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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 .
Opioids have traditionally been used in the treatment of the acute pulmonary edema that results from acute decompensated heart failure. A 2006 review, however, found little evidence to support this practice. [17] The National Institutes for Health and Care Excellence (NICE) guidelines do not recommend routinely offering opioids in acute heart ...
An acute exacerbation of COPD is associated with increased frequency and severity of coughing. [5] It is often accompanied by worsened chest congestion and discomfort. Shortness of breath and wheezing are present in many cases. [5] Exacerbations may be accompanied by increased amount of cough and sputum productions, and a change in appearance ...
The causes of pulmonary heart disease (cor pulmonale) are the following: Acute respiratory distress syndrome (ARDS) [10] COPD [2] Primary pulmonary hypertension [2] Blood clots in lungs/Pulmonary embolism [2] Kyphoscoliosis [2] Interstitial lung disease [2] Cystic fibrosis [2] Sarcoidosis [11] Obstructive sleep apnea (untreated) [2] Sickle cell ...
Acute bronchitis can be defined as acute bacterial or viral infection of the larger airways in healthy patients with no history of recurrent disease. [8] It affects over 40 adults per 1000 each year and consists of transient inflammation of the major bronchi and trachea. [ 9 ]
Lobar pneumonia usually has an acute progression. Classically, the disease has four stages: [1] Congestion in the first 24 hours: This stage is characterized histologically by vascular engorgement, intra-alveolar fluid, and small numbers of neutrophils, often numerous bacteria. Grossly, the lung is heavy and hyperemic.
Current recommendations in acute asthma symptoms are utilization of diuretics such as furosemide, venodilators such as nitroglycerin, and morphine. [1] The initial strategy should focus on decreasing patient fluid retention with diuretic therapy, thereby decreasing cardiac preload and overall fluid load in pulmonary circuit (pulmonary ...
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]