Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pulmonary Diffusing Capacity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,225 records · Page 68Linked to original sources
PubMed1995

[Lung problems in acute to subacute exposure to medium altitudes].

The hypobaric hypoxia of moderate altitude elicits various mechanisms of acute to subacute physiologic adaptations of the healthy lung: First of all it causes a hyperventilation, which increases the diminished arterial pO2. Because of hypoxemia-induced vasoconstriction, pulmonary arterial hypertension develops. The adrenergic stimulation of the cardiac output also increases the pulmonary perfusion. Most likely because of the diminished density of ambient air there is a measurable increase of exspiratory bronchial flow or, respectively, a diminution of the peripheral airway resistance. In higher altitudes, limitation of oxygen-diffusion under physical exertion is observed. The consequences of acute hypobaric hypoxia for diseased lungs depend on preexisting ventilation/perfusion mismatch or diffusion impairment. Arterial hypoxemia and hence also pulmonary arterial hypertension are increased. In the presence of normal chemoreceptor sensitivity (type pink puffer), a hyperventilation, which is often perceived as dyspnea by the patient, is induced. Mostly patients with chronic obstructive pulmonary disease adapt, however, surprisingly well to moderate altitude. Bronchial asthma improves frequently because allergen concentrations are low and air density is diminished. On the other hand, physical exertion in dry and cold ambient air may also elicit acute asthmatic exacerbations. The assessment of moderate altitude tolerance by patients with chronic lung diseases and prophylactic precautions before the ascent are discussed. The only altitude-specific disease of the healthy lung is the so-called high-altitude pulmonary edema. The major pathogenetic factor for its development is an inadequate or overshooting response to hypobaric hypoxia (nonuniform pulmonary arterial vasoconstriction, diminished hypoxic ventilatory drive, retention of fluid, centralization of blood volume and capillary leak). Prophylactic and therapeutic implications are discussed.

Altitude↗
PubMed1995

[Generalized side effects with the use of carbamazepine].

Since 1973, 42 cases of generalized adverse reactions to carbamazepine were reported to the Netherlands Centre for Monitoring of Adverse Reactions to Drugs and the Belgian Centre for Drug Monitoring. The organ involvement can be very diverse in an allergic reaction to carbamazepine. Serious and protracted disturbances in pulmonary diffusion capacity may be present even in the absence of changes on the chest X-ray. Analysis of the type IV mechanism involved suggests that caution is warranted with regard to administration of other drugs during the acute phase of the allergic reaction particularly if these drugs have a propensity to cause type IV allergic reactions themselves.

Adult↗
PubMed1995

The PIO2 vs. SpO2 diagram: a non-invasive measure of pulmonary oxygen exchange.

A non-invasive method for measuring pulmonary oxygen exchange is described using a plot of inspired oxygen partial pressure (PIO2) vs. oxygen saturation (SpO2). This method was assessed using nine normal subjects and 35 patients undergoing major surgery, including five thoracotomies. In each patient PIO2 was varied to produce a range of values of SpO2 between 85% and 99%. A model based on the inspired to arterial oxygen difference involving the shunt equation, solved by simultaneous numerical methods, was used to show how the PIO2 vs. SaO2 relationship could be used to derive two parameters of oxygen exchange, the PIO2-Pco2 difference and the Virtual Shunt. The model allows the inspired to arterial difference in PO2 to be divided into (a) an inspired to 'ideal' alveolar difference attributable to the balance between alveolar ventilation and oxygen uptake; (b) an 'ideal' alveolar to end-capillary difference attributable to inhomogeneity in ventilation/perfusion ratios; and (c) end-capillary to arterial difference attributable to true shunt, which was termed 'virtual shunt' because of the uncertainties of assuming fixed values for haemoglobin concentration and arteriovenous oxygen content difference. The coefficient of determination showed that there was a good fit of the model to the data. Because the method is model-based it enables extrapolation to different PIO2 values as well as the study of the evolution of changes in gas exchange under varying conditions.

Adult↗
PubMed1979

Collateral ventilation.

Ventilation may bypass obstructed airways through collateral channels, including interalveolar pores of Kohn, bronchiole-alveolar communications of Lambert, and interbronchiolar pathways of Martin. Resistance through these channels, like resistance through small airways, increases with decreasing lung volume and with hypocapnia. But whereas the distention of collateral channels and small airways by a variety of factors is similar, the efficiency of ventilation through collateral channels is less than the efficiency through airways. Gas inspired through collateral channels is contaminated with alveolar gas from surrounding lung so that the dead space for collateral ventilation is increased. When one part of the lung ventilates out of phase with the surrounding lung, pulmonary interdependence promotes more homogeneous ventilation. In the presence of airways obstruction, interdependence may be a primary factor governing the rate of collateral ventilation. In man, collateral ventilation is unimportant in normal lungs. However, with disease, it may be critical in producing or compensating for abnormalities. For example, the long time constant for collateral ventilation in the middle lobe may be responsible for atelectasis, which results in the middle lobe syndrome. On the other hand, the short time constant for collateral ventilation in emphysema may be essential for the distribution of ventilation beyond obstructed airways.

Airway Resistance↗
PubMed1993

Transfer lung factor for Co (TLCO) and its components (DM & VC) in flour mill workers.

Tlco, Kco (Tlco/Va), Va, Vc and Dm were measured in 25 flour mill workers (non-smoker 9, smoker 16) and 50 healthy control subjects (25 non-smoker, 25 smoker) of similar anthropometric parameters and socio-economic status. Tlco (P < 0.05) was decreased significantly and rest of the parameters were decreased insignificantly in flour mill workers as compared to control subjects. In non-smoker flour mill workers none of the parameters altered significantly as compared to non-smoker control subjects. Statistically significant reduction was seen in smoker workers only in Tlco (P < 0.05) and its component Dm (P < 0.05) as compared to smoker control subjects. Further it has been observed that less duration of flour dust exposure (< 5 years) in all flour mill workers and smoker flour mill workers caused negligible fall in Tlco, whereas longer duration of flour dust exposure (> 5 years) in both the groups caused highly significant fall in Tlco (P < 0.01) which was contributed to by highly significant fall in Dm (P < 0.001).

Carbon Monoxide↗
PubMed1994

[The value of studies of pulmonary gas exchange during exercise for evaluation of reduced arterial oxygenation at rest in asymptomatic long-term smokers].

The aim of this study was to elucidate extent and nature of an impairment of gas exchange after long time cigarette-smoking. Pulmonary gas exchange at rest as well as during steady state exercise and conventional lung function tests (LFTs) were studied in 32 clinically healthy, asymptomatic severe cigarette-smokers (S; 48.1 +/- 15.7 pack-years) and 32 healthy lifetime nonsmokers (N) between 40 and 60 years of age, respectively, individually matched for age, body height, body weight and gender. Pulmonary function tests of all subjects were within the limits of normal values. Except for a slight reduction of MEF25 in S (p < 0.05) and a slight increase of FRC (p < 0.05), the groups did not differ with respect to LFTs. At rest, however, S had markedly lower values for PaO2, TLO2, DCO and KCO, and higher values for AaDO2 and QVA/Qt. Resting measurements for VD/VE and PaCO2 did not differ between N and S. During ergometry PaO2 and TLO2 increased respectively; AaDO2 and QVA/Qt fell concomitantly with VD/VE and PaCO2. On termination of exercise no significant difference between N and S for the above variables could be discerned any longer. Our findings confirm that even in clinically healthy asymptomatic cigarette-smokers a distinct impairment of gas exchange is present. Their improvement during physical exercise primarily indicates the presence of reversible ventilation-perfusion mismatching and excludes relevant morphologic changes in the lung in these cases.

Adult↗
PubMed1993

[Effect of diffusion limitation on gas exchange in the lung--analysis in oleic acid-induced lung injury].

To assess the effect of diffusion limitation on gas exchange in injured lungs with non-cardiogenic pulmonary edema, an experimental model of acute lung injury with alveolar flooding was produced in six mongrel dogs by intravenously injecting oleic acid at 0.06 ml/kg. The effect of diffusion limitation was quantitatively examined by measuring the excretion (E) of three indicator gases (acetylene, ethylene and freon-22) with differing solubility (lambda) and tissue diffusivity (d). The indicator gases were dissolved in normal saline and infused at a constant rate through a peripheral vein. Since acetylene and ethylene have nearly identical of d but differing lambda, the difference in E values of these two gases may solely reflect the effect of uneven distribution of ventilation-perfusion ratios (VA/Q) in the lung. Thus, measured E values of acetylene and ethylene allowed us to approximately predict the E of freon-22, the value corresponding to the condition where d of freon-22 was taken to be equal to that of acetylene or ethylene. The difference between predicted and measured E values of freon-22 is indicative of the limitation of diffusion in the lung periphery. In all the lungs studied, measured E values of freon-22 were consistently smaller than those predicted from acetylene and ethylene, leading to the conclusion that gas exchange in injured lungs with widespread pulmonary edema was partly impaired by diffusion in aqueous media.

Animals↗
PubMed1993

Cyclophosphamide and low-dose prednisone therapy in patients with systemic sclerosis (scleroderma) with interstitial lung disease.

Fourteen patients with systemic sclerosis (SSc, scleroderma) and interstitial lung disease were treated with oral cyclophosphamide (1-2 mg/kg/day) and low dose prednisone (< 10 mg/day). There was a significant improvement in FVC after 6 months compared to entry values (2.21 +/- 0.19 l vs. 2.03 +/- 0.15 l, p < 0.02). Improvement was maintained at 12 months (2.27 +/- 0.27 l, p < 0.05) and 18-24 months (2.60 +/- 0.28 l, p < 0.001). In 12 cases followed for 18-24 months, FVC was stable or improved. No significant improvement or decline was noted for the DLCO. Side effects included cytopenia (2), infection (1), and hemorrhagic cystitis (2), and one possible related malignancy. A controlled prospective trial of cyclophosphamide is warranted in patients with SSc and active interstitial lung disease.

Adult↗
PubMed1995

[Quantitative computerized tomography of the lung--respiration controlled diagnosis of diffuse lung diseases].

STUDY OBJECTIVE: Computed tomography provides measurements of lung attenuation which reflect changes in the air to tissue ratio and can thereby be employed for diagnosis of diffuse lung disease. In this prospective study, we quantitatively analyzed lung density by high resolution computed tomography (HRCT) in 26 healthy volunteers, 15 patients with chronic obstructive pulmonary disease (COPD), and 15 patients with idiopathic lung fibrosis (IPF). The procedure was standardized by examination of 3 scans at the carina +/- 5 cm and by defining inflation levels by %VC using an on-line hand held spirometer. RESULTS: Performance of HRCT at 50% VC provides not only significant and distinguishable group data, but is the easiest to carry out for dyspneic patients. The mean lung density at 50% VC for healthy subjects was -820 +/- 4.2 (mean +/- SEM) Hounsfield units (HU). It was significantly lower (p < 0.01) in COPD patients (-865 +/- 9.2 HU), and considerably higher (-697 +/- 17.8 HU, p < 0.001) in the IPF group. At an inflation level of 20% VC, mean lung density values were similarly distributed, at significantly lower values relative to those at 50% VC, but the procedure was more difficult to perform for patients with dyspnea. In contrast, at 80% VC, lung density values for the COPD and control groups were not significantly different (p = 0.08). The sensitivity to detect COPD was improved by selecting HRCT values lower than -900 HU, which represent the part of the lung with an increased air/tissue ratio. For IPF patients an increase of lung density values above -699 HU was characteristic, indicating a decrease of the air/tissue relationship. CONCLUSION: From our data we propose to perform quantitative HRCT measurements at 50% VC. Diagnosis of diffuse lung disease can be further improved by consideration of specific CT -value intervals. Spirometrically controlled quantitative HRCT is a clinically meaningful tool for the assessment of diffuse parenchymal lung disease.

Adult↗
PubMed1998

Lung diffusion estimated by oxygen and carbon monoxide.

The study was objected to the comparison of the results of lung diffusion estimated by oxygen to those of routinely used single breath carbon monoxide method. The method described is based on the analysis of the speed of response of arterial partial oxygen pressure (paO2) to increasing inspiratory fraction of oxygen (Fi). The transcutaneous oximetry was used to follow paO2 by means of transcutaneous oxygen pressure (ptCO2). The study was performed on 35 patients of both sexes with interstitial lung involvement with normal or only slightly decreased FVC and FEV1. The close correlation between the results of both methods was proved (r = 0.848, p < 0.0001).

Adult↗
PubMed1998

[The sickle cell anemia lung from childhood to adulthood].

The pulmonary complications remain the prime cause of morbidity and mortality in sickle cell disease. The pathogenetic mechanisms consists both of an alteration of the rheological properties of the blood, the existence of a hypercoagulability state and above all specific interactions between the abnormal sickle cells and the vascular endothelium and a dysregulation of the vascular reactivity in which nitrous oxide intervenes. The acute chest syndrome (ACS) is characterised by chest pain with dyspnoea and recent radiological abnormalities and it is an acute lung complication whose problem is one of aetiology. The infectious pneumonias are rarely documented. On the other hand, alveolar hypoventilation linked to infarcts of the thoracic ribs, thoracoabdominal trauma, subdiaphragmatic pain, the administration of analgesics causing respiratory depression, obesity or sleep disturbance are frequent causes of ACS. Bronchoalveolar lavage has revealed a frequency of fat emboli following infarcts in the long bones. Pulmonary emboli is rarely a cause. Pulmonary thrombosis is a serious complication, the diagnosis is difficult and is seen in a predisposed clinical setting. The treatment of ACS rests on controlled hydration and antibiotic therapy, oxygen therapy and controlled analgesic therapy. The indications for blood transfusion and for exchange transfusion merits a better evaluation. In the long term patients with sickle cell disease present with a failure of normal thoracopulmonary growth with a restrictive ventilatory defect and progressive diminution in the transfer factor of carbon monoxide with age. A history of ACS favours chronic lung disease. Pulmonary arterial hypertension is less frequent.

Acute Disease↗
PubMed1990

Pulmonary mechanical function and diffusion capacity after deep saturation dives.

To assess the effects of deep saturation dives on pulmonary function, static and dynamic lung volumes, transfer factor for carbon monoxide (T1CO), delta-N2, and closing volume (CV) were measured before and after eight saturation dives to pressures of 3.1-4.6 MPa. The atmospheres were helium-oxygen mixtures with partial pressures of oxygen of 40-60 kPa. The durations of the dives were 14-30 days. Mean rate of decompression was 10.5-13.5 kPa/hour. A total of 43 divers were examined, six of whom took part in two dives, the others in one only. Dynamic lung volumes did not change significantly but total lung capacity (TLC) increased significantly by 4.3% and residual volume (RV) by 14.8% (p less than 0.05). CV was increased by 16.7% (p less than 0.01). The T1CO was reduced from 13.0 +/- 1.6 to 11.8 +/- 1.7 mmol/min/kPa (p less than 0.01) when corrected to a haemoglobin concentration of 146 g/l. Effective alveolar volume was unchanged. The increase in TLC and decrease in T1CO were correlated (r = -0.574, p less than 0.02). A control examination of 38 of the divers four to six weeks after the dives showed a partial normalisation of the changes. The increase in TLC, RV, and CV, and the decrease in T1CO, could be explained by a loss of pulmonary elastic tissue caused by inflammatory reactions induced by oxygen toxicity or venous gas emboli.

Adult↗