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.
Citations
More filters
01 Jan 2005
TL;DR: This document is intended to help clarify the role of Twitter in the operation of this website and its role in the social media landscape.
Abstract: Морфологическими методами исследованы легкие людей, погибших в результате тяжелой черепно7мозговой, со7 четанной травмы и массивной кровопотери (92 наблюдения), а также легкие экспериментальных животных (крыс, n= 117) при системных нарушениях кровообращения и тромбозе сосудов микроциркуляторного русла малого кру7 га кровообращения Цель исследования — оценить характер, интенсивность и сроки развития морфологических признаков, характеризующих острое повреждение легких Установлено, что ранними структурными изменениями при травме и массивной кровопотере являются расстройства кровообращения (в том числе микроциркуляции), повреждение слизистой оболочки бронхов и бронхиол, развитие ателектазов, дистелектазов и очаговой эмфизе7 мы Отек легких и признаки системной воспалительной реакции формируются в первые часы после травмы и мас7 сивной кровопотери Экспериментальные исследования подтверждают важную роль нарушений микроциркуля7 ции и индивидуальных особенностей в развитии острого повреждения легких Morphological studies were used to examine the lungs from 92 persons who had died from brain and concomitant injuries and massive blood loss and from 117 experimental animals (rats) in systemic circulatory disorders and vascu7 lar thrombosis of the pulmonary microcirculatory bed The purpose of the study was to assess the nature, intensity, and developmental periods of the morphological signs characterizing acute pulmonary lesion Disorders of circulation (including microcirculation), damages to bronchial and bronchiolar mucosae, the development of atelectases, dyst7 electases, and focal emphysema were found to be early structural changes in injury and massive blood loss Pulmonary edema and the signs of a systemic inflammatory reactions form within the first hours following injury and massive blood loss Experimental studies confirm that microcirculatory disorders and individual traits play an important role in the development of acute pulmonary lesion
2 citations
Additional excerpts
...Нарушения кровотока подтверждаются опреде лением давления в легочных капиллярах при ОПЛ и ОРДС [13]....
[...]
TL;DR: Patients presenting with pathologies characterized by different distributions of pulmonary vascular resistance are studied, suggesting that no single method for estimating pulmonary capillary pressure is adequate for all disease processes.
Abstract: In the absence of a direct method with which to measure pulmonary capillary pressure in humans, various methods for analyzing the pulmonary artery pressure decay following balloon occlusion have been described. In this issue of Critical Care, Souza and coworkers investigate the adequacy of these methods for assessing various pathophysiological processes. They studied patients presenting with pathologies characterized by different distributions of pulmonary vascular resistance. Their findings suggest that no single method for estimating pulmonary capillary pressure is adequate for all disease processes.
1 citations
Cites background from "Pulmonary capillary pressures durin..."
...However, data on the behaviour of pulmonary artery pressure decay after balloon occlusion in different stages of ALI/ARDS are scarce [10]....
[...]
Journal Article•
TL;DR: Alveolar flooding is commonly dependent on the balance of pulmonary edema formation and clearance, so that the dysfunction of any of the components needed for alveolar fluid clearance can promptly predispose to the development of pulmonary Edema.
Abstract: The proper regulation and maintenance of pulmonary fluid balance is crucial to health. In utero, the lungs are net fluid secretors with the volume of fluid being vital for optimal lung growth. Pulmonary hypoplasia occurs when too little fluid is produced, such as in oligohydramnios, whereas excess fluid produces pulmonary hyperplasia. Importantly, fetal fluid secretion is under the control of Cl- secretion by the respiratory epithelium. At birth the sudden dependency on pulmonary gas exchange requires a dramatic change in lung fluid dynamics. As gaseous exchange requires a relatively dry alveolus the respiratory epithelium transforms to a net fluid absorber in a remarkably short space of time. In the few days before birth the lungs begin to produce less fluid, and during labor the physical passage of the fetus through the birth canal forces fluid from the lungs. Simultaneous increases in fetal sympathetic output and catecholamine levels help activate alveolar Na+ channels necessary for fluid absorption. Additionally, the manifold increase in fetal oxygenation ex utero further stimulates Na+ channels. The optimal alveolar gas exchange is dependent on an even thinner alveolar lining fluid of 0.1- 0.2 ?m height. The alveolar lining fluid consists of an analogous dual layer, with surfactant covering an aqueous subphase. Alveolar lining fluid evens the air-liquid interface, enables surfactant precursors to reach the surfactant layer, and allows movement of surfactant within this layer. Pulmonary edema results in fluid deposition in the alveolar region. The resolution of pulmonary edema is vitally dependent on the active absorption of Na+ and Cl- from the alveolar air space into the interstitium creating an osmotic gradient for the movement of water out of the alveolar air space and thereafter from the interstitium, water is cleared by the lymphatic system (Ware 2005). Generally the ALI/ARDS were results from an inflammatory injury to the alveolar epithelial-interstitial-endothelial complex caused by either a pulmonary or extrapulmonary insult. The neutrophil-mediated disruption of this physical barrier causes increased permeability pulmonary edema. The alveolar flooding is commonly dependent on the balance of pulmonary edema formation and clearance, so that the dysfunction of any of the components needed for alveolar fluid clearance can promptly predispose to the development of pulmonary edema.
1 citations
Cites background from "Pulmonary capillary pressures durin..."
...This is the case in the classical non-cardiogenic pulmonary edemas such as ARDS (Figures 18) and high altitude pulmonary edema or neurogenic pulmonary edema, in which there is an increase predominantly of the venous pulmonary resistance [16]....
[...]
01 Jan 2005
TL;DR: The PCP in IPAH patients is greater than normal but methodological limitations related to the occlusion technique may limit interpretation of these data in isolation.
Abstract: Introduction Pulmonary capillary pressure (PCP), together with the time constants of the various vascular compartments, define the dynamics of the pulmonary vascular system. Our objective in the present study was to estimate PCPs and time constants of the vascular system in patients with idiopathic pulmonary arterial hypertension (IPAH), and compare them with these measures in patients with acute respiratory distress syndrome (ARDS). Methods We conducted the study in two groups of patients with pulmonary hypertension: 12 patients with IPAH and 11 with ARDS. Four methods were used to estimate the PCP based on monoexponential and biexponential fitting of pulmonary artery pressure decay curves. Results PCPs in the IPAH group were considerably greater than those in the ARDS group. The PCPs measured using the four methods also differed significantly, suggesting that each method measures the pressure at a different site in the pulmonary circulation. The time constant for the slow component of the biexponential fit in the IPAH group was significantly longer than that in the ARDS group. Conclusion The PCP in IPAH patients is greater than normal but methodological limitations related to the occlusion technique may limit interpretation of these data in isolation. Different disease processes may result in different times for arterial emptying, with resulting implications for the methods available for estimating PCP.
References
More filters
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]....
[...]
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)...
[...]
...Demographic and clinical data [11] are presented in Table 1....
[...]