Patterns of Chest Wall Kinematics During Volitional Pursed-Lip Breathing in COPD at Rest

ARTICLE IN PRESS

Respiratory Medicine (2007) 101, 1412–1418

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

Roberto Bianchi, Francesco Gigliotti, Isabella Romagnoli, Barbara Lanini, Carla Castellani, Barbara Binazzi, Loredana Stendardi, Michela Grazzini, Giorgio ScanoÃ

Fondazione Don C. Gnocchi (IRCCS), Via Imprunetana, 124, 50020 Pozzolatico, Firenze, Italy

Received 23 November 2006; accepted 29 January 2007 Available online 12 March 2007

KEYWORDS Summary Chronic obstructive Background: Analysis of chest wall kinematics can contribute to identifying the reasons pulmonary disease why some patients benefit from pursed-lip breathing (PLB). (COPD); Material and methods: We evaluated the displacement of the chest wall and its Rehabilitation; compartments, the rib cage and abdomen, by optoelectronic plethysmography (OEP), Chest wall; during supervised PLB maneuver in 30 patients with mild to severe chronic obstructive Dyspnea; pulmonary disease (COPD). Breathing exercises Results: 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 (r2 ¼ 0.5, po0.00002). Conclusions: OEP helps identifying the reason why patients with COPD may benefit from PLB at rest. & 2007 Elsevier Ltd. All rights reserved.

ÃCorresponding author. Tel.: +39 055 260 11; fax: +39 055 260 1272. E-mail address: [email protected] (G. Scano).

Thoracic kinematics and pursed lip breathing 1413

Introduction 0.8 0.8 0.7 7 7 Pursed-lip breathing (PLB) performed as nasal inspiration 7

followed by expiratory blowing against partially closed lips is MRC a breathing retraining strategy employed by patients with chronic obstructive pulmonary disease (COPD).1 Not all 10.5 2.9 10.5 2.9 patients, however, employ PLB, or report beneﬁting from it. 9.9 2.9 7 7 7 Some apply this technique spontaneously, whereas other 2 patients do not use it even when they are taught. PaO Studies on patients who naturally incorporate PLB into their breathing pattern may provide additional information 7.2 73.2 7.7 71.0 on whether changes in chest volume help identify the 6.4 76.9 2 7 7 reasons why PLB relieves dyspnea in patients with COPD. It 7 has been reported that the relief from dyspnea provided by PLB is related to its ability to promote a slower and deeper breathing.2,3 In contrast, an increase in tidal volume with 56 41.7 54 42.6 unchanged end-expiratory-lung-volume variably affects 36 40.2 7 7 7 0.004

dyspnea during exercise either by enhancing it or leaving o it unmodiﬁed.4 p An increased tidal volume, however, may be obtained in 20 156 19 177 two different ways: (i) by decreasing end-expiratory volume 16 119 7 7 7 of the abdomen and limiting the increase in end-inspiratory 0.02 o volume of both the rib cage and abdomen. This would limit p pressure production of rib cage muscles and the diaphragm 38 111 38 118 to a small fraction of their maximal pressure-generating 27 100 7 7 7 capacity, therefore, attenuating the sensation of dyspnea in 0.009

3,5,6 o

symptomatic patients ; (ii) in contrast, without the p abdominal contribution, the tidal volume of the chest wall is the result of a higher rib cage inspiratory muscle /VC FRC TLC RV PaCO 11 138 9 152 fractional pressure; this, conceivably, would not attenuate 12 115 1 5,6 0.005 7 7 7

the dyspnea. o FEV Thus, the question arises: do changes in operational chest p wall volumes help identify the reason for dyspnea relief with /VC: Tiffeneau ratio; FRC: functional residual capacity; RV: residual volume; MRC: Medical Research PLB in patients with COPD? 1 16 38 13 34 14 45 1 We hypothesized that an increase in tidal volume of the 0.002 7 7 7 o

chest wall promoted by PLB at the exclusive expense of tidal p volume of the rib cage would not be associated with dyspnea relief in COPD patients. 21 45 22 38 19 56 7 7 To assess whether the volume changes of chest wall can 7 help identify the reason why some patients beneﬁt from PLB while others do not, we applied a recently well-developed technique based on optoelectronic plethysmography (OEP) 15 87 12 84 17 92 0.05 7 7 which allows the evaluation of volume changes of chest wall 7

7–9 o compartments. We performed direct measurements of p end-expiratory and end-inspiratory chest wall volumes ) (py) (%p.v.) (%p.v.) (%) (%p.v.) (%p.v.) (%p.v.) (Torr) (Torr) (a.u.) : forced expiratory volume in 1 s; FEV 2

during natural breathing while avoiding measurements 1 346 351 based on wearing a mouthpiece and nose clip. Breathing 338 0.009 7 7 7 through a mouthpiece with a nose clip in place is known to o alter the pattern of breathing, primarily by increasing tidal p volume.10,11 726 725 828 7 7 7 (years) (kg m Methods Age BMI Smoke VC FEV

Patients SD. VC: vital capacity; FEV 7 Thirty COPD patients with moderate to severe airway obstruction and mild to moderate hyperinﬂation and Anthropometric, clinical, and functional data. hypoxemia participated in the study (Table 1). They were selected from a pulmonary rehabilitation program if they Group (30 subj.) 71 Table 1 Values are mean Council Dyspnea Scale; p.v.: predicted value; a.u.: arbitrary units. Subgroup 1 (19 subj.) 72 satisﬁed each of three criteria: (i) long history of smoking Subgroup 2 (11 subj.) 71 and moderate to severe chronic dyspnea score (MRC4II), ARTICLE IN PRESS

1414 R. Bianchi et al.

(ii) clinically stable condition, with no exacerbation, or each compartment was measured at the beginning and end hospital admission in the preceding four weeks, (iii) free from of inspiratory flow (zero-flow points). The difference other significant disease potentially contributing to dyspnea. between the end-inspiratory and end-expiratory volume of each compartment was calculated as the tidal volume (VT) Protocol contribution by each compartment. Thus, VCW ¼ VRC+VAb, and changes in VCW can be calculated as

Routine lung function was measured first and then patients DVCW ¼ DVRC þ DVAb, were familiarized with procedures and scales for rating assuming that the only factor causing chest wall volume symptom intensity. Compartmental lung volumes were changes is gas movement. OEP calculates absolute volumes evaluated with subjects in a seated position at rest during and the absolute volume of each compartment at FRC in both quiet breathing (QB) defined as a patient’s habitual control conditions was considered as the reference volume. comfortable breathing, and PLB. A physiotherapist gave Volumes are reported either in absolute values or as changes every patient the same instructions about PLB execution. from the volume at FRC in control conditions. Patients were instructed to make a nasal inspiration followed by expiratory blowing against partially closed lips, avoiding forceful exhalation.1 Dyspnea No patient had difficulty in learning this technique. Three trials of both QB and PLB maneuvers, performed correctly Subjects were asked to quantify the following: (i) chronic 15 and with care in random order, were recorded for at least exertional dyspnea by MRC questionnaire and, (ii) the 6 min with the exclusion of sighing and coughing, and then sensation of nonspecific discomfort associated with the act averaged. Dyspnea sensation was measured before, during of breathing by pointing to a score on a modified Borg scale 16 and after QB and PLB. The study was approved by the Ethics from 0 (none) to 10 (maximal) arbitrary units (a.u.). Committee of the Institution and informed consent was obtained from subjects. Data analysis

Lung function Values are means 7SD. Statistical procedure was used to test differences for paired and unpaired samples. Simple Routine spirometry obtained with subjects in a seated regression analysis was performed using Pearson’s correla- position was measured as previously reported.12 FRC tion coefﬁcient. The level of signiﬁcance was set at po0.05. (functional residual capacity) was measured by a constant All statistical procedures were carried out using the Statgraphics Plus 5.1 statistical package (Manugistics, volume whole-body plethysmograph (Autobox DL 6200 Sensor Medics; Yorba Linda, CA, USA.). The normal values Rockville, MD, USA). for lung volumes are those proposed by the European Respiratory Society.13 Results

Chest wall kinematics and compartmental volumes Chest wall kinematics

The volume of the chest wall (VCW) was modeled as the sum The analysis of the time course of volume changes in chest of the volumes of the rib cage (VRC), and abdomen (VAb). The wall compartments allowed us to identify two different PLB volumes of the chest wall and its compartments were patterns. The first pattern (left panels of Fig. 1 and Table 2) assessed by applying a noninvasive OEP technique, used as characterized 19 patients we called euvolumics in whom the previously described.14 Briefly, 89 reflecting markers were PLB maneuver decreased end-expiratory volumes of both placed front and back over the trunk from the clavicles to chest wall ðVCWee Þ and abdomen ðVAbee Þ, and increased, to a the anterior superior iliac spines along pre-defined vertical lesser extent, end-inspiratory volumes of both chest wall and horizontal lines. To measure the volume of chest wall ðVCWei Þ and rib cage ðVRCei Þ, but not abdomen ðVAbei Þ.As compartments from surface markers we defined the follow- shown in Fig. 2 expiratory deflation of chest wall ðVCWee Þ and ing: (1) the boundaries of rib cage as extending from the abdominal compartment ðVAbee Þ down to the FRC line (the clavicles to the costal margin anteriorly down from the dotted line in the fig), and mild inspiratory inflation of rib xiphisternum, and to the level of the lowest point of the cage compartment ðVRCei Þ contributed to increasing the tidal lower costal margin posteriorly; and (2) the boundaries of volume of the chest wall ðVTRC þ VTAb ¼ VTCW ¼þ the abdomen as extending caudally from the lower rib cage 0:63 0:52 LÞ. Also, VCWei and VRCei , but not VAbei , increased to a horizontal line at the level of the anterior superior iliac with PLB. This pattern was also associated with a decrease spine. The landmark coordinates were measured with a in Borg score (PLB vs QB, po0.0007) (Fig. 3). system configuration of four infrared TV-cameras, two The second pattern (right panels of Fig. 1 and left panels placed 4 m behind and two 4 m in front of the subject, at of Table 3) characterized 11 patients, called hyperinflators, a sampling rate of 50 Hz. Starting from these coordinates the with lower VTRC (po0.01), VTAb (po0.05) and their sum VTCW volume of the chest wall was computed by triangulating the (po0.01) than euvolumics at QB. In these patients, PLB surface and then using Gauss’s theorem to convert the increased end-expiratory volumes of the chest wall and rib volume integral to an integral over this surface, as described cage up to FRC (dotted line) (VCWee : þ0:15 0:21 L; 14 previously. Flow signal was obtained by integrating volume VRCee : þ0:11 0:14 L), and increased, to a greater extent track. The end-expiratory and end-inspiratory volume of than in the euvolumics, end-inspiratory volumes of the chest ARTICLE IN PRESS

Thoracic kinematics and pursed lip breathing 1415

Euvolumic Hyperinflator

31 31

30 30 VCW (L) 29 29 VCW (L)

20 18

19 17 VRC (L) 18 16 VRC (L)

12 14

11 13 VAb (L) 10 QB PLB QB PLB 12 VAb (L)

0 102030405060700 10203040506070 Time (s)

Figure 1 Time course of breathing pattern during QB and PLB in two representative patients. From top to bottom: volumes of chest wall (VCW), rib cage (VRC) and abdomen (VAb). QB is quiet breathing; PLB is pursed lip breathing.

Table 2 Effects of PLB on volumes of chest wall compartments and breathing pattern in euvolumic patients.

Euvolumics (19 subj.) QB PLB–QB p QB PLB–QB p

7 7 1 7 7 VCWei ðLÞ 30.24 3.71 +0.25 0.44 o0.05 VE (L min ) 10.12 2.78 +0.30 2.75 n.s. 7 7 1 7 7 VRCei ðLÞ 19.00 2.31 +0.23 0.31 o0.005 Rf (min ) 14.91 4.91 6.78 4.40 o0.000003 7 7 7 7 VAbei ðLÞ 11.24 2.19 +0.02 0.22 n.s. VT (L) 0.74 0.26 +0.63 0.52 o0.00005 7 7 7 7 VCWee ðLÞ 29.50 3.66 0.37 0.23 o0.00001 Ti (s) 1.61 0.56 +0.95 1.13 o0.002 7 7 7 7 VRCee ðLÞ 18.71 2.28 0.06 0.18 n.s. Te (s) 2.91 1.03 +2.72 1.57 o0.00001 7 7 7 7 VAbee ðLÞ 10.79 2.16 0.31 0.22 o0.00001 Ttot (s) 4.52 1.50 +3.67 2.57 o0.00001 7 7 1 7 7 VTCW ðLÞ 0.74 0.26 +0.63 0.52 o0.00005 VT/Ti (L s ) 0.48 0.16 +0.10 0.17 o0.03 7 7 1 7 7 VTRC ðLÞ 0.28 0.16 +0.29 0.31 o0.001 VT/Te Ls ) 0.27 0.08 0.01 0.07 n.s. 7 7 7 7 VTAb ðLÞ 0.46 0.16 +0.33 0.25 o0.00005 Ti/Ttot 0.36 0.06 0.05 0.05 o0.0002 Borg (a.u.) 1.6171.13 0.4270.45 o0.0007

Values are mean7SD. VE: minute ventilation; Rf: respiratory frequency; VT: tidal volume; Ti: inspiratory time; Te: expiratory time; Ttot:

total time of the respiratory cycle; VT/Ti: mean inspiratory ﬂow; VT/Te: mean expiratory ﬂow; Ti/Ttot: duty cycle. VCWei : chest wall

end-inspiratory volume; VRCei : rib cage end-inspiratory volume; VAbei : abdomen end-inspiratory volume; VCWee : chest wall end-

expiratory volume; VRCee : rib cage end-expiratory volume; VAbee : abdomen end-expiratory volume; VTCW : tidal volume of the chest

wall; VTRC : tidal volume of the rib cage; VTAb : tidal volume of the abdomen.

wall (VCWei , po0.000001) and its compartments Important clinical differences were associated with the two

ðVAbei ; VRCei Þ. As shown in Fig. 4 the average increase in pattern groups. Euvolumics were more severely obstructed

VTCW ðþ0:36 0:30 LÞ was exclusively due to an increase in (FEV1/VC and FEV1) and hyperinflated (FRC, TLC, RV) at end-inspiratory compartmental volumes ðVAbei ; VRCei Þ.No baseline (Table 1). They appeared to adopt PLB during common change in Borg score was associated with this pattern (PLB activities of the pulmonary rehabilitation program. In contrast, vs QB, p ¼ ns) (Fig. 3). hyperinflators did not use PLB if not specifically requested.

Moreover, a greater decrease in VCWee was correlated with a greater level of airway obstruction (r ¼ 0.45, po0.02). Finally, Breathing pattern change in VCWee positively correlated with change in Borg score (r2 ¼ 0.50, po0.00002) (Fig. 5). Tables 2 and 3 (right panels) show the effects of PLB on QB pattern in euvolumics and hyperinﬂators, respectively. Analysis of the variance indicated greater PLB increase in Discussion VT (po0.0004), inspiratory time (Ti)(po0.005), expiratory time (Te)(po0.0009) and total time of the respiratory cycle The OEP analysis of chest wall kinematics shows why not all (Ttot)(po0.003) in euvolumics than in hyperinﬂators. patients with COPD obtain symptom relief from PLB at rest. ARTICLE IN PRESS

1416 R. Bianchi et al.

VCW(L) VRC(L) VAb (L)

1.0 1.0 1.0

0.8 0.8 0.8

0.6 0.6 0.6

0.4 0.4 0.4

0.2 0.2 0.2

0.0 0.0 0.0

-0.2 -0.2 -0.2

-0.4 -0.4 -0.4

QB PLB QB PLB QB PLB

Figure 2 Changes in volumes of chest wall (CW) and its compartments with PLB in euvolumics. Left panel: changes in the volumes of the chest wall (VCW); middle panel: volumes of the rib cage (VRC); right panel: volumes of the abdomen (VAb). Closed symbols: end- expiratory volume, open symbols: end-inspiratory volume. The dotted line: functional respiratory capacity. Bars are means 7SEM. For explanation see Results.

4 4

3 3

2 2 BORG (a.u.) BORG (a.u.)

1 1

0 0

QBPLB QB PLB

Figure 3 Change in dyspnea sensation with PLB in euvolumics (left panel) and hyperinﬂators (right panel).

The most severely affected patients who deﬂate the chest The increased VTCW was, therefore the result of both VTAb , wall during volitional PLB reported improvement in their by exploiting the expiratory reserve volume, and VTRC ,by sensation of breathlessness. This was not the case in the exploiting the inspiratory reserve volume. This strategy group who hyperinﬂated during PLB. exploits the stores of elastic energy of the most compliant 18 The major difference between the two PLB patterns was chest wall compartment, the abdomen, and prevents VCWei the ability of euvolumics to decrease VCWee by decreasing from reaching total chest wall capacity.

VAbee , while limiting the increase in VRCei . In line with In contrast, the increase in tidal volume of the chest wall 3 previous data of ours, changes in VCWee and VAbee are in hyperinflators was due to an increase in the tidal volume directly related to increase in Te in that the greater of the rib cage without the contribution of abdominal tidal the latter the greater is the reduction in the volume. In volume. End-inspiratory volume of the chest wall mainly particular, we explain the decrease in VCWee in hyperinflated resulted from rib cage inspiratory muscles; in these patients with lengthening Te and Ttot, not with increasing circumstances esophageal pressure may reach a higher mean expiratory flow (VT/Te see Tables 2 and 3). fraction of maximal inspiratory muscle pressure capacity This mechanism is similar to that expected to reduce and generate a greater dyspnea score19 (see also fig. 34). thoracic gas volume entrapment and exercise breathlessness Most importantly, in the conditions of the present study the after pulmonary rehabilitation programs in patients with lack of decrease in VAbee along with increase in VAbei suggest COPD.17 a lower abdominal muscle contribution, and higher ARTICLE IN PRESS

Thoracic kinematics and pursed lip breathing 1417

Table 3 Effects of PLB on volumes of chest wall compartments and breathing pattern in hyperinﬂator patients

Hyperinﬂators (11 subj.) QB PLB–QB p QB PLB–QB p

7 7 1 7 7 VCWei ðLÞ 31.42 4.37 +0.51 0.15 o0.000001 VE (L min ) 9.85 2.87 +0.30 2.88 n.s. 7 7 1 7 7 VRCei ðLÞ 18.40 2.90 +0.34 0.10 o0.000001 Rf (min ) 22.29 5.69 9.06 5.14 o0.0002 7 7 7 7 VAbei ðLÞ 13.02 2.09 +0.17 0.07 o0.00005 VT (L) 0.47 0.22 +0.36 0.30 o0.003 7 7 7 7 VCWee ðLÞ 30.95 4.28 +0.15 0.21 o0.05 Ti (s) 1.15 0.33 +0.64 0.68 o0.02 7 7 7 7 VRCee ðLÞ 18.25 2.85 +0.11 0.14 o0.05 Te (s) 1.82 0.77 +1.49 1.28 o0.00004 7 7 7 7 VAbee ðLÞ 12.70 2.02 +0.04 0.10 n.s. Ttot (s) 2.97 1.06 +2.14 1.82 o0.003 7 7 1 7 7 VTCW ðLÞ 0.47 0.22 +0.36 0.30 o0.005 VT/Ti (L s ) 0.41 0.10 +0.07 0.12 n.s.(o0.06) 7 7 1 7 7 VTRC ðLÞ 0.15 0.08 +0.23 0.18 o0.005 VT/Te Ls ) 0.28 0.10 0.01 0.09 n.s. 7 7 7 7 VTAb ðLÞ 0.32 0.19 +0.13 0.14 o0.05 Ti/Ttot 0.40 0.06 0.05 0.08 n.s. Borg (a.u.) 0.9670.57 +0.0970.38 n.s.

Values are mean7SD. VE: minute ventilation; Rf: respiratory frequency; VT: tidal volume; Ti: inspiratory time; Te: expiratory time; Ttot:

total time of the respiratory cycle; VT/Ti: mean inspiratory ﬂow; VT/Te: mean expiratory ﬂow; Ti/Ttot: duty cycle. VCWei : chest wall

end-inspiratory volume; VRCei : rib cage end-inspiratory volume; VAbei : abdomen end-inspiratory volume; VCWee : chest wall end-

expiratory volume; VRCee : rib cage end-expiratory volume; VAbee : abdomen end-expiratory volume; VTCW : tidal volume of the chest

wall; VTRC : tidal volume of the rib cage; VTAb : tidal volume of the abdomen.

VCW (L) VRC (L) VAb (L)

1.2 1.2 1.2

1.0 1.0 1.0

0.8 0.8 0.8

0.6 0.6 0.6

0.4 0.4 0.4

0.2 0.2 0.2

0.0 0.0 0.0

-0.2 -0.2 -0.2

QB PLB QB PLB QB PLB

Figure 4 Changes in volumes of chest wall (CW) and its compartments with PLB in hyperinﬂators. Left panel: changes in the volumes of the chest wall (VCW); middle panel: volumes of the rib cage (VRC); right panel: volumes of the abdomen (VAb). Closed symbols: end-expiratory volume; open symbols: end-inspiratory volume. The dotted line: functional respiratory capacity. Bars are means 7SEM. For explanation see Results. 1.5 inspiratory diaphragmatic contribution to abdominal tidal 20 volume, respectively. 1.0 EUVOLUMICS The mechanisms of apparent symptomatic improvement HYPERINFLATORS 2,21,22 p<0.00002 with PLB have not been fully elucidated. Dynamic 0.5 airway compression by itself may produce afferent sensory r2=0.50 information that contributes to the sense of dyspnea 0.0 experienced.23 Assumption of a slower, deeper-breathing pattern during PLB would reduce intrinsic end-expiratory- -0.5

positive-alveolar-pressure (PEEPi) and, thereby, the inspira- BORG (a.u.) tory work of breathing.24 By using PLB, COPD patients Δ -1.0 breathe larger tidal volumes2,22 which correlate with symptomatic relief of dyspnea.2 Nonetheless, the issue of -1.5 whether and to what extent PLB affects dyspnea is still a matter of debate, since the efficacy of PLB in relieving 4,25 -2.0 dyspnea varies greatly among COPD patients. -1.2 -1.0 -0.8 -0.6 -0.4 -0.2 0.0 0.2 0.4 0.6 Our present and previous findings3 of decreased V CWee ΔVCWee (L) associated with a lower Borg score are in line with the effect 26 of hyperinflation on dyspnea and, conversely, with the Figure 5 Relationship between change in end-expiratory attenuation of the symptom with chest wall deflation.18,27 volume of the chest wall ðVCWee Þ and change in Borg score. The net effect of decreased VCWee is an improvement in the Open circles: euvolumics; closed circles: hyperinflators. ARTICLE IN PRESS

1418 R. Bianchi et al. length–tension relationship of the inspiratory muscles so 10. Gilbert R, Auchincloss Jr JH, Brodsky J, Boden W. Changes in that, for any given neural input, lung expansion (VT)is tidal volume, frequency, and ventilation induced by their commensurate with the degree of pressure generated when measurement. J Appl Physiol 1972;33(2):252–4. the muscle shortens. This is a physiological mechanism of 11. McCool FD, Kelly KB, Loring SH, Greaves IA, Mead J. Estimates neuromuscular coupling of the ventilatory pump.26 In of ventilation from body surface measurements in unrestrained contrast and for opposite reasons lung hyperinflation, which subjects. J Appl Physiol 1986;61(3):1114–9. 12. Scano G, Garcia-Herreros P, Stendardi D, Degre S, De Coster A, promotes the shortening of the inspiratory muscle along Sergysels R. Cardiopulmonary adaptation to exercise in coal with a higher than normal neural motor output, results in miners. 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