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Flash pulmonary edema is a clinical syndrome that begins suddenly and accelerates rapidly. Essentially all patients will present to the emergency department by ambulance. The initiating acute event often a vascular event such as intense vasoconstriction and not a cardiac event such as myocardial infarction.
Mouth breathing as a result of decreased nasal breathing also increases lung surface exposure to irritants, pollutants, and allergens, causing neutrophilic inflammation in response to reactive oxygen species formation; research has found that individuals with genetically hindered glutathione counteraction of this oxidative stress are likely at ...
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]
Cardiac symptoms of heart failure include chest pain/pressure and palpitations.Common noncardiac signs and symptoms of heart failure include loss of appetite, nausea, weight loss, bloating, fatigue, weakness, low urine output, waking up at night to urinate, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion.
Alcohol excess appears to increase the risk of ARDS. [47] Diabetes was originally thought to decrease the risk of ARDS, but this has shown to be due to an increase in the risk of pulmonary edema. [48] [49] Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS, particularly during mechanical ventilation.
Patients in shock often experience respiratory distress due to pulmonary edema (e.g., in cardiogenic shock). Lactic acidosis and anemia can also result in type 4 respiratory failure. [1] However, type 1 and 2 are the most widely accepted. [1] [4] [5]
Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. [3] [4] Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase.
A common response cascade to a variety of irritant gases includes inflammation, edema and epithelial sloughing, which if left untreated can result in scar formation and pulmonary and airway remodeling. Currently, mechanical ventilation remains the therapeutic mainstay for pulmonary dysfunction following acute inhalation injury.