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Journal ArticleDOI

Pulmonary capillary pressures during the acute respiratory distress syndrome

29 Oct 2003-Intensive Care Medicine (Springer-Verlag)-Vol. 29, Iss: 12, pp 2174-2179

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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Journal ArticleDOI
TL;DR: Results suggest that indexes of pulmonary permeability provided by transpulmonary thermodilution may be useful for determining the mechanism of pulmonary edema in the critically ill.
Abstract: To test whether assessing pulmonary permeability by transpulmonary thermodilution enables to differentiate increased permeability pulmonary edema (ALI/ARDS) from hydrostatic pulmonary edema. Retrospective review of cases. A 24-bed medical intensive care unit of a university hospital. Forty-eight critically ill patients ventilated for acute respiratory failure with bilateral infiltrates on chest radiograph, a PaO2/FiO2 ratio < 300 mmHg and extravascular lung water indexed for body weight ≥ 12 ml/kg. We assessed pulmonary permeability by two indexes obtained from transpulmonary thermodilution: extravascular lung water/pulmonary blood volume (PVPI) and the ratio of extravascular lung water index over global end-diastolic volume index. The cause of pulmonary edema was determined a posteriori by three experts, taking into account medical history, clinical features, echocardiographic left ventricular function, chest radiography findings, B-type natriuretic peptide serum concentration and the time-course of these findings with therapy. Experts were blind for pulmonary permeability indexes and for global end-diastolic volume. ALI/ARDS was diagnosed in 36 cases. The PVPI was 4.7 ± 1.8 and 2.1 ± 0.5 in patients with ALI/ARDS and hydrostatic pulmonary edema, respectively (p < 0.05). The extravascular lung water index/global end-diastolic volume index ratio was 3.0 × 10−2 ± 1.2 × 10−2 and 1.4 × 10−2 ± 0.4 × 10−2 in patients with ALI/ARDS and with hydrostatic pulmonary edema, respectively (p < 0.05). A PVPI ≥ 3 and an extravascular lung water index/global end-diastolic index ratio ≥ 1.8 × 10−2 allowed the diagnosis of ALI/ARDS with a sensitivity of 85% and specificity of 100%. These results suggest that indexes of pulmonary permeability provided by transpulmonary thermodilution may be useful for determining the mechanism of pulmonary edema in the critically ill.

183 citations


Additional excerpts

  • ...filtration (pulmonary microvessels) [17, 18]....

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Journal ArticleDOI
TL;DR: PVPI may be a useful quantitative diagnostic tool for ARDS in patients with hypoxemic respiratory failure and radiographic infiltrates and was weakly correlated with intrathoracic blood volume in ALI/ARDS and cardiogenic edema patients.
Abstract: Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by features other than increased pulmonary vascular permeability. Pulmonary vascular permeability combined with increased extravascular lung water content has been considered a quantitative diagnostic criterion of ALI/ARDS. This prospective, multi-institutional, observational study aimed to clarify the clinical pathophysiological features of ALI/ARDS and establish its quantitative diagnostic criteria. The extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI) were measured using the transpulmonary thermodilution method in 266 patients with PaO2/FiO2 ratio ≤ 300 mmHg and bilateral infiltration on chest radiography, in 23 ICUs of academic tertiary referral hospitals. Pulmonary edema was defined as EVLWI ≥ 10 ml/kg. Three experts retrospectively determined the pathophysiological features of respiratory insufficiency by considering the patients' history, clinical presentation, chest computed tomography and radiography, echocardiography, EVLWI and brain natriuretic peptide level, and the time course of all preceding findings under systemic and respiratory therapy. Patients were divided into the following three categories on the basis of the pathophysiological diagnostic differentiation of respiratory insufficiency: ALI/ARDS, cardiogenic edema, and pleural effusion with atelectasis, which were noted in 207 patients, 26 patients, and 33 patients, respectively. EVLWI was greater in ALI/ARDS and cardiogenic edema patients than in patients with pleural effusion with atelectasis (18.5 ± 6.8, 14.4 ± 4.0, and 8.3 ± 2.1, respectively; P < 0.01). PVPI was higher in ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 ± 1.4, 2.0 ± 0.8, and 1.6 ± 0.5; P < 0.01). In ALI/ARDS patients, EVLWI increased with increasing pulmonary vascular permeability (r = 0.729, P < 0.01) and was weakly correlated with intrathoracic blood volume (r = 0.236, P < 0.01). EVLWI was weakly correlated with the PaO2/FiO2 ratio in the ALI/ARDS and cardiogenic edema patients. A PVPI value of 2.6 to 2.85 provided a definitive diagnosis of ALI/ARDS (specificity, 0.90 to 0.95), and a value < 1.7 ruled out an ALI/ARDS diagnosis (specificity, 0.95). PVPI may be a useful quantitative diagnostic tool for ARDS in patients with hypoxemic respiratory failure and radiographic infiltrates. UMIN-CTR ID UMIN000003627

115 citations


Journal ArticleDOI
Jukka Takala1
TL;DR: The presence and relevance of increased pulmonary capillary hydrostatic pressures to values in excess of pulmonary artery occlusion pressure are often overlooked.
Abstract: Pulmonary capillary pressure is a primary determinant of fluid flux across the pulmonary capillary wall [1]. Increasing pulmonary capillary pressure increases fluid flux out of the capillaries into the interstitium and in the extreme induces pulmonary edema. Pulmonary capillary pressure is itself determined by the mean pulmonary artery pressure, pulmonary vascular resistance, and total blood flow. The distribution of the pulmonary vascular resistance from precapillary arterial to postcapillary venous compartments varies. Accordingly, at any given blood flow rate the hydrostatic pressure in the pulmonary capillaries depends on the magnitude of the resistance to blood flow across the pulmonary circulation and its distribution between precapillary and postcapillary vessels. Since pulmonary capillary pressure cannot be directly measured, the presence and relevance of increased pulmonary capillary hydrostatic pressures to values in excess of pulmonary artery occlusion pressure are often overlooked.

37 citations



Journal ArticleDOI
TL;DR: This review will focus on the mechanisms responsible for the RV dysfunction/failure during ARDS and on the strategy, which allows improving the right ventricular function.
Abstract: Purpose of reviewCirculatory failure is a frequent complication during acute respiratory distress syndrome (ARDS) and is associated with a poor outcome. This review aims at clarifying the mechanisms of circulatory failure during ARDS.Recent findingsFor the past decades, the right ventricle (RV) has

31 citations


Cites background from "Pulmonary capillary pressures durin..."

  • ...However, a large fluid overload induced during the first hours of resuscitation, especially in patients with septic cardiomyopathy, could be another explanation of this much unexpected PAOP....

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  • ...ARDS is usually defined with a PAOP under 18 mmHg....

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  • ...Besides ARDS-associated circulatory failure, another issue regarding the heart and the circulation in ARDS is the controversy on the level of high pulmonary artery occlusion pressure (PAOP) in ARDS....

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  • ...Nevertheless, some authors have raised the issue of the possible association between authenticable ARDS and high PAOP [21]....

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References
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Journal ArticleDOI
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.
Abstract: In clinical measurement comparison of a new measurement technique with an established one is often needed to see whether they agree sufficiently for the new to replace the old. Such investigations are often analysed inappropriately, notably by using correlation coefficients. The use of correlation is misleading. An alternative approach, based on graphical techniques and simple calculations, is described, together with the relation between this analysis and the assessment of repeatability.

41,576 citations


Journal ArticleDOI
Abstract: In clinical measurement comparison of a new measurement technique with an established one is often needed to see whether they agree sufficiently for the new to replace the old. Such investigations are often analysed inappropriately, notably by using correlation coefficients. The use of correlation is misleading. An alternative approach, based on graphical techniques and simple calculations, is described, together with the relation between this analysis and the assessment of repeatability.

7,315 citations


Journal ArticleDOI
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.

6,031 citations


Journal ArticleDOI
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...

3,184 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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Journal ArticleDOI
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

2,298 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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