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PubMed1988

A simple method for rapid estimate of pulmonary venous admixture.

Data from 2,298 measurements of pulmonary venous admixture (QS/QT) performed in 733 patients were analyzed and processed in order to develop a method for rapid and reliable estimation of QS/QT by a simplified approach. Formulae and charts were obtained, which are easily suitable for use in all settings, and permit estimation of QS/QT with an 85%-93% control of its variability (r2 = 0.85-0.93, p less than 0.0001) simply on the basis of the measured arterial and central venous O2 tensions or saturations.

Adolescent↗
PubMedDate not supplied

Lipid infusion in premature infants suffering from sepsis.

In as much as possible side effects attributing to insufficient fat clearance with hyperlipemia, parenteral lipid administration to septic premature infants is controversial. In this study serum triglyceride and free fatty acid concentrations of nine low birth weight infants with septicemia and 21 low birth weight infants without septicemia were measured. Acidosis, hypoxia, hyperglycemia, and cardiovascular insufficiency were treated before parenteral lipid infusion was started. There was no occurrence of septic shock. In the course of fat infusion with 3 g/kg body weight per day in low birth weight infants without systemic infection we only found triglyceride concentrations of 1.15 mmol/liter and free fatty acid levels of 1.05 mmol/liter. Premature infants with septicemia showed, under fat application of 2 g/kg body weight per day, mean triglyceride levels of 1.67 mmol/liter and free fatty acid values of 1.94 mmol/liter. The highest concentrations occurred at 3 g fat/kg body weight per day with triglycerides of 2.02 mmol/liter and free fatty acids of 2.06 mmol/liter. They indicate a reduced clearance and support earlier findings of reduced utilization of infused fat in premature infants with septicemia. Triglyceride concentrations more than 1.7 mmol/liter probably induce an increase of phagocytosis of the fat particles with the effect of a partial block of the reticuloendothelial system and an impairment of pulmonary diffusion capacity. Therefore, we suggest dosages no higher than 2 g fat/kg body weight per day to low birth weight infants and we advise to check the triglycerides daily. Hypertriglyceridemia implicates an immediate reduction or total interruption of the lipid infusion until normal triglyceride values are regained.

Bacterial Infections↗
PubMed2005

Interventions during donor care before lung transplantation.

Improvement in the ratio of PaO2 to the fraction of inspired oxygen and treatment of pulmonary infections in donors have been cited as important goals for improving lungs before implantation and restoring marginal lungs to the donor pool. Likewise, improving donor PaO2 is often critical for other organs during donor care. The common physiological mechanisms responsible for hypoxemia are ventilation/perfusion mismatching, abnormal oxygen diffusion, and hypoventilation. These mechanisms are discussed and treatment options are considered.

Apnea↗
PubMed2000

The measurement of exhaled carbon monoxide is influenced by airflow obstruction.

The concentration of carboxyhaemoglobin (COHb) is often estimated from measurements of carbon monoxide in the exhaled air (COexh). This study investigates whether the presence of airflow obstruction significantly alters the relationship between COexh and COHb. Eighty-one regular smokers were prospectively studied and divided in four groups according to the presence and severity of airflow obstruction (none, mild, moderate, severe). In each subject, the authors measured in this order: 1) arterial blood gases; 2) haemoglobin concentration and COHb (by co-oxymetry); 3) COexh; 4) lung volumes; and 5) forced spirometry. The size of the measurement error (deltaCO) was calculated from the difference between COHb and COexh. Neither the smoking history nor COexh were different in the four groups of subjects studied. In contrast, deltaCO increased in parallel to the degree of airflow obstruction. DeltaCO was >2% (a threshold value normally used in the clinic to separate smokers from nonsmokers) only in patients with severe airflow obstruction. A stepwise multivariate analysis showed that both forced expiratory volume in one second (FEV1) (percentage reference) and COHb contributed significantly (p<0.0001) to predict deltaCO. This study shows that the estimation of carboxyhaemoglobin from exhaled carbon monoxide measurements can be inaccurate in patients with severe airflow obstruction. In these patients, the direct measurement of carboxyhaemoglobin seems advisable in clinical practice.

Adult↗
PubMed2005

Effects of exacerbations and seasonality on exhaled nitric oxide in COPD.

Exhaled nitric oxide (eNO) appears to be associated with airway inflammation seen in chronic obstructive pulmonary disease (COPD). The present authors studied the effects of exacerbation, season, temperature and pollution on eNO. eNO was measured seasonally and at exacerbations in 79 outpatients suffering from COPD (mean forced expiratory volume in one second=42%). The effects of exacerbation symptoms, physiological and environmental parameters were analysed. Stable eNO levels were correlated positively with arterial oxygen tension. Median levels were found to be lower in smokers (5.3 ppb) than in ex- or nonsmokers (6.8 ppb). Levels were higher during October to December (6.9 ppb) than in April to June (4.6 ppb). Levels were also higher during 68 exacerbations in 38 patients (7.4 ppb) than in stable conditions (5.4 ppb), independent of the effects of smoking. The rise in eNO was greater in exacerbations that were associated with colds, a sore throat or dyspnoea combined with a cold. In conclusion, exhaled nitric oxide levels were higher in colder weather and in the autumn, perhaps related to the increased prevalence of viral infection at this time of year. The levels were lower in more severe chronic obstructive pulmonary disease. Exhaled nitric oxide levels were raised at the onset of exacerbation, particularly in the presence of a cold.

Age Distribution↗
PubMed2006

Cardiopulmonary stress during exercise training in patients with COPD.

Exercise training is an essential component of pulmonary rehabilitation. However, the cardiopulmonary stress imposed during different modalities of exercise training is not yet known. In the present study, the cardiopulmonary stress of a 12-week exercise training programme in 11 chronic obstructive pulmonary disease (COPD) patients (forced expiratory volume in one second 42+/-12%pred, age 69+/-6 yrs) was measured. Pulmonary gas exchange and cardiac frequency (f(C)) of three training sessions were measured with a portable metabolic system at the beginning, mid-term and end of the programme. Symptoms were assessed with Borg scores. The exercise intensity was compared with the recommendations for exercise training by the American College of Sports Medicine (ACSM). Training effects were significant (maximum change in work: 14+/-11 Watts, 6-min walk test: 44+/-36 m). Whole body exercises (cycling, walking and stair climbing) consistently resulted in higher cardiopulmonary stress (oxygen uptake (V'(O(2))), minute ventilation and f(C)) than arm cranking and resistance training. Dyspnoea was higher during cycling than resistance training. Patients exercised for >70% (>20 min) of the total exercise time at >40% of the V'(O(2)) reserve and f(C) reserve ("moderate" intensity according to the ACSM) throughout the programme. The cardiopulmonary stress resistance training is lower than during whole-body exercise and results in fewer symptoms. In addition, exercise testing based on guidelines using a fixed percentage of baseline peak performance and symptom scores achieves and sustains training intensities recommended according to the American College of Sports Medicine.

Aged↗
PubMed1998

Cysteine proteinases and cystatin C in bronchoalveolar lavage fluid from subjects with subclinical emphysema.

This study examined the role of cysteine proteinases and their inhibitor in the development of emphysema in comparison with neutrophil elastase (NE) complexed with alpha1-protease inhibitor (NE-alpha1-PI), which was previously demonstrated to be increased in bronchoalveolar lavage (BAL) fluid from subjects with subclinical emphysema. Eight nonsmokers and 31 current smokers with (n=17) and without (n=14) emphysema, as evidenced by lung computed tomographic scans, were studied. The concentrations of immunologically detected cathepsin L and cystatin C, but not cathepsin B, were significantly increased in BAL fluid from the smokers with emphysema compared with those without emphysema, although the activity of cathepsin L, measured using a synthetic substrate and cathepsin L, released from cultured alveolar macrophages at 24 h, did not show any significant difference between the two groups. When comparison was made only for the subjects aged <60 yrs, the difference between the two groups disappeared for cathepsin L, but remained for NE-alpha1-PI. There was no significant correlation between the level of cathepsin L and that of NE-alpha1-PI in BAL fluid from the subjects with emphysema. In conclusion, increased levels of cathepsin L and cystatin C were demonstrated in bronchoalveolar lavage fluid from subjects with subclinical emphysema. However, the roles of cathepsin L and neutrophil elastase in the development of emphysema may vary between subjects and between the young and the old.

Adult↗
PubMed1980

1,3-Bis(2-chloroethyl)-1-nitrosourea (BCNU)-induced pulmonary fibrosis.

Clinical data are presented on 14 patients undergoing BCNU therapy for a primary intracranial glioma (11 biopsied, 3 suspected) in whom pulmonary fibrosis developed as a consequence of the therapy. Pulmonary diffusion abnormalities, dry hacking cough, and chest x-ray changes herald the onset of the process. Microscopic evaluation of lung specimens revealed a wide spectrum of change including hyaline membrane formation, alveolar septal thickening, interstitial fibrosis, and granuloma formation. It is concluded that BCNU causes pulmonary fibrosis that is primarily but not necessarily dose-related and may not be reversible.

Adolescent↗
PubMed1992

A prospective study of pulmonary function and gas exchange following liver transplantation.

Pulmonary function and gas exchange were prospectively studied in 95 patients before and 9 to 15 months following liver transplantation. Pretransplant, the most common PF abnormality was impaired efficiency of gas exchange as measured by Dss. As a group, the mean Dss was 78.0 +/- 16.6 percent predicted and was found to be less than 80 percent predicted in 50 patients. As a group, patients with the most severe liver diseases clinically (Child's C classification) had the lowest mean Dss pretransplant. Posttransplant, three findings were of clinical importance: PaCO2 significantly improved posttransplantation, suggesting a resolution of pretransplant respiratory alkalosis. Expiratory airflow obstruction, measured by a change in the FEV1/FVC, was extremely uncommon posttransplant. Mean Dss improved significantly in patients with Child's C severity of liver disease. The most frequent deteriorations in Dss statistically were associated with posttransplant thoracotomy, ARDS, nonspecific pneumonitis, significant pleural effusions and hepatic retransplantation.

Female↗
PubMed1993

Colchicine in the treatment of pulmonary fibrosis.

There is no standard or known optimal treatment for idiopathic pulmonary fibrosis. Corticosteroids have been used with widely variable benefit. Colchicine has been reported to suppress fibroblast growth factors and to inhibit collagen deposition. A potential role has been proposed for colchicine in the treatment of fibrotic pulmonary diseases. We retrospectively assessed the outcome of 23 patients with idiopathic pulmonary fibrosis in whom colchicine was used as empiric treatment. Eighteen patients had received prior corticosteroid therapy. By clinical and pulmonary function criteria, five patients (22 percent) improved following colchicine, nine (39 percent) remained stable, and nine (39 percent) worsened. The average duration of follow-up was 22 months. Despite limitations of this retrospective analysis, colchicine may be of benefit in pulmonary fibrosis and should be considered for further clinical trials.

Adult↗
PubMed1993

Outcome of subjects with idiopathic pulmonary fibrosis who fail corticosteroid therapy. Implications for further studies.

To evaluate the outcome of subjects with idiopathic pulmonary fibrosis (IPF) whose conditions clinically deteriorate while receiving corticosteroid therapy, we studied 12 of these subjects (7 male, 5 female) who received subsequent therapy with intravenous (IV) pulse cyclophosphamide (CPX). Seven of the 12 study subjects died during the course of therapy. Six of these subjects died of respiratory failure, and one died of cholecystitis. Among those who died, the mean age at diagnosis was 63 years compared with 57 years in those who have continued to survive (p = 0.29). Smoking status and pack-years of cigarette smoking were similar between those subjects who died and those who continue to survive. However, subjects who died received CPX for a mean of 6 months, while subjects still living have received CPX for a mean of 16 months (p = 0.01). Subjects who died were given a CPX a mean of 64 months after the onset of symptoms, compared with a mean of 50 months for subjects who are still alive (p = 0.57). Interestingly, there were no significant differences in measures of pulmonary function between living and dead subjects. In fact, measures of lung function and gas exchange remained stable in both groups throughout the period of observation. These data suggest that (1) measures of lung function may not be a reliable indicator of patient mortality in end-stage IPF, and (2) while not statistically significant, these data raise the possibility that duration of symptomatic disease may play a role in the outcome of IPF patients receiving alternative therapeutic agents after failure of corticosteroid therapy. In future intervention trails, controlling entry criteria for duration of disease may prove helpful in determining the effects of these agents on the disease process. These data do not permit a determination of the effect of CPX in patients with IPF.

Administration, Oral↗
PubMed1993

Mast cells in fibrotic lung disorders.

Fibrotic lung disorders are chronic inflammatory diseases in which inflammatory processes in the lower respiratory tract injure the lung and modulate the proliferation of mesenchymal cells that form the basis of the fibrotic scar. The pathogenesis of fibrosis in fibrotic lung disorders remains unclear; however, recent attention has focused on the potential role of the mast cell in the genesis of fibrosis. To determine whether mast cells are implicated in the pathogenesis of lung fibrosis, mast cells were compared with the degree of fibrosis in transbronchial lung biopsy specimens from 49 patients with fibrotic lung disorders (16 sarcoidosis, 15 farmer's lung disease, 9 cryptogenic fibrosing alveolitis, 6 bronchiolitis obliterans organizing pneumonia, 3 histiocytosis X). In lung tissue of patients with fibrotic lung disorders, there was an increased number of mast cells in respect to the control group (98.6 +/- 7.7 vs 27.8 +/- 5.1 mast cells per square millimeter, p < 0.01). Mast cell counts in lung biopsy specimens were significantly correlated with the degree of fibrosis (r = 0.87, p < 0.001); 80.8 percent of mast cells were found in the alveolar septa, 9.6 percent within alveoli, 1.9 percent among alveolar lining cells, and 5 percent along blood vessels. No mast cells were located within alveoli in controls. Our data suggest that mast cells participate in chronic inflammation and that their presence is related to interstitial fibrosis in a much broader spectrum of fibrotic lung disorders.

Adult↗
PubMed1994

Clubbing of the fingers and smooth-muscle proliferation in fibrotic changes in the lung in patients with idiopathic pulmonary fibrosis.

In our study of 52 patients with idiopathic pulmonary fibrosis (IPF), we found that the incidence of clubbing of the fingers was significantly more frequent in male than in female patients and in patients who showed lesser grades of honeycombing and higher grades of smooth-muscle proliferation in the pulmonary fibrotic changes (p < 0.01). Smooth-muscle proliferation in fibrotic changes of open lung biopsy specimens correlated with the mode of detection of IPF and the presence of clubbing of the fingers, duration of symptoms of the lower respiratory tract, and a higher extent of pulmonary infiltrates on chest radiographs (p < 0.05). However, the presence of clubbing of the fingers or grades of smooth-muscle proliferation in the pulmonary fibrotic changes did not correlate with the 2-year survival after open lung biopsy.

Adult↗
PubMed1996

Prevalence of pulmonary hypertension in limited and diffuse scleroderma.

STUDY OBJECTIVES: To characterize the prevalence of undiagnosed pulmonary hypertension in patients with limited and diffuse scleroderma. DESIGN: Prospective cross-sectional study. SETTING: University-based outpatient clinic. PATIENTS: Thirty-four consecutive patients with limited (n = 29) or diffuse (n = 5) scleroderma but without the clinical diagnosis of pulmonary hypertension. MEASUREMENTS AND RESULTS: All patients had 12-lead ECGs and two-dimensional and Doppler echocardiograms. The pulmonary artery systolic pressure (PAs) was calculated as the sum of the Doppler transtricuspid pressure gradient and the right atrial pressure as estimated by the caval respiratory index. Thirty-three patients (97%) had adequate spectral signals of tricuspid regurgitation. The velocity of tricuspid regurgitation ranged from 1.6 to 4.5 m/s. The calculated PAs ranged from 15 to 95 (mean +/- SD = 30 +/- 14 mm Hg). Twelve patients (35% of the total cohort) had pulmonary hypertension defined as PAs of 30 mm Hg or greater. CONCLUSIONS: Undiagnosed elevation of PAs is common in patients with scleroderma. Noninvasive assessment of PAs can be performed accurately in most patients independent of clinical signs of pulmonary hypertension. If successful treatment strategies are identified, it may be possible to identify patients early in the development of pulmonary hypertension and intervene before significant end-organ damage occurs.

Adult↗
PubMed1997

Effects of noninvasive positive pressure ventilation on gas exchange and sleep in COPD patients.

STUDY OBJECTIVE: The role of nocturnal noninvasive positive pressure ventilation (NPPV) in the treatment of patients with hypercapnic COPD remains controversial. Beneficial effects reported after prolonged use have included an improvement in gas exchange. The purpose of this study was to examine the short-term effects of NPPV on gas exchange and sleep characteristics in patients with hypercapnic COPD and to determine if similar acute changes in gas exchange are associated with improved sleep quality. DESIGN: Prospective, randomized, controlled trial. SETTING: Sleep laboratory of a university hospital. PATIENTS: Six patients with severe but stable hypercapnic COPD (PaCO2=58+/-4 [SE] mm Hg). Mean age was 63+/-6 (SD) with an FEV1=0.58+/-0.09 L. INTERVENTIONS AND MEASUREMENTS: Patients were studied in the sleep laboratory for a total of three nights. On nights 2 and 3, arterial catheters were placed prior to the study. Following an acquaintance night, patients were randomized to either a control-sham night on 5 cm H2O nasal continuous positive airway pressure (CPAP) or an NPPV night using a ventilatory support system (BiPAP; Respironics Inc; Murrysville, Pa) at previously determined optimal settings. The third night consisted of the opposite for each patient, either a control-sham or an NPPV night. On the second and third nights, three arterial blood gas readings were obtained: (1) baseline wakefulness; (2) non-rapid eye movement (NREM) sleep; and (3) rapid eye movement (REM) sleep. RESULTS: During NREM sleep, NPPV in comparison to the control-sham night on low level CPAP caused no significant change in PaCO2 (60+/-4 to 59+/-3 mm Hg [p=0.6]) and a decrease in PaO2 (96+/-9 to 72+/-5 mm Hg [p=0.04]). During REM sleep, NPPV in comparison to the control-sham night on low level CPAP caused no significant change in either PaCO2 (63+/-7 to 57+/-2 mm Hg [p=0.46]) or PaO2 (67+/-7 to 75+/-8 mm Hg [p=0.51]). Sleep efficiency and total sleep time (TST) increased significantly with NPPV in comparison to the control-sham night on low level CPAP: from 63+/-7% to 81+/-4% (p<0.05) and from 205+/-32 to 262+/-28 min (p<0.05), respectively. Sleep architecture, expressed as a percentage of TST, was unchanged on the NPPV night compared to the control-sham night on low level CPAP. The number of arousals during the night was also unchanged with NPPV in comparison to the control-sham night on low level CPAP (45+/-11 to 42+/-9 [p=not significant]). CONCLUSIONS: NPPV acutely improved sleep efficiency and TST in patients with hypercapnic COPD without significantly improving gas exchange. Other sleep parameters, including sleep architecture and the number of arousals during the night, remained unchanged during NPPV. These data suggest that the beneficial effects of NPPV in patients with hypercapnic respiratory failure are not solely due to an improvement in gas exchange but may be more complex with other factors potentially having contributing roles.

Aged↗
PubMed1998

Postpneumonectomy pulmonary edema: can it be predicted preoperatively?

Postpneumonectomy pulmonary edema (PPE) is a rarely reported form of acute lung injury which occurs in up to 4% of all pneumonectomies. The details of two well-documented cases of PPE are described with special emphasis paid to the preoperative lung functions. Both cases illustrated a striking disparity between preserved spirometric lung function and advanced emphysema as detected by quantitative CT emphysema scores and single-breath diffusion of carbon monoxide measurements. Though retrospective in nature, these results suggest a restricted capillary volume plays a critical role in the development of PPE.

Aged↗