EDUARDO LEITE VIEIRA COSTA

(Fonte: Lattes)
Índice h a partir de 2011
26
Lattes
ResearcherID
ORCID
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/09 - Laboratório de Pneumologia, Hospital das Clínicas, Faculdade de Medicina

Filtros

Mostrar mais
Limpar filtros

Configurações

Autor e Coautores FMUSP-HC Normalizados: MAURO ROBERTO TUCCI ×

Resultados de Busca

Agora exibindo 1 - 10 de 22
  • bookPart 0 Citação(ões) na Scopus
    Noninvasive ventilation interface: Influence on patient-ventilator interaction
    (2020) TUCCI, M. R.; COSTA, E. L. V.; FERREIRA, J. C.; NAKAMURA, M. A. M.; SOUSA, M. L. de Araújo
    Noninvasive ventilation (NIV) is an efficient treatment for acute respiratory failure (ARF), especially for hypercapnic patients and those with congestive heart failure. In patients at high risk of extubation failure, NIV can also be used prophylactically to avoid reintubation. Unfortunately, NIV failure can occur in up to 40% of patients, half of the time due to issues associated with the interface. In this chapter, we discuss the performance of the NIV interfaces in adult patients with ARF, the factors associated with NIV failures and strategies to avoid interface problems. We discuss the use of different types of interface, including the oronasal mask, total-face mask, and helmet and we discuss on what conditions we favor the use of each one. Additionally, we detail the influence of the ventilator type, ventilator settings, and amount of leak on NIV tolerance. © 2020 Nova Science Publishers, Inc.
  • article 32 Citação(ões) na Scopus
    F-18-FDG Kinetics Parameters Depend on the Mechanism of Injury in Early Experimental Acute Respiratory Distress Syndrome
    (2014) PROST, Nicolas de; FENG, Yan; WELLMAN, Tyler; TUCCI, Mauro R.; COSTA, Eduardo L.; MUSCH, Guido; WINKLER, Tilo; HARRIS, R. Scott; VENEGAS, Jose G.; CHAO, Wei; MELO, Marcos F. Vidal
    PET with F-18-FDG allows for noninvasive assessment of regional lung metabolism reflective of neutrophilic inflammation. This study aimed at determining during early acute lung injury whether local F-18-FDG phosphorylation rate and volume of distribution were sensitive to the initial regional inflammatory response and whether they depended on the mechanism of injury: endotoxemia and surfactant depletion. Methods: Twelve sheep underwent homogeneous unilateral surfactant depletion (alveolar lavage) and were mechanically ventilated for 4 h (positive end-expiratory pressure, 10 cm H2O; plateau pressure, 30 cm H2O) while receiving intravenous endotoxin (lipopolysaccharide-positive [LPS+] group; n = 6) or not (lipopolysaccharide-negative group; n = 6). F-18-FDG PET emission scans were then acquired. F-18-FDG phosphorylation rate and distribution volume were calculated with a 4-compartment model. Lung tissue expression of inflammatory cytokines was measured using real-time quantitative reverse transcription polymerase chain reaction. Results: F-18-FDG uptake increased in LPS+ (P = 0.012) and in surfactant-depleted sheep (P < 0.001). These increases were topographically heterogeneous, predominantly in dependent lung regions, and without interaction between alveolar lavage and LPS. The increase of F-18-FDG uptake in the LPS+ group was related both to increases in the F-18-FDG phosphorylation rate (P < 0.05) and to distribution volume (P < 0.01). F-18-FDG distribution volume increased with infiltrating neutrophils (P < 0.001) and phosphorylation rate with the regional expression of IL-1 beta (P = 0.026), IL-8 (P = 0.011), and IL-10 (P = 0.023). Conclusion: Noninvasive F-18-FDG PET-derived parameters represent histologic and gene expression markers of early lung injury. Pulmonary metabolism assessed with F-18-FDG PET depends on the mechanism of injury and appears to be additive for endotoxemia and surfactant depletion. F-18-FDG PET may be a valuable imaging biomarker of early lung injury.
  • conferenceObject
    Regional Lung Perfusion and Tissue Density with Different Long Term Mechanical Ventilation Strategies and Endotoxemia Levels
    (2019) RIBEIRO, G. C. Motta; WINKLER, T.; TUCCI, M. R.; PROST, N. de; HASHIMOTO, S.; COSTA, E. L. V.; SANTOS, A. D.; MELO, M. F. Vidal
  • conferenceObject
    Peep Titration In Severe Acute Respiratory Distress Syndrome: Different Physiological Consequences When Guided By Electrical Impedance Tomography Versus Esophageal Pressure
    (2017) ROLDAN, R.; LIMA, C.; YOSHIDA, T.; SANTIAGO, R. R. D. S.; GOMES, S.; TUCCI, M. R.; BERALDO, M. A.; COSTA, E. L. V.; TORSANI, V.; NAKAMURA, M. A. M.; CARVALHO, C. R. R.; AMATO, M. B. P.
  • conferenceObject
    Higher Positive End-Expiratory Pressures Affect The Distribution Of Lung Inflammation During Spontaneous Breathing In An Experimental Model Of Severe Acute Respiratory Distress Syndrome
    (2017) MORAIS, C. C. A.; PLENS, G.; TUCCI, M. R.; YOSHIDA, T.; BORGES, J. B.; RAMOS, O. P.; PEREIRA, S. M.; LIMA, C. A. S.; GOMES, S.; MELO, M. Vidal; AMATO, M. B. P.; COSTA, E. L. V.
  • article 3 Citação(ões) na Scopus
    Effect of Cardiogenic Oscillations on Trigger Delay During Pressure Support Ventilation
    (2018) PLENS, Glauco M.; MORAIS, Caio C. A.; NAKAMURA, Maria A.; SOUZA, Patricia N.; AMATO, Marcelo B. P.; TUCCI, Mauro R.; V, Eduardo L. Costa
    BACKGROUND: Sensitive flow or pressure triggers are usually applied to improve ventilator response time. Conversely, too sensitive triggers can incur risk of auto-triggering, a type of asynchrony in which a breath is triggered without inspiratory muscle activity. A frequent cause of auto-triggering is cardiogenic oscillations, characterized by cyclical variations in pressure and flow waveforms caused by cardiac contractions. Our goal was to test trigger performance and capacity to abolish auto-triggering in 5 different ICU ventilators using different simulated levels of cardiogenic oscillations. METHODS: A mechanical breathing simulator was used to test 5 different ICU ventilators' trigger response time and capacity to minimize auto-triggering in conditions with 0, 0.25, 0.5, and 1 cm H2O cardiogenic oscillation. Each ventilator was evaluated until an ideal trigger was found (the most sensitive that abolished auto-triggering). When the least sensitive flow trigger was unable to avoid auto-triggering, a pressure trigger was used. We compared time delay, airway pressure drop until triggering, and work of breathing before each trigger, all at the ideal trigger level fur each cardiogenic oscillation amplitude. We also assessed the proportion of auto-triggered breaths in the whole range of trigger levels tested. RESULTS: Larger cardiogenic oscillations were associated with more frequent auto-triggering. To avoid auto-triggering, less sensitive triggers were required ( +2.51 L/min per 1 cm H2O increase in cardiogenic oscillation; 95% CI 2.26-2.76, P < .001). Time delay increased with larger cardiogenic oscillations, because less sensitive trigger levels were required to abolish auto-triggering (4.79-ms increase per 1 L/min increment on flow trigger). CONCLUSIONS: More sensitive triggers led to faster ventilator response, but also to more frequent auto-triggering. To avoid auto-triggering, less sensitive triggers were required, with consequent slower trigger response. To compare trigger performance in a scenario that more closely represents clinical practice, evaluation of the tradeoff between time delay and frequency of auto-triggering should be considered.
  • article 2 Citação(ões) na Scopus
    Inflammatory Activity in Atelectatic and Normally Aerated Regions During Early Acute Lung Injury
    (2020) HINOSHITA, Takuga; RIBEIRO, Gabriel Motta; WINKLER, Tilo; PROST, Nicolas de; TUCCI, Mauro R.; COSTA, Eduardo Leite Vieira; WELLMAN, Tyler J.; HASHIMOTO, Soshi; ZENG, Congli; CARVALHO, Alysson R.; MELO, Marcos Francisco Vidal
    Rationale and Objectives: Pulmonary atelectasis presumably promotes and facilitates lung injury. However, data are limited on its direct and remote relation to inflammation. We aimed to assess regional 2-deoxy-2-[F-18]-fluoro-D-glucose (F-18-FDG) kinetics representative of inflammation in atelectatic and normally aerated regions in models of early lung injury. Materials and Methods: We studied supine sheep in four groups: Permissive Atelectasis (n = 6)-16 hours protective tidal volume (VT) and zero positive end-expiratory pressure; Mild (n = 5) and Moderate Endotoxemia (n = 6)- 20-24 hours protective ventilation and intravenous lipopolysaccharide (Mild = 2.5 and Moderate = 10.0 ng/kg/min), and Surfactant Depletion (n = 6)-saline lung lavage and 4 hours high V-T. Measurements performed immediately after anesthesia induction served as controls (n = 8). Atelectasis was defined as regions of gas fraction <0.1 in transmission or computed tomography scans. F-18-FDG kinetics measured with positron emission tomography were analyzed with a three-compartment model. Results: F-18-FDG net uptake rate in atelectatic tissue was larger during Moderate Endotoxemia (0.0092 +/- 0.0019/min) than controls (0.0051 +/- 0.0014/min, p = 0.01). F-18-FDG phosphorylation rate in atelectatic tissue was larger in both endotoxemia groups (0.0287 +/- 0.0075/min) than controls (0.0198 +/- 0.0039/min, p = 0.05) while the F-18-FDG volume of distribution was not significantly different among groups. Additionally, normally aerated regions showed larger F-18-FDG uptake during Permissive Atelectasis (0.0031 +/- 0.0005/min, p < 0.01), Mild 0.0028 +/- 0.0006/min, p = 0.04), and Moderate Endotoxemia (0.0039 +/- 0.0005/min, p < 0.01) than controls (0.0020 +/- 0.0003/min). Conclusion: Atelectatic regions present increased metabolic activation during moderate endotoxemia mostly due to increased F-18-FDG phosphorylation, indicative of increased cellular metabolic activation. Increased F-18-FDG uptake in normally aerated regions during permissive atelectasis suggests an injurious remote effect of atelectasis even with protective tidal volumes.
  • conferenceObject
    Electrical Impedance Tomography and Ventilation Heterogeneity on a Silicosis Patient
    (2019) BEDER, T. N.; TAKIZAWA, D. B.; QUIZHPE, P. J.; MACEDO, B. R.; GARCIA, M.; TUCCI, M. R.; COSTA, E. L. V.; AMATO, M. B. P.
  • article 129 Citação(ões) na Scopus
    Spontaneous Effort During Mechanical Ventilation: Maximal Injury With Less Positive End-Expiratory Pressure
    (2016) YOSHIDA, Takeshi; ROLDAN, Rollin; BERALDO, Marcelo A.; TORSANI, Vinicius; GOMES, Susimeire; SANTIS, Roberta R. De; COSTA, Eduardo L. V.; TUCCI, Mauro R.; LIMA, Raul G.; KAVANAGH, Brian P.; AMATO, Marcelo B. P.
    Objectives: We recently described how spontaneous effort during mechanical ventilation can cause ""pendelluft,"" that is, displacement of gas from nondependent (more recruited) lung to dependent (less recruited) lung during early inspiration. Such transfer depends on the coexistence of more recruited (source) liquid-like lung regions together with less recruited (target) solid-like lung regions. Pendelluft may improve gas exchange, but because of tidal recruitment, it may also contribute to injury. We hypothesize that higher positive end-expiratory pressure levels decrease the propensity to pendelluft and that with lower positive end-expiratory pressure levels, pendelluft is associated with improved gas exchange but increased tidal recruitment. Design: Crossover design. Setting: University animal research laboratory. Subjects: Anesthetized landrace pigs. Interventions: Surfactant depletion was achieved by saline lavage in anesthetized pigs, and ventilator-induced lung injury was produced by ventilation with high tidal volume and low positive end-expiratory pressure. Ventilation was continued in each of four conditions: positive end-expiratory pressure (low or optimized positive end-expiratory pressure after recruitment) and spontaneous breathing (present or absent). Tidal recruitment was assessed using dynamic CT and regional ventilation/perfusion using electric impedance tomography. Esophageal pressure was measured using an esophageal balloon manometer. Measurements and Results: Among the four conditions, spontaneous breathing at low positive end-expiratory pressure not only caused the largest degree of pendelluft, which was associated with improved ventilation/perfusion matching and oxygenation, but also generated the greatest tidal recruitment. At low positive end-expiratory pressure, paralysis worsened oxygenation but reduced tidal recruitment. Optimized positive end-expiratory pressure decreased the magnitude of spontaneous efforts (measured by esophageal pressure) despite using less sedation, from -5.6 +/- 1.3 to -2.0 +/- 0.7 cm H2O, while concomitantly reducing pendelluft and tidal recruitment. No pendelluft was observed in the absence of spontaneous effort. Conclusions: Spontaneous effort at low positive end-expiratory pressure improved oxygenation but promoted tidal recruitment associated with pendelluft. Optimized positive end-expiratory pressure (set after lung recruitment) may reverse the harmful effects of spontaneous breathing by reducing inspiratory effort, pendelluft, and tidal recruitment.
  • article 139 Citação(ões) na Scopus
    High Positive End-Expiratory Pressure Renders Spontaneous Effort Noninjurious
    (2018) MORAIS, Caio C. A.; KOYAMA, Yukiko; YOSHIDA, Takeshi; PLENS, Glauco M.; GOMES, Susimeire; LIMA, Cristhiano A. S.; RAMOS, Ozires P. S.; PEREIRA, Sergio M.; KAWAGUCHI, Naomasa; YAMAMOTO, Hirofumi; UCHIYAMA, Akinori; BORGES, Joao B.; MELO, Marcos F. Vidal; TUCCI, Mauro R.; AMATO, Marcelo B. P.; KAVANAGH, Brian P.; COSTA, Eduardo L. V.; FUJINO, Yuji
    Rationale: In acute respiratory distress syndrome (ARDS), atelectatic solid-like lung tissue impairs transmission of negative swings in pleural pressure (Ppl) that result from diaphragmatic contraction. The localization of more negative Ppl proportionally increases dependent lung stretch by drawing gas either from other lung regions (e.g., nondependent lung [pendelluft]) or from the ventilator. Lowering the level of spontaneous effort and/or converting solid-like to fluid-like lung might render spontaneous effort noninjurious. Objectives: To determine whether spontaneous effort increases dependent lung injury, and whether such injury would be reduced by recruiting atelectatic solid-like lung with positive end-expiratory pressure (PEEP). Methods: Established models of severe ARDS (rabbit, pig) were used. Regional histology (rabbit), inflammation (positron emission tomography; pig), regional inspiratory Ppl (intrabronchial balloon manometry), and stretch (electrical impedance tomography; pig) were measured. Respiratory drive was evaluated in 11 patients with ARDS. Measurements and Main Results: Although injury during muscle paralysis was predominantly in nondependent and middle lung regions at low (vs. high) PEEP, strong inspiratory effort increased injury (indicated by positron emission tomography and histology) in dependent lung. Stronger effort (vs. muscle paralysis) caused local overstretch and greater tidal recruitment in dependent lung, where more negative Ppl was localized and greater stretch was generated. In contrast, high PEEP minimized lung injury by more uniformly distributing negative Ppl, and lowering the magnitude of spontaneous effort (i.e., deflection in esophageal pressure observed in rabbits, pigs, and patients). Conclusions: Strong effort increased dependent lung injury, where higher local lung stress and stretch was generated; effort-dependent lung injury was minimized by high PEEP in severe ARDS, which may offset need for paralysis.