On their own, COPD and obstructive sleep apnea contribute to tens of thousands of American deaths every year, but the conditions can occur together and the overlap can have increased deleterious effects on the health of patients.

By Bill Pruitt, MBA, RRT, CPFT, AE-C, FAARC

It’s well known that chronic obstructive pulmonary disease (COPD) is a major worldwide disease and ranks as the third leading cause of death in the world—killing some 2.7 million people annually.1

COPD is closely related to cigarette exposure in those who smoke or those who have secondhand exposure to smoke. Meanwhile, obstructive sleep apnea (OSA) is a steadily emerging disease and is closely related to obesity and snoring. OSA is estimated to affect from 9% to 26% of the population.9 According to the World Health Organization, obesity is expected to rise dramatically and the association with OSA will likely result in a dramatic increase in this problem.2

Independent of one another, these conditions directly and indirectly contribute to tens of thousands of American deaths every year. However, these two diseases can occur in a comorbid relationship known as OLDOSA syndrome (obstructive lung disease and obstructive sleep apnea), also known as OVS (overlap syndrome). Together, their negative effects can be even greater than their impact alone. The disease is an important topic for respiratory therapists to understand because it occurs frequently in the population, and—with the increase in obesity, improved awareness of OSA, and the current number of COPD patients—OLDOSA will be more and more prevalent. This article will explore OLDOSA syndrome and provide a guide for RTs to consider as they care for and educate this population.


According to the 2014 release of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, COPD is defined as “a common preventable and treatable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individuals.”3 COPD is most often associated with smoking, but outdoor, indoor, and occupational air pollution are also significant risk factors.

As people live longer and as more women are being diagnosed with COPD, the demographic characteristics of the disease are changing to reflect greater numbers, older patients, and increasing numbers of women. The increase of COPD in women has been linked to increases in female smokers, but women also appear to have a higher susceptibility to lung damage due to exposure to smoke.3

COPD involves many pathological changes that occur in varying degrees depending on severity and on susceptibility to damage. These include inflammation, hypersecretion of mucus, changes in the lung parenchyma (leading to formation of blebs and bullae), limitation of airflow, and increased airtrapping and hyperinflation. In addition, COPD leads to abnormalities in gas exchange (leading to increased PaCO2 and decreased PaO2 with ventilation/perfusion [V/Q] abnormalities), pulmonary hypertension, and exacerbations that bring worsening of airflow, V/Q abnormalities, increased sputum production, and increased dyspnea.3

Diagnosis of COPD is based on clinical symptoms (eg, increased dyspnea, cough with or without sputum production), history of exposure to risk factors (cigarette smoke being the first consideration), and a family history of COPD. Spirometry is a reliable, reproducible, and objective measurement of lung function and is recommended to confirm a clinical diagnosis. Further assessment is evaluated by the scores from validated tests such as the COPD Assessment Test (CAT) and the Modified Medical Research Council (mMRC) questionnaire.3

Depending on the severity of the disease, treatment may involve short and long acting beta-2 agonists and anticholinergics, inhaled corticosteroids, phosphodiesterase-4 inhibiters, oxygen therapy, antibiotic therapy, and systemic corticosteroids. Non-pharmacologic treatment of COPD may include pulmonary rehabilitation, noninvasive ventilation, and surgery (or a bronchoscopic procedure) for lung-volume reduction—reserved for a very limited subgroup of patients with COPD).3

Obstructive Sleep Apnea

OSA involves repeated intermittent collapse of the upper airway and tongue, which blocks the opening of the pharynx and stops airflow. Often the person has loud snoring while asleep prior to having a sleep disturbance. (Assessment of the snoring pattern is included in the Berlin Sleep Questionnaire,4 which is used to look for possible apnea.) To be considered apnea, the airflow must stop for at least 10 seconds. Another similar issue is hypopnea, which involves an event lasting longer than 10 seconds in which there is a ≥30% reduction in nasal pressure tracing swings along with a ≥4% desaturation in the SpO2 from the baseline prior to the event.

When these events occur, the brain is stimulated and the stage of sleep changes (this is called an arousal). The brain signals muscle contractions to reopen the airway, while the person having this event occurring normally doesn’t “wake up” but continues to sleep and often snores loudly until the next episode of apnea. OSA and hypopnea events are counted over the course of an hour and that number divided by the number of hours slept to give an apnea-hypopnea index (AHI). OSA syndrome is defined as an AHI >5.

A polysomnograph (PSG) is the gold standard for diagnosing sleep disturbances. The PSG is an all-night recording of many parameters including electroencephalography (EEG, for brain wave activity), electrooculogram (EOG, for eye movement), and submental electromyelography (EMG, for grinding teeth or bruxism). In addition, a thermistor and pressure sensor are placed at the nose to monitor airflow by temperature and pressure swings, belts or electrodes on the chest and abdomen record chest and abdomen movement, pulse oximetry monitors Spo2, heart rate and rhythm are recorded via electrocardiography (ECG), and EMG sensors on the legs record leg jerks (myoclonus).1,5

When apnea occurs, airflow ceases while chest and abdomen efforts continue. Hypoxemia and hypercapnia can occur with each apneic period while the heart may experience arrhythmias such as atrial and ventricular premature beats, atrial fibrillation or flutter, ventricular tachycardia, and bradyarrhythmias.6 Due to the repeated arousals, the person suffers from fragmented sleep and excessive daytime sleepiness, neurocognitive issues (including lack of concentration and focus), and increased risk of motor-vehicle accidents. Long-term health consequences include risk of hypertension, coronary artery disease, stroke, pulmonary hypertension, and insulin resistance.5-7

Continuous positive airway pressure (CPAP) is the preferred initial treatment for OSA. In addition, alternative treatment options include oral mandibular advancement devices (and mandibular advancement surgery), weight loss, avoidance of alcohol and sleeping pills, nasal sprays, and nasal surgery.8


With the high number of people suffering from OSA and COPD, the belief is that there is a large group of people who are affected by both diseases. COPD is estimated to be present in some 13.9% of adults in the United States, and OSA is estimated to occur in 9% to as much as 26% of adults in the United States.9 It is estimated that a patient with one of these diseases has a 10% chance of suffering from the other as well.7,10 Examining prevalence figures in the general population, in those over 70 years of age diagnosed with COPD, OSA is estimated to be a comorbid disease in some 15% of the cases.11

When both COPD and OSA are present, there may be an additive (synergistic) effect on the clinical picture, but it has not been established at what level of severity this occurs. For example, it is not clear if patients with severe COPD and mild OSA should be treated in a similar fashion to those with the opposite pattern—mild COPD concurrent with severe OSA. Both COPD and OSA have been linked to vascular endothelial dysfunction, increased levels of inflammatory mediators, and more rapid development of atherosclerosis.9 Other factors that link the two diseases include a worsening of both entities with increasing age, the shared risk factor of smoking, and worsening conditions when gastrointestinal reflux disease (GERD) is present.12

There are many possible reasons why COPD can either cause OSA or make it worse in patients already suffering from the disease, and vice versa. COPD often involves chronic hypoxemia, which worsens during the night. (In addition, hypercapnia increases during the night for OLDOSA patients, linking to greater nighttime desaturation and higher AHI.13)

Meanwhile, OSA involves hypoxemia related to the apneic periods. In combination, it appears that the OLDOSA patients have a greater risk of prolonged oxygen desaturation at night and more risk of pulmonary hypertension, right-heart failure, and cor pulmonale than those who have one or the other disease. Nocturnal desaturations cause both systemic and pulmonary blood pressure to increase, which may be a cause for developing pulmonary hypertension.7 In a study published in 2004, researchers found that 16% of patients with OSA only had pulmonary hypertension, while 86% of those with OLDOSA had this comorbidity.14

Notably, mortality for patients with OLDOSA syndrome appears to be greater than patients suffering from only one of the conditions. One study looking at OSA patients found the mortality risks were multiplied sevenfold when COPD was a comorbid condition.15 In another study published in 2010, scientists examined outcomes data on patients with COPD versus those with OLDOSA covering a 9-year period. They found that in OLDOSA patients who were not treated with CPAP, all-cause mortality was 42.2%. In contrast, for COPD patients with no OSA, all-cause mortality was 24.2%.9

Treatment for OLDOSA

CPAP is the preferred treatment for OSA and it appears that CPAP improves outcomes in OLDOSA patients. Marin et al found that CPAP therapy in those with OLDOSA had an all-cause mortality of 31.6% compared to an all-cause mortality of 42.2% in the OLDOSA patients who were not treated with CPAP.9 When examining specific causes for death in these two groups, cardiovascular events were greatly affected by CPAP. The OLDOSA patients in the group using CPAP (n=228 with CVS mortality occurring in 17) had a 7.5% mortality due to cardiovascular issues compared to a 14.6% mortality in the non-CPAP group (n=213 with CVS mortality occurring in 31).9

The Marin study also found that CPAP reduced COPD exacerbations in patients with OLDOSA.9 This finding occurred when the baseline reports of exacerbation were compared to results over a 9-year monitoring period for CPAP and non-CPAP groups. These groups were similar in many baseline characteristics (including body mass index, smoking history, alcohol use, cardiac and respiratory medications, spirometry measurements, and AHI) and both groups received similar medical care and medications over the course of time.9

In addition, Toraldo et al published a study in 2010 that tracked the effects of CPAP therapy in OLDOSA patients. Over a 3-month period of therapy, arterial blood gas results improved along with mean pulmonary artery pressure, as well as the percentage of sleep time spent with Spo2 greater than 90%.16 Additional treatment options are studied in reviews of OLDOSA syndrome, including weight loss, oxygen therapy to treat hypoxemia (but this should be used along with CPAP and not be used alone to treat OLDOSA), bronchodilators, and corticosteroids.7


OLDOSA is an emerging disease in the US population but it often remains undiagnosed. Respiratory therapists may be the first line of defense in identifying this overlapped condition, as the RT often deals with both the COPD patient and the OSA patient. Importantly, the leading tools for diagnosing both diseases fall into the realm of the RT, specifically polysomnography and pulmonary function testing. Patient history and physical exam findings may not call clear attention to the presence of an overlap syndrome, but the alert, astute RT should be able to discern the comorbid conditions.

Treatment for OLDOSA also falls squarely into the realm of the RT, specifically, any approach involving administration of inhaled pharmacotherapy or respiratory therapy appliances or devices such as CPAP and oxygen therapy. Be aware of the daytime somnolent patient, of those who snore at night (or day), and call for the healthcare team to act when you observe apnea. RTs must be proactive—if you suspect OLDOSA in the hospitalized patient or in the home or assisted-living environment patient, strive to get protocols in place for nighttime screening with overnight pulse oximetry and respiratory effort recordings. Push for protocols to perform overnight recordings with auto-titrating CPAP for those with high suspicion of OLDOSA and urge the provider to obtain full polysomnography when the situation calls for this.

As research has shown, effective CPAP can literally save the lives of patients with OLDOSA, and as RTs, there is no greater responsibility than saving lives. Look closely at those with a diagnosis of COPD or OSA and ask, “Is there anything that may point to a diagnosis of OLDOSA in this patient and we just haven’t looked closely, performed the right screenings or tests?” As RTs, we can make a huge difference in these areas of overlapping respiratory problems that carry on through the day and strike hard at night.


Bill Pruitt, MBA, RRT, CPFT, AE-C, FAARC, is a senior instructor and director of clinical education in the department of Cardiorespiratory Sciences, College of Allied Health Sciences, at the University of South Alabama in Mobile. He also works as a PRN therapist at Springhill Medical Center. For further information, contact editor@RTmagazine.com.


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