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Edema of the lungs should be thought of as the result of a disease such as congestive heart failure and not a disease in and of itself. In this case it would be a cardiac disease and not a pulmonary disease. Cardiogenic pulmonary edema is typically caused by either volume overload or impaired left ventricular function.
Hypervolemia, also known as fluid overload, is the medical condition where there is too much fluid in the blood. The opposite condition is hypovolemia, which is too little fluid volume in the blood. Fluid volume excess in the intravascular compartment occurs due to an increase in total body sodium content and a consequent increase in ...
In the lungs, the extra fluid accumulates into the air sacs within the lung, causing difficulties in oxygen getting into the blood. This results in low blood oxygen levels and shortness of breath. In the arms and legs, the fluid accumulates in the tissues, causing swelling. This is most prominent in the legs due to the effects of gravity.
Heart failure is usually associated with a volume overloaded state. Therefore, those with evidence of fluid overload should be treated initially with intravenous loop diuretics. In the absence of symptomatic low blood pressure intravenous nitroglycerin is often used in addition to diuretic therapy to improve congestive symptoms. [8]
A pleural effusion is accumulation of excessive fluid in the pleural space, the potential space that surrounds each lung.Under normal conditions, pleural fluid is secreted by the parietal pleural capillaries at a rate of 0.6 millilitre per kilogram weight per hour, and is cleared by lymphatic absorption leaving behind only 5–15 millilitres of fluid, which helps to maintain a functional ...
Chest Imaging: either chest x-ray or CT scan, must show bilateral opacities that cannot be fully explained by other conditions such as effusion, lung/lobar collapse, or lung nodules. Origin of Edema: respiratory failure that cannot be fully explained by cardiac failure or fluid overload, this needs objective assessment such as an echocardiogram.
It is often impossible to distinguish TRALI from acute respiratory distress syndrome (ARDS). The typical presentation of TRALI is the sudden development of shortness of breath, severe hypoxemia (O 2 saturation <90% in room air), low blood pressure, and fever that develop within 6 hours after transfusion and usually resolve with supportive care within 48 to 96 hours.
The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. [1]