Intra-abdominal Pressure and Chest Wall Interaction
Acute lung injury (ALI) is characterized by of a reduction in functional residual capacity (FRC) and an increase in static elastance of the respiratory system [1]. Such increase in static elastance of the respiratory system is mostly due to alterations in
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I Introduction Acute lung injury (ALI) is characterized by of a reduction in functional residual capacity (FRC) and an increase in static elastance of the respiratory system [1]. Such increase in static elastance of the respiratory system is mostly due to alterations in the mechanical properties of the lung because of the leading role of the underlying pulmonary injury. However, recent studies [2, 3] have reported that chest wall elastance may also be increased in patients with ALI probably through the increase in abdominal pressure. This chapter will • discuss the physiology of the abdomen-chest wall interaction, • describe the gold standard technique to measure intra-thoracic and abdominal pressures, and • discuss the mechanisms and potential clinical implications of increased intra-abdominal pressure (lAP).
I Physiology of Abdomen-chest Wall Interaction The chest wall operates in series with the lung being divided into two parallel pathways, the rib cage and the diaphragm-abdomen. The diaphragm forms the caudal distensible boundary of the chest cavity and is mechanically coupled to the abdominal wall and contents. The abdomen mechanically behaves like a closed fluid system and transmission of abdominal pressure is nearly homogeneous. The average density of abdominal contents is similar to that of water, and, therefore, under static conditions the walls are subjected to a surface pressure gradient that approximates a hydrostatic gradient. The change in pressure across the chest wall, when the muscle are relaxed (static condition), with the airway closed, is considered the change in pleural pressure, which is the surface pressure between the opposite surface of the thorax separated by the visceral and parietal pleural. Pleural pressure exhibits a hydrostatic pressure gradient along the height of the lungs and it is higher in gravity-dependent portions of the pleural space, being similar to the alveolar pressure at end expiration. The degree of lung distension is greater in the non-dependent than in the dependent portion of the chest wall. In the upright posture, at the end of a normal expiration, the pressure beneath the dome of the diaphragm and at the surface of the lungs above the diaphragm is approximately -3 or -4 cmHzO. In the upright posture, gravity acts in the inspiratory direction on the abdomen-diaphragm and in the expiratory direction on the rib cage, and the hydrostatic effect of the abdomen is greater at small than at large vol-
J.-L. Vincent (ed.), Yearbook of Intensive Care and Emergency Medicine 2002 © Springer-Verlag Berlin Heidelberg 2002
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