Skip to main content

Value of incentive spirometry in routine management of COPD patients and its effect on diaphragmatic function



Incentive spirometry (IS) is mostly used postoperatively to avoid pulmonary complications, but its effect on COPD patients and its effect on diaphragmatic functions are still not fully studied. The current study aimed to evaluate the value of IS on arterial blood gases, mMRC dyspnea scale, spirometry, and diaphragmatic functions by ultrasound in patients hospitalized for COPD exacerbation.

Methods and patients

Forty patients (37 males, 3 females) were admitted for COPD exacerbations and divided randomly into 2 groups: Group1 (G1) =20 patients (mean age 60.7±5.99) used incentive spirometry (IS) for 2 months with medical treatment. Group 2 as a control group (G2) = 20 patients (mean age 60.3±6.44) were given medical treatment only. ABG, spirometry, mMRC dyspnea scale, and diaphragmatic ultrasound functions were assessed on admission and after 2 months of treatment in the groups.


There were statistically significant differences between G1 and G2 after 2 months regarding PaCO2, FEV1/FVC (p=0.001 and 0.042, respectively), and Lt diaphragmatic excursion and diaphragm thickness ratio. There was a statistically significant increase in results of PaO2, PaCO2, FEV1/FVC, PEFR, and all diaphragmatic findings in group I before and after 2 months of IS but no difference in FVC and mMRC dyspnea scale.


Incentive spirometry in COPD patients seems to improve ABG, and spirometry functions together with improving diaphragmatic functions.

Trial registration NCT05679609. Retrospectively egistered on 10 January 2023


Chronic obstructive pulmonary disease (COPD) is considered a common cause of mortality and morbidity all over the world [1]. The airflow limitation in COPD promotes air trapping together with a decrease in inspiratory capacity, an increase in end-expiratory lung volume (EELV), and finally leads to lung hyperinflation [2]. This will reduce the diaphragmatic contraction in the inspiration which decreases the generation of inspiratory flow and lead to dyspnea and limitation of exercise [3]. The patients experience dysfunctions of inspiratory muscle from the effect of hyperinflation, malnutrition, increased the work of breathing, impairment of gas exchange, and possible use of corticosteroids [4].

The incentive spirometer (IS) is a device that is used to maximally inflate the lungs and hold on to that inflation. It encourages patients with visual feedback. It is a common respiratory therapy postoperative because it prevents and resolves atelectasis by increasing the lung inflation that thoughts to open the collapsed lung alveoli [5, 6].

In COPD patients, it is recommended to use IS postoperative [7]. But still its effect in COPD patients is unknown independently on surgery.

Exercise training lowers ventilatory requirements and reduces dynamic lung hyperinflation that leads to improving oxygen content and so, the systemic oxygen availability in muscles increases [8].

Diaphragm excursion (DE) can be determined by ultrasound which can help to detect diaphragmatic dysfunction [9]. Ultrasound can also detect the thickness of the diaphragm in the zone of apposition [10]. Thickening measuring during deep breathing can reflect the magnitude of the effort of the diaphragm, similar to the ejection fraction of the heart [11]. In cases of air trapping, there was a progressive decrease in both the thickening and thickness of the diaphragm with increasing the severity of this air trapping [12].

Patients and methods

This study was a prospective randomized trial done on 40 patients diagnosed with COPD admitted to the Chest Department in Menoufia University Hospital from the period of March 2021 to May 2022. Written informed consent was taken from the patients; after obtaining ethics committee approval from Menoufia University Hospital (IRB: 6/2022CHES4-1).

This current study aimed to evaluate the effect of IS on ABG, spirometry, and on diaphragmatic function using ultrasound in patients hospitalized for COPD exacerbation and then follow-up 2 months later.

The inclusion criteria were as follows: a confirmed case of COPD according to the criteria of the global initiative for COPD (GOLD) with a post-bronchodilator forced expiratory volume/forced vital capacity (FEV1/FVC) ratio of <70% of patients [13]. The age of all patients was over 40 years.

Patients with a bad acoustic window by ultrasound (US) that interferes with US measurements, significant reactivity after bronchodilator use, other chronic chest diseases that result in hypoxia, neurological disease, pleural effusion, lung cancer, recent myocardial infarction, medical history of the chest, or abdominal major surgical operation or inability to complete the study procedures were excluded from this study.

The population of the study consisted of 40 patients who were hospitalized with an acute exacerbation of COPD and the patients were randomized and divided into two groups: Group 1: used the incentive spirometer plus medical treatment (G1 group = 20 patients) and group 2: used only medical treatment (G2 group= 20 patients). GOLD staging systems were used to classify all patients from stages I to IV [13].


All patients underwent a history taking including past medical history, drug history, any comorbidity, and smoking history. After a physical examination, a chest X-ray was obtained. Dyspnea was assessed by The modified Medical Research Council (mMRC) dyspnea scale which is a 5-point (0 to 4) scale depending on dyspnea severity and was explained in Arabic to all patients [14], then arterial blood gases (ABG), spirometry, and US assessment of the diaphragm were done on admission for all patients, and after 2 months of IS use and medical treatment in G1 and after medical treatment in only G2. The patients were hospitalized for about 10 days (6–14 days). The discharge criteria and hospital and home medications were the same for both groups according to GOLD guidelines.


ABG samples were taken by percutaneous puncture of the radial artery, during breathing room air, and analyzed on the gas analyzer (the Stat Profile pHOx series blood gases analyzers, USA) obtaining data were collected with an emphasis on PaO2 and PaCO2.


The spirometry was done in the pulmonary function Unit of Menoufia University Hospital (THOR Laboratories Kft Spirometer, Hungary) measuring data were collected with an emphasis on FEV1/FVC, FVC, and peak expiratory flow rate (PEFR).

Diaphragmatic ultrasonography

US was performed using a machine (Philips Affiniti 50 G; Germany), and the patients were asked to sit in a semi-recumbent position.

For the diaphragmatic excursion (DE), we examined by a convex probe (2–5 MHz) using B-mode (Fig. 1), then the M-mode was used to measure the amplitude of DE in quiet breathing and deep breathing [15].

Fig. 1
figure 1

Diaphragmatic excursion by m-mode (a): during quit breathing and (b): during deep inspiration. DE = distance A-distance B

The right hemidiaphragm was obtained by putting the probe subcostal or in the low intercostal area, in between the midclavicular and the mid-axillary lines. In the left hemidiaphragm, it is placed subcostal or more posteriorly than on the Rt side in between the anterior and the posterior axillary lines, and at least three different breathing cycles were recorded and take the average measurement.

Examination of the right hemidiaphragm is made by visualization of the liver window, but on the left side, the narrow window of the spleen makes it more difficult. In this case, we can place the probe in a more coronal position and parallel to the ribs [16].

Measurements of the diaphragmatic thickness (DT) were done at the zone of apposition, near the costophrenic angle in between the anterior and mid-axillary lines like the technique of Ueki et al. [17]. The diaphragm appeared as a structure of three layers. A non-echogenic muscle layer in-between 2 echogenic layers (diaphragmatic pleura and peritoneal serosa) [18]. DT was measured at the end of inspiration and the end of expiration bilaterally (Fig. 2). The examination was done by the linear probe (6–12 MHz).

Fig. 2
figure 2

Measurement of diaphragmatic thickness by the linear probe (a): during end expiration, (b) during end inspiration

The percentage of DT fraction done by the formula: (DT at end inspiration) - (DT at end-expiration)/(DT at end-expiration) × 100% [11].

Incentive spirometry (IS)

Inspiratory muscle training (IMT) is done by threshold loading or by resistive breathing in most studies. But it was not available for us to do it. The IS is an easy and cheap device that can easily be used for inspiratory muscle training at the bedside.

The IS used was a flow-oriented incentive spirometer (UNICARE, model UNA01, China), which had three chambers, 600, 900, and 1200 cc/s, with a ball in each chamber and a mouthpiece (Fig. 3). The patients were first trained to use it by one of the chest physicians. After a quiet exhalation, they were instructed to take slow full inspirations and to keep it for as long as they can (at least for 5 s) and then expire slowly. The balls were raised and suspended up by the sustained inspiration that corresponded to the inspiratory flow. The device is used during wake time every hour at least 5–10 times in the session [7]. IS was used for 2 months from the 1st day of admission. Every 2 weeks, telephone contact with the patients was done to ensure compliance, and also one of the patient’s relatives who is the main health caregiver has been instructed for the maneuver to follow up with the patient.

Fig. 3
figure 3

Incentive spirometer used in the study (UNICARE, China)

Statistical analysis

Data were collected, tabulated, and statistically analyzed using an IBM personal computer with Statistical Package of Social Science (SPSS) version 20 (SPSS, Inc., Chicago, Illinois, USA). Quantitative data were presented as mean, standard deviation (SD), range, and qualitative data were presented as numbers and percentages.

Chi-square test (χ2) is used to study the association between two qualitative variables; when the expected cell count of more than 25% of cases was less than 5, Fischer’s exact test for 2 × 2 tables were used, t test was used for comparison between two groups having quantitative variables, and Mann-Whitney test (nonparametric test) was used for comparison between two groups not normally distributed having quantitative variables. Paired t test was used for comparison between two related groups having quantitative variables, and Wilcoxon signed-rank test (nonparametric test) was used for comparison between two related groups not normally distributed having quantitative variables. The significance level was set at a P value of <0.05.


Forty patients diagnosed with COPD were admitted to the Chest Department in Menoufia University Hospital by exacerbation. The patients were randomly divided into 2 groups: group 1 (20 patients, 19 males and 1 female, age 60.7±5.99 years) and group 2 (20 patients with 18 males and 2 females, age 60.3±6.44 years). There were no statistically significant differences between both groups regarding socio-demographics, comorbidities, and clinical data (Table 1) and between both groups on admission regarding ABG, spirometry (Table 2), and diaphragmatic ultrasound finding (Table 3).

Table 1 Socio-demographic and comorbidities of the studied groups (N=40)
Table 2 Comparison between the studied groups regarding ABG finding and spirometry finding (N=40)
Table 3 Comparison between the studied groups regarding diaphragm finding by ultrasound (N=40)

After 2 months of the study, there were statistically significant differences between both groups regarding FEV1/FVC and Lt DE in deep inspiration (P value 0.04 and 0.048, respectively) and highly statistically significant differences regarding PaCO2 and Rt and Lt DT ratio (P value 0.001, 0.007 and 0.001, respectively) (Tables 4 and 5).

Table 4 Comparison between the studied groups regarding ABG finding and spirometry finding after 2 months (N=40)
Table 5 Comparison between the studied groups regarding diaphragm by ultrasound finding after 2 months (N=40)

G1 showed high statistically significant differences before and after the IS used with medical treatment regarding PaO2, PaCO2 (P value 0.002 and 0.003, respectively), FEV1/FVC, and PEFR (P value 0.001) together with all diaphragmatic findings by US (P value 0.001) but no statistically significant differences regarding FVC. The dyspnea scale improved but did not reach a significant level (P=0.235) (Tables 6 and 7).

Table 6 ABG and spirometry before and after 2 months of IS use and medical treatment among group I (N=20)
Table 7 Comparison between diaphragm finding by ultrasound before and after 2 months among group I

G2 showed statistically significant differences regarding PaO2 (P value 0.011) and highly statistically significant differences regarding Rt DE in quit breathing (P value 0.008), but no statistically significant differences regarding other parameters.


This study aimed to evaluate the effect of IS use for 2 months on ABG, spirometry functions, and diaphragmatic excursion and thickness ratio in COPD patients hospitalized by acute exacerbation. The results showed that in COPD patients, incentive spirometry for a short duration can improve some respiratory functions, and blood gases and can improve diaphragmatic functions, so it can be a supplemental therapy in a COPD management program.

There were statistically significant differences between both groups after 2 months regarding PaCO2 and FEV1/FVC (P=0.001 and 0.042, respectively). There was a statistically significant improvement in the results of PaO2, PaCO2, FEV1/FVC, and PEFR in group I before and after 2 months of IS but the mMRC dyspnea scale did not reach a significant level although its value improved.

Igarashi et al. studied the effects of IS on pulmonary functions and ABG (that were measured at the start of the program, and 2 and 4 weeks after the start) in normal advanced age and COPD groups, they found that there were significant increases in vital capacity, FEV1, PEFR, the flow at 75 % VC (V75), maximal voluntary ventilation MVV and PaO2, and a significant decline in alveolar-arterial oxygen gradient D(A-a) O2 at both 2 and 4 weeks after the start in both groups. In addition, V25 increased significantly in the COPD group [19].

In another study that evaluated the effect of incentive breathing exercise that was given for half an hour every day for 6 weeks on patients of COPD in a controlled study, there was a significant increase in vital capacity and a decrease in air trapping in the exercise group. Also, there was a remarkable improvement in the feeling of well-being and breathlessness [20].

Scherer et al. studied the effects of inspiratory muscle training by using a portable device in COPD patients for an 8-week duration, and the control group used the IS to perform breathing exercises. The study showed that the breathing exercises improved dyspnea and the maximum inspiratory pressure (PImax) in the IS group because of an improvement in their inspiratory muscle performance [21].

Ahmad et al. found that there were significant changes from baseline after a 4-week intervention of a combination of inspiratory muscle training (IMT) and chest physiotherapy treatments in pulmonary function, exercise tolerance, the strength of inspiratory muscle, and quality of life among hospitalized patients with mild to moderate COPD [22]. Also, it is reported by Cortopassi et al. and Barakat et al. with changes of 2.6% and 16.2%, respectively in FEV1/FVC [23, 24].

The study of Tout et al. showed a significant increase in FEV1 and PEFR in COPD patients who underwent a protocol of rehabilitation utilizing Threshold® inspiratory muscle training (IMT) [25].

Smart et al. studied COPD patients and the study showed that besides increasing respiratory muscle strength, IMT improved the functional capacity, exercise capacity, dyspnea, and quality of life [26].

These effects may be explained by the fact that IS can assist the subject to inspire lung capacity through sustained maximal inhalation, helped by visual feedback. This will increase transpulmonary pressure and lung volume together with diaphragmatic mobility. The collapsed areas in the lungs will expand that preventing alveolar collapse together with inducing greater lower inspiratory muscle activity that improves breathing capacity [7, 27,28,29,30].

In comparison with the study of Basoglu et al. who studied the efficacy of IS in COPD patients, there were no significant differences in pulmonary functions between the IS group and the post-treatment group but the use of IS for 2 months with medical treatment improved the arterial blood gases and health-related quality of life [31].

In this study, there was a statistically significant difference between the studied groups after 2 months regarding left DE in deep inspiration, and Rt & Lt diaphragm thickness ratio.

There was a statistically significant improvement in all diaphragmatic findings by the US before and after 2 months among group I

The contractile force of all respiratory muscles is proportional to the increase in the intra-alveolar pressure which explains the fact that to obtain the total lung capacity, intense muscle activity should occur [32].

To make breathing exercises with the IS, the person mobilizes a large tidal volume (TV) with a low respiratory rate, which increases the muscle strength by increasing the inspiration/expiration ratio [33].

There are limited studies that study the value of IS on both diaphragmatic excursion and thickness in COPD patients.

Various research studied the effects of IS on a diaphragmatic excursion in different studying groups that came following our study, e.g., Udayamala et al. found that IS exercise promotes a greater DE assessed by ultrasonography in healthy participants during both rest and breathing exercises [34]. Also, Darnley et al. reported that IMT may improve exercise capacity, diaphragmatic function, and feelings of dyspnea in individuals with chronic coronary artery disease [35].

Hala et al. studied chronic kidney disease (CKD) patients; their results showed that IS training for 8 weeks had significant good effects on DE and quality of life in CKD patients on regular hemodialysis [36].

The effect of IS on DE may be due to the improvement of diaphragm power and mechanics together with the strength of inspiratory muscles.

On the other hand, the results of this study conflict with the results of the study of Barbalho-Moulim et al. who stated that there was a non-significant change in DE with the IMT program for 4 weeks, but the difference could be explained by the short study duration and different in studying group [37].

The study of Ramírez-Sarmiento et al. studied the effect of pressure threshold IMT on the structural changes in the respiratory muscles of patients with COPD. The muscle fibers from the external intercostal muscle before and after 5 weeks showed significant increases in the proportion of type I fibers (by 38%) and the size of type II fibers (by 21%). This structural remodeling leads to functional improvement [38].

Many studies observed that breathing exercises against load increase maximum inspiratory pressure (MIP) together with the endurance capacity of inspiratory muscles as it leads to significant hypertrophy of type I and type II fibers of the diaphragm [39, 40].

Cheng et al stated that after respiratory muscle training, COPD patients exhibited a significant increase in FEV1, MIP, maximum expiratory pressure (MEP), SpO2 at rest, DT fraction, and DE (all P < 0.01) [41].

We considered US measurements obtained from the right and left sides, although some studies studied only the right side of the patients, as the left side has a poor acoustic window [42].

We tried to assess the left diaphragmatic function and found that the left diaphragmatic excursion improved better than the right side in G1 before and after IS use and between both groups after 2 months. This needs to be evaluated in future studies.

There was a statistically significant increase in the results of PaO2 and Rt DE in quit inspiration in group II before and after 2 months of medical treatment. This can be explained by the improvement of oxygenation after treatment in the exacerbation. The PaCO2 improved more in G1 this may be explained by more effect on respiratory muscle function by IS.

The pulmonary function parameters did not show significant differences although improvements in lung function were stated in studies on long-acting B agonists as maintenance therapy; this may be due to the short duration of the study and the unknown actual start of medications in each patient [43,44,45].


It was concluded that the IS improves ABG, some parameters in pulmonary functions, and diaphragmatic functions in COPD patients who are hospitalized by acute exacerbations. Further studies are needed to assess the value of IS in COPD patients and to compare it with other respiratory therapy modalities for a longer period and its correlation with GOLD classifications. Also, evaluation of diaphragmatic function after IS in COPD patients with more facilities, e.g., pressure-derived parameters and electromyography.

Limitation of the study

There were some limitations to this study. The number of patients needs to be increased. The study did not include stable COPD patients or the effect of IS on the quality of life, and these are recommended in future studies. Not all parameters of pulmonary functions had been studied.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.



Arterial blood gases


Chronic obstructive pulmonary disease


Diaphragmatic excursion


Diaphragmatic thickness


End-expiratory lung volume


Forced expiratory volume


Forced vital capacity


Inspiratory muscle training


Incentive spirometry


Modified Medical Research Council


Peak expiratory flow rate




  1. Soriano JB, Kendrick PJ, Paulson KR, Gupta V, Abrams EM, Adedoyin RA et al (2020) Prevalence and attributable health burden of chronic respiratory diseases, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Respir Med 8(6):585–596

    Article  Google Scholar 

  2. Petrovic M, Reiter M, Zipko H, Pohl W, Wanke T (2012) Effects of inspiratory muscle training on dynamic hyperinflation in patients with COPD. Int JChronic ObstructPulmonary Dis 7:797–805

    Google Scholar 

  3. McKenzie DK, Butler JE, Gandevia SC (2009) Respiratory muscle function and activation in chronic obstructive pulmonary disease. J Appl Physiol 107(2):621–629

    Article  Google Scholar 

  4. Geddes EL, Reid WD, Crowe J, O”Brien K, Brooks D (2005) Inspiratory muscle training in adults with chronic obstructive pulmonary disease: a systematic review. Respir Med 99(11):1440–1458

    Article  Google Scholar 

  5. Stock MC, Downs JB, Gauer PK, Alster JM, Imrey PB (1985) Prevention of postoperative pulmonary complications with CPAP, incentive spirometry, and conservative therapy. Chest 87:151–157

    Article  CAS  Google Scholar 

  6. Chutter TAM, Weissman C, Starker PM, Gump FE (1989) Effect of incentive spirometry on diaphragmatic function after surgery. Surgery 105:488–493

    Google Scholar 

  7. American Association for Respiratory Care (1991) Clinical practice guideline. Incentive Spirometry Respir Care 36:1402–1405

    Google Scholar 

  8. Casaburi R, Porszasz J, Burns MR, Carithers ER, Chang RS, Cooper CB (1997) Physiologic benefits of exercise training in rehabilitation of patients with severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med 155(5):1541–1551

    Article  CAS  Google Scholar 

  9. Boussuges A, Gole Y, Blanc P (2009) Diaphragmatic motion studied by m-mode ultrasonography: methods, reproducibility, and normal values. Chest 135:391–400

    Article  Google Scholar 

  10. Wait JL, Nahormek PA, Yost WT, Rochester DP (1989) Diaphragmatic thickness-lung volume relationship in vivo. J Appl Physiol 67:1560–1568

    Article  CAS  Google Scholar 

  11. DiNino E, Gartman EJ, Sethi JM, McCool FD (2014) Diaphragm ultrasound as a predictor of successful extubation from mechanical ventilation. Thorax 69:423–427

    Article  Google Scholar 

  12. Smargiassi A, Inchingolo R, Tagliaboschi L, di Marco BA, Valente S, Corbo GM (2014) Ultrasonographic assessment of the diaphragm in chronic obstructive pulmonary disease patients: relationships with pulmonary function and the influence of body composition – a pilot study. Respiration 87(5):364–371

    Article  Google Scholar 

  13. Vestbo J, Hurd SS, Agustí AG, Jones PW, Vogelmeier C, Anzueto A et al (2013) Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med 187(4):347–365

    Article  CAS  Google Scholar 

  14. Bestall JC, Paul EA, Garrod R, Garnham R, Jones PW, Wedzicha JA (1999) Usefulness of the Medical Research Council (MRC) dyspnoea scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 54(7):581–586.

    Article  CAS  Google Scholar 

  15. Testa A, Soldati G, Giannuzzi R, Berardi S, Portale G, Silveri NG (2011) Ultrasound M-mode assessment of diaphragmatic kinetics by anterior transverse scanning in healthy subjects. Ultrasound Med Biol 37(1):44–52

    Article  Google Scholar 

  16. Gerscovich EO, Cronan M, McGahan JP, Jain K, Jones CD, McDonald C (2001) Ultrasonographic evaluation of diaphragmatic motion. J Ultrasound Medi 20(6):597–604

    Article  CAS  Google Scholar 

  17. Ueki J, De Bruin PF, Pride NB (1995) In vivo assessment of diaphragm contraction by ultrasound in normal subjects. Thorax 50(11):1157–1161

    Article  CAS  Google Scholar 

  18. Fantini R, Mandrioli J, Zona S, Antenora F, Iattoni A, Monelli M et al (2016) Ultrasound assessment of diaphragmatic function in patients with amyotrophic lateral sclerosis. Respirology 21(5):932–938

    Article  Google Scholar 

  19. Igarashi T, Konishi A, Suwa K (1994) [The effects of incentive spirometry on pulmonary functions] Masui. Japan J Anesthesiol 43(5):770–773 PMID: 8015170

    CAS  Google Scholar 

  20. Tiwary RS, Lakhera SC, Kain TC, Sinha KC (1989) Effect of incentive breathing on lung functions in chronic obstructive pulmonary disease (COPD). J Assoc Phys India 37(11):689–691

    CAS  Google Scholar 

  21. Scherer TA, Spengler CM, Owassapian D, Imhof E, Boutellier U (2000) Respiratory muscle endurance training in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 162:1709–1714

    Article  CAS  Google Scholar 

  22. Ahmad H, Justine M, Othman Z, Mohan V and Mirza FT (2013) The outcomes of short-term inspiratory muscle training (IMT) combined with chest physiotherapy in hospitalized COPD patients. Bangladesh J Med Sci 12(4);398–404.

  23. Barakat S, Michele G, George P, Nicole V, Guy A (2008) Outpatient pulmonary rehabilitation in patients with chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis 3:155–162

    Article  Google Scholar 

  24. Cortopassi F, Castro AA, Porto EF, Colucci M, Fonseca G, Torre-Bouscoulet L et al (2009) Comprehensive exercise training improves ventilatory muscle function and reduces dyspnea perception in patients with COPD. Monaldi Arch Chest Dis 71:106–112

    CAS  Google Scholar 

  25. Tout R, Tayara L, Halimi M (2013) The effects of respiratory muscle training on improvement of the internal and external thoraco-pulmonary respiratory mechanism in COPD patients. Ann Phys Rehabil Med 56(3):193–211

    Article  CAS  Google Scholar 

  26. Smart N, And GF, Dieberg G (2013) Efficacy of inspiratory muscle training in chronic heart failure patients: a systematic review and meta-analysis. Int J Cardiol 167:1502–1507

    Article  Google Scholar 

  27. Overend TJ, Anderson CM, Lucy SD, Bhatia C, Jonsson BI, Timmermans C (2001) The effect of incentive spirometry on postoperative pulmonary complications: a systematic review. Chest 120(3):971–978

    Article  CAS  Google Scholar 

  28. Tomich G, França D, Diório A, Britto R, Sampaio R, Parreira V (2007) Breathing pattern, thoracoabdominal motion and muscular activity during three breathing exercises. Braz J Med Biol Res 40:1409–1417

    Article  CAS  Google Scholar 

  29. Yamaguti WP, Sakamoto ET, Panazzolo D, Peixoto CaC, Cerri GG, Albuquerque AL (2010) Diaphragmatic mobility in healthy subjects during incentive spirometry with a flow-oriented device and with a volume-oriented device. J Bras Pneumol 36:738–745

    Article  Google Scholar 

  30. Santos TV, Ruas G, Sande de Souza LA, Volpe MS (2012) Influence of forward leaning and incentive spirometry on inspired volumes and inspiratory electromyographic activity during breathing exercises in healthy subjects. J Electromyogr Kinesiol 22:961–967

    Article  Google Scholar 

  31. Basoglu OK, Atasever A, Bacakoglu F (2005) The efficacy of incentive spirometry in patients with COPD. Respirology 10(3):349–353.

    Article  Google Scholar 

  32. Wattie J (1998) Incentive spirometry following coronary artery bypass surgery. Physiotherapy 84:508–514.

    Article  Google Scholar 

  33. Parreira VF, Tomich GM, Britto RR, Sampaio RF (2005) Assessment of tidal volume and thoracoabdominal motion using volume and flow-oriented incentive spirometers in healthy subjects. Braz J Med Biol Res 38:1105–1112

    Article  CAS  Google Scholar 

  34. Udayamala E, Alaparthi GK, Augustine AJ, Anand R, Mahale A, Zulfeequer CP, Shyam KK (2016) Comparison of diaphragmatic excursion during diaphragmatic breathing exercise, volume and flow oriented incentive spirometer in healthy subjects: a randomized cross over trial. Online J Health Allied Scs 15(3):7 Available at URL:

    Google Scholar 

  35. Darnley GM, Gray AC, McClure SJ et al (1999) Effects of resistive breathing on exercise capacity and diaphragm function in patients with ischaemic heart disease. Eur J Heart Fail 1(3):297–300.

    Article  CAS  Google Scholar 

  36. Hala M, Hadeer SM, Tarek FA, Fatma AM (2018) Efficacy of incentive spirometer training on diaphragmatic excursion and quality of life in hemodialysis patients. Med J Cairo Univ 86:3997–4002

    Article  Google Scholar 

  37. Barbalho-Moulim MC, Miguel GP, Forti EM, Campos Fdo A, Costa D (2011) Effects of preoperative inspiratory muscle training in obese women undergoing open bariatric surgery: respiratory muscle strength, lung volumes, and diaphragmatic excursion. Clinics (Sao Paulo) 66(10):1721–1727

    Article  Google Scholar 

  38. Ramírez-Sarmiento A, Orozco-Levi M, Güell R, Barreiro E, Hernandez N, Mota S et al (2002) Inspiratory muscle training in patients with chronic obstructive pulmonary disease: structural adaptation and physiologic outcomes. Am J Respir Crit Care Med 166(11):1491–1497

    Article  Google Scholar 

  39. Andrew H, Donald AM, Andrew D (1989) Targeted inspiratory muscle training improves respiratory muscle function and reduces dyspnoea in patients with chronic, Obstructive Pulmonary Disease. Annals of Int Med 111:117–124

    Article  Google Scholar 

  40. Belman MJ, Mittman C (1980) Ventilatory muscle training improves exercise capacity in chronic obstructive pulmonary disease patients. Am Rev Respiratory Dis. 121(2):273–280

    CAS  Google Scholar 

  41. Cheng YY, Lin SY, Hsu CY, Fu PK (2022) Respiratory muscle training can improve cognition, lung function, and diaphragmatic thickness fraction in male and non-obese patients with chronic obstructive pulmonary disease: a prospective study. Journal of. Pers Med 12(3):475

    Article  Google Scholar 

  42. Tobin MJ, Laghi F, Brochard L (2009) Role of the respiratory muscles in acute respiratory failure of COPD: lessons from weaning failure. J Appl Physiol 107(3):962–970

    Article  Google Scholar 

  43. Boyd G, Morice AH, Pounsford JC, Siebert M, Peslis N, Crawford C (1997) An evaluation of salmeterol in the treatment of chronic obstructive pulmonary disease (COPD). Eur Respir J 10:815–821

    Article  CAS  Google Scholar 

  44. Szafranski W, Cukier A, Ramirez A, Menga G, Sansores R, Nahabedian S et al (2003) Efficacy and safety of budesonide/formoterol in the management of chronic obstructive pulmonary disease. Eur Respir J 21:74–81

    Article  CAS  Google Scholar 

  45. Tashkin DP, Fabbri LM (2010) Long-acting beta-agonists in the management of chronic obstructive pulmonary disease: current and future agents. Respir Res 11(1):1–14

    Article  Google Scholar 

Download references


Not applicable.


No financial support or sponsorship.

Author information

Authors and Affiliations



Study design: M.E. Data collection: A.E, H.E, and M.E . Data analysis: S.A and M.E. Interpretation of results: A.E, S.A and M.E. Initial draft: A.E and H.E. final review of the manuscript content: all authors. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Amal A. El-Koa.

Ethics declarations

Ethics approval and consent to participate

The study was approved by the Ethics Committee of Menoufia University Hospital. Written informed consent was obtained from all participants.

Consent for publication


Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit

Reprints and Permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

El-Koa, A.A., Eid, H.A., Abd Elrahman, S.R. et al. Value of incentive spirometry in routine management of COPD patients and its effect on diaphragmatic function. Egypt J Bronchol 17, 8 (2023).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI:


  • Chronic obstructive pulmonary disease
  • Incentive spirometry
  • Arterial blood gases
  • Spirometry
  • Diaphragmatic ultrasound