Susimeire Gomes

Spontaneous Effort Causes Occult Pendelluft during Mechanical Ventilation

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.

Real-time detection of pneumothorax using electrical impedance tomography*

Objectives:Pneumothorax is a frequent complication during mechanical ventilation. Electrical impedance tomography (EIT) is a noninvasive tool that allows real-time imaging of regional ventilation. The purpose of this study was to 1) identify characteristic changes in the EIT signals associated with pneumothoraces; 2) develop and fine-tune an algorithm for their automatic detection; and 3) prospectively evaluate this algorithm for its sensitivity and specificity in detecting pneumothoraces in real time. Design:Prospective controlled laboratory animal investigation. Setting:Experimental Pulmonology Laboratory of the University of São Paulo. Subjects:Thirty-nine anesthetized mechanically ventilated supine pigs (31.0 ± 3.2 kg, mean ± sd). Interventions:In a first group of 18 animals monitored by EIT, we either injected progressive amounts of air (from 20 to 500 mL) through chest tubes or applied large positive end-expiratory pressure (PEEP) increments to simulate extreme lung overdistension. This first data set was used to calibrate an EIT-based pneumothorax detection algorithm. Subsequently, we evaluated the real-time performance of the detection algorithm in 21 additional animals (with normal or preinjured lungs), submitted to multiple ventilatory interventions or traumatic punctures of the lung. Measurements and Main Results:Primary EIT relative images were acquired online (50 images/sec) and processed according to a few imaging-analysis routines running automatically and in parallel. Pneumothoraces as small as 20 mL could be detected with a sensitivity of 100% and specificity 95% and could be easily distinguished from parenchymal overdistension induced by PEEP or recruiting maneuvers. Their location was correctly identified in all cases, with a total delay of only three respiratory cycles. Conclusions:We created an EIT-based algorithm capable of detecting early signs of pneumothoraces in high-risk situations, which also identifies its location. It requires that the pneumothorax occurs or enlarges at least minimally during the monitoring period. Such detection was operator-free and in quasi real-time, opening opportunities for improving patient safety during mechanical ventilation.

Spontaneous Effort During Mechanical Ventilation: Maximal Injury With Less Positive End-Expiratory Pressure.

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.

Volume-controlled Ventilation Does Not Prevent Injurious Inflation during Spontaneous Effort

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.

Cell Therapy for Fibrotic Interstitial Pulmonary Disease: Experimental Study

Parte superior do formulário Digite um texto ou endereço de um site ou traduza um documento. The aim of this study is to evaluate the histological changes in lung parenchyma of pigs affected by interstitial lung disease induced after the infusion of bone marrow mononuclear cells (BMMCs). Ten female swines were submitted to pulmonary fibrosis induced by a single dose of intratracheal bleomicine sulfate. Animals were arranged into two groups: Group 1: induced‐disease control and Group 2: cell therapy using BMMCs. Both groups were clinically evaluated for 180 days. High‐resolution computed tomography (HRCT) was performed at 90 and 180 days. BMMC sampling was performed in cell therapy group at 90 days. Euthanasia was performed, and samples were collected for histology and immunohistochemistry. The 90‐days HRCT demonstrated typical interstitial lesions in pulmonary parenchyma similarly to human disease. The 180‐days HRCT in Group 1 demonstrated advanced stages of the disease when compared with Group 2. Immunohistochemistry analysis suggests the presence of pre‐existent vessels and neoformed vessels as well as predominant young cells in the injured parenchyma of Group 2. Immunohistochemistry analysis suggests that cell therapy would promote a reconstructive response. Histology and HRCT analysis suggest a positive application of swine as a model for a bleomicine inducing of fibrotic interstitial pulmonary disease. Microsc. Res. Tech., 2011.

High Positive End-Expiratory Pressure Renders Spontaneous Effort Noninjurious

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.

Esophageal Manometry and Regional Transpulmonary Pressure in Lung Injury

Rationale: Esophageal manometry is the clinically available method to estimate pleural pressure, thus enabling calculation of transpulmonary pressure (PL). However, many concerns make it uncertain in which lung region esophageal manometry reflects local PL. Objectives: To determine the accuracy of esophageal pressure (Pes) and in which regions esophageal manometry reflects pleural pressure (Ppl) and PL; to assess whether lung stress in nondependent regions can be estimated at end‐inspiration from PL. Methods: In lung‐injured pigs (n = 6) and human cadavers (n = 3), Pes was measured across a range of positive end‐expiratory pressure, together with directly measured Ppl in nondependent and dependent pleural regions. All measurements were obtained with minimal nonstressed volumes in the pleural sensors and esophageal balloons. Expiratory and inspiratory PL was calculated by subtracting local Ppl or Pes from airway pressure; inspiratory PL was also estimated by subtracting Ppl (calculated from chest wall and respiratory system elastance) from the airway plateau pressure. Measurements and Main Results: In pigs and human cadavers, expiratory and inspiratory PL using Pes closely reflected values in dependent to middle lung (adjacent to the esophagus). Inspiratory PL estimated from elastance ratio reflected the directly measured nondependent values. Conclusions: These data support the use of esophageal manometry in acute respiratory distress syndrome. Assuming correct calibration, expiratory PL derived from Pes reflects PL in dependent to middle lung, where atelectasis usually predominates; inspiratory PL estimated from elastance ratio may indicate the highest level of lung stress in nondependent “baby” lung, where it is vulnerable to ventilator‐induced lung injury.

Abordagem clínica e laboratorial do bócio uninodular sólido: vantagens da determinaçäo da calcitonina sérica por métodos distintos no rastreamento do carcinoma medular de tireóide, forma esporádica

Sporadic medullary thyroid carcinoma (MTC) usually presents as a single nodule (SNT), a presentation common to other thyroid tumors. The establishment of its frequency in SNT has diagnostic and therapeutic implications, since surgery for MTC differs from other tumors. Serum calcitonin (CT), the standard marker for MTC, were measured in 60 cases of SNT (55 females, 22-75 years of age). Fine needle aspiration biopsy (FNAB) of the nodules was also performed, being 100% specific and 67% sensitive for detecting thyroid carcinomas. Sixty percent of clinically suspected malignancies were confirmed post-surgically. MTC was diagnosed by serum CT in 1 of 59 cases (1.69%), confirmed by FNAB and submitted to appropriate surgery. It accounted for 12.5% of thyroid malignancies of this group, since 6 papillary and 1 undifferentiated cases were also diagnosed. Therefore, routine serum CT measurement in SNT is a strong tool in the diagnosis and adequate surgery of MTC. Both IRMA and RIA were useful in this screening. The latter, however, can detect MTC earlier, due to its ability to measure non-monomeric forms of CT, abundant in this condition.

Physiologic effects of alveolar recruitment and inspiratory pauses during moderately-high-frequency ventilation delivered by a conventional ventilator in a severe lung injury model

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]cmH2O), but had lower driving pressures (13 [13,11] vs 16 [14, 17]cmH2O), 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.

Ischemia/reperfusion-induced lung injury prevention: many options, no choices

1. Divisão de Pneumologia, Instituto do Coração – InCor – Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo (SP) Brasil. 2. Unidade de Terapia Intensiva, A.C.Camargo Cancer Center, São Paulo (SP) Brasil. The pulmonary parenchyma is prone to injuries caused by indirect insults, such as sepsis, pancreatitis, burn, blood transfusion, bypass surgery, intoxication, and ischemia followed by reperfusion (ischemia/reperfusion injury). Approximately 20% of all cases of acute respiratory distress syndrome (an extreme case of lung injury) are the result of an indirect insult to the lung parenchyma. (1)