Pneumomediastinum in a 63-year-old woman with asthma exacerbation.
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Abdominal Abscess↗
Biomedical subjects
B R Celli
Publications and source records attributed to B R Celli.
Long-term controlled trial of nocturnal nasal positive pressure ventilation in patients with severe COPD.
STUDY OBJECTIVES: To determine the 1-year efficacy of noninvasive positive pressure ventilation (NPPV) added to long-term oxygen therapy (LTOT) in patients with stable severe COPD. PATIENT SELECTION AND METHODS: We prospectively randomized 52 patients with severe COPD (FEV(1) < 45%) to either NPPV plus "standard care" (96% patients with LTOT) or to standard care alone (93% patients with LTOT). The outcomes measured included the following: rate of acute COPD exacerbations; hospital admissions; intubations; and mortality at 3 months, 6 months, and 12 months. The patients were also evaluated at 3 months and 6 months for dyspnea using the Medical Research Council and Borg scales, gas exchange, hematocrit, pulmonary function, cardiac function with echocardiogram, and neuropsychological performance. RESULTS: One-year survival was similar in both groups (78%). The number of acute exacerbations was similar at all time points in patients receiving NPPV, compared with control subjects. The number of hospital admissions was decreased at 3 months in the NPPV group (5% vs 15% of patients, p < 0.05), but this difference was not seen at 6 months (18% vs 19%, respectively). The only beneficial differences were observed in the Borg dyspnea rating, which dropped from 6 to 5 (p < 0.039), and in one of the neuropsychological tests (psychomotor coordination) for the NPPV group at 6 months. CONCLUSIONS: Our study indicates that over 1 year, NPPV does not affect the natural course of the disease and is of marginal benefit in outpatients with severe COPD who are in stable condition.
Acute Disease↗
Weaning from mechanical ventilation.
In this review, traditional weaning parameters, integrative indexes, and experimental methods of predicting weaning outcomes have been reviewed. All have limitations; however, judicious application of these parameters may guide clinical decisions regarding timing of weaning trials. Of the parameters reviewed, the RSBI has several advantages and may identify patients who are candidates for weaning. Likewise, application of tools such as the daily screen or implementation of multidisciplinary weaning teams may assist clinicians in weaning patients earlier in their ICU course. Most patients will be successfully extubated after a single SBT, and weaning methods that focus on sequential decrements in ventilator support appear to needlessly prolong ventilation. However, for patients who fail, identification of potential causes of continued ventilator dependence should focus on the various pathophysiological causes outlined. Although a number of patients will require prolonged ventilator support beyond the critical care setting, the growing experience with this population demonstrates that a large percentage have favorable outcomes.
Humans↗
Ventilatory drive at rest and perception of exertional dyspnea in severe COPD.
BACKGROUND: The reasons for exertional dyspnea in severe COPD are not well established, but they are not solely related to the mechanical load. We tested the hypothesis that breathlessness may be determined, in part, by the response of an individual's central output. METHODS: In 26 patients with severe COPD (FEV1 < 50% predicted) and 22 matched control subjects, we assessed at rest the ventilatory and mouth occlusion pressure (P0.1) response to hyperoxic progressive hypercapnia. At rest and during a symptom-limited exercise test, routine cardiopulmonary variables were measured, and respiratory muscle function was evaluated using esophageal and gastric pressure. Dyspnea was assessed with a visual analog scale. RESULTS: Dyspnea with or without leg discomfort limited exercise in 73% of patients. Peak exercise dyspnea correlated only with dyspnea at rest (r = 0.5, p < 0.008) and P0.1 response to CO2 (deltaP0.1/delta[end-tidal PCO2]PETCO2) (r = 0.48, p = 0.02). Multiple regression analysis including resting and exercise data as independent variables revealed that 47% of the variance for dyspnea at peak exercise was explained by a model including dyspnea at rest and deltaP0.1/deltaPETCO2. Again, deltaP0.1/deltaPETCO2 was the only predictor for the change in dyspnea from rest to peak exercise (delta Dyspnea, r2 = 0.28, p = 0.005). There was no correlation between exercise dyspnea and any metabolic variable, pulmonary function, or respiratory muscle function test. CONCLUSION: In severe COPD, exertional dyspnea is not simply related to respiratory muscle load or mechanical impairment, but also to an individual's central motoneural output to the respiratory system.
Adult↗
Use of transfer impedance measurements for clinical assessment of lung mechanics.
Respiratory transfer impedance (Ztr) measured using the forced oscillation technique requires virtually no patient cooperation and provides a noninvasive approach for acquiring data reflective of lung mechanics. Also, model analysis of Ztr provides reliable estimates of separate airway and tissue properties (1), but only if data out to 64 Hz are acquired. The current study evaluated the clinical utility of Ztr from 1-80 Hz for assessing the degree and type of impaired lung function. Spirometry and Ztr measurements were made on 37 individuals: 11 healthy subjects and 26 patients with lung disease including chronic obstructive pulmonary disease (COPD), asthma, lung cancer, and sarcoidosis. Over the entire patient group, 12 were also smokers. We first established normal ranges for several Ztr features and model estimated mechanical properties. The COPD and smokers groups showed significant differences in portions of their Ztr spectra from that of the healthy group. Key Ztr spectral features included R0, the frequency at which the real part of impedance is zero; and Re4, the real part of impedance at 4 Hz. The key model parameter was airway resistance, Raw. We found Raw, Re4, and R0 to be significantly elevated during disease (p < 0.0005) and to significantly decrease with bronchodilator therapy (p < 0.025). Moreover, we found moderate to strong correlations between R0, Raw, and Re4 versus FVC and R0 versus FEV1. After bronchodilator, changes in R0, Re4, and Raw were correlated with changes in several spirometric indices. The R0 feature has not been previously evaluated since it is typically above 32 Hz (well above 32 Hz in diseased individuals) and not encompassed in previous clinical studies.
Adolescent↗
Mouth occlusion pressure, CO2 response and hypercapnia in severe chronic obstructive pulmonary disease.
The resting mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) and minute ventilation (V'E) and their response to CO2 in patients with chronic obstructive pulmonary disease (COPD) remain controversial. The ventilatory drive and the factors that predict resting arterial CO2 tension (Pa,CO2) were studied in 19 eucapnic and 14 hypercapnic severe COPD patients, and 20 controls. The CO2 response was evaluated by the Read technique. The V'E, and P0.1 as a function of end-tidal CO2 tension (Pet,CO2) was used to study the ventilatory (deltaV'E/deltaPet,CO2) and P0.1 response (deltaP0.1/deltaPet,CO2). In the patients, respiratory muscle function and pleural occlusion pressure 0.1 s after onset of inspiration (Ppl,0.1) were evaluated with simultaneous measurement of pleural (Ppl) and gastric (Pga) pressures. Hypercapnic patients had lower forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and arterial O2 tension (Pa,O2). Resting P0.1 was higher in patients than in controls, whereas deltaP0.1/deltaPet,CO2 was similar in the three groups. There was no difference in resting P0.1 (3.6+/-2.0 versus 4.3+/-2.8 kPa (2.7+/-1.5 versus 3.2+/-2.1 cmH2O), p=0.2) and Ppl,0.1 (1.4+/-2.3 versus 5.2+/-3.3 kPa (4.08+/-1.7 versus 3.9+/-2.5 cmH2O), p=0.22) between eucapnic and hypercapnic COPD, whereas deltaV'E/deltaPet,CO2 was lower in the hypercapnic group (0.29+/-0.24 versus 0.66+/-0.5 L x min(-1) x kPa, p<0.001). By logistic regression only FEVI and increased diaphragmatic load, and not respiratory drive, predicted resting Pa,CO2. Irrespective of CO2 level, baseline central drive (represented by the mouth occlusion and pleural pressures) and CO2 response are preserved in most patients with severe chronic obstructive pulmonary disease. Effective ventilation is inadequate in the more severely obstructed patients and this results in hypercapnia. Neuroventilatory coupling failure is an attractive explanation for chronic hypercapnia in these patients.
Aged↗
Standards for the optimal management of COPD: a summary.
Tobacco smoking is the main cause of COPD, and encouragement and support in smoking cessation is the best way to help the patient with COPD. The three major goals of COPD management are to lessen airflow limitation, to prevent and treat secondary medical complications, and to decrease respiratory symptoms and improve quality of life. Outpatient pharmacotherapy should be organized in a stepwise manner according the severity of disease, the aims being to induce bronchodilation, reduce inflammation, and facilitate expectoration, although the role of anti-inflammatory and mucolytic treatment of COPD has not been clearly established. Patients whose conditions are not well controlled with optimal pharmacotherapy are candidates for enrollment in a pulmonary rehabilitation program. Correction or prevention of hypoxemia is a priority, and long-term oxygen therapy supplementation prolongs survival in hypoxemic patients. With only limited data on criteria for hospital admission and the objectives of hospitalization, the published standards on the management of COPD include an expert consensus statement on these aspects of hospital care. Surgery, special considerations such as sleep, nutrition, and air travel, and ethical issues are discussed.
Combined Modality Therapy↗
Pulmonary rehabilitation for COPD. A practical approach for improving ventilatory conditioning.
Pulmonary rehabilitation has gradually become the "gold standard" for patients with severe lung disease, especially chronic obstructive pulmonary disease (COPD). Because some newer therapeutic strategies, such as lung volume reduction surgery and lung transplantation, require well-conditioned patients, pulmonary rehabilitation is now considered essential for many patients formerly deemed untreatable. In this article, Dr Celli reviews the basic goals, components, and benefits of pulmonary rehabilitation for COPD and other chronic respiratory diseases.
Breathing Exercises↗
Pathophysiology of chronic obstructive pulmonary disease.
The prevalence of COPD has increased as mortality from the two organ systems affected by the same risk factors of smoking, heart attacks and strokes, has decreased. Once diagnosed, COPD is progressive and may lead to disability, usually due to dyspnea, at a relatively early age (60 to 80 years of age). COPD is usually caused by destruction of the lung parenchyma or by disease affecting the airways. In most patients both processes exist simultaneously. Less often recognized is the fact that the disease does not affect all portions of the lung alike, which causes different physiologic behaviors in different parts of the lung. This article integrates the pathologic changes of COPD with the known adaptive and maladaptive consequences of those changes. An understanding of these changes should result in an increased capacity to comprehend the different therapeutic strategies that have been developed to decrease the symptoms and improve the well-being of patients with COPD.
Dyspnea↗
Training in the rehabilitation of pulmonary patients with chronic obstructive pulmonary disease.
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Breathing Exercises↗
Pulmonary rehabilitation and lung volume reduction surgery in the treatment of patients with chronic obstructive pulmonary disease.
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Humans↗
Pulmonary rehabilitation for patients with advanced lung disease.
Pulmonary rehabilitation has gradually become a cornerstone of treatment for patients with advanced lung disease. Although most of the data that has resulted in the acceptance of this therapeutic modality has been obtained from studies of patients with chronic obstructive pulmonary disease, the basic principles and tools are applicable to patients with many other limiting chronic diseases of the respiratory system. Because new therapeutic strategies, such as lung volume reduction surgery and lung transplantation, require well-conditioned patients, pulmonary rehabilitation is becoming a crucial component of the overall treatment strategy of many patients who heretofore were deemed untreatable. This article reviews the basic definitions, objectives, components, and outcomes of pulmonary rehabilitation in order to provide the reader with a practical and inclusive overview of the topic.
Exercise Therapy↗
Is pulmonary rehabilitation an effective treatment for chronic obstructive pulmonary disease? Yes.
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Exercise Therapy↗
Lung-volume reduction improves dyspnea, dynamic hyperinflation, and respiratory muscle function.
Lung-volume reduction surgery (LVRS) improves static lung elastic recoil in selected patients with severe chronic obstructive pulmonary disease (COPD). This explains the increase in FEV1 in many COPD patients who undergo LVRS, but fails to explain clinical improvement in those without changes in FEV1. We prospectively evaluated 17 patients after pulmonary rehabilitation but prior to and again at least 3 mo after bilateral LVRS done via median sternotomy. In addition to pulmonary function, lung elastic recoil, walking distance, and exercise capacity, we evaluated static and dynamic respiratory muscle (RM) function, and dyspnea. In 12 patients we also quantified dynamic hyperinflation (end-expiratory and end-inspiratory lung volume [EELV and EILV, respectively]). After LVRS, FEV1 rose from 26.7 +/- 1.8 to 39.0 +/- 3.7% predicted (p < 0.004), whereas TLC dropped from 134.7 +/- 4.8 to 118.3 +/- 4.4% predicted (p < 0.0002), and RV from 239.6 +/- 14.8 to 180.3 +/- 8.7% predicted (p < 0.0002). Isowork dyspnea decreased as assessed with a visual analogue scale (VAS) (79.6 +/- 5.2 versus 49.3 +/- 7.5 mm, p < 0.005) and the Borg scale (7.1 +/- 0.6 versus 3.5 +/- 0.6, p = 0.002). Walking distance improved significantly and, in the 12 patients in whom they were measured, EELV and EILV decreased at rest and at isowork. Maximal transdiaphragmatic pressure rose from 67.1 +/- 8.3 to 92.0 +/- 7.5 cm H2O (p < 0.03). Resting RM function changed little, but at isowork improved significantly after LVRS. Excluding one outlier, there was a strong linear correlation between the change in Borg-scale score at equivalent work loads before and after LVRS and the change in EELV (% predicted TLC, r = 0.75, p < 0.001), as well as between the change in Borg-scale score and the absolute decrease in end-expiratory pleural pressure (Ppl(e)) (r = 0.78, p = 0.004). Successful LVRS improves not only lung recoil, but also respiratory muscle function, and reduces dynamic hyperinflation. These changes help explain the decreased dyspnea and improved exercise capacity seen after LVRS, and add to current understanding of the mechanisms by which this procedure may help selected patients with severe emphysema.
Cohort Studies↗
Noninvasive positive pressure ventilation and not oxygen may prevent overt ventilatory failure in patients with chest wall diseases.
Some patients with chest wall diseases (CWD) without respiratory failure manifest important alterations in nocturnal gas exchange, as a previous stage to the future development of daytime respiratory failure. The purpose of this study was to evaluate the efficacy of nasal intermittent positive pressure ventilation (NIPPV) during sleep in a group of obese patients and in another group with restrictive thoracic diseases (RTD), comparing the results with those obtained from conventional nocturnal oxygen therapy. From a total of 42 patients with CWD free of daytime respiratory failure, 27 (64%) were considered nocturnal oxygen desaturators without sleep apnea and were included in the study. The study protocol was completed by 21 of these patients. After 2 weeks of treatment, symptoms of dyspnea, morning headaches, and morning obnubilation improved significantly (p<0.05) in both groups of patients after NIPPV but not with oxygen. Baseline daytime PaO2 was 68+/-7 mm Hg in the obese group of patients and 73+/-11 mm Hg in the RTD group. It improved significantly with NIPPV to 73+/-5 mm Hg in obese patients (p<0.05) and to 77+/-12 mm Hg in the RTD group (p<0.05) but did not change with oxygen (68+/-8 mm Hg in the obese group and 73+/-12 mm Hg in the RTD group). Both treatments improved oxygen saturation during sleep, but oxygenation tends to be higher with oxygen than with NIPPV. Only NIPPV was able to normalize the baseline nocturnal alveolar hypoventilation. From the 21 patients treated, 19 decided to continue with long-term NIPPV, one with oxygen, and one refused treatment. We conclude that in patients with CWD who manifest nighttime oxygen desaturation and hypoventilation, early initiation of NIPPV is preferable to supplemental oxygen. Our results also suggest that NIPPV initiated before overt ventilatory failure could prevent its onset.
Female↗
Lung reduction surgery in severe COPD decreases central drive and ventilatory response to CO2.
BACKGROUND AND OBJECTIVES: Lung volume reduction surgery (LVRS) improves ventilatory function in selected patients with severe COPD. The reasons for the observed benefits include the following: increased elastic recoil, improved airflow, and lesser dynamic hyperinflation and decreased lung volumes. We reasoned that these changes could also alter respiratory drive. METHODS: Respiratory central drive was prospectively assessed using the mouth occlusion pressure (P0.1), and the P0.1 response to increasing CO2 (P0.1/PETCO2 [end-tidal CO2 pressure]), in eight sequential patients before and 3 to 5 months after LVRS. Results were compared with those from 13 control subjects. RESULTS: LVRS decreased total lung capacity from 7.44+/-1.8 L to 5.92+/-1.3 L (p<0.05) and residual volume from 4.97+/-1.5 L to 3.56+/-1.1 L (p<0.05). It also significantly improved FEV1 from 0.85+/-0.26 L to 0.99+/-0.26 L (p<0.05). Baseline P0.1 (3.4+/-1.8 vs 1.4+/-0.4 cm H2O, p<0.01) and P0.1/PETCO2 (0.24+/-0.07 vs 0.11+/-0.04 cm H2O/mm Hg, p<0.05) were higher in patients than in control subjects. After LVRS, P0.1 decreased from 3.4+/-1.8 to 1.3+/-0.75 cm H2O (p<0.01) and P0.1/PETCO2 from 0.24+/-0.07 to 0.16+/-0.06 cm H2O/mm Hg (p<0.05). These postoperative values were similar to those of control subjects. There were no correlations between changes in the factors known to influence central drive (PaO2, PaCO2, age, weight, height, FVC, and FEV1) and changes in P0.1. CONCLUSIONS: We conclude that decreased ventilatory drive should be added to the list of benefits of LVRS, and may help explain the symptomatic improvement reported by many patients after this surgery.
Age Factors↗
ATS standards for the optimal management of chronic obstructive pulmonary disease.
Tobacco smoking is the main cause of chronic obstructive pulmonary disease (COPD), and the provision of encouragement and support in smoking cessation is the best way to help patients with COPD. The three major goals of COPD management are to lessen airflow limitation, to prevent and treat secondary medical complications and to decrease respiratory symptoms and improve quality of life. Outpatient pharmacotherapy should be organized in a stepwise manner according the severity of disease, the aims being to induce bronchodilation, reduce inflammation and facilitate expectoration, although the role of anti-inflammatory and mucolytic treatment in COPD has not been clearly established. Patients who are not well controlled on optimal pharmacotherapy are candidates for enrollment in a pulmonary rehabilitation programme. Correction or prevention of hypoxaemia is a priority, and long-term oxygen therapy may prolong survival in hypoxaemic patients. With only limited data on criteria for hospital admission and the objectives of hospitalization, the published ATS standards on the management of COPD include expert consensus statements on these aspects of hospital care. Special considerations, such as surgery in the COPD patient, sleep disorders, nutrition, air travel, and ethical issues, are discussed.
Ambulatory Care↗
[Progress of respiratory muscle dysfunction in patients with severe chronic obstructive disease].
The altered function of respiratory muscle function in chronic obstructive pulmonary disease (COPD) has been documented by short term studies but not by prospective follow-up. To evaluate the progression of muscle dysfunction and its relation to hyperinflation, air flow obstruction and generalized muscle weakness, we studied seven patients upon admission and 10 to 25 months later. We measured peak inspiratory (PImax) and expiratory (PEmax) pressures in the mouth, peak pleural inspiratory pressure (Pplimax) and peak transdiaphragmatic pressure (Pdimax). Pdimax was measured using gastric (Pg) and esophageal (Ppl) balloons. The slope of excursion of Pg and Ppl measured at the end of inspiration and expiration (Pg/Ppl) was used to assess respiratory muscle recruitment. Nutritional status was indexed as the ratio of weight to height (W/H). FEV1 remained unchanged (1.0 +/- 0.1 to 0.8 +/- 0.3 L), while functional residual capacity (FRC) increased from 7.1 +/- 1.0 to 8.9 +/- 2.0 L (p < 0.05). W/H, PImax, Pplimax and PEmax remained unchanged, while Pdimax decreased significantly from 83 +/- 35 to 47 +/- 16 cmH2O. Diaphragm loading (TTDI and Pdi/Pdimax) were found to increase and Pg/Ppl shifted toward increased use of accessory muscles. The last finding was significantly related to changes in FRC (r = 0.87; p < 0.05). We conclude that diaphragm function deteriorates progressively in patients with severe COPD, even though overall inspiratory muscle strength is preserved, apparently as a consequence of the effect of mechanical factors (hyperinflation) but not of air flow obstruction or generalized muscle weakness.
Data Interpretation, Statistical↗