Pulmonary capillary pressures during the acute respiratory distress syndrome
TL;DR: Pulmonary capillary pressure cannot be predicted from PAOP during early and established ARDS, and the high variability in Pcap−PAOP increases the risk for underestimation of filtration pressures and consequently the risk of lung edema.
Abstract: (1)To describe the evolution of pulmonary capillary pressure (Pcap) and of the pressure drop across the pulmonary venous bed from early to established acute respiratory distress syndrome (ARDS), (2) to assess Pcap under different levels of positive end-expiratory pressure (PEEP) and (3) to compare the visual method and a mathematical model to determine Pcap. Prospective, intervention study. Intensive care unit in a teaching institution. Nine ARDS patients, according to the ARDS Consensus Conference criteria. Pulmonary arterial pressures were measured during routine respiratory mechanics measurements throughout ARDS. Four PEEP levels (6, 9, 12 and 15 cmH2O) were studied. Pulmonary artery occlusions were made in triplicate at each PEEP level. Pcap was determined for every occlusion trace by three observers (visual method) and a mathematical model. Diastolic pulmonary artery pressure (PAPd) and pulmonary artery occlusion pressure (PAOP) were measured. The visually determined Pcap showed a bias of 2.5±2.1 mmHg as compared to the mathematical estimation. PAPd, Pcap and PAOP tended to decrease from early to late ARDS (p=0.128, 0.265, 0.121). Pcap−PAOP (6.3±2.7 mmHg) did not change throughout ARDS. Higher PEEP levels were associated with increased PAPd, Pcap and PAOP, as well as with larger Pcap−PAOP throughout ARDS. Pulmonary capillary pressure cannot be predicted from PAOP during early and established ARDS. The high variability in Pcap−PAOP increases the risk for underestimation of filtration pressures and consequently the risk for lung edema. Pcap can be estimated at the bedside by either the visual or mathematical methods.
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15 citations
TL;DR: Treatment of severely hypoxemic patients should aim to improve oxygenation while limiting ventilator-induced lung injury and a physiopathological approach that accounts for the underlying mechanisms of hypoxemia, and physiological and clinical effects of different treatments is likely the best guide.
Abstract: Purpose of review To describe a physiopathological-based approach to clinical management of severely hypoxemic patients that integrates the most recent findings on the use of rescue therapies. Recent findings Several techniques are available to improve oxygenation in severely hypoxemic patients. Survival benefits have not been proved for most of these techniques. In a recent randomized trial, centralization of acute respiratory distress syndrome patients to a specialized center able to provide extracorporeal membrane oxygenation showed better survival as compared to conventional treatment. Randomized trials failed to prove survival benefits with the use of high levels of positive end-expiratory pressure (PEEP) or prone positioning. However, pooled data from two meta-analyses showed significant higher survival in the most severe patients both with the use of higher PEEP and prone positioning. Summary Treatment of severely hypoxemic patients should aim to improve oxygenation while limiting ventilator-induced lung injury. A physiopathological approach that accounts for the underlying mechanisms of hypoxemia, and physiological and clinical effects of different treatments is likely the best guide we have to treat severely hypoxemic patients.
12 citations
TL;DR: A monitorizacao de funcoes vitais e uma das mais importantes e essenciais ferramentas no manuseio de pacientes criticos na UTI, considerando a relacao risco-beneficio da tecnica.
Abstract: JUSTIFICATIVA E OBJETIVOS: A monitorizacao de funcoes vitais e uma das mais importantes e essenciais ferramentas no manuseio de pacientes criticos na UTI. Hoje e possivel detectar e analisar uma grande variedade de sinais fisiologicos atraves de diferentes tecnicas, invasivas e nao-invasivas. O intensivista deve ser capaz de selecionar e executar o metodo de monitorizacao mais apropriado de acordo com as necessidades individuais do paciente, considerando a relacao risco-beneficio da tecnica. Apesar do rapido desenvolvimento de tecnicas de monitorizacao nao-invasiva, a monitorizacao hemodinâmica invasiva com o uso do cateter de arteria pulmonar (CAP) ainda e um dos procedimentos fundamentais em UTI. O objetivo destas recomendacoes e estabelecer diretrizes para o uso adequado dos metodos basicos de monitorizacao hemodinâmica e CAP. METODO: O processo de desenvolvimento de recomendacoes utilizou o metodo Delphi modificado para criar e quantificar o consenso entre os participantes. A AMIB determinou um coordenador para o consenso, o qual escolheu seis especialistas para comporem o comite consultivo. Outros 18 peritos de diferentes regioes do pais foram selecionados para completar o painel de 25 especialistas, medicos e enfermeiros. Um levantamento bibliografico na MedLine de artigos na lingua inglesa foi realizado no periodo de 1966 a 2004. RESULTADOS: Foram apresentadas recomendacoes referentes a 55 questoes sobre monitorizacao da pressao venosa central, pressao arterial invasiva e cateter de arteria pulmonar. Com relacao ao CAP, alem de recomendacoes quanto ao uso correto foram discutidas as indicacoes em diferentes situacoes clinicas. CONCLUSOES: A avaliacao da pressao venosa central e da pressao arterial, alem das variaveis obtidas com o CAP permite o entendimento da fisiologia indispensavel para o cuidado de pacientes graves. Entretanto, a correta utilizacao dessas ferramentas e fundamental para os possiveis beneficios decorrentes do uso.
8 citations
Dissertation•
01 Dec 2015
TL;DR: It is demonstrated that vitamin D deficiency is a potential modifiable risk factor and should be identified and treated in patients at risk of sepsis and ARDS.
Abstract: The acute respiratory distress syndrome (ARDS) remains a major cause of morbidity and mortality in the critically ill patient. There are no effective strategies for identifying those most at risk or therapeutic interventions proven to prevent its occurrence. Vitamin D deficiency is common and has important functions besides calcium homeostasis with profound effects on human immunity. Preliminary data suggests in the high-risk sepsis and oesophagectomy groups that vitamin D deficiency may be a pre-existing risk factor and mechanistic driver of ARDS.
This thesis investigated in an animal model and in-vitro studies whether vitamin D influences the innate immune response to sepsis and resolution of neutrophilic injury. In addition, it reports a proof of concept phase II study to determine if vitamin D therapy in patients undergoing oesophagectomy is anti-inflammatory and protective of markers of lung injury.
Vitamin D deficiency significantly increased the bacterial load, bacteraemia and translocation to the lung in a murine model of peritonitis. This was associated with a rise in tissue permeability locally and within the lung, reduced antimicrobial peptide and defective peritoneal macrophage phagocytosis. These data support pre-existing vitamin D deficiency as a determinant of the severity of bacteraemic sepsis.
In-vivo high dose vitamin D supplementation was a safe, well-tolerated preoperative intervention with reduced biomarkers of alveolar oedema, capillary leak and macrophage efferocytosis. In-vitro culture with vitamin D increased macrophage efferocytosis and promoted monocyte differentiation to a pro-resolution phenotype. This suggests a potential mechanism for vitamin D on protecting barrier integrity and resolution of neutrophilic inflammation, a hallmark of ARDS.
This body of work demonstrates that vitamin D deficiency is a potential modifiable risk factor and should be identified and treated in patients at risk of sepsis and ARDS. Larger trials powered to evaluate the effect of vitamin D on preventing and improving clinical outcomes in sepsis and ARDS are warranted.
4 citations
01 Jan 2005
TL;DR: Pulmonary oedema is classified according to its main aetiologies: hydrostatic pulmonary Oedema (increased capillary pressure due to hypervolaemia, left heart failure, or left-to-right cardiac shunt), permeability pulmonary oingema ( increased permeability of the alveolar–capillary barrier), and lung oedma due to decreased osmotic pressure of the plasma proteins (reduced plasma albumin concentration).
Abstract: Lung oedema occurs when transudation or exudation from the pulmonary capillaries exceeds the capacity of the lymphatic drainage. In itsmore severe forms there is free fluid in the alveoli [1]. The alveolar–capillary barrier is formed by themicrovascular endothelium and the alveolar epithelium.Alveolar oedema results thus from(1) transudation of fluid from the pulmonary microcirculation into the interstitial space (across the endothelium), (2) movement of fluid within the interstitium and (3) movement of fluid from the interstitial space into the alveoli (across the epithelium). Passage of fluid across the pulmonarymicrovascular endothelium is promoted by the hydrostatic pressure differential between capillary and interstitium, but counteracted by the osmotic pressure of the plasma proteins. This relationship is described by the Starling equation [1]. Transudation across the alveolar epithelium seems to occur only in the presence of epithelial damage or when the interstitial pressure increases above a critical level [2]. On the basis of this knowledge, it is possible to classify pulmonary oedema according to itsmain aetiologies: (1) hydrostatic pulmonary oedema (increased capillary pressure due to hypervolaemia, left heart failure, or left-to-right cardiac shunt), (2) permeability pulmonary oedema (increased permeability of the alveolar–capillary barrier) and (3) lung oedema due to decreased osmotic pressure of the plasma proteins (reduced plasma albumin concentration).
2 citations
Cites background from "Pulmonary capillary pressures durin..."
...Recent data point to the presence of high pulmonary capillary pressures throughout the course of ALI and ARDS [55]....
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References
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TL;DR: An alternative approach, based on graphical techniques and simple calculations, is described, together with the relation between this analysis and the assessment of repeatability.
43,884 citations
TL;DR: In this article, an alternative approach, based on graphical techniques and simple calculations, is described, together with the relation between this analysis and the assessment of repeatability, which is often used in clinical comparison of a new measurement technique with an established one.
9,160 citations
TL;DR: The acute respiratory distress syndrome (ARDS), a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies, carries a high morbidity, mortality, and financial cost.
Abstract: The acute respiratory distress syndrome (ARDS), a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies, carries a high morbidity, mortality (10 to 90%), and financial cost. The reported annual incidence in the United States is 150,000 cases, but this figure has been challenged, and it may be different in Europe. Part of the reason for these uncertainties are the heterogeneity of diseases underlying ARDS and the lack of uniform definitions for ARDS. Thus, those who wish to know the true incidence and outcome of this clinical syndrome are stymied. The American-European Consensus Committee on ARDS was formed to focus on these issues and on the pathophysiologic mechanisms of the process. It was felt that international coordination between North America and Europe in clinical studies of ARDS was becoming increasingly important in order to address the recent plethora of potential therapeutic agents for the prevention and treatment of ARDS.
6,233 citations
TL;DR: As compared with conventional ventilation, the protective strategy was associated with improved survival at 28 days, a higher rate of weaning from mechanical ventilation, and a lower rate of barotrauma in patients with the acute respiratory distress syndrome.
Abstract: Background In patients with the acute respiratory distress syndrome, massive alveolar collapse and cyclic lung reopening and overdistention during mechanical ventilation may perpetuate alveolar injury. We determined whether a ventilatory strategy designed to minimize such lung injuries could reduce not only pulmonary complications but also mortality at 28 days in patients with the acute respiratory distress syndrome. Methods We randomly assigned 53 patients with early acute respiratory distress syndrome (including 28 described previously), all of whom were receiving identical hemodynamic and general support, to conventional or protective mechanical ventilation. Conventional ventilation was based on the strategy of maintaining the lowest positive end-expiratory pressure (PEEP) for acceptable oxygenation, with a tidal volume of 12 ml per kilogram of body weight and normal arterial carbon dioxide levels (35 to 38 mm Hg). Protective ventilation involved end-expiratory pressures above the lower inflection poin...
3,323 citations
"Pulmonary capillary pressures durin..." refers background in this paper
...The protective approach to ventilation in ARDS advocates high positive end-expiratory pressure (PEEP) levels and low tidal volumes [8]....
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TL;DR: An expanded definition of ARDS is proposed that takes into account new knowledge about adult respiratory distress syndrome and its clinical features, physiologic disturbances, prognosis, and pathologic findings.
Abstract: More than twenty years ago, Ashbaugh and coworkers, (1), in a now classic article, described. 12 patients whose striking but uniform clinical, physiologic, roentgenographic,and pathologic abnormalities distinguished them from among 272adult patients who had received respiratory support in the intensive care units of Colorado General Hospital and Denver General Hospital. The 12patients all had severedyspnea, tachypnea, cyanosis that was refractory to oxygen therapy, decreased respiratory system compliance, and diffuse alveolar infiltrations on their chest radiographs. Pathologic examination in seven patients who died revealed atelectasis, vascular congestion and hemorrhage, severe pulmonary edema and hyaline membranes. Shortly afterward, Petty and coworkers (2), called this constellation of findings the adult respiratory distress syndrome (ARDS). Since then, ARDS has been recognized as an entity throughout the world and has been the subject of numerous conferences, hundreds of articles, and several books. As a result of this activity, much descriptive information has been obtained about ARDS, and we have learned a lot about its clinical features, physiologic disturbances, prognosis, and pathologic findings. And yet formidable problems remain: there is disagreement about exactly what ARDS is and on what causes it; more importantly, available empiric treatment is inadequate, and mortality remains unacceptably high (600/0 or more) (3). This appears to be one of the few points of agreement among investigators, but even that statement is arguable (4). We believe that much of the controversy concerning ARDS is explained by the lack of a satisfactory definition of this elusivesyndrome. How can you collect, much less compare, epidemiologicdata and mortality figures when there is no uniformly accepted (and used) definition? How can you study basic pathophysiologic mechanisms, understand natural history, and above all, evaluate new therapeutic approaches in what appears now to be an amalgam of many different disorders? The purpose of this article, therefore, is to propose an expanded definition of ARDS that takes into account new knowledge about
2,372 citations
"Pulmonary capillary pressures durin..." refers background in this paper
.../sex) (year) diagnosis (cmH2O) compliance [11] (ml/cmH2O)...
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...Demographic and clinical data [11] are presented in Table 1....
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