Prevention and treatment of small airway and alveolar instability leading to atelectasis formation

Anesthesia, intubation, and muscle paralysis cause atelectasis in dependent lung zones. Intermittent tidal volumes that are larger than normal (sigh), and/or the use of PEEP, and/or postural changes can prevent or reverse closure of peripheral airways and collapse of alveoli. This results in an improvement of regional

ventilation-perfusion ratios ( VlQ) in dependent lung zones and hence improvement of systemic arterial oxygenation. However, when too much PEEP is used,

overdistension of non-dependent lung zones and areas of high VlQ can be created, thereby increasing alveolar dead-space. The most appropriate level of PEEP

results in an acceptable balance between sufficient recruitment and tolerable overdistension in other lung areas. The dead-space effect of overdistended areas can

be enhanced by PEEP-induced decreases in cardiac output, creating very high VlQ ratios by increasing V and lowering Q by lung inflation.

In acute lung injury such as acute respiratory distress syndrome, small airway and alveolar instability are magnified by the important additional effects of interstitial edema, gravitational characteristics of ventilation distribution, and global or regional inflammatory changes.

For all the above reasons, a certain amount of PEEP (or CPAP in the spontaneously breathing patient) can be considered 'physiological' up to the time of extubation in all forms of acute lung failure. Breathing through a T-piece during weaning is associated with a lower FRC than unassisted breathing after extubation; this is because of the impossibility of closing the vocal cords, owing to the presence of the endotracheal tube, and producing an efficient cough.

Massive edema creating areas of low V/Q

Pulmonary edema, acute respiratory distress syndrome, severe pneumonia, and lung contusion are characterized by gravity-dependent massive parenchymal edema with or without additional tissue consolidation. FRC is severely impaired and, for many years, its increase by PEEP has been considered essential for improved lung function (Fajkeefa/ 1972). PEEP increases lung volume and the gas exchange surface in two different ways: firstly, by recruitment of collapsed areas and, secondly, by distension of already open regions. The relative importance of both these effects can be assessed by the pressure-volume ( P-V) curve. Recruitment of collapsed regions results in a curvilinear P-V relationship (concave towards the volume axis) with a lower inflection point and an increasing compliance, i.e. a biphasic curve. When open units are distended by PEEP (or tidal volume), the P-V curve is linear, at least up to the point where overdistension begins. This latter area is characterized by the upper inflection point (convex towards the volume axis).

Typical P-V curves for a normal subject, an emphysematous patient, and a patient with acute respiratory distress syndrome are presented in Fig 1(Suter et ai 1975).

In non-dependent lung areas, i.e. in the parasternal regions in the supine position, PEEP produces essentially a linear increase in gas volume and VlQ; most units are open at zero PEEP in these regions. In severe lung edema or acute respiratory distress syndrome, most alveolar spaces are collapsed in paravertebral areas and there is a biphasic P-V relationship, corresponding to an important recruitment occurring at a certain level of PEEP in these regions. This 'critical' level of PEEP corresponds to the lower inflection point of the P-V curve (Pflex). This recruitment phenomenon increases progressively from the parasternal to the paravertebral areas, and the 'opening' pressure Pflex increases linearly along this axis, being highest in dependent lung zones. These effects of PEEP are most striking in the early phases of acute respiratory distress syndrome when lung edema is predominant. In pneumonia or later phases of acute respiratory distress syndrome, when fibrotic changes and remodeling of lung structures are more important, other mechanisms play essential roles in determining the distribution of ventilation with and without PEEP. In addition, PEEP is not solely responsible for the recruitment of alveolar space; tidal volume and end-inspiratory airway pressure also contribute to this effect. Furthermore, postural changes, which are frequently used in the current management of such patients, also influence gravity-dependent mechanisms and their localization, and thus the effects of PEEP and the level of Pflex in different lung regions. Lung size, i.e. the distance between the sternum and the vertebrae, is another important variable influencing regional lung weight and the pressure required to counteract compression airway closure and atelectasis.

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Trade-offs between PEEP, tidal volume, and Fi<2

Fig. 1 P-V curves for the respiratory system in normal lungs (N) and in those of patients with emphysema (E) and acute respiratory failure (ARF) of the early acute respiratory distress syndrome type: FRC, functional residual capacity; RV, residual volume; TLC, total lung capacity.The shaded areas represent the P-V relation during an identical tidal volume at two different PEEP levels. Lower and upper infection zones can be recognized on the P-V curve corresponding to acute pulmonary failure.

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