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The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. [1]
Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. [1] Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). [ 1 ]
Acute respiratory distress syndrome : a potentially life-threatening condition where the alveoli are damaged thereby letting fluid leak into the lungs which makes it difficult to exchange gases and oxygenate the blood. [3] It is the general practice of the medical community to use the Berlin criteria to diagnose ARDS.
Acute respiratory distress syndrome (ARDS), a severe lung condition occurring in response to a critical illness or injury. Infant respiratory distress syndrome due to a deficiency of surfactant in the lungs of a baby born prematurely. Tuberculosis [4] Many cases of restrictive lung disease are idiopathic (have no known cause).
Respiratory distress syndrome (RDS) - is a breathing problem that sometimes affects babies born six weeks or more before their due dates. Their lungs aren't developed enough to make surfactant, a liquid that coats the inside of the lungs and keeps them open so that the baby can breathe in air once he or she is born.
The pathophysiology of type 3 respiratory failure often includes lung atelectasis, which is a term used to describe a collapsing of the functional units of the lung that allow for gas exchange. Because atelectasis occurs so commonly in the perioperative period, this form is also called perioperative respiratory failure.
The widely accepted pathophysiology of respiratory distress syndrome is it caused by insufficient surfactant production and immature lung and vascular development. The lack of surfactant makes the lungs atelectatic causing a ventilation to perfusion mismatch, lowered compliance, and increased air resistance.
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.