Surfactant dramatically reduces surface tension.High surface tension of liquid lining the alveoli tends to collapse them. Separates abdominal and thoracic contents.Peripheral afferents from intercostal and subcostal nerves.Efferent and central afferent: phrenic nerve (C3-5).Back attaches to T12 vertebral body, descents to L1/L2 on sides.Front arises from xiphoid process, costal margins.3 Openings: Aorta (T12), oesophagus (T10) and vena caval (T8).Muscle fibres arise from peripheral attachment to form central tendon →Ĭrest of diaphrgam (thin but strong aponeurosis).C- shaped structure of muscle and fibrous tissues.Dome shaped muscle that inserts into the lower ribs.Perfusion vs Diffusion Limited Gas Transfer.Time Dependence of Pulmonary Elastic Behaviour.Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V'A/Q' ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces. For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V'A/Q') heterogeneity has been the most important pathophysiological mechanism. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure.
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