RESUMO
This pilot study aimed to investigate the relation between cardio-respiratory parameters derived from Central Venous Pressure (CVP) waveform and Extubation Failure (EF) in mechanically ventilated ICU patients during post-extubation period. This study also proposes a new methodology for analysing these parameters during rest/sleep periods to try to improve the identification of EF. We conducted a prospective observational study, computing CVP-derived parameters including breathing effort, spectral analyses, and entropy in twenty critically ill patients post-extubation. The Dynamic Warping Index (DWi) was calculated from the respiratory component extracted from the CVP signal to identify rest/sleep states. The obtained parameters from EF patients and patients without EF were compared both during arbitrary periods and during reduced DWi (rest/sleep). We have analysed data from twenty patients of which nine experienced EF. Our findings may suggest significantly increased respiratory effort in EF patients compared to those successfully extubated. Our study also suggests the occurrence of significant change in the frequency dispersion of the cardiac signal component. We also identified a possible improvement in the differentiation between the two groups of patients when assessed during rest/sleep states. Although with caveats regarding the sample size, the results of this pilot study may suggest that CVP-derived cardio-respiratory parameters are valuable for monitoring respiratory failure during post-extubation, which could aid in managing non-invasive interventions and possibly reduce the incidence of EF. Our findings also indicate the possible importance of considering sleep/rest state when assessing cardio-respiratory parameters, which could enhance respiratory failure detection/monitoring.
Assuntos
Extubação , Pressão Venosa Central , Unidades de Terapia Intensiva , Respiração Artificial , Sono , Humanos , Masculino , Feminino , Projetos Piloto , Pessoa de Meia-Idade , Extubação/métodos , Estudos Prospectivos , Idoso , Monitorização Fisiológica/métodos , Respiração Artificial/métodos , Estado Terminal , Descanso , Desmame do Respirador/métodos , Adulto , Insuficiência Respiratória/terapia , Insuficiência Respiratória/fisiopatologia , Respiração , Cuidados Críticos/métodosRESUMO
Lung physiology research advanced significantly over the last 100 years. Respiratory mechanics applied to animal models of lung disease extended the knowledge of the workings of respiratory system. In human research, a better understanding of respiratory mechanics has contributed to development of mechanical ventilators. In this review, we explore the use of respiratory mechanics in basic science to investigate asthma and chronic obstructive pulmonary disease (COPD). We also discuss the use of lung mechanics in clinical care and its role on the development of modern mechanical ventilators. Additionally, we analyse some bench-developed technologies that are not in widespread use in the present but can become part of the clinical arsenal in the future. Finally, we explore some of the difficult questions that intensive care doctors still face when managing respiratory failure. Bringing back these questions to bench can help to solve them. Interaction between basic and translational science and human subject investigation can be very rewarding, as in the conceptualization of "Lung Protective Ventilation" principles. We expect this interaction to expand further generating new treatments and managing strategies for patients with respiratory disease.
RESUMO
Flow sensors are required for monitoring patients on mechanical ventilation and in respiratory research. Proper calibration is important for ensuring accuracy and can be done with a precision syringe. This procedure, however, becomes complex for nonlinear flow sensors, which are commonly used. The objective of the present work was to develop an algorithm to allow the calibration of nonlinear flow sensors using an accurate syringe. We first noticed that a power law equation could properly fit the pressure-flow relationship of nonlinear flow sensors. We then developed a software code to estimate the parameters for this equation using a 3 L syringe (calibration syringe). Finally, we tested the performance of a calibrated flow sensor using a different 3 L syringe (testing syringe) and a commercially available spirometer. After calibration, the sensor had a bias ranging from −1.7% to 3.0% and precision from 0.012 L to 0.039 L for volumes measured with the 3 L testing syringe. Calibrated sensor performance was at least as good as the commercial sensor. This calibration procedure can be done at the bedside for both clinical and research purposes, therefore improving the accuracy of nonlinear flow sensors.
Assuntos
Calibragem , Espirometria/instrumentação , Seringas/normas , Humanos , Respiração Artificial , SoftwareRESUMO
Acute lung injury (ALI) is a common complication associated with septic shock that directly influences the prognosis of sepsis patients. Currently, one of the main supportive treatment modalities for septic shock is fluid resuscitation. The use of hypertonic saline (HS: 7.5% NaCl) for fluid resuscitation has been described as a promising therapy in experimental models of sepsis-induced ALI, but it has failed to produce similar results in clinical practice. Thus, we compared experimental timing versus clinical timing effectiveness (i.e., early vs. late fluid resuscitation) after the inflammatory scenario was established in a rat model of bacterial lipopolysaccharide-induced ALI. We found that late fluid resuscitation with hypertonic saline (NaCl 7.5%) did not reduce the mortality rates of animals compared with the mortality late associated with early treatment. Late fluid resuscitation with both hypertonic and normal saline increased pulmonary inflammation, decreased pulmonary function, and induced pulmonary injury by elevating metalloproteinase-2 and metalloproteinase-9 activity and collagen deposition in the animals, unlike early treatment. The animals with lipopolysaccharide-induced ALI that received late resuscitation with any kind of fluids demonstrated aggravated pulmonary injury and respiratory function. Moreover, we showed that the therapeutic window for a beneficial effect of fluid resuscitation with hypertonic saline is very narrow.
Assuntos
Lesão Pulmonar Aguda/sangue , Lesão Pulmonar Aguda/induzido quimicamente , Lipopolissacarídeos/efeitos adversos , Ressuscitação/métodos , Solução Salina Hipertônica/uso terapêutico , Animais , Colágeno/química , Citocinas/metabolismo , Modelos Animais de Doenças , Endotoxinas/química , Hidratação/métodos , Proteínas de Choque Térmico/metabolismo , Inflamação , Pulmão/fisiopatologia , Lesão Pulmonar/fisiopatologia , Masculino , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Prognóstico , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase em Tempo Real , Sepse/fisiopatologia , Choque Séptico/fisiopatologia , Cloreto de Sódio/química , Fatores de TempoRESUMO
Acute respiratory distress syndrome (ARDS) is the most severe lung inflammatory manifestation and has no effective therapy nowadays. Sepsis is one of the main illnesses among ARDS causes. The use of fluid resuscitation is an important treatment for sepsis, but positive fluid balance may induce pulmonary injury. As an alternative, fluid resuscitation with hypertonic saline ((HS) NaCl 7.5%) has been described as a promising therapeutical agent in sepsis-induced ARDS by the diminished amount of fluid necessary. Thus, we evaluated the effect of hypertonic saline in the treatment of LPS-induced ARDS. We found that hypertonic saline (NaCl 7.5%) treatment in rat model of LPS-induced ARDS avoided pulmonary function worsening and inhibited type I collagen deposition. In addition, hypertonic saline prevented pulmonary injury by decreasing metalloproteinase 9 (MMP-9) activity in tissue. Focal adhesion kinase (FAK) activation was reduced in HS group as well as neutrophil infiltration, NOS2 expression and NO content. Our study shows that fluid resuscitation with hypertonic saline decreases the progression of LPS-induced ARDS due to inhibition of pulmonary remodeling that is observed when regular saline is used.
Assuntos
Lesão Pulmonar Aguda/prevenção & controle , Remodelação das Vias Aéreas , Hidratação/métodos , Lipopolissacarídeos , Pulmão , Síndrome do Desconforto Respiratório/terapia , Solução Salina Hipertônica/administração & dosagem , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/metabolismo , Lesão Pulmonar Aguda/fisiopatologia , Resistência das Vias Respiratórias , Animais , Colágeno Tipo I/metabolismo , Modelos Animais de Doenças , Quinase 1 de Adesão Focal/metabolismo , Pulmão/metabolismo , Pulmão/patologia , Pulmão/fisiopatologia , Masculino , Metaloproteinase 9 da Matriz/metabolismo , Infiltração de Neutrófilos , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/prevenção & controle , Ratos Wistar , Síndrome do Desconforto Respiratório/induzido quimicamente , Síndrome do Desconforto Respiratório/metabolismo , Síndrome do Desconforto Respiratório/fisiopatologia , Fatores de TempoRESUMO
Vários mecanismos que participam do desenvolvimento da DPOC (Doença Pulmonar Obstrutiva Crônica) não são ainda bem esclarecidos. Neste estudo, expusemos camundongos C57/Bl6, por 2 meses, à fumaça de cigarro e/ou à ROFA (resíduo de óleo diesel). Os animais expostos à fumaça de cigarro desenvolveram aumento da resistência de grandes vias aéreas, provavelmente por espessamento da sua parede, resultante de alterações nas células epiteliais. Estes animais também desenvolveram enfisema inicial, com distensão de espaços aéreos em algumas regiões pulmonares. Não houve recrutamento de células inflamatórias, alteração de fibras elásticas ou colágenas ou aumento do estresse oxidativo, medido pelo Isoprostano 8. Este trabalho sugere que há uma lesão pulmonar inicial que se caracteriza por alterações nas células epiteliais e algum grau de enfisema, que pode ser mediado pelas próprias células epiteliais.
Many of the mechanisms leading to CPOD (Chronic Pulmonary Obstructive Disease) are not completely understood. In the present study, we exposed C57/Bl6 mice, for two months, to cigarette smoke and/or ROFA (Residual Oil Fly Ash). Animals exposed to cigarette smoke had an increased in proximal airways resistance, probably due to the thickening of airways walls that followed changes in epithelial cells. These animals also had a small degree of emphysema, once air spaces enlargement could be noticed in circumscribed lung areas. We observed no inflammatory cells recruitment, elastic or collagen fibers deposition or increases in oxidative stress, measured by staining Isoprotane8. This study shows an early stage of the CPOD development, in which we can detect changes in epithelial cells and a small degree of emphysema, which could be mediated by these same epithelial cells.
Assuntos
Humanos , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Poluição Ambiental , Camundongos , Enfisema Pulmonar , NicotianaRESUMO
O raciocínio clínico diagnóstico mudou muito ao longo dos anos, partindo de diagnóstico (e tratamento) de sinais para, nos dias de hoje, fazermos diagnósticos mais precisos, visando o melhor tratamento. A partir da anamnese e usando técnicas de raciocínio diagnóstico hipotético-dedutivo ou reconhecimento de padrão (as duas mais utilizadas) procura-se, a partir de diagnósticos sindrômicos, chegar a diagnósticos etiológicos / Clinical diagnosis changed a lot in history, starting with diagnosing (and treating) signs and symptoms to, in modern times, making more precise diagnosis, seeking the best treatment. Starting with clinical history and using hypothetic-deductive way of thinking or pattern recognition (the two most used techniques), we seek, through syndromic diagnosis, the etiologic diagnosis...