What causes pulmonary edema in acute respiratory distress syndrome,strengths of good communication skills,bridesmaid survival kit diy poem - Downloads 2016

Acute pulmonary edema is a pathological condition defined by the presence of large amounts of fluid in pulmonary alveoli and in pulmonary interstitium. Cardiogenic acute pulmonary edema by decreasing blood evacuation from the left atrium: atrial fibrillation, acute mitral regurgitation, mitral stenosis, thrombus or myxoma in the left atrium. Cardiogenic acute pulmonary edema caused by left ventricular diastolic dysfunction: aortic stenosis, hypertension, hypertrophic cardiomyopathy, acute myocardial ischemia. Cardiogenic acute pulmonary edema caused by left ventricular systolic dysfunction: acute myocardial ischemia, myocarditis, dilated cardiomyopathy, heart failure. Increased capillary permeability (acute respiratory distress syndrome): pneumonia, aspiration syndrome, inhalation of toxic gases, disseminated intravascular coagulation, anaphylaxis shock, acute pancreatitis. Incompletely understood causes: altitude acute pulmonary edema, neurogenic acute pulmonary edema, eclamsie, post anesthesia and post cardio-conversion.
Cardiogenic acute pulmonary edema is caused due to the increase pulmonary capillary pressure from 8-12 mm Hg (normal) to over 18 mm Hg. The main symptoms of acute pulmonary edema are the shortness of breath, cough, marked anxiety, cold and increased sweating and symptoms of the background heart disease.
Dyspnea is very intense, may occur in a patient who had until then no charge of this symptom (for example, a acute pulmonary edema that occurs after the onset of a myocardial infarction), or can overlap with the symptoms of preexisting heart failure .
A patient that is restless, anxious or confused with sweaty, pale or mottled skin, with central type cyanosis, the patient is breathing typically standing at the edge of the bed and using accessory respiratory muscles.
Marked dyspnea, possibly vesicular murmur and prolonged expiration, rales crackles, of which level increases from the bases of the lungs to tops and can include the entire lung field.
Tachycardia, hypertension or hypotension and, depending on the case, rhythm disturbances or different heart murmurs. In some cases, may appear signs of right heart failure: hepatomegaly, jugular turgor, hepato-jugular reflux, lower limb edema.
Echocardiography can detect the presence of valvulopathies, of thrombus or myxoma in the left atrium, impaired function of the left ventricle. Positive diagnosis of cardiogenic acute pulmonary edema is relatively simple, it is based on patient history and symptoms. General measures: keep the patient in a sitting position, administration of oxygen on mask or nasal tube, dyspnea sedation with morphine. Furosemide, administrated intravenous in dose of 80-120 mg or more, divided into four doses of 40 mg, each, is the primary mean of treatment of cardiogenic acute pulmonary edema. Nitroglycerin, vasodilator with rapid effect, administrated sublingual (0.5 mg tablets, the dose can be repeated in 5-10 minutes) or intravenously, in the conditions of systolic blood pressure higher than 100 mm Hg.
Administration of digoxin can bring benefits by improving the cardiac tonus or by decreasing the heart rate in case of atrial fibrillation.
Other therapeutic measures in cardiogenic acute pulmonary edema are: miofilin administration or the administration of angiotensin converting enzyme inhibitors, assisted ventilation, circulatory support with counterpulsation balloon and the treatment of the cause that led to the installation of cardiogenic acute pulmonary edema. Anteroposterior chest radiograph shows bilateral alveolar opacities in a patient with subarachnoid hemorrhage who developed neurogenic pulmonary edema. Axial, contrast-enhanced computed tomography (CT) scan shows alveolar and interstitial pulmonary edema. The correct diagnosis relies on clinical and radiologic findings, despite some overlap in the clinical and imaging findings between the different causes.
An initial and rapid increase in pulmonary vascular pressure due to pulmonary vasoconstriction or pulmonary blood flow can lead to pulmonary microvascular injury. Two major components contribute to the pathogenesis of NPE: elevated intravascular pressure and pulmonary capillary leak. Whether the hemodynamic changes produce a pulmonary capillary leak through pressure-induced mechanical injury to the pulmonary capillaries or whether some direct nervous system control over pulmonary capillary permeability exists remains uncertain.
Gadolinium-based MRI contrast agents has been associated with several adverse effects, some of which can be serious. In conjunction with the clinical presentation, radiographic findings are generally sufficient to arrive at a diagnosis of NPE.
The specificity of chest radiographs, particularly portable, anteroposterior (AP) images, is low, and it may not be possible to differentiate the various causes of lung parenchymal shadowing on radiographs alone. Most patients with NPE are generally ill, and there may be transportation problems to computed tomography (CT) scanning and magnetic resonance imaging (MRI) units.
The heart is usually enlarged in cardiogenic pulmonary edema, but it may be normal in lung injury and NPE.
The infiltrates of cardiogenic pulmonary edema are usually diffuse, and air bronchograms are rare. One of 3 patterns is seen: a normal chest, bilateral perihilar pulmonary edema, or generalized pulmonary edema.
Another feature that may be seen is cardiac enlargement, in cases of previous cardiac failure. NPE is a known complication of lung transplantation.[2, 3] Herman and colleagues, however, found chest radiography to be helpful, but not definitive, in distinguishing problems after bilateral lung transplantation and found CT scanning to be excellent for the demonstration of airway problems. The reimplantation response (NPE due to ischemia, trauma, denervation, and lymphatic interruption) occurred in 12 patients and usually consisted of bilateral perihilar and basal consolidation.
Radiographic findings associated with the reimplantation response and rejection were nonspecific and were mimicked by fluid overload and infection.
The 3 principal features found were the distribution of pulmonary flow, the distribution of pulmonary edema, and the width of the vascular pedicle. A study by Liebman et al indicated that it is hazardous to accept a portable radiographic diagnosis of congestive heart failure as a cause of pulmonary edema.
CT scanning is seldom used in assessing patients with NPE and ARDS, mostly because of problems in transporting and monitoring these severely ill individuals. Tagliabue and colleagues reviewed the findings of 74 patients with ARDS who underwent chest CT scanning.[9] Lung opacities were bilateral in almost all patients and in most cases (86%) were dependent.
In contrast with previous reports, pleural effusion was a frequent finding (50%) that did not worsen the patients' prognosis. Gattinoni and co-authors examined 10 patients with full-blown ARDS who were receiving mechanical ventilation with positive end-expiratory pressure (PEEP) and who underwent lung CT scanning.[10] Seven healthy subjects also were included in the study. Stark and colleagues described the CT scan features of 28 patients with ARDS.[11] Diffuse lung consolidation, lobar or segmental disease, and multifocal, patchy involvement were observed. Research indicates that a variety of nuclear imaging techniques can be used to diagnose NPE. Raijmakers and co-investigators concluded that a 67Ga pulmonary leak index can be used in distinguishing ARDS from hydrostatic pulmonary edema. According to a study by Chen and Schuster, fluorodeoxyglucose (FDG)a€“positron emission tomography (PET) FDG-PET scanning may be useful for studying neutrophil kinetics during oleic acida€“induced lung injury.
Iodine-123 meta-iodobenzylguanidine (MIBG) results can be considered indicators of pulmonary endothelial cell function. Koizumi and colleagues studied serial scintigraphic assessment of 123I MIBG lung uptake in a patient with high-altitude pulmonary edema.[15] The initial evaluation was performed 7 days after the patient's admission. Medscape's clinical reference is the most authoritative and accessible point-of-care medical reference for physicians and healthcare professionals, available online and via all major mobile devices. The clinical information represents the expertise and practical knowledge of top physicians and pharmacists from leading academic medical centers in the United States and worldwide. More than 6000 evidence-based and physician-reviewed disease and condition articles are organized to rapidly and comprehensively answer clinical questions and to provide in-depth information in support of diagnosis, treatment, and other clinical decision-making. More than 1000 clinical procedure articles provide clear, step-by-step instructions and include instructional videos and images to allow clinicians to master the newest techniques or to improve their skills in procedures they have performed previously. More than 100 anatomy articles feature clinical images and diagrams of the human body's major systems and organs. More than 7100 monographs are provided for prescription and over-the-counter drugs, as well as for corresponding brand-name drugs, herbals, and supplements. Our Drug Interaction Checker provides rapid access to tens of thousands of interactions between brand and generic drugs, over-the-counter drugs, and supplements. Access health plan drug formulary information when looking up a particular drug, and save time and effort for you and your patient.
Medscape Reference features 129 medical calculators covering formulas, scales, and classifications. Hundreds of image-rich slideshow presentations visually engage and challenge readers while expanding their knowledge of both common and uncommon diseases, case presentations, and current controversies in medicine. Click on citations within drug and disease topics in our clinical reference to review the clinical evidence on MEDLINE. Medscape is the leading online destination for healthcare professionals seeking clinical information. All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. A chest X-ray (CXR) or chest radiograph is an image obtained by passing ionizing X-rays (electromagnetic radiation) through the chest (thorax). The x-ray of chest is may be taken from different angles based on the direction of passing the ionizing X-rays.
Posterior-anterior (PA) view refers to X-ray images taken by allowing x-rays to pass from the back side of the body to the front side of chest and fall on the x-ray film placed in front of chest. Anterior-posterior (AP) view refers to X-ray images taken by allowing the ionizing rays to pass from front to the back of the chest where the x-ray film is placed. Lateral view refers to films obtained by pass X-rays from one side of the patient towards the other side where film is placed. Other occasionally used views of chest X-ray include decubitus view (lying down position), oblique and expiratory view.
Structures which can be examined in chest X-rays are airways, cardiac shadow, ribs and thoracic vertebra, position of trachea, costophrenic angle (angle between diaphragm and rib cage), cardiophrenic angle, diaphragm, lung parenchyma, breast shadow and other soft tissue shadows.

Localised opacities are seen in pneumonia (inflammation of lung parenchyma), lung inflammation due to radiation exposure (radiation pneumonitis), infarction of lung, and certain lung malignancies. Single well-defined opacities are seen in lung cancer, tuberculosis, localized bacterial and fungal infections, cyst arising from the bronchus, blood vessel malformation and in autoimmune diseases (rheumatoid arthritis and Wegener’s granulomatosis). Multiple diffuse patchy opacities are seen in lung fibrosis, Pneumocystitis carnii pneumonia, allergic pneumonitis, and in occupational lung diseases (pneumoconiosis). Diffuse alveolar patchy opacities are seen in lung edema in heart failure, alveolar haemorrhage, acute respiratory distress syndrome and sarcoidosis. Diffuse nodular opacities are seen in metastatic cancer of the lung, haematogenous (blood) spread of bacteria, virus and fungus to lung, and in occupational lung diseases.
Bronchial asthma can cause hyperinflation in patients with severe bronchial asthma, whereas in mild and moderate bronchial asthma it appears normal. Acute and sub-acute allergic pneumonitis can present with poorly defined, diffuse and patchy infiltration of lung. Lung fibrosis is usually secondary to pulmonary tuberculosis, hence more common near the apex of the lungs.
Pleural effusion (collection of fluid in pleural sac) presents with uniform homogenous opacity which is obliquely inclined with more opacities towards the outer end of the lung margin. Chronic obstructive pulmonary disease (COPD): Increased translucency, diminished lung marking, flattening of the diaphragm, hyperinflation of lung and presence of bullae suggest emphysema.
Pneumothorax (collection of air in pleural sac): There will be uniform opacity on one side of lung and trachea and heart will be pushed towards the opposite side of pneumothorax. Hydropneumothorax presents with uniform opacities with the meniscus exactly transverse to the line of patient. Empyema which is characterized by collection of pus in the pleural cavity shows the fluid level similar to the hydropneumothorax.
Lung abscess is characterized by collection of pus in the lungs which is characterized by presence of cavity filled with fluid and air in the X-ray. Bronchiectasis (destructive dilatation of larger airways): This may appear normal on X-ray, but certain types of bronchiectasis may show cystic dilatations with or without air fluid levels.
Pulmonary embolism : This may present with focal reduced blood flow (oligemia), wedge shaped opacities, and sometimes there might be enlargement of right pulmonary artery.
Lung cancer may present as solitary pulmonary nodule mainly near the apex of lung, and serial x-ray show characteristic doubling time of 6 to 18 months in malignant cancers, and doubling time of more than 24 months in case of benign cancers.
Pneumoconiosis (occupational lung diseases) are due to chronic exposure to minerals, metals and organic material which characteristically present with allergic pneumonitis. Heart failure may be associated with enlargement of heart, prominence of vascular marking in lungs, and variation in shape of heart.
Coarctation of aorta is constriction of aorta distal to left subclavian artery and this presents with dilatation of left subclavian artery and ascending aorta.
Tetrology of fallot is a congenital heart disease characterized by pulmonary stenosis, right ventricular hypertrophy, ventricular septal defect and overriding of aorta.
Pulmonary stenosis is obstruction to the flow of blood from right ventricle to pulmonary artery due to narrowing of the pulmonary artery, and is associated with enlargement of the right ventricle.
Mitral stenosis is a narrowing of the mitral valve opening hence it causes resistance to flow of blood from left atrium to left ventricle.
Mitral regurgitation is back flow of blood from left ventricle back to left atrium due to incomplete closure of mitral valve. Aortic stenosis is narrowing of aortic opening hence left ventricle may not pump sufficient blood into aorta with each heart beat. Tricuspid stenosis is characterised by obstruction of blood flow from right atrium to right ventricle due narrowing of opening of tricuspid valve.
Perforation of the intestines or perforated gastric ulcer can show presence of gas under diaphragm on x-ray.
Other features due to traumatic injury like pneumothorax, hemorrhage in thoracic cavity and hydropneumothrorax may be diagnosed using a chest X-ray. Please note that any information or feedback on this website is not intended to replace a consultation with a health care professional and will not constitute a medical diagnosis. Grant Support: By the National Heart, Lung, and Blood Institute, National Institutes of Health (PO1 HL 31992-18). The lung's alveolar–capillary structure normally provides a large surface for gas exchange and a tight barrier between alveolar gas and pulmonary capillary blood. Cardiogenic acute pulmonary edema is an acute form of heart failure caused by increased pressure in the pulmonary capillary.
In severe forms may be present hypercapnia and respiratory acidosis, which constitute signs of gravity. Its beneficial effects are explained by the occurrence of venous dilation, which will lead to decreased preload (quickly installed) and diuresis (which occurs in 20-90 minutes after the administration of furosemide). Digoxin administration is contraindicated in cardiogenic acute pulmonary edema associated with mitral stenosis or with acute myocardial infarction. The latter, noncardiogenic pulmonary edema (NPE), is caused by changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult (see the images below).
An increase in vascular permeability consequently results in edema formation, as suggested by the frequent observation of pulmonary hemorrhage in NPE (ie, the blast theory).
The neuro-effector site for nervous systema€“induced pulmonary edema appears to be relatively well established in regions about the caudal medulla, where nuclei regulating systemic arterial pressure, as well as afferent and efferent pathways to and from the lungs, are located.
The use of chest radiography and other tests is key to establishing the diagnosis and to distinguishing between the 2 types of pulmonary edema. It has extremely rare life-threatening systemic complications, which can lead to bronchospasm, hypersensitivity reactions, and cardiovascular arrest. Conventional chest radiography is readily and universally available, and it has the added advantage of portability; chest radiography is the examination of choice. Moreover, because these patients may be restless, sedation may be required to obtain images that are not degraded by motion artifacts.
However, the heart may also be of normal size in cardiogenic edema after acute myocardial infarction. Infiltrates in nephrogenic pulmonary edema are classically described as having a bat-wing distribution, whereas those in lung injury tend to be more peripheral. The early signs of pulmonary edema (interstitial edema) are the septal lines (Kerley B lines), which are horizontal lines seen laterally in the lower zones. In their study, the authors reviewed the postoperative chest radiographic and CT scan findings in 13 patients who underwent bilateral lung transplantation.[4] Portable chest radiography was performed daily for about 10 days, after which upright posteroanterior studies were performed daily for about 10 days and then as clinically required. Twelve episodes of acute rejection, an imprecise clinical diagnosis, occurred in 10 patients. The cause of the pulmonary edema can be determined with a high degree of accuracy by paying careful attention to certain radiographic features. The ancillary features were pulmonary blood volume, peribronchial cuffing, septal lines, pleural effusions, air bronchograms, lung volume, and cardiac size. In their report, the authors assessed the usefulness of portable chest radiographs in defining the amount of physiologic shunting and the severity of NPE.[6, 7] Ten of their 11 patients had acute respiratory failure. High-resolution CT (HRCT) scanning demonstrates widespread airspace consolidation, which may have predominant distribution in the dependent lung regions.
Large lung cysts and small cysts producing a Swiss-cheese appearance of the parenchyma were detected.
In their study, the investigators examined the effectiveness of a noninvasive, bedside, dual-radionuclide method (67Ga circulating transferrin and technetium-99m [99mTc]a€“labeled RBCs) of measuring pulmonary microvascular permeability, in differentiating between hydrostatic pulmonary edema and pulmonary edema due to ARDS.[13] Patients in the study suffered from respiratory insufficiency and bilateral, alveolar pulmonary edema, as demonstrated on chest radiographs.
With various definitions, a supranormal pulmonary leak index for ARDS had a sensitivity of 100%, while its specificity ranged from 46-75%. The investigators measured neutrophil glucose uptake with FDGa€“PET scanning in anesthetized dogs after intravenous, oleic acida€“induced, acute lung injury (n = 6) or after low-dose, intravenous endotoxin (which is known to activate neutrophils without causing lung injury) followed by oleic acid (n = 7).
Lung transplantation: indications, donor and recipient selection, and imaging of complications. Limitations of portable roentgenography of the chest in patients with acute respiratory failure. Adult respiratory distress syndrome due to pulmonary and extrapulmonary causes: CT, clinical, and functional correlations. Positron emission tomography with [18F]fluorodeoxyglucose to evaluate neutrophil kinetics during acute lung injury. Serial scintigraphic assessment of iodine-123 metaiodobenzylguanidine lung uptake in a patient with high-altitude pulmonary edema. Topics are richly illustrated with more than 40,000 clinical photos, videos, diagrams, and radiographic images. The articles assist in the understanding of the anatomy involved in treating specific conditions and performing procedures.
Check mild interactions to serious contraindications for up to 30 drugs, herbals, and supplements at a time.
Plus, more than 600 drug monographs in our drug reference include integrated dosing calculators. This is helpful in screening and diagnosing various diseases of the organs in the thoracic cavity including the airways and alveoli (lungs), pleura, heart and blood vessels, bones, diaphragm, and certain gastrointestinal conditions. This is the least commonly used view as the interpretation of the information in these films is difficult.
Presence of pneumatoceles indicates that the cause of pneumonia as staphylococcal infection.
Chronic allergic pneumonitis and progressive allergic pneumonitis present with honey comb appearance. Other findings suggestive of COPD on X-ray include pneumonic opacities and heart failure features.

Dilated airways may appear to run parallel giving tram track appearance when viewed longitudinally, or may show ring shadows when seen in cross section. Alveoli are typically deflated and exert negative pressure which pulls the trachea and heart towards the side of atelactasis. Silica and coal dust exposure is characterized by small round opacities, and asbestosis exposure is characterized by linear opacities. There might be notching of 3rd to 9th rib due to erosion of inferior rib by dilated collateral blood vessels.
Hypertrophic and restrictive cardiomyopathy may show very mild cardiac enlargement on X-ray.
In chest X-ray heart appears boot-shaped and vascular marking in the lung may be diminished.
X-ray shows straightening of left upper border of heart, pulmonary arteries will be very prominent, and the esophagus will be pushed back. X-ray characteristically shows enlargement of left atrium, there will be increased prominence of pulmonary blood vessels. Hypertrophy of left ventricle of heart may present with rounding off of apex of heart in chest X-ray.
Large hernia may be made out in normal chest X-ray, and there might be features suggestive of aspiration in lower lobes of lung.
Piantadosi: Division of Pulmonary and Critical Care Medicine, Box 3315, Duke University Medical Center, Durham, NC 27710.
Schwartz: Division of Pulmonary and Critical Care Medicine, Box 2629, Duke University Medical Center, Durham, NC 27710.
Diffuse damage to the alveolar region occurs in the acute or exudative phase of acute lung injury and ARDS (Figure 2). The hydraulic conductance (Kf,c) is the capacity to filter fluid as filtration pressure increases relative to number and size of endothelial openings per unit surface area.
These components often work in concert, as in pulmonary edema after epileptic convulsions or intracranial pressure elevation.
Pulmonary vascular plethora often occurs with upper lobe blood diversion in cardiogenic cases; vessels of the upper lobe are balanced to cephalic in fluid overload but are normal in lung injury. Although the peripheral infiltrate is fairly specific for lung injury, the diffuse variety is seen with equal frequency in lung injury. The septal lines arise from the pleural surface and are typically 1 mm thick and 10 mm long; unlike blood vessels, these reach the edge of the lung. However, over the course of 24-48 hours following the onset of tachypnea, dyspnea, and hypoxia, ARDS becomes more widespread and uniform. Radiographic changes consisted of bibasal (n = 2) and right middle and lower (n = 2) or left basal consolidation (n = 1); no changes were observed in 7 episodes. In general, chest radiography was inaccurate in the assessment of these complications, and CT scanning was accurate in such assessments.
Differing constellations of these features, each characteristic of a specific type of edema, were found. Radiographic assessment of the amount of pulmonary edema and the severity of left ventricular failure was compared with the physiologic shunt fraction, tracer-measured lung water, and pulmonary arterial wedge pressure. Therefore, the radiographic findings were predictive for the shunt value of the preceding day. The most consistent morphologic finding in ARDS was attenuating in the dependent regions of the lung. On receiver operating characteristic curves, the pulmonary leak index performed best when ARDS and hydrostatic pulmonary edema were defined only on the basis of risk factors.
The authors concluded that the rate of FDG uptake in the lungs during lung injury reflects the state of neutrophil activation.
Customize your Medscape account with the health plans you accept, so that the information you need is saved and ready every time you look up a drug on our site or in the Medscape app. Although the chest X-ray is the most widely performed diagnostic imaging study, it does have several limitations. Hence this view is preferred only in bed ridden patients, in conditions to see posterior parts of lungs and for abnormalities of vertebrae and scapula.
Patchy opacity with cavitary lesion in apex of lung is usually due to tubercular infection.
This damage involves both the endothelial and epithelial surfaces and disrupts the lung's barrier function, flooding alveolar spaces with fluid, inactivating surfactant, causing inflammation, and producing severe gas exchange abnormalities and loss of lung compliance. The osmotic reflection coefficient (? ) determines osmotic permeability to specific proteins (0 is permeable and 1 is impermeable).
As filtration pressure increases, dilute fluid is forced into the interstitial space, which increases the absorption force (arrowhead) opposing it (square 1). Pulmonary arterial (PA) blood entering such units cannot be oxygenated and decreases the oxygen saturation of blood returning to the left atrium (LA ). The hemodynamic component is relatively brief and may unmask pure NPE, such as that seen in experimental seizures. As the edema progresses, alveolar edema is observed in a butterfly pattern characterized by the central predominance of shadows, with a clear zone at periphery lobes.
A useful characteristic for differentiating cardiac pulmonary edema from NPE, as well as from pneumonia and other widespread exudates, is the amount of time it takes for the edema to develop and to vanish.
Following the intravenous administration of steroids, radiographic resolution occurred in 4 cases. The radiographic scores for edema were not predictive for the shunt fraction or for the tracer-measured lung water. Pulmonary air cysts (30%), always multiple and mostly bilateral, were associated with a mortality rate (55%) higher than that of the whole study group (35%). Assuming that the 3 levels were a representative sample of the whole lung, the authors computed lung weight from the mean CT scan number and lung gas volume.
The index was better than hemodynamic measures, and its performance equaled that of ventilatory variables in discriminating between edema types (if definitions were based primarily on hemodynamic and ventilatory variables, respectively). Easily compare tier status for drugs in the same class when considering an alternative drug for your patient. However, several other imaging studies are available as a follow up to the chest X-ray thereby providing better visualization of underlying disease.
These events are reflected in the presence of bilateral infiltrates, which are indistinguishable by conventional radiology from cardiogenic pulmonary edema (11). Capillary damage in the acute respiratory distress syndrome may increase Kf,c and decrease ? , increasing capillary fluid flux at constant hydrostatic pressure. The increase in interstitial fluid volume causes perivascular swelling (square 2), and interstitial fluid is removed at a greater rate (square 3) by lung lymphatics (Ly). Local hypoxic pulmonary vasoconstriction diverts PA blood flow to better ventilated alveoli, which improves ventilation–perfusion matching. Septal lines indicative of interstitial edema are more frequent with cardiogenic causes than with others.
If substantial improvement occurs within 24 hours, this is virtually diagnostic of cardiac pulmonary edema.
The highest accuracy was obtained in distinguishing capillary permeability edema from all other varieties (91%). The radiographic score for congestive heart failure was correlated with the wedge pressure but not well enough to be clinically useful. Compared with chest radiography, CT scanning often yielded additional information (66%), with direct influence on patient treatment in 22% of cases.
Computed tomography of the chest often demonstrates heterogeneous areas of consolidation and atelectasis, predominantly in the dependent lung (12–13), although areas of apparent sparing may still show inflammation. A breech of the alveolar epithelium allows plasma and interstitial fluid to leak into the airspaces faster than salt and water can be pumped back into the interstitial space. If hypoxic pulmonary vasoconstriction is absent or large areas of lung are flooded, pulmonary venous oxygen saturation decreases and hypoxemia occurs.
The lowest accuracy (81%) was obtained in distinguishing chronic cardiac failure from renal failure.
Pathologic findings consist of diffuse alveolar damage, including capillary injury, and areas of exposed alveolar epithelial basement membrane (14–16). The right half of the diagram illustrates the effect of PEEP, which stabilizes alveoli that are then better able to exchange gas because they have more surface area. In 15 patients, CT scans provided additional information not obvious on bedside chest radiographs and led to a change in care for 5 patients. The alveolar spaces are lined with hyaline membranes and are filled with protein-rich edema fluid and inflammatory cells.
When pulmonary venous oxygen saturation increases, hypoxic pulmonary vasoconstriction is relieved, allowing more uniform distribution of blood flow. The interstitial spaces, alveolar ducts, small vessels, and capillaries also contain macrophages, neutrophils, and erythrocytes.
However, PEEP may overdistend healthy alveoli, thereby damaging functional gas exchange units and redirecting blood flow toward damaged alveoli, worsening the capillary leak rate.

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