The dark side of the lung: unveiling regional lung ventilation with electrical impedance tomography.

I N this issue of ANESTHESIOLOGY, we can read the results of a study of the distribution of lung ventilation performed with electrical impedance tomography (EIT). The authors collected data during awake state and during lower limb surgery under general anesthesia in three randomized groups of surgical patients breathing spontaneously or receiving either pressure-support ventilation (PSV) or pressure-controlled ventilation. Two observations of interest emerged from the study. The first concerns the effects of the three ventilatory modes on the distribution of pulmonary ventilation. The second is the potential value of EIT monitoring during anesthesia. The study’s main finding was that when patients breathe spontaneously, gas was distributed similarly in anesthetized and awake states. During pressure-controlled ventilation, on the other hand, the distribution shifted to more ventral regions of the lung, and surprisingly, this shift also occurred in patients assigned to PSV. That atelectasis develops during general anesthesia in dependent zones is well known, and we also know that it leads to ventilation-perfusion mismatching and impaired gas exchange. In the early 1980s, Hedenstierna’s group in Sweden showed that this effect occurs both in patients breathing spontaneously and those under mechanical ventilation. However, Nyrén et al., using single-photon emission computed tomography, recently showed that the distribution of ventilation is similar during inhalational anesthesia in spontaneous breathing and during awake state. In the critical care setting, when patients with acute lung injury are initially allowed to breathe spontaneously with airway pressure release ventilation, better cardiopulmonary function has been observed and patients have required ventilation support for shorter periods. It seems that when diaphragm contraction is preserved at least to some extent, it is able to generate a transpulmonary pressure that exceeds the critical alveolar pressure. This pressure is transmitted to lung regions near the diaphragm, specifically to the more caudal and dorsal zones, where alveolar collapse tends to occur; spontaneous breathing would therefore open lung units where recruitment is most useful, improving aeration. These observations seem to call into question the findings of Radke et al. in patients under general anesthesia and PSV. First, certain design limitations may explain the discrepancy, given that the anesthetic techniques used and the duration of surgery were not entirely homogeneous in the authors’ three patient groups. The differences, though not statistically significant in this small study, may have been clinically significant. We are referring to slight variations in the combination of regional block techniques and general anesthesia, the amount of sufentanil administered, and the depth of anesthesia recorded. As a result, it is possible that automatic ventilator adjustments in the PSV group may have led to enough loss of ventilatory stimulus to diminish diaphragm activity. PSV levels set from 10 to 20 cm H2O are too high to produce enough diaphragm contraction to provide spontaneous ventilation benefits. Second, spontaneous ventilation during airway pressure release ventilation has been shown to be more efficient than PSV in decreasing atelectasis in patients with acute respiratory distress syndrome, even when both ventilator modes are set at the same mean airway pressure. During airway pressure release ventilation, patients