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Respiratory failure
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===Type 2=== [[Hypoxemia]] (PaO<sub>2</sub> <8kPa or normal) with hypercapnia (PaCO<sub>2</sub> >6.0kPa). The basic defect in type 2 respiratory failure is characterized by: :::{| class="wikitable" |P<sub>a</sub>O<sub>2</sub> || decreased (< {{convert|60|mmHg|kPa|abbr=on}})or normal |- | P<sub>a</sub>CO<sub>2</sub> || increased (> {{convert|50|mmHg|kPa|abbr=on}}) |- | P<sub>A-a</sub>O<sub>2</sub> || normal |- |pH || <7.35 |} Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the buildup of carbon dioxide levels (P<sub>a</sub>CO<sub>2</sub>) that has been generated by the body but cannot be eliminated. The underlying causes include: * Increased airways resistance ([[chronic obstructive pulmonary disease]], [[asthma]], suffocation) * Reduced breathing effort (drug effects, brain stem lesion, extreme obesity) * A decrease in the area of the lung available for gas exchange (such as in [[Bronchitis#Chronic bronchitis|chronic bronchitis]]) * Neuromuscular problems ([[Guillain–Barré syndrome]],<ref name="Burt 475–479">{{cite journal| vauthors = Arrowsmith J, Burt C |title=Respiratory failure |journal=Surgery | location = Oxford |date=1 November 2009 |volume=27 |issue=11 |pages=475–479 |doi=10.1016/j.mpsur.2009.09.007}}</ref> [[motor neuron disease]]) * Deformed ([[kyphoscoliosis]]), rigid ([[ankylosing spondylitis]]), or [[flail chest]].<ref name="Burt 475–479"/>
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