In this cohort of patients with AHRF, an increasing HFNC flow rate progressively decreased inspiratory effort and improved lung aeration, dynamic compliance and oxygenation. Most of the effect on inspiratory workload and CO clearance was already obtained at the lowest flow rate.

In acute hypoxemic respiratory failure (AHRF) and acute respiratory distress syndrome (ARDS) patients, spontaneous breathing is associated with multiple physiologic benefits: it prevents muscles atrophy, avoids paralysis, decreases sedation needs and is associated with improved hemodynamics. On the other hand, in the presence of uncontrolled inspiratory effort, severe lung injury and asynchronies, spontaneous ventilation might also worsen lung edema, induce diaphragm dysfunction and lead to muscles exhaustion and prolonged weaning. In the present review article, we present physiologic mechanisms driving spontaneous breathing, with emphasis on how to implement basic and advanced respiratory monitoring to assess lung protection during spontaneous assisted ventilation. Then, key benefits and risks associated with spontaneous ventilation are described. Finally, we propose some clinical means to promote protective spontaneous breathing at the bedside. In summary, early switch to spontaneous assisted breathing of acutely hypoxemic patients is more respectful of physiology and might yield several advantages. Nonetheless, risk of additional lung injury is not completely avoided during spontaneous breathing and careful monitoring of target physiologic variables such as tidal volume (Vt) and driving transpulmonary pressure should be applied routinely. In clinical practice, multiple interventions such as extracorporeal CO removal exist to maintain inspiratory effort, Vt and driving transpulmonary pressure within safe limits but more studies are needed to assess their long-term efficacy.

BackgroundSevere hypoperfusion can cause lung damage. We studied the effects of regional perfusion block in normal lungs and in the lungs that had been conditioned by lavage with 500 ml saline and high V T (20 ml kg−1) ventilation.MethodsNineteen pigs (61.2 ± 2.5 kg) were randomized to five groups: controls (n = 3), the right lower lobe block alone (n = 3), lavage and high V T (n = 4), lung lavage, and high V T plus perfusion block of the right (n = 5) or left (n = 4) lower lobe. Gas exchange, respiratory mechanics, and hemodynamics were measured hourly. After an 8-h observation period, CT scans were obtained at 0 and 15 cmH2O airway pressure.ResultsPerfusion block did not damage healthy lungs. In conditioned lungs, the left perfusion block caused more edema in the contralateral lung (777 ± 62 g right lung vs 484 ± 204 g left; p < 0.05) than the right perfusion block did (581 ± 103 g right lung vs 484 ± 204 g left; p n.s.). The gas/tissue ratio, however, was similar (0.5 ± 0.3 and 0.8 ± 0.5; p n.s.). The lobes with perfusion block were not affected (gas/tissue ratio right 1.6 ± 0.9; left 1.7 ± 0.5, respectively). Pulmonary artery pressure, PaO2/FiO2, dead space, and lung mechanics were more markedly affected in animals with left perfusion block, while the gas/tissue ratios were similar in the non-occluded lobes.ConclusionsThe right and left perfusion blocks caused the same “intensity” of edema in conditioned lungs. The total amount of edema in the two lungs differed because of differences in lung size. If capillary permeability is altered, increased blood flow may induce or increase edema.Electronic supplementary materialThe online version of this article (10.1186/s40635-017-0161-2) contains supplementary material, which is available to authorized users.

A pneumothorax (PTX) is a potentially lethal condition in high-risk intensive care patients. Electrical impedance tomography (EIT) has been proven to detect PTX at the bedside. A so far not described pattern in the course of thoracic impedance at an early state of PTX was observed in a pig model of ventilator-induced lung injury (VILI) used for a more extensive study. EIT was performed at a framerate of 50 Hz. Beginning of PTX at normal ventilation, manifestation of PTX at VILI ventilation (plateau pressure 42 cm H O) and final pleural drainage were documented. At ventilation with 8·6 ml kg , early PTX findings prior to any clinical deterioration consisted in a spike-like pattern in the time course of impedance (relative impedance change referred to initial end-expiratory level). Spike amplitudes (mean ± SD) were the following: 0·154 ± 0·059 (right lung) and 0·048 ± 0·050 (left lung). At this state, end-expiratory levels (mean ± SD) were still similar, -0·035 ± 0·010 (right) and -0·058 ± 0·022 (left). After application of VILI ventilation (38 ml kg ), a PTX developed slowly, being confirmed by a continuous increase in the end-expiratory level on the right side and diverging levels of +0·320 ± 0·057 (right) and -0·193 ± 0·147 (left) at full manifestation. We assume that spikes reflect a temporary change in the electrical pathway caused by leakage into the pleural cavity. This newly described phenomenon of spikes is considered to be a potentially useful indicator for a very early detection of an evolving PTX in high-risk ICU patients.