Chronic obstructive pulmonary disease (COPD) is an unremitting disease characterized by a decline in lung function over the time and insidiously progressive respiratory disability. In the global burden of disease study conducted under the auspices of WHO and World Bank, the worldwide prevalence of COPD in 1990 was estimated to be 9.34/1000 in men and 7.33/1000 in women for all age
groups1. The COPD is also common in India as prevalence rate is about 5% in male and 2.7% in female adult population over 30 years of age and total disease burden was calculated as 12.36 million based on 1991 census23. COPD is currently fourth leading cause of death in the world and
further increase in the prevalence and mortality of disease can be predicted in the coming decades4. COPD is also the biggest cause of unnatural death in rural India and its prevalence is increasing continuously because of widespread habit of smoking and the use of cowdung, wood and residual crop as cooking fuels. The impact of COPD on morbidity is even greater then on mortality. According to the projections of the global burden of disease study,
COPD will be the fifth leading cause of DALY′S lost world wide in year 2020 behind ischemic heart disease, major depression, traffic accidents and cerebrovascular accidents, which was ranked 12 in year 199014. Dyspnea, the hallmark symptom of COPD is the reason the most patient seek medical attention and is a major cause of disability and anxiety associated with the disease. This
breathlessness is characteristically persistent and progressive. Initially, dyspnea is noted only on unusual effort but eventually, present during every day activities like dressing, walking, cooking etc. or even at rest, leaving the patient confined to the home. Exercise intolerance is an another troubling manifestation of this disease6. There are pieces of evidences point to the fact that features of impaired exercise tolerance
are not simple consequences of loss of pulmonary functions but because of combination of exertional dyspnea, cardiovascular limitation, nutritional impairment, psychological factors and skeletal muscle dysfunctions which are commonly encountered in COPD patients7. Because of exercise intolerance patients typically limit their activity to avoid these uncomfortable sensation of dyspnea, leg fatigue and
discomfort8. Activity limitation reduces social interaction and promotes depression and anxiety9 which further worsens the impact of dyspnea. This vicious cycle of exertional dyspnea, immobility, social isolation, depression and lack of fitness in COPD is responsible for morbidity4. People suffering from severe form of this disease usually spent their
remaining years of life in bed and have impaired health related quality of life and high utilization of health care resources1410. There is currently no cure for COPD, and much attention has been paid to smoking cessation as the sole beneficial measures for both development and
prognosis of COPD. Because this is effective only in 20% patients11, symptomatic treatment with bronchodilator is the mainstream of therapy24. Although modern medicines can alleviate symptoms and can improve exercise capacity but they have a limited role in overall management of
COPD1213. Years ago, patients with chronic pulmonary disease were given a standard prescription for rest and avoidance of exercises. The stress imposed by exercise was considered deleterious to people with pulmonary disorders. They were treated as invalids, sometime being referred to as “respiratory
cripples”. Breathing and physical exercises, as accessories to medical and surgical treatment, were described by MacMahon in 191514. By 1919, “a very large experience of chest cases” had shown how very important it is that when there is serious lung collapse and chest deformity, following wounds or illness, breathing and physical exercise should, in certain cases, be given as accessories to medical and surgical treatment, if the best possible
recovery is to be assured15. This philosophy continues today and is supported by an increasing evidence base47161718. Most commonly used pursed lip
breathing (PLB) is a breathing strategy often spontaneously employed by patient with COPD and claims an immediate subjective benefits1619202122. Breathing exercises has been shown to improve gas
exchanges18202122, efficiency of ventilation23 and exercise performance18 but the efficacy of breathing exercises in relieving dyspnea varies greatly among
patients21232425. Active cycle of breathing techniques (ACBT) and variants of diaphragmatic breathing e.g. forced-exhalation abdominal breathing, forced inhalation abdominal breathing, forced exhalation with walking and mobilization of lower ribs are other types of breathing exercises used in clinical
practices. Since dyspnea is the symptom mostly associated with dysfunction for patients with COPD26, a reasonable ′hypothesis is that treatment of dyspnea which is mainly due to a limited ventilatory capacity will result in improved functional outcome and ultimately health related quality of life. Though the mechanism of dyspnea is not clearly understood and there is no universal theory that completely explains its physiological basis, there are several reasons for ventilatory limitation78. In patients with COPD expiratory airway obstruction may arise as a results of the airway collapse during
expiration27. Airway collapse may arise when pleural pressure is higher than bronchial pressure and overcomes the rigidity of the airway wall28. The pressure difference over the airway wall, the “transmural pressure” becomes negative as expiration in COPD is not passive but is the result of active muscular effort. The resulting airway collapse consequently leads to increased airway resistance and
expiratory flow limitation that increases the work of breathing. Severe airflow obstruction can also lead to dynamic hyperinflation due to impaired lung emptying and higher end expiratory lung volume that worsens during exercises as well as hyperpnea of any other cause (anxiety)29. This hyperinflation limits the tidal volume response (Vt) to exercise, increases the elastic load to the
inspiratory muscle, and leads to mechanical disadvantage of the respiratory muscle by forcing them into a shortened position (altered length- tension relationship). Indeed the degree of hyperinflation is an important predictor of exertional dyspnea. Ventilatory limitation also occurs as a result of, gas exchange abnormalities that arises from excess physiological dead space to tidal volume ratio (dv/ dt), ventilation perfusion (V/Q) mismatch, reduction in diffusing capacity and hypoxemia30. Pursed lip breathing results in a positive expiatory pressure (PEP) and is thought to have similarities with continuous positive airway pressure (CPAP) and positive end expiratory pressure
(PEEP)19. By creating an obstruction at the lip, this active expiration may be intensified and the resulting greater increase in positive expiratory pressure (PEP) may increase bronchial pressure and thus “tansmural” pressure, leading to a diminution of airway collapse: In various studies there was a linear relationship between the effectiveness of PEP breathing in decreasing the nonelastic resistance across the lung and airway and the collapsibility of
airways19. Barach et al.22 performed bronchograms in asthmatic patients and evaluated radiologically the diameter of the tracheobronchial tree, with or without positive pressure breathing using pressure of 4-8 cm of water. He demonstrated less constriction of bronchi occurred with the use of positive expiratory pressure (PEP). As the PEP of 5 cm
H2O is within the range of mouth pressure reached during expiration with pursed lips in patients with COPD, he advocated the use of pursed lip expiration in both asthma and emphysema. Prevention of airway collapse may result in more homogenous ventilation because of a shift of ventilation of relatively hyperventilated parts of the lung to relatively
hypoventilated parts. This improved ventilation in hypoventilated parts of the lung probably results in an improved alveolar ventilation and an augmentation of the local PO2. This consequently leads to a reduction of the local hypoxic vasoconstriction and a decrease in physiological dead space ventilation (VD/VT) or
decrease in volume of trapped gases (VTG) without significant change in forced residual capacity as found by Schans et al in their study of effect of positive expiratory pressure breathing during exercises in patients with COPD19. Ventilation in poorly ventilated parts of the lung may also improve when functional residual capacity (FRC) increases leading to a decrease resistance of the small peripheral and collateral
airways31. Parsons et al observed that there is a more homogenous ventilation and perfusion distribution due to the effect of intermittent positive pressure breathing and continuous positive airway pressure on ventilation and perfusion in healthy subjects. This effect seems to be more pronounced in COPD than the healthy subjects32. Thoman R22, proposed that those segments of lungs with greatest fall and/or greater increase in flow resistance will receive disproportionately less of the tidal volume. Therefore, the abnormal and uneven distribution of gases in emphysema will be accentuated with increased respiratory rate. Work of breathing increases disproportionately and there is increased
CO2production with increasing respiratory rate. So the slowing of respiration alone would be expected to enhance the ventilation of those subdivisions of the lung which normally are underventilated. They found that tidal volume (VT) increases while respiratory rate decreases and CO2elimination improves without
significant change in forced residual capacity and volume of slow space (VS) by pulsed lip breathing. They found that indeed there was an increase in ventilatory rates (Vs) of those most slowly ventilated lung components, when respiratory rate slowed down with pursed lip breathing. Mueller et al21 also observed that pursed lip breathing was accompanied by both increased tidal volume and decreased respiratory rate, more so in subjects who claimed benefit from pursed lip breathing (PLB) in comparison to the subjects who did not feel improvement with pursed lip breathing. An improvement in PO2and
PCO2was observed in both groups during rest, but not during exercise and he concluded that benefits of pursed lip breathing (PLB) were due to decreased airway collapse, decreased respiratory rate, and increased tidal volume but found no relationship between symptomatic benefit from pursed lip breathing (PLB) and improvement in ABG. Mueller as well as other investigators2021 found that although pursed lip breathing was more effective in the sense that less air exchange was required to absorb a given amount of oxygen, there was no increase in oxygen uptake. This suggests that PLB does not significantly
alter the work of breathing. It is known that hyperactivity of the inspiratory muscles is a cause for the sensation of dyspnea. Their assumption that decrease in dyspnea sensation which is often thought to be related to pursed lip breathing might be caused by reduced activity of respiratory muscle is still a matter of debate19. Through encouraging the use of diaphragm, the principal and efficient
muscle of inspiration, the oxygen cost of breathing can be decreased. Decreasing the use of accessory muscles also decreases the work of breathing. The biofeed can be used to discourage accessory muscle firing during the ventilatory cycles. Because use of the diaphragm as in diaphragmatic breathing was found to increase rather than decrease the level of dyspnea at present routine use of diaphragmatic breathing in pulmonary rehabilitation is not
recommended16 but recently Jones et al.33 compared the oxygen cost (i.e., work of breathing) in three common breathing exercises i.e. diaphragmatic breathing (DB), pursed lip breathing (PLB) and combination of both (CB) with that of spontaneous breathing in COPD patients and found that mean VO2 ± S.D. was lower during the breathing exercise (165.8 ± 22.3
ml O2/min for DB, 164.8 ± 20.9 ml O2/ min for PLB and 165.7 ± 20.7 ml O2/min for C.B.) compared with spontaneous breathing 174.5 ± 25.7 ml O2/min. Correspondingly mean respiratory rate (±SD) was higher during SB (17.3 ± 4.32 breaths/min), followed by DB
(15.0±4.32 breaths/min), PLB 12.8 ± 3.53 breath/min and CB (11.2 ± 2.7 breath/min). Bianchi R et al34 assessed the volumes of chest wall compartments (rib cage and abdomen) using an optoelectronic plethysmograph and concluded that by decreasing respiratory frequency and lengthening expiratory time
(TE), pursed lip breathing decreases end expiratory volume of chest wall (Vcwee), which is mostly at the abdominal level et al. decrease in end expiratory volume of abdomen (VAbee) and modulates the breathlessness. Changes in end expiratory volume of chest wall is
related to baseline airway obstruction (FEV1) but not due to hyperinflation (forced residual capacity). So, improvement in dyspnea observed after breathing exercises can be attributed to the decrease in respiratory rate, increase in tidal volume, decreased physiological dead space to tidal volume ratio (dv/dt), improved blood gases and decrease the work of breathing by decreasing or preventing airway collapse and
promoting more homogenous ventilation as observed in various clinical trials of breathing exercises. Though true values of these techniques have not yet been established16172535 even then they are usually advise by physicians and physiotherapists in an attempts to achieve improvement. Esteve et al36 found that breathing pattern training, enhanced with visual feedback increased the FEV1, and FVC in patients with COPD. At present there is no other documented reports of improvement in FEV2, even following
pulmonary rehabilitation having breathing exercises as a component573738 and this area needs further evaluation by more clinical trials. Killian and coworkers showed that exercise capacity in COPD patient is
mainly limited by subjective symptoms such as muscle fatigue and dyspnea without the patient reaching their physiological limitations89. Now as this is well known that a “vicious cycle” of exertional dyspnea, exercise and activity limitation, psychosocial illness are the major causes of poor health related quality of life in COPD patients, there are increasing evidence that physical reconditioning which
is most essential component of pulmonary rehabilitation can improve the exercise capacity and health related quality of lifes5716173738. Casciari RJ et al18 found in
their study that breathing retraining increases exercise performance in subjects with severe chronic obstructive pulmonary disease. Schans et al19 observed that positive expiratory pressure breathing of 5 cm H2O which is in range of mouth pressure reached during expiration with pursed lip in patients with COPD increases the efficiency of ventilation at rest and during exercise, since same
work load is achieved with less ventilation. So the improvement in exercise tolerance seems to be due to the decrease in the sensation of dyspnea. That′s why these patients do not feel panic at the time of respiratory distress. Their self-confidence could be improved, which progressively increases activities of daily living that mimics exercise of physical reconditioning that can ultimately restore the patient to the highest level of functional capacity and improved health related quality of
life. However, the effect on quality of life has not been evaluated by other workers. Results of various clinical trials indicates that breathing exercises are the effective and economical methods for alleviating the symptoms and can improve health related quality of life (HRQL) if given as an adjuvant in the management of COPD along with standard medical treatment. 1. Murray CJL, Lopez AD. Alternative projections of mortality and disability by cause, 1990-2020.Global burden of disease study Lancet. 1997;349:1498–1504 2. Guidelines for management of chronic obstructive pulmonary disease (COPD) in India: A guide for physicians (2003). Indian J. Chest Dis. Allied Sci. 2004;46:137–153 3. Jindal SK, Agarwal AN, Gupta D. A review of population studies from India
to estimate national burden of COPD and its association with smoking Indian J Chest Dis Allied Sci. 2001;43:139–47 4. Global Initiative for Chronic Obstructive Lung Disease, 2004. Global Strategy for the diagnosis management and prevention of chronic obstructive pulmonary disease (updated 2005). Available from: www.goldcopd.org
5. Singh V, Khandelwal DC, Khandelwal R, Abusaria S. Pulmonary rehabilitation in patients with chronic obstructive pulmonary disease Indian J Chest Dis Allied Sci. 2003;45:13–17 6. Nici L. Mechanism and measures of exercise intolerance in chronic obstructive pulmonary disease Clin. Chest. Med. 2000;21(4):G93–704 7. Rochester CL. Exercise training in chronic obstructive pulmonary disease Journal of Rehabilitation
research & development. 2003;40(3)(Suppl 2):59–80 8. Killian KJ, LeBlanc P, Martin DH, Summers E, Jones NL, Campbell EJ. Exercise capacity and ventilatory, circulatory and symptoms limitation in patients with chronic airflow obstruction Am. Rev. Respir Disord. 1992;146:935–40 9. VanEde L, Yzermans CJ, Brouwer HJ. Prevalence of depression in patients with chronic obstructive pulmonary disease: a systemic review Thorax. 1999;54:688–92DISEASE AND ITS BURDEN
IMPACT OF DISEASE
ROLE OF PHARMACOTHERAPY
HISTORICAL BACKGROUND OF BREATHING EXERCISES
Rationales for Breathing Exercises: Pathophysiology of COPD
Airway
collapse, dynamic hyperinflation and Increase work of Breathing
EFFECT OF PURSED LIP BREATHING: PREVENTION OF AIRWAY COLLAPSE
HOMOGENOUS VENTILATION
INCREASE IN TIDAL
VALUE AND DECREASE IN RESPIRATORY RATE
Decrease in Work of Breathing ?
DECREASE IN END EXPIRATORY VOLUME OF ABDOMEN
EFFECT ON FEV1
EFFECT ON EXERCISE CAPACITY AND QUALITY OF LIFE
CONCLUSION
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Keywords:
Breathing exercises; COPD; HRQL; Dyspnea; Pursed lip breathing