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PubMed1984

Prospective evaluation of amiodarone pulmonary toxicity.

Reports of pulmonary infiltrates in patients taking amiodarone, initiated the study of 69 patients for pulmonary toxicity using serial chest roentgenograms (CXRs), pulmonary function tests (PFTs), and symptoms before and during therapy. Mean PFTs did not significantly change from their baseline normal values, but 10 percent of patients had a greater than or equal to 15 percent fall in total lung capacity, and 28 percent a greater than or equal to 15 percent fall in diffusion capacity (DCO) following treatment. Initial abnormalities in pulmonary function or CXR were predictive of risk of developing pulmonary toxicity. Degree of exposure to amiodarone (dose plus duration) correlated only weakly with development of pulmonary toxicity, which could occur in patients taking relatively small doses of the drug. Pulmonary complications of amiodarone are common, in most cases reversible, and often confused with congestive heart failure or pneumonia. Patients should be evaluated before treatment by assessing symptoms, CXRs, and DCO. Patients with initial abnormalities in these parameters, particularly both CXR and DCO abnormalities, should be considered for alternative therapy.

Adult↗
PubMed2005

[Pulmonary hypertension during exercise in toxic oil syndrome].

BACKGROUND AND OBJECTIVE: Toxic oil syndrome is a risk factor for pulmonary arterial hypertension (PAH) and new cases of this entity are emerging after more than 20 years since the initial toxic oil epidemic. Abnormal elevation of pulmonary systolic pressure with exercise may be considered an early marker of PAH in populations at risk. We aimed to analyze the pulmonary systolic pressure with exercise echocardiography in toxic oil syndrome patients. PATIENTS AND METHOD: 50 toxic oil syndrome patients (cases), and 20 healthy control subjects were submitted to rest and peak exercise echocardiography (semi supine cycloergometer) measuring pulmonary systolic pressure. In toxic oil syndrome patients, pulmonary carbon monoxide diffusion capacity was also analyzed. RESULTS: Peak exercise pulmonary systolic pressure was statistically similar in cases and controls. Nevertheless, 8% of cases reached a pulmonary systolic pressure > or = 80 mmHg and this fact was associated with mild pulmonary arterial hypertension, reduced right ventricular function and abnormal pulmonary diffusion capacity in the rest study. A rest pulmonary systolic pressure cut-off value > or = 27 mmHg had a 100% sensitivity and 71% specificity to predict a peak exercise systolic pulmonary pressure > or = 80 mmHg. CONCLUSIONS: A minority of toxic oil syndrome patients develop severe pulmonary arterial hypertension during exercise. This abnormal response is associated with other markers of pulmonary vasculopathy. Further studies are needed to elucidate the relation between these findings and the likelihood to develop pulmonary arterial hypertension in the future.

Adult↗
PubMed1989

Retrospective studies in scleroderma: pulmonary findings and effect of potassium p-aminobenzoate on vital capacity.

The principal clinical pulmonary findings were extracted from University of Michigan Hospital records of 390 patients with scleroderma. Dyspnea was the most frequent symptom and strongly correlated with pulmonary fibrosis and with decreased vital capacity (FVC) and CO diffusing capacity (DLCO). The mean value for FVC was 84% of the predicted normal for 326 patients, and that of the initial DLCO 56.8% of the predicted normal (323 patients). Pulmonary fibrosis was diagnosed on first chest X-ray in 80 of 382 patients. An additional 48 patients developed fibrosis detected on subsequent X-rays. Analyses were performed to determine whether the deterioration of pulmonary function over time was less for scleroderma patients who were adequately treated with potassium p-aminobenzoate (KPAB) than for those inadequately or never treated with KPAB, The average decrease for both FVC and DLCO was found to be less for KPAB-treated patients. However, only in the case of vital capacity was the difference significant. In the presence of radiological evidence of pulmonary fibrosis FVC decreased more rapidly (p = 0.002), but the decline in DLCO was not affected. When adjusting for the presence or absence of fibrosis the average slopes of the logarithm of vital capacity were significantly less negative (p = 0.003) for patients on KPAB.

4-Aminobenzoic Acid↗
PubMed1993

Measurement of carbon monoxide transfer and lung volume in ventilated subjects.

A simple method for measuring lung volume and carbon monoxide transfer factor (TLCO) by a rebreathing technique was assessed in nine healthy volunteers undergoing intermittent positive pressure ventilation (IPPV). Measurements of TLCO, alveolar volume (VA) and carbon monoxide transfer coefficient (KCO) made at three inspired oxygen concentrations (21, 35 and 70%) during IPPV were compared to those obtained during spontaneous breathing. The effects of 10 cmH2O positive end expiratory pressure (PEEP) were also studied. Pulmonary capillary blood volume (Vc) and the diffusing capacity of the alveolar capillary membrane (Dm) were derived. There was a close correlation between measurements of TLCO during IPPV (TLCOIPPV) and spontaneous breathing (TLCOSV) (r = 0.92). Ventilated TLCO was 64 +/- 8% of spontaneously breathing TLCO. There was a close agreement between ventilated and spontaneously breathing measurements of KCO (r = 0.95; mean difference 0.14, 95% limits of agreement +0.37 to -0.09 mmol.min-1 x kPa-1 x l-1). Vc was 92 +/- 23 ml during spontaneous breathing and 72 +/- 21 ml during IPPV (p < 0.05). PEEP of 10 cmH2O significantly increased functional residual capacity (2.3 +/- 0.5 to 3.5 +/- 0.6 l) and decreased TLCO (5.9 +/- 1.0 to 5.3 +/- 1.2 mmol.min-1 x kPa-1), KCO (1.7 +/- 0.2 to 1.1 +/- 0.3 mmol.min-1 x kPa-1 x l-1) and Vc (82 +/- 22 to 56 +/- 20 ml). Dm did not change with PEEP. This simple method may be a useful means of assessing gas exchange and lung volume in ventilated subjects. It showed that PEEP increased lung volume but reduced TLCO and that this reduction appeared to be due to a reduction in capillary blood volume.

Adult↗
PubMed1986

Change in O2 uptake during rebreathing in hyperoxia in man.

In pertaining to PO2 dependency of the pulmonary CO diffusing capacity during rebreathing, the O2 uptake (VO2) and cardiac output (Q) were measured at three different PO2 levels between 100 and 500 Torr. Since the VO2 measured by an O2 injection method is strongly influenced in hyperoxia by a gas exchange ratio (R), a simulation method using a R-PCO2 relation during rebreathing was developed. Gas volume in the lung-bag-system needed in the computation was measured from the difference in O2 concentration between before and after injecting a known amount of O2 into the rebreathing circuit. The accuracy of the volume was checked by comparing it with the volume measured successively with a body box. The VO2 was determined by comparing the simulated O2 and CO2 concentrations in rebreathing gas with the measured ones. The VO2 significantly increased by rebreathing in hyperoxia. To analyze the VO2 increase, the Q was computed by dividing the VO2 by the arteriovenous O2 content difference, which in turn was obtained by dividing the slope of the CO2 dissociation curve by that of the R-PCO2 line. The Q was almost linearly related to the VO2. Since there was no difference in VO2 in steady state breathing between normoxia and hyperoxia, the increase in VO2 and Q seemed to occur transiently. This finding is very important in evaluating the PO2 dependency of the pulmonary diffusing capacity for CO.

Adult↗
PubMed1989

Effect of cold pressor test on carbon monoxide diffusing capacity in normal subjects.

We investigated changes in the pulmonary carbon monoxide diffusing capacity (DLco) during the cold pressor test (CPT) on 25 normal subjects. In 10 of them we also observed changes in circulatory parameters by a computerized dual cadmium telluride detector system, using an equilibrium radionuclide blood-pool label. DLco and DLco per unit of alveolar volume (DLco/VA) averaged in the control period were 29.4 +/- 4.1 ml/min/mm Hg, 6.1 +/- 0.8 ml/min/mm Hg/l (mean +/- SD). During the 2nd minute of CPT, DLco increased by 3.6 +/- 1.5% and DLco/VA by 5.1 +/- 1.5% (mean +/- SE). The systemic blood pressure increased by 17% (mean increase) whereas the heart rate and the stroke volume remained unchanged. The increases were small but significant (p less than 0.05, p less than 0.01, respectively). We conclude that the increase in DLco is due to cold-induced systemic vasoconstriction followed by a passive shift of blood into the pulmonary vasculature.

Adult↗
PubMed2000

Lack of improvement of lung diffusing capacity following fluid withdrawal by ultrafiltration in chronic heart failure.

OBJECTIVES: We sought to investigate the possibility that lung diffusing capacity reduction observed in chronic heart failure is reversible in the short term. BACKGROUND: Mechanical properties of the lung usually ameliorate with antifailure treatment including drugs, ultrafiltration and heart transplantation, whereas lung diffusion rarely improves. METHODS: We studied the mechanical properties of the lung (pulmonary function tests with determination of alveolar volume, extravascular lung fluids and lung tissue), lung diffusion for carbon monoxide (DLco), including membrane diffusing capacity (Dm), pulmonary capillary blood volume (Vc) and pulmonary hemodynamics, in 28 patients with stable chronic heart failure, before a single session of extracorporeal ultrafiltration (3,973 +/- 2200 ml) and four days thereafter. Lung mechanics and diffusion were also evaluated in 18 normal subjects. RESULTS: Vital capacity, forced expiratory volume (1 s) and maximal voluntary ventilation were lower in patients when compared with normal subjects, and increased after ultrafiltration from 2.1 +/- 0.7 to 2.5 +/- 0.7(1)*, 1.7 +/- 0.5 to 2.0 +/- 0.6(1)* and 67 +/- 25 to 79 +/- 26 (1/min)*, respectively (* p < 0.02 vs. pre-ultrafiltration). Post-ultrafiltration alveolar volume was augmented, while lung tissue, body weight (approximately 6 kg), chest X-ray extravascular lung water score and pulmonary vascular pressure were reduced. Heart dimensions (echocardiography) remained unchanged. DLco, Dm and Vc were 29.0 +/- 5.0 ml/min/mm Hg, 47.0 +/- 11.0 ml/min/mm Hg, 102 +/- 20 ml in normal subjects and 17.1 +/- 4.0#, 24.1 +/- 6.5#, 113 +/- 38 and 17.0 +/- 5.0#, 24.8 +/- 7.9#, 100 +/- 39 in patients before and after ultrafiltration, respectively (# = p < 0.01 vs. controls). CONCLUSIONS: In chronic heart failure, ultrafiltration improves volumes and mechanical properties of the lung by reducing lung fluids. Diffusion is unaffected by ultrafiltration, suggesting that, in chronic heart failure, the alveolar-capillary membrane abnormalities are fluid-independent.

Chronic Disease↗
PubMed1997

Inhomogeneities of ventilation and the diffusing capacity to perfusion in various chronic lung diseases.

Although impairment of gas exchange caused by ventilation-perfusion (VA/Q) mismatch has been extensively analyzed, there have been no systematic studies focused on determining the distributions of diffusion properties in dose connection with those of VA/Q. We attempted to clarify the simultaneous distributions of VA/Q and diffusion capacity to perfusion (D/Q) in patients with idiopathic pulmonary fibrosis (IPF) or chronic obstructive pulmonary disease (COPD). To assess pathologic determinants causing functional abnormalities, we compared VA/Q and D/Q distributions with the findings on high-resolution computed tomography. O2, CO2, and CO together with six foreign inert gases were used as indicator gases. We transformed the measured data on indicator gases in arterial blood into a continuous distribution of Q in the VA/Q-D/Q field. In IPF, active alveolitis or acinitis played a major role in producing low D/Q regions impeding gas exchange via a diffusion limitation, whereas extensive fibrosis with minimal inflammation accounted for low D/Q as well as low VA/Q regions. In COPD, no regions with low D/Q ratios were observed, but an abnormality in the VA/Q distribution with low or high VA/Q ratios was identified. Emphysematous lesions produced high VA/Q regions, whereas peripheral airway involvement yielded low VA/Q regions. These findings suggest that hypoxemia in patients with IPF is caused by inhomogeneous distributions of D/Q in combination with those of VA/Q. Hypoxemia in patients with COPD is attributable primarily to inhomogeneities in VA/Q rather than in D/Q distributions.

Aged↗
PubMedDate not supplied

[Early detection of fibrosing alveolitis in collagenoses].

Lung function tests during a five-year follow-up were performed on 29 patients with various collagen diseases. At the beginning of the study none of the patients had signs of any pulmonary dysfunction. The onset of fibrosing alveolitis was accompanied by a marked reduction of the diffusing capacity for CO and a more minor alteration of the static specific compliance. The vital capacity and the pO2 at rest changed only in cases of advanced pulmonary fibrosis.

Airway Resistance↗
PubMed2006

Short-term variability of nitric oxide diffusing capacity and its components.

When monitoring nitric oxide diffusing capacity (DL(NO)) in patients, it is necessary to distinguish natural biological variation from a real change in alveolar-membrane conductance. The short-term variability of single-breath DL(NO) has not been established. The aim was to determine the short-term variability DL(NO) in healthy subjects. Twelve healthy subjects performed single-breath hold diffusing capacity tests at rest over a 2-month period (eight separate sessions with 8+/-3 days between each session). Each subject inhaled 41+/-4 ppm NO and a standard diffusion mixture. DL(NO), which is a multiple of the membrane diffusing capacity for carbon monoxide (Dm(CO)), as well as carbon monoxide diffusing capacity (DL(CO)) and pulmonary capillary blood volume (V(c)) remained unaltered over the 2-month period (P>0.05). Reproducibility (calculated as 2.77 multiplied by the within-subject standard deviation) over eight sessions was 20, 5 and 8 mL min(-1)mmHg(-1) for DL(NO), DL(CO) and Dm(CO), respectively, and 19 mL for V(c) (when Dm(CO)=DL(NO)/2.42). DL(NO), DL(CO), Dm(CO) and V(c) remain unchanged over a period of 2 months. Since the inter-session variability is 20, 5 and 8 mL min(-1)mmHg(-1) for DL(NO), DL(CO) and Dm(CO), and 19 mL for V(c), a meaningful change should equal or exceed those values. While there is a small chance that week-to-week variation can also be partly due to mild pathophysiological changes, any differences that are below the reproducibility values are likely to be natural biological variation or technical variation of the equipment, rather than true physiological change.

Adult↗
PubMed1977

Pulmonary gas transfer 20 years after pneumonectomy for pulmonary tuberculosis.

The changes in pulmonary function after pneumonectomy in 13 patients with pulmonary tuberculosis have been studied. The data at the time of two follow-up studies are compared with those obtained before the pneumonectomy. The first follow-up was carried out between 5 and 30 months postoperatively and the second between 20 and 24 years later. The results of this second follow-up show a relatively normal arterial oxygen saturation and gas transfer factor but an increased residual volume which cannot be explained by increasing age alone.

Adult↗