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PPHN can range from mild to severe disease. In the most severe form, infants experience severe hypoxemia resulting in cardiac and pulmonary complications. [4] As a result of low oxygen levels, infants with PPHN are at an increased risk of developing complications, such as asphyxia, chronic lung disease, neurodevelopment issues, and death.
The test is not infallible and many factors can cause the test to give false positive or negative results. Decomposition may result in postmortem gas formation, allowing a non-aerated lung to float. [2] During labor, air can be introduced to a deceased infant's lungs while moving through the birth canal. Lungs exposed to air do not always float ...
Major aortopulmonary collateral arteries (MAPCAs) develop early in embryonic life but regress as the normal pulmonary arteries (vessels that will supply deoxygenated blood to the lungs) develop. [2] In certain heart conditions the pulmonary arteries do not develop. The collaterals continue to grow, and can become the main supply of blood to the ...
These tests include the lungs' capability of air intake and outtake, and gas flow of oxygen and carbon dioxide between the body and environment. Following these function tests a special type of Chest CT scan or a bronchoscopy will be ordered. The results of the scan and bronchoscopy [9] will display the status of the condition. A mild case of ...
Medical diagnosis of pulmonary hypoplasia in utero may use imaging, usually ultrasound or MRI. [12] [13] The extent of hypoplasia is a very important prognostic factor. [14]One study of 147 fetuses (49 normal, 98 with abnormalities) found that a simple measurement, the ratio of chest length to trunk length, was a useful predictor of postnatal respiratory distress. [15]
Breathing sharply increases O 2 in the lungs, thus quickly reverting hypoxic pulmonary vasoconstriction that had held the pulmonary vascular resistance high during the uterine life. Lung ventilation also extends the so far convoluted, shrunk pulmonary vessels, also contributing to the quick and marked drop in the pulmonary vascular resistance.
Congenital pulmonary airway malformation (CPAM), formerly known as congenital cystic adenomatoid malformation (CCAM), is a congenital disorder of the lung similar to bronchopulmonary sequestration. In CPAM, usually an entire lobe of lung is replaced by a non-working cystic piece of abnormal lung tissue.
Positive end-expiratory pressure (PEEP) is the pressure in the lungs (alveolar pressure) above atmospheric pressure (the pressure outside of the body) that exists at the end of expiration. [1] The two types of PEEP are extrinsic PEEP (PEEP applied by a ventilator) and intrinsic PEEP (PEEP caused by an incomplete exhalation).