Tidal Hyperinflation during Low Tidal Volume Ventilation in Acute Respiratory Distress Syndrome

University of Milan, Milano, Lombardy, Italy
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 13). 02/2007; 175(2):160-6. DOI: 10.1164/rccm.200607-915OC
Source: PubMed


Tidal volume and plateau pressure limitation decreases mortality in acute respiratory distress syndrome. Computed tomography demonstrated a small, normally aerated compartment on the top of poorly aerated and nonaerated compartments that may be hyperinflated by tidal inflation.
We hypothesized that despite tidal volume and plateau pressure limitation, patients with a larger nonaerated compartment are exposed to tidal hyperinflation of the normally aerated compartment.
Pulmonary computed tomography at end-expiration and end-inspiration was obtained in 30 patients ventilated with a low tidal volume (6 ml/kg predicted body weight). Cluster analysis identified 20 patients in whom tidal inflation occurred largely in the normally aerated compartment (69.9 +/- 6.9%; "more protected"), and 10 patients in whom tidal inflation occurred largely within the hyperinflated compartments (63.0 +/- 12.7%; "less protected"). The nonaerated compartment was smaller and the normally aerated compartment was larger in the more protected patients than in the less protected patients (p = 0.01). Pulmonary cytokines were lower in the more protected patients than in the less protected patients (p < 0.05). Ventilator-free days were 7 +/- 8 and 1 +/- 2 d in the more protected and less protected patients, respectively (p = 0.01). Plateau pressure ranged between 25 and 26 cm H(2)O in the more protected patients and between 28 and 30 cm H(2)O in the less protected patients (p = 0.006).
Limiting tidal volume to 6 ml/kg predicted body weight and plateau pressure to 30 cm H(2)O may not be sufficient in patients characterized by a larger nonaerated compartment.

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    • "First, measures of lung injury will not perform well as prognostic measures because non-pulmonary factors including age, severity of sepsis, co-morbidities and non-pulmonary organ failure remain the most influential predictors of hospital mortality in ARDS, [25-39] and non-resolving respiratory failure accounts for less than 20% of ARDS deaths [34-36]. Also, although the finding that PaO2/FiO2 level is associated with mortality is consistent with the findings reported from cohorts used for empirical analysis in the development of the Berlin ARDS definition, [40-46] this has not been demonstrated consistently, a finding that may be attributable, in part, to practice variability in mechanical ventilation settings, which is known to have a large effect on PaO2/FiO2 levels [5,6,24,47,48]. Furthermore, post-mortem studies highlight the poor accuracy that clinical definitions such as the Berlin criteria have for histological definitions of diffuse alveolar damage, which are found in only a minority of patients with clinical ARDS [49,50]. "
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    ABSTRACT: The Lung Injury Score (LIS) remains a commonly utilized measure of lung injury severity though the additive value of LIS to predict ARDS outcomes over the recent Berlin definition of ARDS, which incorporates severity, is not known. We tested the association of LIS (in which scores range from 0 to 4, with higher scores indicating more severe lung injury) and its four components calculated on the day of ARDS diagnosis with ARDS morbidity and mortality in a large, multi-ICU cohort of patients with Berlin-defined ARDS. Receiver Operator Characteristic (ROC) curves were generated to compare the predictive validity of LIS for mortality to Berlin stages of severity (mild, moderate and severe). In 550 ARDS patients, a one-point increase in LIS was associated with 58% increased odds of in-hospital death (95% CI 14 to 219%, P = 0.006), a 7% reduction in ventilator-free days (95% CI 2 to 13%, P = 0.01), and, among patients surviving hospitalization, a 25% increase in days of mechanical ventilation (95% CI 9 to 43%, P = 0.001) and a 16% increase (95% CI 2 to 31%, P = 0.02) in the number of ICU days. However, the mean LIS was only 0.2 points higher (95% CI 0.1 to 0.3) among those who died compared to those who lived. Berlin stages of severity were highly correlated with LIS (Spearman's rho 0.72, P < 0.0001) and were also significantly associated with ARDS mortality and similar morbidity measures. The predictive validity of LIS for mortality was similar to Berlin stages of severity with an area under the curve of 0.58 compared to 0.60, respectively (P-value 0.49). In a large, multi-ICU cohort of patients with ARDS, both LIS and the Berlin definition severity stages were associated with increased in-hospital morbidity and mortality. However, predictive validity of both scores was marginal, and there was no additive value of LIS over Berlin. Although neither LIS nor the Berlin definition were designed to prognosticate outcomes, these findings suggest that the role of LIS in characterizing lung injury severity in the era of the Berlin definition ARDS may be limited.
    Full-text · Article · Feb 2014 · Annals of Intensive Care
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    • "Indeed, when large tidal volumes are delivered, this can lead to repeated over-distension of alveoli and further aggravate injury by volutrauma [6,35]. When lung protective ventilation is used, the aggravation of lung injury may depend on the degree of the reduction in aerated lung volume and the tidal volume used [36]. In the present study, the degree of the reduction in aerated lung volume following lung lavage was not severe as indicated by the mean P/F ratio above 400 on the high PEEP in experimental groups. "
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    ABSTRACT: Although endotracheal suctioning induces alveolar derecruitment during mechanical ventilation, it is not clear whether repeated endotracheal suctioning exacerbates lung injuries. The present study aimed to determine whether repeated open endotracheal suctioning (OS) exacerbates lung injury compared to closed endotracheal suctioning (CS) during mechanical ventilation in an animal model of acute respiratory distress syndrome (ARDS). Briefly, thirty six Japanese white rabbits were initially ventilated in pressure-controlled mode with a constant tidal volume (6 mL/kg). Then, lung injury was induced by repeated saline lavage. The rabbits were divided into four groups, namely: a) OS; b) CS; c) control with ARDS only; d) and healthy control (HC) without ARDS. Animals in all the groups were then ventilated with positive end expiratory pressure (PEEP) at 10 cm H2O. CS was performed using 6 French-closed suctioning catheters connected to endotracheal tube under the following conditions: a) a suctioning time and pressure of 10 sec and 140 mm Hg, respectively; and b) a suction depth of 2 cm (length of adapter) plus tracheal tube. OS was performed using the same conditions described for CS, except the ventilator was disconnected from the animals. Each endotracheal suctioning was performed at an interval of 30 min. PaO2/FIO2 (P/F) ratio for CS, control and HC groups remained at >400 for 6 hours, whereas that of the OS group progressively declined to 300 (p < 0.05), with each suctioning. However, no difference was observed either in lung injury score (histology) or in the expression pattern of inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6) after 6 hours between the OS and CS groups in the circulatory as well as the pulmonary tissues. Progressive arterial desaturation under conditions of repeated endotracheal suctioning is greater in OS than in CS time-dependently. However, OS does not exacerbate lung injury during mechanical ventilation when observed over a longer time span (6 hours) of repeated endotracheal suctioning, based on morphological and molecular analysis.
    Full-text · Article · Dec 2013 · BMC Anesthesiology
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    • "These findings, however, are not in contrast with the hypothesis that lung inhomogeneity may lead to pressure multiplication because the introduction of unphysiologic strain may lead to capillary lesions. The potential benefit of PEEP in the framework of lung protective strategy is to maintain open, at end-expiration, the lung parenchyma that has been recruited during inspiration phase, thus decreasing the lung inhomogeneity and the VILI(15,16,23). Actually, we found that the lung inhomogeneities decreased increasing PEEP and, in addition, were significantly but weakly related with lung recruitability. In individual patients, however, recruitability, PEEP, and lung inhomogeneity pattern were not associated. "
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    ABSTRACT: Rationale: Pressures and volumes needed to induce ventilator-induced lung injury in healthy lungs are far greater than applied in diseased lungs. A possible explanation may be the presence of local inhomogeneities acting as pressure multipliers (stress raisers). Objectives: quantify lung inhomogeneities in patients with Acute Respiratory Distress Syndrome (ARDS). Methods: Retrospective quantitative analysis of CT scan images of 148 patient with ARDS and 100 control subjects. A ideally homogeneous lung would have the same expansion in all regions; lung expansion was measured by CT scan as gas/tissue ratio and lung inhomogenities were measured as lung regions with lower gas/tissue ratio than their neighboring lung regions. We defined as the extent of lung inhomogenities the fraction of the lung showing an inflation ratio greater than 95th percentile of the control group (1.61). Measurments 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 physiological dead space (r2=0.34, p<0.0001). The application of PEEP reduced the extent of lung inhomogeneities from 18±8 to 12±7% (p < 0.0001) going from 5 to 45 cmH2O airway pressure. Lung inhomogeneities were greater in non-survivor patients than in survivor patients (17±7 vs 20±9% 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 not abolished the extent of lung inhomogeneities.
    Full-text · Article · Nov 2013 · American Journal of Respiratory and Critical Care Medicine
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