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Pulmonary edema (British English: oedema), also known as pulmonary congestion, is excessive fluid accumulation in the tissue or air spaces (usually alveoli) of the lungs. [1] This leads to impaired gas exchange , most often leading to shortness of breath ( dyspnea ) which can progress to hypoxemia and respiratory failure .
A chest x-ray showing pulmonary edema with bilateral pleural effusions. Along with: Elevations in brain-natriuretic peptide (BNP) or N-terminal (NT)-pro BNP. Evidence of cardiovascular system changes (tachycardia, hypertension, widened pulse pressure, jugular venous distension, peripheral edema) Evidence of fluid overload.
NPPE develops as a result of significant negative pressure generated in the chest cavity by inspiration against an upper airway obstruction. These negative pressures in the chest lead to increase venous supply to the right side of the heart while simultaneously creating more resistance for the left side of the heart to supply blood to the rest of the body (). [4]
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.
Acute lung injury (ALI), also called non-cardiogenic pulmonary edema, is characterized by the abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates in the absence of cardiac failure. The core pathology is disruption of the capillary-endothelial interface: this actually refers to two separate barriers – the endothelium and ...
Lower airway: may occur from bronchospasm, drowning, or airspace filling disorders (e.g. pneumonia, pulmonary edema, pulmonary hemorrhage). [7] Obstructive conditions of the lower airway, including severe asthma or COPD episodes, can also lead to respiratory arrest. During these episodes, known as exacerbations, airway resistance is increased ...
It may often be misdiagnosed as pulmonary edema (fluid in the lungs), pneumonia, or tuberculosis. Using workplace controls, silicosis is almost always a preventable disease. [5] Silicosis resulted in at least 43,000 deaths globally in 2013, down from at least 50,000 deaths in 1990. [6]
This is known as low-pressure oxygen poisoning, pulmonary toxicity, or the Lorrain Smith effect. This form of exposure leads to lung airway congestion, pulmonary edema, and atelectasis caused by damage to the linings of the bronchi and alveoli. Fluid accumulation in the lungs causes a feeling of shortness of breath, a burning sensation is felt ...