**3. How Optoelectronic Plethysmography (OEP) can help answer the above questions**

*OEP allows us to demonstrate that dyspnea, chest wall dynamic hyperinflation, and rib cage distor‐*

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Georgiadou *et al*. [12] studied the effect of pulmonary rehabilitation on the regulation of to‐ tal chest wall and compartmental volumes during exercise in patients with COPD. Twenty patients undertook high-intensity exercise 3 days week-1 for 12 weeks. Before and after reha‐ bilitation, the changes in chest wall (cw) volumes at the end of expiration (Vcw,ee) and in‐ spiration (Vcw,ei) were computed by OEP during incremental exercise to the limit of tolerance (Wpeak). Rehabilitation significantly improved Wpeak In the post-rehabilitation peri‐ od and at identical work rates, significant reductions were observed in minute ventilation, breathing frequency and Vcw,ee and Vcw,ei. Inspiratory reserve volume was significantly increased. Volume reductions were attributed to significant changes in abdominal Vcw,ee and Vcw,ei. The improvement in Wpeak was similar in patients who progressively hyperin‐ flated during exercise and those who did not. The authors concluded that pulmonary reha‐ bilitation lowers chest wall volumes during exercise by decreasing the abdominal volumes.

*The study indicates that improvement in exercise capacity following rehabilitation is independent of*

Preliminary laboratory data indicate that OEP substantially assists in clarifying the link be‐ tween chest wall dynamic hyperinflation and breathlessness following pulmonary rehabili‐ tation. The volume of the chest wall and its compartments were evaluated in 14 patients by OEP during constant load cycle exercise before and after pulmonary rehabilitation. Prior to rehabilitation exercise increased end-expiratory chest wall volumes in eight patients, but de‐ flated the chest wall in six [11]. Rehabilitation increased exercise endurance. Relief in both dyspnea and leg effort at iso-time were associated with a decrease in ventilation regardless of whether patients hyperinflated or not. Also, the effect of pulmonary rehabilitation on rib

**Figure 2.** Effect of pulmonary rehabilitation (PRP) on phase angle and dyspnea in patients with and without ribcage

*tion are not interrelated phenomena.*

*the pattern of exercise-induced dynamic hyperinflation.*

distortion (RCD).

cage distortion and dyspnea were independent of each other (Fig 2).

The use of Optoelectronic Plethysmography (OEP) has allowed us to understand some of the mechanisms underlying the efficacy of rehabilitative treatment in patients with COPD. Rehabilitation interventions such as oxygen supplementation reduce ventilation and the rate of dynamic hyperinflation, but whether and to what extent reduction in lung volume con‐ tributes to dyspnea relief remains uncertain in these patients [13,14,27]. Innocenti Bruni *et al*. [11] tried to (i) determine whether and how hyperoxia would affect exercise dyspnea, chest wall dynamic hyperinflation, and rib cage distortion in normoxic COPD patients, and (ii) in‐ vestigate whether these phenomena are interrelated. It was speculated that they are not, based on the following observations: (i) significant dyspnea relief and improvement in exer‐ cise endurance can occur even in the absence of an effect on dynamic lung hyperinflation [27]; (ii) externally imposed expiratory flow limitation is associated with no rib cage distor‐ tion during strenuous incremental exercise, with indexes of hyperinflation not being corre‐ lated with dyspnea [16]; (iii) 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 [10]; (iv) a similar level of dyspnea is associated with differ‐ ent increases in chest wall dynamic hyperinflation at the limits of exercise tolerance [28]. The volume of chest wall (Vcw) and its compartments: the upper rib cage (Vrcp), lower rib cage (Vrca), and abdomen (Vab) were evaluated by OEP in 16 patients breathing either room air or 50% supplemental O2 at 75% of peak exercise in randomized order; rib cage distortion was assessed by measuring the phase angle shift between Vrcp and Vrca. Ten patients in‐ creased end-expiratory Vcw (Vcw,ee) on air. In 7 *hyperinflators* and 3 *non-hyperinflators* the lower rib cage paradoxed inward during inspiration with a phase angle of 63.4° (30.7) com‐ pared with a normal phase angle of 16.1° (2.3) recorded in patients without rib cage distor‐ tion. Dyspnea by a modified Borg scale from zero (no dyspnea), to ten (maximum dyspnea) averaged 8.2 and 9 at end-exercise on air in patients with and without rib cage distortion, respectively. At iso-time during exercise with oxygen, dyspnea relief was associated with a decrease in ventilation regardless of whether patients distorted the rib cage, dynamically hy‐ perinflated or deflated the chest wall. (Fig 1).

**Figure 1.** Oxygen supplementation decreses ventilation and dyspnea at isotime during constant load cycling exercise.

*OEP allows us to demonstrate that dyspnea, chest wall dynamic hyperinflation, and rib cage distor‐ tion are not interrelated phenomena.*

**3. How Optoelectronic Plethysmography (OEP) can help answer the**

The use of Optoelectronic Plethysmography (OEP) has allowed us to understand some of the mechanisms underlying the efficacy of rehabilitative treatment in patients with COPD. Rehabilitation interventions such as oxygen supplementation reduce ventilation and the rate of dynamic hyperinflation, but whether and to what extent reduction in lung volume con‐ tributes to dyspnea relief remains uncertain in these patients [13,14,27]. Innocenti Bruni *et al*. [11] tried to (i) determine whether and how hyperoxia would affect exercise dyspnea, chest wall dynamic hyperinflation, and rib cage distortion in normoxic COPD patients, and (ii) in‐ vestigate whether these phenomena are interrelated. It was speculated that they are not, based on the following observations: (i) significant dyspnea relief and improvement in exer‐ cise endurance can occur even in the absence of an effect on dynamic lung hyperinflation [27]; (ii) externally imposed expiratory flow limitation is associated with no rib cage distor‐ tion during strenuous incremental exercise, with indexes of hyperinflation not being corre‐ lated with dyspnea [16]; (iii) 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 [10]; (iv) a similar level of dyspnea is associated with differ‐ ent increases in chest wall dynamic hyperinflation at the limits of exercise tolerance [28]. The volume of chest wall (Vcw) and its compartments: the upper rib cage (Vrcp), lower rib cage (Vrca), and abdomen (Vab) were evaluated by OEP in 16 patients breathing either room air or 50% supplemental O2 at 75% of peak exercise in randomized order; rib cage distortion was assessed by measuring the phase angle shift between Vrcp and Vrca. Ten patients in‐ creased end-expiratory Vcw (Vcw,ee) on air. In 7 *hyperinflators* and 3 *non-hyperinflators* the lower rib cage paradoxed inward during inspiration with a phase angle of 63.4° (30.7) com‐ pared with a normal phase angle of 16.1° (2.3) recorded in patients without rib cage distor‐ tion. Dyspnea by a modified Borg scale from zero (no dyspnea), to ten (maximum dyspnea) averaged 8.2 and 9 at end-exercise on air in patients with and without rib cage distortion, respectively. At iso-time during exercise with oxygen, dyspnea relief was associated with a decrease in ventilation regardless of whether patients distorted the rib cage, dynamically hy‐

**Figure 1.** Oxygen supplementation decreses ventilation and dyspnea at isotime during constant load cycling exercise.

**above questions**

474 Optoelectronics - Advanced Materials and Devices

perinflated or deflated the chest wall. (Fig 1).

Georgiadou *et al*. [12] studied the effect of pulmonary rehabilitation on the regulation of to‐ tal chest wall and compartmental volumes during exercise in patients with COPD. Twenty patients undertook high-intensity exercise 3 days week-1 for 12 weeks. Before and after reha‐ bilitation, the changes in chest wall (cw) volumes at the end of expiration (Vcw,ee) and in‐ spiration (Vcw,ei) were computed by OEP during incremental exercise to the limit of tolerance (Wpeak). Rehabilitation significantly improved Wpeak In the post-rehabilitation peri‐ od and at identical work rates, significant reductions were observed in minute ventilation, breathing frequency and Vcw,ee and Vcw,ei. Inspiratory reserve volume was significantly increased. Volume reductions were attributed to significant changes in abdominal Vcw,ee and Vcw,ei. The improvement in Wpeak was similar in patients who progressively hyperin‐ flated during exercise and those who did not. The authors concluded that pulmonary reha‐ bilitation lowers chest wall volumes during exercise by decreasing the abdominal volumes.

#### *The study indicates that improvement in exercise capacity following rehabilitation is independent of the pattern of exercise-induced dynamic hyperinflation.*

Preliminary laboratory data indicate that OEP substantially assists in clarifying the link be‐ tween chest wall dynamic hyperinflation and breathlessness following pulmonary rehabili‐ tation. The volume of the chest wall and its compartments were evaluated in 14 patients by OEP during constant load cycle exercise before and after pulmonary rehabilitation. Prior to rehabilitation exercise increased end-expiratory chest wall volumes in eight patients, but de‐ flated the chest wall in six [11]. Rehabilitation increased exercise endurance. Relief in both dyspnea and leg effort at iso-time were associated with a decrease in ventilation regardless of whether patients hyperinflated or not. Also, the effect of pulmonary rehabilitation on rib cage distortion and dyspnea were independent of each other (Fig 2).

**Figure 2.** Effect of pulmonary rehabilitation (PRP) on phase angle and dyspnea in patients with and without ribcage distortion (RCD).

*These data suggest that pulmonary rehabilitation reduces dyspnea regardless of rib cage distortion and dynamic chest wall hyperinflation.*

**4. Comparing OEP with spirometric operational volumes**

OEP may provide complementary information on operational volumes to that provided by spirometry. Vogiatzis *et al.* [28] found a good relationship between changes in inspiratory capacity (ΔICpn) and changes in end expiratory chest wall volume (ΔVcw,ee). By contrast we have not found any significant relationship between the two measurements (Fig 3).

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**Figure 3.** Plots of change in inspiratory capacity (IC) vs change in end-expiratory-chest wall-volumes (CWee) from rest to end exercise, before (closed circles) and after (triangles) pulmonary rehabilitation. Continuous line is the identity

The decrease in ICpn is much greater than the increase in Vcw,ee in most patients. The rea‐ sons for this discrepancy are probably due to: i) error measurements with the pneumotacho‐ graph possibly linked to leakage and elevation of temperature in the system, and to spirometric drift resulting in spurious increments or decrements in volume measurements; ii) spirometry measures the volume of the gas entering or leaving the lungs at the mouth, while OEP measures the volume of the trunk which includes changes in gas volume, gas compression and blood volume shifts [16]. Arguably, activity of the abdominal muscles pro‐ ducing various amounts of gas compression and blood shifts might account for the preva‐ lence of one method over the other. For instance, high gas compression and blood shift would result in a greater decrease in Vcw,ee than an increase in the next ICpn manoeuvre [44]. It has been postulated that OEP would not detect 89% of the reduction in inspiratory

Pectus excavatum, the most common congenital chest wall deformity, is characterized by a depression of the anterior chest wall and sternum. Some patients will develop cardiopulmo‐

capacity measured with spirometry in some conditions [44].

**5. OEP and reparative deformity of the rib cage**

line.

Many COPD patients complain of severe dyspnea while performing simple daily-life activi‐ ties using their arms. The increased demand during simple arm elevation may play a role in the development of dyspnea and in the limitation that is frequently reported by these patients when performing activities involving their arms [29,30]. Unsupported arm exercise training (UAET) is increasingly recognized as an important component of pulmonary rehabilitation in these patients [31]. Although some studies have demonstrated improvement in unsupported arm exercise after UAET [32-34], suggesting that the test can be sensitive to changes in arm ex‐ ercise capacity, the impact of upper extremity training on arm exercise related-dyspnea and fa‐ tigue remains unclear [35-38] or undemonstrated [32,38-40]. Surprisingly, few studies [32,35,37-39] have investigated the effect of upper extremity training on ratings of perceived dyspnea by applying psychophysical methods, that is, the quantitative study of the relation‐ ship between stimuli and evoked conscious sensory responses. On this basis we have recently demonstrated that neither chest wall dynamic hyperinflation nor dyssynchronous breathing *per se* are the major contributors to dyspnea during unsupported arm exercise in COPD pa‐ tients [25]. Using the same approach we have recently tried to document the impact of arm training on arm exercise-related perceptions. The finding that before rehabilitation patients stop arm exercise namely because of arm symptoms, makes a case for the excessive effort felt by subjects being elicited by arm/torso afferent information (from the muscles performing the excessive effort) conveyed to the motor-sensory cortex [25].

These findings may explain why even a very small decrease in ventilatory demand, reflec‐ tive of a decrease in central motor output to ribcage/torso muscles, has a salutary effect on arm symptoms during arm training in patients with COPD [41].

OEP has also helped to clarify mechanisms by which some techniques of pulmonary rehabil‐ itation such as breathing retraining, namely "pursed lip breathing" (PLB), act in reducing the sensation of dyspnea. Bianchi *et al*. [42] hypothesized that the effect of PLB on breathless‐ ness relies on its deflationary effects on the chest wall. They found that patients exhibited a significant reduction in end-expiratory volume of the chest wall (Vcw,ee) and a significant increase in end-inspiratory volume of the chest wall in comparison with spontaneous breathing. In a stepwise multiple regression analysis, a decrease in end expiratory volume of the chest wall accounted for 27% of the variability in the Borg score.

#### *These data indicate that by lengthening the expiratory time, PLB deflates the chest wall and reduces dyspnea.*

In a further paper Bianchi *et al.* [43] identified the reasons why some patients benefit from PLB while others do not. The OEP analysis of chest wall kinematics shows why not all patients with COPD obtain symptom relief from PLB at rest. The most severely affected patients who de‐ flate the chest wall during volitional PLB reported improvement in their sensation of breath‐ lessness. This was not the case in the group who hyperinflated during PLB.
