Elisabetta Gallazzi

Lung Inhomogeneity in Patients with Acute Respiratory Distress Syndrome

RATIONALE Pressures and volumes needed to induce ventilator-induced lung injury in healthy lungs are far greater than those applied in diseased lungs. A possible explanation may be the presence of local inhomogeneities acting as pressure multipliers (stress raisers). OBJECTIVES To quantify lung inhomogeneities in patients with acute respiratory distress syndrome (ARDS). METHODS Retrospective quantitative analysis of CT scan images of 148 patients with ARDS and 100 control subjects. An ideally homogeneous lung would have the same expansion in all regions; lung expansion was measured by CT scan as gas/tissue ratio and lung inhomogeneities were measured as lung regions with lower gas/tissue ratio than their neighboring lung regions. We defined as the extent of lung inhomogeneities the fraction of the lung showing an inflation ratio greater than 95th percentile of the control group (1.61). MEASUREMENTS AND MAIN RESULTS The extent of lung inhomogeneities increased with the severity of ARDS (14 ± 5, 18 ± 8, and 23 ± 10% of lung volume in mild, moderate, and severe ARDS; P < 0.001) and correlated with the physiologic dead space (r(2) = 0.34; P < 0.0001). The application of positive end-expiratory pressure reduced the extent of lung inhomogeneities from 18 ± 8 to 12 ± 7% (P < 0.0001) going from 5 to 45 cm H2O airway pressure. Lung inhomogeneities were greater in nonsurvivor patients than in survivor patients (20 ± 9 vs. 17 ± 7% of lung volume; P = 0.01) and were the only CT scan variable independently associated with mortality at backward logistic regression. CONCLUSIONS Lung inhomogeneities are associated with overall disease severity and mortality. Increasing the airway pressures decreased but did not abolish the extent of lung inhomogeneities.

Bedside selection of positive end-expiratory pressure in mild, moderate, and severe acute respiratory distress syndrome.

Objective:Positive end-expiratory pressure exerts its effects keeping open at end-expiration previously collapsed areas of the lung; consequently, higher positive end-expiratory pressure should be limited to patients with high recruitability. We aimed to determine which bedside method would provide positive end-expiratory pressure better related to lung recruitability. Design:Prospective study performed between 2008 and 2011. Setting:Two university hospitals (Italy and Germany). Patients:Fifty-one patients with acute respiratory distress syndrome. Interventions:Whole lung CT scans were taken in static conditions at 5 and 45 cm H2O during an end-expiratory/end-inspiratory pause to measure lung recruitability. To select individual positive end-expiratory pressure, we applied bedside methods based on lung mechanics (ExPress, stress index), esophageal pressure, and oxygenation (higher positive end-expiratory pressure table of lung open ventilation study). Measurements and Main Results:Patients were classified in mild, moderate and severe acute respiratory distress syndrome. Positive end-expiratory pressure levels selected by the ExPress, stress index, and absolute esophageal pressures methods were unrelated with lung recruitability, whereas positive end-expiratory pressure levels selected by the lung open ventilation method showed a weak relationship with lung recruitability (r2 = 0.29; p < 0.0001). When patients were classified according to the acute respiratory distress syndrome Berlin definition, the lung open ventilation method was the only one which gave lower positive end-expiratory pressure levels in mild and moderate acute respiratory distress syndrome compared with severe acute respiratory distress syndrome (8 ± 2 and 11 ± 3 cm H2O vs 15 ± 3 cm H2O; p < 0.05), whereas ExPress, stress index, and esophageal pressure methods gave similar positive end-expiratory pressure values in mild, moderate, and severe acute respiratory distress syndrome. The positive end-expiratory pressure selected by the different methods were unrelated to each other with the exception of the two methods based on lung mechanics (ExPress and stress index). Conclusions:Bedside positive end-expiratory pressure selection methods based on lung mechanics or absolute esophageal pressures provide positive end-expiratory pressure levels unrelated to lung recruitability and similar in mild, moderate, and severe acute respiratory distress syndrome, whereas the oxygenation-based method provided positive end-expiratory pressure levels related with lung recruitability progressively increasing from mild to moderate and severe acute respiratory distress syndrome.

Pleural effusion in patients with acute lung injury : a CT scan study

Objectives:Pleural effusion is a frequent finding in patients with acute respiratory distress syndrome. To assess the effects of pleural effusion in patients with acute lung injury on lung volume, respiratory mechanics, gas exchange, lung recruitability, and response to positive end-expiratory pressure. Design, Setting, and Patients:A total of 129 acute lung injury or acute respiratory distress syndrome patients, 68 analyzed retrospectively and 61 prospectively, studied at two University Hospitals. Interventions:Whole-lung CT was performed during two breath-holding pressures (5 and 45 cm H2O). Two levels of positive end-expiratory pressure (5 and 15 cm H2O) were randomly applied. Measurements:Pleural effusion volume was determined on each CT scan section; respiratory system mechanics, gas exchange, and hemodynamics were measured at 5 and 15 cm H2O positive end-expiratory pressure. In 60 patients, elastances of lung and chest wall were computed, and lung and chest wall displacements were estimated. Results:Patients were divided into higher and lower pleural effusion groups according to the median value (287 mL). Patients with higher pleural effusion were older (62 ± 16 yr vs. 54 ± 17 yr, p < 0.01) with a lower minute ventilation (8.8 ± 2.2 L/min vs. 10.1 ± 2.9 L/min, p < 0.01) and respiratory rate (16 ± 5 bpm vs. 19 ± 6 bpm, p < 0.01) than those with lower pleural effusion. Both at 5 and 15 cm H2O of positive end-expiratory pressure PaO2/FIO2, respiratory system elastance, lung weight, normally aerated tissue, collapsed tissue, and lung and chest wall elastances were similar between the two groups. The thoracic cage expansion (405 ± 172 mL vs. 80 ± 87 mL, p < 0.0001, for higher pleural effusion group vs. lower pleural effusion group) was greater than the estimated lung compression (178 ± 124 mL vs. 23 ± 29 mL, p < 0.0001 for higher pleural effusion group vs. lower pleural effusion group, respectively). Conclusions:Pleural effusion in acute lung injury or acute respiratory distress syndrome patients is of modest entity and leads to a greater chest wall expansion than lung reduction, without affecting gas exchange or respiratory mechanics.

Estimation of dead space fraction can be simplified in the acute respiratory distress syndrome.

Acute lung injury and acute respiratory distress syndrome are characterized by a non-cardiogenic pulmonary edema responsible for a significant impairment of gas exchange. The pulmonary dead space increase, which is due primarily to an alteration in pulmonary blood flow distribution, is largely responsible for carbon dioxide retention. Previous studies, computing the pulmonary dead space by measuring the expired carbon dioxide and the Enghoff equation, found that the dead space fraction was significantly higher in the non-survivors; it was even an independent risk of death. The computation of the dead space not by measuring the expired carbon dioxide but by applying a rearranged alveolar gas equation that takes into account only the weight, age, height, and temperature of the patient could lead to widespread clinical diffusion of this measurement at the bedside.

The Effects of Pleural Effusion

In healthy subjects, the pleural space, which is delimited by the visceral and parietal pleura, contains only a small amount of fluid, ranging from 10 to 20 ml [1]. This liquid usually originates from the capillaries of the parietal pleura and is drained by the lymphatics of the parietal pleura. However, in ill patients the fluid can originate from the visceral pleura or directly from the peritoneal cavity through the diaphragm. Basically, liquid accumulates every time there is an excess in liquid formation or a reduction in drainage. Medical or surgical patients are rarely admitted to the intensive care unit (ICU) for primary pleural disease; however, the pleura can be affected by various pulmonary or extrapulmonary conditions that promote the development of pleural effusions, which can affect the respiratory system [2].