Where Lp is a unit of membrane permeability, S is the surface area available for fluid movement, Õcap is capillary fluid pressure and Õif is the interstitial fluid pressure, and s is the reflection coefficient of proteins across the capillary wall. Noncardiogenic pulmonary edema is thought to occur due to increased capillary permeability, whereas cardiogenic pulmonary edema is secondary to increased pulmonary venous pressure causing increased capillary pressure in the lungs.[3,4] Obviously noncardiogenic pulmonary edema can only be diagnosed in the absence of evidence of an underlying cardiogenic etiology. Some etiologies of noncardiogenic pulmonary edema include ARDS, high altitude pulmonary edema, neurogenic pulmonary edema, salicylate toxicity, pulmonary embolism, reexpansion pulmonary edema, reperfusion pulmonary edema, transfusion associated lung injury, and opioid overdose. [5]. It is well known that opioids act on mu2 receptors to decreased sensitivity of medullary chemoreceptors to ...
NONCARDIOGENIC PULMONARY EDEMA Noncardiogenic pulmonary edema(NCPE) results from elevated pulmonary capillary hydrostatic pressure damage to vascular
Purpose: The present study proposes the comprehensive ultrasound evaluation of a consecutive batch of patients with acute cardiogenic pulmonary edema. Method: The registry included all patients with acute pulmonary edema from 2 emergency hospitals between February and May 2016. During the first 3 days of admission, a transthoracic ultrasound was performed which included the parameters of systolic and diastolic function of the left ventricle, right ventricular systolic function, heart cavity dimensions, estimated pulmonary pressure, and the presence and severity of valvular disease. Results: A total of 70 patients were enrolled in the registry. The mean ejection fraction of the left ventricle was 39.5±11.4% and the average indexed end-diastolic volume was 77.7±29.5ml/m2, above the upper limit of normal. All patients in whom diastolic function could be evaluated had a degree of diastolic dysfunction. Functional parameters of the right ventricle were normalized as average, and the mean pulmonary artery
We believe that Dr. Siegels concern about osmotic demyelination is unfounded. There is no actual evidence that "osmotic demyelination" has ever been caused by any rate of correction of hyponatremia (1). A recent prospective study showed no relationship (2). More important, in patients with hyponatremic encephalopathy, therapy with small increases in plasma sodium, as suggested by Dr. Siegel, leads to 100% mortality (2). With symptomatic hyponatremia, increased intracranial pressure secondary to cerebral edema is the critical factor, and its management determines patient outcome. Thus, such patients must be treated with hypertonic sodium chloride, which increases plasma sodium levels sufficiently to relieve brain edema (1). Such a maneuver was used in the six patients in our report who survived and were neurologically intact after 1 year of follow-up. More important, the patient who received no therapy died of brain stem herniation, without demyelination lesions ...
Identifying the underlying etiology of the first episode of pulmonary edema can sometimes be challenging as all causes of pulmonary edema share the same clinical features to some extent. The first step in approaching pulmonary edema is to differentiate cardiac etiologies from non-cardiac etiologies. Clinical features that point toward cardiogenic pulmonary edema include history of acute coronary syndrome or congestive heart failure and the finding of S3, JVD, or peripheral pitting edema on physical examination. Other features of cardiogenic pulmonary edema include elevated cardiac enzymes and enlarged cardiac silhouette or the presence of Kerley B lines in CXR (3). In contrast, non-cardiac etiologies of pulmonary edema should be suspected in patients with ongoing pulmonary or non-pulmonary infection and sleep apnea syndrome (SAS), those at the risk of aspiration pneumonia or inhalation injury, and after multiple blood transfusions (3). The gold standard test to differentiate cardiogenic ...
Cardiogenic Pulmonary Edema (Cardiogenic Pulmonary Oedema): Read more about Symptoms, Diagnosis, Treatment, Complications, Causes and Prognosis.
TY - JOUR. T1 - Neurogenic pulmonary edema. T2 - Another multiple-hit model of acute lung injury. AU - Gajic, Ognjen. AU - Manno, Edward M.. PY - 2007/8/1. Y1 - 2007/8/1. KW - Acute lung injury. KW - Complications. KW - Head injury. KW - Outcome assessment. KW - Pulmonary edema. UR - http://www.scopus.com/inward/record.url?scp=34547657611&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=34547657611&partnerID=8YFLogxK. U2 - 10.1097/01.CCM.0000277254.12230.7D. DO - 10.1097/01.CCM.0000277254.12230.7D. M3 - Editorial. C2 - 17667244. AN - SCOPUS:34547657611. VL - 35. SP - 1979. EP - 1980. JO - Critical Care Medicine. JF - Critical Care Medicine. SN - 0090-3493. IS - 8. ER - ...
Two patients have been observed to develop acute repetitive pulmonary edema in the absence of left ventricular failure as evidenced by a normal or near normal left atrial pressure recorded during these periods. Continuous monitoring of the left atrial pressure was made possible by a catheter inserted during open-heart surgery. Both patients suffered brain damage, presumably secondary to cerebral air embolism, and eventually succumbed.. Although the authors think that a causal relationship between cerebral damage and pulmonary edema best explains the mechanism in these two patients, this must remain conjectural. Neurogenic pulmonary edema, however, has been assumed to be secondary to elevated left atrial and left ventricular end-diastolic pressures. If a specific relation exists in these patients, the findings herein described strongly suggest that this may not be the mechanism.. ...
Transfusion-related acute lung injury (TRALI) is defined as noncardiogenic pulmonary edema temporally related to the transfusion of blood products. We present a patient who, while undergoing orthotopic liver transplantation, developed acute pulmonary edema within minutes of administration of fresh frozen plasma (FFP).
Free Online Library: The role of early diagnosis in Neurogenic Pulmonary edema.(STUDENT PAPERS) by FOCUS: Journal for Respiratory Care & Sleep Medicine; Health care industry Health, general Diagnosis
Peacock W. Peacock W Peacock, W. Frank.Chapter 57. Congestive Heart Failure and Acute Pulmonary Edema. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. Tintinalli J.E., Stapczynski J, Ma O, Cline D.M., Cydulka R.K., Meckler G.D., T Eds. Judith E. Tintinalli, et al.eds. Tintinallis Emergency Medicine: A Comprehensive Study Guide, 7e New York, NY: McGraw-Hill; 2011. http://accessmedicine.mhmedical.com/content.aspx?bookid=348§ionid=40381522. Accessed December 10, 2017 ...
Presented by Dr. Anand Swaminathan, NYU/Bellevue. A 65 yo M pt with PMH of ESRD, HTN, CAD comes in c/o SOB x3 days after missing hemodialysis twice in the past week. A portable CXR is ordered, and it looks similar to this: http://radiopaedia.org/cases/apo-arrowsjpg Acute Pulmonary Edema. Causes: MI, PE, dysrhythmia, infection, tox, therapy non-compliance Managment:…
There is no one single test for confirming that breathlessness is caused by pulmonary edema; indeed, in many cases, the cause of shortness of breath is probably multifactorial. Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema[2] Lung ultrasound, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema.[18] Especially in the case of cardiogenic pulmonary edema, urgent ...
There is no single test for confirming that breathlessness is caused by pulmonary edema - there are many causes of shortness of breath. Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. A chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema[2] Lung ultrasound, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema.[20] Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the ...
High-altitude pulmonary edema (HAPE) is a form of noncardiogenic pulmonary edema, generally beginning within the first 2 to 4 days after ascent above 2500 m (8200 ft). The earliest symptoms are fatigue, weakness, dyspnea on exertion, and decreased exercise performance. Symptoms of Acute mountain sickness (AMS) such as headache, anorexia, and lassitude may also be present, but HAPE may develop without AMS. First symptoms usually include persistent dry cough and dyspnea followed by tachycardia, tachypnea, and cyanosis at rest. Patients suffering from HAPE often experience sudden onset of symptoms upon awakening after the second night at altitude. Eventually the victim develops dyspnea at ...
Cardiogenic pulmonary edema (CPE) is defined as pulmonary edema due to increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure. CPE reflects the accumulation of fluid with a low-protein content in the lung interstitium and alveoli as a result of cardiac dysfunction (see the image below).
Isoflurane and sevoflurane protect lungs with ischemia-reperfusion (IR) injury. We examined the influence of desflurane on IR lung injury using isolated rabbit lungs perfused with a physiological salt solution. The isolated lungs were divided into three groups: IR, desflurane-treated ischemia-reperfusion (DES-IR), and ventilation/perfusion-continued control (Cont) groups (n = 6 per group). In the DES-IR group, inhalation of desflurane at 1 minimum alveolar concentration (MAC) was conducted in a stable 30-min phase. In the IR and DES-IR groups, ventilation/perfusion was stopped for 75 min after the stable phase. Subsequently, they were resumed. Each lung was placed on a balance, and weighed. Weight changes were measured serially throughout this experiment. The coefficient of filtration (Kfc) was determined immediately before ischemia and 60 min after reperfusion. Furthermore, bronchoalveolar lavage fluid (BALF) was collected from the right bronchus at the completion of the experiment. After the
CPAP has become a widely accepted treatment in respiratory medicine for obstructive sleep apnea (OSA). With this study, Bersten and colleagues add evidence for the emerging role of CPAP in the treatment of acute pulmonary edema. Earlier work by Vaisanen and Rasanen showed a reduction of respiratory rate with CPAP, but no effect on PaO2 or PaCO2 (1). In the current study, however, significant improvement was seen in the respiratory rate as well as PaCO2, pH, and the PaO2 to FIO2 ratio within the critical first hour of treatment. This study shows that early implementation of CPAP can decrease both the need for intubation as well as length of stay in the intensive care unit (ICU) for a patient who develops acute pulmonary edema. Future studies should examine whether nasal CPAP affords the same benefit as mask CPAP in the treatment of acute pulmonary edema. The benefits of long-term nasal CPAP on left ventricular function in patients with OSA and congestive heart failure have been shown (2). Nasal ...
Wolters Kluwer Health may email you for journal alerts and information, but is committed to maintaining your privacy and will not share your personal information without your express consent. For more information, please refer to our Privacy Policy ...
As the pulmonary edema progresses, alveolar edema develops with disruption of the alveolar capillary membrane. There is bi-basal diffuse haziness of lung fields, Kerley B lines, loss of distinct vascular margins, increased bronchovascular margins (bats wing sign) and ares of consolidation, lung mottling and pleural effusion on chest x-ray. Cardiomegaly may also be present. Acute respiratory distress syndrome, a type of non cardiogenic pulmonary edema may resemble cardiac pulmonary edema. But within next 24-48 hours following the onset of symptoms, ARDS becomes more uniform. Differentiation of cardiac pulmonary edema from non cardiogenic pulmonary edema, can be done by the time it takes for the edema to develop and to vanish. If substantial improvement occurs within 24 hours, it is usually cardiac pulmonary edema ...
Non-cardiogenic pulmonary edema (NCPE) is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest radiograph, without evidence of left atrial hypertension/congestive heart failure/fluid
Cardiogenic pulmonary edema (CPE) is a frequent presenting process for acute out-of-hospital practice. Acute left heart failure may occur from a variety of processes that rapidly deteriorates to this generalized cardiopulmonary disorder. The classical treatment of out-of-hospital CPE includes supplemental oxygen, vasodilators, loop diuretics, and morphine. If not effective, or because of the associated respiratory depression, tracheal intubation and mechanical ventilation are often needed, which, by themselves are associated with a worse prognosis. Continuous positive airway pressure (CPAP) has been proposed as an alternative to mechanical ventilation in CPE. This technique not only improves alveolar recruitment and decreases the work of breathing 4 but also reduces left ventricular afterload, and both right and left ventricular preload. The overall effect of CPAP in the acute management of CPE is to improve cardio-respiratory function and sustained tissue oxygenation. Furthermore, the ...
GAMMAKED is contraindicated in patients who have had an anaphylactic or severe systemic reaction to human immunoglobulin. It is also contraindicated in IgA deficient patients with antibodies against IgA and history of hypersensitivity. Have epinephrine available immediately to treat any acute severe hypersensitivity reactions.. Hyperproteinemia, increased serum viscosity, and hyponatremia may occur in patients receiving IGIV therapy, including GAMMAKED.. Aseptic Meningitis Syndrome (AMS) may occur infrequently, especially with high doses or rapid infusion.. Hemolysis, either intravascular or due to enhanced red blood cell (RBC) sequestration, can develop subsequent to GAMMAKED treatment. Risk factors include high doses and non-O blood group. Closely monitor patients for hemolysis and hemolytic anemia, especially in patients with pre-existing anemia and/or cardiovascular or pulmonary compromise.. Noncardiogenic pulmonary edema may occur in patients following treatment with IGIV products, ...
GAMMAKED is contraindicated in patients who have had an anaphylactic or severe systemic reaction to human immunoglobulin. It is also contraindicated in IgA deficient patients with antibodies against IgA and history of hypersensitivity. Have epinephrine available immediately to treat any acute severe hypersensitivity reactions.. Hyperproteinemia, increased serum viscosity, and hyponatremia may occur in patients receiving IGIV therapy, including GAMMAKED.. Aseptic Meningitis Syndrome (AMS) may occur infrequently, especially with high doses or rapid infusion.. Hemolysis, either intravascular or due to enhanced red blood cell (RBC) sequestration, can develop subsequent to GAMMAKED treatment. Risk factors include high doses and non-O blood group. Closely monitor patients for hemolysis and hemolytic anemia, especially in patients with pre-existing anemia and/or cardiovascular or pulmonary compromise.. Noncardiogenic pulmonary edema may occur in patients following treatment with IGIV products, ...
Elderly patients or those with diabetes, alcoholism, uremia, or congestive heart failure are at risk for severe disease characterized by neurologic involvement, respiratory distress, and gangrene of the digits. Mortality rates associated with this severe form of disease approach 50%. Epidemic typhus, caused by Rickettsia prowazekii, is transmitted in louse-infested environments and emerges in conditions of extreme poverty, war, and natural disaster. Patients experience a sudden onset of high fevers, severe headache, cough, myalgias, and abdominal pain. A maculopapular rash develops (primarily on the trunk) in more than half of patients and can progress to petechiae and purpura. Serious signs include delirium, coma, seizures, noncardiogenic pulmonary edema, skin necrosis, and peripheral gangrene. Mortality rates approached 60% in the preantibiotic era 159 and continue to exceed 10-15% in contemporary outbreaks. Scrub typhus, caused by Orientia tsutsugamushi-a separate genus in the family ...
Sigma-Aldrich offers abstracts and full-text articles by [P Bauer, M Weber, J M Mur, J C Protois, P E Bollaert, A Condi, A Larcan, H Lambert].
The demand for lung transplantation exceeds the supply of donor lungs, leading to protracted waiting times and a high death rate on the waiting list [4-6]. Although the use of extended donors who do not meet traditional criteria for lung donation has improved donor lung utilization rates at selected centers [7-10], the national donor lung utilization rate remains low [4]. The most common reasons for failure to utilize donor lungs are donor hypoxemia and/or pulmonary infiltrates [4]. Acute pulmonary edema occurs commonly in association with acute brain injury [4] and is a potentially reversible cause of donor hypoxemia and pulmonary infiltrates. In lungs from 29 donors that were rejected for transplantation, lung wet-to-dry weight ratio, a measure of pulmonary edema, was normal in only 7 (24%), indicating that pulmonary edema is very common in organ donors [11]. Strategies to enhance the resolution of pulmonary edema could lead to improved donor oxygenation and higher rates of donor lung ...
... (POPE) is a noncardiogenic cause of pulmonary edema with an incidence of 0.05-0.1%. Risk factors include male gender, head and neck surgeries, OSA, acromegaly, difficult intubation, and young age (probably associated to the ability to generate a significant pressure change).. POPE is categorized as type I (inhalation against an obstruction) or type II (exhalation against an obstruction).. Type I has a multifactorial etiology, which include negative pressure pulmonary, hypoxia, and hyperadrenergic states. During inhalation against an obstruction pressures up to -140 cmH2O (normal -4 cmH2O) are generated. This leads to an increase in right ventricular preload and afterload. These increases generate higher pulmonary venous pressures, which in turn increases capillary hydrostatic pressures. This, along with the negative intrapleural pressures being transmitted to alveoli, drives flow into the interstitium causing edema. Hypoxia adds to this effect by increase ...
Signs of Pulmonary edema including medical signs and symptoms of Pulmonary edema, symptoms, misdiagnosis, tests, common medical issues, duration, and the correct diagnosis for Pulmonary edema signs or Pulmonary edema symptoms.
We report the case of a 42-year-old female with a history of hypothyroidism and asthma presenting with progressive dyspnea and orthopnea after 2 days of an upper respiratory tract infection (URTI). Based on the clinical and radiological findings, the patient was admitted as a case of cardiogenic pulmonary edema secondary to possible viral myocarditis. However, a normal brain natriuretic peptide (BNP) level with a normal ejection fraction (EF) on echocardiogram changed our working diagnosis from cardiogenic to non-cardiogenic pulmonary edema. Further questioning revealed a history of nocturnal snoring, frequent awakening, and daytime fatigue, suggesting a possible sleep apnea syndrome (SAS). In conclusion, we believe that SAS was the missing link between our patients hypothyroidism and non-cardiogenic pulmonary edema. ...
Nephrology was consulted for acute kidney injury and hypervolemia in a chronically ill nursing home resident. You decide to perform lung POCUS to assess extravascular lung water. Multiple B-lines per rib interspace are noted bilaterally consistent with pulmonary edema. Chest X-ray shown for comparison. Right upperLeft upperChest radiograph But would you stop there? No. Focused…
Topical phenylephrine, an agent used to facilitate nasotracheal intubation and prevent nasal mucosal bleeding, can cause severe hypertension in some patients, secondary to its stimulation of alpha-adrenergic receptors. Moreover, a high incidence of pulmonary edema is found in patients whose phenylep...
A differential diagnosis of the pulmonary oedema is important because the therapeutic approach is quite different. In cardiogenic pulmonary oedema, a negative fluid balance is sought, while in cases of permeability pulmonary oedema treating the cause of inflammation has priority. The Pulmonary Vascular Permeability Index (PVPI) enables this differential diagnosis. This parameter is calculated from the relation between Extravascular Lung Water (EVLW) and Pulmonary Blood Volume (PBV). A PVPI value in the range of 1 to 3 points to a cardiogenic pulmonary oedema, while a PVPI value greater than 3 suggests a permeability pulmonary oedema.. ...
Body fluid in the lungs while swimming. Swimming induced pulmonary edema (SIPE), also known as immersion pulmonary edema, occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli). SIPE usually occurs during exertion in conditions of water immersion, such as swimming and diving. With the recent surge in popularity of triathlons and swimming in open water events there has been an increasing incidence of SIPE. It has been reported in scuba divers, apnea (breath hold) free-diving competitors combat swimmers, and triathletes. The causes are incompletely understood at the present time. As with other forms of pulmonary edema, the hallmark of SIPE is a cough which may lead to frothy or blood-tinged sputum. Symptoms include: Shortness of breath out of proportion to effort being expended. Crackles, rattling or junky feelings deep in the chest associated with breathing effort - usually progressively worsening with increasing ...
Treatment for Pulmonary Edema in Sai Snehdeep Hospital, Mumbai. Find Doctors Near You, Book Appointment, Consult Online, View Doctor Fees, Address, Phone Numbers and Reviews. Doctors for Pulmonary Edema in Sai Snehdeep Hospital, Mumbai | Lybrate
Do you want to learn about pulmonary edema? Discover what pulmonary edema is at 10FAQ Health and stay better informed to make healthy living decisions.
After working within the Operational Research section of ScHARR for four years, I joined the Health Services Research section in 2000 to work on a Department of Health funded project looking at the scale of, and reasons for, removal of patients from GPs lists. Since then I have worked on a number of projects funded by the DH and other funders, including evaluations of NHS Direct, Advanced Access in primary care, NHS 111 and PCT commissioning.. More recently I have worked on projects in the area of emergency care, including working as project manager for the evaluation of the National Infarct Angioplasty Project Pilots (NIAPP) and on a trial for interventions for acute cardiogenic pulmonary oedema (3CPO study). In 2011 I was awarded a NIHR doctoral research fellowship to look at improving pain management in Emergency Departments.. ...
RBW Let me preface this by stating in no way shape or form am I an expert in this field! However I have been doing some research and feel that this is an extremely important topic that we should discuss in further detail. More and more people suffer from sleep apnea. A lot of you that are reading this may suffer from it as well. Sleep apnea syndrome can lead to many cardiorespiratory problems. Acute pulmonary edema is one of them. It appears that the cause of the PE is from
Other names: pulmonary congestion, congestion of blood in the lungs Pulmonary congestion is not a classic symptom of subjective, but rather a sign of a disease on chest radiograph, which alerts the clinician to either lung disease or heart. However, it may manifest dyspnea and bloody sputum secretion. Technically this phenomenon called pulmonary congestion (stasis of blood in the lungs). It may mean that the heart can not handle pump blood into the large circulation and it then accumulates in the small circulation - in pulmonary vessels. These radiographic appears to be widespread, highlighted. When judgment is advanced to pulmonary edema (pulmonary edema when the fluid passes from the blood vessels into the lung tissue). Such heart failure are often elderly people from various causes (degenerative valvular defects, heart attack, high blood pressure, …) or even small children from birth if they have some developmental heart defects often more serious nature. At other times, however, slight pulmonary
Pulmonary edema is fluid buildup in the lung. Its usually due to mitral stenosis or left ventricular failure. Symptoms of pulmonary edema include difficulty breathing, coughing up blood-tinged sputum, excessive sweating, anxiety and pale skin. ...
This middle-aged patient has a history of CVA and hypertension. He presented with a two hour onset of pulmonary edema and chest pressure, severely elevated blood pressure, and very tachycardic. His prehospital BP was 280/150, and it was 230/150 in the ED. He had not been taking his antihypertensives He was speaking in 1-2 word sentences and had diffuse rales. Chest xray confirmed pulmonary edema. Here is his initial ECG ...
Pulmonary Edema Definition Pulmonary edema is a condition in which fluid accumulates in the lungs, usually because the hearts left ventricle does not
Pulmonary edema is a disorder wherein fluid accumulates in the lungs leading to lack of oxygen in the body. The usual cause of pulmonary edema is c...
Pulmonary edema in cats, as in anyone, tends to indicate a heart problem. Heart problems used to be rare in cats, but as with all diseases, old, new and rare, they are all on the increase. The heart isnt the only cause of pulmonary edema; toxins and medical/veterinary drugs can be, too, as can trauma to the chest wall.
Chest ultrasonography can be a useful diagnostic tool for respiratory physicians. It can be used to complete and widen the general objective examination also in emergency situations, at the patients bedside. The aim of this document is to promote better knowledge and more widespread use of thoracic ultrasound among respiratory physicians in Italy.This document II is focused on advanced approaches to chest ultrasonography especially in diagnosing sonographic interstitial syndrome with physical hypotheses about the genesis of vertical artifacts, differential diagnosis of cardiogenic pulmonary edema and non-cardiogenic pulmonary edema, raising diagnostic suspicion of pulmonary embolism, ultrasound characterization of lung consolidations and the use of ultrasonography to guide procedural interventions in pulmonology ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Due to the large surface area of the capillary network, all extra-vascular pulmonary fluid has traditionally been thought to result from pathological fluid movement across the capillary endothelium. In this model, fluid leaking from capillaries is drawn by negative interstitial pressure to the extra-alveolar interstitium, and moves into alveoli only when interstitial pressure reaches some critical value which forces fluid across the alveolar epithelium [1]. However, there is considerable evidence from animal models to suggest that extra-vascular pulmonary fluid may result from fluid flux across arteries or veins as well as capillaries. Rat pulmonary venules are more permeable than capillaries when edema is induced with alpha-naphthylthiourea [2]. Arteries have been shown to be the primary source of extra-vascular fluid in models of hypoxic pulmonary edema [3]. Under conditions of increased vascular pressure in excised or in situ dog lungs, fluid movement across extra-alveolar vessels accounts ...
The donor lung utilization rate in the United States remains less than 15%, and the demand for donor lungs far exceeds the available supply. The most common reasons for failure to utilize donor lungs are donor hypoxemia and/or pulmonary infiltrates. Since pulmonary edema is a common, reversible cause of hypoxemia and infiltrates in patients with brain injury, strategies to treat pulmonary edema in organ donors should lead to improved donor oxygenation and higher rates of donor lung utilization. Inhaled beta-2 agonists increase the rate of alveolar fluid clearance and reduce pulmonary edema in both animal and human lungs. In addition, our group has recently reported that the majority of human donor lungs that are rejected for transplantation have measurable pulmonary edema and respond to beta-2 agonists with increased rates of alveolar fluid clearance. Based on this compelling scientific evidence, we propose to test the efficacy of an inhaled beta-2 agonist to increase the rate of alveolar fluid ...
BACKGROUND Left cardiac chambers dilation, interstitial lung changes and pleural effusions are the characteristics of cardiogenic pulmonary oedema on computed tomography (CT) of the chest but mensuration of the left atrial size is not routinely performed. Cardiac chambers normal dimensions are known to be proportional to the patients build and anthropomorphic data but adjustment of chambers dimensions to available elements seen on the axial CT images has never been evaluated before. OBJECTIVES Our objective was to use data easily available on axial images to directly scale the left atrium. We chose to divide the left atrial diameter by the thoracic vertebral diameter, using the latter as a body-mass indicator. As a preliminary study, we aimed to evaluate the range of values of this left atrio-vertebral ratio (LAVR) by comparing patients suffering from cardiogenic pulmonary oedema with patients free of cardiac disease. We hypothesized that if the difference of values in these two populations of
This is a basic article for medical students and other non-radiologists Pulmonary edema refers to the abnormal accumulation of fluid in the extravascular compartments of the lung. This initially results in interstitial edema and perihilar airspa...