MAURO ROBERTO TUCCI
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
LIM/09 - Laboratório de Pneumologia, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Changes in Regional Lung Perfusion Along Time and with Different Lung Volume During Mechanical Ventilation of Supine Healthy Swine(2020) TUCCI, M. R.; RIBEIRO, B. M.; VICTOR JUNIOR, M.; MELO, J. R.; BERALDO, M.; MORAIS, C. C.; NAKAMURA, M. A.; GOMES, S.; LIMA, C.; ALCALA, G. C.; AMATO, M. B.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 AraújoNoninvasive 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.- 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. VidalPET 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. VidalconferenceObject 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.- 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. CostaBACKGROUND: 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.
- 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 VidalRationale 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.
- Cycling-off modes during pressure support ventilation: Effects on breathing pattern, patient effort, and comfort(2014) HOFF, Fabricia C.; TUCCI, Mauro R.; AMATO, Marcelo B. P.; SANTOS, Laura J.; VICTORINO, Josue A.Purpose: Expiratory asynchrony during pressure support ventilation (PSV) has been recognized as a cause of patient discomfort, increased workload, and impaired weaning process. We evaluated breathing pattern, patient comfort, and patient effort during PSV comparing 2 flow termination criteria: fixed at 5% of peak inspiratory flow vs automatic, real-time, breath-by-breath adjustment within the range of 5% to 55%. Materials and methods: Randomized crossover clinical trial. Sixteen awake patients, in the process of weaning, under PSV for more than 24 hours were subjected to 3 phases of PSV, each lasting 1 hour and using 1 of the 2 aforementioned termination criteria. Results: Effective pressure support during automatic adjustment (AA) was 12.5 +/- 3.2 cm H2O vs 12.5 +/- 3.9 cm H2O (P =. 9) with the fixed termination criterion, and external positive end-expiratory pressure was 6.2 +/- 1.8 vs 6.8 +/- 2 (P < .05). The effective termination criterion was higher during AA (31% [23-39] vs 12% [6-23]; P < .01), but without producing premature breath terminations. Pressure overshoots and alternative cycling-off were also decreased. Throughout the AA period, we observed a higher respiratory rate (24 +/- 8 breaths/min vs 19 +/- 6 breaths/min; P < .001), lower tidal volume (484 +/- 88 mL vs 518 +/- 102 mL; P b.001), and shorter inspiratory times (1.0 +/- 0.3 seconds vs 1.3 +/- 0.3 seconds; P < .001). Automatic adjustment was associated with lower airway occlusion pressure after 0.1 second (P < 0.1) (1.8 +/- 0.9 cm H2O vs 2.4 +/- 1 cm H2O; P < .01), lower pressure-time product to trigger the ventilator, and lower subjective discomfort (visual analog scale, 3.7 +/- 1.3 vs 4.5 +/- 1.2; P < .001). Conclusions: When compared with a fixed termination criterion, the use of a variable, real-time-adjusted termination criterion improved some indices of patient-ventilator synchrony, producing better breathing pattern, less discomfort, and slightly lower patient effort during PSV.
- Manual Hyperinflation: Is It Effective?(2019) TUCCI, Mauro R.; NAKAMURA, Maria A. M.; CARVALHO, Nadja C.; VOLPE, Marcia S.