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Pulmonary edema is an abnormal accumulation of fluid in the air sacs (alveoli) and lung tissue, leading to impaired gas exchange and difficulty breathing. It is most commonly caused by heart conditions such as congestive heart failure but can also result from non-cardiac causes including pneumonia, sepsis, kidney failure, exposure to toxins or high altitude, trauma, or drug reactions. Symptoms include shortness of breath—especially when lying down—coughing up frothy sputum that may be blood-stained, wheezing, chest pain or tightness, anxiety and restlessness. Acute pulmonary edema is a medical emergency requiring immediate intervention with oxygen therapy and medications to address the underlying cause. Chronic forms may develop more slowly but still require prompt management to prevent life-threatening complications.[1][2][3] **Note:** "Airway edema" is not a molecular target but rather a clinical condition describing swelling due to fluid accumulation within the airway structures. The correct canonical term for this context is "pulmonary edema," which refers specifically to fluid buildup in the lungs' alveoli rather than just any airway swelling. There are no specific receptors or molecules named "airway edema"; thus it should not be considered a therapeutic target like an enzyme or receptor would be.[2]
Diuretics reduce fluid overload by increasing urine output. - Vasodilators decrease cardiac preload and afterload, reducing pulmonary capillary pressure. - Oxygen therapy increases oxygenation when gas exchange is impaired.[1][3]
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