Barbara Lanini

Exercise training improves exertional dyspnea in patients with COPD: evidence of the role of mechanical factors.

BACKGROUND To our knowledge, no data have been reported on the effects of exercise training (EXT) on central respiratory motor output or neuromuscular coupling (NMC) of the ventilatory pump, and their potential association with exertional dyspnea. Accurate assessment of these important clinical outcomes is integral to effective management of breathlessness of patients with COPD. MATERIAL AND METHODS Twenty consecutive patients with stable moderate-to-severe COPD were tested at 6-week intervals at baseline, after a nonintervention control period (pre-EXT), and after EXT. Patients entered an outpatient pulmonary rehabilitation program involving regular exercise on a bicycle. Incremental symptom-limited exercise testing (1-min increments of 10 W) was performed on an electronically braked cycle ergometer. Oxygen uptake (O(2)), carbon dioxide output (CO(2)), minute ventilation (E), time, and volume components of the respiratory cycle and, in six patients, esophageal pressure swings (Pessw), both as actual values and as percentage of maximal (most negative in sign) esophageal pressure during sniff maneuver (Pessn), were measured continuously over the runs. Exertional dyspnea and leg effort were evaluated by administering a Borg scale. RESULTS Measurements at baseline and pre-EXT were similar. Significant increase in exercise capacity was found in response to EXT: (1) peak work rate (WR), O(2), CO(2), E, tidal volume (VT), and heart rate increased, while peak exertional dyspnea and leg effort did not significantly change; (2) exertional dyspnea/O(2) and exertional dyspnea/CO(2) decreased while E/O(2) and E/CO(2) remained unchanged. The slope of both exertional dyspnea and leg effort relative to E fell significantly after EXT; (3) at standardized WR, E, and CO(2), exertional dyspnea and leg effort decreased while inspiratory capacity (IC) increased. Decrease in E was accomplished primarily by decrease in respiratory rate (RR) and increase in both inspiratory time (TI) and expiratory time; VT slightly increased, while inspiratory drive (VT/TI) and duty cycle (TI/total time of the respiratory cycle) remained unchanged. The decrease in Pessw and the increase in VT were associated with lower exertional dyspnea after EXT; (4) at standardized E, VT, RR, and IC, Pessw and Pessw(%Pessn)/VT remained unchanged while exertional dyspnea and leg effort decreased with EXT. CONCLUSION In conclusion, increases in NMC, aerobic capacity, and tolerance to dyspnogenic stimuli and possibly breathing retraining are likely to contribute to the relief of both exertional dyspnea and leg effort after EXT.

Clinical InvestigationsCOPDExercise Training Improves Exertional Dyspnea in Patients With COPDa: Evidence of the Role of Mechanical Factors

BACKGROUND To our knowledge, no data have been reported on the effects of exercise training (EXT) on central respiratory motor output or neuromuscular coupling (NMC) of the ventilatory pump, and their potential association with exertional dyspnea. Accurate assessment of these important clinical outcomes is integral to effective management of breathlessness of patients with COPD. MATERIAL AND METHODS Twenty consecutive patients with stable moderate-to-severe COPD were tested at 6-week intervals at baseline, after a nonintervention control period (pre-EXT), and after EXT. Patients entered an outpatient pulmonary rehabilitation program involving regular exercise on a bicycle. Incremental symptom-limited exercise testing (1-min increments of 10 W) was performed on an electronically braked cycle ergometer. Oxygen uptake (O(2)), carbon dioxide output (CO(2)), minute ventilation (E), time, and volume components of the respiratory cycle and, in six patients, esophageal pressure swings (Pessw), both as actual values and as percentage of maximal (most negative in sign) esophageal pressure during sniff maneuver (Pessn), were measured continuously over the runs. Exertional dyspnea and leg effort were evaluated by administering a Borg scale. RESULTS Measurements at baseline and pre-EXT were similar. Significant increase in exercise capacity was found in response to EXT: (1) peak work rate (WR), O(2), CO(2), E, tidal volume (VT), and heart rate increased, while peak exertional dyspnea and leg effort did not significantly change; (2) exertional dyspnea/O(2) and exertional dyspnea/CO(2) decreased while E/O(2) and E/CO(2) remained unchanged. The slope of both exertional dyspnea and leg effort relative to E fell significantly after EXT; (3) at standardized WR, E, and CO(2), exertional dyspnea and leg effort decreased while inspiratory capacity (IC) increased. Decrease in E was accomplished primarily by decrease in respiratory rate (RR) and increase in both inspiratory time (TI) and expiratory time; VT slightly increased, while inspiratory drive (VT/TI) and duty cycle (TI/total time of the respiratory cycle) remained unchanged. The decrease in Pessw and the increase in VT were associated with lower exertional dyspnea after EXT; (4) at standardized E, VT, RR, and IC, Pessw and Pessw(%Pessn)/VT remained unchanged while exertional dyspnea and leg effort decreased with EXT. CONCLUSION In conclusion, increases in NMC, aerobic capacity, and tolerance to dyspnogenic stimuli and possibly breathing retraining are likely to contribute to the relief of both exertional dyspnea and leg effort after EXT.

Chest wall kinematics and respiratory muscle action in ankylosing spondylitis patients

No direct measurements of the pressures produced by the ribcage muscles, the diaphragm and the abdominal muscles during hyperventilation have been reported in patients with ankylosing spondylitis. Based on recent evidence indicating that abdominal muscles are important contributors to stimulation of ventilation, it was hypothesised that, in ankylosing spondylitis patients with limited ribcage expansion, a respiratory centre strategy to help the diaphragm function may involve coordinated action of this muscle with abdominal muscles. In order to validate this hypothesis, the chest wall response to a hypercapnic/hyperoxic rebreathing test was assessed in six ankylosing spondylitis patients and seven controls by combined analysis of: 1) chest wall kinematics, using optoelectronic plethysmography, this system is accurate in partitioning chest wall expansion into the contributions of the ribcage and the abdomen; and 2) respiratory muscle pressures, oesophageal, gastric and transdiaphragmatic (Pdi); the pressure/volume relaxation characteristics of both the ribcage and the abdomen allowed assessment of the peak pressure of both inspiratory and expiratory ribcage muscles, and of the abdominal muscles. During rebreathing, chest wall expansion increased to a similar extent in patients to that in controls; however, the abdominal component increased more and the ribcage component less in patients. Peak inspiratory ribcage, but not abdominal, muscle pressure was significantly lower in patients than in controls. End-inspiratory Pdi increased similarly in both groups, whereas inspiratory swings in Pdi increased significantly only in patients. No pressure or volume signals correlated with disease severity. The diaphragm and abdominal muscles help to expand the chest wall in ankylosing spondylitis patients, regardless of the severity of their disease. This finding supports the starting hypothesis that a coordinated response of respiratory muscle activity optimises the efficiency of the thoracoabdominal compartment in conditions of limited ribcage expansion.

Breathing pattern and kinematics in normal subjects during speech, singing and loud whispering

Aims:  We used for the first time a non‐invasive optoelectronic plethysmography to assess breathing movements and to provide a quantitative description of chest wall kinematics during phonation.

Chest wall kinematics, respiratory muscle action and dyspnoea during arm vs. leg exercise in humans

Aim:  We hypothesize that different patterns of chest wall (CW) kinematics and respiratory muscle coordination contribute to sensation of dyspnoea during unsupported arm exercise (UAE) and leg exercise (LE).

Chest wall kinematics and Hoover's sign

BACKGROUND No attempt has been made to quantify the observed rib cage distortion (Hoovers sign) in terms of volume displacement. We hypothesized that Hoovers sign and hyperinflation are independent quantities. METHODS Twenty obstructed stable patients were divided into two groups according to whether or not they exhibited Hoovers sign during clinical examination while breathing quietly. We evaluated the volumes of chest wall and its compartments: the upper rib cage, the lower rib cage and the abdomen, using optoelectronic plethysmography. RESULTS The volumes of upper rib cage, lower rib cage and abdomen as a percentage of absolute volume of the chest wall were similar in patients with and without Hoovers sign. In contrast, the tidal volume of the chest wall, upper rib cage, lower rib cage, their ratio and abdomen quantified Hoovers sign, but did not correlate with level of hyperinflation. CONCLUSIONS Rib cage distortion and hyperinflation appear to define independently the functional condition of these patients.

Chest wall kinematics and respiratory muscle coordinated action during hypercapnia in healthy males

The present study was designed to verify whether during hypercapnic stimulation, as we had previously found during exercise or walking, the partitioning of the respiratory motor output is equally distributed to the muscles of chest wall compartments to assist diaphragm function. We studied chest wall kinematics and respiratory muscle recruitment in seven healthy men during rebreathing of a hypercapnic-hyperoxic gas mixture (CO2 RT). Data were compared with those previously obtained during either cycling exercise or walking. The chest wall volume (Vcw), assessed by optoelectronic plethysmography (OEP), was modeled as the sum of the volumes of the lung-apposed rib cage (Vrc,p), diaphragm-apposed rib cage (Vrc,a) and abdomen (Vab). Esophageal (Pes), gastric (Pga) and transdiaphragmatic (Pdi=Pga−Pes) pressures were simultaneously recorded. Velocity of shortening (V′) and power (W′=PxV′) of the diaphragm (W′di), rib cage muscles (W′rcm) and abdominal muscles (W′abm) were also calculated. During CO2 RT the progressive increase in end-inspiratory Vcw resulted from an increase in both end-inspiratory Vrc,p and Vrc,a, while the progressive decrease in end-expiratory Vcw was entirely due to the decrease in end-expiratory Vab. The increase in Vrc,p was proportionally slightly greater than that in Vrc,a. The end-inspiratory increase and end-expiratory decrease in Vcw were accounted for by inspiratory rib cage (RCM,i) and abdominal (ABM) muscle recruitment, respectively. W′di, W′rcm and W′abm progressively increased. However, while most of W′di was expressed in terms of velocity of shortening, most of W′rcm and W′abm was expressed as force or pressure. A comparison of CO2 results with data obtained during exercise revealed: (1) a gradual vs. an immediate response, (2) a similar decrease in Vab,e and Pabm, (3) an apparent lack of any difference in ABM recruitment, (4) less gradual ABM relaxation, (5) no drop in Pdi but a similar Wdi change and decrease in pressure-to-velocity ratio of the diaphragm. We have found that in healthy humans: (1) the increased motor output with hypercapnia is equally distributed between RCM and ABM to minimize transdiaphragmatic pressure and (2) data on chest wall kinematics and respiratory muscle recruitment are only partly in line with those obtained during walking or cycling exercise.

Chest wall kinematics during voluntary cough in neuromuscular patients

Muscular diseases are characterized by progressive loss of muscle strength, resulting in cough ineffectiveness with its deleterious effects on the respiratory system. Assessment of cough effectiveness is therefore a prominent component of the clinical evaluation and respiratory care in these patients. Owing to uneven distribution of muscle weakness in neuromuscular patients, we hypothesized that forces acting on the chest wall may impact on the compartmental distribution of gas volume resulting in a decrease in cough effectiveness. Pulmonary volumes, respiratory muscle strength, peak cough flow and chest wall kinematics by optoelectronic plethysmography were studied in 8 patients and 12 healthy subjects as controls. Chest wall volume was modeled as the sum of volumes of the rib cage and abdomen. The plot of the volumes of upper to lower rib cage allowed assessment of rib cage distortion. Unlike controls, patients were unable to reduce end-expiratory chest wall volume, and exhibited greater rib cage distortion during cough. Peak cough flow was negatively correlated with rib cage distortion (the greater the former, the smaller the latter), but not with respiratory muscle strength. In conclusion, insufficient deflation of chest wall compartments and marked rib cage distortion resulted in cough ineffectiveness in these neuromuscular patients.

Chest wall kinematics and breathlessness during unsupported arm exercise in COPD patients

We hypothesised that chest wall displacement inappropriate to increased ventilation contributes to dyspnoea more than dynamic hyperinflation or dyssynchronous breathing during unsupported arm exercise (UAE) in COPD patients. We used optoelectronic plethysmography to evaluate operational volumes of chest wall compartments, the upper rib cage, lower rib cage and abdomen, at 80% of peak incremental exercise in 13 patients. The phase shift between the volumes of upper and lower rib cage (RC) was taken as an index of RC distortion. With UAE, no chest wall dynamic hyperinflation was found; sometimes the lower RC paradoxed inward while in other patients it was the upper RC. Phase shift did not correlate with dyspnoea (by Borg scale) at any time, and chest wall displacement was in proportion to increased ventilation. In conclusions neither chest wall dynamic hyperinflation nor dyssynchronous breathing per se were major contributors to dyspnoea. Unlike our prediction, chest wall expansion and ventilation were adequately coupled with each other.

Optoelectronic Plethysmography has Improved our Knowledge of Respiratory Physiology and Pathophysiology

It is well known that the methods actually used to track thoraco-abdominal volume displacement have several limitations. This review evaluates the clinical usefulness of measuring chest wall kinematics by optoelectronic plethysmography [OEP]. OEP provides direct measurements (both absolute and its variations) of the volume of the chest wall and its compartments, according to the model of Ward and Macklem, without requiring calibration or subject cooperation. The system is non invasive and does not require a mouthpiece or nose-clip which may modify the pattern of breathing, making the subject aware of his breathing. Also, the precise assessment of compartmental changes in chest wall volumes, combined with pressure measurements, provides a detailed description of the action and control of the different respiratory muscle groups and assessment of chest wall dynamics in a number of physiological and clinical experimental conditions.