Pulmonary Perfusion Research Articles

Impact of pulmonary perfusion defects by scintigraphy on pulmonary vascular resistances, functional capacity and right ventricular systolic function in chronic thromboembolic pulmonary hypertension

Chronic thromboembolic pulmonary hypertension (CTEPH) is a specific subtype of pulmonary hypertension. Pulmonary ventilation/perfusion single-photon emission computed tomography (V/Q SPECT) is the reference diagnostic examination of CTPEH showing mismatch in at least one segment or two sub-segments. To investigate the relationship between the extent of pulmonary perfusion defects and hemodynamic, echocardiographic, biological and functional parameters. Between 2012 and 2019, 46 patients with CTEPH were retrospectively enrolled in the study. The diagnosis of pulmonary hypertension was made by the referral team of the expert centre according European Society of Cardiology and European Respiratory Society guidelines. All patients underwent pulmonary V/Q SPECT, right heart catheterisation, transthoracic echocardiography (TTE), functional tests and natriuretic peptides assays during the same stay. There was a slight correlation between the extent of pulmonary perfusion defects and pulmonary vascular resistances ( r = 0.510, P < 0.001; Fig. 1 ). However, there was no correlation between the extent of pulmonary perfusion defects or hemodynamic measurements and right ventricular function assessed by TTE, the functional parameters (6 minutes walk distance [6MWD], NYHA class and NT-proBNP level). In contrast, there was a correlation between right ventricular function assessed in TTE (i.e. tricuspid antero-posterior systolic excursion and tricuspid annular S wave) and 6MWD ( r = 0.586, P < 0.001 and r = 0.471, P < 0.01, respectively), functional class (NYHA III or IV) ( r = 0.427, P < 0.01 and r = 0.377, P < 0.01, respectively) and the NT-proBNP level ( r = 0.513, P < 0.001 and r = 0.485, P < 0.001, respectively). Pulmonary perfusion defects extension by V/Q SPECT can provide information on pulmonary vascular resistances. However, it is not correlated with right ventricular function and functional parameters.

Regional Lung Perfusion Analysis in Experimental ARDS by Electrical Impedance and Computed Tomography.

Electrical impedance tomography is clinically used to trace ventilation related changes in electrical conductivity of lung tissue. Estimating regional pulmonary perfusion using electrical impedance tomography is still a matter of research. To support clinical decision making, reliable bedside information of pulmonary perfusion is needed. We introduce a method to robustly detect pulmonary perfusion based on indicator-enhanced electrical impedance tomography and validate it by dynamic multidetector computed tomography in two experimental models of acute respiratory distress syndrome. The acute injury was induced in a sublobar segment of the right lung by saline lavage or endotoxin instillation in eight anesthetized mechanically ventilated pigs. For electrical impedance tomography measurements, a conductive bolus (10% saline solution) was injected into the right ventricle during breath hold. Electrical impedance tomography perfusion images were reconstructed by linear and normalized Gauss-Newton reconstruction on a finite element mesh with subsequent element-wise signal and feature analysis. An iodinated contrast agent was used to compute pulmonary blood flow via dynamic multidetector computed tomography. Spatial perfusion was estimated based on first-pass indicator dilution for both electrical impedance and multidetector computed tomography and compared by Pearson correlation and Bland-Altman analysis. Strong correlation was found in dorsoventral (r = 0.92) and in right-to-left directions (r = 0.85) with good limits of agreement of 8.74% in eight lung segments. With a robust electrical impedance tomography perfusion estimation method, we found strong agreement between multidetector computed and electrical impedance tomography perfusion in healthy and regionally injured lungs and demonstrated feasibility of electrical impedance tomography perfusion imaging.

Exercise training modalities for heart transplant recipients: a systematic review and network meta-analysis protocol

IntroductionHeart transplantation is the gold standard treatment for selected patients with end-stage heart failure. Although this procedure can improve quality and prolong life expectancy, several of these patients persist with...

Myocardial involvement in eosinophilic granulomatosis with polyangiitis evaluated with cardiopulmonary magnetic resonance

Patients with eosinophilic granulomatosis with polyangiitis (EGPA) most commonly die from cardiac causes, however, cardiac involvement remains poorly characterised and the relationship between cardiac and pulmonary disease is not known. This study aimed to characterise myocardial and pulmonary manifestations of EGPA, and their relationship. Prospective comprehensive cardiopulmonary investigation, including a novel combined cardiopulmonary magnetic resonance imaging (MRI) technology, was performed in 13 patients with stable EGPA. Comparison was made with 11 prospectively recruited matched healthy volunteers. Stable EGPA was associated with focal replacement and diffuse interstitial myocardial fibrosis (myocardial extracellular volume 26.9% vs. 24.7%; p = 0.034), which drove a borderline increase in left ventricular mass (56 ± 9 g/m2 vs. 49 ± 8 g/m2; p = 0.065). Corrected QT interval was significantly prolonged and was associated with the severity of myocardial fibrosis (r = 0.582, p = 0.037). Stable EGPA was not associated with increased myocardial capillary permeability or myocardial oedema. Pulmonary tissue perfusion and capillary permeability were normal and there was no evidence of pulmonary tissue oedema or fibrosis. Forced expiratory volume in one second showed a strong inverse relationship with myocardial fibrosis (r = −0.783, p = 0.038). In this exploratory study, stable EGPA was associated with focal replacement and diffuse interstitial myocardial fibrosis, but no evidence of myocardial or pulmonary inflammation or pulmonary fibrosis. Myocardial fibrosis was strongly associated with airway obstruction and abnormal cardiac repolarisation. Further investigation is required to determine the mechanisms underlying the association between heart and lung disease in EGPA and whether an immediate immunosuppressive strategy could prevent myocardial fibrosis formation.

Heparin-binding protein levels correlate with aggravation and multiorgan damage in severe COVID-19.

BackgroundCritically ill coronavirus disease 2019 (COVID-19) patients may suffer persistent systemic inflammation and multiple organ failure, leading to a poor prognosis.Research questionTo examine the relevance of the novel inflammatory factor heparin-binding protein (HBP) in critically ill COVID-19 patients, and evaluate the correlation of the biomarker with disease progression.Study design and methods18 critically ill COVID-19 patients who suffered from respiratory failure and sepsis, including 12 cases who experienced a rapidly deteriorating clinical condition and six cases without deterioration, were investigated. They were compared with 15 age- and sex- matched COVID-19-negative patients with respiratory failure. Clinical data were collected and HBP levels were investigated.ResultsHBP was significantly increased in critically ill COVID-19 patients following disease aggravation and tracked with disease progression. HBP elevation preceded the clinical manifestations for up to 5 days and was closely correlated with patients’ pulmonary ventilation and perfusion status.InterpretationHBP levels are associated with COVID-19 disease progression in critically ill patients. As a potential mediator of disease aggravation and multiple organ injuries that are triggered by continuing inflammation and oxygen deficits, HBP warrants further study as a disease biomarker and potential therapeutic target.

Evaluation of intramuscular sodium nitroprusside injection to improve oxygenation in white-tailed deer (Odocoileus virginianus) anesthetized with medetomidine–alfaxalone–azaperone

ObjectiveIn ungulates, α2-adrenergic agonists can decrease oxygenation possibly through alteration of pulmonary perfusion. Sodium nitroprusside can decrease pulmonary vascular resistance (PVR) and increase cardiac output (Q˙t) through vasodilation. The objective was to determine if sodium nitroprusside would improve pulmonary perfusion and attenuate the increased alveolar–arterial (a–a) gradient resulting from medetomidine–azaperone–alfaxalone (MAA) administration. Study designProspective, randomized, crossover study with a 2 week rest period. AnimalsA group of eight adult female captive white-tailed deer (Odocoileus virginianus). MethodsDeer were administered MAA intramuscularly (IM), and auricular artery and pulmonary artery balloon catheters were placed. Deer spontaneously breathed air. Saline or sodium nitroprusside (0.07 mg kg–1) were administered IM 40 minutes after MAA injection. Heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), pulmonary artery occlusion pressure (PAOP), right atrial pressure (RAP), Q˙t, arterial pH, PaCO2 and PaO2 were obtained immediately before nitroprusside injection (baseline) and 5, 10 and 15 minutes afterwards. Mixed venous blood samples were obtained at baseline and at 5 minutes. Systemic vascular resistance (SVR), PVR, intrapulmonary shunt fraction (Q˙s/Q˙t), a–a gradient, oxygen delivery (D˙O2) and oxygen extraction ratio (O2ER) were calculated. Statistical analysis was performed with repeated measures analysis of variance with correction factors. A p value < 0.05 was considered significant. ResultsWith nitroprusside, MAP, MPAP, PAOP, RAP, SVR and O2ER significantly decreased and HR, Q˙t and D˙O2 increased compared with baseline and between treatments. There was a significant decrease in PVR and a–a gradient and increase in PaO2 compared with baseline and saline treatment. Changes were not sustained. Conclusions and clinical relevanceNitroprusside temporarily changed hemodynamic variables, increased PaO2 and decreased a–a gradient. Nitroprusside possibly led to better pulmonary perfusion of ventilated alveoli. However, IM nitroprusside at this dose is not recommended because of severe systemic hypotension and short action.

Case report: hepatobronchial lymphatic communications in single ventricle patients as a pathophysiological mechanism of plastic bronchitis: diagnosis and treatment.

Background Plastic bronchitis is a rare but devastating complication in single ventricle patients after Fontan completion. Recent advances in dynamic contrast-enhanced magnetic resonance lymphangiogram demonstrate the typical pathophysiological mechanism of the thoracic duct leaking lymphatic fluid towards the bronchi resulting in intraluminal casts. This has been termed abnormal pulmonary lymphatic perfusion and has been successfully treated in 94% of patients with thoracic duct occlusion. However, in some cases, this aberrant flow is not identified and therefore no intervention is available. This case report identifies a newly discovered origin of abnormal lymphatic flow from the liver to the bronchi and the treatment of these patients.Case summary We report two cases of plastic bronchitis in single ventricle patients with no identified abnormal lymphatic pulmonary perfusion from the thoracic duct. Both patients underwent liver lymphangiogram and demonstrated aberrant flow from the hepatic lymphatic ducts to the bronchi. These were successfully occluded, and plastic bronchitis symptoms resolved in both cases.Discussion The recent discovery of the abnormal pulmonary lymphatic perfusion from the thoracic duct to the bronchi has allowed successful treatment of 94% of single ventricle patients with plastic bronchitis. The discovery of hepatobronchial lymphatic perfusion reveals an occult aetiology of plastic bronchitis and a second target for embolization and successful treatment.

Pulmonary vascular improvement in severe COVID-19 patients treated with tocilizumab

As of October 2020 management of Coronavirus disease 2019 (COVID-19) is based on supportive care and off-label or compassionate-use therapies. On March 2020 tocilizumab - an anti-IL-6 receptor monoclonal antibody - was suggested as immunomodulatory treatment in severe COVID-19 because hyperinflammatory syndrome occurs in many patients similarly to the cytokine release syndrome that develops after CAR-T cell therapy. In our retrospective observational study, 20 severe COVID-19 patients requiring intensive care were treated with tocilizumab in addition to standard-of-care therapy (SOC) and compared with 13 COVID-19 patients receiving only SOC. Clinical respiratory status, inflammatory markers and vascular radiologic score improved after one week from tocilizumab administration. On the contrary, these parameters were stable or worsened in patients receiving only SOC. Despite major study limitations, improvement of alveolar-arterial oxygen gradient as well as vascular radiologic score after one week may account for improved pulmonary vascular perfusion and could explain the more rapid recovery of COVID-19 patients receiving tocilizumab compared to controls.

Efficacy of interventional treatment for patients with chronic thromboembolic pulmonary hypertension with microvasculopathy

Abstract Background The existence of microvasculopathy in chronic thromboembolic pulmonary hypertension (CTEPH) had been suggested. However, the impact of microvasculopathy for pathophysiology had been unknown. Recently dual-energy computed tomography (DECT) can produce a sensitive iodine distribution map in lung fields to quantify lung perfusion, which may indicate the existence of microvasculopathy according to poor subpleural perfusion. This study aimed to examine the therapeutic efficacy of interventional treatment (pulmonary endarterectomy or/and balloon pulmonary angioplasty) in CTEPH with microvasculopathy. Methods We retrospectively reviewed poor subpleural perfusion (defined as subpleural spaces either not or minimally perfused in all segments) and hemodynamics of 70 consecutive CTEPH patients who underwent DECT before and after interventional therapy from January 2014 to January 2020. Patients were divided according to poor subpleural perfusion in DECT images before treatment: a microvasculopathy group (MV group, n=37) or a non-microvasculopathy group (Non-MV group, n=33). We evaluated clinical parameters as WHO functional class (WHO-Fc), 6-min walk distance, respiratory function test, cardiopulmonary exercise test, hemodynamic parameters, and DECT parameters at baseline and after the treatments. DECT parameters as quantitative evaluation of pulmonary blood volume (PBV) calculated as the average of entire lung iodine density. Results After interventional treatments, WHO-Fc improved in 33 patients in MV group, and 27 patients in Non-MV group (p=0.50). In MV group, baseline mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR) and VE/VCO2 slope were higher (38.3±9.3 vs. 33.2±10.8 mmHg p=0.04, 818±394 vs. 539±289 dyne*sec/cm5 p&amp;lt;0.01 and 43.7±11.3 vs. 35.2±6.9 p&amp;lt;0.01, respectively) and PBV were lower (43.7±11.3 vs. 35.2±6.9 Hounsfield Unit p&amp;lt;0.01) After the treatments, mPAP, PVR, VE/VCO2 slope and PBV showed almost equivalent between the groups (19.5±4.1 vs. 20.6±5.1 mmHg p=0.35, 272±111 vs 251±109 dyne*sec/cm5 p=0.42, 29.2±6.3 vs. 26.0±6.1 p=0.06 and 27.1±6.6 vs. 29.6±6.6 Hounsfield Unit p=0.13). Diffusing capacity for carbon monoxide (%DLCO/VA) did not improve after treatment in both groups (MV group: 59.5±13.1 to 58.8±11.9% p=0.43. Non-MV group: 77.8±13.4% to 70.5±10.8% P&amp;lt;0.01). Conclusion Hemodynamics, pulmonary perfusion, exercise capacities significantly improved after the treatments in spite of the existence or absence of microvasculopathy. However, DLCO which might indicate the existence of microvasculopathy did not improve. Interventional treatments could not improve microvasculopathy because of their limit of accessibilities. Funding Acknowledgement Type of funding source: None

Abnormal pulmonary perfusion heterogeneity in patients with Fontan circulation and pulmonary arterial hypertension.

The distribution of pulmonary perfusion is affected by gravity, vascular branching structure and active regulatory mechanisms, which may be disrupted by cardiopulmonary disease, but this is not well studied, particularly in rare conditions. We evaluated pulmonary perfusion in patients who had undergone Fontan procedure, patients with pulmonary arterial hypertension (PAH) and two groups of controls using a proton magnetic resonance imaging technique, arterial spin labelling to measure perfusion. Heterogeneity was assessed by the relative dispersion (SD/mean) and gravitational gradients. Gravitational gradients were similar between all groups, but heterogeneity was significantly increased in both patient groups compared to controls and persisted after removing contributions from large blood vessels and gravitational gradients. Patients with Fontan physiology and patients with PAH have increased pulmonary perfusion heterogeneity that is not explainable by differences in mean perfusion, gravitational gradients, or large vessel anatomy. This probably reflects vascular remodelling in PAH and possibly in Fontan physiology. Many factors affect the distribution of pulmonary perfusion, which may be disrupted by cardiopulmonary disease, but this is not well studied, particularly in rare conditions. An example is following the Fontan procedure, where pulmonary perfusion is passive, and heterogeneity may be increased because of the underlying pathophysiology leading to Fontan palliation, remodelling, or increased gravitational gradients from low flow. Another is pulmonary arterial hypertension (PAH), where gravitational gradients may be reduced secondary to high pressures, but remodelling may increase perfusion heterogeneity. We evaluated regional pulmonary perfusion in Fontan patients (n=5), healthy young controls (Fontan control, n=5), patients with PAH (n=6) and healthy older controls (PAH control) using proton magnetic resonance imaging. Regional perfusion was measured using arterial spin labelling. Heterogeneity was assessed by the relative dispersion (SD/mean) and gravitational gradients. Mean perfusion was similar (Fontan=2.50±1.02mlmin-1 ml-1 ; Fontan control=3.09±0.58, PAH=3.63±1.95; PAH control=3.98±0.91, P=0.26), and the slopes of gravitational gradients were not different (Fontan=-0.23±0.09mlmin-1 ml-1 cm-1 ; Fontan control=-0.29±0.23, PAH=-0.27±0.09, PAH control=-0.25±0.18, P=0.91) between groups. Perfusion relative dispersion was greater in both Fontan and PAH than controls (Fontan=1.46±0.18; Fontan control=0.99±0.21, P=0.005; PAH=1.22±0.27, PAH control=0.91±0.12, P=0.02) but similar between patient groups (P=0.13). These findings persisted after removing contributions from large blood vessels and gravitational gradients (all P<0.05). We conclude that patients with Fontan physiology and PAH have increased pulmonary perfusion heterogeneity that is not explained by differences in mean perfusion, gravitational gradients, or large vessel anatomy. This probably reflects the effects of remodelling in PAH and possibly in Fontan physiology.

Pulmonary perfusion by chest digital dynamic radiography: Comparison between breath-holding and deep-breathing acquisition.

PurposePulmonary perfusion is an important factor for gas exchange. Chest digital dynamic radiography (DDR) by the deep‐breathing protocol can evaluate pulmonary perfusion in healthy subjects. However, respiratory artifacts may affect DDR in patients with respiratory diseases. We examined the feasibility of a breath‐holding protocol and compared it with the deep‐breathing protocol to reduce respiratory artifacts.Materials and methodsA total of 42 consecutive patients with respiratory diseases (32 males; age, 68.6 ± 12.3 yr), including 21 patients with chronic obstructive pulmonary disease, underwent chest DDR through the breath‐holding protocol and the deep‐breathing protocol. Imaging success rate and exposure to radiation were compared. The correlation rate of temporal changes in each pixel value between the lung fields and left cardiac ventricles was analyzed.ResultsImaging success rate was higher with the breath‐holding protocol vs the deep‐breathing protocol (97% vs 69%, respectively; P < 0.0001). The entrance surface dose was lower with the breath‐holding protocol (1.09 ± 0.20 vs 1.81 ± 0.08 mGy, respectively; P < 0.0001). The correlation rate was higher with the breath‐holding protocol (right lung field, 41.7 ± 9.3%; left lung field, 44.2 ± 8.9% vs right lung field, 33.4 ± 6.6%; left lung field, 36.0 ± 7.1%, respectively; both lung fields, P < 0.0001). In the lower lung fields, the correlation rate was markedly different (right, 15.3% difference; left, 14.1% difference; both lung fields, P < 0.0001).ConclusionThe breath‐holding protocol resulted in high imaging success rate among patients with respiratory diseases, yielding vivid images of pulmonary perfusion.

Dual-Energy Computed Tomography of the Lung in COVID-19 Patients: Mismatch of Perfusion Defects and Pulmonary Opacities.

To evaluate contrast-enhanced dual-energy computed tomography (DECT) chest examinations regarding pulmonary perfusion patterns and pulmonary opacities in patients with confirmed COVID-19 disease. Fourteen patients with 24 DECT examinations performed between April and May 2020 were included in this retrospective study. DECT studies were assessed independently by two radiologists regarding pulmonary perfusion defects, using a Likert scale ranging from 1 to 4. Furthermore, in all imaging studies the extent of pulmonary opacities was quantified using the same rating system as for perfusion defects. The main pulmonary findings were ground glass opacities (GGO) in all 24 examinations and pulmonary consolidations in 22 examinations. The total lung scores after the addition of the scores of the single lobes showed significantly higher values of opacities compared to perfusion defects, with a median of 12 (9–18) for perfusion defects and a median of 17 (15–19) for pulmonary opacities (p = 0.002). Furthermore, mosaic perfusion patterns were found in 19 examinations in areas with and without GGO. Further studies will be necessary to investigate the pathophysiological background of GGO with maintained perfusion compared to GGO with reduced perfusion, especially regarding long-term lung damage and prognosis.

COVID-19: What Iodine Maps From Perfusion CT can reveal\u2014A Prospective Cohort Study

BackgroundSubtraction CT angiography (sCTA) is a technique used to evaluate pulmonary perfusion based on iodine distribution maps. The aim of this study is to assess lung perfusion changes with sCTA seen in patients with COVID-19 pneumonia and correlate them with clinical outcomes.Material and methodsA prospective cohort study was carried out with 45 RT-PCR-confirmed COVID-19 patients that required hospitalization at three different hospitals, between April and May 2020. In all cases, a basic clinical and demographic profile was obtained. Lung perfusion was assessed using sCTA. Evaluated imaging features included: Pattern predominance of injured lung parenchyma in both lungs (ground-glass opacities, consolidation and mixed pattern) and anatomical extension; predominant type of perfusion abnormality (increased perfusion or hypoperfusion), perfusion abnormality distribution (focal or diffuse), extension of perfusion abnormalities (mild, moderate and severe involvement); presence of vascular dilatation and vascular tortuosity. All participants were followed-up until hospital discharge searching for the development of any of the study endpoints. These endpoints included intensive-care unit (ICU) admission, initiation of invasive mechanical ventilation (IMV) and death.ResultsForty-one patients (55.2 ± 16.5 years, 22 men) with RT-PCR-confirmed SARS-CoV-2 infection and an interpretable iodine map were included. Patients with perfusion anomalies on sCTA in morphologically normal lung parenchyma showed lower Pa/Fi values (294 ± 111.3 vs. 397 ± 37.7, p = 0.035), and higher D-dimer levels (1156 ± 1018 vs. 378 ± 60.2, p < 0.01). The main common patterns seen in lung CT scans were ground-glass opacities, mixed pattern with predominant ground-glass opacities and mixed pattern with predominant consolidation in 56.1%, 24.4% and 19.5% respectively. Perfusion abnormalities were common (36 patients, 87.8%), mainly hypoperfusion in areas of apparently healthy lung. Patients with severe hypoperfusion in areas of apparently healthy lung parenchyma had an increased probability of being admitted to ICU and to initiate IMV (HR of 11.9 (95% CI 1.55–91.9) and HR 7.8 (95% CI 1.05–61.1), respectively).ConclusionPerfusion abnormalities evidenced in iodine maps obtained by sCTA are associated with increased admission to ICU and initiation of IMV in COVID-19 patients.

PAY ATTENTION! AN UNUSUAL CASE OF DYSPNEA

SESSION TITLE: Medical Student/Resident Cardiothoracic Surgery Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Platypnea-orthodeoxia is an uncommon syndrome characterized by dyspnea and hypoxemia in upright position that improves with recumbent position. It can occur due to intracardiac shunts, pulmonary arteriovenous shunts and ventilation perfusion mismatch. We present a unique and rare cause of platypnea-orthodeoxia syndrome. CASE PRESENTATION: A 68 years old man with history of coronary artery disease and COPD presented with acute onset chest pain and associated difficulty breathing. Patient did have several months’ history of exertional dyspnea which did not improve with rest this time. On presentation, patient was noted to be hypoxic with oxygen saturation of 88% and ABG showed PH 7.41, PaO2 47 mmHg and PaCO2 22.4 mmHg. Oxygen saturation improved to 94% with 3L of supplemental oxygen. EKG and troponin were unremarkable. CT PE was unremarkable for pulmonary embolism as well. IV heparin drip was started for suspected unstable angina and patient underwent cardiac catheterization that revealed non-obstructive coronary artery disease. Echocardiography showed ejection fraction of 55-60% with mild mitral and tricuspid regurgitationDuring the course of hospitalization, patient was noted to have intermittent positional hypoxemia. He had normal resting saturation on 2 L of oxygen which dropped to 88% sitting upright and dropped to 84% on 2 L of oxygen upon raising both arms. Platypnea-orthodeoxia syndrome was strongly suspected with possible intra-cardiac or intrapulmonary shunt. Meanwhile, CT chest was unremarkable for interstitial lung disease. Right heart catheterization revealed normal right atrial RA (68.9%) and pulmonary arterial PA (68.3%) saturation at rest but reduced RA (42.5%) and PA (43.2%) saturation with sitting up. Echocardiography with bubble study showed right-to-left shunting and trans-esophageal echocardiography revealed a small 0.5 cm atrial septal defect (ASD) with bidirectional shunting. Patient was diagnosed with Platypnea-orthodeoxia syndrome secondary to ASD. He was discharged home on supplemental oxygen and outpatient follow-up for ASD closure. DISCUSSION: Platypnea-orthodeoxia is a rare syndrome. Patent foramen ovale is the most common cardiac cause of platypnea-orthodeoxia syndrome followed by ASD. Transesophageal echocardiography is the best test to diagnose atrial septal defect but it is important to rule out pulmonary causes of platypnea-orthodeoxia syndrome as well. ASD is successfully treated with percutaneous closure and prognosis of is good after correction of the defect. CONCLUSIONS: Platypnea-orthodeoxia syndrome is rare syndrome but it can be easily recognized with careful history and physical examination. Reference #1: Henkin S, Negrotto S, Pollak PM, Cullen MW, O'Cochlain DF, Wright RS. Platypnea-Orthodeoxia Syndrome: Diagnostic Challenge and the Importance of Heightened Clinical Suspicion. Tex Heart Inst J. 2015;42(5):498-501. Published 2015 Oct 1. doi:10.14503/THIJ-14-4596 Reference #2: Kazawa S, Enomoto T, Suzuki N, et al. Platypnea-orthodeoxia Syndrome in a Patient with an Atrial Septal Defect: The Diagnosis and Choice of Treatment. Intern Med. 2017;56(2):169-173. doi:10.2169/internalmedicine.56.7728 Reference #3: PLATYPNEA ORTHODEOXIA SYNDROME: A RARE COMPLICATION OF IATROGENIC ATRIAL SEPTAL DEFECT. Bharat Avirneni, Christopher Rosse, Joseph Choo, Kalpan Desai. J Am Coll Cardiol. 2020 Mar, 75 (11 Supplement 1) 2799. DISCLOSURES: No relevant relationships by Muhammad Aamir, source=Web Response No relevant relationships by Muhammad Afzal, source=Web Response No relevant relationships by Saleha Dar, source=Web Response

New Technology for the Use of Inhaled Nitric Oxide to Protect the Heart and Lungs during Operations with Cardiopulmonary Bypass.

The aim of the study was to evaluate the effectiveness of a new technology for the use of inhaled nitric oxide (NO) for the heart and lung protection during operations with cardiopulmonary bypass (СРВ).Materials and Methods.The study included 90 patients who underwent heart valve surgery and combined procedures under CPB and pharmacological cardioplegia. Three groups were created: group 1 (control, n=30); group 2 (n=30) — NO inhalation (20 ppm) was conducted traditionally, that is, before and after CPB; group 3 (n=30) — NO inhalation was performed using a new technology — during the entire operation, with pulmonary artery perfusion and lung ventilation performed during CPB. Troponin I (cTn I) level, changes in the pulmonary function parameters, and clinical indicators were studied.Results.Statistically significant lower levels of postoperative cTn I were registered in the patients of groups 2 and 3, at the same time, the levels were significantly lower in group 3 compared to group 2. The patients in group 1 (standardized anesthesia protocol) demonstrated an increase in the alveolar-arterial oxygen difference, an increase in intrapulmonary shunting, a decrease in blood oxygenation, and static lung compliance after СРВ. In both cases, NO inhalation retained the values of lung compliance and pulmonary oxygenating function after CPB, and in the patients of group 3, it also significantly reduced intrapulmonary shunting and alveolar-arterial difference after CPB. NO inhalation allowed a statistically significant decrease in the incidence of pulmonary dysfunction, acute respiratory failure, as well as the time of respiratory support in the ICU.Conclusion.The developed technology for the use of inhaled NO in surgery with CPB provides a clinically marked protective effect on the heart and lungs. The effectiveness of the protective action of NO depends on the duration of its administration and is most pronounced when used during the entire operation, including CPB time.

Diagnostic Value of the Dual Source CT Dual Energy Pulmonary Perfusion Imaging for Pulmonary Embolism

Objective To assess the diagnostic value of dual energy pulmonary perfusion imaging(DEPI)for pulmonary embolism.Methods The clinical data of 87 patients with suspected pulmonary embolism who had received DEPI between August 2017 and July 2018 in Jiaxing Second Hospital were retrospectively analyzed.With the findings of CT pulmonary angiography(CTPA)as the reference standard and with patients and pulmonary lobes as evaluation units,respectively,a diagnostic test was performed to calculate the diagnostic coincidence rate,sensitivity,specificity,positive predictive value,negative predictive value,Youden index,positive likelihood ratio,negative likelihood ratio,and Kappa coefficient value for the diagnosis of DEPI and CTPA.Results The coincidence rate,sensitivity,specificity,positive predictive value,negative predictive value,Youden index,positive likelihood ratio,and negative likelihood ratio were 85.06%,88.41%,72.22%,92.42%,61.90%,0.61,3.18,and 0.16,respectively,when applying the patients as evaluation units.When the pulmonary lobes were invoked as evaluation units,the above-mentioned indexes were 89.57%,76.80%,96.82%,93.20%,88.02%,0.74,24.15,and 0.24,respectively.The diagnostic results of DEPI and CTPA had a good and excellent consistency,respectively(Kappa value=0.571,0.765).Conclusions DEPI has high accuracy,sensitivity,and specificity in the detection of pulmonary embolism.The combination of DEPI with CTPA can simultaneously obtain the anatomical structure and functional information images,greatly improving the diagnostic accuracy for pulmonary embolism.Thus,it can be used as the preferred examination for patients with clinically suspected pulmonary embolism.

THE POWER OF PERFUSION: A UNIQUE PRESENTATION OF UNILATERAL PULMONARY EDEMA

SESSION TITLE: Medical Student/Resident Transplantation Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Unilateral pulmonary edema in lung transplant is a unique entity that requires a broad differential including evaluation for infection, acute graft rejection, cardiovascular, and pulmonary vascular pathology. CASE PRESENTATION: A 74-year-old male with history of right single lung transplant in 2011 for severe emphysema, chronic kidney injury, and avascular necrosis of the hip underwent uncomplicated left total hip arthroplasty. On post-operative day 1, he developed acute hypoxemic respiratory failure requiring high-flow nasal cannula. He was otherwise afebrile and normotensive on arrival. Physical examination revealed crackles in the right lung and bedside lung ultrasound demonstrated diffuse unilateral B-lines in the right lung. Labs were unremarkable other than NT-pro BNP level of 2200 pg/mL. ECG was unremarkable, and chest x-ray showed diffuse interstitial airspace opacities on the right. He was started on antibiotics for possible aspiration pneumonia. Review of post-operative fluid balanced revealed he was net positive 3.5 L since the admission. Ventilation and perfusion scan from 2 months prior demonstrated dominant right lung perfusion at 91% compared to 9% to the left lung. Echocardiogram showed ejection fraction of 54% without significant valvular pathology. Overall, his presentation was thought secondary to volume overload presenting as unilateral pulmonary edema secondary to selective perfusion of his transplanted lung. Diuretic therapy was started, and over the next day, the patient was weaned off supplemental oxygen entirely. The following day, his antibiotics and diuresis were discontinued and his unilateral pulmonary edema had completely resolved (Figure 1). DISCUSSION: The differential diagnoses for single lung interstitial infiltrates include infection, pneumonitis, and pulmonary edema from acute mitral regurgitation, pulmonary artery hypoplasia, or pulmonary vein stenosis (reference 1-2). Additionally, lung transplant patients require thorough evaluation for infection and acute graft rejection, which necessitate an invasive procedure, such as bronchoscopy with transbronchial biopsy. This case demonstrates the importance of the considering vascular etiologies, as it avoided an unnecessary invasive procedure. A case study by Akindipe et al. described 3 cases of single lung transplant patients presenting with unilateral pulmonary edema (reference 3). Two of these cases occurred in the context of acute renal failure and the other after acute mitral regurgitation. In our patient, no evidence of acute on chronic renal injury, coronary disease, or valve pathology was noted. CONCLUSIONS: We believe this is a unique, but often unrecognized case of unilateral pulmonary edema in a single lung transplant patient with asymmetric pulmonary perfusion. Reference #1: Attias David et al. Prevalence, Characteristics, and Outcomes of Patients Presenting With Cardiogenic Unilateral Pulmonary Edema. Circulation 122, 1109–1115 (2010). Reference #2: Handagala, R., Ralapanawa, U. & Jayalath, T. Unilateral pulmonary edema: a case report and review of the literature. J. Med. Case Reports 12, (2018). Reference #3: Akindipe, O., Fernandez-Bussy, S., Staples, E. D. & Baz, M. Late Unilateral Pulmonary Edema in Single Lung Transplant Recipients. J. Heart Lung Transplant. 27, 1055–1058 (2008). DISCLOSURES: No relevant relationships by Samuel Falde, source=Web Response No relevant relationships by Hiroshi Sekiguchi, source=Web Response No relevant relationships by Yosuf Subat, source=Web Response

Physiological mechanism and spatial distribution of increased alveolar dead-space in early ARDS: An experimental study.

We aimed to investigate the physiological mechanism and spatial distribution of increased physiological dead-space, an early marker of ARDS mortality, in the initial stages of ARDS. We hypothesized that: increased dead-space results from the spatial redistribution of pulmonary perfusion, not ventilation; such redistribution is not related to thromboembolism (ie, areas with perfusion=0 and infinite ventilation-perfusion ratio, ), but rather to moderate shifts of perfusion increasing in non-dependent regions. Five healthy anesthetized sheep received protective ventilation for 20hours, while endotoxin was continuously infused. Maps of voxel-level lung ventilation, perfusion, , CO2 partial pressures, and alveolar dead-space fraction were estimated from positron emission tomography at baseline and 20hours. Alveolar dead-space fraction increased during the 20hours (+0.05, P=.031), mainly in non-dependent regions (+0.03, P=.031). This was mediated by perfusion redistribution away from non-dependent regions (-5.9%, P=.031), while the spatial distribution of ventilation did not change, resulting in increased in non-dependent regions. The increased alveolar dead-space derived mostly from areas with intermediate (0.5≤ ≤10), not areas of nearly "complete" dead-space ( >10). In this early ARDS model, increases in alveolar dead-space occur within 20hours due to the regional redistribution of perfusion and not ventilation. This moderate redistribution suggests changes in the interplay between active and passive perfusion redistribution mechanisms (including hypoxic vasoconstriction and gravitational effects), not the appearance of thromboembolism. Hence, the association between mortality and increased dead-space possibly arises from the former, reflecting gas-exchange inefficiency due to perfusion heterogeneity. Such heterogeneity results from the injury and exhaustion of compensatory mechanisms for perfusion redistribution.

Perioperative CTEPH patient monitoring with 2D phase-contrast MRI reflects clinical, cardiac and pulmonary perfusion changes after pulmonary endarterectomy.

Magnetic resonance imaging (MRI) is an emerging tool for diagnosis and treatment monitoring of chronic thromboembolic pulmonary hypertension (CTEPH). The current study aims to identify central pulmonary arterial hemodynamic parameters that reflect clinical, cardiac and pulmonary changes after PEA. 31 CTEPH patients, who underwent PEA and received pre- and postoperative MRI, were analyzed retrospectively. Central pulmonary arterial blood flow, lung perfusion and right heart function data were derived from MRI. Mean pulmonary arterial pressure (mPAP) and 5-month follow-up six-minute walk-distance (6MWD) were assessed. After PEA, mPAP decreased significantly and patients achieved a higher 6MWD. Central pulmonary arterial blood flow velocities, pulmonary blood flow (PBF) and right ventricular function increased significantly. Two-dimensional (2D) phase-contrast (PC) MRI-derived average mean velocity, maximum mean velocity and deceleration volume changes after PEA correlated with changes of 6MWD and right heart ejection fraction (RVEF). Deceleration volume is a novel 2D PC MRI parameter showing further correlation with PBF changes. In conclusion, 2D PC MRI-derived main pulmonary hemodynamic changes reflect changes of RVEF, PBF and 5-month follow-up 6MWD and may be used for future CTEPH patient monitoring after PEA.

Neonatal lymphatic flow disorders: impact of lymphatic imaging and interventions on outcomes.

We conducted a retrospective study of 35 neonates with pulmonary lymphatic abnormalities at our institution who underwent lymphatic evaluation between December 2015 and September 2018. Patients with only pulmonary lymphatic perfusion syndrome were classified as NCTx and those with multiple flow abnormalities were classified as CLFD. Demographics, clinical characteristics, and outcomes were compared using t-tests/Wilcoxon rank sum tests and Fisher's exact tests. All 35 patients had intranodal MR lymphangiography and 14 (40%) also had conventional fluoroscopic lymphangiography. Fifteen (42.8%) patients were diagnosed with NCTx and 20 (57.1%) were diagnosed with CLFD. Thirty-four (97.1%) patients had pleural effusions. None of the NCTx group had ascites, anasarca, or dermal backflow compared to 17 (85%) (p < 0.001), 8 (42.1%) (p: 0.004), and 20 (100%) (p < 0.001) of the CLFD group, respectively. In the NCTx group, 11 (73.3%) had ethiodized oil embolization and 4 (26.7%) received conservative therapy. Ten (50%) of the CLFD patients had an intervention; of those, two (10%) had ethiodized oil-only embolization. Eight had non-ethiodized oil embolizations (two (25%) had embolization with glue, three (37.5%) underwent surgical lymphovenous anastomosis, two (25%) underwent thoracic duct (TD) externalization, and one (12.5%) had a non-TD lymphatic channel drain placed). Complete resolution of pleural effusions was achieved in all 15 NCTx patients, whereas 9 (45%) of 20 CLFD patients had resolution of chylothorax (p: 0.001). Establishing a diagnosis of NCTx or CLFD is paramount in selecting treatment options and providing prognostic information. Development of lymphatic interventions represents a paradigm shift in our understanding of neonatal lymphatic flow disorders and may be associated with improved survival.