Lung Volume Restriction Research Articles

Disturbance of respiratory muscle function in patients with mitral valve disease

A reduced total lung capacity associated with a normal or decreased lung recoil pressure at full inflation (Pel max) has been noted in patients with valvular heart lesions. In order to investigate the mechanism underlying this inappropriately low Pel max, we measured respiratory mechanics in a group of 15 patients with mitral valve disease uncomplicated by other illness. The total lung capacity was 81 percent of control. The static pressure-volume curve of the long intersected the normal one in the vicinity of functional residual capacity (i.e., the recoil pressure was increased at large lung volumes and diminished at low lung volumes), and both expiratory compliance and Pel max were significantly decreased. In 13 of the 15 patients, the minimal (inspiratory) pleural pressure-volume curve was shifted so that the pressures generated by the inspiratory muscles were less negative than normal at any given lung volume. The decrease in Pel max was proportional to the alteration in muscle pressures. These findings indicate (1) that patients with mitral valve disease have compromised function of the inspiratory muscles, and (2) that this alteration is responsible for the low Pel max. Respiratory muscle weakness contributes to the restriction of lung volume in patients with pulmonary vascular congestion and is probably implicated in cardiac dyspnea.

Rib cage and abdominal restrictions have different effects on lung mechanics

The effects of a variety of restrictive procedures on lung mechanics were studied in eight healthy subjects. Rib cage restriction decreased total lung capacity (TLC) by 43% and significantly increased elastic recoil and maximum expiratory flow (MEF). Subsequent immersion of four subjects with rib cage restriction resulted in no further change in either parameter; shifts of blood volume did not reverse recoil changes during rib cage restriction. Abdominal restriction decreased TLC by 40% and increased MEF and elastic recoil, but recoil was increased significantly less than was the case with rib cage restriction. Further, at a given recoil pressure, MEF was less during rib cage restriction than during either abdominal restriction or no restriction. Measurements of the unevenness of inspired gas distribution by the single-breath nitrogen technique showed increased unevenness during rib cage restriction, which was significantly greater than that during abdominal restriction. We conclude that lung volume restriction induces changes in lung function, but the nature of these changes depends on how the restriction is applied and therefore cannot be ascribed to low lung volume breathing per se.

Analysis of lung volume restriction in patients with respiratory muscle weakness.

We investigated pulmonary mechanics in 25 patients, 9 to 55 years of age, with a variety of generalised neuromuscular diseases and variable degrees of respiratory muscle weakness. The average degree of inspiratory muscle force was 39.2% (range 8-83%) of predicted. The lung volume restriction far exceeded that expected for the degree of muscle weakness: the observed decrement in respiratory muscle force should, theoretically, decrease vital capacity to 78% of its control value, while the mean VC in our patients was only 50% of predicted. Analysis of lung pressure-volume curves indicated that the two principal causes of the disproportionate loss of lung volume were a reduction in lung distensibility probably caused by widespread microatelectasis, and a decrease in the outward pull of the chest wall. Because it reflects both direct (loss of distending pressure) and secondary (alterations in the elastic properties of the lungs and chest wall) effects of respiratory muscle weakness on lung function, we conclude that, in these patients, the vital capacity remains the most useful measurement to follow evolution of the disease process or response to treatment.

Paraquat Poisoning<subtitle>SERIEL STUDIES OF LUNG FUNCTION</subtitle>

Serial lung-function studies on six patients with paraquat poisoning are presented. Five patients died, two after lung transplantation; one survived, but it is highly improbable that he had developed ‘paraquat lung’. The usual pattern of change indicating progressive lung damage due to paraquat was restriction of lung volumes at an early stage, a falling arterial oxygen tension, and increasing alveolar to arterial oxygen tension gradient with the later development of a significant intrapulmonary shunt. However, these abnormalities are not specific for ‘paraquat lung’, and we stress that serial changes must be interpreted with attention to the clinical state of the patient before attributing them to damage by paraquat. We consider serial studies essential in patients poisoned with the liquid paraquat concentrate, so that early warning of lung involvement may be given. Early warning is necessary if a suitable donor for lung transplantation is to be found. Our experience and a review of the published cases indicate that the lung damage is progressive and we consider treatment by lung transplantation the only hope of success at the present time. The first patient to die following ingestion of the granular form of paraquat is described.

Respiratory function after lung homotransplantation with a ten-month survival in man.

In a patient surviving for 10 months after homotransplantation of the right lung, respiratory function was studied repeatedly before and after surgery. The results indicated an improvement in ventilatory function and gas exchange. The persistence of lung volume restriction and the appearance of an associated airway obstruction still severely limited the patient's postoperative function and his ability to perform physical effort. The effects of chronic infection and rejection on respiratory function were observed. An attempt was made to study possible effects of the denervation of the transplanted lung.

Talc pneumoconiosis: Significance of sublight microscopic mineral particles

Described herein is a patient with talc pneumoconiosis whose symptoms began fifteen years after heavy exposure and who progressed to massive fibrosis and death seven years later from cardiopulmonary insufficiency. Studies of pulmonary function showed restriction of lung volumes, loss of pulmonary compliance and increased venous admixture with moderate hypoxemia. Cardiac catheterization revealed pulmonary hypertension. Lung tissue was analyzed for mineral content by x-ray diffraction and electron microscopy, which established the presence of talc in the absence of histologic demonstration of mineral particles by conventional light microscopy. The significance of submicroscopic talc particles in the production of disease is demonstrated and related to similar findings in asbestosis.

Early lipoid pneumonia: Roentgenologic, anatomic and physiologic characteristics

The clinical variability of lipoid pneumonia is illustrated by three cases. The evolution of the disease has been demonstrated by serial roentgenograms. Rosettes and stippling are seen on the early roentgenograms and correspond to acinar consolidations in the experimental disease. When aspiration of oil continues, recent foci of disease are found together with areas of granuloma and fibrosis. That this disease can produce significant functional disturbance has been demonstrated in an asymptomatic patient with diffusely distributed lesions. Significant restriction of lung volume with poor gas exchange was present at a time when gross distortion of the lung had not taken place. Diagnostic methods for the demonstration of oil in the sputum are illustrated and briefly discussed; an alternative method utilizing fluorescence microscopy has been introduced.

Lung volume restriction as a ventilatory stimulus during breath holding.

Experiments on breath holding in man are presented which demonstrate that a restriction in the volume of gas in the lungs is an independent ventilatory stimulus which limits breath holding. This reflex stimulus interacts with the chemical stimuli from hypercapnia and hypoxia to determine the breaking point of breath holding. Previous work by others failed to demonstrate a relationship between lung volume restriction and hypoxia at the breaking point of breath holding with air. Experiments are presented which explain this and show that when hypoxia is present at the breaking point of breath holding, a time correction must be introduced to relate lung volume at the breaking point with the PaOO2 that existed several seconds before. When this is done the relationship between lung volume restriction and hypoxia becomes apparent. Submitted on March 2, 1959

Lung Volume Restriction, Hypoxia and Hypercapnia as Interrelated Respiratory Stimuli in Normal Man

<i>Lung Volume Restriction, Hypoxia and Hypercapnia as Interrelated Respiratory Stimuli in Normal Man</i>