Cardiogenic Edema Research Articles

Chloride secretion across adult alveolar epithelial cells contributes to cardiogenic edema

In utero, fetal lung epithelial cells actively secrete chloride (Cl−) ions into the lung airspaces. Cl− ions enter the basolateral membranes through Na+/K+/2Cl− (NKCC) transporters (1), down an electrochemical gradient generated by the basolateral Na+/K+/ATPase, and exit through apical anion channels, including the cAMP- activated cystic fibrosis transmembrane regulator (CFTR) (2). Na+ ions follow passively through the paracellular junctions to preserve electroneutrality. The vectorial transport of NaCl generates an oncotic pressure, which drives fetal fluid secretion into the airway lumen. Shortly before birth, Cl− secretion diminishes and active Na+ transport begins: Na+ ions enter lung epithelial cells through amiloride-sensitive Na+ channels (ENaC) and are extruded across the basolateral membranes by the Na+/K+/ATPase (3, 4). This process is critical for the reabsorption of fetal lung fluid and the establishment of gas exchange. In the adult lung active Na+ reabsorption limits the degree of alveolar edema in hyperoxic lung injury (5) and in patients with acute respiratory distress syndrome (6, 7).

Chloride transport-driven alveolar fluid secretion is a major contributor to cardiogenic lung edema

Alveolar fluid clearance driven by active epithelial Na(+) and secondary Cl(-) absorption counteracts edema formation in the intact lung. Recently, we showed that impairment of alveolar fluid clearance because of inhibition of epithelial Na(+) channels (ENaCs) promotes cardiogenic lung edema. Concomitantly, we observed a reversal of alveolar fluid clearance, suggesting that reversed transepithelial ion transport may promote lung edema by driving active alveolar fluid secretion. We, therefore, hypothesized that alveolar ion and fluid secretion may constitute a pathomechanism in lung edema and aimed to identify underlying molecular pathways. In isolated perfused lungs, alveolar fluid clearance and secretion were determined by a double-indicator dilution technique. Transepithelial Cl(-) secretion and alveolar Cl(-) influx were quantified by radionuclide tracing and alveolar Cl(-) imaging, respectively. Elevated hydrostatic pressure induced ouabain-sensitive alveolar fluid secretion that coincided with transepithelial Cl(-) secretion and alveolar Cl(-) influx. Inhibition of either cystic fibrosis transmembrane conductance regulator (CFTR) or Na(+)-K(+)-Cl(-) cotransporters (NKCC) blocked alveolar fluid secretion, and lungs of CFTR(-/-) mice were protected from hydrostatic edema. Inhibition of ENaC by amiloride reproduced alveolar fluid and Cl(-) secretion that were again CFTR-, NKCC-, and Na(+)-K(+)-ATPase-dependent. Our findings show a reversal of transepithelial Cl(-) and fluid flux from absorptive to secretory mode at hydrostatic stress. Alveolar Cl(-) and fluid secretion are triggered by ENaC inhibition and mediated by NKCC and CFTR. Our results characterize an innovative mechanism of cardiogenic edema formation and identify NKCC1 as a unique therapeutic target in cardiogenic lung edema.

Risk of weaning failure with PAOP ≥15 versus PAOP ≥18

Despite 18 mmHg being recognized as a classical cutoff value, there is no definite value of PAOP above which cardiogenic oedema develops. We aimed to assess the risks of weaning failure with PAOP ≥15 and with PAOP ≥18.

Abstract TP423: Postoperative Hemodynamics is Different between Clipping and Coiling after Aneurismal Subarachnoid Hemorrhage -A Multicenter Prospective Cohort Study -

Background and Purpose: Volume management is critical for the assessment of the vasospasm after aneurismal subarachnoid hemorrhage (SAH). In this study, we investigate the difference in the postoperative systemic hemodynamics between surgical clipping and endovascular coiling. Methods: In a multicenter prospective cohort study, multiple hemodynamic parameters were calculated by single indicator transpulmonary thermodilution system (Picco®) from day 1 to 14 in the patients with SAH. Results: Two hundred and four patients were enrolled in this study, and 176 patients with ruptured anterior circulation aneurysm were analyzed. Clipping was performed in 155 patients and coiling was performed in 21 patients. The patient characteristics were similar in both groups except higher preoperative grade in coiling than clipping. Regarding hematological parameters, clipping group had higher CRP and lower hemoglobin and hematocrits. Preload and afterload were similar in both groups. Coiling group had significantly less cardiac function index compared with clipping indicating that coiling was preferably selected for severe cases. Interestingly, extravascular lung water index (EVLWI) was significantly higher in clipping than coiling group without elevation of the pulmonary vascular permeability index. Moreover, elevation of Brain Natriuretic Peptide did not affect EVLWI. Conclusions: We first show that postoperative hemodynamics is different depending on the treatment option: clipping or coiling after aneurysmal SAH. Clipping can enhances cardiogenic lung edema due to hemodynamic stress rather than coiling. Bedside monitoring with Picco® system is a powerful tool for the volume management of patients with SAH.

Extravascular lung water and the pulmonary vascular permeability index may improve the definition of ARDS

The recent Berlin definition has made some improvements in the older definition of acute respiratory distress syndrome (ARDS), although the concepts and components of the definition remained largely unchanged. In an effort to improve both predictive and face validity, the Berlin panel has examined a number of additional measures that may reflect increased pulmonary vascular permeability, including extravascular lung water. The panel concluded that although extravascular lung water has improved face validity and higher values are associated with mortality, it is infeasible to mandate on the basis of availability and the fact that it does not distinguish between hydrostatic and inflammatory pulmonary edema. However, the results of a multi-institutional study that appeared in the previous issue of Critical Care show that this latter reservation may not necessarily be true. By using extravascular lung water and the pulmonary vascular permeability index, both of which are derived from transpulmonary thermodilution, the authors could successfully differentiate between patients with ARDS and other patients in respiratory failure due to either cardiogenic edema or pleural effusion with atelectasis. This commentary discusses the merits and limitations of this study in view of the potential improvement that transpulmonary thermodilution may bring to the definition of ARDS.

Impact of noninvasive ventilation failure upon patient prognosis. Subanalysis of a multicenter study

ObjectiveNoninvasive ventilation (NIV) constitutes first-line treatment for the exacerbation of obstructive pulmonary disease and cardiogenic lung edema. Several studies suggest that NIV failure could increase the risk of mortality, mainly due to the delay in tracheal intubation. We aimed to evaluate the negative impact of NIV failure in routine practice among Spanish ICUs. PatientsA subanalysis was made of the multicenter validation of the Sabadell Score study, extracting patients with acute respiratory failure requiring either invasive or noninvasive mechanical ventilation, with the exclusion of patients presenting “do not resuscitate and/or do not intubate” orders. VariablesWe recorded demographic parameters, ICU-specific treatments and the development of acute renal failure or infections during ICU stay. Patients were followed-up on until hospital discharge or death. The statistic analysis included Cox multiple logistic regression. ResultsWe analyzed 4132 patients, of whom 1602 (39%) received only invasive mechanical ventilation (IMV), while 529 (13%) received NIV. The latter succeeded in 50% of the patients, but the other 50% required intubation. NIV failure was more common in neurological and postsurgical patients. Mortality was lower than predicted in NIV patients (22% vs 33%) and similar to predicted in IMV patients (27% vs 29%). Mortality was lower than predicted in patients in whom NIV proved successful (12% vs 28%), and in those in whom NIV failed (32% vs 38%). ConclusionNIV failure and the need of intubation as routinely used do not seem to imply a poorer patient prognosis.

Impacto del fracaso de la ventilacion no invasiva en el pronóstico de los pacientes. Subanálisis de un estudio multicéntrico

Noninvasive ventilation (NIV) constitutes first-line treatment for the exacerbation of obstructive pulmonary disease and cardiogenic lung edema. Several studies suggest that NIV failure could increase the risk of mortality, mainly due to the delay in tracheal intubation. We aimed to evaluate the negative impact of NIV failure in routine practice among Spanish ICUs.A subanalysis was made of the multicenter validation of the Sabadell Score study, extracting patients with acute respiratory failure requiring either invasive or noninvasive mechanical ventilation, with the exclusion of patients presenting "do not resuscitate and/or do not intubate" orders.We recorded demographic parameters, ICU-specific treatments and the development of acute renal failure or infections during ICU stay. Patients were followed-up on until hospital discharge or death. The statistic analysis included Cox multiple logistic regression.We analyzed 4132 patients, of whom 1602 (39%) received only invasive mechanical ventilation (IMV), while 529 (13%) received NIV. The latter succeeded in 50% of the patients, but the other 50% required intubation. NIV failure was more common in neurological and postsurgical patients. Mortality was lower than predicted in NIV patients (22% vs. 33%) and similar to predicted in IMV patients (27% vs. 29%). Mortality was lower than predicted in patients in whom NIV proved successful (12% vs. 28%), and in those in whom NIV failed (32% vs. 38%).NIV failure and the need of intubation as routinely used do not seem to imply a poorer patient prognosis.

Relationship between CT Findings and the Plasma Levels of Brain Natriuretic Peptide in 29 Patients with Acute Cardiogenic Pulmonary Edema

Brain natriuretic peptide (BNP) is a useful biomarker for the assessment of cardiogenic pulmonary edema. This study evaluated the relationship between computed tomography (CT) findings and plasma BNP levels in patients with cardiogenic pulmonary edema. Twenty-nine consecutive outpatients with severe respiratory failure from cardiogenic edema presenting to emergency departments were enrolled. They underwent chest CT and plasma BNP levels were measured in the emergency room. CT findings were independently evaluated by two radiologists who were unaware of the patients' clinical information. The plasma BNP levels only correlated with the volume of pleural effusion in each side (right: r(s) = 0.519, P = .004; left: r(s) = 0.460, P = .012). No significant correlation was observed between the BNP levels and the findings of lung parenchyma or cardiovascular enlargement. Estimating the pleural effusion volume with CT may be a feasible method as well as measuring the plasma BNP level in the assessment of acute cardiogenic pulmonary edema.

The clinical usefulness of extravascular lung water and pulmonary vascular permeability index to diagnose and characterize pulmonary edema: a prospective multicenter study on the quantitative differential diagnostic definition for acute lung injury/acute respiratory distress syndrome

IntroductionAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by features other than increased pulmonary vascular permeability. Pulmonary vascular permeability combined with increased extravascular lung water content has been considered a quantitative diagnostic criterion of ALI/ARDS. This prospective, multi-institutional, observational study aimed to clarify the clinical pathophysiological features of ALI/ARDS and establish its quantitative diagnostic criteria.MethodsThe extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI) were measured using the transpulmonary thermodilution method in 266 patients with PaO2/FiO2 ratio ≤ 300 mmHg and bilateral infiltration on chest radiography, in 23 ICUs of academic tertiary referral hospitals. Pulmonary edema was defined as EVLWI ≥ 10 ml/kg. Three experts retrospectively determined the pathophysiological features of respiratory insufficiency by considering the patients' history, clinical presentation, chest computed tomography and radiography, echocardiography, EVLWI and brain natriuretic peptide level, and the time course of all preceding findings under systemic and respiratory therapy.ResultsPatients were divided into the following three categories on the basis of the pathophysiological diagnostic differentiation of respiratory insufficiency: ALI/ARDS, cardiogenic edema, and pleural effusion with atelectasis, which were noted in 207 patients, 26 patients, and 33 patients, respectively. EVLWI was greater in ALI/ARDS and cardiogenic edema patients than in patients with pleural effusion with atelectasis (18.5 ± 6.8, 14.4 ± 4.0, and 8.3 ± 2.1, respectively; P < 0.01). PVPI was higher in ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 ± 1.4, 2.0 ± 0.8, and 1.6 ± 0.5; P < 0.01). In ALI/ARDS patients, EVLWI increased with increasing pulmonary vascular permeability (r = 0.729, P < 0.01) and was weakly correlated with intrathoracic blood volume (r = 0.236, P < 0.01). EVLWI was weakly correlated with the PaO2/FiO2 ratio in the ALI/ARDS and cardiogenic edema patients. A PVPI value of 2.6 to 2.85 provided a definitive diagnosis of ALI/ARDS (specificity, 0.90 to 0.95), and a value < 1.7 ruled out an ALI/ARDS diagnosis (specificity, 0.95).ConclusionPVPI may be a useful quantitative diagnostic tool for ARDS in patients with hypoxemic respiratory failure and radiographic infiltrates.Trial registrationUMIN-CTR ID UMIN000003627

Case Scenario: Acute Postoperative Negative Pressure Pulmonary Edema

A 25-yr-old man (weight, 68 kg; height, 183 cm) presentedto the surgery center for excision of back and thigh schwan-nomas on the same day. The patient’s medical history wassignificant only for his history of multiple schwannoma re-sections and a history of smoking one pack of cigarettes perweek for the past 5 yr. He denied previous problems withgeneral anesthesia, and his baseline peripheral oxygen satu-ration was 99% on ambient air.Thepatientwaspremedicatedwith2mgmidazolam,andanesthesia was induced with 250 mg fentanyl, 500 mg thio-pental, and 8 mg vecuronium given for facilitation of tra-cheal intubation. He was atraumatically intubated with a7-mm ID endotracheal tube using a no. 3 Macintosh laryn-goscope (Teleflex Medical, Research Triangle Park, NC) onthe first attempt with direct visualization of the vocal cords.The patient was turned prone, bilateral breath sounds werereconfirmed, and schwannoma excisions were performed ontheleftthighandtheleftflank.Atotalof0.5mghydromor-phone was administered for analgesia. The intraoperativecoursewasunremarkable.Thepatientwashemodynamicallystable with minimal blood loss and was easily ventilated andoxygenated. A total of 500 ml lactated Ringer’s solution wasadministeredduringthe65-minsurgicalprocedure.Thepa-

Kardiales und nicht kardiales Lungenödem: Pathomechanismen und Ursachen

The development of pulmonary edema is divided in cardiogenic and non-cardiogenic. Cardiogenic edema pathogenically is caused by elevated hydrostatic pressure in the pulmonary capillaries due to left sided congestive heart failure. Non-cardiogenic pulmonary edema is categorized depending on the underlying pathogenesis in low-alveolar pressure, elevated permeability or neurogenic edema. Some important examples of causes are upper airway obstruction like in laryngeal paralysis or strangulation for low alveolar pressure, leptospirosis and ARDS for elevated permeability, and epilepsy, brain trauma and electrocution for neurogenic edema. The differentiation between cardiogenic versus non-cardiogenic genesis is not always straightforward, but most relevant, because treatment markedly differs between the two. Of further importance is the identification of the specific underlying cause in non-cardiogenic edema, not only for therapeutic but particularly for prognostic reasons. Depending on the cause the prognosis ranges from very poor to good chance of complete recovery.

Prediction of outcome in patients with acute respiratory distress syndrome by bronchoalveolar lavage inflammatory mediators

Acute respiratory distress syndrome (ARDS) is characterized by overwhelming lung inflammation. This study explored the inflammatory mediators in bronchoalveolar lavage fluid (BALF) for prognostic relevance in patients with infection-induced ARDS. Thirty-nine patients with infection-induced ARDS (28 pneumonia and 11 extrapulmonary sepsis) and two patients with cardiogenic lung edema as the control were included. The expression profiles of inflammatory mediators in BALF were compared between ARDS and cardiogenic lung edema. A group of inflammatory mediators that showed higher expression in ARDS was analyzed for their relationships with clinical features and outcome. We found that 17 patients who died had higher levels of interleukin (IL)-6 (P = 0.012), IL-8 (P = 0.001) and monocyte chemoattractant protein-1 (P = 0.036) in BALF compared with those who survived. Furthermore, there was an inverse relationship between the BALF levels of IL-6 (P = 0.026), IL-8 (P = 0.008) and macrophage inflammatory protein (MIP)-1 alpha (P = 0.048) and the changes of lung compliance between days 1 and 4, whereas the BALF levels of IL-8 (P = 0.033) and MIP-1 alpha (P = 0.029) were positively correlated with the changes of sequential organ failure assessment scores between days 1 and 4. In multivariate logistic regression analysis, only IL-8 (P = 0.013) and lung injury score (LIS) (P = 0.017) independently predicted the mortality, and IL-8 (P = 0.002) was most likely predictive of mortality in analysis of area under the receiver operating characteristic curve. In conclusion, we show the expression profiles of inflammatory mediators in BALF of infection-induced ARDS. Among the mediators, IL-8 is the most significant predictor for mortality, and several mediators are correlated with clinical severity. However, potential selection bias due to limited control subjects and lack of serum inflammatory mediator data suggest a necessity of further studies to confirm our findings.

Applanation tonometry application in ICU patients with acute cardiogenic edema

The incidence of acute cardiogenic pulmonary edema (ACPE) is increasing and it is now one of the leading causes of morbidity and mortality in our society. As the global population of European countries is getting older, the impact of arterial stiffness is becoming more and more important in the pathophysiology of ACPE, besides coronary vascular disease and valvular disease. The aim of the study was to evaluate whether acute modifications in elastic artery distensibility can be involved in the pathogenesis of ACPE.

Imagerie des pneumopathies infiltrantes diffuses

Subacute and chronic diffuse interstitial lung diseases Computed tomography (CT) plays an important role in all stages of management: positive diagnosis, etiological diagnosis, evaluation of lesions, ongoing monitoring, screening for complications, and prognosis. The etiological diagnosis is based on the imaging and analysis of patterns or groups of basic lesions often characteristics of a disease. Assessment of the images, the patient history, and the epidemiologic, clinical, laboratory, functional and cytologic data generally make it possible to reach a diagnosis. A pulmonary biopsy is rarely necessary. Acute diffuse interstitial lung diseases In the absence of an obvious clinical direction, CT, electrocardiography, and echocardiography are the first-line examinations to identify or rule out cardiogenic edema. CT can be used to guide bronchoalveolar lavage (BAL), widely used when the patient's respiratory condition permits. BAL can provide a diagnosis of diverse infections or help determine the cytologic type of alveolitis. CT also makes it possible to evaluate the lesions and plays a role in assessing severity. It makes it possible to choose the best sampling method and in principle directs sampling towards the most useful areas. It allows monitoring of disease course, screening of some complications, and precise localizing of tubes, drains, and catheters. Finally, it is used to assess the sequelae.

Continuous positive airway pressure increases haemoglobin O2 saturation after acute but not prolonged altitude exposure

It is unknown whether subclinical high-altitude pulmonary oedema reduces spontaneously after prolonged altitude exposure. Continuous positive airway pressure (CPAP) removes extravascular lung fluids and improves haemoglobin oxygen saturation in acute cardiogenic oedema. We evaluated the presence of pulmonary extravascular fluid increase by assessing CPAP effects on haemoglobin oxygen saturation under acute and prolonged altitude exposure. We applied 7 cm H(2)O CPAP for 30 min to healthy individuals after acute (Capanna Margherita, CM, 4559 m, 2 days permanence, and <36 h hike) and prolonged altitude exposure (Mount Everest South Base Camp, MEBC, 5350 m, 10 days permanence, and 9 days hike). At CM, CPAP reduced heart rate and systolic pulmonary artery pressure while haemoglobin oxygen saturation increased from 80% (median), 78-81 (first to third quartiles), to 91%, 84-97 (P < 0.001). After 10 days at MEBC, haemoglobin oxygen saturation spontaneously increased from 77% (74-82) to 86% (82-89) (P < 0.001) while heart rate (from 79, 64-92, to 70, 54-81; P < 0.001) and respiratory rate (from 15, 13-17, to 13, 13-15; P < 0.001) decreased. Under such conditions, these parameters were not influenced by CPAP. After ascent excessive lung fluids accumulate affecting haemoglobin oxygen saturation and, in these circumstances, CPAP is effective. Acclimatization implies spontaneous haemoglobin oxygen saturation increase and, after prolonged altitude exposure, CPAP is not associated with HbO(2)-sat increase suggesting a reduction in alveolar fluids.

The role of continuous positive airway pressure in acute cardiogenic edema with preserved left ventricular systolic function

Objective The objective of the study was to compare the effect of continuous positive airway pressure (CPAP) in patients with acute cardiogenic pulmonary edema (ACPE) with preserved or impaired left ventricular systolic function with regard to resolution time. Methods In a prospective, preliminary observational cohort study, 18 patients with preserved left ventricular systolic function (group A) and 18 patients with systolic heart dysfunction (group B) with ACPE underwent CPAP (10 cmH 20) through a face mask with standard medical therapy after a morphologic echocardiographic investigation shortly before CPAP. Results Resolution time did not differ significantly between the 2 groups of patients (64 ± 25 minutes in diastolic group vs 80 ± 33 minutes in systolic group). One patient in preserved left ventricular systolic function group required endotracheal intubation (not statistically significant). No patient died during hospital stay. Arterial blood gases improved after a trial of CPAP in both groups of patients. Conclusions The results of this preliminary study show that resolution time is not significantly different in patients with ACPE with preserved or impaired systolic function submitted to CPAP.

Cardiogenic Unilateral Pulmonary Edema: An Unreported Complication of a Digestive Endoscopic Procedure

Unilateral pulmonary edema is an uncommon clinical situation that may be difficult to distinguish from other conditions that cause lung infiltrates. Most cases occur in the right lung, and there are no reports about cardiogenic unilateral pulmonary edema as a complication of an endoscopic procedure of gastrointestinal tract. The authors describe a case of a 79-year-old woman with acute cardiac heart failure that developed soon after a diagnostic upper and lower digestive endoscopy. Continuous positive airway pressure, intravenous nitroglycerin, and furosemide treatment resulted in rapid improvement of symptoms and the progressive resolution of left-sided infiltrates on chest radiography. This case is of particular importance because of the rarity of cardiogenic unilateral edema in the left lung. This clinical finding was associated with the prolonged rest on the left side during the gastrointestinal endoscopic procedure.

Keratinocyte growth factor expression is suppressed in early acute lung injury/acute respiratory distress syndrome by smad and c-Abl pathways*

Keratinocyte growth factor (KGF) is expressed primarily by fibroblasts, is important for alveolar epithelial proliferation/function, and protects against lung injury in multiple animal models. We wished to determine whether acute lung injury/acute respiratory distress syndrome (ALI/ARDS) alveolar fluid induces KGF and fibroblast genes important for alveolar repair. A single-center cohort study enrolling patients between 2004 and 2006. A medical intensive care unit of a tertiary care medical center. Adult patients meeting the American-European Consensus Conference definition of ALI/ARDS. Patients with ALI/ARDS were enrolled, and lavage fluid was collected within 48 hours of intubation. Lavage fluid was also collected from two control cohorts. The patients with ALI/ARDS were followed for 28 days or until death. Fifteen patients with ALI/ARDS, five patients with cardiogenic edema, and five normal lung parenchyma controls were enrolled from 2004 to 2006. Primary normal human lung fibroblasts were incubated with bronchoalveolar lavage fluid and assessed for KGF, connective tissue growth factor, alpha-smooth muscle actin, and collagen 1 expression by real-time reverse transcriptase-polymerase chain reaction. Fibroblasts incubated with ALI/ARDS lavage fluid expressed 50% less KGF messenger RNA than those incubated with lavage fluid from CE patients (p < 0.01) and 33% than normal parenchymal controls (p < 0.03). Lavage fluid from patients with ALI/ARDS induced more connective tissue growth factor (p < 0.05), collagen 1 (p < 0.03), and alpha-smooth muscle actin (p < 0.04) than from CE patients. Preincubation of normal human lung fibroblasts with the transforming growth factor (TGF)-beta1 receptor/smad phosphorylation inhibitor SB431542 increased ALI/ARDS-induced KGF expression by 40% (p < 0.04). In cultured human lung fibroblasts, TGF-beta1 suppressed KGF messenger RNA and protein expression, which were reversed by SB431542 and by the c-Abl inhibitor, imatinib mesylate, but not by the p38 map kinase inhibitor, SB203580. ALI/ARDS alveolar fluid suppresses KGF expression, in part, due to TGF-beta1. TGF-beta1 suppression of KGF requires both smad phosphorylation and c-Abl activation.

Noninvasive positive-pressure ventilation for extubation failure after cardiac surgery: Pilot safety evaluation

Extubation failure is a serious complication after cardiac surgery. The role of noninvasive positive-pressure ventilation for acute respiratory failure in patients undergoing cardiac surgery is unknown. This study aimed to assess the safety of implementing noninvasive positive-pressure ventilation in this setting and its impact on lung function and operative outcomes. In a 6-month pilot prospective survey, the study population comprised 43 patients (32 were male with a mean age of 65.73 +/- 9 years; 3 heart transplantations, 18 coronary artery bypass grafts, 5 aortic dissections, and 17 valvular procedures; 34 active smokers, 25 with medically treated chronic obstructive pulmonary disease, 21 emergency/urgency procedures) who required noninvasive positive-pressure ventilation for acute respiratory failure after initial weaning from a respirator. The cause of acute respiratory failure (classified as post-cardiopulmonary bypass lung injury in 48.8% [21 patients], cardiogenic edema in 30.2% [13 patients], and pneumonia in 21% [9 patients]), length of noninvasive positive-pressure ventilation support, respiratory ratios (arterial oxygen tension/fraction of inspired oxygen assessed immediately before noninvasive positive-pressure ventilation, and every 6 hours after institution of pressure ventilation), and need for reintubation along with a set of predefined safety parameters were recorded. The mean length of noninvasive positive-pressure ventilation support was 33.8 +/- 24.04 hours. Plotting respiratory ratios with length of noninvasive positive-pressure ventilation supports a significant improvement was already evident within the first 6-hour frame (133.6 +/- 39.5 vs 205 +/- 65.7; P < .001) for all causes. Noninvasive positive-pressure ventilation prevented intubation in 74.4% of the patients, with satisfactory recovery for post-cardiopulmonary bypass lung injury and cardiogenic dysfunction (90.5% and 69.2%, respectively) and poor results (55% reintubated) in those treated for pneumonia. Noninvasive positive-pressure ventilation safety approached 97.7%. In appropriate candidates, noninvasive positive-pressure ventilation exerts favorable effects on lung function, preventing reintubation. The cost-effectiveness of its systematic use in this setting should be assessed.

Comparison of two non-bronchoscopic methods for evaluating inflammation in patients with acute hypoxaemic respiratory failure

IntroductionThe simple bedside method for sampling undiluted distal pulmonary edema fluid through a normal suction catheter (s-Cath) has been experimentally and clinically validated. However, there are no data comparing non-bronchoscopic bronchoalveolar lavage (mini-BAL) and s-Cath for assessing lung inflammation in acute hypoxaemic respiratory failure. We designed a prospective study in two groups of patients, those with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and those with acute cardiogenic lung edema (ACLE), designed to investigate the clinical feasibility of these techniques and to evaluate inflammation in both groups using undiluted sampling obtained by s-Cath. To test the interchangeability of the two methods in the same patient for studying the inflammation response, we further compared mini-BAL and s-Cath for agreement of protein concentration and percentage of polymorphonuclear cells (PMNs).MethodsMini-BAL and s-Cath sampling was assessed in 30 mechanically ventilated patients, 21 with ALI/ARDS and 9 with ACLE. To analyse agreement between the two sampling techniques, we considered only simultaneously collected mini-BAL and s-Cath paired samples. The protein concentration and polymorphonuclear cell (PMN) count comparisons were performed using undiluted sampling. Bland-Altman plots were used for assessing the mean bias and the limits of agreement between the two sampling techniques; comparison between groups was performed by using the non-parametric Mann-Whitney-U test; continuous variables were compared by using the Student t-test, Wilcoxon signed rank test, analysis of variance or Student-Newman-Keuls test; and categorical variables were compared by using chi-square analysis or Fisher exact test.ResultsUsing protein content and PMN percentage as parameters, we identified substantial variations between the two sampling techniques. When the protein concentration in the lung was high, the s-Cath was a more sensitive method; by contrast, as inflammation increased, both methods provided similar estimates of neutrophil percentages in the lung. The patients with ACLE showed an increased PMN count, suggesting that hydrostatic lung edema can be associated with a concomitant inflammatory process.ConclusionsThere are significant differences between the s-Cath and mini-BAL sampling techniques, indicating that these procedures cannot be used interchangeably for studying the lung inflammatory response in patients with acute hypoxaemic lung injury.