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Respiratory Physiology & Neurobiology 210 (2015) 1–6

Contents lists available at ScienceDirect

Respiratory Physiology & Neurobiology

jou rn al h om epa ge: www.elsev ier .com/ locate / resphys io l

nxiety and depression are related to dyspnea and clinical control butot with thoracoabdominal mechanics in patients with COPD

rickson Borges-Santosa,1, Juliano Takashi Wadaa,1, Cibele Marques da Silvaa,1,onaldo A. Silvaa,1, Rafael Stelmachb,1, Celso R. Carvalhoa,1, Adriana C. Lunardia,∗,1

Department of Physical Therapy, School of Medicine, University of Sao Paulo, Sao Paulo, BrazilDepartment of Pneumology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil

r t i c l e i n f o

rticle history:ccepted 16 January 2015vailable online 22 January 2015

eywords:OPDhoracic mechanicsnxietyepression

a b s t r a c t

Objective: To investigate the relationship between the presence of symptoms of anxiety or depressionwith breathing pattern and thoracoabdominal mechanics at rest and during exercise in COPD.Methods: Cross-sectional study enrolled 54 patients with COPD ranked according to Hospital Anxiety andDepression Scale (HAD) score and compared to dyspnea, clinical control, hypercapnia, breathing patternand thoracoabdominal mechanics at rest and during exercise.Results: Seventeen patients with COPD had no symptoms, 12 had anxiety symptoms, 13 had depressivesymptoms and 12 had both symptoms. COPD with depressive symptoms presented greater degree ofdyspnea (p < 0.01). Poor clinical control was observed in COPD with anxious and/or depressive symptoms

yspnealinical control

(p < 0.05). Breathing pattern and thoracoabdominal mechanics were similar among all groups at rest andduring exercise.Conclusions: COPD with symptoms of depression report more dyspnea. Anxiety and depression are asso-ciated with poor clinical control without impact on breathing pattern and thoracoabdominal mechanicsin COPD.

© 2015 Elsevier B.V. All rights reserved.

. Introduction

In patients with chronic obstructive pulmonary disease (COPD)ir trapping and chronic lung hyperinflation lead to reducediaphragmatic mobility and its contribution to thoracoabdominalovement. This, in turn, increases the activity of other muscles on

ibcage movement (dos Santos Yamaguti et al., 2008). Early or latenset of dynamic pulmonary hyperinflation, when it occurs, mayimit exercise and it appears to be correlated with paradoxical tho-acoabdominal movement (Aliverti et al., 2009) and symptoms ofyspnea (Vogiatzis et al., 2005).

Dyspnea is often associated with reduction in the levels of phys-cal activity that reduces patient’s exercise capacity and thereby

reating the “negative spiral in COPD” (Polkey and Moxham, 2006).nticipation of discomfort caused by physical exertion and sub-equent limitations in activities of daily living (ADL) are related

∗ Corresponding author at: Department of Physical Therapy, School of Medicinef University of Sao Paulo, R. Cipotanea 51, Sao Paulo, SP 05360-160, Brazil.el.: +55 11 3091 7451.

E-mail address: adrianalunardi@usp.br (A.C. Lunardi).1 All authors have contributed at all stages of this study.

ttp://dx.doi.org/10.1016/j.resp.2015.01.011569-9048/© 2015 Elsevier B.V. All rights reserved.

to psychosocial symptoms such as anxiety and depression (Godoyand Godoy, 2002). Increased levels of anxiety can occur in up to 74%of patients with COPD (Yohannes et al., 2010) which, in turn, cancontribute to multiple somatic symptoms including restlessness,signs of motor tension, insomnia, difficulty swallowing, palpita-tions, shortness of breath, appetite suppression and decreased bodyweight, quality of sleep, attention deficit and pronounced feeling offatigue (Simms et al., 2012). The prevalence of these symptoms inpatients with COPD ranges between 16% and 88% (Yohannes et al.,2010). Furthermore, the presence of psychosocial symptoms areassociated with the severity of obstructive pulmonary disease (Luet al., 2013), dyspnea (Neuman et al., 2006), levels of physical activ-ity (Nguyen et al., 2013) and with higher chances of exacerbationrequiring hospitalization (Gudmundsson et al., 2005) in patientswith COPD.

The impact of anxiety and depression on breathing patternhas been investigated in patients with various diseases since thebeginning of the last century (Boiten, 1998). Mador and Tobin(1991) and Masaoka and Homma (1997) showed that healthy

individuals with increased levels of anxiety have changes in breath-ing pattern parameters such as increased respiratory rate andtidal volume and decreased respiratory time. However, the roleof anxiety and depression on breathing pattern parameters of

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atients with chronic respiratory diseases including COPD remainsnknown.

Faulkner (1941) investigated the relationship between thora-oabdominal mechanics and psychosocial symptoms by evaluatingiaphragmatic motion using fluoroscopy in five subjects duringhich the subjects had to imagine pleasant or adverse situa-

ions. Authors concluded that pleasant feelings tended to increaseiaphragmatic displacement, whereas negative emotions tendedo decrease it. Faulkner’s study, despite its pioneering spirit, wasimited not only by not having a description of the sample eval-ated but also by the small number of subjects (Faulkner, 1941).

n brief communications, other authors described increased ampli-ude of the thoracic signal and reduced amplitude of the abdominalignal during noxious stimuli or unpleasant sensations in healthyeople (Boiten, 1998).

Although the association between psychosocial and respiratoryymptoms have been previously described (Chetta et al., 2005)nvestigation into the relationship between symptoms of anxietynd depression and ventilation mechanics in patients with COPDas not been studied. In addition, variations in PaCO2 (partial pres-ure of carbon dioxide) could be another factor related to anxiousymptoms due to hyperventilation even in healthy people (Hant al., 2000; Ramos, 2001); however, it has not been previouslytudied in COPD patients.

Changes in breathing pattern significantly influence exercisentolerance and disability in patients with COPD (Aliverti et al.,009); therefore, research that identifies factors that contributeo decreased lung function is critical to prevention and treat-

ent. Thus, the aim of this study was to evaluate the impact ofnxiety and depression on the severity of dyspnea and clinicalanagement, as well as on the breathing pattern and thora-

oabdominal mechanics of COPD patients at rest and duringxercise.

. Methods

.1. Study design

This cross-sectional observational study was approved by theospital Research Ethics Committee of University of Sao Paulo (no.295/09) and the volunteer participants provided written informedonsent prior to study participation.

.2. Subjects

Fifty-four patients with COPD (defined as forced expiratory vol-me in the first second (FEV1)/forced vital capacity (FVC) <70%f predicted value) (GOLD, 2014) were recruited from the clini-al outpatient follow-up of obstructive disease in the Universityospital. Patients over than 40 years of age, with a body mass

ndex (BMI) between 20 and 30 kg/m2, not oxygen-dependent,linically stable (no respiratory symptoms or seek medicalervice beyond the usual for at least one month) and receivingptimized medical treatment (bronchodilator and inhaled cortico-teroid) were included according to international guidelines (GOLD,014).

.3. Study protocol

After study inclusion, all subjects were submitted to an initial

ssessment of clinical history, lung function, presence of symptomsf anxiety and depression, arterial blood gas, level of dyspnea, clin-cal control and thoracoabdominal mechanics at rest and duringxercise on a cycle ergometer.

ogy & Neurobiology 210 (2015) 1–6

2.4. Outcomes assessment

2.4.1. Lung functionSpirometry (Koko Club Legend, USA) was performed in

accordance with the American Thoracic Society and EuropeanRespiratory Society criteria (Miller et al., 2005) and normalizedto the standard Brazilian population as described by Pereira et al.(2007). The variables of forced vital capacity (FVC), forced expira-tory volume in the first second of a forced exhale (FEV1) and theFEV1/FVC ratio were analysed.

2.4.2. Anxiety and depressionAnxiety and depression symptoms were assessed by the Hospi-

tal Anxiety and Depression Scale (HADS). Patients were consideredanxious if their (HAD-A) score was greater than 8 (HAD-A ≥ 9), theywere considered depressed if their (HAD-D) score was greater than8 (HAD-D ≥ 9) and they were considered anxious and depressed iftheir score was greater than 8 in both HAD-A and HAD-D (Zigmondand Snaith, 1983). If patients score less than 8 in HAD-S, they wereconsiderate without psychological symptoms (control group).

2.5. Breathlessness and clinical control of the disease

Dyspnea was objectively evaluated using the modified Medi-cal Research Council (mMRC) scale. The higher the score meansthe greater degree of difficulty in daily living activities due to dys-pnea (Kovelis et al., 2008). The Clinical COPD Questionnaire (CCQ)was used to assess clinical control. Higher scores were indicative ofpoorer clinical control (Van der Molen et al., 2003).

2.5.1. Arterial blood gasValues of partial pressures of oxygen (PaO2) and carbon diox-

ide (PaCO2) in the arterial blood were obtained from the hospitalrecords that were performed during patient’s regular medical visit.

2.5.2. Thoracoabdominal mechanicsSimultaneous analysis of thoracoabdominal kinematics and

respiratory muscle activity was performed during quiet breathingfor 30 s and subsequently during cycle ergometer exercise. First,patients performed exercise without charging at a fixed speed of60 rpm for 3 min. This was followed by cycling for two more min-utes, with an initial load of 0 and ending at 25% of maximumpredicted load for the patient (Jones et al., 1985). Upon reaching 25%of the maximum predicted load, the patient continued pedalling for30 s to allow for variable acquisition.

2.5.3. Thoracoabdominal kinematicsThoracoabdominal kinematics were analysed by optoelectronic

plethysmography (OEP System, BTS Bioengineering, GarbagnateMilanese, Italy) according to the standards proposed by Alivertiet al. (2009). The following variables were obtained: volume ofthe chest wall (VT), pulmonary rib cage volume (RCp), abdominalrib cage volume (RCa), abdomen volume (Ab), the relative contrib-utions of the pulmonary rib cage, abdominal rib cage and abdomento the total tidal volume (%RCp, %RCa, %Ab, respectively), respi-ratory rate (RR) in inspirations per minute, inspiratory time (TI),expiratory time (TE) and total time of breath (TTOT) in seconds(Aliverti et al., 2009).

The thoracoabdominal synchrony was calculated by the differ-ence between the end time of inspiration of pulmonary rib cage and

abdominal rib cage (RCp-RCa) and from the pulmonary rib cage andabdomen (RCp-Ab), divided by the total length of the respiratorycycle and multiplied by 360◦ as previously described (Agostoni andMognoni, 1966; Strömberg and Nelson, 1998).

E. Borges-Santos et al. / Respiratory Physiology & Neurobiology 210 (2015) 1–6 3

Table 1Anthropometric and clinical data of both groups (n = 54).

Control (n = 17) Anxiety (n = 12) Depression (n = 13) Anxiety + Depression (n = 12)

Age (years) 63 ± 6 66 ± 6 62 ± 5 62 ± 5Gender (M/F) 10/7 7/5 9/4 6/6BMI (kg/m2) 25.7 ± 3.3 27.1 ± 4.3 24.3 ± 2.0 25.7 ± 2.6FEV1 (%) 49 (36–72) 50 (43–60) 48 (35–63) 47 (35–67)FEV1/FVC 0.68 (0.55–0.96) 0.53 (0.44–1.03) 0.54 (0.39–1.05) 0.62 (0.38–1.16)BODE (I/II/III/IV) 4/7/5/1 1/5/4/2 2/4/6/1 2/5/2/3pH 7.40 (7.40–7.42) 7.42 (7.41–7.44) 7.38 (7.36–7.38) 7.40 (7.39–7.42)PaCO2 40.9 ± 5.5 38.4 ± 3.6 44.5 ± 3.6 41.0 ± 5.9PaO2 60.7 ± 12.6 81.6 ± 18.8 54.6 ± 16.1 61.7 ± 17.1Wmax (W) 35.0 (25.0–41.3) 35.0 (27.5–40.0) 40.0 (23.8–42.5) 27.5 (20.0–35.0)

Data are presented as average ± SD except for gender and BODE presented as absolute number and FEV1% and pH presented as median (interquartile range). M, male; F,f percefi structa dioxid

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emale; BMI, body mass index; FEV1, forced expiratory volume in the first second inrst second and forced vital capacity ratio; BODE, BMI (body mass index), airway obccording to Jones et al. (1985); pH, acidity level; PaCO2, partial pressure of carbon

.5.4. Respiratory muscle activityActivity of the sternocleidomastoid muscles (RSL), higher

xternal intercostal (RIC), lower external intercostal (LIC) andectus abdominis (RA) was analysed by surface electromyogra-hy (FreeEMG 300, OEP System, BTS Bioengineering, Garbagnateilanese, Italy). Ag/AgCl electrodes were attached with an adhesive

onductive hydrogel (Maxicor, Brazil). The electrodes were placedccording to European recommendations for surface EMG for non-nvasive assessment of muscles (SENIAM) (Hermens et al., 2000).he electrode of the right RSL was positioned 5 cm from the mastoidrocess in muscle belly (Kallenberg et al., 2009). For RIC, the elec-rode was placed on the second intercostal space on the right andor LIC, the electrode was placed on the seventh intercostal spacen the left (Maarsingh et al., 2000). For the RA, the electrode wasositioned on the right side of the abdomen, 4 cm from the umbili-us (Maarsingh et al., 2000). The positions of the electrodes werealidated by signal strength and the resulting data were processedy specific software for further analysis.

.6. Statistical analysis

The sample size calculation was performed considering theverage difference in tidal volume (Vt) of 64 ml, with an averagetandard deviation of 45 ml (Tobin et al., 1983) and a power of 80%s the primary variable. The sample size estimation was 12 sub-ects per each group. The data normality was verified using thehapiro–Wilk test. Groups were compared by one-way ANOVA,ruskal–Wallis One Way Analysis of Variance on Ranks followedy Tukey post hoc test and Chi-square tests. Multiple linear regres-ion models were performed testing which independent variablesPCO2, FEV1, HAD score, presence of depression or anxiety symp-om, age, gender and BMI) could be related with thoracoabdominal

echanics or breathing pattern (dependent variables). Resultsere considered significant for p < 0.05. All data analysis was per-

ormed with the statistic software Sigma Stat (version 12.1, Jandelcientific, San Rafael, CA).

able 2yspnea and clinical control between groups (n = 54).

Control (n = 17) Anxiety (n = 12)

Dyspnea (mMRC) 2 (2–3) 3 (2–3.5)

CCQ – symptoms 1.2 (1–1.9) 2.4 (2–4)*

CCQ – Functional 1.1 ± 0.9 2.4 ± 1.1*

CCQ – mental 1 (0–1.5) 2.1 (0.25–3.8)

CCQ – total 1.3 (0.9–1.7) 2.7 (1.8–3.1)*

ata are presented as median (interquartile range) except for CCQ – functional presenteOPD Questionnaire.

* p < 0.001.# p < 0.05 compared to control.

ntage of predicted (Pereira et al., 2007); FEV1/FVC, forced expiratory volume in theion, dyspnea and exercise capacity index; Wmax, maximum load in exercise testinge in arterial blood; PaO2, partial pressure of oxygen in arterial blood.

3. Results

Seventeen patients with COPD had no symptoms, 12 had anx-iety symptoms, 13 had depressive symptoms and 12 had bothsymptoms. No differences were observed between the groupsin age, gender, anthropometry, lung function, disease severity,partial pressure of oxygen and carbon dioxide or exercise load(Table 1). Patients with anxiety and/or depression symptoms pre-sented poorer clinical control of the disease compared to patientswithout these symptoms; however, patients with COPD only withdepression symptoms presented higher dyspnea level (Table 2).

Breathing pattern parameters (tidal volume, respiratory rate,inspiratory and expiratory time and total time of the respiratorycycle) were not influenced by anxiety symptoms or depressionsymptoms either at rest or during exercise (Table 3). Likewise, thecontribution of each compartment in the total pulmonary ventila-tion (RCp, RCa and Ab) or thoracoabdominal synchrony (RCp-Ab,RCp-RCa) at rest or during exercise were not affected by symptomsof anxiety or depression (Table 4). In addition, muscular activity ofRSL, RIC, LIC and RA also revealed no differences between groupsat rest or during exercise (Table 5).

In regression models, none of the analysed variables wererelated to the respiratory pattern or parameters of thoracoabdom-inal mechanics.

4. Discussion

The present study demonstrates that symptoms of anxiety anddepression are associated with poorer clinical disease control anddepressive symptom is associated with dyspnea in patients withCOPD. However, the presence of these symptoms is not related tochanges in breathing pattern and thoracoabdominal mechanics at

rest or while performing exercise.

Most of the previous studies that assessed the influence of anxi-ety or depression on respiratory variables only described few casesin which patients were exposed to a visual, auditory or imaginative

Depression (n = 13) Anxiety + depression (n = 12)

3 (3–4.7)* 3 (2–4)3.7 (1.9–4.7)* 1.3 (1.2–3.2)2.7 ± 0.7* 1.8 ± 1.0#

2.5 (1.6–3)* 2 (1.1–3.8)#

2.9 (2.2–4.1)* 2.1 (1.5–2.7)*

d as average ± SD. mMRC, modified Medical Research Council scale; CCQ, Clinical

4 E. Borges-Santos et al. / Respiratory Physiology & Neurobiology 210 (2015) 1–6

Table 3Breathing pattern between groups at rest and during exercise (n = 54).

Control (n = 17) Anxiety (n = 12) Depression (n = 13) Anxiety + depression (n = 12)

At restVT (L) 0.42 (0.34–0.49) 0.48 (0.44–0.63) 0.49 (0.33–0.54) 0.42 (0.38–0.50)RR (bpm) 19 (17–21) 16 (15–17) 24 (20–25) 18 (17–20)TI (s) 1.16 ± 0.25 1.28 ± 0.29 1.06 ± 0.26 1.22 ± 0.13TE (s) 2.04 ± 0.43 2.51 ± 0.16 1.82 ± 0.72 2.11 ± 0.40TTOT (s) 3.20 ± 0.61 3.79 ± 0.18 2.88 ± 0.94 3.32 ± 0.49

ExerciseVT (L) 0.86 (0.63–1.03) 0.99 (0.77–1.06) 0.96 (0.83–1.15) 0.94 (0.71–1.03)RR (bpm) 30 ± 5 30 ± 5 29 ± 5 27 ± 6TI (s) 0.91 ± 0.2 0.84 ± 0.26 0.88 ± 0.14 0.97 ± 0.15TE (s) 1.12 (1.02–1.38) 1.15 (1.10–1.44) 1.18 (1.01–1.43) 1.20 (1.11–1.46)TTOT (s) 2.12 ± 0.40 2.09 ± 0.40 2.11 ± 0.34 2.31 ± 0.49

Data are presented as average ± SD or as median (interquartile range). VT, tidal volume; L, litre; RR, respiratory rate; bpm, breaths per minute; TI, inspiratory time; s, seconds;TE, expiratory time; TTOT, total time of the respiratory cycle.

Table 4Compartmental volumes and contribution of each one on total chest wall volume and thoracoabdominal synchrony between groups at rest and during exercise (n = 54).

Control (n = 17) Anxiety (n = 12) Depression (n = 13) Anxiety + Depression (n = 12)

At restRCp (L) 0.09 (0.07–0.13) 0.07 (0.06–0.15) 0.09 (0.07–0.12) 0.08 (0.07–0.12)RCa (L) 0.05 (0.04–0.07) 0.06 (0.01–0.09) 0.03 (0.01–0.08) 0.06 (0.05–0.10)Ab (L) 0.27 ± 0.10 0.38 ± 0.16 0.33 ± 0.17 0.26 ± 0.10%RCp 24.6 ± 8.1 18.2 ± 8.9 21.0 ± 7.3 22.2 ± 6.4%RCa 13.9 (8.8–15.9) 11.3 (2.1–20.1) 7.7 (1.3–16.1) 16.9 (10.5–23.9)%Ab 62.5 (54.1–67.4) 74.2 (63.7–79.2) 70.1 (52.6–80.9) 63.9 (47.4–71.8)RCp-Ab 4.9 (2.8–10.9) 3.2 (2.3–22.2) 5.2 (1.4–8.1) 7.1 (4.4–13.2)RCp-RCa 14.1 (3.3–20.0) 14.5 (2.4–36.7) 31.9 (21.9–69.3) 15.5 (5.0–33.4)

ExerciseRCp (L) 0.20 ± 0.09 0.17 ± 0.12 0.17 ± 0.09 0.16 ± 0.10RCa (L) 0.11 ± 0.08 0.12 ± 0.10 0.03 ± 0.14 0.15 ± 0.10Ab (L) 0.55 ± 0.21 0.65 ± 0.20 0.75 ± 0.30 0.56 ± 0.17%RCp 11.3 (7.8–17.6) 10.2 (6.9–17.9) 2.1 (-7.2–15.6) 16.2 (9.1–30.9)%RCa 13.9 (8.8–15.9) 11.3 (2.1–20.1) 7.7 (1.3–16.1) 16.9 (10.5–23.9)%Ab 63.6 ± 15.2 68.5 ± 15.9 76.6 ± 24.3 64.5 ± 12.7RCp-Ab (◦) 7.2 (4.2–14.5) 6.1 (4.4–24.8) 12.5 (6.1–13.2) 8.5 (6.6–17.5)RCp-RCa (◦) 25.7 (6.3–41.3) 19.5 (3.9–29.5) 58.5 (22.9–151.8) 18.5 (6.9–39.3)

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ata are presented as average ± SD or as median (interquartile range). L, litre; RCp,

olume;◦ , degrees.

timulation (Feleky, 1916; Stevenson and Ripley, 1952). In addi-ion, these studies had conducted a momentary provocation inatients, which is not representative of baseline symptoms pre-ented by these individuals (Boiten, 1998). Recently, researchersoncluded that the personality of the individual promotes changesn breathing pattern during mental or physical stress. They alsoeported different patterns of cortical stimulation in individuals

ith feelings of fear or anxiety, resulting in increased respiratory

ate (Masaoka and Homma, 1997).The relationship between symptoms of depression and greater

cores of dyspnea in the MRC scale corroborates with previous

able 5espiratory muscular activity between groups at rest and during exercise (n = 54).

Control (n = 17) Anxiety (n = 12)

At restRSL (�V) 5.65 (4.09–6.51) 8.80 (7.85–36.50)

RIC (�V) 6.97 (5.47–7.67) 15.80 (12.80–178.00)

LIC (�V) 6.77 (5.57–8.57) 6.31 (4.59–59.71)

RA (�V) 7.01 (5.92–8.41) 6.59 (5.87–20.34)

ExerciseRSL (�V) 11.00 (7.39–20.20) 24.30 (14.00–25.10)

RIC (�V) 9.54 (7.02–13.20) 18.40 (15.70–25.40)

LIC (�V) 10.40 (7.67–13.40) 11.80 (7.69–23.00)

RA (�V) 8.03 (5.99–9.40) 10.60 (5.82–15.20)

ata are presented as median (interquartile range). RSL, sternocleidomastoid electromyower external intercostal electromyographic activity; RA, rectus abdominis electromyog

ribcage; RCa, lower ribcage; Ab, abdomen; %, relative contribution to the total tidal

studies (Chetta et al., 2005; Quint et al., 2008). The cortical andsubcortical mechanisms that enrol in the spatial components ofthe respiratory input (respiratory frequency and intensity) as wellas emotional components (feelings) (Davenport and Vovk, 2009;Von Leopouldt and Dahme, 2007). The involvement of all thesecomponents might explain the relationship between chronic respi-ratory disease with the emotional impact and a greater sense

of dyspnea. However, this hypothetical model might has twodirections, either the intensity of dyspnea leads to the devel-opment of anxious or depression symptoms or the presence ofthese symptoms intensifies the subjective perception of dyspnea

Depression (n = 13) Anxiety + depression (n = 12)

4.98 (4.70–10.90) 5.73 (4.58–9.49)8.48 (5.75–12.30) 6.41 (5.76–7.36)7.36 (6.00–8.39) 6.47 (5.07–8.12)6.97 (5.70–7.08) 6.10 (4.52–8.65)

26.80 (22.80–30.60) 19.00 (7.90–28.00)13.10 (9.79–17.30) 8.43 (7.36–10.30)

9.33 (7.68–16.40) 8.39 (7.25–13.50)10.20 (8.13–24.60) 8.68 (5.27–11.80)

ographic activity; RIC, higher external intercostal electromyographic activity; LIC,raphic activity; �V, microvolts.

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E. Borges-Santos et al. / Respiratory P

hat is already present in patients with CPOD (Neuman et al.,006).

Our data also demonstrate that individuals with psychologicalymptoms exhibit poorer clinical control of the disease (Clelandt al., 2007). These results are consistent with previous findingshowing that low CCQ scores in patients with COPD have a stronginear association with symptoms of anxiety and depression asssessed by HAD. Clinically, the presence of psychosocial symptomss related to poorer quality of life (Cleland et al., 2007), difficultiesn adherence to treatment (Katon et al., 2007), changes in the levelf physical activity in daily life (Nguyen et al., 2013), increased fre-uency of exacerbations and increased rates of mortality in COPDatients (Lou et al., 2012). The association between anxiety andepression and clinical disease control was partly mediated byOPD severity (Eisner et al., 2010) and impact to the ability to copeith living with the disease and hence the development of moodisorders (Cleland et al., 2007); therefore, more severe patientshould have more mood disorders. However, in our patients we didot observe an association between disease severity and psychoso-ial disorders mainly due to the reduced number sample there wereot many critically ill patients making it difficult that a strong linearelationship was shown by our results.

Regarding the breathing pattern, our results showed no differ-nces between patients with and without symptoms of anxiety orepression. The values of tidal volume and respiratory time (inspi-atory and expiratory) presented by our population were similaro those reported by Tobin et al. (1983) in COPD patients at rest.his similarity between groups was also observed during exer-ise. The respiratory rate and time observed in our patients areimilar to those observed by Aliverti et al. (2004). Our patientsresented increased volumes during exercise in all thoracoabdom-

nal compartments but we did not observed the installation ofhoracoabdominal asynchrony, regardless the presence of symp-oms of anxiety or depression. The increase in compartmentalolumes was the same as found by other investigators (Alivertit al., 2004) in COPD patients presenting pulmonary hyperinfla-ion. Since our patients had normal values of pH and PaCO2 and thathese variables were similar between the groups with and withoutymptoms, we believe that this also was not a determining factorn our results.

Unlike our population, patients with asthma have changes inreathing pattern and thoracoabdominal mechanics when they areubjected to psychological stress (Ritz et al., 2000, 2012). Theseatients have reduced inspiratory time, increased expiratory time,otal respiratory time and tidal volume with a higher share of theverall ventilation in thoracic compartment, commensurate withn increase of thoracoabdominal asynchrony (Ritz et al., 2012).hese abnormalities are caused by airway obstruction triggered byegative stimuli (Ritz et al., 2000).

The limitation of this study was the absence of analysis accord-ng to the disease phenotype due to the small sample size withnxious or depression symptoms, although we believe that the sim-larity between the groups for the degree of pulmonary obstruction,rterial blood gas and degree of dyspnea partially off sets this limi-ation. Furthermore, although we used a compliant load (25% load,n watts) consistent with the requirements needed to perform mostveryday activities that do not require high energy consumption, its possible that the load used in the stress test was not enough torigger changes in thoracoabdominal mechanics. To date, no stud-es exist in the literature with accurate methodology to assess thempact of symptoms of anxiety or depression on breathing pat-ern and thoracoabdominal mechanics of COPD patients. This study

s innovative in that it used optoelectronic plethysmography inhe assessment of thoracoabdominal mechanics and its associationith symptoms of anxiety or depression. The aim of this novel studyas to contribute to a better understanding of the impact of extra

ogy & Neurobiology 210 (2015) 1–6 5

pulmonary factors that may influence the respiratory pattern ofCOPD patients.

5. Conclusions

Our results suggest that symptoms of anxiety or depressioninterfere in sensation of dyspnea and clinical control of the disease,without any impact on breathing pattern or on thoracoabdominalmechanics at rest or during exercise in COPD patients.

Acknowledgements

The authors gratefully acknowledge the valuable help of Denisede Moraes Paisani and Desiderio Cano Porras who were instrumen-tal to the achievement of this study.

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