Ventilator hyperinflation associated with flow bias optimization in the bronchial hygiene of mechanically ventilated patients.

BACKGROUND: Ventilation configurations are of great clinical importance for adequate outcomes in mechanically ventilated patients, and they may even be used as specific physical therapy techniques. OBJECTIVES: To compare the effectiveness of lung hyperinflation through mechanical ventilation (HMV) with HMV plus flow bias optimization regarding respiratory mechanics, hemodynamics, and volume of secretion. METHODS: Patients mechanically ventilated > 24 h were included in this randomized crossover clinical trial. The following techniques were applied: HMV alone (control group) and HMV plus flow bias optimization (intervention group). RESULTS: The 20 included patients underwent both techniques, totaling 40 collections. A total of 52 % were women, the mean age was 60.8 (SD, 15.7) years, and the mean mechanical ventilation time was 4.3 (SD, 3.0) days. The main cause of mechanical ventilation was sepsis (44 %). Expiratory flow bias in optimized HMV was higher. than conventional HMV (p < 0.001). The volume of tracheal secretions collected was higher during optimized than conventional HMV. (p = 0.012). Significant differences in peak flow occurred at the beginning of the technique and a there was a significant decrease in respiratory system resistance immediately and 30 min after applying the technique in the intervention group. CONCLUSIONS: The volume of tracheal secretions collected was higher during optimized HMV, and, HMV with flow bias optimization resulted in lower respiratory system resistance and flow peaks and produced expiratory flow bias.

The Association Between Lung Hyperinflation and Coronary Artery Disease in Smokers.

BACKGROUND: Smokers manifest varied phenotypes of pulmonary impairment. RESEARCH QUESTION: Which pulmonary phenotypes are associated with coronary artery disease (CAD) in smokers? STUDY DESIGN AND METHODS: We analyzed data from the University of Pittsburgh COPD Specialized Center for Clinically Oriented Research (SCCOR) cohort (n = 481) and the Genetic Epidemiology of COPD (COPDGene) cohort (n = 2,580). Participants were current and former smokers with > 10 pack-years of tobacco exposure. Data from the two cohorts were analyzed separately because of methodologic differences. Lung hyperinflation was assessed by plethysmography in the SCCOR cohort and by inspiratory and expiratory CT scan lung volumes in the COPDGene cohort. Subclinical CAD was assessed as the coronary artery calcium score, whereas clinical CAD was defined as a self-reported history of CAD or myocardial infarction (MI). Analyses were performed in all smokers and then repeated in those with airflow obstruction (FEV1 to FVC ratio, < 0.70). RESULTS: Pulmonary phenotypes, including airflow limitation, emphysema, lung hyperinflation, diffusion capacity, and radiographic measures of airway remodeling, showed weak to moderate correlations (r < 0.7) with each other. In multivariate models adjusted for pulmonary phenotypes and CAD risk factors, lung hyperinflation was the only phenotype associated with calcium score, history of clinical CAD, or history of MI (per 0.2 higher expiratory and inspiratory CT scan lung volume; coronary calcium: OR, 1.2; 95% CI, 1.1-1.5; P = .02; clinical CAD: OR, 1.6; 95% CI, 1.1-2.3; P = .01; and MI in COPDGene: OR, 1.7; 95% CI, 1.0-2.8; P = .05). FEV1 and emphysema were associated with increased risk of CAD (P < .05) in models adjusted for CAD risk factors; however, these associations were attenuated on adjusting for lung hyperinflation. Results were the same in those with airflow obstruction and were present in both cohorts. INTERPRETATION: Lung hyperinflation is associated strongly with clinical and subclinical CAD in smokers, including those with airflow obstruction. After lung hyperinflation was accounted for, FEV1 and emphysema no longer were associated with CAD. Subsequent studies should consider measuring lung hyperinflation and examining its mechanistic role in CAD in current and former smokers.

Brazilian studies on pulmonary function in COPD patients: what are the gaps?

BACKGROUND: COPD is a major cause of death and morbidity worldwide, and is characterized by persistent airflow obstruction. The evaluation of obstruction is critically dependent on sensitive methods for lung-function testing. A wide body of knowledge has been accumulated in recent years showing that these methods have been significantly refined and seems promising for detection of early disease. OBJECTIVES: This review focuses on research on pulmonary function analysis in COPD performed in Brazil during this century. MATERIALS AND METHODS: The literature was searched using a systematic search strategy limited to English language studies that were carried out in Brazil from the year 2000 onward, with study objectives that included a focus on lung function. RESULTS: After we applied our inclusion and exclusion criteria, 94 articles addressed our stated objectives. Among the new methods reviewed are the forced-oscillation technique and the nitrogen-washout test, which may provide information on small-airway abnormalities. Studies investigating the respiratory muscles and thoracoabdominal motion are also discussed, as well as studies on automatic clinical decision-support systems and complexity measurements. We also examined important gaps in the present knowledge and suggested future directions for the cited research fields. CONCLUSION: There is clear evidence that improvements in lung-function methods allowed us to obtain new pathophysiological information, contributing to improvement in our understanding of COPD. In addition, they may also assist in the diagnosis and prevention of COPD. Further investigations using prospective and longitudinal design may be of interest to elucidate the use of these new methods in the diagnosis and prevention of COPD.

Avaliação do impacto da aplicação de manobra de hiperinsuflação pulmonar sobre a resposta inflamatória sistêmica e colapso pulmonar em pacientes submetidos a procedimentos cirúrgicos sob ventilação espontânea / Assessing the impact of lung hyperinflation maneuver on systemic inflammatory response and lung collapse in patients undergoing surgeries under spontaneous ventilation

JUSTIFICATIVA E OBJETIVOS: O uso de manobras de hiperinsuflação pulmonar (MHP) reverte atelectasias intraoperatórias. Contudo, pode induzir resposta inflamatória sistêmica de origem pulmonar. O objetivo deste estudo foi testar o impacto da aplicação de MHP sobre a resposta inflamatória sistêmica e sobre a estrutura pulmonar em pacientes submetidos à anestesia subaracnoidea. MÉTODO: Após aprovação do Comitê de Ética institucional e obtenção do consentimento escrito pós-informado, 20 pacientes submetidos a procedimentos cirúrgicos de pequeno e médio porte foram alea torizados em dois grupos: 1) Controle (GC) e 2) MHP (GMHP). Uma hora após a instalação do bloqueio espinhal, foi realizada MHP no GMHP aplicando-se pressão positiva nas vias aéreas em dois níveis (BIPAP) com pressão expiratória de 20 cmH2O e pressão inspiratória de 20 cmH2O durante 1 a 2 minutos. TNFα, IL-1, IL-6, IL-8, IL-10 e IL-12 foram medidos no sangue através de técnica de citometria de fluxo nos momentos basal, 90, 180 e 780 minutos. Os volumes e peso pulmonares foram computados a partir de tomografias computadorizadas obtidas imediatamente após a cirurgia. RESULTADOS: A aplicação de MHP resultou em redução da fração de parênquima pulmonar não aerado (7,5 ± 4,3 por cento no Grupo Controle versus 4 ± 2,1 por cento no Grupo MHP, p = 0,02), sem alterações nos volumes pulmonares. Foi observada elevação progressiva nos valores plasmáticos das interleucinas IL-1, IL-6, IL-8 e IL-10, similar nos dois grupos. Os níveis plasmáticos de TNFα e IL-12 foram indetectáveis durante o estudo. CONCLUSÕES: A aplicação de MHP única reduziu a fração de atelectasias, porém não amplificou a resposta inflamatória observada em pacientes com pulmões normais submetidos a cirurgias de pequeno e médio portes sob anestesia subaracnoidea.

BACKGROUND AND OBJECTIVES: Lung hyperinflation maneuvers (LHM) reverse intraoperative atelectasis; however, they can lead to pulmonary-induced systemic inflammatory response. The objective of this study was to determine the impact of LHM on systemic inflammatory response and lung structure in patients undergoing subarachnoid block. METHODS: After approval by the Ethics Committee of the institution and signing the informed consent, 20 patients undergoing small and medium surgical procedures were randomly separated into two groups: 1) control (CG), and 2) LHM (LHMG). One hour after the spinal anesthesia, LHM was performed in LHMG by applying bilevel positive pressure in the airways (BIPAP) with an expiratory pressure of 20 cmH2O and inspiratory pressure of 20 cmH2O for 1 to 2 minutes. Blood levels of TNFα, IL-1, IL-6, IL-8, IL-10, and IL-12 were determined by flow cytometry at baseline and at 90, 180, and 780 minutes. Lung volumes and weights were determined using CT scans obtained immediately after the surgery. RESULTS: The use of LHM resulted in a reduction in the fraction of non-aerated pulmonary parenchyma (7.5 ± 4.3 percent, in the Control Group, vs. 4 ± 2.1 percent, in the LHM Group, p = 0.02) without changing pulmonary volumes. A progressive increase in plasma levels of IL-1, IL-6, IL-8, and IL-10, similar in both groups, was observed. Plasma levels of TNFα and IL-12 were undetectable during the study. CONCLUSIONS: The use of LHM reduced the incidence of atelectasis, but it did not amplify the inflammatory response in patients with normal lungs undergoing small and medium surgeries under subarachnoid block.

JUSTIFICATIVA Y OBJETIVOS: El uso de maniobras de hiperinsuflación pulmonar (MHP), revierte las atelectasias intraoperatorias, pero puede conllevar a una respuesta inflamatoria sistémica de origen pulmonar. Los objetivos de este estudio fueron comprobar el impacto de la aplicación de MHP sobre la respuesta inflamatoria sistémica y sobre la estructura pulmonar en pacientes sometidos a la anestesia subaracnoidea. MÉTODO: Después de la aprobación del Comité de Ética institucional y de la obtención del consentimiento informado, 20 pacientes sometidos a procedimientos quirúrgicos de pequeño y mediano porte, se separaron aleatoriamente en dos grupos: 1) control (GC) y 2) MHP (GMHP). Una hora después de la instalación del bloqueo espinal, fue realizada MHP en el GMHP aplicando una presión positiva en las vías aéreas en los niveles (BIPAP) con una presión espiratoria de 20 cmH2O y una presión inspiratoria de 20 cmH2O durante 1 a 2 minutos. FNTα, IL-1, IL-6, IL-8, IL-10 y IL-12 se midieron en la sangre a través de la técnica de citometría de flujo en los momentos basal, 90, 180 y 780 minutos. Los volúmenes y el peso pulmonares fueron computados a partir de tomografías computadorizadas obtenidas inmediatamente después de la operación. RESULTADOS: La aplicación de MHP resultó en una reducción de la fracción del parénquima pulmonar no aerado (7,5 ± 4,3 por ciento en el Grupo Control vs 4 ± 2,1 por ciento en el Grupo MHP, p = 0,02), sin alteraciones en los volúmenes pulmonares. Se observó una elevación progresiva en los valores plasmáticos de las interleucinas IL-1, IL-6, IL-8 y IL-10, similar en los dos grupos. Los niveles plasmáticos de FNT< y IL-12 no se detectaron durante el estudio. CONCLUSIONES: La aplicación de MHP única redujo la fracción de atelectasias, sin embargo, no amplificó la respuesta inflamatoria observada en pacientes con pulmones normales sometidos a cirugías de pequeño y mediano porte bajo anestesia subaracnoidea.

Lung hyperinflation stimulates the release of inflammatory mediators in spontaneously breathing subjects

Lung hyperinflation up to vital capacity is used to re-expand collapsed lung areas and to improve gas exchange during general anesthesia. However, it may induce inflammation in normal lungs. The objective of this study was to evaluate the effects of a lung hyperinflation maneuver (LHM) on plasma cytokine release in 10 healthy subjects (age: 26.1 ± 1.2 years, BMI: 23.8 ± 3.6 kg/m²). LHM was performed applying continuous positive airway pressure (CPAP) with a face mask, increased by 3-cmH2O steps up to 20 cmH2O every 5 breaths. At CPAP 20 cmH2O, an inspiratory pressure of 20 cmH2O above CPAP was applied, reaching an airway pressure of 40 cmH2O for 10 breaths. CPAP was then decreased stepwise. Blood samples were collected before and 2 and 12 h after LHM. TNF-á, IL-1â, IL-6, IL-8, IL-10, and IL-12 were measured by flow cytometry. Lung hyperinflation significantly increased (P < 0.05) all measured cytokines (TNF-á: 1.2 ± 3.8 vs 6.4 ± 8.6 pg/mL; IL-1â: 4.9 ± 15.6 vs 22.4 ± 28.4 pg/mL; IL-6: 1.4 ± 3.3 vs 6.5 ± 5.6 pg/mL; IL-8: 13.2 ± 8.8 vs 33.4 ± 26.4 pg/mL; IL-10: 3.3 ± 3.3 vs 7.7 ± 6.5 pg/mL, and IL-12: 3.1 ± 7.9 vs 9 ± 11.4 pg/mL), which returned to basal levels 12 h later. A significant correlation was found between changes in pro- (IL-6) and anti-inflammatory (IL-10) cytokines (r = 0.89, P = 0.004). LHM-induced lung stretching was associated with an early inflammatory response in healthy spontaneously breathing subjects.