Expiratory and inspiratory chest computed tomography and pulmonary function tests in cigarette smokers. (1/343)

This study evaluated small airway dysfunction and emphysematous destruction of lung parenchyma in cigarette smokers, using chest expiratory high-resolution computed tomography (HRCT) and pulmonary function tests (PFT). The degree of emphysematous destruction was classified by visual scoring (VS) and the average HRCT number at full expiration/full inspiration (E/I ratio) calculated in 63 male smokers and 10 male nonsmokers (group A). The Brinkman smoking index (BI), defined as cigarettes x day(-1) x yrs, was estimated. Sixty-three smokers were divided into three groups by PFT: group B1 (n=7), with normal PFT; group B2 (n=21), with diffusing capacity of the lung for carbon monoxide (DL,CO) > or = 80% predicted, forced expiratory volume in one second (FEV1) < 80% pred and/or residual volume (RV) > 120% pred; and group B3 (n=35), with DL,CO < 80% pred, FEV1 < 80% pred and/or RV > 120% pred. Heavy smokers (BI > or = 600) (n=48) showed a significant increase in emphysema by both VS and E/I. E/I was significantly elevated in both group B2 (mean+/-SD 0.95+/-0.05) and B3 (0.96+/-0.06) compared with group B1 (0.89+/-0.03). VS could not differentiate group B2 (3.9+/-5.0) from B1 (1.1+/-1.6). These findings suggest that the expiration/inspiration ratio reflects hyperinflation and airway obstruction, regardless of the functional characteristics of emphysema, in cigarette smokers.  (+info)

Red cell distribution and the recruitment of pulmonary diffusing capacity. (2/343)

The distribution of red blood cells in alveolar capillaries is typically nonuniform, as shown by intravital microscopy and in alveolar tissue fixed in situ. To determine the effects of red cell distribution on pulmonary diffusive gas transport, we computed the uptake of CO across a two-dimensional geometric capillary model containing a variable number of red blood cells. Red blood cells are spaced uniformly, randomly, or clustered without overlap within the capillary. Total CO diffusing capacity (DLCO) and membrane diffusing capacity (DmCO) are calculated by a finite-element method. Results show that distribution of red blood cells at a fixed hematocrit greatly affects capillary CO uptake. At any given average capillary red cell density, the uniform distribution of red blood cells yields the highest DmCO and DLCO, whereas the clustered distribution yields the lowest values. Random nonuniform distribution of red blood cells within a single capillary segment reduces diffusive CO uptake by up to 30%. Nonuniform distribution of red blood cells among separate capillary segments can reduce diffusive CO uptake by >50%. This analysis demonstrates that pulmonary microvascular recruitment for gas exchange does not depend solely on the number of patent capillaries or the hematocrit; simple redistribution of red blood cells within capillaries can potentially account for 50% of the observed physiological recruitment of DLCO from rest to exercise.  (+info)

Effects of side lying on lung function in older individuals. (3/343)

BACKGROUND AND PURPOSE: Body positioning exerts a strong effect on pulmonary function, but its effect on other components of the oxygen transport pathway are less well understood, especially the effects of side-lying positions. This study investigated the interrelationships between side-lying positions and indexes of lung function such as spirometry, alveolar diffusing capacity, and inhomogeneity of ventilation in older individuals. SUBJECTS AND METHODS: Nineteen nonsmoking subjects (mean age=62.8 years, SD=6.8, range=50-74) with no history of cardiac or pulmonary disease were tested over 2 sessions. The test positions were sitting and left side lying in one session and sitting and right side lying in the other session. In each of the positions, forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), single-breath pulmonary diffusing capacity (DLCO/VA), and the slope of phase III (DN2%/L) of the single-breath nitrogen washout test to determine inhomogeneity of ventilation were measured. RESULTS: Compared with measurements obtained in the sitting position, FVC and FEV1 were decreased equally in the side-lying positions, but no change was observed in DLCO/VA or DN2%/L. CONCLUSION AND DISCUSSION: Side-lying positions resulted in decreases in FVC and FEV1, which is consistent with the well-documented effects of the supine position. These findings further support the need for prescriptive rather than routine body positioning of patients with risks of cardiopulmonary compromise and the need to use upright positions in which lung volumes and capacities are maximized.  (+info)

Does the cellular bronchoalveolar lavage fluid profile reflect the severity of sarcoidosis? (4/343)

The aim of this study was to assess whether the cellular bronchoalveolar lavage fluid (BALF) profile, particularly the number of polymorphonuclear neutrophils (PMNs), is associated with disease severity of sarcoidosis and its usefulness in determining remission. Twenty-six nonsmoking outpatients with sarcoidosis were included in this study. The patients were divided into two subgroups according to the absolute number of PMNs in BALF: < or =0.2x10(4) cells x mL(-1) (group 1; n = 15) and >0.2x10(4) cells x mL(-1) (group 2; n = 11). The radiographic stage, high-resolution computed tomography (HRCT) findings, 67Ga lung uptake as well as lung function tests differed significantly between group 1 and 2. Follow-up revealed that 14 (93.3%) patients of group 1 compared to four (36.4%) of group 2 recovered spontaneously without the help of corticosteroids. In contrast, no differences were found in the number of lymphocytes in BALF nor in the serum angiotensin converting enzyme (sACE) level between both groups. The number of PMNs, the transfer factor of the lungs for carbon monoxide (TL,CO), the forced expiratory volume in one second (FEV1) and one of the HRCT subscores discriminated between patients with different disease progression. Of these parameters the PMNs appeared to be the only one which differentiated patients who demonstrated remission and those who deteriorated. In conclusion, these results indicate that the number of polymorphonuclear neutrophils in bronchoalveolar lavage fluid distinguish between sarcoidosis patients who demonstrated remission and those having a more severe course of the disease. Whether polymorphonuclear neutrophils may be considered as markers of disease activity and/or prognosis in sarcoidosis needs further investigation.  (+info)

Intrapulmonary gas mixing and the sloping alveolar plateau in COPD patients with macroscopic emphysema. (5/343)

Chronic obstructive pulmonary disease patients, especially those with emphysema, show steep slopes of the alveolar plateau (S). This study tested the hypothesis that continued gas exchange between poorly and well-ventilated lung units by means of collateral ventilation would contribute to S in these patients. Nine young volunteers, nine older volunteers and 11 patients with macroscopic emphysema performed wash-out tests with helium (He) and sulphur hexafluoride (SF6). S was determined for breaths 1-5 (range 1), and for breaths between 95% and 98% of complete wash-out (range 2). An unequal ventilation index (UVI) was defined as the ratio between the estimated mean alveolar pressure and the end tidal pressure (PET) of each tracer gas, calculated over range 2. Over the same range, a phase III ratio was calculated by dividing PET by the estimated pressure at Fowler dead space. In all groups of subjects, the S for He and SF6 were greater for range 2 than for range 1 (p< or =0.012). In the emphysema patients, the correlations between S and UVI were 0.72 for He (p=0.012) and 0.81 for SF6 (p=0.002), while the mean phase III ratios were 1.7 for He and 2.4 for SF6, much less than their theoretical maxima. It was concluded that in patients collateral ventilation may account for only a small part of the increase in the alveolar plateau slope between ranges 1 and 2, and that this increase was mainly caused by unequal ventilation in combination with sequential emptying of lung units. The degree of sequential emptying, however, was modest compared with its full potential.  (+info)

Impaired pulmonary diffusion during exercise in patients with chronic heart failure. (6/343)

BACKGROUND: Pulmonary diffusion is impaired at rest in patients with chronic heart failure (CHF) and has been implicated in the generation of symptoms and exercise intolerance. The aim of this study was to determine whether pulmonary diffusion is impaired during exercise in CHF, to examine its relationship to pulmonary blood flow, and to consider its functional significance in relation to metabolic gas exchange. METHODS AND RESULTS: Carbon monoxide transfer factor (TLCO) and pulmonary blood flow (Q(C)) were measured by a rebreathe technique at rest and during steady-state cycling at 30 W in 24 CHF patients and 10 control subjects. Both patients and control subjects were able to raise TLCO and Q(C) during exercise. However, the patient group had a lower diffusion for a given blood flow (TLCO/Q(C)) both at rest (3.6+/-0.16 and 4.8+/-0.23 mL x L(-1) x mm Hg(-1); P<0.001) and during exercise (2.8+/-0.16 and 3.4+/-0.13 mL x L(-1) x mm Hg(-1) for CHF patients and control subjects, respectively; P<0.05). TLCO/Q(C) was related to the ventilatory equivalent for carbon dioxide (VEVCO(2)) production at 30 W (TLCO/Q(c) versus VEVCO(2), r = -0.58, P<0.01) and to peak exercise oxygen consumption measured during a progressive test (TLCO/Qc versus VO(2peak), r = 0.57, P<0.01) in these patients. CONCLUSIONS: Patients with CHF are able to recruit reserves of TLCO and Q(C) during exercise. However, the TLCO/Q(C) ratio is consistently impaired in these patients and relates to both exercise hyperpnea and peak exercise oxygen consumption. Whether this impairment in alveolar gas exchange is reversible in CHF and therefore is a potential target for therapy has yet to be determined.  (+info)

Simultaneous measurement of nitric oxide production by conducting and alveolar airways of humans. (7/343)

Human airways produce nitric oxide (NO), and exhaled NO increases as expiratory flow rates fall. We show that mixing during exhalation between the NO produced by the lower, alveolar airways (VL(NO)) and the upper conducting airways (VU(NO)) explains this phenomenon and permits measurement of VL(NO), VU(NO), and the NO diffusing capacity of the conducting airways (DU(NO)). After breath holding for 10-15 s the partial pressure of alveolar NO (PA) becomes constant, and during a subsequent exhalation at a constant expiratory flow rate the alveoli will deliver a stable amount of NO to the conducting airways. The conducting airways secrete NO into the lumen (VU(NO)), which mixes with PA during exhalation, resulting in the observed expiratory concentration of NO (PE). At fast exhalations, PA makes a large contribution to PE, and, at slow exhalations, NO from the conducting airways predominates. Simple equations describing this mixing, combined with measurements of PE at several different expiratory flow rates, permit calculation of PA, VU(NO), and DU(NO). VL(NO) is the product of PA and the alveolar airway diffusion capacity for NO. In seven normal subjects, PA = 1.6 +/- 0.7 x 10(-6) (SD) Torr, VL(NO) = 0.19 +/- 0.07 microl/min, VU(NO) = 0.08 +/- 0.05 microl/min, and DU(NO) = 0.4 +/- 0.4 ml. min(-1). Torr(-1). These quantitative measurements of VL(NO) and VU(NO) are suitable for exploring alterations in NO production at these sites by diseases and physiological stresses.  (+info)

Serial measurements of exhaled nitric oxide during exacerbations of chronic obstructive pulmonary disease. (8/343)

Excessive inflammation seems important in chronic obstructive pulmonary disease (COPD), particularly during exacerbations of the disease. Exhaled nitric oxide concentration ([NOexh]) is a sensitive marker of bronchial inflammation in asthma; it is unclear if this is also the case in COPD. This study: 1) quantifies [NOexh] in patients with COPD (during an exacerbation and while clinically stable); 2) investigates the response of [NOexh] to i.v. steroid therapy, and its potential relationship with other relevant physiological variables; and 3) assesses the relative contributions of the central and peripheral airways to [NOexh] by collecting exhaled air in two different bags connected in series. Seventeen COPD patients (forced expiratory volume in one second (FEV1) 37.6+/-3.4% of the predicted value (+/-SEM)) hospitalized because of an exacerbation of the disease (arterial oxygen tension (Pa,O2) (7.46+/-0.72 kPa 56.1+/-5.4 mmHg), arterial carbon dioxide tension (Pa,CO2) 5.63+/-0.37 kPa 42.3+/-2.8 mmHg), pH 7.41+/-0.02) and 10 healthy subjects that served as controls were studied. On admission, [NOexh] in COPD was higher than normal (41.0+/-5.1 versus 13.3+/-0.8 parts per billion (ppb), respectively, p<0.001). Despite i.v. steroid therapy, [NOexh] remained elevated throughout recovery (37.9+/-4.8 ppb, p<0.001) until discharge (40.9+/-4.3 ppb, p<0.001). In contrast, when the patients were clinically stable (several months later), [NOexh] was significantly reduced (15.8+/-3.8 ppb, p<0.001), and no longer different from control values. [NOexh] was not related to any of the physiological variables measured during recovery (pulmonary gas exchange) or at discharge (forced spirometry, lung volumes, diffusing capacity). Finally, the contribution of the central and peripheral airways to [NOexh] was not different at any point in time. These results indicate that during exacerbations of chronic obstructive pulmonary disease, the exhaled nitric oxide concentration: 1) is higher than normal; 2) is not reduced acutely by i.v. steroids but is normalized several months after discharge; 3) is unrelated to several physiological indices of disease severity; and 4) appears to be produced homogeneously in central and peripheral airways. Overall, these results are different from those reported in asthma, suggesting that different inflammatory mechanisms are operating in both diseases.  (+info)