Effect of body position on measurements of diffusion capacity after exercise.
(17/343)
BACKGROUND: Pulmonary diffusing capacity for carbon monoxide (D1co), alveolar capillary membrane diffusing capacity (Dm), and pulmonary capillary blood volume (Vc) are all significantly reduced after exercise. OBJECTIVE: To investigate whether measurement position affects this impaired gas transfer. METHODS: Before and one, two, and four hours after incremental cycle ergometer exercise to fatigue, single breath D1co, Dm, and Vc measurements were obtained in 10 healthy men in a randomly assigned supine and upright seated position. RESULTS: After exercise, D1co, Dm, and Vc were significantly depressed compared with baseline in both positions. The supine position produced significantly higher values over time for D1co (5.22 (0.13) v. 4.66 (0.15) ml/min/mm Hg/l, p = 0.022) and Dm (6.78 (0.19) v. 6.03 (0.19) ml/min/mm Hg/l, p = 0.016), but there was no significant position effect for Vc. There was a similar pattern of change over time for D1co, Dm, and Vc in the two positions. CONCLUSIONS: The change in D1co after exercise appears to be primarily due to a decrease in Vc. Although the mechanism for the reduction in Vc cannot be determined from these data, passive relocation of blood to the periphery as the result of gravity can be discounted, suggesting that active vasoconstriction of the pulmonary vasculature and/or peripheral vasodilatation is occurring after exercise. (+info)
Lung sounds in asbestos induced pulmonary disorders.
(18/343)
The aim of the study was to compare the lung sounds in patients with asbestos related pulmonary disorders with findings in high-resolution computed tomography (HRCT), and with lung function variables, in order to find out associations of acoustic changes with radiological fibrosis, emphysema or with pulmonary gas transfer functions. Sixty-four patients with asbestos-related pleural disease, with or without pulmonary disease, were studied. Lung sound recording and analysis was carried out with a computerized lung sound analyser, and HRCT of the chest, as well as forced spirometry and diffusing capacity measurement were performed. The fibrosis score correlated positively with the quartile frequencies of the power spectrum of lung sounds in inspiration (f50) and expiration (f50) and crackle count in inspiration, as well as negatively with diffusing capacity. When the patients with crackling sounds and significant fibrosis were excluded (n=18), emphysema correlated negatively with expiratory quartile frequencies of the power spectrum, with f25 and f50. Furthermore, diffusing capacity correlated with inspiratory f25 and forced expiratory volume in one second with inspiratory f50 when crackles and fibrosis were excluded. Changes in lung sounds were significantly associated with radiologically verified abnormalities and gas transfer of pulmonary tissue. High sound frequencies were associated with fibrotic changes of the lung while low sound frequencies with pulmonary emphysema. Acoustic analysis gives complementary clinical information for evaluation of asbestos-related pulmonary disorders. (+info)
Changes in the carbon monoxide diffusing capacity of the lung in ulcerative colitis.
(19/343)
The aim of this study was to investigate lung function in patients with ulcerative colitis and to assess the incidence of latent pulmonary involvement in subjects with active and inactive disease. After full colonscopic assessment with multiple mucosal biopsy, the clinical disease activity of each patient was quantified, using the simple index of Harvey and Bradshaw. The patients were divided into 2 equal groups: subjects with active disease (group 1; n=16); and those with inactive disease (group 2; n=16). Global spirometry was then performed. A latent pulmonary involvement was found in 17 of 32 patients (53%), the incidence was higher in the group 1 patients (81%). The majority of patients presented a reduction in the carbon monoxide diffusing capacity of the lungs (DL,CO). The mean DL,CO value was 73.87+/-14.87 in group 1 and 87.31+/-11.23 in group 2. The DL,CO and KCO reduction correlated significantly with intestinal histopathological grading in the group of patients with active disease (r=0.87, p<0.001; r=0.603, p=0.015). To conclude, a high incidence of pulmonary function abnormalities were identified, despite the lack of radiological alterations (High Resolution Computed Tomography) and pulmonary symptoms, in ulcerative colitis patients. These alterations were more common in patients with active disease. The strong correlation between DL,CO values and histopathological grading suggests that this test may reflect bowel disease activity. (+info)
Relative contribution of resting haemodynamic profile and lung function to exercise tolerance in male patients with chronic heart failure.
(20/343)
OBJECTIVE: To clarify the relative contribution of resting haemodynamic profile and pulmonary function to exercise capacity in patients with heart failure. SETTING: Cardiology department and cardiac rehabilitation unit in a tertiary centre. DESIGN: 161 male patients (mean (SD) age 59 (9) years) with heart failure (New York Heart Association class II-IV, left ventricular ejection fraction 23 (7)%) underwent spirometry, alveolar capillary diffusing capacity (DLCO), and mouth inspiratory and expiratory pressures (MIP, MEP, respectively, in 100 patients). Right heart catheterisation and a symptom limited cardiopulmonary exercise test were performed in 137 patients within 3-4 days. RESULTS: Mean peak exercise oxygen consumption (VO(2)) was 13 (3.9) ml/kg/min. Among resting haemodynamic variables only cardiac index showed a significant correlation with peak VO(2). There were no differences in haemodynamic variables between patients with peak VO(2) 14 ml/kg/min. There was a moderate correlation (p < 0.05) between several pulmonary function variables and peak VO(2). Forced vital capacity (3.5 (0.9) v 3.2 (0.8) l, p < 0.05) and DLCO (21.6 (6.9) v 17.7 (5.5) ml/mm Hg/min, p < 0.05) were higher in patients with peak VO(2) > 14 ml/kg/min than in those with peak VO(2) +info)
Steady-state measurement of NO and CO lung diffusing capacity on moderate exercise in men.
(21/343)
Using a rapidly responding nitric oxide (NO) analyzer, we measured the steady-state NO diffusing capacity (DL(NO)) from end-tidal NO. The diffusing capacity of the alveolar capillary membrane and pulmonary capillary blood volume were calculated from the steady-state diffusing capacity for CO (measured simultaneously) and the specific transfer conductance of blood per milliliter for NO and for CO. Nine men were studied bicycling at an average O(2) consumption of 1.3 +/- 0.2 l/min (mean +/- SD). DL(NO) was 202.7 +/- 71.2 ml. min(-1). Torr(-1) and steady-state diffusing capacity for CO, calculated from end-tidal (assumed alveolar) CO(2), mixed expired CO(2), and mixed expired CO, was 46.9 +/- 12.8 ml. min(-1). Torr(-1). NO dead space = (VT x FE(NO) - VT x FA(NO))/(FI(NO) - FA(NO)) = 209 +/- 88 ml, where VT is tidal volume and FE(NO), FI(NO), and FA(NO) are mixed exhaled, inhaled, and alveolar NO concentrations, respectively. We used the Bohr equation to estimate CO(2) dead space from mixed exhaled and end-tidal (assumed alveolar) CO(2) = 430 +/- 136 ml. Predicted anatomic dead space = 199 +/- 22 ml. Membrane diffusing capacity was 333 and 166 ml. min(-1). Torr(-1) for NO and CO, respectively, and pulmonary capillary blood volume was 140 ml. Inhalation of repeated breaths of NO over 80 s did not alter DL(NO) at the concentrations used. (+info)
Modulation of alveolar-capillary sodium handling as a mechanism of protection of gas transfer by enalapril, and not by losartan, in chronic heart failure.
(22/343)
OBJECTIVES: We sought to compare the protective efficacy of enalapril and losartan on lung diffusion in chronic heart failure (CHF). BACKGROUND: In CHF, hydrostatic overload causes disruption of the alveolar-capillary membrane and depression of carbon monoxide diffusion (DCO); enalapril improves DCO through mechanisms still undefined; and saline infusion in the pulmonary circulation worsens DCO, putatively because of an upregulated sodium transport to the alveolar interstitium. We investigated whether enalapril modulates sodium handling and whether losartan shares the same properties. METHODS: In 29 patients with CHF, DCO, its membrane diffusion subcomponent (DM) and right atrial and pulmonary wedge pressures were monitored during saline infusion, in the control condition, during enalapril therapy (20 mg/day) for two weeks and after crossover to losartan (50 mg/day) for two weeks (first 20 patients), or after the combination of enalapril with aspirin (325 mg/day) for one week (last 9 patients). RESULTS: Saline, 150 ml, lowered DCO (-7.9%; p < 0.01) and DM (-9.9%; p < 0.01) without hydrostatic variations. Responses to 750 ml of saline were qualitatively similar. After treatment with enalapril, baseline DCO (p < 0.01) and DM (p < 0.01) were augmented; after sodium loading, the percent reductions of DCO (p < 0.01) and DM (p < 0.01) were comparable to those before it, resulting in higher absolute values. This suggests that the greater the gas conductance improvement with enalapril, the lower the impedance with saline. Losartan was ineffective on gas transfer at rest and under salt challenge. Aspirin counteracted the benefits of enalapril. CONCLUSIONS: In CHF, enalapril protects lung diffusion, possibly through a prostaglandin-mediated modulation of sodium overfiltration to the alveolar interstitium; losartan does not share this ability. (+info)
In defence of the carbon monoxide transfer coefficient Kco (TL/VA).
(23/343)
The carbon monoxide transfer factor (TL,co) is the product of the two primary measurements during breath-holding, the CO transfer coefficient (Kco) and the alveolar volume (VA). Kco is essentially the rate constant for alveolar CO uptake (Krogh's kco), and in healthy subjects, increases when VA is reduced by submaximal inflation, or when pulmonary blood flow increases. Recently, new reference values were proposed for clinical use which included the observed VA at full inflation; this was claimed to "eliminate the need for Kco". In this commentary, some mechanisms e.g. respiratory muscle weakness, lung resection, diffuse alveolar damage and airflow obstruction, which decrease or increase total lung capacity (TLC) are reviewed. Even when alveolar structure and function are normal, the change in Kco at a given VA varies according to the underlying pathophysiological mechanism. The advantages and disadvantages of normalizing Kco and TL,co to predisease predicted TLC or to the patient's actual VA (using lack of expansion or loss of alveolar units models) are considered. Examination of carbon monoxide transfer coefficient and alveolar volume separately provides information on disease pathophysiology which cannot be obtained from their product, the carbon monoxide transfer factor. (+info)
A single-breath technique with variable flow rate to characterize nitric oxide exchange dynamics in the lungs.
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Current techniques to estimate nitric oxide (NO) production and elimination in the lungs are inherently nonspecific or are cumbersome to perform (multiple-breathing maneuvers). We present a new technique capable of estimating key flow-independent parameters characteristic of NO exchange in the lungs: 1) the steady-state alveolar concentration (C(alv,ss)), 2) the maximum flux of NO from the airways (J(NO,max)), and 3) the diffusing capacity of NO in the airways (D(NO,air)). Importantly, the parameters were estimated from a single experimental single-exhalation maneuver that consisted of a preexpiratory breath hold, followed by an exhalation in which the flow rate progressively decreased. The mean values for J(NO,max), D(NO,air), and C(alv,ss) do not depend on breath-hold time and range from 280-600 pl/s, 3.7-7.1 pl. s(-1). parts per billion (ppb)(-1), and 0.73-2.2 ppb, respectively, in two healthy human subjects. A priori estimates of the parameter confidence intervals demonstrate that a breath hold no longer than 20 s may be adequate and that J(NO,max) can be estimated with the smallest uncertainty and D(NO,air) with the largest, which is consistent with theoretical predictions. We conclude that our new technique can be used to characterize flow-independent NO exchange parameters from a single experimental single-exhalation breathing maneuver. (+info)