SUSIMEIRE GOMES

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LIM/09 - Laboratório de Pneumologia, Hospital das Clínicas, Faculdade de Medicina

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  • article 1 Citação(ões) na Scopus
  • article 20 Citação(ões) na Scopus
    Driving pressure and long-term outcomes in moderate/severe acute respiratory distress syndrome
    (2018) TOUFEN JUNIOR, Carlos; SANTIAGO, Roberta R. De Santis; HIROTA, Adriana S.; CARVALHO, Alysson Roncally S.; GOMES, Susimeire; AMATO, Marcelo Brito Passos; CARVALHO, Carlos Roberto Ribeiro
    BackgroundAcute respiratory distress syndrome (ARDS) patients may present impaired in lung function and structure after hospital discharge that may be related to mechanical ventilation strategy. The aim of this study was to evaluate the association between functional and structural lung impairment, N-terminal-peptide type III procollagen (NT-PCP-III) and driving pressure during protective mechanical ventilation. It was a secondary analysis of data from randomized controlled trial that included patients with moderate/severe ARDS with at least one follow-up visit performed. We obtained serial measurements of plasma NT-PCP-III levels. Whole-lung computed tomography analysis and pulmonary function test were performed at 1 and 6months of follow-up. A health-related quality of life survey after 6months was also performed.ResultsThirty-three patients were enrolled, and 21 patients survived after 6months. In extubation day an association between driving pressure and NT-PCP-III was observed. At 1 and 6months forced vital capacity (FVC) was negatively correlated to driving pressure (p<0.01). At 6months driving pressure was associated with lower FVC independently on tidal volume, plateau pressure and baseline static respiratory compliance after adjustments (r(2)=0.51, p=0.02). There was a significant correlation between driving pressure and lung densities and nonaerated/poorly aerated lung volume after 6months. Driving pressure was also related to general health domain of SF-36 at 6months.ConclusionEven in patients ventilated with protective tidal volume, higher driving pressure is associated with worse long-term pulmonary function and structure.
  • article 34 Citação(ões) na Scopus
    High Pleural Pressure Prevents Alveolar Overdistension and Hemodynamic Collapse in Acute Respiratory Distress Syndrome with Class III Obesity A Clinical Trial
    (2021) SANTIAGO, Roberta De Santis; DROGHI, Maddalena Teggia; FUMAGALLI, Jacopo; MARRAZZO, Francesco; FLORIO, Gaetano; GRASSI, Luigi G.; GOMES, Susimeire; MORAIS, Caio C. A.; RAMOS, Ozires P. S.; BOTTIROLI, Maurizio; PINCIROLI, Riccardo; IMBER, David A.; BAGCHI, Aranya; SHELTON, Kenneth; SONNY, Abraham; BITTNER, Edward A.; AMATO, Marcelo B. P.; KACMAREK, Robert M.; BERRA, Lorenzo
    Rationale: Obesity is characterized by elevated pleural pressure (Ppl) and worsening atelectasis during mechanical ventilation in patients with acute respiratory distress syndrome (ARDS). Objectives: To determine the effects of a lung recruitment maneuver (LRM) in the presence of elevated Ppl on hemodynamics, left and right ventricular pressure, and pulmonary vascular resistance. We hypothesized that elevated Ppl protects the cardiovascular system against high airway pressure and prevents lung overdistension. Methods: First, an interventional crossover trial in adult subjects with ARDS and a body mass index >= 35 kg/m(2) (n = 21) was performed to explore the hemodynamic consequences of the LRM. Second, cardiovascular function was studied during low and high positive end-expiratory pressure (PEEP) in a model of swine with ARDS and high Ppl (n = 9) versus healthy swine with normal Ppl (n = 6). Measurements and Main Results: Subjects with ARDS and obesity (body mass index = 57612 kg/m(2)) after LRM required an increase in PEEP of 8 (95% confidence interval [95% CI], 7-10) cm H2O above traditional ARDS Network settings to improve lung function, oxygenation and V/Q matching, without impairment of hemodynamics or right heart function. ARDS swine with high Ppl demonstrated unchanged transmural left ventricular pressure and systemic blood pressure after the LRM protocol. Pulmonary arterial hypertension decreased (8 [95% CI, 13-4] mm Hg), as did vascular resistance (1.5 [95% CI, 2.2-0.9] Wood units) and transmural right ventricular pressure (10 [95% CI, 15-6] mm Hg) during exhalation. LRM and PEEP decreased pulmonary vascular resistance and normalized the V/Q ratio. Conclusions: High airway pressure is required to recruit lung atelectasis in patients with ARDS and class III obesity but causes minimal overdistension. In addition, patients with ARDS and class III obesity hemodynamically tolerate LRM with high airway pressure.
  • 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.
  • article 25 Citação(ões) na Scopus
    Effects of different mechanical ventilation strategies on the mucociliary system
    (2011) PICCIN, Vivien S.; CALCIOLARI, Christiane; YOSHIZAKI, Kelly; GOMES, Susimeire; ALBERTINI-YAGI, Claudia; DOLHNIKOFF, Marisa; MACCHIONE, Mariangela; CALDINI, Elia G.; SALDIVA, Paulo H. N.; NEGRI, Elnara M.
    To evaluate the effects of different mechanical ventilation (MV) strategies on the mucociliary system. Experimental study. Twenty-seven male New Zealand rabbits. After anesthesia, animals were tracheotomized and ventilated with standard ventilation [tidal volume (Vt) 8 ml/kg, positive end expiratory pressure (PEEP) 5 cmH(2)O, flow 3 L/min, FiO(2) 0.4] for 30 min. Next, animals were randomized into three groups and ventilated for 3 h with low volume (LV): Vt 8 ml/kg, PEEP 5 cmH(2)O, flow 3 L/min (n = 6); high volume (HV): Vt 16 ml/kg, PEEP 5 cmH(2)O, flow 5 L/min (n = 7); or high pressure (HP): Ppeak 30 cmH(2)O, PEEP 12 cmH(2)O (n = 8). Six animals (controls) were ventilated for 10 min with standard ventilation. Vital signals, blood lactate, and respiratory system mechanics were verified. Tracheal tissue was collected before and after MV. Lung and tracheal tissue sections were stained to analyze inflammation and mucosubstances by the point-counting method. Electron microscopy verified tracheal cell ultrastructure. In situ tracheal ciliary beating frequency (CBF), determined using a videoscopic technique, and tracheal mucociliary transport (TMCT), assessed by stereoscopic microscope, were evaluated before and after MV. Respiratory compliance decreased in the HP group. The HV and HP groups showed higher lactate levels after MV. Macroscopy showed areas of atelectasis and congestion on HV and HP lungs. Lung inflammatory infiltrate increased in all ventilated groups. Compared to the control, ventilated animals also showed a reduction of total and acid mucus on tracheal epithelium. Under electron microscopy, injury was observed in the ciliated cells of the HP group. CBF decreased significantly after MV only in the HP group. TMCT did not change significantly in the ventilated groups. Different MV strategies induce not only distal lung alterations but also morphological and physiological tracheal alterations leading to mucociliary system dysfunction.
  • article 79 Citação(ões) na Scopus
    Transpulmonary Pressure Describes Lung Morphology During Decremental Positive End-Expiratory Pressure Trials in Obesity
    (2017) FUMAGALLI, Jacopo; BERRA, Lorenzo; ZHANG, Changsheng; PIRRONE, Massimiliano; SANTIAGO, Roberta R. De Santis; GOMES, Susimeire; MAGNI, Federico; SANTOS, Glaucia A. B. dos; BENNETT, Desmond; TORSANI, Vinicius; FISHER, Daniel; MORAIS, Caio; AMATO, Marcelo B. P.; KACMAREK, Robert M.
    Objectives: Atelectasis develops in critically ill obese patients when undergoing mechanical ventilation due to increased pleural pressure. The current study aimed to determine the relationship between transpulmonary pressure, lung mechanics, and lung morphology and to quantify the benefits of a decremental positive end-expiratory pressure trial preceded by a recruitment maneuver. Design: Prospective, crossover, nonrandomized interventional study. Setting: Medical and Surgical Intensive Care Units at Massachusetts General Hospital (Boston, MA) and University Animal Research Laboratory (Sao Paulo, Brazil). Patients/Subjects: Critically ill obese patients with acute respiratory failure and anesthetized swine. Interventions: Clinical data from 16 mechanically ventilated critically ill obese patients were analyzed. An animal model of obesity with reversible atelectasis was developed by placing fluid filled bags on the abdomen to describe changes of lung mechanics, lung morphology, and pulmonary hemodynamics in 10 swine. Measurements and Main Results: In obese patients (body mass index, 48 +/- 11 kg/m(2)), 21.7 +/- 3.7 cm H2O of positive end-expiratory pressure resulted in the lowest elastance of the respiratory system (18.6 +/- 6.1 cm H2O/L) after a recruitment maneuver and decremental positive end-expiratory pressure and corresponded to a positive (2.1 +/- 2.2 cm H2O) end-expiratory transpulmonary pressure. Ventilation at lowest elastance positive end-expiratory pressure preceded by a recruitment maneuver restored end-expiratory lung volume (30.4 +/- 9.1 mL/kg ideal body weight) and oxygenation (273.4 +/- 72.1 mm Hg). In the swine model, lung collapse and intratidal recruitment/derecruitment occurred when the positive end-expiratory transpulmonary pressure decreased below 2-4 cm H2O. After the development of atelectasis, a decremental positive end-expiratory pressure trial preceded by lung recruitment identified the positive end-expiratory pressure level (17.4 +/- 2.1 cm H2O) needed to restore poorly and nonaerated lung tissue, reestablishing lung elastance and oxygenation while avoiding increased pulmonary vascular resistance. Conclusions: In obesity, low-to-negative values of transpulmonary pressure predict lung collapse and intratidal recruitment/derecruitment. A decremental positive end-expiratory pressure trial preceded by a recruitment maneuver reverses atelectasis, improves lung mechanics, distribution of ventilation and oxygenation, and does not increase pulmonary vascular resistance.
  • article 2 Citação(ões) na Scopus
    Physiologic effects of alveolar recruitment and inspiratory pauses during moderately-high-frequency ventilation delivered by a conventional ventilator in a severe lung injury model
    (2017) CORDIOLI, Ricardo Luiz; COSTA, Eduardo Leite Vieira; AZEVEDO, Luciano Cesar Pontes; GOMES, Susimeire; AMATO, Marcelo Britto Passos; PARK, Marcelo
    Background and aims To investigate whether performing alveolar recruitment or adding inspiratory pauses could promote physiologic benefits (VT) during moderately-high-frequency positive pressure ventilation (MHFPPV) delivered by a conventional ventilator in a porcine model of severe acute respiratory distress syndrome (ARDS). Methods Prospective experimental laboratory study with eight pigs. Induction of acute lung injury with sequential pulmonary lavages and injurious ventilation was initially performed. Then, animals were ventilated on a conventional mechanical ventilator with a respiratory rate (RR) = 60 breaths/minute and PEEP titrated according to ARDS Network table. The first two steps consisted of a randomized order of inspiratory pauses of 10 and 30% of inspiratory time. In final step, we removed the inspiratory pause and titrated PEEP, after lung recruitment, with the aid of electrical impedance tomography. At each step, PaCO2 was allowed to stabilize between 57-63 mmHg for 30 minutes. Results The step with RR of 60 after lung recruitment had the highest PEEP when compared with all other steps (17 [16,19] vs 14 [10, 17]cmH(2)O), but had lower driving pressures (13 [13,11] vs 16 [14, 17]cmH(2)O), higher P/F ratios (212 [191,243] vs 141 [105, 184] mmHg), lower shunt (23 [20, 23] vs 32 [27, 49]%), lower dead space ventilation (10 [0, 15] vs 30 [20, 37]%), and a more homogeneous alveolar ventilation distribution. There were no detrimental effects in terms of lung mechanics, hemodynamics, or gas exchange. Neither the addition of inspiratory pauses or the alveolar recruitment maneuver followed by decremental PEEP titration resulted in further reductions in VT. Conclusions During MHFPPV set with RR of 60 bpm delivered by a conventional ventilator in severe ARDS swine model, neither the inspiratory pauses or PEEP titration after recruitment maneuver allowed reduction of VT significantly, however the last strategy decreased driving pressures and improved both shunt and dead space.
  • article 111 Citação(ões) na Scopus
    Volume-controlled Ventilation Does Not Prevent Injurious Inflation during Spontaneous Effort
    (2017) YOSHIDA, Takeshi; NAKAHASHI, Susumu; NAKAMURA, Maria Aparecida Miyuki; KOYAMA, Yukiko; ROLDAN, Rollin; TORSANI, Vinicius; SANTIS, Roberta R. De; GOMES, Susimeire; UCHIYAMA, Akinori; AMATO, Marcelo B. P.; KAVANAGH, Brian P.; FUJINO, Yuji
    Rationale: Spontaneous breathing during mechanical ventilation increases transpulmonary pressure and VT, and worsens lung injury. Intuitively, controlling VT and transpulmonary pressure might limit injury caused by added spontaneous effort. Objectives: To test the hypothesis that, during spontaneous effort in injured lungs, limitation of VT and transpulmonary pressure by volume-controlled ventilation results in less injurious patterns of inflation. Methods: Dynamic computed tomography was used to determine patterns of regional inflation in rabbits with injured lungs during volume-controlled or pressure-controlled ventilation. Transpulmonary pressure was estimated by using esophageal balloon manometry [PL(es)] with and without spontaneous effort. Local dependent lung stress was estimated as the swing (inspiratory change) in transpulmonary pressure measured by intrapleural manometry in dependent lung and was compared with the swing in PL(es). Electrical impedance tomography was performed to evaluate the inflation pattern in a larger animal (pig) and in a patient with acute respiratory distress syndrome. Measurements and Main Results: Spontaneous breathing in injured lungs increased PL(es) during pressure-controlled (but not volume-controlled) ventilation, but the pattern of dependent lung inflation was the same in both modes. In volume-controlled ventilation, spontaneous effort caused greater inflation and tidal recruitment of dorsal regions (greater than twofold) compared with during muscle paralysis, despite the same VT and PL(es). This was caused by higher local dependent lung stress (measured by intrapleural manometry). In injured lungs, esophageal manometry underestimated local dependent pleural pressure changes during spontaneous effort. Conclusions: Limitation of VT and PL(es) by volume-controlled ventilation could not eliminate harm caused by spontaneous breathing unless the level of spontaneous effort was lowered and local dependent lung stress was reduced.
  • article 367 Citação(ões) na Scopus
    Spontaneous Effort Causes Occult Pendelluft during Mechanical Ventilation
    (2013) YOSHIDA, Takeshi; TORSANI, Vinicius; GOMES, Susimeire; SANTIS, Roberta R. De; BERALDO, Marcelo A.; COSTA, Eduardo L. V.; TUCCI, Mauro R.; ZIN, Walter A.; KAVANAGH, Brian P.; AMATO, Marcelo B. P.
    Rationale: In normal lungs, local changes in pleural pressure (P-pl) are generalized over the whole pleural surface. However, in a patient with injured lungs, we observed (using electrical impedance tomography) a pendelluft phenomenon (movement of air within the lung from nondependent to dependent regions without change in tidal volume) that was caused by spontaneous breathing during mechanical ventilation. Objectives: To test the hypotheses that in injured lungs negative P-pl generated by diaphragm contraction has localized effects (in dependent regions) that are not uniformly transmitted, and that such localized changes in P-pl cause pendelluft. Methods: We used electrical impedance tomography and dynamic computed tomography (CT) to analyze regional inflation in anesthetized pigs with lung injury. Changes in local P-pl were measured in nondependent versus dependent regions using intrabronchial balloon catheters. The airway pressure needed to achieve comparable dependent lung inflation during paralysis versus spontaneous breathing was estimated. Measurements and Main Results: In all animals, spontaneous breathing caused pendelluft during early inflation, which was associated with more negative local P-pl in dependent regions versus nondependent regions (-13.0 +/- 4.0 vs. -6.4 +/- 3.8 cm H2O; P < 0.05). Dynamic CT confirmed pendelluft, which occurred despite limitation of tidal volume to less than 6 ml/kg. Comparable inflation of dependent lung during paralysis required almost threefold greater driving pressure (and tidal volume) versus spontaneous breathing (28.0 +/- 0.5 vs. 10.3 +/- 0.6 cm H2O, P < 0.01; 14.8 +/- 4.6 vs. 5.8 +/- 1.6 ml/kg, P < 0.05). Conclusions: Spontaneous breathing effort during mechanical ventilation causes unsuspected overstretch of dependent lung during early inflation (associated with reciprocal deflation of nondependent lung). Even when not increasing tidal volume, strong spontaneous effort may potentially enhance lung damage.