat exchange was measured as respiratory enthalpy using the novel, pre-commercial VQm™ monitor (development stage, Rostrum Medical Innovations, Vancouver, CA). According to MIGET, shunt perfusion of low V/Q compartments increased during single lung ventilation, high cardiac output and whole-lung lavage, whereas dead space and ventilation of high V/Q compartments increased during occlusion of the left pulmonary artery and whole-lung lavage.ResultsBohr dead space increased after pulmonary artery occlusion and whole-lung lavage, venous admixture increased during single lung ventilation and whole-lung lavage, PaO2/FiO2 was decreased during all interventions. MIGET confirmed acute V/Q-mismatch. Respiratory enthalpy did not change significantly despite significant acute V/Q-mismatch.ConclusionClinically relevant V/Q-mismatch does not impair respiratory heat exchange in the absence of additional thermal stressors and may not have clinical utility in the detection of acute changes.

Гепатопульмональный синдром. Обзор литературы

Liver cirrhosis is often accompanied by complications from the pulmonary system. These include hydrothorax, portopulmonary hypertension and hepatopulmonary syndrome. Hepatic hydrothorax affects about 6-10% of patients with end-stage disease, which results in the passage of ascetic fluid into the pleural space through diaphragm defects. The common cause of the hepatopulmonary syndrome and portopulmonary hypertension is portal hypertension and portosystemic shunting, indicating that vasoactive and angiogenetic factors originating from the liver normally control the pulmonary circulation. Portopulmonary hypertension is like pulmonary arterial hypertension, which develops against the background of portal hypertension as a result of chronic liver disease or without other causes of increased pressure in the pulmonary vessels. The prevalence of portopulmonary hypertension ranges from 2% to 8.5% among patients with portal hypertension and is associated with a poor prognosis. Hepatopulmonary syndrome is characterized by intrapulmonary dilatation of microvessels, which causes intrapulmonary shunting and leads to impaired gas exchange in liver diseases, and is associated with a decrease in the quality and duration of life in patients with cirrhosis. Nitric oxide overproduction and angiogenesis seem to be the hallmarks of a complicated pathogenetic mechanism, leading to intrapulmonary shunting and ventilation-perfusion mismatch. A classification of hepatopulmonary syndrome according to the severity of hypoxemia has been suggested. Hepatopulmonary syndrome includes a triad: hepatic dysfunction and / or portal hypertension, dilatation of intrapulmonary vessels, and increased alveolar-arterial oxygen gradient. The prevalence of hepatopulmonary syndrome varies depending on the study groups from 5% to 30%. The most common symptom of the complication is shortness of breath, but in most cases, hepatopulmonary syndrome is asymptomatic. A decrease in oxygen saturation less than 96% corresponds to a decrease in PaO2&lt;70 mm Hg and testifies to the possible development of hepatopulmonary syndrome. In the case of a positive screening, the patient should undergo arterial blood gas analysis, which helps to determine PaO2 and alveolar to arterial oxygen gradient. Conclusion. Contrast-enhanced echocardiography with agitated saline is the gold standard in the diagnosis of intrapulmonary dilatation. The only effective treatment for hepatopulmonary syndrome is liver transplantation. Complete recovery of hepatopulmonary syndrome after liver transplantation is observed within a year in most patients with cirrhosis and hepatopulmonary syndrome

Fatal COVID-19 is Characterized by Distinct Vasculopathic Features and Increased Congestion of the Alveolar Capillary-Bed

Background: Clinical and radiologic studies investigating Coronavirus disease 2019 (COVID-19) indicate that a possible cause of severe hypoxia is marked ventilation-perfusion (VA/Q) mismatch. Published histopathology reports diffuse alveolar damage (DAD) in fatal COVID-19 is indistinguishable from other causes of DAD. We compared lung parenchymal and vascular alterations between COVID-19 and DAD of other etiologies using a multidimensional approach. Methods: This autopsy cohort consisted of consecutive COVID-19 patients (n=20) and patients with clinical acute respiratory distress syndrome and histologic DAD (n=21; non-COVID-19 viral and non-viral etiologies). Premortem chest CTs were evaluated for mosaic attenuation and vascular changes. Postmortem lung tissues were compared using histopathological, immunohistochemical, transcriptomics and computational analyses. Machine-learning-derived morphometric analysis of microvasculature was performed, with a random forest classifier quantifying vascular congestion (VSCong), in different microscopic compartments. Findings: On premortem CT, COVID-19 patients showed more mosaic attenuation (p<0·020), and subsegmental dilated vasculature (p=0·003) compared to controls. Histopathology revealed vasculopathic changes including: capillary-congestion and hemangiomatosis-like changes (p=0·043), microthrombi (p=0·026), thromboemboli (p=0·0036), infarcts (p=0·048), and perivascular inflammation(p <0·001). Immunohistochemistry revealed increased CD4+ T-cells(p=0·023), TIM3+ lymphocytes/macrophages (p=0·037/0·019), and PD-1+ cells(p=0·008). Morphometric analysis in COVID-19 revealed significantly higher bronchiolar VS Cong (p <0·0001) and alveolar-septal VSCong (p<0·0001), with larger overall VSCong range (p=0·002). Septal-congestion was associated with a significantly shorter time-to-death from symptom onset (p=0·02). Interpretation: Severe COVID-19 is characterized by significant vasculopathy and aberrant alveolar septal-congestion, which may be associated with shorter time-to-death. Dilated sublobar vessels and heterogeneously increased septal-congestion may translate to VA/Q mismatch in COVID-19. These findings warrant further investigation in larger multi-institutional autopsy cohorts. Funding Information: Supported by Internal Sundry, and Vickery-Colvin Award from the Department of Pathology, Massachusetts General Hospital. Declaration of Interests: LPH reports grants from Boehringer Ingelheim and has received personal consulting fees from Boehringer Ingelheim, Pliant Therapeutics, and Biogen Idec, all of which are not related to this study. SET have received CDC funding for other COVID-related work which are not related to this study. JAB has received grant support from Zeus Scientific, bioMerieux, Immunetics, the Bay Area Lyme Foundation and the Lyme Disease Biobank Foundation for work not related to this study, and has been a consultant for T2 Biosystems, DiaSorin and Roche Diagnostics, not related to this study. BPL reports royalties from Elsevier, Inc. for his work as an associate textbook editor, not related to this study. MMK has served as a compensated consultant for H3 Biomedicine and AstraZeneca and has received research (institutional) funding from Novartis and loyalty from Elsevier, all of which are not related to this study. The other authors declare no competing interests. Ethics Approval Statement: Analysis of patient autopsy material was reviewed and approved by the Partners Human Research IRB (Protocol #: 2020P001146).

A new look at the correction of COVID-19-mediated pulmonary gas exchange disorders

Aim. To assess the effect of meglumine sodium succinate on the effectiveness of basic therapy in correcting gas exchange abnormalities in patients with severe COVID-19 infection complicated by bilateral community-acquired pneumonia.&#x0D; Methods. The analysis of the effectiveness of therapy of 12 patients with a diagnosis of New coronavirus infection COVID-19 (confirmed), severe form U07.1. Complication: bilateral multifocal pneumonia was carried out. The patients were divided into two groups: 7 received, as part of standard therapy, a solution of meglumine sodium succinate in a daily dose of 5 ml/kg during stay in the intensive care unit; 5 patients received a similar volume of Ringer's solution and formed the control group. In the arterial and venous blood of all patients, the indicators of acid-base state and water-electrolyte balance, glycemia and lactatemia were measured at several stages: (1) at admission to the intensive care unit, (2) 24 hours after the start of intensive therapy, (3) after 812 hours, (4) after 24 hours. On the 28th day of observation, mortality, the duration of treatment in the intensive care unit and the incidence of thrombotic complications in the groups were assessed. The Friedman nonparametric hypothesis test was used to assess intragroup dynamics, and the nonparametric Mannhitney U test for intergroup comparisons.&#x0D; Results. In the group of patients who received meglumine sodium succinate, there was a significant decrease in the incidence of thromboembolic events during 28 days of treatment: myocardial ischemia event rate ratio from 0.89 [95% confidence interval (CI) 0.191.16] in the control group to 0.55 (95% CI 0.060.81) in the study group at p=0.043; pulmonary embolism event from 0.50 (95% CI 01.0) in the control group to 0.28 (95% CI 01.0) in the study group at p=0.041. There was also a decrease in the duration of intensive care unit length of stay to 6.11.1 days in the study group versus 8.91.3 days in the control group.&#x0D; Conclusion. Compared with standard infusion therapy, the use of meglumine sodium succinate leads to a faster normalization of ventilation-perfusion ratios in patients with severe coronavirus infection.

Severe COVID-19 pneumonia: Perfusion analysis in correlation with pulmonary embolism and vessel enlargement using dual-energy CT data.

Gas exchange in COVID-19 pneumonia is impaired and vessel obstruction has been suspected to cause ventilation-perfusion mismatch. Dual-energy CT (DECT) can depict pulmonary perfusion by regional assessment of iodine uptake. The purpose of this study was the analysis of pulmonary perfusion using dual-energy CT in a cohort of 27 consecutive patients with severe COVID-19 pneumonia. We retrospectively analyzed pulmonary perfusion with DECT in 27 consecutive patients (mean age 57 years, range 21-73; 19 men and 8 women) with severe COVID-19 pneumonia. Iodine uptake (IU) in regions-of-interest placed into normally aerated lung, ground-glass opacifications (GGO) and consolidations was measured using a dedicated postprocessing software. Vessel enlargement (VE) within opacifications and presence of pulmonary embolism (PE) was assessed by subjective analysis. Linear mixed models were used for statistical analyses. Compared to normally aerated lung 106/151 (70.2%) opacifications without upstream PE demonstrated an increased IU, 9/151 (6.0%) an equal IU and 36/151 (23.8%) a decreased IU. The estimated mean iodine uptake (EMIU) in opacifications without upstream PE (GGO 1.77 mg/mL; 95%-CI: 1.52-2.02; p = 0.011, consolidations 1.82 mg/mL; 95%-CI: 1.56-2.08, p = 0.006) was significantly higher compared to normal lung (1.22 mg/mL; 95%-CI: 0.95-1.49). In case of upstream PE, EMIU of opacifications (combined GGO and consolidations) was significantly decreased compared to normal lung (0.52 mg/mL; 95%-CI: -0.07-1.12; p = 0.043). The presence of VE in opacifications correlated significantly with iodine uptake (p<0.001). DECT revealed the opacifications in a subset of patients with severe COVID-19 pneumonia to be perfused non-uniformly with some being hypo- and others being hyperperfused. Mean iodine uptake in opacifications (both ground-glass and consolidation) was higher compared to normally aerated lung except for areas with upstream pulmonary embolism. Vessel enlargement correlated with iodine uptake: In summary, in a cohort of 27 consecutive patients with severe COVID-19 pneumonia, dual-energy CT demonstrated a wide range of iodine uptake in pulmonary ground-glass opacifications and consolidations as a surrogate marker for hypo- and hyperperfusion compared to normally aerated lung. Applying DECT to determine which pathophysiology is predominant might help to tailor therapy to the individual patient´s needs.

Intrapleural Steroid Instillation for Critically Ill Patients With Covid-19 Severe Adult Respiratory Distress Syndrome.

Within a very short period, outbreaks of a novel coronavirus disease (COVID-19) have affected 183 countries worldwide. COVID-19 resolves acutely, but it has resulted in thousands of deaths, with an overall fatality rate of 2% to 5% (1). Among the fatal cases, over 50% of patients died from respiratory failure with massive alveolar damage due to virus-activated “cytokine storm syndrome” (2). Of these patients, 67% developed adult respiratory distress syndrome (ARDS), 29% developed acute kidney injury, 23% developed cardiac injury, and 29% experienced liver dysfunction (3). The intensive care unit (ICU) mortality rate among those who required invasive mechanical ventilation was 86% (4), and the mortality of patients who received extracorporeal membrane oxygenation was also extremely high (5). Until now, there have been no proven effective specific treatment strategies and so methylprednisolone may be the best option for COVID-19 patients who develop ARDS (6). Although interferon alfa-2b, antiviral therapy, antibiotics for the prevention of secondary infection, and methylprednisolone were all administered to attenuate lung inflammation, histological examination still revealed bilateral diffuse alveolar damage with hyaline membrane formation in an autopsy of a patient (7). According to the imaging changes and pathological findings associated with ARDS, a tubular and enlarged appearance of the pulmonary vessels with a sudden caliber reduction seen within ground glass opacity lesions showing partial consolidation and fibrosis should be expected in severe cases of COVID-19 (8, 9). Fortunately, corticosteroids have a greater anti-inflammatory effect when administered intrapleurally, rather than via the intravenous route, because the permeability of the damaged visceral pleural membrane increases during pulmonary edema and steroid treatment, with the characteristic of fat-solubility, further permits infiltration into the lung parenchyma. Glucocorticoids can easily pass through the visceral pleura and bind to steroid hormone receptors, thereby allowing them to reach the injured areas and avoiding the problems of a ventilation–perfusion mismatch and the need for a shunt via intratracheal instillation or intravenous instillation. Glucocorticoids can normalize the ion pump (Na-K pump) and increase the synthesis of Na+/K+-ATPase, thus contributing to reductions in lung edema and optimization of oxygenation because alveolar fluid clearance is impaired in the majority of patients with ARDS (10). In COVID-19 severe refractory ARDS, more aggressive management is required to reduce the inflammatory reaction and consequent lung injury. The results of our study provide more evidence supporting the efficacy of intrapleural steroid instillation (IPSI) in the treatment of ARDS with multiple organ failure (11). This alternative treatment resulted in significant improvement in oxygenation and survival benefits after 5 days of treatment. The dosing schedule of intrapleural methylprednisolone was initially 40 mg q6 h in both pleural cavities, but the dose was reduced on the basis of chest radiography appearance, inspired oxygen concentration demand, and positive end-expiratory pressure of the ventilator. Thoracic catheterization was easily performed because COVID-19 patients usually had significant pleural effusion. Although managing COVID-19 pneumonia is currently a major issue for ICU healthcare providers around the world, IPSI will greatly improve the ability to respond effectively to current needs. Our recommendation in this severe case of COVID-19 might help physicians implement suitable therapeutic strategies for similar severe patients and reduce mortality.

Large difference between Enghoff and Bohr dead space in ventilated infants with hypoxemic respiratory failure.

Ventilated neonates with hypoxemic respiratory failure (HRF) may show a ventilation-perfusion (V/Q) mismatch. To evaluate the difference between the Bohr (Vd, Bohr ) and Enghoff (Vd, Enghoff ) dead spaces in infants by using volumetric capnography based on ventilator graphics and capnograms. This study enrolled 46 ventilated infants (mean birth weight, 2239 ± 640 g; mean gestational age, 35.5 ± 3.3 weeks). We performed volumetric capnography and calculated Vd, Bohr and Vd, Enghoff when arterial blood sampling was necessary for treatment. According to the oxygenation index (OI) based on the Montreux definition of neonatal acute respiratory distress syndrome, each measurement was classified into the HRF (OI ≥ 4) or control (OI < 4) group. Then, a regression analysis was performed to evaluate the correlation between the OI and the difference between Vd, Enghoff and Vd, Bohr . The median Vd, Enghoff /tidal volume (VT ) was significantly higher in the HRF group (0.55 [interquartile range, 0.47-0.68]) than in the control group (0.46 [0.37-0.57]). The HRF group showed a larger difference between Vd, Enghoff /VT and Vd, Bohr /VT than the control group (median, 0.22 [0.15-0.29] vs. 0.10 [0.06-0.14], respectively). Moreover, the regression analysis of the relationship between OI and Vd, Enghoff /VT - Vd, Bohr /VT showed a positive correlation (r = .60, p < .001). Ventilated neonates with hypoxemic respiratory failure showed a large difference between Vd, Enghoff and Vd, Bohr , possibly reflecting a low V/Q mismatch and right-to-left shunting.

An Automated Jet Nebulizer with Dynamic Flow Regulation.

PurposeThe present study is focused on designing an automated jet nebulizer that possesses the capability of dynamic flow regulation. In the case of existing equipment, 50% of the aerosol is lost to the atmosphere through the vent, during the exhalation phase of respiration. Desired effects of nebulization may not be achieved by neglecting this poor administration technique. There may be adverse effects like bronchospasm and exposure to high drug concentrations. MethodsThe proposed nebulizer is composed of two modes as “Compressed Air” mode and the “Oxygen Therapy” mode. The automated triggering from one mode to another will be dependent upon the percentage of oxygen saturation of the patient, monitored from the SpO2 sensor. The compressed airflow will be delivered to the patient according to the minute ventilation, derived with the aid of a temperature sensor–based algorithm. The compressor controller circuitry ensures that the patient receives optimum level of compressed air as per the flow rate. At the end of the drug delivery, if the liquid level sensor detects the absence of medication within the nebulizer chamber, the nebulization process will be terminated. The dynamic regulation of the motor speed with respect to the minute ventilation was accomplished.ResultsA laminar flow was obtained from the outlet of the compressor towards the nebulizer tubing, and a turbulent flow was obtained within the chamber. No excessive turbulent flows or rotational flow patterns were detected.ConclusionDetecting the drug levels in the nebulizing chamber will prevent continuous workup and useful in situations where back-to-back nebulization is required. Oxygen therapy mode identifies the patient’s desaturation and important where the patient can be already hypoxic or have a ventilation-perfusion mismatch, but may be disadvantageous in severe COPD patients. The aforesaid results could certainly lead to the improvements of the existing nebulizers.

Non-invasive assessment of intrapulmonary shunt and ventilation to perfusion ratio in children with hepatopulmonary syndrome before and after liver transplantation.

To use the oxyhaemoglobin dissociation curve (ODC) to non-invasively measure the ventilation perfusion ratio (VA/Q) and right-to-left intrapulmonary vascular shunt before and after liver transplantation (LT) in children with hepatopulmonary syndrome (HPS). To investigate whether the right-to-left shunt derived by ODC correlated with the shunt derived by technetium-99 labelled macroaggregated albumin lung perfusion scan (MAA). A retrospective cohort study at King's College Hospital NHS Foundation Trust, London, UK was performed between 1998 and 2016. The VA/Q and right-to-left shunt were non-invasively measured pre and post LT. The pre-LT right-to-left intrapulmonary shunt was also measured by MAA. The non-invasively derived pre-LT shunt was correlated with the shunt derived by MAA. Fifteen children with HPS were studied with a median (IQR) age at LT of 8.8 (6.6-12.9) years. The median (IQR) pre-LT VA/Q [0.49 (0.42-0.65)] was lower compared to the post-LT VA/Q [0.61 (IQR 0.54-0.72), p=0.012]. The median (IQR) pre-LT shunt was 19 (3-24) % which decreased to zero in all but one children post-LT, (p=0.001). The MAA-derived shunt was significantly positively correlated with the ODC-derived shunt (r=0.783, p=0.001). The mean (SD) difference between shunt derived by ODC and shunt derived by MAA was 0.5 (7.2) %. Ventilation/perfusion impairment reverses but not completely resolves after liver transplantation in children with hepatopulmonary syndrome. The non-invasive method for estimating intrapulmonary shunting could be used as an alternative to the macroaggregated albumin scan in this population.

Novel pulmonary perfusion imaging using chest digital dynamic radiography for pulmonary artery sarcoma.

Key messageChest digital dynamic radiography (DDR) is a novel method for evaluating pulmonary perfusion and ventilation. It could depict ventilation–perfusion mismatch in a pulmonary artery sarcoma with severe stenosis in the right pulmonary artery. This report is the first demonstration of ventilation–perfusion mismatch in a malignant neoplasm using DDR.