End-expiratory Chest Wall Volume Research Articles

Thoracoabdominal Asynchrony Contributes to Exercise Limitation in Mild Asthmatic Subjects

This study aimed to better understand how subjects with stable asthma and without exercise-induced bronchoconstriction respond to mild exercise. Breathing pattern, chest wall compartmental and operational volumes, and thoracoabdominal asynchrony were assessed in 11 stable asthmatic subjects and 10 healthy subjects at rest and during exercise in a cycle-ergometer through optoelectronic plethysmography. Dyspnea and sensation of leg effort were assessed through Borg scale. During exercise, with similar minute ventilation, a significant lower chest wall tidal volume (p = 0.003) as well as a higher respiratory rate (p < 0.05) and rapid shallow breathing (p < 0.05) were observed in asthmatic when compared to healthy subjects. Asthmatic subjects exhibited a significantly lower inspiratory (p < 0.05) and expiratory times (p < 0.05). Intergroup analysis found a significant higher end-expiratory chest wall volume in asthmatic subjects, mainly due to a significant increase in volume of the pulmonary ribcage (RCp; 170 ml, p = 0.002), indicating dynamic hyperinflation (DH). Dyspnea and sensation of leg effort were both significantly greater (p < 0.0001) in asthmatic when compared to healthy subjects. In addition to a higher thoracoabdominal asynchrony found between RCp and abdominal (AB) (p < 0.005) compartments in asthmatic subjects, post-inspiratory action of the inspiratory ribcage and diaphragm muscles were observed through the higher expiratory paradox time of both RCp (p < 0.0001) and AB (p = 0.0002), respectively. Our data suggest that a different breathing pattern is adopted by asthmatic subjects without exercise-induced bronchoconstriction during mild exercise and that this feature, associated with DH and thoracoabdominal asynchrony, contributes significantly to exercise limitation.

Effects of positive expiratory pressure on chest wall volumes in subjects with stroke compared to healthy controls: a case–control study

BackgroundAlterations in respiratory system kinematics in stroke lead to restrictive pattern associated with decreased lung volumes. Chest physical therapy, such as positive expiratory pressure, may be useful in the treatment of these patients;however, the optimum intensity to promote volume and motion changes of the chest wall remains unclear. ObjectiveTo assess the effect of different intensities of positive expiratory pressure on chest wall kinematics in subjects with stroke compared to healthy controls. Methods16 subjects with chronic stroke and 16 healthy controls matched for age, gender, and body mass index were recruited. Chest wall volumes were assessed using optoelectronic plethysmography during quiet breathing, 5 minutes,and recovery. Three different intensities of positive expiratory pressure (10, 15, and 20cmH2O) were administered in a random order with a 30 minutes rest interval between intensities. ResultsDuring positive expiratory pressure, tidal chest wall expansion increased in both groups compared to quiet breathing; however, this increase was not significant in the subjects with stroke (0.41 vs. 1.32L, 0.56 vs. 1.54L, 0.52 vs. 1.8L, at 10, 15, 20cmH2O positive expiratory pressure, for stroke and control groups; p<0.001). End-expiratory chest wall volume decreased in controls, mainly due to the abdomen, and increased in the stroke group, mainly due the pulmonary rib cage. ConclusionPositive expiratory pressure administration facilitates acute lung expansion of the chest wall and its compartments in restricted subjects with stroke. Positive expiratory pressure intensities above 10cmH2O should be used with caution as the increase in end-expiratory volume led to hyperinflation in subjects with stroke.

Limitation in tidal volume expansion partially determines the intensity of physical activity in COPD.

In patients with chronic obstructive pulmonary disease (COPD), reduced levels of daily physical activity are associated with the degree of impairment in lung, peripheral muscle, and central hemodynamic function. There is, however, limited evidence as to whether limitations in tidal volume expansion also, importantly, determine daily physical activity levels in COPD. Eighteen consecutive patients with COPD [9 active (forced expiratory volume in 1 s, FEV1: 1.59 ± 0.64 l) with an average daily movement intensity >1.88 m/s(2) and 9 less active patients (FEV1: 1.16 ± 0.41 l) with an average intensity <1.88 m/s(2)] underwent a 4-min treadmill test at a constant speed corresponding to each individual patient's average movement intensity, captured by a triaxial accelerometer during a preceding 7-day period. When chest wall volumes, captured by optoelectronic plethysmography, were expressed relative to comparable levels of minute ventilation (ranging between 14.5 ± 4.3 to 33.5 ± 4.4 l/min), active patients differed from the less active ones in terms of the lower increase in end-expiratory chest wall volume (by 0.15 ± 0.17 vs. 0.45 ± 0.21 l), the greater expansion in tidal volume (by 1.76 ± 0.58 vs. 1.36 ± 0.24 l), and the larger inspiratory reserve chest wall volume (IRVcw: by 0.81 ± 0.25 vs. 0.39 ± 0.27 l). IRVcw (r(2) = 0.420), expiratory flow (r(2) change = 0.174), and Borg dyspnea score (r(2) change = 0.123) emerged as the best contributors, accounting for 71.7% of the explained variance in daily movement intensity. Patients with COPD exhibiting greater ability to expand tidal volume and to maintain adequate inspiratory reserve volume tend to be more physically active. Thus interventions aiming at mitigating restrictions on operational chest wall volumes are expected to enhance daily physical activity levels in COPD.

Assessment of the acute effects of different PEP levels on respiratory pattern and operational volumes in patients with Parkinson's disease

The aim of the study was to determine the acute effects of positive expiratory pressure (PEP) on breathing pattern, operational volumes and shortening velocity of respiratory muscles on patients with Parkinson's disease. It was evaluated 15 patients and healthy controls, by optoelectronic plethysmography, using PEP in three different levels (10, 15 and 20cmH2O). Breathing pattern changed in both groups. Parkinson group increased tidal volume in all PEP levels (p<0.001), but with lower values compared to control. End-inspiratory chest wall volume increased in the Parkinson group at all PEP levels (p<0.001), end-expiratory chest wall volume show a slightly increase when we compared QB to all PEP levels in Parkinson's. There was an intergroup difference in the index of shortening velocity of abdominal, diaphragm and inspiratory muscles of the rib cage at all PEP levels (p<0.01). We conclude that Parkinson's disease promotes important alterations in different breathing pattern components and PEP has significant effects on these alterations.

Influence of Tracheal Obstruction on the Efficacy of Superimposed High-frequency Jet Ventilation and Single-frequency Jet Ventilation.

Both superimposed high-frequency jet ventilation (SHFJV) and single-frequency (high-frequency) jet ventilation (HFJV) have been used with success for airway surgery, but SHFJV has been found to provide higher lung volumes and better gas exchange than HFJV in unobstructed airways. The authors systematically compared the ventilation efficacy of SHFJV and HFJV at different ventilation frequencies in a model of tracheal obstruction and describe the frequency and obstruction dependence of SHFJV efficacy. Ten anesthetized animals (weight 25 to 31.5 kg) were alternately ventilated with SHFJV and HFJV at a set of different fHF from 50 to 600 min. Obstruction was created by insertion of interchangeable stents with ID 2 to 8 mm into the trachea. Chest wall volume was measured using optoelectronic plethysmography, airway pressures were recorded, and blood gases were analyzed repeatedly. SHFJV provided greater than 1.6 times higher end-expiratory chest wall volume than HFJV, and tidal volume (VT) was always greater than 200 ml with SHFJV. Increase of fHF from 50 to 600 min during HFJV resulted in a more than 30-fold VT decrease from 112 ml (97 to 130 ml) to negligible values and resulted in severe hypoxia and hypercapnia. During SHFJV, stent ID reduction from 8 to 2 mm increased end-expiratory chest wall volume by up to 3 times from approximately 100 to 300 ml and decreased VT by up to 4.2 times from approximately 470 to 110 ml. Oxygenation and ventilation were acceptable for 4 mm ID or more, but hypercapnia occurred with the 2 mm stent. In this in vivo porcine model of variable severe tracheal stenosis, SHFJV effectively increased lung volumes and maintained gas exchange and may be advantageous in severe airway obstruction.

Heliox increases quadriceps muscle oxygen delivery during exercise in COPD patients with and without dynamic hyperinflation

Some reports suggest that heliox breathing during exercise may improve peripheral muscle oxygen availability in patients with chronic obstructive pulmonary disease (COPD). Besides COPD patients who dynamically hyperinflate during exercise (hyperinflators), there are patients who do not hyperinflate (non-hyperinflators). As heliox breathing may differently affect cardiac output in hyperinflators (by increasing preload and decreasing afterload of both ventricles) and non-hyperinflators (by increasing venous return) during exercise, it was reasoned that heliox administration would improve peripheral muscle oxygen delivery possibly by different mechanisms in those two COPD categories. Chest wall volume and respiratory muscle activity were determined during constant-load exercise at 75% peak capacity to exhaustion, while breathing room air or normoxic heliox in 17 COPD patients: 9 hyperinflators (forced expiratory volume in 1 s = 39 ± 5% predicted), and 8 non-hyperinflators (forced expiratory volume in 1 s = 48 ± 5% predicted). Quadriceps muscle blood flow was measured by near-infrared spectroscopy using indocyanine green dye. Hyperinflators and non-hyperinflators demonstrated comparable improvements in endurance time during heliox (231 ± 23 and 257 ± 28 s, respectively). At exhaustion in room air, expiratory muscle activity (expressed by peak-expiratory gastric pressure) was lower in hyperinflators than in non-hyperinflators. In hyperinflators, heliox reduced end-expiratory chest wall volume and diaphragmatic activity, and increased arterial oxygen content (by 17.8 ± 2.5 ml/l), whereas, in non-hyperinflators, heliox reduced peak-expiratory gastric pressure and increased systemic vascular conductance (by 11.0 ± 2.8 ml·min(-1)·mmHg(-1)). Quadriceps muscle blood flow and oxygen delivery significantly improved during heliox compared with room air by a comparable magnitude (in hyperinflators by 6.1 ± 1.3 ml·min(-1)·100 g(-1) and 1.3 ± 0.3 ml O(2)·min(-1)·100 g(-1), and in non-hyperinflators by 7.2 ± 1.6 ml·min(-1)·100 g(-1) and 1.6 ± 0.3 ml O(2)·min(-1)·100 g(-1), respectively). Despite similar increase in locomotor muscle oxygen delivery with heliox in both groups, the mechanisms of such improvements were different: 1) in hyperinflators, heliox increased arterial oxygen content and quadriceps blood flow at similar cardiac output, whereas 2) in non-hyperinflators, heliox improved central hemodynamics and increased systemic vascular conductance and quadriceps blood flow at similar arterial oxygen content.

Dyspnea, Chest Wall Hyperinflation, and Rib Cage Distortion in Exercising Patients with Chronic Obstructive Pulmonary Disease

Whether dyspnea, chest wall dynamic hyperinflation, and abnormalities of rib cage motion are interrelated phenomena has not been systematically evaluated in patients with chronic obstructive pulmonary disease (COPD). Our hypothesis that they are not interrelated was based on the following observations: (i) externally imposed expiratory flow limitation is associated with no rib cage distortion during strenuous incremental exercise, with indexes of hyperinflation not being correlated with dyspnea, and (ii) end-expiratory chest wall volume may either increase or decrease during exercise in patients with COPD, with those who hyperinflate being as breathless as those who do not. Sixteen patients breathed either room air or 50% supplemental O2 at 75% of peak exercise in randomized order. We evaluated the volume of chest wall (V(cw)) and its compartments: the upper rib cage (V(rcp)), lower rib cage (V(rca)), and abdomen (V(ab)) using optoelectronic plethysmography; rib cage distortion was assessed by measuring the phase angle shift between V(rcp) and V(rca). Ten patients increased end-expiratory V(cw) (V(cw,ee)) on air. In seven hyperinflators and three non-hyperinflators, the lower rib cage paradoxed inward during inspiration with a phase angle of 63.4° ± 30.7° compared with a normal phase angle of 16.1° ± 2.3° recorded in patients without rib cage distortion. Dyspnea (by Borg scale) averaged 8.2 and 9 at the end of exercise on air in patients with and without rib cage distortion, respectively. At iso-time during exercise with oxygen, decreased dyspnea was associated with a decrease in ventilation regardless of whether patients distorted the rib cage, dynamically hyperinflated, or deflated the chest wall. Dyspnea, chest wall dynamic hyperinflation, and rib cage distortion are not interrelated phenomena.

Comparison of superimposed high-frequency jet ventilation with conventional jet ventilation for laryngeal surgery

New ventilators have simplified the use of supraglottic superimposed high-frequency jet ventilation (SHFJV(SG)), but it has not been systematically compared with other modes of jet ventilation (JV) in humans. We sought to investigate whether SHFJV(SG) would provide more effective ventilation compared with single-frequency JV techniques. A total of 16 patients undergoing minor laryngeal surgery under general anaesthesia were included. In each patient, four different JV techniques were applied in random order for 10-min periods: SHFJV(SG), supraglottic normal frequency (NFJV(SG)), supraglottic high frequency (HFJV(SG)), and infraglottic high-frequency jet ventilation (HFJV(IG)). Chest wall volume variations were continuously measured with opto-electronic plethysmography (OEP), intratracheal pressure was recorded and blood gases were measured. Chest wall volumes were normalized to NFJV(SG) end-expiratory level. The increase in end-expiratory chest wall volume (EEV(CW)) was 239 (196) ml during SHFJV(SG) (P<0.05 compared with NFJV(SG)). EEV(CW) was 148 (145) and 44 (106) ml during HFJV(SG) and HFJV(IG), respectively (P<0.05 compared with SHFJV(SG)). Tidal volume (V(T)) during SHFJV(SG) was 269 (149) ml. V(T) was 229 (169) ml (P=1.00 compared with SHFJV(SG)), 145 (50) ml (P<0.05), and 110 (33) ml (P<0.01) during NFJV(SG), HFJV(SG), and HFJV(IG), respectively. Intratracheal pressures corresponded well to changes in both EEV(CW) and V(T). All JV modes resulted in adequate oxygenation. However, was lowest during HFJV(SG) [4.3 (1.3) kPa; P<0.01 compared with SHFJV(SG)]. SHFJV(SG) was associated with increased EEV(CW) and V(T) compared with the three other investigated JV modes. All four modes provided adequate ventilation and oxygenation, and thus can be used for uncomplicated laryngeal surgery in healthy patients with limited airway obstruction.

Effects of propofol anaesthesia on thoraco-abdominal volume variations during spontaneous breathing and mechanical ventilation

Anaesthesia based on inhalational agents has profound effects on chest wall configuration and breathing pattern. The effects of propofol are less well characterised. The aim of the current study was to evaluate the effects of propofol anaesthesia on chest wall motion during spontaneous breathing and positive pressure ventilation. We studied 16 subjects undergoing elective surgery requiring general anaesthesia. Chest wall volumes were continuously monitored by opto-electronic plethysmography during quiet breathing (QB) in the conscious state, induction of anaesthesia, spontaneous breathing during anaesthesia (SB), pressure support ventilation (PSV) and pressure control ventilation (PCV) after muscle paralysis. The total chest wall volume decreased by 0.41 ± 0.08 l immediately after induction by equal reductions in the rib cage and abdominal volumes. An increase in the rib cage volume was then seen, resulting in total chest wall volumes 0.26 ± 0.09, 0.24 ± 0.10, 0.22 ± 0.10 l lower than baseline, during SB, PSV and PCV, respectively. During QB, rib cage volume displacement corresponded to 34.2 ± 5.3% of the tidal volume. During SB, PSV and PCV, this increased to 42.2 ± 4.9%, 48.2 ± 3.6% and 46.3 ± 3.2%, respectively, with a corresponding decrease in the abdominal contribution. Breathing was initiated by the rib cage muscles during SB. Propofol anaesthesia decreases end-expiratory chest wall volume, with a more pronounced effect on the diaphragm than on the rib cage muscles, which initiate breathing after apnoea.

Paradoxical movement of the lower ribcage at rest and during exercise in COPD patients

Paradoxical inward displacement of the costal margin during inspiration is observed in many chronic obstructive pulmonary disease patients at rest but its importance is unclear. The current authors studied 20 patients (forced expiratory volume in one second 32.6+/-11.7, functional residual capacity 186+/-32% predicted) and 10 healthy controls at rest and during symptom-limited incremental exercise. With optoelectronic plethysmography, the phase shift between pulmonary and abdominal ribcage volumes and the percentage of inspiratory time the ribcage compartments moved in opposite directions were quantified, using control data to define the normal range of movement. Eight patients showed lower ribcage inspiratory paradox at rest (P+), while 12 patients did not (P-). This was unrelated to resting lung function or exercise tolerance. Total end-expiratory chest wall volume (EEV(cw)) increased immediately when exercise began in P+ patients, but later in exercise in P- patients. This difference in EEV(cw) was mainly due to a greater increase of end-expiratory pulmonary ribcage volume in P+ patients. During exercise, dyspnoea increased similarly in the two groups, while leg effort increased more markedly in the patients without paradox. In conclusion, lower ribcage paradox at rest is reproducible and associated with early-onset hyperinflation of the chest wall and predominant dyspnoea at end-exercise. When paradox is absent, the sense of leg effort becomes a more important symptom limiting 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.

Acute effects of thixotropy conditioning of inspiratory muscles on end-expiratory chest wall volume

Acute effects of thixotropy conditioning of inspiratory muscles on end-expiratory chest wall volume

Patterns of chest wall kinematics during volitional pursed-lip breathing in COPD at rest

Analysis of chest wall kinematics can contribute to identifying the reasons why some patients benefit from pursed-lip breathing (PLB). We evaluated the displacement of the chest wall and its compartments, the rib cage and abdomen, by optoelectronic plethysmography (OEP), during supervised PLB maneuver in 30 patients with mild to severe chronic obstructive pulmonary disease (COPD). OEP showed two different patterns. A first pattern characterized the 19 most severely obstructed and hyperinflated patients in whom PLB decreased end-expiratory volumes of the chest wall and abdomen, and increased end-inspiratory volumes of the chest wall and rib cage. Deflation of the abdomen and inflation of the rib cage contributed to increasing tidal volume of the chest wall. The second pattern characterized 11 patients in whom, compared to the former group, PLB resulted in the following: (i) increased end-expiratory volume of the rib cage and chest wall, (ii) greater increase in end-inspiratory volume of the rib cage and abdomen, and (iii) lower tidal volume of the chest wall. In the patients as a whole changes in end-expiratory chest wall volume were related to change in Borg score (r(2)=0.5, p<0.00002). OEP helps identifying the reason why patients with COPD may benefit from PLB at rest.

Acute effects of thixotropy conditioning of inspiratory muscles on end-expiratory chest wall and lung volumes in normal humans

Thixotropy conditioning of inspiratory muscles consisting of maximal inspiratory effort performed at an inflated lung volume is followed by an increase in end-expiratory position of the rib cage in normal human subjects. When performed at a deflated lung volume, conditioning is followed by a reduction in end-expiratory position. The present study was performed to determine whether changes in end-expiratory chest wall and lung volumes occur after thixotropy conditioning. We first examined the acute effects of conditioning on chest wall volume during subsequent five-breath cycles using respiratory inductive plethysmography (n = 8). End-expiratory chest wall volume increased after conditioning at an inflated lung volume (P < 0.05), which was attained mainly by rib cage movements. Conditioning at a deflated lung volume was followed by reductions in end-expiratory chest wall volume, which was explained by rib cage and abdominal volume changes (P < 0.05). End-expiratory esophageal pressure decreased and increased after conditioning at inflated and deflated lung volumes, respectively (n = 3). These changes in end-expiratory volumes and esophageal pressure were greatest for the first breath after conditioning. We also found that an increase in spirometrically determined inspiratory capacity (n = 13) was maintained for 3 min after conditioning at a deflated lung volume, and a decrease for 1 min after conditioning at an inflated lung volume. Helium-dilution end-expiratory lung volume increased and decreased after conditioning at inflated and deflated lung volumes, respectively (both P < 0.05; n = 11). These results suggest that thixotropy conditioning changes end-expiratory volume of the chest wall and lung in normal human subjects.

Chest Wall Motion after Thixotropy Conditioning of Inspiratory Muscles in Healthy Humans

Inspiratory muscle conditioning at a lower or higher lung volume based on the principles of muscle thixotropy causes acute changes in end-expiratory chest wall and lung volumes. The present study aimed to demonstrate the time course of effects of this conditioning on both end-expiratory chest wall volume and thoracoabdominal synchrony. We measured chest wall motion with respiratory induction plethysmography at 0.5, 1, 2, 3, and 6 min after conditioning at three different lung volumes in 15 healthy men. After conditioning at total lung capacity - 20% inspiratory capacity, increases in end-expiratory chest wall volume were significant at 0.5, 1, and 2 min (P < 0.05), being most obvious at 0.5 min (Delta 0.24 +/- 0.20 liter). After conditioning at residual volume, reductions in end-expiratory chest wall volume were significant at any time point (P < 0.05), being most obvious at 0.5 min (Delta 0.16 +/- 0.08 liter). Conditioning at functional residual capacity had little effect on the volume. Spirometric inspiratory capacity at 6 min after conditioning at residual volume (2.68 +/- 0.35 liter) was higher than the baseline value (2.53 +/- 0.31 liter, P < 0.05). Reductions in the phase angle, quantified by the Konno-Mead diagram, occurred after conditioning at residual volume at any time point (P < 0.05), being most obvious at 2 min (Delta 3.47 +/- 3.02 degrees). In conclusion, there is a 6-min time course of changes in end-expiratory chest wall volume after conditioning. More synchronous motion between the rib cage and abdomen occurs after conditioning at residual volume.