Electrical impedance tomography and trans-pulmonary pressure measurements in a patient with extreme respiratory drive

Preserving spontaneous breathing during mechanical ventilation prevents muscle atrophy of the diaphragm, but may lead to ventilator induced lung injury (VILI). We present a case in which monitoring of trans-pulmonary pressure and ventilation distribution using Electrical Impedance Tomography (EIT) provided essential information for preventing VILI

Excessive extracellular ATP desensitizes P2Y2 and P2X4 ATP receptors provoking surfactant impairment ending in ventilation-induced lung injury

Stretching the alveolar epithelial type I (AT I) cells controls the intercellular signaling for the exocytosis of surfactant by the AT II cells through the extracellular release of adenosine triphosphate (ATP) (purinergic signaling). Extracellular ATP is cleared by extracellular ATPases, maintaining its homeostasis and enabling the lung to adapt the exocytosis of surfactant to the demand. Vigorous deformation of the AT I cells by high mechanical power ventilation causes a massive release of extracellular ATP beyond the clearance capacity of the extracellular ATPases. When extracellular ATP reaches levels >100 μM, the ATP receptors of the AT II cells become desensitized and surfactant impairment is initiated. The resulting alteration in viscoelastic properties and in alveolar opening and collapse time-constants leads to alveolar collapse and the redistribution of inspired air from the alveoli to the alveolar ducts, which become pathologically dilated. The collapsed alveoli connected to these dilated alveolar ducts are subject to a massive strain, exacerbating the ATP release. After reaching concentrations >300 μM extracellular ATP acts as a danger-associated molecular pattern, causing capillary leakage, alveolar space edema, and further deactivation of surfactant by serum proteins. Decreasing the tidal volume to 6 mL/kg or less at this stage cannot prevent further lung injury

Clinical implication of monitoring regional ventilation using electrical impedance tomography

Abstract Mechanical ventilation can initiate ventilator-associated lung injury (VALI) and contribute to the development of multiple organ dysfunction. Although a lung protective strategy limiting both tidal volume and plateau pressure reduces VALI, uneven intrapulmonary gas distribution is still capable of increasing regional stress and strain, especially in non-homogeneous lungs, such as during acute respiratory distress syndrome. Real-time monitoring of regional ventilation may prevent inhomogeneous ventilation, leading to a reduction in VALI. Electrical impedance tomography (EIT) is a technique performed at the patient’s bedside. It is noninvasive and radiation-free and provides dynamic tidal images of gas distribution. Studies have reported that EIT provides useful information both in animal and clinical studies during mechanical ventilation. EIT has been shown to be useful during lung recruitment, titration of positive end-expiratory pressure, lung volume estimation, and evaluation of homogeneity of gas distribution in a single EIT measure or in combination with multiple EIT measures. EIT-guided mechanical ventilation preserved the alveolar architecture and maintained oxygenation and lung mechanics better than low-tidal volume ventilation in animal models. However, careful assessment is required for data analysis owing to the limited understanding of the results of EIT interpretation. Previous studies indicate monitoring regional ventilation by EIT is feasible in the intensive care setting and has potential to lead to lung protective ventilation. Further clinical studies are warranted to evaluate whether monitoring of regional ventilation using EIT can shorten the duration of ventilation or improve mortality in patients with acute respiratory distress syndrome

Personalisation of Therapies in COVID-19 Associated Acute Respiratory Distress Syndrome, Using Electrical Impedance Tomography

Each patient suffering from severe coronavirus COVID-19-associated acute respiratory distress syndrome (ARDS), requiring mechanical ventilation, shows different lung mechanics and disease evolution. Therefore, lung protective strategies should be personalised for the individual patient

Regional overdistension during prone positioning in a patient with acute respiratory failure who was ventilated with a low tidal volume: a case report

Abstract Background Prone positioning may provide a uniform distribution of transpulmonary pressure and contribute to prevent ventilator-induced lung injury. However, despite moderate positive end-expiratory pressure and low tidal volumes, there is still a risk of regional overdistension. Case presentation A man with refractory hypoxemia was mechanically ventilated with prone positioning. Although prone positioning with a plateau pressure of 18 cmH2O and a positive end-expiratory pressure of 8 cmH2O promptly improved oxygenation, regional ventilation monitoring using electrical impedance tomography initially detected decreased distribution in the dorsal region but increased in the ventral, suggesting overdistension. Conclusions Our experience indicates monitoring regional ventilation distribution is useful for decreasing the risk of overdistension during prone positioning

Whole lung lavage decreases physiological dead space in patients with pulmonary alveolar proteinosis: two case reports

Abstract Background Pulmonary alveolar proteinosis (PAP) is a rare disease characterized by progressive accumulation of the alveolar surfactant. Whole lung lavage (WLL) using a high volume of warmed saline remains the standard therapy. However, no established bedside monitoring tool can evaluate the physiological effect of WLL in the perioperative period. Indirect calorimetry, which is generally used to measure resting energy expenditure, can detect carbon dioxide (CO2) production and mixed-expired partial pressure of CO2 breath by breath. In this physiological study, we calculated CO2 elimination per breath (VTCO2,br) and Enghoff’s dead space using indirect calorimetry and measured the extravascular lung water index to reveal the effect of WLL. Case presentation We measured VTCO2,br, Enghoff’s dead space, and the extravascular lung water and cardiac indices before and after WLL to assess the reduction in shunt by washing out the surfactant. A total of four WLLs were performed in two PAP patients. The first case involved an Asian 62-year-old man who presented with a 3-month history of dyspnea on exertion. The second case involved an Asian 48-year-old woman with no symptoms. VTCO2,br increased, and the Enghoff’s dead space decreased at 12 h following WLL. An increase in the extravascular lung water was detected immediately following WLL, leading to a transient increase in Enghoff’s dead space. Conclusion WLL can increase efficient alveolar ventilation by washing out the accumulated surfactant. However, the lavage fluid may be absorbed into the lung tissues immediately after WLL and result in an increase in the extravascular lung water

Clinical Implications of Determining Individualized Positive End-Expiratory Pressure Using Electrical Impedance Tomography in Post-Cardiac Surgery Patients: A Prospective, Non-Randomized Interventional Study

Optimal positive end-expiratory pressure (PEEP) can induce sustained lung function improvement. This prospective, non-randomized interventional study aimed to investigate the effect of individualized PEEP determined using electrical impedance tomography (EIT) in post-cardiac surgery patients (n = 35). Decremental PEEP trials were performed from 20 to 4 cmH2O in steps of 2 cmH2O, guided by EIT. PEEP levels preventing ventilation loss in dependent lung regions (PEEPONLINE) were set. Ventilation distributions and oxygenation before the PEEP trial, and 5 min and 1 h after the PEEPONLINE setting were examined. Furthermore, we analyzed the saved impedance data offline to determine the PEEP levels that provided the best compromise between overdistended and collapsed lung (PEEPODCL). Ventilation distributions of dependent regions increased at 5 min after the PEEPONLINE setting compared with those before the PEEP trial (mean ± standard deviation, 41.3 ± 8.5% vs. 49.1 ± 9.3%; p < 0.001), and were maintained at 1 h thereafter (48.7 ± 9.4%, p < 0.001). Oxygenation also showed sustained improvement. Rescue oxygen therapy (high-flow nasal cannula, noninvasive ventilation) after extubation was less frequent in patients with PEEPONLINE ≥ PEEPODCL than in those with PEEPONLINE < PEEPODCL (1/19 vs. 6/16; p = 0.018). EIT-guided individualized PEEP stabilized the improvement in ventilation distribution and oxygenation. Individual PEEP varies with EIT measures, and may differentially affect oxygenation after cardiac surgery