Ware L and Matthay M. N Engl J Med 2005;353:2788-2796
Fisiopatologia do Edema de Pulmão - Cardíaco
Presenter
Presentation Notes
Figure 1. Physiology of Microvascular Fluid Exchange in the Lung. In the normal lung (Panel A), fluid moves continuously outward from the vascular to the interstitial space according to the net difference between hydrostatic and protein osmotic pressures, as well as to the permeability of the capillary membrane. The following Starling equation for filtration of fluid across a semipermeable membrane describes the factors that determine the amount of fluid leaving the vascular space: Q = K[(Pmv - Ppmv) - ({pi}mv - {pi}pmv)], where Q is the net transvascular flow of fluid, K is the membrane permeability, Pmv is the hydrostatic pressure in the microvessels, Ppmv is the hydrostatic pressure in the perimicrovascular interstitium, {pi}mv is the plasma protein osmotic pressure in the circulation, and {pi}pmv is the protein osmotic pressure in the perimicrovascular interstitium. When hydrostatic pressure increases in the microcirculation, the rate of transvascular fluid filtration rises (Panel B). When lung interstitial pressure exceeds pleural pressure, fluid moves across the visceral pleura, creating pleural effusions. Since the permeability of the capillary endothelium remains normal, the filtered edema fluid leaving the circulation has a low protein content. The removal of edema fluid from the air spaces of the lung depends on active transport of sodium and chloride across the alveolar epithelial barrier. The primary sites of sodium and chloride reabsorption are the epithelial ion channels located on the apical membrane of alveolar epithelial type I and II cells and distal airway epithelia. Sodium is actively extruded into the interstitial space by means of the Na+/K+-ATPase located on the basolateral membrane of type II cells. Water follows passively, probably through aquaporins, which are water channels that are found predominantly on alveolar epithelial type I cells.6 Noncardiogenic pulmonary edema (Panel C) occurs when the permeability of the microvascular membrane increases because of direct or indirect lung injury (including the acute respiratory distress syndrome), resulting in a marked increase in the amount of fluid and protein leaving the vascular space. Noncardiogenic pulmonary edema has a high protein content because the more permeable microvascular membrane has a reduced capacity to restrict the outward movement of larger molecules such as plasma proteins. The degree of alveolar flooding depends on the extent of interstitial edema, the presence or absence of injury to the alveolar epithelium, and the capacity of the alveolar epithelium to actively remove alveolar edema fluid. In edema due to acute lung injury, alveolar epithelial injury commonly causes a decrease in the capacity for the removal of alveolar fluid, delaying the resolution of pulmonary edema.6
Edema
Ware L and Matthay M. N Engl J Med 2000;342:1334-1349
Edema Pulmonar Não Cardíaco - ARDS
Presenter
Presentation Notes
Table 1. Definitions of the Acute Respiratory Distress Syndrome.
Edema
Ware L and Matthay M. N Engl J Med 2000;342:1334-1349
Fase Aguda da ARDS
Presenter
Presentation Notes
Figure 3. The Normal Alveolus (Left-Hand Side) and the Injured Alveolus in the Acute Phase of Acute Lung Injury and the Acute Respiratory Distress Syndrome (Right-Hand Side). In the acute phase of the syndrome (right-hand side), there is sloughing of both the bronchial and alveolar epithelial cells, with the formation of protein-rich hyaline membranes on the denuded basement membrane. Neutrophils are shown adhering to the injured capillary endothelium and marginating through the interstitium into the air space, which is filled with protein-rich edema fluid. In the air space, an alveloar macrophage is secreting cytokines, interleukin-1, 6, 8, and 10, (IL-1, 6, 8, and 10) and tumor necrosis factor {alpha} (TNF-{alpha}), which act locally to stimulate chemotaxis and activate neutrophils. Macrophages also secrete other cytokines, including interleukin-1, 6, and 10. Interleukin-1 can also stimulate the production of extracellular matrix by fibroblasts. Neutrophils can release oxidants, proteases, leukotrienes, and other proinflammatory molecules, such as platelet-activating factor (PAF). A number of antiinflammatory mediators are also present in the alveolar milieu, including interleukin-1-receptor antagonist, soluble tumor necrosis factor receptor, autoantibodies against interleukin-8, and cytokines such as interleukin-10 and 11 (not shown). The influx of protein-rich edema fluid into the alveolus has led to the inactivation of surfactant. MIF denotes macrophage inhibitory factor.
Edema
Ware L and Matthay M. N Engl J Med 2000;342:1334-1349
Fase Aguda e Fase Fibrosante da ARDS
Presenter
Presentation Notes
Figure 1. Radiographic and Computed Tomographic (CT) Findings in the Acute, or Exudative, Phase (Panels A and C) and the Fibrosing-Alveolitis Phase (Panels B and D) of Acute Lung Injury and the Acute Respiratory Distress Syndrome. Panel A shows an anteroposterior chest radiograph from a 42-year-old man with the acute respiratory distress syndrome associated with gram-negative sepsis who was receiving mechanical ventilation. The pulmonary-artery wedge pressure, measured with a pulmonary-artery catheter, was 4 mm Hg. There are diffuse bilateral alveolar opacities consistent with the presence of pulmonary edema. Panel B shows an anteroposterior chest radiograph from a 60-year-old man with acute lung injury and the acute respiratory distress syndrome who had been receiving mechanical ventilation for seven days. Reticular opacities are present throughout both lung fields, a finding suggestive of the development of fibrosing alveolitis. Panel C shows a CT scan of the chest obtained during the acute phase. The bilateral alveolar opacities are denser in the dependent, posterior lung zones, with sparing of the anterior lung fields. The arrows indicate thickened interlobular septa, consistent with the presence of pulmonary edema. The bilateral pleural effusions are a common finding.1415 Panel D shows a CT scan of the chest obtained during the fibrosing-alveolitis phase. There are reticular opacities and diffuse ground-glass opacities throughout both lung fields, and a large bulla is present in the left anterior hemithorax. Panels C and D are reprinted from Goodman16 with the permission of the publisher.
Edema
Ware L and Matthay M. N Engl J Med 2005;353:2788-2796
Edema Pulmonar Cardiogênico x Não Cardiogênico
Presenter
Presentation Notes
Figure 2. Representative Chest Radiographs from Patients with Cardiogenic and Noncardiogenic Pulmonary Edema. Panel A shows an anteroposterior chest radiograph from a 51-year-old man who presented with acute anterior myocardial infarction and acute cardiogenic pulmonary edema. Note the enlargement of the peribronchovascular spaces (arrowheads) and the prominent septal lines (Kerley's B lines) (arrows) as well as acinar areas of increased opacity that coalesce into frank consolidations. The periphery is relatively spared, a common finding in cardiogenic edema.31 Panel B shows an anteroposterior chest radiograph from a 22-year-old woman whose blood culture was positive for Streptococcus pneumoniae, causing pneumonia complicated by septic shock and acute respiratory distress syndrome. Diffuse alveolar infiltrates appear patchy and bilateral with air bronchograms (arrows), findings that are characteristic of, but not specific for, noncardiogenic edema and acute lung injury.31 Although involved, the left upper lobe is relatively spared. There is no evidence of vascular engorgement or redistribution of pulmonary blood flow.
Edema
Ware L and Matthay M. N Engl J Med 2005;353:2788-2796
Edema Pulmonar Cardiogênico x Não Cardiogênico
Presenter
Presentation Notes
Table 1. Radiographic Features That May Help to Differentiate Cardiogenic from Noncardiogenic Pulmonary Edema.
Edema
Ware L and Matthay M. N Engl J Med 2005;353:2788-2796
Algoritmo Para diferenciar Edema Cardiogênico de Não Cardiogênico
Presenter
Presentation Notes
Figure 3. Algorithm for the Clinical Differentiation between Cardiogenic and Noncardiogenic Pulmonary Edema.
Edema
Renal
Nefrite Glomerular Aguda
Síndrome Nefrótica
Falência Renal Crônica
Estágio final de doença renal em diálise
Edema
Nefrite Glomerular
Retenção de Sódio e água resultante da insuf. Renal
Permeabilidade Capilar Aumentada
– Urina, Sangue, US e Biopsia
– Hematúria, Proteinúria
Edema
Investigação Renal
Edema
Síndrome Nefrótica
Proteinúria maciça > 3,5g / d
Hipoalbuminemia
Lipídios aumentado, Hipercoagulabilidade
Etiologia
– Doença Renal
Membranosa - GN focal segmentar mínimas alterações
