Clinical Physiology of Chronic Obstructive Pulmonary Disease

Ali Al Talag, MD, Pearce Wilcox, MD, FRCP Clinical physiology of chronic obstructive pulmonary disease A variety of methods can be used to assess disturbances and dys- functions common in COPD, including pulse oximetry and exercise testing. ABSTRACT: The symptoms and func- lthough many different compression of these airways.5,6 Other tional limitations of chronic obstruc- factors may be involved in factors such as respiratory muscle tive pulmonary disease (COPD) are the development of COPD, dys function can further limit airflow a direct result of airway and lung A smoking is the most sig- in some patients. parenchymal processes. These pro - nificant. Exposure to tobacco smoke Hyperinflation can also occur in cesses lead to airflow obstruction, provokes a series of inflammatory COPD, leading to an increase in func- increased work of breathing, and gas processes involving the small as well tional residual capacity (FRC)—the exchange abnormalities. When ad- as the large airways and can also amount of air that remains in the lungs vanced, these can in turn cause pul- impair host defence mechanisms. In at the end of tidal exhalation. This can monary hypertension, cor pulmonale, predisposed individuals this leads to lead to gas trapping and an increase and left heart dysfunction. Catalogu- pathological processes that we have in residual volume (RV). As a conse- ing of symptoms, physical examina- come to recognize as chronic bronchi- quence, there is an augmentation of tion, and routine radiology are of lim- tis and emphysema. It is important to the inspiratory work of breathing, ited utility in the early diagnosis and note that bronchial inflammation can which is an important factor in pro- assessment of response to therapy be detected long before the disease is ducing dyspnea. As the expiratory for COPD. Patients can benefit from evident clinically1 and persists long time is essential for lung emptying, the use of laboratory measurements after the cessation of smoking,2 and factors that decrease this time, such as to manage this disorder. Spirometry that the inflammatory processes of an increasing respiratory rate during and oximetry have the broadest COPD are readily distinguishable exercise, result in a progressive in - application, while arterial blood gas from those of asthma.3,4 crease in FRC (Figure 1 ).7 This phe- and exercise testing have selected nomenon is called dynamic hyperin- utility. Physiological defects flation, and is largely responsible for Airflow limitation exercise limitation in COPD.7-11 and hyperinflation Expiratory airflow limitation is the principal physiological defect in COPD. Intrinsic airway factors re - Dr Al Talag is a fellow in the division of late to bronchial wall inflammation Respirology Medicine at the University of and include mucosal inflammation/ British Columbia. Dr Wilcox is a respirolo- edema, bronchial wall remodeling/ gist at St. Paul's Hospital, associate pro- fibrosis, and increased mucosal secre- fessor of medicine at UBC, the director for tions. Extrinsic factors involve the Respirology Training at UBC, and the med- loss of elastic tissue support for small ical director of the Pulmonary Function Lab- airways and the dynamic expiratory oratory St. Paul’s Hospital. VOL. 50 NO. 2, MARCH 2008 BC MEDICAL JOURNAL 97 Clinical physiology of chronic obstructive pulmonary disease Gas exchange disturbances more advanced disease can also con- function, which can lead to reduced Perturbations in gas exchange are tribute to hypercapnia and chronic res- mixed venous oxygenation. caused primarily by regional inequal- piratory acidosis. Other contributing ities of ventilation and perfusion (VQ factors to gas exchange disturbances Ventilatory muscle dysfunction mismatching).12 This process com- in advanced COPD are pulmonary A number of factors contribute to ven- monly produces hypoxemia, but in hypertension and impaired cardiac tilatory muscle dysfunction in COPD. A major factor is a consequence of hyperinflation, which limits force gener- ation and endurance,13 and places the inspiratory muscles at a mechan ical e is disadvantage. Other factors include TLC rc nutritional alterations, a sustained ring exe inflammatory response that affects the contractile apparatus, tissue hypoxia, and loss of muscle mass.14,15 These fac- inflation du r tors also affect other skeletal muscles, ise hype c rc which may further contribute to exer- me (L) 16,17 u cise limitation. Dynami Vol Cardiovascular disturbances eases with exe Cardiovascular disturbances are com- cr in mon in COPD and may represent a High FRC to start with C FR complication of COPD itself or may be triggered by the same factor, that is, smoking. Recently it has been pro- Time (sec) posed that lung inflammation may directly affect atherogenesis by dri- ving systemic inflammation. Figure 1. Dynamic hyperinflation in patients with emphysema during exercise. Pulmonary hypertension is a late FRC: functional residual capacity TLC: total lung capacity complication of COPD and indepen- Predicted curve Patient’s volume-time curve FVC me (L) u Vol FEV1 1234567891011 Figure 2. Volume-time curve of a patient with COPD. Airway obstruction is indicated by the significant straightening of the patient’s curve compared with the predicted curve. FEV1: forced expiratory volume in 1 second FVC: forced vital capacity 98 BC MEDICAL JOURNAL VOL. 50 NO. 2, MARCH 2008 Clinical physiology of chronic obstructive pulmonary disease dently worsens its prognosis.18-24 A major factor is chronic hypoxia, which can result in pulmonary vasoconstric- tion. Other factors include endothelial Predicted curve dysfunction, remodeling of pulmonary Low PEF arteries, and pulmonary capillary bed destruction. Right ventricular dysfunction and failure (cor pulmonale) may eventually develop and add to the Scooped out flow-volume curve morbidity and mortality of this disease. Flow (L/s) Reduced exercise capacity Volume (L) Deconditioning may result from lack of physical activity and can be an independent factor in exercise limitation. Fortunately, this is amenable to a pulmonary rehabilitation program. Normal inspiratory flow Management of deconditioning, like the management of other physiological defects of COPD, begins with Figure 3. Maximal inspiratory and expiratory flow-volume curve. In emphysema, the loss of assessment of function. supportive tissues means the airways tend to collapse with forced exhalation, giving a char- acteristic concave appearance in the expiratory portion of the flow-volume curve. This can also be seen in other obstructive disorders such as asthma. Assessment of airflow limitation and PEF: peak expiratory flow hyperinflation Spirometry with measurements derived from a maximal forced ex - New technology has allowed the there is a reduction in FVC and a need piratory maneuver is the most clini- development of portable hand-held to determine whether there is a con- cally relevant test in assessing COPD. spirometers that are robust, simple to comitant restrictive disorder such as Airway obstruction is diagnosed when use, and reasonable in cost ($500 to interstitial lung disease. In pure the FEV1/FVC (forced expiratory vol- $1500), making spirometry a test that COPD, FVC is modestly decreased ume in 1 second to forced vital capac- can be performed in the office setting. if there is air trapping and hyper - ity) ratio is less than 0.7 L, a situation Accreditation can be obtained in BC inflation (RV increased). Diffusing usually accompanied by a reduction through the Diagnostic Accreditation capacity (DLCO) is very sensitive in in FEV1 to less than 80% of predicted Program, and once you have the re - detecting gas exchange abnormalities. ().Figure 2 FEV1 has tra ditionally quired pulmonary function test (PFT) It is usually reduced in emphysema been used to grade severity of COPD credentials you may bill for perform- (whereas it is normal or high in asth- (see “Pharmacological management,” ing this test. Spirometry should be ma) and correlates reasonably well Table 2 , page 86).25-26 In COPD the routine in COPD for the following: with the pathological severity of expiratory flow-volume curve is char- • Diagnosis (particularly of early dis- emphysema.28 Full pulmonary func- acteristically concave (Figure 3 ). This ease or to differentiate from asthma). tion tests should therefore be consid- appearance is typical for emphysema • Establishing severity. ered when spirometry indicates a (but not specific) and implies the • Determining prognosis. reduced FVC to determine if there is a dynamic airway collapse with forced • Monitoring disease progression and restrictive disorder present, and when exhalation.27 Significant response to response to therapy. spirometry is normal despite the pres- bronchodilators, defined as an in - More detailed lung function tests are ence of dyspnea to determine if there crease in FEV1 by 12% and 180 mL, available in most PFT labs. These are is an impairment in DLCO that might is common in asthma but uncommon utilized in select instances in COPD. suggest another pulmonary parenchy- in COPD. Most commonly this occurs when mal or vascular disorder. VOL. 50 NO. 2, MARCH 2008 BC MEDICAL JOURNAL 99 Clinical physiology of chronic obstructive pulmonary disease Assessment of ventilatory muscle dysfunction none Grade 1 Breathless with strenuous exercise Tests for ventilatory muscle function may be considered in select cases, Grade 2 Short of breath when hurrying on the level or walking up a slight hill including those where ventilatory muscle involvement is suspected in a Grade 3 Walks slower than people of the same age on the level or neuromuscular disorder, or where stops for breath while walking at own pace on the level dyspnea or hypercapnia are out of pro- 12 portion to the patient’s FEV1. Other Grade 4 Stops for breath after walking 100 yards assessment methods for muscle dysfunction may include measuring lung Grade 5 Too breathless to leave the house or volumes (restrictive disorder), blood breathless when dressing severe gases (elevated PCO2), and maximal inspiratory and expiratory pressures. Figure 4. The Medical Research Council dyspnea scale. 26 EMG and nerve conduction studies may also be considered.

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