Chronic obstructive pulmonary disease (COPD) is defined by airway obstruction and alveolar damage caused by exposure to harmful airborne particles. Physiologic findings include varying degrees of abnormal gas exchange and mechanical respiratory limitation, often in the form of dynamic hyperinflation. However, there is a third major contributor: breathlessness. That’s how it is, skeletal muscle deconditioning. Only one of these abnormalities responds to inhalers.
When your COPD patients report dyspnea or exercise intolerance, what do you do? Are you trying to determine its character to pinpoint its origin? Do you quiz them on their baseline activity levels to quantify their conditioning? I bet he cuts to the chase and orders a cardiopulmonary exercise test (CPET). That way, you will be able to figure out all the taxpayers. No. You will most likely add a inhaler before moving on to COPD quality metrics: Vaccines? Check. Lung cancer screening? Check. Give up smoking? Check.
physiology of Dyspnea and exercise limitation in COPD has been extensively studied. Work of breathing inefficiencies, dynamic hyperinflation, and gas exchange interact with each other in complex ways to produce symptoms. The presence of deconditioning simply magnifies existing abnormalities within the respiratory system by creating more strain at lower work rates. Acute exacerbations (COPD) and oral corticosteroids aggravate skeletal muscle dysfunction.
the Report of the Global Strategy for the diagnosis, treatment and prevention of chronic obstructive pulmonary disease (GOLD) tells doctors to use inhalers to control breathlessness. If they’re already on one inhaler, they get another one. This continues until they are stabilized with a long-acting beta agonist (LABA), a long-acting muscarinic antagonist (LAMA), and a inhaled corticosteroid (ICS). The GOLD report also advises pulmonary rehabilitation for any patient with grade B to D disease. Unfortunately, the recommendation for pulmonary rehabilitation is hidden in the text and does not appear within the popularized pharmacological algorithms in the report figures.
The data on adding inhalers on top of each other to reduce AECOPD and improve overall quality of life (QoL) is good. However, although GOLD tells us to continue to add inhalers for the dyspneic patient with COPD, the authors acknowledge that this has not been systematically tested. It is important to remember that GOLD is a “statement” rather than a clinical practice guideline. The difference? A declaration does not require the same formal and rigorous scientific analysis known as the DEGREE approach. Using this type of analysis, a recent clinical practice guideline of the American Thoracic Society found no benefit in breathlessness or respiratory quality of life with augmentation of inhaler monotherapy.
Inhalers won’t do anything for gas exchange inefficiencies and deconditioning, at least not directly. A recent CPET study of the CanCOLD network found ventilatory inefficiency in 23% of GOLD 1 and 26% of GOLD 2 to 4 patients with COPD. The numbers were higher for those who reported breathlessness. Skeletal muscle dysfunction rates are similarly high.
Therefore, dyspnea and exercise intolerance are the main determinants of QoL in COPD, but inhalers will only take it so far. At a minimum, make sure you get a activity/exercise history of your COPD patients. For those who are sedentary, provide a exercise prescription (really, it’s not that hard to do). If dyspnea persists despite LABA or LAMA monotherapy, clarify the problem before doubling the dose. Finally, try to get the patient into a good pulmonary rehabilitation program. They will thank you later.
Aaron B. Holley, MD, is an associate professor of medicine at the Uniformed Services University and director of the critical care and pulmonary medicine program at Walter Reed National Military Medical Center. he covers a wide range of topics in pulmonary, critical care and sleep medicine.