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Liquid breathing is a form of respiration in which a normally air-breathing organism breathes an oxygen-rich liquid which is capable of CO 2 gas exchange (such as a perfluorocarbon). [ 1 ] The liquid involved requires certain physical properties, such as respiratory gas solubility, density, viscosity, vapor pressure and lipid solubility, which ...
As the pulmonary venous pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. [14] Depending on whether the cause is acute or chronic determines how fast pulmonary edema develops and the severity of symptoms. [ 12 ]
This is known as outgassing, and occurs during decompression, when the reduction in ambient pressure or a change of breathing gas reduces the partial pressure of the inert gas in the lungs. [2] The combined concentrations of gases in any given tissue will depend on the history of pressure and gas composition.
Pulmonary function testing (PFT) is a complete evaluation of the respiratory system including patient history, physical examinations, and tests of pulmonary function. The primary purpose of pulmonary function testing is to identify the severity of pulmonary impairment. [ 1 ]
Rapid breathing helps the patient compensate for the decrease in blood pH by increasing the amount of exhaled carbon dioxide, which helps prevent further acid accumulation in the blood. [ 11 ] Cheyne–Stokes respiration is a breathing pattern consisting of alternating periods of rapid and slow breathing, which may result from a brain stem ...
Thermal injury combined with inhalation injury compromises pulmonary function, producing microvascular hyperpermeability that leads to a significant increase in lung lymph flow and pulmonary edema. The terrorist attack on the World Trade Center on September 11, 2001 left many people with impaired lung function.
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]
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.