Jean-Jacques Rouby

Comparative Diagnostic Performances of Auscultation, Chest Radiography, and Lung Ultrasonography in Acute Respiratory Distress Syndrome

BackgroundLung auscultation and bedside chest radiography are routinely used to assess the respiratory condition of ventilated patients with acute respiratory distress syndrome (ARDS). Clinical experience suggests that the diagnostic accuracy of these procedures is poor. MethodsThis prospective study of 32 patients with ARDS and 10 healthy volunteers was performed to compare the diagnostic accuracy of auscultation, bedside chest radiography, and lung ultrasonography with that of thoracic computed tomography. Three pathologic entities were evaluated in 384 lung regions (12 per patient): pleural effusion, alveolar consolidation, and alveolar-interstitial syndrome. ResultsAuscultation had a diagnostic accuracy of 61% for pleural effusion, 36% for alveolar consolidation, and 55% for alveolar-interstitial syndrome. Bedside chest radiography had a diagnostic accuracy of 47% for pleural effusion, 75% for alveolar consolidation, and 72% for alveolar-interstitial syndrome. Lung ultrasonography had a diagnostic accuracy of 93% for pleural effusion, 97% for alveolar consolidation, and 95% for alveolar-interstitial syndrome. Lung ultrasonography, in contrast to auscultation and chest radiography, could quantify the extent of lung injury. Interobserver agreement for the ultrasound findings as assessed by the &kgr; statistic was satisfactory: 0.74, 0.77, and 0.73 for detection of alveolar-interstitial syndrome, alveolar consolidation, and pleural effusion, respectively. ConclusionsAt the bedside, lung ultrasonography is highly sensitive, specific, and reproducible for diagnosing the main lung pathologic entities in patients with ARDS and can be considered an attractive alternative to bedside chest radiography and thoracic computed tomography.

Regional distribution of gas and tissue in acute respiratory distress syndrome. III. Consequences for the effects of positive end-expiratory pressure

Objective: To determine whether differences in lung morphology assessed by computed tomography (CT) affect the response to positive end-expiratory pressure (PEEP).¶Design: Prospective study over a 53-month period.¶Setting: Fourteen-bed surgical intensive care unit of a university hospital.¶Patients and participants: Seventy-one consecutive patients with early adult respiratory distress syndrome (ARDS).¶Measurements and results: Fast spiral thoracic CT was performed at zero end-expiratory pressure (ZEEP) and after implementation of PEEP 10 cmH2O. Hemodynamic and respiratory parameters were measured in both conditions. PEEP-induced overdistension and alveolar recruitment were quantified by specifically designed software (Lungview). Overdistension occurred only in the upper lobes and was significantly correlated with the volume of lung, characterized by a CT attenuation ranging between –900 and –800 HU in ZEEP conditions. Cardiorespiratory effects of PEEP were similar in patients with primary and secondary ARDS. PEEP-induced alveolar recruitment of the lower lobes was significantly correlated with their lung volume (gas + tissue) at functional residual capacity. PEEP-induced alveolar recruitment was greater in the lower lobes with “inflammatory atelectasis” than in the lower lobes with “mechanical atelectasis.” Lung morphology as assessed by CT markedly influenced the effects of PEEP: in patients with diffuse CT attenuations PEEP induced a marked alveolar recruitment without overdistension, whereas in patients with lobar CT attenuations PEEP induced a mild alveolar recruitment associated with overdistension of previously aerated lung areas. These results can be explained by the uneven distribution of regional compliance characterizing patients with lobar CT attenuations (compliant upper lobes and stiff lower lobes) contrasting with a more even distribution of regional compliances observed in patients with diffuse CT attenuations.¶Conclusions: In patients with ARDS, the cardiorespiratory effects of PEEP are affected by lung morphology rather than by the cause of the lung injury (primary versus secondary ARDS). The regional distribution of the loss of aeration and the type of atelectasis –“mechanical” with a massive loss of lung volume, or “inflammatory” with a preservation of lung volume – characterizing the lower lobes are the main determinants of the cardiorespiratory effects of PEEP.

Bedside Ultrasound Assessment of Positive End Expiratory Pressure–induced Lung Recruitment

RATIONALE In the critically ill patients, lung ultrasound (LUS) is increasingly being used at the bedside for assessing alveolar-interstitial syndrome, lung consolidation, pneumonia, pneumothorax, and pleural effusion. It could be an easily repeatable noninvasive tool for assessing lung recruitment. OBJECTIVES Our goal was to compare the pressure-volume (PV) curve method with LUS for assessing positive end-expiratory pressure (PEEP)-induced lung recruitment in patients with acute respiratory distress syndrome/acute lung injury (ARDS/ALI). METHODS Thirty patients with ARDS and 10 patients with ALI were prospectively studied. PV curves and LUS were performed in PEEP 0 and PEEP 15 cm H₂O₂. PEEP-induced lung recruitment was measured using the PV curve method. MEASUREMENTS AND MAIN RESULTS Four LUS entities were defined: consolidation; multiple, irregularly spaced B lines; multiple coalescent B lines; and normal aeration. For each of the 12 lung regions examined, PEEP-induced ultrasound changes were measured, and an ultrasound reaeration score was calculated. A highly significant correlation was found between PEEP-induced lung recruitment measured by PV curves and ultrasound reaeration score (Rho = 0.88; P < 0.0001). An ultrasound reaeration score of +8 or higher was associated with a PEEP-induced lung recruitment greater than 600 ml. An ultrasound lung reaeration score of +4 or less was associated with a PEEP-induced lung recruitment ranging from 75 to 450 ml. A statistically significant correlation was found between LUS reaeration score and PEEP-induced increase in Pa(O₂) (Rho = 0.63; P < 0.05). CONCLUSIONS PEEP-induced lung recruitment can be adequately estimated with bedside LUS. Because LUS cannot assess PEEP-induced lung hyperinflation, it should not be the sole method for PEEP titration.

Clinical review: Bedside lung ultrasound in critical care practice.

Lung ultrasound can be routinely performed at the bedside by intensive care unit physicians and may provide accurate information on lung status with diagnostic and therapeutic relevance. This article reviews the performance of bedside lung ultrasound for diagnosing pleural effusion, pneumothorax, alveolar-interstitial syndrome, lung consolidation, pulmonary abscess and lung recruitment/derecruitment in critically ill patients with acute lung injury.

Regional distribution of gas and tissue in acute respiratory distress syndrome. I. Consequences for lung morphology

Objective: To compare the computed tomographic (CT) analysis of the distribution of gas and tissue in the lungs of patients with ARDS with that in healthy volunteers. Design: Prospective study over a 53-month period.¶Setting: Fourteen-bed surgical intensive care unit of a university hospital. Patients and participants: Seventy-one consecutive patients with early ARDS and 11 healthy volunteers. Measurements and results: A lung CT was performed at end-expiration in patients with ARDS (at zero PEEP) and healthy volunteers. In patients with ARDS, end-expiratory lung volume (gas + tissue) and functional residual capacity (FRC) were reduced by 17 % and 58 % respectively, and an excess lung tissue of 701 ± 321 ml was observed. The loss of gas was more pronounced in the lower than in the upper lobes. The lower lobes of 27 % of the patients were characterized by “compression atelectasis,” defined as a massive loss of aeration with no concomitant excess in lung tissue, and “inflammatory atelectasis,” defined as a massive loss of aeration associated with an excess lung tissue, was observed in 73 % of the patients. Three groups of patients were differentiated according to the appearance of their CT: 23 % had diffuse attenuations evenly distributed in the two lungs, 36 % had lobar attenuations predominating in the lower lobes, and 41 % had patchy attenuations unevenly distributed in the two lungs. The three groups were similar regarding excess lung tissue in the upper and lower lobes and reduction in FRC in the lower lobes. In contrast, the FRC of the upper lobes was markedly lower in patients with diffuse or patchy attenuations than in healthy volunteers or patients with lobar attenuations. Conclusions: These results demonstrate that striking differences in lung morphology, corresponding to different distributions of gas within the lungs, are observed in patients whose respiratory condition fulfills the definition criteria of ARDS.

Acute respiratory distress syndrome: lessons from computed tomography of the whole lung.

ObjectiveThis review aims to show how computed tomography of the whole lung has modified our view of acute respiratory distress syndrome, and why it impacts on the optimization of the ventilatory strategy. Data sourcesComputed tomography allows an accurate assessment of the volumes of gas and lung tissue, respectively, and lung aeration. If computed tomographic sections are contiguous from the apex to the lung base, quantitative analysis can be performed either on the whole lung or, regionally, at the lobar level. Analysis requires a manual delineation of lung parenchyma and is facilitated by software, including a color-coding system that allows direct visualization of overinflated, normally aerated, poorly aerated, and nonaerated lung regions. In addition, lung recruitment can be measured as the amount of gas that penetrates poorly aerated and nonaerated lung regions after the application of positive intrathoracic pressure. Data SummaryThe lung in acute respiratory distress syndrome is characterized by a marked increase in lung tissue and a massive loss of aeration. The former is homogeneously distributed, although with a slight predominance in the upper lobes, whereas the latter is heterogeneously distributed. The lower lobes are essentially nonaerated, whereas the upper lobes may remain normally aerated, despite a substantial increase in regional lung tissue. The overall lung volume and the cephalocaudal lung dimensions are reduced primarily at the expense of the lower lobes, which are externally compressed by the heart and abdominal content when the patient is in the supine position. Two opposite radiologic presentations, corresponding to different lung morphologies, can be observed. In patients with focal computed tomographic attenuations, frontal chest radiography generally shows bilateral opacities in the lower quadrants and may remain normal, particularly when the lower lobes are entirely atelectatic. In patients with diffuse computed tomographic attenuations, the typical radiologic presentation of “white lungs” is observed. If these patients lie supine, lung volume is preserved in the upper lobes and reduced in the lower lobes, although the loss of aeration is equally distributed between the upper and lower lobes. This observation does not support the “opening and collapse concept” described as the “sponge model.” In fact, interstitial edema, alveolar flooding, or both, not collapse, are histologically present in all regions of the lung in acute respiratory distress syndrome. Compression atelectasis is observed only in caudal parts of the lung, where external forces (such as cardiac weight, abdominal pressure, and pleural effusion) tend to squeeze the lower lobes. When a positive intrathoracic pressure is applied to patients with focal acute respiratory distress syndrome, poorly aerated and nonaerated lung regions are recruited, whereas lung regions that are normally aerated at zero end-expiratory pressure tend to be rapidly overinflated, increasing the risk of ventilator-induced lung injury. ConclusionSelection of the optimal positive end-expiratory pressure level should not only consider optimizing alveolar recruitment, it should also focus on limiting lung overinflation and counterbalancing compression of the lower lobes by maneuvers such as appropriate body positioning. Prone and semirecumbent positions facilitate the reaeration of dependent and caudal lung regions by partially relieving cardiac and abdominal compression and may improve gas exchange.

Inhaled nitric oxide in acute respiratory failure : dose-response curves

ObjectiveTo determine the dose-response curve of inhaled nitric oxide (NO) in terms of pulmonary vasodilation and improvement in PaO2 in adults with severe acute respiratory failure.DesignProspective randomized study.SettingA 14-bed ICU in a teaching hospital.Patients6 critically ill patients with severe acute respiratory failure (lung injury severity score ≥2.5) and pulmonary hypertension.Interventions8 concentrations of inhaled NO were administered at random: 100, 400, 700, 1000, 1300, 1600, 1900 and 5000 parts per billion (ppb). Control measurements were performed before NO inhalation and after the last concentration administered. After an NO exposure of 15–20 min, hemodynamic parameters obtained from a fiberoptic Swan-Ganz catheter, blood gases, methemoglobin blood concentrations and intratracheal NO and nitrogen dioxide (NO2) concentrations, continuously monitored using a bedside chemiluminescence apparatus, were recorded on a Gould ES 1000 recorder. In 2 patients end-tidal CO2 was also recorded.ResultsThe administration of 100–2000 ppb of inhaled NO induced: i) a dose-dependent decrease in pulmonary artery pressure and in pulmonary vascular resistance (maximum decrease −25%); ii) a dose-dependent increase in PaO2 via a dose-dependent reduction in pulmonary shunt; iii) a slight but significant decrease in PaCO2 via a reduction in alveolar dead space; iv) a dose-dependent increase in mixed venous oxygen saturation (SVO2). Systemic hemodynamic variables and methemoglobin blood concentrations did not change. Maximum NO2 concentrations never exceeded 165 ppb. In 2 patients, 91% and 74% of the pulmonary vasodilation was obtained for inhaled NO concentrations of 100 ppb.ConclusionIn hypoxemic patients with pulmonary hypertension and severe acute respiratory failure, therapeutic inhaled NO concentrations are in the range 100–2000 ppb. The risk of toxicity related to NO inhalation is therefore markedly reduced. Continuous SVO2 monitoring appears useful at the bedside for determining optimum therapeutic inhaled NO concentrations in a given patient.

Inhaled Nitric Oxide Reverses the Increase in Pulmonary Vascular Resistance Induced by Permissive Hypercapnia in Patients with Acute Respiratory Distress Syndrome

BackgroundThe aim of this prospective study was to determine if inhaled nitric oxide (NO) would reverse the increase in pulmonary arterial pressures and in pulmonary vascular resistance induced by acute permissive hypercapnia in patients with acute respiratory distress syndrome. MethodsIn 11 critically ill patients (mean age 59 ± 22 yr) with acute respiratory distress syndrome (Murray Score 2.5), the lungs were mechanically ventilated with NO 2 ppm during both normocapnic and hypercapnic conditions. Four phases were studied: normocapnla (arterial carbon dioxide tension 38 ± 6 mmHg, tidal volume 655 ± 132 ml); normocapnia plus inhaled NO 2 ppm; hypercapnia (arterial carbon dioxide tension 65 ± 15 mmHg, tidal volume 330 ± 93 ml); and hypercapnia plus inhaled NO 2 ppm. Continuous recordings were made of heart rate, arterial pressure, pulmonary artery pressure, tracheal pressure, and tidal volume (by pneumotachograph). At the end of each condition, arterial pressure, pulmonary artery pressure, cardiac filling pressures, and cardiac output were measured. Simultaneous arterial and mixed venous blood samples were obtained to measure arterial oxygen tension, arterial carbon dioxide tension, mixed venous oxygen tension, arterial hemoglobin oxygen saturation, mixed venous hemoglobin oxygen saturation, pH, and blood hemoglobin and methemoglobin concentrations (by hemoximeter). In addition, plasma concentrations of catecholamines were measured with a radioenzymatic assay. In 5 patients, end-tidal carbon dioxide tension was measured with a nonaspirative infrared capnometer. Calculations were made of pulmonary vascular resistance index, systemic vascular resistance index, true pulmonary shunt, and alveolar dead space. ResultsDuring hypercapnia, NO decreased pulmonary vascular resistance Index from 525 ± 223 to 393 ± 142 dyn. s. cm−5. m−2 (P < 0.01), a value similar to that measured in normocapnic conditions (391 ± 122 dyn. s. cm−5. m−2). It also reduced mean pulmonary artery pressure from 40 ± 9 to 35 ± 8 mmHg (P < 0.01). NO increased arterial oxygen tension (inspired oxygen fraction 1) from 184 ± 67 to 270 ± 87 mmHg during normocapnia and from 189 ± 73 to 258 ± 101 mmHg during hypercapnia (P < 0.01). NO decreased true pulmonary shunt during normocapnia (from 34 ± 3% to 28 ± 4%, P < 0.001) but had no significant effect on it during hypercapnia (39 ± 7% vs. 38 ± 8.5%). In five patients, NO resulted in a decrease in alveolar dead space from 34 ± 7% to 28 ± 10% in normocapnic conditions and from 30 ± 9% to 22 ± 10% in hypercapnic conditions (P < 0.05). ConclusionsInhaled NO completely reversed the increase in pulmonary vascular resistance Index induced by acute permissive hypercapnia. It only partially reduced the pulmonary hypertension induced by acute permissive hypercapnia, probably because the flow component of the Increase in pulmonary pressure (i.e., the increase in cardiac output) was not reduced by inhaled NO. A significant increase in arterial oxygenation after NO administration was observed during normocapnic and hypercapnic conditions. A ventilation strategy combining permissive hypercapnia and inhaled NO may reduce the potentially deleterious effects that permissive hypercapnia alone has on lung parenchyma and pulmonary circulation.

Histologic aspects of pulmonary barotrauma in critically ill patients with acute respiratory failure

ObjectiveTo describe histologically pulmonary barotrauma in mechanically ventilated patients with severe acute respiratory failure.DesignAssessment of histologic pulmonary barotrauma.SettingA 14-bed surgical intensive care unit (SICU).PatientsThe lungs of 30 young critically ill patients (mean age 34±10 years) were histologically examined in the immediate post-mortem period. None of them were suspected of pre-existing emphysema.Measurements and resultsClinical events and ventilatory settings used during mechanical ventilation were compared with lung histology. Airspace enlargement, defined as the presence of either alveolar overdistension in aerated lung areas or intraparenchymal pseudocysts in nonaerated lung areas, was found in 26 of the 30 lungs examined (86%). Patients with severe airspace enlargement (2.6–40 mm internal diameter) had a significantly greater incidence of pneumothorax (8 versus 2,p<0.05), were ventilated using higher peak airway pressures (56±18 cmH2O versus 44±10 cmH2O,p<0.05) and tidal volumes (12±3 ml/kg, versus 9±2ml/kg,p<0.05) were exposed significantly longer to toxic levels of oxygen (8.6±9.4 days versus 1.9±2 days at FIO2>0.6,p<0.05) and lost more weight (6.3±9.2 kg versus 0.75±5.8 kg,p<0.05) than patients with mild airspace enlargement (1–2.5 mm internal diameter).ConclusionUnderlying histologic lesions responsible for clinical lung barotrauma consist of pleural cysts, bronchiolar dilatation, alveolar overdistension and intraparenchymal pseudocysts. Mechanical ventilation appears to be an aggravating factor, particularly when high peak airway pressures and large tidal volumes are delivered by the ventilator.

Regional distribution of gas and tissue in acute respiratory distress syndrome. II. Physiological correlations and definition of an ARDS Severity Score

Objectives: (a) To assess whether differences in lung morphology observed in patients with adult respiratory distress syndrome (ARDS) are associated with differences in cardiorespiratory parameters, lung mechanics, and outcome. (b) To propose a new ARDS Severity Score to identify patients with a high mortality risk. Design: Prospective study over a 53-month period. Setting: Fourteen-bed surgical intensive care unit of a university hospital. Patients and participants: Seventy-one consecutive patients with early ARDS. Measurements and results: Cardiorespiratory parameters were measured using a Swan-Ganz catheter, the pressure-volume (PV) curve was measured using the gross syringe method, and fast spiral computed tomography (CT) was performed. Patients with diffuse attenuations (n = 16) differed from patients with lobar attenuations (n = 26) regarding: (a) mortality rate (75 % vs. 42 %, p = 0.05), (b) incidence of primary ARDS (82 % vs. 50 %, p = 0.03), (c) respiratory compliance (47 ± 12 vs. 64 ± 16 ml per cmH2O–1p = 0.04), and (d) lower inflexion point (8.4 ± 2.0 vs. 4.6 ± 2.0 cmH2O, p = 0.001). A third group of patients with patchy attenuations (n = 29) had a mortality rate of 41 %, a respiratory compliance of 56 ± 18 ml per cmH2O–1 and a lower inflexion point of 6.3 ± 2.7 cmH2O. The bedside chest radiograph accurately assessed lung morphology in only 42 % of the patients. In contrast to the scores based on the bedside chest radiograph, a new ARDS Severity Score based on CT lung morphology and cardiorespiratory parameters identified a subgroup of patients with a high mortality rate (≥ 60 %). Conclusions: In patients with ARDS, differences in lung morphology are associated with differences in outcome and lung mechanics. A new ARDS Severity Score based on CT lung morphology and cardiorespiratory parameters accurately identified patients with the most severe forms of ARDS and a mortality rate above 60 %.