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Flash Pulmonary Edema or Crash Pulmonary Edema is a clinical characterization of acute heart failure with a dramatic presentation. [4] It is an acute cardiac disease precipitated by cardiac events and usually associated with severe hypertension.
The symptoms/signs of pulmonary heart disease (cor pulmonale) can be non-specific and depend on the stage of the disorder, and can include blood backing up into the systemic venous system, including the hepatic vein. [7] [8] As pulmonary heart disease progresses, most individuals will develop symptoms like: [1] Shortness of breath; Wheezing ...
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]
Pulmonary edema has multiple causes and is traditionally classified as cardiogenic (caused by the heart) or noncardiogenic (all other types not caused by the heart). [ 2 ] [ 3 ] Various laboratory tests ( CBC , troponin , BNP , etc.) and imaging studies ( chest x-ray , CT scan , ultrasound ) are often used to diagnose and classify the cause of ...
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). [2] HAPE is a severe presentation of altitude sickness. Cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in people who ...
Breast cancer patients are at high risk of heart failure due to several factors. [55] After analyzing data from 26 studies (836,301 patients), the recent meta-analysis found that breast cancer survivors demonstrated a higher risk heart failure within first ten years after diagnosis (hazard ratio = 1.21; 95% CI: 1.1, 1.33). [56]
Patients diagnosed with TACO should have at least 1 of the following two characteristics within 12 hours after the transfusion was ended: Acute or worsening respiratory distress (tachypnea, dyspnea, cyanosis, and/or hypoxemia) in the absence of other causes; Evidence of acute or worsening pulmonary edema (by physical examination or chest imaging)
Patients with left heart failure or hypoxemic lung diseases (groups II or III pulmonary hypertension) should not routinely be treated with vasoactive agents including prostanoids, phosphodiesterase inhibitors, or endothelin antagonists, as these are approved for the different condition called primary pulmonary arterial hypertension. [69]