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Biomedical subjects

G Misuri

Publications and source records attributed to G Misuri.

25 records · Page 2Linked to original sources
PubMed1996

Breathing pattern and carbon dioxide retention in severe chronic obstructive pulmonary disease.

BACKGROUND: The factors leading to chronic hypercapnia and rapid shallow breathing in patients with severe chronic obstructive pulmonary disease (COPD) are not completely understood. In this study the interrelations between chronic carbon dioxide retention, breathing pattern, dyspnoea, and the pressure required for breathing relative to inspiratory muscle strength in stable COPD patients with severe airflow obstruction were studied. METHODS: Thirty patients with COPD in a clinically stable condition with forced expiratory volume in one second (FEV1) of < 1 litre were studied. In each patient the following parameters were assessed: (1) dyspnoea scale rating, (2) inspiratory muscle strength by measuring minimal pleural pressure (PPLmin), and (3) tidal volume (VT), flow, pleural pressure swing (PPLsw), total lung resistance (RL), dynamic lung elastance (ELdyn), and positive end expiratory alveolar pressure (PEEPi) during resting breathing. RESULTS: Arterial carbon dioxide tension (PaCO2) related directly to RL/PPLmin, and ELdyn/PPLmin, and inversely to VT and PPLmin. There was no relationship between PaCO2 and functional residual capacity (FRC), total lung capacity (TLC), or minute ventilation. PEEPi was similar in eucapnic and hypercapnic patients. Expressing PaCO2 as a combined function of VT and PPLmin (stepwise multiple regression analysis) explained 71% of the variance in PaCO2. Tidal volume was directly related to inspiratory time (TI), and TI was inversely related to the pressure required for breathing relative to inspiratory muscle strength (PPLsw, %PPLmin). There was an association between the severity of dyspnoea and both the increase in PPLsw (%PPLmin) and the shortening in TI. CONCLUSIONS: The results indicate that, in stable patients with COPD with severe airflow obstruction, hypercapnia is associated with shallow breathing and inspiratory muscle weakness, and rapid and shallow breathing appears to be linked to both a marked increase in the pressure required for breathing relative to inspiratory muscle strength and to the severity of the breathlessness.

Aged↗
PubMed1995

Mechanical loading and control of breathing in patients with severe chronic obstructive pulmonary disease.

BACKGROUND: High neural drive to the respiratory muscles and rapid and shallow breathing are frequently observed in patients with chronic obstructive pulmonary disease (COPD), and both mechanical and chemical factors are thought to play a part. However, the interrelation between these factors and the modifications in the control of breathing are not clearly defined. The effects of an acute decrease in mechanical load by the administration of a high dose of a beta 2 agonist were studied. METHODS: Nine spontaneously breathing patients with severe COPD took part in the study. Criteria for entry were FEV1 of < 40% of predicted and an improvement in FEV1 of < 200 ml after inhalation of 400 micrograms fenoterol. The following parameters were measured: lung volumes, tidal volume (VT), respiratory frequency (Rf), maximal pleural pressure during a sniff manoeuvre (PPLmax), pleural pressure swings (PPLsw), lung resistance (RL), RL/PPLmax ratio, and surface electromyographic activity (EMG) of diaphragm (EDI) and parasternal (EPS) muscles. Arterial oxygen saturation (SaO2), end tidal carbon dioxide pressure (PETCO2), and the electrocardiogram were also monitored. Each variable was measured under control conditions and 20 and 40 minutes after the inhalation of 800 micrograms fenoterol. In five patients the effects of placebo were also studied. RESULTS: Fenoterol resulted in an increase in FEV1 and decrease in FRC. SaO2 did not change, while PETCO2 fell and heart rate increased. The VT increased, and Rf decreased, PPLsw fell and PPLmax increased, thus the PPLsw/PPLmax ratio fell. Both RL and RL/PPLmax also fell, and a substantial decrease in EDI and EPS was observed. Changes in PPLsw were related to changes in FEV1 and RL. Changes in VT and Rf, and EDI/TI and EPS/TI were also related to changes in PPLsw and RL/PPLmax ratio, but not to changes in FEV1. No variation was observed with placebo. CONCLUSIONS: In patients with severe COPD a decrease in inspiratory muscle loading relative to the maximal available strength, as expressed by the RL/PPLmax and PPLsw/PPLmax ratios, appears to be the major determinant of changes in breathing pattern and inspiratory muscle activity (decrease in EMG).

Aged↗
PubMed1995

Control of breathing in a subset of patients with systemic lupus erythematosus.

BACKGROUND: Inspiratory muscle weakness and abnormalities in breathing pattern and in respiratory drive have been reported in patients with multisystem disorders. In patients with systemic lupus erythematosus (SLE), data on respiratory muscle strength and control of breathing are scarce. METHODS: We studied a subset of nine female patients with SLE with no major findings of cardiovascular, renal, or neurologic involvement, and with a normal routine chest radiograph. An age- and sex-matched normal group was also studied as a control. We evaluated lung volumes, diffusing lung properties (TLCO, TLCO/VA), maximal inspiratory (MIP) and expiratory (MEP) pressures, end-tidal carbon dioxide tension (PCO2), and breathing pattern: ventilation (VE), tidal volume (VT), inspiratory time (TI), and respiratory frequency (Rf). Neural respiratory drive, assessed in terms of mean inspiratory flow (VT/TI), mouth occlusion pressure (P0.1), and surface electromyographic activity of the diaphragm (Edi) and intercostal (Eps) muscles was also evaluated. RESULTS: As a whole, patients exhibited mild decrease in MIP; vital capacity was slightly reduced in two patients and TLCO/VA was moderately reduced in three. During a hypercapnic rebreathing test, delta VT/delta PCO2 was lower, delta P0.1/delta PCO2 was normal, while delta Edi/delta PCO2 and delta Eps/delta PCO2 were higher in patients compared with normal control subjects. delta VT/delta PCO2 significantly related to MIP. At 60 mm Hg of PCO2 patients maintained the rapid and shallow pattern of breathing (RSB) exhibited during room-air breathing: lower VT, shorter TI, and greater Rf, with VE, VT/TI, and Edi being greater compared with the normal control subjects. CONCLUSIONS: These data seem to indicate that in this SLE subset, mild decrease in respiratory muscle strength may accompany an increased respiratory drive, and contribute to a qualitatively abnormal ventilatory response (RSB) to carbon dioxide stimulation.

Adult↗
PubMed1995

Effects of the iron lung on respiratory function in chronic hypercapnic COPD patients.

Whether or not short-term negative pressure ventilation (NPV) improves respiratory function by decreasing the drive to the respiratory muscles in hypercapnic chronic obstructive pulmonary disease (COPD) patients remains to be defined. In six severely obstructed hypercapnic COPD patients (Group A) with grade IV dyspnoea (modified Medical Research Council (MRC) dyspnoea scale), we evaluated pulmonary volumes, arterial blood gases, the pattern of breathing (tidal volume (VT) and respiratory frequency (Rf)) and the neuromuscular respiratory drive (NMRD), before and immediately after a 7 day period with the iron lung (IL). NMRD was assessed by expressing mouth occlusion pressure (P0.1) recorded during quiet breathing as a percentage of maximal P0.1 recorded during exogenous CO2 stimulation (P0.1 max,CO2). A group of six hypercapnic, less dyspnoeic (grade II to III) COPD patients (Group B), with similar mechanical characteristics, and another less obstructed historically normocapnic control group (Group C) were also considered. Before IL, in Group A VT was lower than in C, and P0.1 (%P0.1 max,CO2) was greater than in Group B and C. After a 7 day period with IL, VT increased, Rf decreased, and arterial blood gases and dyspnoea grade improved; P0.1 (%P0.1 max,CO2) significantly decreased remaining, however, greater than in Group C. In Group A the time course of arterial carbon dioxide tension (Pa,CO2) and P0.1 (%P0.1 max,CO2) were significantly related to each other. These data seem to indicate that IL is effective in improving respiratory function and symptoms in chronic hypercapnic severely dyspnoeic COPD patients. The observation that these effects were associated with a decrease in NMRD reflects an improved efficiency of the respiratory system. After IL, respiratory function in Group A was similar or even better than that in Group B. This study also considers the possibility of putting severely dyspnoeic hypercapnic COPD patients into an IL trial before starting a traditional rehabilitation programme.

Aged↗
PubMed1994

Aminophylline and respiratory muscle interaction in normal humans.

The effects of intravenous infusion of aminophylline on respiratory muscle interaction were examined in seven normal subjects breathing at rest. Rib cage (RC-Ap) and abdominal (AB-Ap) volume displacements, pleural (Ppl), gastric (Pg), and transdiaphragmatic (Pdi) pressure swings, and electromyographic activity of the diaphragm (Edi) and the parasternal (Eps) muscles were measured under control and during infusion of either aminophylline or placebo in a double-blind randomized manner. Compared with placebo, aminophylline induced an increase in ventilation (p < 0.01) that was mainly accounted for by an increase in tidal volume (p = 0.01). Aminophylline induced a significant and similar increase in RC-Ap and AB-Ap as associated with increased Ppl and Pg swings (p = 0.002, and p < 0.01, respectively). On the contrary, no changes in end-expiratory RC and AB volume and in Ppl and Pg at end-expiration were observed, indicating that expiratory muscles did not contribute to the increase in tidal volume. Edi and Eps increased significantly with aminophylline, whereas Pdi/Edi ratio remained unchanged. We conclude that in normal humans breathing at rest: (1) aminophylline increases ventilation, promoting larger tidal volume; (2) this effect is due to increased neural drive to inspiratory muscles; (3) aminophylline does not promote any appreciable expiratory muscle recruitment and distortion in the pattern of chest wall motion.

Adult↗
PubMedDate not supplied

Respiratory muscle overloading and dyspnoea during bronchoconstriction in asthma: protective effects of fenoterol.

Whether, and to what extent, beta 2-agonists protect against respiratory muscle overloading and breathlessness during bronchoconstriction remains to be defined in patients with asthma. In a double blind placebo-controlled study, 100 micrograms of fenoterol were administered to six stable asthmatics before a bronchial provocation test, performed by inhaling doubling concentrations of histamine from a Devilbiss 646 nebulizer. We recorded breathing pattern (tidal volume VT, inspiratory time TI, total time of the respiratory cycle TTOT), inspiratory capacity (IC), dynamic pleural pressure swing (Pplsw), total lung resistance (RL) and FEV1. VT was expressed both in actual values and as % of IC. Changes in VT (%IC) during histamine inhalation reflected changes in dynamic end-inspiratory lung volume (EILV). Pplsw was expressed as % of maximal (the most negative in sign) pleural pressure, obtained under control conditions during a sniff manoeuvre (Pplsn). Pplsw (%Pplsn) is an index of inspiratory muscle effort. The test ended when the concentration of histamine which caused a decrease in FEV1 of > or = 40% post-saline was reached. Dyspnoea rating was scored by a modified Borg scale. At the ultimate degree of bronchoconstriction (UDB) with histamine: (i) decrease in FEV1 was similar after placebo and fenoterol, while increase in RL was lower after fenoterol (P < 0.005); (ii) VT(%IC) increased less after fenoterol (P < 0.027); (iii) increases in Pplsw (%Pplsn) was lower after fenoterol (P < 0.001); (iv) delta Borg (from saline) was lower (P < 0.01) after fenoterol; (v) differences in delta Borg, from placebo to fenoterol, related to concurrent changes in VT(%IC) (r2 = 0.67). In conclusion, at UDB 100 micrograms of fenoterol produced a beneficial effect on the degree of inspiratory muscle loading and breathlessness, an effect greater than it would be expected from measuring FEV1 alone.

Adrenergic beta-Agonists↗