Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema

BACKGROUND: Brain natriuretic peptide (BNP) is useful in diagnosing congestive heart failure (CHF) in patients presenting in the emergency department with acute dyspnea. We prospectively tested the utility of BNP for discriminating ARDS vs cardiogenic pulmonary edema (CPE). METHODS: We enrolled ICU patients with acute hypoxemic respiratory failure and bilateral pulmonary infiltrates who were undergoing right-heart catheterization (RHC) to aid in diagnosis. Patients with acute coronary syndrome, end-stage renal disease, recent coronary artery bypass graft surgery, or preexisting left ventricular ejection fraction /= 1,200 pg/mL, BNP had a specificity of 92% for CPE. Higher levels of BNP were associated with a decreased odds for ARDS (odds ratio, 0.4 per log increase; p = 0.007) after adjustment for age, history of CHF, and right atrial pressure. BNP was associated with in-hospital mortality (p = 0.03) irrespective of the final diagnosis and independent of APACHE (acute physiology and chronic health evaluation) II score. CONCLUSION: In ICU patients with hypoxemic respiratory failure, BNP appears useful in excluding CPE and identifying patients with a high probability of ARDS, and was associated with mortality in patients with both ARDS and CPE. Larger studies are necessary to validate these findings.     

CXCR3 and CCR5 chemokines in induced sputum from patients with COPD

BACKGROUND: COPD is associated with increased numbers of CD4(+) and CD8(+) lymphocytes and macrophages in the small airways and lung parenchyma. The chemokines regulating T-cell recruitment into the lung are unknown but may involve CXCR3 and CCR5 chemoattractants. The aims of this study were to determine the concentrations of CXCR3 chemokines CXCL9, CXCL10, CXCL11, and the CCR5 chemokine CCL5 in induced sputum from patients with COPD, smokers, and nonsmokers, and to examine the relationship between chemokine expression, inflammatory cells, and airway obstruction. METHODS: Differential cell counts were performed and concentrations of CXCL9, CXCL10, CXCL11, and CCL5 were measured in induced sputum from nonsmokers (n = 18), smokers (n = 20), and COPD patients (n = 35) using an enzyme-linked immunosorbent assay. RESULTS: Concentrations of CXCL9, CXCL10, CXCL11, and CCL5 were significantly increased in the sputum of patients with COPD when compared with nonsmokers but not smokers without obstruction: CXCL9 (median, 14.3 pg/mL; interquartile range [IQR], 6.5 to 99.3; vs median, 1.4 pg/mL; IQR, 0 to 10.4 [p < 0.001]; vs 8.5 pg/mL; IQR, 0 to 16.0, respectively); CXCL10 (16.9 pg/mL; IQR, 6.2 to 148.8; vs 3.7 pg/mL; IQR, 0 to 18.8 [p < 0.05]; vs 11.3 pg/mL; IQR, 3.7 to 46.7); CXCL11 (58.1 pg/mL; IQR, 34.5 to 85.3; vs 33.5 pg/mL; IQR, 23.2 to 49.7 [p < 0.05]; vs 49.8 pg/mL; IQR, 32.6 to 105.6); and CCL5 (59.9 pg/mL; IQR, 57.1 to 67.8; vs 33.5 pg/mL; IQR, 31.6 to 36.9 [p < 0.001]). CCL5 in sputum from smokers was also significantly increased compared with that from nonsmokers (median, 63.0 pg/mL; IQR, 60.8 to70.2; p < 0.001). There was a negative correlation between FEV(1) percentage of predicted, FEV(1)/FVC ratio, and percentage of macrophages, and all the chemokines analyzed. Neutrophil numbers correlated positively with the concentrations of chemokines. CONCLUSIONS: CXCR3 chemokines and CCL5 are increased in sputum from COPD patients compared with nonsmokers, and may be important in COPD pathogenesis.     

Copeptin, C-reactive protein, and procalcitonin as prognostic biomarkers in acute exacerbation of COPD

BACKGROUND: A novel approach to estimate the severity of COPD exacerbation and predict its outcome is the use of biomarkers. We assessed circulating levels of copeptin, the precursor of vasopressin, C-reactive protein (CRP), and procalcitonin as potential prognostic parameters for in-hospital and long-term outcomes in patients with acute exacerbation of COPD (AECOPD) requiring hospitalization. METHODS: Data of 167 patients (mean age, 70 years; mean FEV(1), 39.9 +/- 16.9 of predicted [+/- SD]) presenting to the emergency department due to AECOPD were analyzed. Patients were evaluated based on clinical, laboratory, and lung function parameters on hospital admission, at 14 days, and at 6 months. RESULTS: Plasma levels of all three biomarkers were elevated during the acute exacerbation (p < 0.001), but levels at 14 days and 6 months were similar (p = not significant). CRP was significantly higher in patients presenting with Anthonisen type I exacerbation (p = 0.003). In contrast to CRP and procalcitonin, copeptin on hospital admission was associated with a prolonged hospital stay (p = 0.002) and long-term clinical failure (p < 0.0001). Only copeptin was predictive for long-term clinical failure independent of age, comorbidity, hypoxemia, and lung functional impairment in multivariate analysis (p = 0.005). The combination of copeptin and previous hospitalization for COPD increased the risk of poor outcome (p < 0.0001). Long-term clinical failure was observed in 11% of cases with copeptin < 40 pmol/L and no history of hospitalization, as compared to 73% of patients with copeptin >/= 40 pmol/L and a history of hospitalization (p < 0.0001). CONCLUSIONS: We suggest copeptin as a prognostic marker for short-term and long-term prognoses in patients with AECOPD requiring hospitalization.     

Systemic cytokines, clinical and physiological changes in patients hospitalized for exacerbation of COPD

BACKGROUND: Systemic inflammation in patients with COPD may worsen during exacerbations, but there is limited information relating levels of systemic inflammatory markers with symptoms and physiologic changes during an exacerbation METHODS: We measured dyspnea using the visual analog scale, pulmonary function tests, hemograms, and plasma levels for interleukin (IL)-6, IL-8, leukotriene B(4) (LTB4), tumor necrosis factor-alpha, and secretory leukocyte protease inhibitor (SLPI) in 20 patients on admission to a hospital for exacerbation of COPD (ECOPD), 48 h later (interim), and 8 weeks after hospital discharge (recovery). RESULTS: Dyspnea was present in all patients. Inspiratory capacity improved faster than FEV(1). Compared to recovery, there was a significant increase in the mean (+/- SD) hospital admission plasma levels of IL-6 (6.38 +/- 0.72 to 2.80 +/- 0.79 pg/mL; p = 0.0001), IL-8 (8.18 +/- 0.85 to 3.72 +/- 0.85 pg/mL; p = 0.002), and LTB4 (8,675 +/- 1,652 to 2,534 +/- 1,813 pg/mL; p = 0.003), and the percentages of segmented neutrophils (79 to 69%; p < 0.02) and band forms (7.3 to 1.0%; p < 0.01) in peripheral blood, with no changes in TNF-alpha and SLPI. There were significant correlations between changes in IL-6 (r = 0.61; p = 0.01) and IL-8 (r = 0.56; p = 0.04) with changes in dyspnea and levels of IL-6 (r = -0.51; p = 0.04) and TNF-alpha (r = -0.71; p < 0.02) with changes in FEV(1.) CONCLUSIONS: Hospitalized patients with ECOPDs experience significant changes in systemic cytokine levels that correlate with symptoms and lung function. An ECOPD represents not only a worsening of airflow obstruction but also increased systemic demand in a host with limited ventilatory reserve.     

Brain natriuretic peptide in patients with congestive heart failure and central sleep apnea

STUDY OBJECTIVE: To assess the possible relationship between Cheyne-Stokes respiration (CSR) associated with central sleep apnea (CSA) syndrome and brain natriuretic peptide (BNP) in an outpatient population presenting with stable congestive heart failure (CHF). MEASUREMENTS AND RESULTS: Ninety patients with CHF due to systolic dysfunction (left ventricular ejection fraction 相似文献   

Ventilator settings and outcome of respiratory failure in chronic interstitial lung disease

BACKGROUND: While patients with interstitial lung disease (ILD) may be particularly susceptible to ventilator-induced lung injury, ventilator strategies have not been studied in this group of patients. PURPOSES: To describe the clinical course and outcome of patients with ILD and acute respiratory failure in relation to ventilatory parameters. METHODS: We retrospectively identified a cohort of ventilated patients with ILD who had been admitted to five ICUs at a single institution. We analyzed demographic data, pulmonary function test results, severity of illness, and the parameters of continuous ventilation for the initial 24 h after admission to the ICU. Primary outcomes were survival to hospital discharge and 1-year survival. Main results: Of 94 patients with ILD, 44 (47%) survived to hospital discharge and 39 (41%) were alive at 1 year. Nonsurvivors were less likely to be postoperative, had higher severity of illness, and were ventilated at higher airway pressures and lower tidal volumes. Step changes in positive end-expiratory pressure (PEEP) of > 10 cm H(2)O were attempted in 20 patients and resulted in an increase in plateau pressure (median difference, + 16 cm H(2)O; interquartile range [IQR], 9 to 24 cm H(2)O) and a decrease in respiratory system compliance (median difference, - 0.28 mL/kg/cm H(2)O; IQR, - 0.43 to - 0.13 mL/kg/cm H(2)O). The Cox proportional hazards model revealed that high PEEP (hazard ratio, 4.72; 95% confidence interval [CI], 2.06 to 11.15), acute physiology and chronic health evaluation (APACHE) III score predicted mortality (hazard ratio 1.33; 95% CI, 1.18 to 1.50), age (hazard ratio, 1.03; 95% CI, 1 to 1.05), and low Pao(2)/fraction of inspired oxygen ratio (hazard ratio, 0.96; 95% CI, 0.92 to 0.99) to be independent determinants of survival. CONCLUSION: Both severity of illness and high PEEP settings are associated with the decreased survival of patients with ILD who are receiving mechanical ventilation.     

Safety of sputum induction during exacerbations of COPD

Sputum induction (SI) is considered to be a safe tool for assessing airway inflammation in stable patients with COPD, but little is known about its safety during exacerbations. We therefore assessed the safety of SI during COPD exacerbations. SI data from 44 COPD patients were assessed both in the stable phase and during exacerbation. The median FEV1 for the stable phase and exacerbation were 61% predicted (interquartile range [IQR], 49 to 74% predicted) and 51% predicted (IQR, 45 to 60% predicted), respectively. The median decrease in FEV(1) with SI during an exacerbation was 0.27 L (IQR, 0.17 to 0.40 L) vs 0.28 L (IQR, 0.22 to 0.44 L) during the stable phase (p = 0.03). The patients experienced the associated dyspnea well; no other adverse events occurred. All FEV1 values returned to within 90% of their initial value within 30 min. A larger decrease in FEV1 due to SI during an exacerbation was associated with the following parameters in the stable phase of disease: lower total sputum cell count (r = -0.37; p = 0.01); higher percentage of eosinophils (r = 0.33; p = 0.04); and a larger decrease in FEV1 after SI (r = 0.39; p = 0.03). In a multivariate analysis, the only independent association was with the larger decrease in FEV1 in the stable phase. We concluded that SI can be safely carried out in patients with mild-to-moderate COPD who experience an exacerbation, and this occurs with no greater risk than in stable patients with COPD.     

Contemporary management of acute exacerbations of COPD: a systematic review and metaanalysis

BACKGROUND: Systemic corticosteroids, antibiotics, and noninvasive positive pressure ventilation (NPPV) are recommended for patients with acute exacerbation of COPD. However, their clinical benefits in various settings are uncertain. We undertook a systematic review and metaanalysis to systematically evaluate the effectiveness of these therapies. METHODS: MEDLINE and EMBASE were searched to identify relevant randomized controlled clinical trials published from January 1968 to November 2006. We identified additional studies by searching bibliographies of retrieved articles. RESULTS: Compared with placebo, systemic corticosteroids reduced treatment failure by 46% (95% confidence interval [CI], 0.41 to 0.71), length of hospital stay by 1.4 days (95% CI, 0.7 to 2.2), and improved FEV(1) by 0.13 L after 3 days of therapy (95% CI, 0.04 to 0.21). Meanwhile, the risk of hyperglycemia significantly increased (relative risk, 5.88; 95% CI, 2.40 to 14.41). Compared with placebo, antibiotics reduced treatment failure by 46% (95% CI, 0.32 to 0.92) and in-hospital mortality by 78% (95% CI, 0.08 to 0.62). Compared with standard therapy, NPPV reduced the risk of intubation by 65% (95% CI, 0.26 to 0.47), in-hospital mortality by 55% (95% CI, 0.30 to 0.66), and the length of hospitalization by 1.9 days (95% CI, 0.0 to 3.9). CONCLUSIONS: For acute COPD exacerbations, systemic corticosteroids are effective in reducing treatment failures, while antibiotics reduce mortality and treatment failures in those requiring hospitalization and NPPV reduces the risk of intubation and in-hospital mortality, especially in those who demonstrate respiratory acidosis.     

Platelet count decline: an early prognostic marker in critically ill patients with prolonged ICU stays

BACKGROUND: Thrombocytopenia is common in ICU patients. The objective of this study was to evaluate possible links between declining platelet counts early in the ICU stay and survival. METHODS: All patients who were admitted to the ICU for at least 5 days and had no thrombocytopenia at the time of admission were included in the study. A multivariable logistic regression model, with hospital mortality as the outcome variable, was built. RESULTS: We included 1,077 patients in the study. At ICU admission, the median platelet count was not significantly different in survivors (256 x 10(9) cells/L; interquartile range [IQR], 206 to 330 x 10(9) cells/L) and nonsurvivors (262 x 10(9) cells/L; 211 to 351 x 10(9) cells/L). Median simplified acute physiology scores II (SAPS II) at ICU admission was worse in nonsurvivors than in survivors (50 [IQR, 37 to 63] vs 37 [IQR, 27 to 48], respectively; p < 0.0001), as was the mean (+/- SD) sequential organ failure assessment (SOFA) score on day 3 (6.3 +/- 3.24 vs 4 +/- 2.8, respectively; p < 0.0001). Absolute platelet counts were lowest on day 4, but differed significantly between survivors and nonsurvivors only on day 7. Conversely, any percentage decline in platelet counts from 10 to 60% on day 4 was significantly associated with mortality. By multivariable analysis, a 30% decline in platelet count independently predicted death (odds ratio, 1.54; 95% confidence interval, 1.12 to 2.14; p = 0.008), in addition to increasing or stable SOFA scores from ICU admission to day 4, older age, male gender, ICU admission for coma, worse SAPS II score at ICU admission, transfer from another ward, and comorbidity. CONCLUSION: In patients who spend > 5 days in the ICU and have normal platelet counts at ICU admission, a decline in platelet counts provides prognostic information. This parameter deserves to be included in new scoring systems.     

The association between body mass index and clinical outcomes in acute lung injury

BACKGROUND: The association between body mass index (BMI) and outcomes in critically ill patients is unclear. Our objective was to determine the association between BMI and outcomes in a population-based cohort of patients with acute lung injury (ALI). METHODS: In a prospective cohort study of all ICU patients in King County, Washington, with ALI in 1 year (1999 to 2000), 825 patients had a BMI recorded. Using multivariate analysis, patients in the abnormal BMI groups were compared to normal patients in the following areas: mortality, hospital length of stay (LOS), ICU LOS, duration of mechanical ventilation, and discharge disposition. RESULTS: There was no mortality difference in any of the abnormal BMI groups compared to normal-weight patients. Severely obese patients had longer hospital LOS than normal-weight patients (mean increase, 10.5 days; 95% confidence interval [CI], 4.8 to 16.2 days; p < 0.001); this was accentuated when analysis was restricted to survivors (mean increase, 14.3 days; 95% CI, 7.1 to 21.6 days; p < 0.001). ICU LOS and duration of mechanical ventilation were also longer in the severely obese group when analysis was restricted to survivors (mean increase, 5.6 days; 95% CI, 1.3 to 9.8 days; p = 0.01; and mean increase, 4.1 days; 95% CI, 0.4 to 7.7 days, respectively; p = 0.03). Severely obese patients were more likely to be discharged to a rehabilitation or skilled nursing facility than to home. CONCLUSIONS: BMI is not associated with mortality in patients with ALI, but severe obesity is associated with increased morbidity and resource utilization in the hospital and after discharge.     

Prognostic value of circulating levels of endothelin-1 in patients after acute myocardial infarction undergoing primary coronary angioplasty

BACKGROUND: The link between increased circulating level of endothelin (ET)-1 and adverse clinical outcomes after acute myocardial infarction (AMI) has been established. Current studies demonstrate that reperfusion therapy by either thrombolysis or primary percutaneous coronary intervention (PCI) can salvage myocardium, improving survival of AMI patients. However, whether reperfusion therapy by primary PCI can prevent the adverse effect of ET-1 on clinical outcomes in patients after AMI remains unclear. Therefore, this study examined the predictive value of circulating ET-1 levels on 30-day outcomes in ST-segment elevated AMI treated with primary PCI. METHODS AND RESULTS: We conducted a prospective cohort study of 186 consecutive patients with ST-segment elevated AMI of onset < 12 h who underwent primary PCI. Blood samples for plasma concentration of ET-1 were collected in the catheterization laboratory following vascular puncture. Patients were classified into a high group (group 1, ET-1 level >or= 0.632 pg/mL, n = 93) and a low group (group 2, ET-1 level < 0.632 pg/mL, n = 93) according to the median value of ET-1 after AMI. Univariate analysis demonstrated that the 30-day composite major adverse clinical outcomes (MACO) [advanced Killip score >or= 3], severe congestive heart failure (CHF) [New York Heart Association functional class 4], and 30-day mortality were strongly associated with high ET-1 level (>or= 0.632 pg/mL; p < 0.0001), unsuccessful reperfusion (final Thrombolysis in Myocardial Infarction flow 相似文献   

N-terminal pro-brain natriuretic peptide and renal insufficiency as predictors of mortality in pulmonary hypertension

BACKGROUND: N-terminal pro-brain natriuretic peptide (NT-proBNP) is a byproduct of the brain natriuretic peptide (BNP) that was shown to be of prognostic value in pulmonary hypertension (PH). The role of NT-proBNP in PH has to be determined, especially under the influence of renal impairment that might lead to an accumulation of the peptide, and may be a sign of increased mortality per se. METHODS: We assessed NT-proBNP, BNP, renal function, and hemodynamic parameters (during right-heart catheterization) in 118 consecutive patients with isolated PH, excluding left-heart disease. Depending on the calculated creatinine clearance, patients were classified into different groups of renal function. Correlation analysis was performed on all key parameters. Results were then compared between the levels of renal function. The prognostic value of each parameter was assessed during a mean follow-up period of 10 months. RESULTS: Twenty-two patients (approximately 19%) had significantly impaired renal function (creatinine clearance < 60 mL/min). Although the overall levels of NT-proBNP were correlated with hemodynamics, we observed no correlation in the group with significant renal dysfunction. Moreover, NT-proBNP was related to creatinine clearance. Finally, NT-proBNP and renal insufficiency were independent predictors of death during univariate and multivariate analysis, whereas BNP only predicted mortality in univariate analysis. CONCLUSIONS: The diagnostic accuracy of NT-proBNP as a parameter of the hemodynamic status is diminished by renal function. However, NT-proBNP could be superior to BNP as a survival parameter in PH because it integrates hemodynamic impairment and renal insufficiency, which serves as a sign of increased mortality per se.     

A comparative study of community-acquired pneumonia patients admitted to the ward and the ICU

BACKGROUND: Limited information is available on the health-care utilization of hospitalized patients with community-acquired pneumonia (CAP) depending on the location of care. Our aim was to compare the clinical characteristics, etiologies, and outcomes of patients with CAP who were admitted to the ICU with those admitted who were to the ward service. METHODS: A retrospective cohort study, at two tertiary teaching hospitals, one of which was a Veterans Affairs hospital, and the other a county hospital. Eligible subjects had been admitted to the hospital with a diagnosis of CAP between January 1, 1999, and December 31, 2001, had a confirmatory chest radiograph, and a hospital discharge International Classification of Diseases, ninth revision, diagnosis of pneumonia. Subjects were excluded from the study if they had designated "comfort measures only" or had been transferred from another acute care hospital or were nursing home patients. Bivariate and multivariable analysis evaluated 30-day and 90-day mortality as the dependent measures. RESULTS: Data were abstracted on 730 patients (ICU, 145 patients; wards, 585 patients). Compared to ward patients, ICU patients were more likely to be male (p = 0.001), and to have congestive heart failure (p = 0.01) and COPD (p = 0.01). ICU patients also had higher mean pneumonia severity index scores (112 [SD, 35] vs 83 [SD, 30], respectively; p = 0.02). Patients admitted to the ICU had a longer mean length of hospital stay (12 days [SD, 10 days] vs 7 days [SD, 17 days], respectively; p = 0.07), and a higher 30-day mortality rate (23% vs 4%, respectively; p < 0.001) and 90-day mortality rate (28% vs 8%, respectively; p < 0.001) compared to ward patients. CONCLUSIONS: ICU patients present with more severe disease and more comorbidities. ICU patients stay longer in the hospital and have a much higher mortality rate when compared to ward patients. Management strategies should be designed to improve clinical outcomes in ICU patients.     

Normal bronchial blood flow in COPD is unaffected by inhaled corticosteroids and correlates with exhaled nitric oxide

BACKGROUND: In COPD patients, there is reduced vascularity and inflammation of the bronchi, which may have opposite effects on bronchial blood flow (QAW). We studied the relationship of QAW with the fraction of exhaled nitric oxide (FENO), which is a potent vasodilator. We also investigated the vascular response to budesonide and a beta(2)-agonist. METHODS: We measured QAW in 17 patients with COPD (mean [+/- SEM] age, 67 +/- 3 years; 10 male patients; mean FEV(1), 57 +/- 3% predicted; mean FEV(1)/FVC ratio, 54 +/- 4%), all of whom were ex-smokers, and in 16 age-matched nonsmoking volunteers (mean age, 64 +/- 4 years) and compared this to FENO. QAW was measured using the acetylene dilution method. RESULTS: Mean QAW was similar in patients with COPD (34.29 +/- 1.09 microL/mL/min) compared to healthy subjects (35.50 +/- 1.74 microL/mL/min; p > 0.05) and was not affected by long-term treatment (35.89 +/- 1.63 microL/mL/min) or short-term treatment (32.50 +/- 1.24 microL/mL/min; p < 0.05) with inhaled budesonide. QAW positively correlated with the diffusion of carbon monoxide (ie, carbon monoxide transfer coefficient: r = 0.74; p < 0.05). FENO levels were mildly elevated in steroid-treated patients (10.89 +/- 0.87 parts per billion [ppb]) and untreated patients (9.40 +/- 0.86 ppb) compared to the control group (8.22 +/- 0.57 ppb; p < 0.05) and were correlated with QAW (r = 0.6; p < 0.05). Ten minutes after the inhalation of 200 microg of albuterol, QAW was more elevated in healthy control subjects (59.33 +/- 2.40 microL/mL/min) compared to COPD patients (38.00 +/- 0.58 microL/mL/min; p < 0.05), indicating that COPD patients may have a reduced bronchial vascular reactivity. CONCLUSIONS: QAW is normal in COPD patients and is not affected by therapy with inhaled corticosteroids or beta(2)-agonists. In addition, QAW correlates with levels of FENO, which may have a regulatory role.     

Survival of chronic hypercapnic COPD patients is predicted by smoking habits, comorbidity, and hypoxemia

STUDY OBJECTIVES: Chronic hypercapnia in patients with COPD has been associated with a poor prognosis. We hypothesized that, within this group of chronic hypercapnic COPD patients, factors that could mediate this hypercapnia, such as decreased maximum inspiratory mouth pressure (P(I(max))), decreased maximum expiratory mouth pressure (P(E(max))), and low hypercapnic ventilatory response (HCVR), could be related to survival. Other parameters, such as arterial blood gas values, airway obstruction (FEV1), body mass index (BMI), current smoking status, and the presence of comorbidity were studied as well. METHODS: A cohort of 47 chronic hypercapnic COPD patients recruited for short-term trials (1 to 3 weeks) in our institute was followed up for 3.8 years on average. Survival was analyzed using a Cox proportional hazards model. The risk factors considered were analyzed, optimally adjusted for age and gender. RESULTS: At the time of analysis 18 patients (10 male) were deceased. After adjusting for age and gender, P(I(max)), P(E(max)), and HCVR were not correlated with survival within this hypercapnic group. Current smoking (hazard ratio [HR], 7.0; 95% confidence interval [CI], 1.4 to 35.3) and the presence of comorbidity (HR, 5.5; 95% CI, 1.7 to 18.7) were associated with increased mortality. A higher Pa(O2) affected survival positively (HR, 0.6 per 5 mm Hg; 95% CI, 0.4 to 1.0). Pa(CO2) tended to be lower in survivors, but this did not reach statistical significance (HR, 2.0 per 5 mm Hg; 95% CI, 0.9 to 4.3). FEV1 and BMI were not significantly related with survival in hypercapnic COPD patients. CONCLUSION: In patients with chronic hypercapnia, only smoking status, the presence of comorbidity, and Pa(O2) level are significantly associated with survival. Airway obstruction, age, and BMI are known to be predictors of survival in COPD patients in general. However, these parameters do not seem to significantly affect survival once chronic hypercapnia has developed.     

The effect of body mass index on patient outcomes in a medical ICU

STUDY OBJECTIVES: To examine the effect of patient body mass index (BMI) on outcome in intensive care. DESIGN: In a prospective study, the patients were classified into groups based on the calculated BMI, as follows: BMI < 19.0 (n = 350), > or = 19.0 and < 25.0 (n = 663), > or = 25.0 and < 29.9 (n = 585), > or = 30.0 and < 40.0 (n = 396), and > or = 40.0 (n = 154). Groups were compared by age, APACHE (acute physiology and chronic health evaluation) II score, mortality, ICU length of stay (LOS), hospital LOS, number receiving ventilation, and ventilator-days. Adverse events including nosocomial pneumonia, ventilator-days per patient, failed extubations, and line-related complications were recorded. SETTING: The study was conducted in a 9-bed medical ICU of a 650-bed tertiary care hospital. MEASUREMENTS: Height and weight were prospectively recorded for the first ICU admission during a hospital stay. RESULTS: Between January 1, 1997, and August 1, 2001, 2,148 of 2,806 patients admitted to the ICU had height and weight recorded. There were no differences in APACHE II score, mortality, ICU LOS, hospital LOS, number receiving ventilation, ventilator-days, average total cost, or average variable cost among the five groups. However, the severely obese patients were more frequently female and younger than those who were overweight and obese (p < 0.001). Adverse events were infrequent, but there were no differences between the obese/very obese compared with others. CONCLUSION: BMI has minimal effects on ICU outcome after patients are admitted to a critical care unit.     

Granulocyte chemotactic activity in exhaled breath condensate of healthy subjects and patients with COPD

BACKGROUND: Several chemoattractants have been measured in exhaled breath condensate (EBC) from patients with COPD. The aim of this study was to compare the eosinophil and neutrophil chemotactic activity contained in EBC from healthy subjects and patients with COPD. METHODS: EBC collected using a commercially available condenser (EcoScreen; Erich Jaeger Viasys; Hoechberg, Germany) was compared in 45 COPD patients and 65 healthy subjects. EBC chemotactic activity for eosinophils and neutrophils was assessed using microchambers (Boyden; Neuro Probe; Cabin John, MD). Chemotactic index (CI) was used to evaluate cell migration. RESULTS: EBC from patients with COPD (CI, 2.21 +/- 0.16 [mean +/- SEM]) and healthy subjects (CI, 1.67 +/- 0.11) displayed significant neutrophil chemotactic activity (p < 0.0001 for both), which was however higher in patients with COPD (p < 0.001). Healthy smokers had a significantly raised CI for neutrophils by comparison with healthy nonsmokers (p < 0.01) and ex-smokers (p < 0.05). Likewise, current COPD smokers tended to have greater neutrophil CI than COPD who stopped smoking (p = 0.08). COPD ex-smokers had raised chemotactic activity by comparison with healthy ex-smokers (p < 0.05). Anti-interleukin-8 (10(-6) g/mL) antibodies reduced neutrophil chemotactic activity by 35.2% (p < 0.05). EBC also contained significant eosinophil chemotactic activity in healthy subjects (CI, 1.68 +/- 0.09; p < 0.0001) and patients with COPD (CI, 1.23 +/- 0.07; p < 0.01), with a significantly lower CI in patients with COPD as compared to healthy subjects (p < 0.001). Smoking did not influence eosinophil chemotactic activity in healthy subjects or patients with COPD. CONCLUSIONS: Current smoking favors neutrophil chemotactic activity. As compared to healthy subjects, EBC from patients with COPD displays a skewed chemotactic activity toward neutrophils vs eosinophils.     

The acute effects of oxygen and carbon dioxide on renal vascular resistance in patients with an acute exacerbation of COPD.

OBJECTIVE: Changes in renal hemodynamics occur in patients with severe COPD, especially during an acute exacerbation. Renal hemodynamics are affected by changes in oxygen and carbon dioxide levels, but these changes have not been well defined, particularly in the acute clinical situation. We wished to determine whether oxygen or carbon dioxide levels have the predominant effect on renal hemodynamics in patients with an acute exacerbation of COPD. DESIGN: Fourteen patients with an acute exacerbation of COPD and a PaO2 < 64 mm Hg were studied. Initially, the patients breathed room air (hypoxemia). Then their arterial oxygen saturation was raised to approximately 95% (normoxemia) and then to 98 to 99% (hyperoxemia). Finally, 1 L/min of carbon dioxide was added to the circuit (hyperoxemic hypercapnia). Using duplex ultrasonography, the pulsatility index (PI) of an intrarenal artery was measured after 10 min at each level of oxygenation. The PI is an index of distal renovascular resistance. RESULTS: The PI fell significantly from room-air values on inducing hyperoxemia (p < 0.05). This suggests decreased renovascular resistance and increased renal blood flow. When hyperoxemic hypercapnia was induced, the PI rose significantly from the hyperoxemia level (p < 0.001). CONCLUSIONS: In hypoxemic patients, renovascular resistance decreased when hyperoxemia was induced. This fall in renovascular resistance was reversed with the addition of carbon dioxide. This suggests that acute changes in carbon dioxide levels might have a more dominant role than oxygen levels in determining renovascular resistance.