Maintenance of eucapnia is sometimes only possible with strategies that increase the risk of ventilator-induced lung injury, including the use of a tidal volume that causes alveolar overdistension. In these situations (e.g. acute lung injury), the risk can be reduced by decreasing tidal volume and therefore peak alveolar pressure. If the respiratory rate, physiological dead-space, and CO 2 production remain constant, Paco2 will rise. This may be appropriate if there is no significant respiratory acidosis (Slutsky 1.994).
If the metabolic rate decreases, Paco2 will decrease if alveolar ventilation remains constant. A reduction in tidal volume (if respiratory rate and physiological dead-space remain the same) may return CO2 tension to normal.
In normal lungs respiring spontaneously, the physiological dead-space ( VD) is approximately 2.2 ml/kg. The tidal volume ( VT) is significantly larger such that the ratio VDVT is between 0.2 and 0.4. Once the lungs become ventilated under positive pressure, deterioration of ventilation-perfusion matching results in an increase in VD/VT to approximately 0.5. In pulmonary disease this ratio can be as high as 0.8 ( SIuis,kY...19.9.4). As VD/VT increases, the effectiveness of ventilation reduces. An increase in tidal volume may restore alveolar ventilation. However, the relationship between VD/VT and tidal volume is not constant. At small tidal volumes, VD/VT is high and it falls as tidal volume is increased. At the point where increases in tidal volume cause airway distension, VD/VT remains constant until the size of the tidal volume causes a rapid increase in alveolar pressure (when the flat segment of the compliance curve is reached). This causes a reduction in venous return, deterioration in ventilation-perfusion matching, and an increase in VD/VT(KacmarekM.and..Venegas...1987). In normal ventilated lungs, VD/VT is lowest when the tidal volume is 10 to 15 ml/kg.
where Vco2 is the C02 production, Vk is alveolar ventilation, Paco2 is arterial C02 tension, and Patm is atmospheric pressure, and
where f is the respiratory rate, VT is the tidal volume, and VD is the physiological dead-space. Ventilator-induced lung injury
Alveolar overdistension increases the likelihood of ventilator-induced lung injury and should be avoided. Limiting the tidal volume to within the steep segment of the compliance curve reduces this possibility (Slutsky. . .1994), as alveolar volume is difficult to measure. The plateau pressure reflects alveolar pressure, and many clinicians attempt to limit it to below approximately 35 cmH2O (Slutsky 1994). However, if the compliance of the chest wall is reduced (e.g. severe kyphoscoliosis), a plateau pressure higher than this value is less likely to cause ventilator-induced lung injury.
The lung should be allowed to return to its resting position between each breath. Failure for this to occur leads to higher alveolar end-expiratory pressure than that selected. This auto-PEEP increases the risk of ventilator-induced lung injury ( Marcy and Marini 1991). The gas volume Vt above functional residual capacity left in the lung at time t after the start of expiration is calculated by the formula
where V0 is the volume at time zero and RC is the respiratory time constant (the product of resistance and compliance). Therefore a rise in tidal volume increases the chance of development of auto-PEEP if expiratory time is unaltered.
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