[Practical approach to respiratory function tests].
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Biomedical subjects
Publications and source records attributed to C Prefaut.
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In view of their own effects and haemodynamic repercussions, abnormalities in blood gas values are increasingly recognized as being of major significance for the prognosis of chronic obstructive respiratory diseases. Controlled trials of low flow rate oxygen therapy have demonstrated that correcting hypoxaemia in such cases significantly improved the vital prognosis. Almitrine bismesylate administered in single or multiple daily doses in short-medium-or long term treatment to patients with chronic bronchitis and hypoxaemia has proved capable of increasing PaO2 and, when hypercapnia is present, decreasing PaCO2. In responsive patients, a 1.5 mg/kg dose brings about a 5 mmHg change in PaO2 values and, when applicable, PaCO2 values. Several studies with a 1 year follow-up have shown that almitrine bismesylate represents a breakthrough in the management of respiratory failure consecutive to chronic obstructive respiratory disease. Only long-term controlled trials will demonstrate whether this drug can really improve the vital prognosis and even alter the natural course of the disease.
Six subjects suffering from chronic airflow obstruction and respiratory failure were treated with oral almitrine bismesylate (3 mg/kg/day). Studies were made before and after 2 and 4 months treatment on: total ventilation, arterial blood gases, pulmonary artery pressure by a micro-catheter and cardiac out-put by rebreathing CO2. The results were compared with those of a placebo group of 3 subjects. While in the almitrine group a significant improvement in blood gases was observed, no change was seen in the two populations in either the haemodynamic or ventilatory variables. The medium term haemodynamic stability observed is contrasting with single dose effects of almitrine. This discrepancy could be due, at least in part, to a balance between the possible vasoconstrictor effect of almitrine bismesylate and vasodilator consequences of blood gases improvement.
In healthy humans, we studied the effect of high-frequency mechanical vibrations applied unilaterally to the tendon of the biceps or triceps brachialis on ventilation and the breathing pattern. This stimulus preferentially activates the muscle spindle afferents. Increase of respiratory frequency and changes in the ventilatory timing started at the first or second inspiration during tendon stimulation, and no adaptation occurred as long as the vibrations continued. The tidal volume and mean inspiratory flow rate were only enhanced in individuals having high-frequency breathing during eupnea. The changes in ventilatory variables were observed when the motor response to vibrations was tested under isometric or isotonic conditions. Various experimental procedures enabled us to induce a tonic reflex contraction in either the vibrated muscle or the antagonist of no reflex contraction in either group of muscles. In all cases the increase in minute ventilation was identical. These changes in breathing pattern was not associated with a significant decrease in alveolar CO2 pressure and did not seem to be responsible for important variations in respiratory gas exchanges. The response to high-frequency vibrations was also studied after ventilation was increased with added dead space. The magnitude of hyperventilation an the pattern of ventilatory response produced by tendon stimulation did not change with increased ventilation. In conclusion, the stimulation of muscle spindles in human induces changes in ventilation and pattern of breathing , and the occurrence of a reflex muscular contraction does not seem necessary in order to obtain such effects.
Spirometry, blood gases, steady state diffusing lung capacity for carbon monoxyde, ductance for carbon monoxyde were determined in 27 obeses. In 13 of them we also measured closing volume. In 80 per cent of these patients we observed a decrease in expiratory reserve volume certainly due to a shift on the right of the chest wall volume-pressure curve. In 50% of the obeses we found an arterial hypoxia, usually observed when the expiratory level was lower than closing volume. Finally in 20% of the subjects we observed a decrease in diffusing lung capacity and/or ductances probably due to an important fall in and expiratory level at the closing volume level with impairment of the distribution of ventilation.
We measured closing volume (CV), expiratory reserve volume (ERV) regional distribution of lung volume (Vr) and perfusion in 7 normal subjects in air and during immersion to the neck in water. In four subjects immersion resulted in a CV greater than ERV and the normal perfusion distribution became inverted. In the other subjects, ERV remained larger than CV and perfusion distribution during immersion was uniform, not inverted. In 5 subjects closing volume increased and in 3 of them, the ratio of apical/basal Vr increased significantly during immersion. One subject had nomeasurable CV and in the other it was not measured. The data suggest: (1) that when CV is greater than ERV during immersion there is an inversion of the normal perfusion distribution, caused by hypoxia and/or an increase in mean alveolar pressure in the alveoli beyond the closed airways, and (2) that an increase in pleural pressure gradient during immersion may contribute to the increase in C.V.
We have studied the maximal expiratory flow volume curves with air and with an 80% helium-oxygen mixture, using 12 normal and 33 asthmatic children chosen according to clinical, functional and immunological criteria. In the normal children, the average delta Vmax (difference between the maximal flow in HeO2 and in air at corresponding lung volumes) was 49% and was similar from 60% to 20% of vital capacity. The iso flow volume (lung volume level at which the HeO2 and air flow volume curves intersect) was 3% of vital capacity. Eleven of the asthmatics were non-responders to the helium mixture (no significant differences in flow between HeO2 and air curves), five at 50% and 25% VC and six at only 25% VC. The other 22 asthmatics were responders, but nine of them showed a rise of the iso flow volume. Eight subjects showed no obstruction according to the flow volume curves in air; three of these had an abnormal response to the helium mixture. All the non-responders at 50% VC and half of the non-responders at 25% VC had a clinical history of recurrent infections. These results suggest, firstly, that when there is no history of recurrent infections, the site of obstruction in asthmatic children is mainly central. This does not exclude a coexisting peripheral obstruction which could persist after recovery of the central component. Secondly, by studying the HeO2 response at 25% VC, we can get more information than by measuring only the delta Vmax50 or iso flow volumes.
We measured lung volumes, closing volume (CV), alveolo-arterial oxygen difference (P(A-a)O2) and steady-state diffusing lung capacity per liter ventilation (DLCO/V) in 18 men immersed up to the neck in water. The subjects were divided into 3 groups, according to relative changes in P(A-a)O2 and DLCO/V. In group 1 (n = 6), P(A-a)O2 decreased and DLCO/V increased, probably because of the hemodynamic changes induced by immersion. Their end expiratory level was above closing volume in water. In group 3 (n = 6), P(A-a)O2 increased and DLCO/V decreased, probably as a result of a decrease in ventilation in the dependent parts of the lung, considering that breathing range (ERV + VT) was less than closing volume. In group 2 (n = 6), P(A-a)O2 increased significantly and DLCO/V, only slightly. Tidal volume was only partially included in closing volume. The increase in exchange surface area was probably unable to compensate for the arterial hypoxia brought on by the decrease in ventilation in the dependent parts of the lung. The relationship between end expiratory level and closing volume, which seemed to explain the results observed during immersion, was itself a consequence of the subjects' age and body build.
The authors compared the effects of a synthetic vagolytic drug, the SCH 1000, and a beta2 sympathicomimetic one (Fenoterol) in two groups of control children (n = 11) and two groups of asthmatic children (n = 23). They studied the following parameters, flow volumes curves, steady state lung diffusing capacity and the blood gases. No difference of efficiency was found between the two types of bronchodilators although the graphic modification of flow volumes curves was different after Fenoterol and after SCH 1000. The modifications consisted in a great improvement in instantaneous flow, a decrease in diffusion capacity and an increase of the Pa O2 significant in the group of asthmatic children after Fenoterol.
Twenty patients having previously had a Mendelson's syndrome were subjected to a respiratory functional test. A syndrome of diffuse interstitial pulmonary fibrosis (DIPF) was found only in 3 cases examined shortly after the pneumopathy. In one of these cases, another examination done later showed signs of regressing fibrosis. The authors concluded that if a functional syndrome of DIPF occurred immediately after a Mendelson's pneumopathy, it eventually disappeared in the long term in most cases.
We measured lung volumes, static deflation pressure-volume curves of the lung, maximum expiratory flow-volume curves, and closing capacities in five men standing immersed to the neck in water. FRC was decreased 27%, while other lung volumes did not change significantly. At high lung volumes immersion tended to increase lung elastic recoil while recoil was decreased at low lung volumes, changes compatible with vascular congestion. Maximum expiratory flow was increased at high lung volumes, probably because of hydrostatic pressure. At low lung volumes maximum expiratory flow was decreased. This was probably due to decreased recoil since the relationship between elastic recoil and maximum flow was unchanged. Closing capacities by the N2 technique were unchanged but the slope of the alveolar plateau and the amplitude of cardiogenic oscillations were decreased in some individuals. Static and dynamic lung properties were unchanged by 5 min of immersion with tidal volume restricted to 0.5 liter. Though immersion produced volume restriction comparable with that reported with chest strapping, it did not produce similar changes in lung mechanics.
The apnoeic response following interruption of the air flow at different levels of the inspiratory capacity (deltaVL) was studied in conscious children and adults. Changes in mouth pressure were used to measured the duration of the apnoe. The total duration of the interrupted breath (T1) was compared to mean value of the ventilatory period of the five preceding breaths (T0). A monoexponential regression could be fitted to the relationship between T1/T0 ratio and change in lung volume (deltaVL) measured at the onset of interruption: T1/T0=k-exp (S-deltaVL), S begin the sensitivity of the response to lung inflation. When T1/T0=1, the intrathoracic lung volume was called threshold volume (VTh.L.). The parameters S and VTh.L. were used for characterization of the individual importance of the Breuer-Hering inspiratory-inhibitory reflex (B.H. reflex). The high reproducibility of the T1/T0 vs. deltaVL relationship in many subjects showed the light influence of voluntary control on apnoea's duration. In each subject, S and VTh.L. were compared with ventilatory variables measured during eupnoea. A fast pattern of breathing (i.e. small inspired volume and short inspiratory duration) was associated with high value of S and low VTh.L. Moreover VTh.L. was near the tidal volume range in subjects where the B.H. reflex was the more potent. Thus, vagal afferents relating to this reflex could modulate the eupnoeic pattern of some subjects.
The individual importance of peripheral chemosensitive afferents was studied using a transient hypercapnia (inhalation of a 5% or a 10% CO2 in air gas mixture respectively during 4 or 2 breaths) in human conscious subjects chosen for their different eupnoeic ventilatory patterns. Calculation of the speed of change in end-tidal CO2 pressure in tracheal gas (sPETCO2) and of the rate of change in tidal volume (sVI) gave assessment for quantifying the sensitivity of arterial chemoreceptors to hypercapnia (sCO2=SVI/SPETCO2). Our results showed that, independently of any outside influence of the eupnoeic ventilatory pattern on the components of the chemical stimulus, sVI and sCO2 were found to be much smaller in subjects whose pattern of breathing was slow (i.e. having a large tidal volume). The possible causes of the weak importance of peripheral chemosensitive afferents in such subjects were discussed.
Lacoste has shown the interest of determination of overall ductance of CO and partial expired alveolar ductance and arterio-alveolar partial ductances in the assessment of the efficacy of gaseous exchanges in the lung. DuCO was, by definition, the product : DuACO X DuaCO, the increase in partial ductance may theoretically compensate reduction in the other, the overall ductance then remains normal. This theory was verified studying the effects of low lung volume ventilation. Under these conditions, the dead space series becomes reduced and the DuACO should increase at the same rate, for ventilation occurs at the level of the closing volume. The inspired air is then directed preferentially towards the lung apices. These artificial changes in distribution of ventilation should produce a reduction in DuaCO. The measurements carried out confirmed these theories during low lung volume ventilation ; whereas the differences observed in overall ductance were not significant, those observed on partial ductance were very definitely significant. It appears that isolated measurement of overall ductance is insufficient and may lead to misdiagnosis of a change in the lung exchanges.
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