Materiały źródłowe

• #1 Pulmonary Edema – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557611/

  Pulmonary edema is defined as an abnormal accumulation of extravascular fluid in the lung parenchyma. […] Its etiology is either due to a cardiogenic process with the inability to remove sufficient blood away from the pulmonary circulation or non-cardiogenic precipitated by injury to the lung parenchyma. […] The resultant pathology of increased extravascular fluid content in the lung remains common to all forms of pulmonary edema. However, the underlying mechanism leading to the edema arises from the disruption of various complex physiologic processes, maintaining a delicate balance of filtration of fluid and solute across the pulmonary capillary membrane. This imbalance can be from one or more of the following factors: Increase in intravascular hydrostatic pressure transmitted in a retrograde fashion to the pulmonary microvasculature, Increase in interstitial hydrostatic pressure, Endothelial injury and disruption of epithelial barriers, Decrease in oncotic pressure due to underlying hepatic, renal, malnutrition, and other protein-losing states, Lymphatic insufficiency, Increased negative interstitial pressure.

• #2 Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis

  https://emedicine.medscape.com/article/157452-overview

  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. […] Pulmonary edema can be caused by the following major pathophysiologic mechanisms: Imbalance of Starling forces – ie, increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure; Damage to the alveolar-capillary barrier; Lymphatic obstruction; Idiopathic (unknown) mechanism. […] Increased hydrostatic pressure leading to pulmonary edema may result from many causes, including excessive intravascular volume administration, pulmonary venous outflow obstruction (eg, mitral stenosis or left atrial [LA] myxoma), and LV failure secondary to systolic or diastolic dysfunction of the left ventricle. CPE leads to progressive deterioration of alveolar gas exchange and respiratory failure.

• #3 Pulmonary edema pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Pulmonary_edema_pathophysiology

  Pulmonary edema is due to either failure of the heart to remove fluid from the lung circulation („cardiogenic pulmonary edema”), or due to a direct injury to the lung parenchyma or increased permeability or leakiness of the capillaries („noncardiogenic pulmonary edema”). […] It is understood that pulmonary edema is the abnormal increase in extravascular lung water (EVLW). This condition may be caused by the following underlying physiologic changes: Imbalance of staling force, Altered valvular capillary membrane permeability, Lymphatic insufficiency, Other factors. […] In cardiogenic pulmonary edema, the most common mechanism for a rise in transcapillary filtration is an increase in pulmonary capillary pressure. […] In noncardiogenic pulmonary edema, the most common mechanism for a rise in transcapillary filtration is an increase in capillary permeability.

• #4 Pulmonary Edema – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557611/

  The relationship between hydrostatic and oncotic forces in relation to net fluid filtration is best explained by Ernest Starlings equation. The rate of fluid filtration is determined by the differences in the hydrostatic and oncotic pressures between the pulmonary capillaries and interstitial space.

• #5 Noncardiogenic pulmonary edema – UpToDate

  https://www.uptodate.com/contents/noncardiogenic-pulmonary-edema

  Pulmonary edema is due to the movement of excess fluid into the alveoli as a result of an alteration in one or more of Starling’s forces. […] In contrast, noncardiogenic pulmonary edema is caused by various disorders in which factors other than elevated pulmonary capillary pressure are responsible for protein and fluid accumulation in the alveoli. […] The distinction between cardiogenic and noncardiogenic causes is not always possible, since the clinical syndrome may represent a combination of several different disorders. The diagnosis is important, however, because treatment varies considerably depending upon the underlying pathophysiologic mechanisms. […] Fluid balance between the interstitium and vascular bed in the lung, as in other microcirculations, is determined by the Starling relationship, which predicts the net flow of liquid across a membrane.

• #6 Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis

  https://emedicine.medscape.com/article/157452-overview

  CPE predominantly occurs secondary to LA outflow impairment or LV dysfunction. For pulmonary edema to develop secondary to increased pulmonary capillary pressure, the pulmonary capillary pressure must rise to a level higher than the plasma colloid osmotic pressure. […] The lymphatics play an important role in maintaining an adequate fluid balance in the lungs by removing solutes, colloid, and liquid from the interstitial space at a rate of approximately 10-20 mL/h. An acute rise in pulmonary arterial capillary pressure (ie, to 18 mm Hg) may increase filtration of fluid into the lung interstitium, but the lymphatic removal does not increase correspondingly. […] The progression of fluid accumulation in CPE can be identified as three distinct physiologic stages. In stage 1, elevated LA pressure causes distention and opening of small pulmonary vessels.

• #7 Cardiogenic Pulmonary Edema in Emergency Medicine

  https://www.mdpi.com/2543-6031/91/5/34

  In patients with CPE, an increase in pulmonary venous and left atrial (LA) pressure, which most frequently occurs from an elevated LV filling pressure, causes the rise in pulmonary capillary of the hydrostatic pressure. According to the Starling law, the pressure must increase higher than the normal value of the plasma colloid osmotic pressure for edema to occur. The functional capacity of the lymphatic system to remove the extra fluid is different from patient to patient and with the severity of the disease. These characteristics influence the rate of accumulation of lung fluid at a given elevation in pulmonary capillary pressure. An acute rise in pulmonary arterial capillary pressure (i.e., to >18 mm Hg) may increase fluid filtration into the lung interstitium, but the lymphatic removal does not increase correspondingly. As a result, pulmonary edema may occur at pulmonary capillary pressures as low as 18 mmHg.

• #8 Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis

  https://emedicine.medscape.com/article/157452-overview

  CPE predominantly occurs secondary to LA outflow impairment or LV dysfunction. For pulmonary edema to develop secondary to increased pulmonary capillary pressure, the pulmonary capillary pressure must rise to a level higher than the plasma colloid osmotic pressure. […] The lymphatics play an important role in maintaining an adequate fluid balance in the lungs by removing solutes, colloid, and liquid from the interstitial space at a rate of approximately 10-20 mL/h. An acute rise in pulmonary arterial capillary pressure (ie, to 18 mm Hg) may increase filtration of fluid into the lung interstitium, but the lymphatic removal does not increase correspondingly. […] The progression of fluid accumulation in CPE can be identified as three distinct physiologic stages. In stage 1, elevated LA pressure causes distention and opening of small pulmonary vessels.

• #9 Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis

  https://emedicine.medscape.com/article/157452-overview

  In stage 2, fluid and colloid shift into the lung interstitium from the pulmonary capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid. […] In stage 3, as fluid filtration continues to increase and the filling of loose interstitial space occurs, fluid accumulates in the relatively noncompliant interstitial space. […] LV systolic dysfunction, a common cause of CPE, is defined as decreased myocardial contractility that reduces cardiac output. […] Diastolic dysfunction signals a decrease in LV diastolic distensibility (compliance). Because of this decreased compliance, a heightened diastolic pressure is required to achieve a similar stroke volume. […] New-onset rapid atrial fibrillation and ventricular tachycardia can be responsible for CPE. […] Elevated systemic blood pressure can be considered an etiology of LV outflow obstruction because it increases systemic resistance against the pump function of the left ventricle.

• #10 Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis

  https://emedicine.medscape.com/article/157452-overview

  In stage 2, fluid and colloid shift into the lung interstitium from the pulmonary capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid. […] In stage 3, as fluid filtration continues to increase and the filling of loose interstitial space occurs, fluid accumulates in the relatively noncompliant interstitial space. […] LV systolic dysfunction, a common cause of CPE, is defined as decreased myocardial contractility that reduces cardiac output. […] Diastolic dysfunction signals a decrease in LV diastolic distensibility (compliance). Because of this decreased compliance, a heightened diastolic pressure is required to achieve a similar stroke volume. […] New-onset rapid atrial fibrillation and ventricular tachycardia can be responsible for CPE. […] Elevated systemic blood pressure can be considered an etiology of LV outflow obstruction because it increases systemic resistance against the pump function of the left ventricle.

• #11 Pulmonary Oedema – Pathophysiology – Approach & Management | PPT

  https://www.slideshare.net/slideshow/pulmonary-oedema-pathophysiology-approach-management/80843033

  Cardiogenic pulmonary edema is defined as pulmonary edema due to increased pulmonary capillary hydrostatic pressure secondary to elevated pulmonary venous pressure. Increased LA pressure increases pulmonary venous pressure and pressure in the lung microvasculature, resulting in pulmonary edema. […] The progression of fluid accumulation in CPE can be identified as 3 distinct physiologic stages. […] Non-cardiogenic pulmonary edema is caused by changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult. […] ARDS is associated with diffuse alveolar damage (DAD) and lung capillary endothelial injury. The early phase is described as being exudative, whereas the later phase is fibroproliferative in character. […] HAPE – Pathogenesis altered permeability of the alveolar-capillary barrier secondary to intense pulmonary vasoconstriction and high capillary pressure.

• #12 Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis

  https://emedicine.medscape.com/article/157452-overview

  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. […] Pulmonary edema can be caused by the following major pathophysiologic mechanisms: Imbalance of Starling forces – ie, increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure; Damage to the alveolar-capillary barrier; Lymphatic obstruction; Idiopathic (unknown) mechanism. […] Increased hydrostatic pressure leading to pulmonary edema may result from many causes, including excessive intravascular volume administration, pulmonary venous outflow obstruction (eg, mitral stenosis or left atrial [LA] myxoma), and LV failure secondary to systolic or diastolic dysfunction of the left ventricle. CPE leads to progressive deterioration of alveolar gas exchange and respiratory failure.

• #13 Pathophysiology of cardiogenic pulmonary edema – UpToDate

  https://www.uptodate.com/contents/pathophysiology-of-cardiogenic-pulmonary-edema

  Pathophysiology of cardiogenic pulmonary edema […] Cardiogenic pulmonary edema is a common and potentially fatal cause of acute respiratory failure. Cardiogenic pulmonary edema is most often a result of acute decompensated heart failure (ADHF). The clinical presentation is characterized by the development of dyspnea associated with the rapid accumulation of fluid within the lung’s interstitial and/or alveolar spaces, which is the result of acutely elevated cardiac filling pressures. […] ADHF is most commonly due to left ventricular (LV) systolic and/or diastolic impairment, with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions or events can cause cardiogenic pulmonary edema in the absence of heart disease, including primary fluid overload (eg, due to blood transfusion), severe hypertension, renal artery stenosis, and severe renal disease.

• #14 Cardiogenic Pulmonary Edema: Background, Etiology, Prognosis

  https://emedicine.medscape.com/article/157452-overview

  In stage 2, fluid and colloid shift into the lung interstitium from the pulmonary capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid. […] In stage 3, as fluid filtration continues to increase and the filling of loose interstitial space occurs, fluid accumulates in the relatively noncompliant interstitial space. […] LV systolic dysfunction, a common cause of CPE, is defined as decreased myocardial contractility that reduces cardiac output. […] Diastolic dysfunction signals a decrease in LV diastolic distensibility (compliance). Because of this decreased compliance, a heightened diastolic pressure is required to achieve a similar stroke volume. […] New-onset rapid atrial fibrillation and ventricular tachycardia can be responsible for CPE. […] Elevated systemic blood pressure can be considered an etiology of LV outflow obstruction because it increases systemic resistance against the pump function of the left ventricle.

• #15 Pulmonary edema: new insight on pathogenesis and treatment – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11357010/

  Pulmonary edema is one of the most serious and life-threatening situations in emergency medicine. Lately it has become apparent that in most cases pulmonary edema is not caused by fluid accumulation but rather fluid redistribution that is directed into the lungs because of heart failure. Based on a series of recently published studies, we propose that often the pathogenesis of pulmonary edema is related to a combination of marked increase in systemic vascular resistance superimposed on insufficient systolic and diastolic myocardial functional reserve. This resistance results in increased left ventricular diastolic pressure causing increased pulmonary venous pressure, which yields a fluid shift from the intravascular compartment into the pulmonary interstitium and alveoli, inducing the syndrome of pulmonary edema.

• #16 Pulmonary Oedema—Therapeutic Targets

  https://www.cfrjournal.com/articles/pulmonary-oedema-therapeutic-targets?language_content_entity=en

  Pulmonary oedema (PO) is a common manifestation of acute heart failure (AHF) and is associated with a high-acuity presentation and with poor in-hospital outcomes. […] The pathogenesis of hydrostatic PO has been attributed predominantly to a difference in Starling forces (i.e. fluid extravasation attributable to an increased hydrostatic or reduced oncotic pressure gradient across the intact alveolo-capillary barrier). […] In a recent study, the mechanism of PO was described as a consequence of acutely increased afterload in patients with decreased systolic and diastolic capacity to adapt to changes in loading in the presence of maintained right ventricular function. […] Although pressure-related mechanisms were considered sufficient to explain PO, recent studies show that cardiogenic PO is critically regulated by active signalling processes, suggesting that endothelial and alveolar responses may contribute critically to the formation of hydrostatic PO.

• #17 Pulmonary edema: new insight on pathogenesis and treatment – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11357010/

  Pulmonary edema is one of the most serious and life-threatening situations in emergency medicine. Lately it has become apparent that in most cases pulmonary edema is not caused by fluid accumulation but rather fluid redistribution that is directed into the lungs because of heart failure. Based on a series of recently published studies, we propose that often the pathogenesis of pulmonary edema is related to a combination of marked increase in systemic vascular resistance superimposed on insufficient systolic and diastolic myocardial functional reserve. This resistance results in increased left ventricular diastolic pressure causing increased pulmonary venous pressure, which yields a fluid shift from the intravascular compartment into the pulmonary interstitium and alveoli, inducing the syndrome of pulmonary edema.

• #18 Pathophysiology of cardiogenic pulmonary edema – UpToDate

  https://www.uptodate.com/contents/pathophysiology-of-cardiogenic-pulmonary-edema

  „Flash” pulmonary edema is a term that is used to describe a particularly dramatic form of cardiogenic alveolar pulmonary edema. In „flash” pulmonary edema, the underlying pathophysiologic principles, etiologic triggers, and initial management strategies are similar to those of less severe ADHF, although there is a greater degree of urgency to the implementation of initial therapies and the search for triggering causes. Often, „flash” pulmonary edema is related to a sudden rise in left-sided intracardiac filling pressures in the setting of hypertensive emergency, acute ischemia, new onset tachyarrhythmia, or obstructive valvular disease. In addition to standard therapies for cardiogenic pulmonary edema, this condition responds well to combined venous and arterial vasodilators. […] General issues related to the pathophysiology and etiology of cardiogenic pulmonary edema will be reviewed here.

• #19 Pathophysiology of cardiogenic pulmonary edema – UpToDate

  https://www.uptodate.com/contents/pathophysiology-of-cardiogenic-pulmonary-edema

  „Flash” pulmonary edema is a term that is used to describe a particularly dramatic form of cardiogenic alveolar pulmonary edema. In „flash” pulmonary edema, the underlying pathophysiologic principles, etiologic triggers, and initial management strategies are similar to those of less severe ADHF, although there is a greater degree of urgency to the implementation of initial therapies and the search for triggering causes. Often, „flash” pulmonary edema is related to a sudden rise in left-sided intracardiac filling pressures in the setting of hypertensive emergency, acute ischemia, new onset tachyarrhythmia, or obstructive valvular disease. In addition to standard therapies for cardiogenic pulmonary edema, this condition responds well to combined venous and arterial vasodilators. […] General issues related to the pathophysiology and etiology of cardiogenic pulmonary edema will be reviewed here.

• #20 Pulmonary edema – Wikipedia

  https://en.wikipedia.org/wiki/Pulmonary_edema

  Noncardiogenic causes are associated with the oncotic pressure as discussed above causing malfunctioning barriers in the lungs (increased microvascular permeability). […] Cardiogenic pulmonary edema is typically caused by either volume overload or impaired left ventricular function. […] As the pulmonary venous pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. […] Flash pulmonary edema is a clinical syndrome that begins suddenly and accelerates rapidly. […] Noncardiogenic pulmonary edema is caused by increased microvascular permeability (increased oncotic pressure) leading to increased fluid transfer into the alveolar spaces. […] Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. […] Acute lung injury may cause pulmonary edema directly through injury to the vasculature and parenchyma of the lung.

• #21 Pulmonary edema – Wikipedia

  https://en.wikipedia.org/wiki/Pulmonary_edema

  Noncardiogenic causes are associated with the oncotic pressure as discussed above causing malfunctioning barriers in the lungs (increased microvascular permeability). […] Cardiogenic pulmonary edema is typically caused by either volume overload or impaired left ventricular function. […] As the pulmonary venous pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. […] Flash pulmonary edema is a clinical syndrome that begins suddenly and accelerates rapidly. […] Noncardiogenic pulmonary edema is caused by increased microvascular permeability (increased oncotic pressure) leading to increased fluid transfer into the alveolar spaces. […] Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. […] Acute lung injury may cause pulmonary edema directly through injury to the vasculature and parenchyma of the lung.

• #22 Pulmonary edema–pathophysiology and therapy (Proceedings)

  https://www.dvm360.com/view/pulmonary-edema-pathophysiology-and-therapy-proceedings

  Pulmonary edema is the accumulation of fluids in the interstitium and alveoli of the lung. There are two main basic mechanisms for edema development: increased hydrostatic pressure in the lung capillaries (high-pressure edema) and increase vascular permeability (low-pressure edema). […] Disruption of some or all layers of the alveolar-capillary unit occurs during elevated capillary hydrostatic pressures, a phenomenon termed pulmonary capillary stress failure. […] Pulmonary capillary stress failure represents a process that blurs the distinction between high-pressure and low-pressure pulmonary edema, as the disruption of the alveolar-capillary membrane by high hydrostatic pressures may render it more permeable to fluid and proteins. […] High-pressure edema is usually secondary to left-sided congestive heart failure and many times called cardiogenic pulmonary edema, whereas low-pressure pulmonary edema are termed noncardiogenic.

• #23 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/html

  Appearance of alveolar protein-rich edema is an early event in the development of acute respiratory distress syndrome (ARDS). […] Damage of the alveolar epithelium is considered a major mechanism responsible for the increased pulmonary permeability, which results in edema fluid containing high concentrations of extravasated macromolecules in the alveoli. […] The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of pro-coagulant processes, cell death and mechanical stretch. […] The disruption of tight junction (TJ) complexes at the lateral contact of epithelial cells, the loss of contact between epithelial cells and extracellular matrix (ECM), and relevant changes in the communication between epithelial and immune cells, are deleterious alterations that mediate the disruption of the alveolar epithelial barrier and thereby the formation of lung edema in ARDS.

• #24 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/html

  Appearance of alveolar protein-rich edema is an early event in the development of acute respiratory distress syndrome (ARDS). […] Damage of the alveolar epithelium is considered a major mechanism responsible for the increased pulmonary permeability, which results in edema fluid containing high concentrations of extravasated macromolecules in the alveoli. […] The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of pro-coagulant processes, cell death and mechanical stretch. […] The disruption of tight junction (TJ) complexes at the lateral contact of epithelial cells, the loss of contact between epithelial cells and extracellular matrix (ECM), and relevant changes in the communication between epithelial and immune cells, are deleterious alterations that mediate the disruption of the alveolar epithelial barrier and thereby the formation of lung edema in ARDS.

• #25 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/html

  Appearance of alveolar protein-rich edema is an early event in the development of acute respiratory distress syndrome (ARDS). […] Damage of the alveolar epithelium is considered a major mechanism responsible for the increased pulmonary permeability, which results in edema fluid containing high concentrations of extravasated macromolecules in the alveoli. […] The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of pro-coagulant processes, cell death and mechanical stretch. […] The disruption of tight junction (TJ) complexes at the lateral contact of epithelial cells, the loss of contact between epithelial cells and extracellular matrix (ECM), and relevant changes in the communication between epithelial and immune cells, are deleterious alterations that mediate the disruption of the alveolar epithelial barrier and thereby the formation of lung edema in ARDS.

• #26 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/html

  Appearance of alveolar protein-rich edema is an early event in the development of acute respiratory distress syndrome (ARDS). […] Damage of the alveolar epithelium is considered a major mechanism responsible for the increased pulmonary permeability, which results in edema fluid containing high concentrations of extravasated macromolecules in the alveoli. […] The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of pro-coagulant processes, cell death and mechanical stretch. […] The disruption of tight junction (TJ) complexes at the lateral contact of epithelial cells, the loss of contact between epithelial cells and extracellular matrix (ECM), and relevant changes in the communication between epithelial and immune cells, are deleterious alterations that mediate the disruption of the alveolar epithelial barrier and thereby the formation of lung edema in ARDS.

• #27 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/18485

  Appearance of alveolar protein-rich edema is an early event in the development of acute respiratory distress syndrome (ARDS). Alveolar edema in ARDS results from a significant increase in the permeability of the alveolar epithelial barrier, and represents one of the main factors that contribute to the hypoxemia in these patients. Damage of the alveolar epithelium is considered a major mechanism responsible for the increased pulmonary permeability, which results in edema fluid containing high concentrations of extravasated macromolecules in the alveoli. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of pro-coagulant processes, cell death and mechanical stretch. The disruption of tight junction (TJ) complexes at the lateral contact of epithelial cells, the loss of contact between epithelial cells and extracellular matrix (ECM), and relevant changes in the communication between epithelial and immune cells, are deleterious alterations that mediate the disruption of the alveolar epithelial barrier and thereby the formation of lung edema in ARDS.

• #28 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/html

  In patients with ARDS, in contrast, the alveolar edema results from the loss of the alveolar endothelial and epithelial barriers, allowing fluid and large plasma proteins to move into the interstitial tissue and to flood the alveolar airspaces. […] The alveolar epithelial damage is a critical factor that promotes the development of increased-permeability edema in ARDS. […] Potential operative mechanisms of alveolar epithelial damage include cell death, the loss of adequate tight junction (TJ)-mediated cell-to-cell contact, changes in extracellular matrix (ECM) components and in their contact with epithelial cells, and changes in the communication between epithelial and immune cells. […] Damage of TJs is a major cause of epithelial barrier breakdown during lung inflammation. […] Dysfunction of the TJs results in increased permeability to water and proteins and in the deterioration of the AFC capacity of the epithelium, leading to the formation and perpetuation of lung edema.

• #29 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/18485

  In patients with ARDS, in contrast, the alveolar edema results from the loss of the alveolar endothelial and epithelial barriers, allowing fluid and large plasma proteins to move into the interstitial tissue and to flood the alveolar airspaces. The alveolar epithelial damage is a critical factor that promotes the development of increased-permeability edema in ARDS. Potential operative mechanisms of alveolar epithelial damage include cell death, the loss of adequate tight junction (TJ)-mediated cell-to-cell contact, changes in extracellular matrix (ECM) components and in their contact with epithelial cells, and changes in the communication between epithelial and immune cells. […] Damage of TJs is a major cause of epithelial barrier breakdown during lung inflammation. Dysfunction of the TJs results in increased permeability to water and proteins and in the deterioration of the AFC capacity of the epithelium, leading to the formation and perpetuation of lung edema.

• #30 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/html

  The ECM is also crucial for the epithelial and endothelial barrier function, since it regulates cell-cell interactions and controls the trafficking of fluid and molecules in the interstitial space. […] Changes in the composition and mechanic properties of the ECM have been shown to modify the expression of TJs and the barrier function in alveolar epithelial and endothelial cells, contributing to lung edema formation. […] The degradation of protein components in the alveolar epithelial and endothelial barriers, including intercellular TJ proteins and ECM, is considered a critical process in the development of protein-rich edema in ARDS, and constitutes an attractive therapeutic target for maintaining the integrity and function of the alveolar epithelial barrier.

• #31 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/18485

  The ECM is also crucial for the epithelial and endothelial barrier function, since it regulates cell-cell interactions and controls the trafficking of fluid and molecules in the interstitial space. Changes in the composition and mechanic properties of the ECM have been shown to modify the expression of TJs and the barrier function in alveolar epithelial and endothelial cells, contributing to lung edema formation. […] The normal alveolar epithelium is composed of type I and type II pneumocytes. Type I pneumocytes are squamous, cover 90-95% of the alveolar surface area, mediate gas exchange and barrier function, and are easily injured. […] Cell death occurs in the alveolar walls of patients with ARDS as well as of animal models of acute lung injury (ALI) induced by hyperoxia, lipopolysaccharide (LPS), bleomycin, cecal ligation and puncture, ischemia/reperfusion injury, and mechanical ventilation. In patients with ARDS, epithelial necrosis is present and can be directly caused by mechanical factors, hyperthermia, local ischemia, or bacterial products and viruses in the airspaces.

• #32 New insights into the mechanisms of pulmonary edema in acute lung injury

  https://atm.amegroups.org/article/view/17773/html

  The ECM is also crucial for the epithelial and endothelial barrier function, since it regulates cell-cell interactions and controls the trafficking of fluid and molecules in the interstitial space. […] Changes in the composition and mechanic properties of the ECM have been shown to modify the expression of TJs and the barrier function in alveolar epithelial and endothelial cells, contributing to lung edema formation. […] The degradation of protein components in the alveolar epithelial and endothelial barriers, including intercellular TJ proteins and ECM, is considered a critical process in the development of protein-rich edema in ARDS, and constitutes an attractive therapeutic target for maintaining the integrity and function of the alveolar epithelial barrier.

• #33 Neurogenic pulmonary edema | Critical Care | Full Text

  https://ccforum.biomedcentral.com/articles/10.1186/cc11226

  Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system (CNS) insult. The etiology is thought to be a surge of catecholamines that results in cardiopulmonary dysfunction. […] The pathophysiology linking the neurologic, cardiac, and pulmonary conditions in NPE has been subject to debate and controversy since the recognition of NPE as a clinical entity. A common thread among all case descriptions of NPE is the severity and acuity of the precipitating CNS event. Neurologic conditions that cause abrupt, rapid, and extreme elevation in intracranial pressure (ICP) appear to be at greatest risk of being associated with NPE. Elevated ICP levels correlate with increased levels of extravascular lung water (EVLW) and NPE.

• #34 Neurogenic Pulmonary Edema – EMCrit Project

  https://emcrit.org/ibcc/npe/

  (1) The primary mechanism appears to be increased sympathetic outflow from the central nervous system. […] Increased sympathetic tone may cause vasoconstriction of the pulmonary veins, which increases the pulmonary capillary wedge pressure. […] Increased sympathetic tone may cause vasoconstriction of systemic capacitance veins, increasing venous return to the heart (shifting blood volume from the systemic circulation into the pulmonary circulation). […] Increased sympathetic output may cause hypertension (which increases the afterload of the left ventricle), increasing the pulmonary capillary wedge pressure. […] (2) Another potential mechanism may be increased pulmonary capillary permeability. This could be caused by various factors: […] The blast theory suggests that a transient increase in transcapillary pressure (due to factors described above) may cause pulmonary microvascular injury, leading to a prolonged increase in pulmonary capillary permeability. Essentially, the pulmonary capillary endothelium gets blasted open.

• #35 Neurogenic Pulmonary Edema – EMCrit Project

  https://emcrit.org/ibcc/npe/

  (1) The primary mechanism appears to be increased sympathetic outflow from the central nervous system. […] Increased sympathetic tone may cause vasoconstriction of the pulmonary veins, which increases the pulmonary capillary wedge pressure. […] Increased sympathetic tone may cause vasoconstriction of systemic capacitance veins, increasing venous return to the heart (shifting blood volume from the systemic circulation into the pulmonary circulation). […] Increased sympathetic output may cause hypertension (which increases the afterload of the left ventricle), increasing the pulmonary capillary wedge pressure. […] (2) Another potential mechanism may be increased pulmonary capillary permeability. This could be caused by various factors: […] The blast theory suggests that a transient increase in transcapillary pressure (due to factors described above) may cause pulmonary microvascular injury, leading to a prolonged increase in pulmonary capillary permeability. Essentially, the pulmonary capillary endothelium gets blasted open.

• #36 Neurogenic pulmonary edema | Critical Care | Full Text

  https://ccforum.biomedcentral.com/articles/10.1186/cc11226

  It is the prevailing view that the autonomic response to elevated ICP plays an important role in the pathogenesis of NPE. However, what occurs mechanistically at the level of the pulmonary vascular endothelium remains enigmatic and theoretical. Several clinicopathologic paradigms have been proposed to explain the clinical syndrome of NPE: 1) Neuro-cardiac; 2) Neuro-hemodynamic; 3) „blast theory”; and 4) pulmonary venule adrenergic hypersensitivity. […] The neuro-cardiac and neuro-hemodynamic theories outlined above both suggest that alterations in hydrostatic and Starling forces are central to the formation of pulmonary edema following CNS injury. […] The „blast theory” further posits that the acute rise in capillary pressure induces a degree of barotrauma capable of damaging the capillary-alveolar membrane. The structural damage to the pulmonary endothelium ultimately leads to vascular leak and persistent protein-rich pulmonary edema. […] An alternative hypothesis is that the massive sympathetic discharge following CNS injury directly affects the pulmonary vascular bed, and that the edema develops regardless of any systemic changes. We refer to this as the 'pulmonary venule adrenergic hypersensitivity’ theory.

• #37 Neurogenic Pulmonary Edema – EMCrit Project

  https://emcrit.org/ibcc/npe/

  Endothelial injury may help explain why pulmonary edema may persist, even after a transient sympathetic surge has passed. […] Central nervous system injury may cause systemic inflammation, which increases the permeability of alveolar capillaries. […] Elevated intracranial pressure (ICP) may be the most common physiological trigger of neurogenic pulmonary edema. […] Thus, neurogenic pulmonary edema should always prompt consideration regarding whether the patient requires therapies to reduce the intracranial pressure. […] The pathophysiology of neurogenic pulmonary edema involves predominantly fluid shifts into the lungs, rather than changes in total body volume. Therefore, aggressive diuresis is generally not indicated. […] Neurogenic pulmonary edema is generally self-limiting, with spontaneous resolution over a few days. Observation and supportive care are generally the primary therapies (especially for more mild cases).

• #38 High-altitude pulmonary edema – Wikipedia

  https://en.wikipedia.org/wiki/High-altitude_pulmonary_edema

  High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). […] The inciting factor of HAPE is the decrease in partial pressure of arterial oxygen caused by the lower air pressure at high altitudes (pulmonary gas pressures). […] The resultant hypoxemia is then thought to precipitate the development of increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction. […] Increased capillary pressure (hydrostatic pressure) with over-distention of the capillary beds and increased permeability of the vascular endothelium, also known as „stress failure.” […] This leads to subsequent leakage of cells and proteins into the alveoli, aka pulmonary edema.

• #39 High-altitude pulmonary edema – Wikipedia

  https://en.wikipedia.org/wiki/High-altitude_pulmonary_edema

  High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). […] The inciting factor of HAPE is the decrease in partial pressure of arterial oxygen caused by the lower air pressure at high altitudes (pulmonary gas pressures). […] The resultant hypoxemia is then thought to precipitate the development of increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction. […] Increased capillary pressure (hydrostatic pressure) with over-distention of the capillary beds and increased permeability of the vascular endothelium, also known as „stress failure.” […] This leads to subsequent leakage of cells and proteins into the alveoli, aka pulmonary edema.

• #40 High-altitude pulmonary edema – Wikipedia

  https://en.wikipedia.org/wiki/High-altitude_pulmonary_edema

  High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). […] The inciting factor of HAPE is the decrease in partial pressure of arterial oxygen caused by the lower air pressure at high altitudes (pulmonary gas pressures). […] The resultant hypoxemia is then thought to precipitate the development of increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction. […] Increased capillary pressure (hydrostatic pressure) with over-distention of the capillary beds and increased permeability of the vascular endothelium, also known as „stress failure.” […] This leads to subsequent leakage of cells and proteins into the alveoli, aka pulmonary edema.

• #41 Update on High-Altitude Pulmonary Edema: Pathogenesis, Prevention, and Treatment

  https://bioone.org/journals/wilderness-and-environmental-medicine/volume-19/issue-4/07-WEME-REV-173.1/Update-on-High-Altitude-Pulmonary-Edema–Pathogenesis-Prevention-and/10.1580/07-WEME-REV-173.1.full

  High-altitude pulmonary edema (HAPE) is a life-threatening noncardiogenic form of pulmonary edema (PE) that afflicts susceptible persons after rapid ascent to high altitude above 2500 m. Its pathogenesis is related to increased sympathetic tone, exaggerated hypoxic pulmonary vasoconstriction, uneven hypoxic pulmonary vasoconstriction with overperfusion of some regions of the pulmonary vascular bed, increased pulmonary capillary pressure, stress failure of pulmonary capillaries, and alveolar fluid leak across capillary endothelium resulting in interstitial and alveolar edema. […] Prevention of HAPE is most effectively achieved by gradual ascent with time for acclimatization, although recent small studies have highlighted a number of pharmacologic options. Inhaled salmeterol prevents HAPE presumably by increasing alveolar fluid clearance, the phosphodiesterase-5 inhibitor tadalafil works by acting as a pulmonary vasodilator, and dexamethasone seems to prevent HAPE by stabilizing the capillary endothelium, along with other potential effects.

• #42 High-altitude pulmonary edema – Wikipedia

  https://en.wikipedia.org/wiki/High-altitude_pulmonary_edema

  Hypoxic pulmonary vasoconstriction (HPV) occurs diffusely, leading to arterial vasoconstriction in all areas of the lung. […] Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of pulmonary hypertension may not in itself be sufficient to explain the development of edema; severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude.

• #43

  https://respiratoryscience.or.id/index.php/journal/article/view/130

  Re-expansion pulmonary edema (RPE) is a rare complication of pleural puncture (thoracentesis) and chest tube insertion. […] The main pathophysiological mechanism is pulmonary edema due to increased permeability and increased hydrostatic pressure in the pulmonary capillaries. […] Risk factors include duration of lung collapse (3 to 7 days), size of pneumothorax (30%), volume of aspirated air or fluid (1.5 to 3 L), excessive negative intrapleural pressure, diabetes mellitus, and chronic hypoxemia. […] Prevention includes limiting the volume of aspirated air or fluid (1.5 L), air or fluid evacuation in a controlled manner, and preventing excessive negative intrapleural pressure. […] Treatment is supportive care through cardiovascular and respiratory monitoring, oxygen and decubitus positioning.

• #44

  https://respiratoryscience.or.id/index.php/journal/article/view/130

  Re-expansion pulmonary edema (RPE) is a rare complication of pleural puncture (thoracentesis) and chest tube insertion. […] The main pathophysiological mechanism is pulmonary edema due to increased permeability and increased hydrostatic pressure in the pulmonary capillaries. […] Risk factors include duration of lung collapse (3 to 7 days), size of pneumothorax (30%), volume of aspirated air or fluid (1.5 to 3 L), excessive negative intrapleural pressure, diabetes mellitus, and chronic hypoxemia. […] Prevention includes limiting the volume of aspirated air or fluid (1.5 L), air or fluid evacuation in a controlled manner, and preventing excessive negative intrapleural pressure. […] Treatment is supportive care through cardiovascular and respiratory monitoring, oxygen and decubitus positioning.

• #45 Re-Expansion Pulmonary Edema as a Life-Threatening Complication in Massive, Long-Standing Pneumothorax: A Case Series and Literature Review

  https://www.mdpi.com/2077-0383/13/9/2667

  Re-expansion pulmonary edema is a rare and potentially life-threatening complication that can occur after the rapid re-expansion of a collapsed lung due to pneumothorax or pleural effusion. It has a multifactorial pathogenesis, and risk factors for re-expansion pulmonary edema, such as chronic lung collapse, rapid re-expansion, and changes in pulmonary vascular permeability, have been identified. […] The pathogenesis of re-expansion pulmonary edema is multifactorial and involves various risk factors. These factors include chronic lung collapse, rapid re-expansion, and alterations in pulmonary vascular permeability. Additionally, observations following large-volume thoracentesis suggest the potential involvement of mechanisms related to ischemia/reperfusion injury and increased capillary permeability in the development of re-expansion pulmonary edema.

• #46 Re-Expansion Pulmonary Edema as a Life-Threatening Complication in Massive, Long-Standing Pneumothorax: A Case Series and Literature Review

  https://www.mdpi.com/2077-0383/13/9/2667

  The pathogenesis of re-expansion pulmonary edema is still unknown and is probably multifactorial, prompting several authors to investigate its potential risk factors. Various hypotheses have been proposed, in particular, in the etiological process of re-expansion pulmonary edema. They involve the chronicity of collapse, the technique of re-expansion, and modifications of pulmonary vascular permeability. […] Although re-expansion pulmonary edema typically manifests in cases of chronic lung collapse and rapid lung expansion following the removal of substantial amounts of air or fluid, it is not a universal rule. […] The majority of studies indicate, as in our series, that patients with re-expansion pulmonary edema experienced a pneumothorax lasting 3 days or more. […] An animal study conducted by Miller et al. supports the hypothesis that the length of pneumothorax’s onset and the application of suction after drainage could be considered risk factors for the development of re-expansion pulmonary edema.

• #47 Re-Expansion Pulmonary Edema as a Life-Threatening Complication in Massive, Long-Standing Pneumothorax: A Case Series and Literature Review

  https://www.mdpi.com/2077-0383/13/9/2667

  Other hypotheses support the idea that changes in vascular permeability may play a role in this process. Re-expansion pulmonary edema may result directly from the traction exerted on blood vessels during rapid lung re-expansion, leading to the increased permeability of damaged pulmonary blood vessels. […] The re-expansion of the parenchyma due to extensive drainage results in the reperfusion injury of the collapsed lung, leading to a substantial generation of reactive oxygen species (ROS). These ROS activate the cascade of ischemia/reperfusion injury, causing severe impairment to cell membranes and simultaneously increasing the permeability of the vessel wall.

• #48 Pulmonary Oedema—Therapeutic Targets

  https://www.cfrjournal.com/articles/pulmonary-oedema-therapeutic-targets?language_content_entity=en

  Pulmonary oedema (PO) is a common manifestation of acute heart failure (AHF) and is associated with a high-acuity presentation and with poor in-hospital outcomes. […] The pathogenesis of hydrostatic PO has been attributed predominantly to a difference in Starling forces (i.e. fluid extravasation attributable to an increased hydrostatic or reduced oncotic pressure gradient across the intact alveolo-capillary barrier). […] In a recent study, the mechanism of PO was described as a consequence of acutely increased afterload in patients with decreased systolic and diastolic capacity to adapt to changes in loading in the presence of maintained right ventricular function. […] Although pressure-related mechanisms were considered sufficient to explain PO, recent studies show that cardiogenic PO is critically regulated by active signalling processes, suggesting that endothelial and alveolar responses may contribute critically to the formation of hydrostatic PO.

• #49 Pulmonary Oedema—Therapeutic Targets

  https://www.cfrjournal.com/articles/pulmonary-oedema-therapeutic-targets?language_content_entity=en

  Active transepithelial transport of sodium from the airspaces to the lung interstitial space is a primary mechanism driving alveolar fluid clearance. […] A major part of cardiogenic PO formation results from active epithelial secretion of chlorine and secondary fluid flux into the alveolar space. […] Regulation of the Na-K-ATPase is elicited by stimulation of dopaminergic, 2 adrenergic receptors, and aldosterone, and inhibited by oabain-like compounds. […] Furthermore, recent data suggest that lung injury and barrier dysfunction may play a role in the formation and resolution of congestion and pulmonary oedema. […] Future research is required to develop innovative pharmacotherapies capable of relieving hemodynamic congestion while simultaneously preserving end-organ function.

• #50 Pulmonary Oedema—Therapeutic Targets

  https://www.cfrjournal.com/articles/pulmonary-oedema-therapeutic-targets?language_content_entity=en

  Active transepithelial transport of sodium from the airspaces to the lung interstitial space is a primary mechanism driving alveolar fluid clearance. […] A major part of cardiogenic PO formation results from active epithelial secretion of chlorine and secondary fluid flux into the alveolar space. […] Regulation of the Na-K-ATPase is elicited by stimulation of dopaminergic, 2 adrenergic receptors, and aldosterone, and inhibited by oabain-like compounds. […] Furthermore, recent data suggest that lung injury and barrier dysfunction may play a role in the formation and resolution of congestion and pulmonary oedema. […] Future research is required to develop innovative pharmacotherapies capable of relieving hemodynamic congestion while simultaneously preserving end-organ function.

• #51 Cardiogenic Pulmonary Edema in Emergency Medicine

  https://www.mdpi.com/2543-6031/91/5/34

  Cardiogenic pulmonary edema (CPE) is characterized by the development of acute respiratory failure associated with the accumulation of fluid in the lung’s alveolar spaces due to an elevated cardiac filling pressure. All cardiac diseases, characterized by an increasing pressure in the left side of the heart, can cause CPE. High capillary pressure for an extended period can also cause barrier disruption, which implies increased permeability and fluid transfer into the alveoli, leading to edema and atelectasis. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of procoagulant processes, cell death, and mechanical stretch. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance.

• #52 Cardiogenic Pulmonary Edema in Emergency Medicine

  https://www.mdpi.com/2543-6031/91/5/34

  Although CPE usually occurs in the absence of change in the permeability of the alveolar-capillary barrier, the capillary wall’s permeability may also be affected during CPE. A sudden increase in pulmonary capillary hydrostatic pressure (i.e., flash pulmonary edema) can cause mechanical damage on the alveoli–capillary barrier through a process known as “stress failure.” Renal artery stenosis, particularly when bilateral, has been identified as a common cause of flash pulmonary edema. In case of stress failure, both hydrostatic pressures and raised permeability increase fluid transfer into alveolar spaces. Finally, inflammation associated with stress failure may cause surfactant alterations. […] From a molecular point of view, another important aspect to consider is the downregulation of the epithelial Sodium channels (ENaC) due to hypoxia and hypercapnia. In addition, cell necrosis and fluid accumulation could trigger an inflammatory response. Pro-apoptotic cellular factors, including Bax, Caspase-3, and p53, are activated in the lung along with the apoptotic alterations, as can be seen with a bronchoalveolar lavage. Another important mechanism underlying pulmonary edema is the activation of the pro-apoptotic Fas/FasL pathway. It has been demonstrated that blocking the activation of this pathway may reduce alveolar damage and the formation of pulmonary edema.

• #53 Cardiogenic Pulmonary Edema in Emergency Medicine

  https://www.mdpi.com/2543-6031/91/5/34

  Although CPE usually occurs in the absence of change in the permeability of the alveolar-capillary barrier, the capillary wall’s permeability may also be affected during CPE. A sudden increase in pulmonary capillary hydrostatic pressure (i.e., flash pulmonary edema) can cause mechanical damage on the alveoli–capillary barrier through a process known as “stress failure.” Renal artery stenosis, particularly when bilateral, has been identified as a common cause of flash pulmonary edema. In case of stress failure, both hydrostatic pressures and raised permeability increase fluid transfer into alveolar spaces. Finally, inflammation associated with stress failure may cause surfactant alterations. […] From a molecular point of view, another important aspect to consider is the downregulation of the epithelial Sodium channels (ENaC) due to hypoxia and hypercapnia. In addition, cell necrosis and fluid accumulation could trigger an inflammatory response. Pro-apoptotic cellular factors, including Bax, Caspase-3, and p53, are activated in the lung along with the apoptotic alterations, as can be seen with a bronchoalveolar lavage. Another important mechanism underlying pulmonary edema is the activation of the pro-apoptotic Fas/FasL pathway. It has been demonstrated that blocking the activation of this pathway may reduce alveolar damage and the formation of pulmonary edema.

• #54 Cardiogenic Pulmonary Edema in Emergency Medicine

  https://www.mdpi.com/2543-6031/91/5/34

  Pulmonary edema leads to progressive deterioration of alveolar gas exchange and respiratory failure. The pathophysiology of respiratory failure includes an increase in extravascular lung water, a reduction in pulmonary compliance, and an increase in airway resistance. These events result in increased work breathing. Moreover, they also cause changes in the ventilation-perfusion ratio and in intrapulmonary shunting, which lead to arterial hypoxemia. Finally, increased work of breathing may induce rapid shallow breathing, leading to hypercapnia.

• #55 Cardiogenic Pulmonary Edema in Emergency Medicine

  https://www.mdpi.com/2543-6031/91/5/34

  Pulmonary edema leads to progressive deterioration of alveolar gas exchange and respiratory failure. The pathophysiology of respiratory failure includes an increase in extravascular lung water, a reduction in pulmonary compliance, and an increase in airway resistance. These events result in increased work breathing. Moreover, they also cause changes in the ventilation-perfusion ratio and in intrapulmonary shunting, which lead to arterial hypoxemia. Finally, increased work of breathing may induce rapid shallow breathing, leading to hypercapnia.

• #56 Pulmonary edema–pathophysiology and therapy (Proceedings)

  https://www.dvm360.com/view/pulmonary-edema-pathophysiology-and-therapy-proceedings

  Pulmonary edema is the accumulation of fluids in the interstitium and alveoli of the lung. There are two main basic mechanisms for edema development: increased hydrostatic pressure in the lung capillaries (high-pressure edema) and increase vascular permeability (low-pressure edema). […] Disruption of some or all layers of the alveolar-capillary unit occurs during elevated capillary hydrostatic pressures, a phenomenon termed pulmonary capillary stress failure. […] Pulmonary capillary stress failure represents a process that blurs the distinction between high-pressure and low-pressure pulmonary edema, as the disruption of the alveolar-capillary membrane by high hydrostatic pressures may render it more permeable to fluid and proteins. […] High-pressure edema is usually secondary to left-sided congestive heart failure and many times called cardiogenic pulmonary edema, whereas low-pressure pulmonary edema are termed noncardiogenic.

• #57 Pulmonary edema–pathophysiology and therapy (Proceedings)

  https://www.dvm360.com/view/pulmonary-edema-pathophysiology-and-therapy-proceedings

  Pulmonary edema is the accumulation of fluids in the interstitium and alveoli of the lung. There are two main basic mechanisms for edema development: increased hydrostatic pressure in the lung capillaries (high-pressure edema) and increase vascular permeability (low-pressure edema). […] Disruption of some or all layers of the alveolar-capillary unit occurs during elevated capillary hydrostatic pressures, a phenomenon termed pulmonary capillary stress failure. […] Pulmonary capillary stress failure represents a process that blurs the distinction between high-pressure and low-pressure pulmonary edema, as the disruption of the alveolar-capillary membrane by high hydrostatic pressures may render it more permeable to fluid and proteins. […] High-pressure edema is usually secondary to left-sided congestive heart failure and many times called cardiogenic pulmonary edema, whereas low-pressure pulmonary edema are termed noncardiogenic.

• #58

  https://www.vin.com/apputil/content/defaultadv1.aspx?pId=11196&catId=30763&id=3854264

  Pulmonary edema is the accumulation of fluids in the interstitium and alveoli of the lung. There are two main basic mechanisms for edema development: increased hydrostatic pressure in the lung capillaries („high-pressure edema”) and increase vascular permeability („low-pressure edema). This classification helps understand the basic pathophysiological differences between the two types of pulmonary edema, but has limitations. Disruption of some or all layers of the alveolar-capillary unit occurs during elevated capillary hydrostatic pressures, a phenomenon termed „pulmonary capillary stress failure”. Pulmonary capillary stress failure represents a process that blurs the distinction between high-pressure and low-pressure pulmonary edema, as the disruption of the alveolar-capillary membrane by high hydrostatic pressures may render it more permeable to fluid and proteins. The resulting edema fluid has a higher concentration of protein than would be expected in conventional high-pressure pulmonary edema. These observations may explain some features seen in high-altitude pulmonary edema and neurogenic pulmonary edema.

• #59

  https://www.vin.com/apputil/content/defaultadv1.aspx?pId=11196&catId=30763&id=3854264

  High-pressure edema is usually secondary to left-sided congestive heart failure and many times called „cardiogenic pulmonary edema”, whereas low-pressure pulmonary edema are termed „noncardiogenic”. Fluid in noncardiogenic pulmonary has a higher concentration of proteins and the edema occurs with normal capillary wedge pressure. The increased vascular permeability can occur with a wide variety of pulmonary and systemic disorders including vasculitis, acute respiratory distress syndrome, electric shock, neurogenic edema and uremic pneumonitis. […] The initial goals of therapy in cardiogenic pulmonary edema include increasing arterial PO2, reducing oxygen demand, establishing a diuresis, and unloading the ventricles while supporting blood pressure, tissue perfusion and renal function. Supplemental oxygen therapy and sedation are used as needed to reduce distress or air hunger. Pulmonary edema sufficient to cause respiratory failure and respiratory muscle fatigue is an indication for artificial ventilation. Diuresis is initiated and maintained with parenterally-administered furosemide. Nitroglycerin ointment can be used to decrease preload, whereas nitroprusside can be used to decrease afterload in dogs with florid pulmonary edema.

• #60 Noncardiogenic pulmonary edema – UpToDate

  https://www.uptodate.com/contents/noncardiogenic-pulmonary-edema

  Pulmonary edema is due to the movement of excess fluid into the alveoli as a result of an alteration in one or more of Starling’s forces. […] In contrast, noncardiogenic pulmonary edema is caused by various disorders in which factors other than elevated pulmonary capillary pressure are responsible for protein and fluid accumulation in the alveoli. […] The distinction between cardiogenic and noncardiogenic causes is not always possible, since the clinical syndrome may represent a combination of several different disorders. The diagnosis is important, however, because treatment varies considerably depending upon the underlying pathophysiologic mechanisms. […] Fluid balance between the interstitium and vascular bed in the lung, as in other microcirculations, is determined by the Starling relationship, which predicts the net flow of liquid across a membrane.

• #61 Pulmonary edema: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/000140.htm

  Pulmonary edema is an abnormal buildup of fluid in the lungs. This buildup of fluid leads to shortness of breath. […] Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the blood vessels that take blood through the lungs. […] As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. This fluid reduces normal oxygen movement through the lungs. These two factors combine to cause shortness of breath. […] The cause of pulmonary edema should be identified and treated quickly. For example, if a heart attack has caused the condition, it must be treated right away. […] The outlook depends on the cause. The condition may get better quickly or slowly. Some people may need to use a breathing machine for a long time. If not treated, this condition can be life threatening.

• #62 Pulmonary Oedema—Therapeutic Targets

  https://www.cfrjournal.com/articles/pulmonary-oedema-therapeutic-targets?language_content_entity=en

  Active transepithelial transport of sodium from the airspaces to the lung interstitial space is a primary mechanism driving alveolar fluid clearance. […] A major part of cardiogenic PO formation results from active epithelial secretion of chlorine and secondary fluid flux into the alveolar space. […] Regulation of the Na-K-ATPase is elicited by stimulation of dopaminergic, 2 adrenergic receptors, and aldosterone, and inhibited by oabain-like compounds. […] Furthermore, recent data suggest that lung injury and barrier dysfunction may play a role in the formation and resolution of congestion and pulmonary oedema. […] Future research is required to develop innovative pharmacotherapies capable of relieving hemodynamic congestion while simultaneously preserving end-organ function.

• #63 A New Mechanism to Prevent Pulmonary Edema in Severe Infections

  https://lungdiseasenews.com/2015/01/14/researchers-discover-a-new-mechanism-to-prevent-pulmonary-edema-in-severe-infections/

  It’s a vicious cycle of inflammation and leakiness of the lung blood vessels that is very hard to control. […] The researchers analyzed several proteins that regulate cell-to-cell contacts, also known as adherens junctions, and found that the VE-PTP protein can increase the integrity of the endothelial barrier. […] The reported mechanism in this study therefore represents a potential new target for the treatment of inflammatory diseases, such as the life-threatening ARDS, by preventing the formation of leaky vessels and edema.

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