Chronic obstructive pulmonary disease (COPD) usually is not diagnosed until clinically apparent and moderately advanced. Patients might not notice chronic dyspnea and smoker’s cough, or might consider their symptoms “normal” and not seek medical care. Delayed diagnosis is particularly prevalent in the psychiatric population, in which co-existing medical problems tend to remain unrecognized and untreated.1
Life expectancy of people with serious mental illness (SMI) is 13 to 30 years less than that of the general population—a gap that has widened over time.2 Pulmonary disease is a leading cause of elevated mortality risk in SMI, along with cardiovascular and infectious disease, diabetes, and barriers to care. Having a comorbid mental illness triples the mortality risk of chronic lower respiratory disease (Table 1).3
This article describes how you can intervene and improve quality of life for your patients with COPD by:
- asking all patients, especially smokers, if they are experiencing classic symptoms of COPD
- advocating for and supporting smoking cessation efforts
- avoiding drug interactions and off-target dosing related to COPD and nicotine replacement therapy
- considering, if feasible, a switch from typical to atypical antipsychotic therapy, which could reduce smoking behavior.
What is COPD?
COPD is preventable and treatable. It is characterized by “persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lungs to inhaled noxious particles or gases.”4
Smoking tobacco is the greatest risk factor for developing COPD.5 An estimated 50% to 80% of people with schizophrenia are smokers, as are 55% of people with bipolar disorder.6 COPD is a leading cause of morbidity and mortality worldwide,7,8 and its prevalence is projected to increase as the global population and smoking rates grow.9
A simplified schema of the pathophysiology of COPD implicates 4 lung areas: parenchyma, pulmonary vasculature, central airways, and peripheral airways.10 Variation in the areas affected and severity of change contributes to the disease’s heterogeneous presentation, which can include pulmonary hypertension, hypersecretion of mucus, ciliary dysfunction, airway hyperinflation, and impaired gas exchange.11,12 Many of these features lead to systemic effects as well, particularly on cardiac function.
When to test a patient for COPD
Early diagnosis and treatment can substantially improve quality-of-life outcomes for patients with COPD. The clinical approach (Figure 1) begins with recognizing classic symptoms. Consider COPD in any patient with:
- dyspnea (particularly if becoming worse, persistent, or associated with exercise)
- chronic cough
- chronic sputum production
- history of risk-factor exposure (particularly tobacco smoke)
- family history of COPD.4
If the history and physical exam suggest COPD (Table 2), spirometry is the most reliable test to quantify and characterize lung dysfunction. It is not indicated as a screening tool for healthy adults or appropriate when a patient is acutely ill. Forced expiratory volume in the first second of expiration divided by the measured forced vital capacity (FEV1/FVC) < 0.7 defines clinical COPD and determines the need for pharmacologic intervention. Laboratory studies could be useful in certain clinical scenarios, such as serum testing for alpha1-antitrypsin deficiency in patients age <45 with emphysema. Plain film imaging might be useful to support a COPD diagnosis or rule out alternate diagnoses.
Psychopharmacology issues with comorbid COPD
Pharmacotherapy for psychiatric disorders can exacerbate comorbid COPD. For example, long-term use of phenothiazine-related typical antipsychotics for schizophrenia has been linked to an increased incidence of COPD.13 Antipsychotic side effects such as acute laryngeal dystonia and tardive dyskinesia, most commonly seen with first-generation antipsychotic use, can aggravate dyspnea caused by COPD. Opioids and most hypnotics, sedatives, and anxiolytics suppress the respiratory drive, and therefore should be used with caution in patients with COPD.
Carefully monitor serum levels of medications before and during attempts at smoking cessation. Nicotine’s induction of the cytochrome P450 1A2 system increases the metabolism of antipsychotics such as clozapine, fluvoxamine, olanzapine, and haloperidol. As a result, potentially toxic drug levels can occur when a smoker tries to quit.14
Screen patients with COPD for comorbid psychiatric conditions. New psychiatric symptoms can emerge after COPD has been diagnosed, even in patients without pre-existing psychopathology.
Anxiety is a particularly common COPD comorbidity that can be difficult to manage. Selective serotonin reuptake inhibitors, buspirone, cognitive-behavioral therapy, and pulmonary rehabilitation can be helpful, although the effect of antidepressants on respiration is controversial. Nortriptyline has been shown to be effective in treating both anxiety and depressive symptoms in patients with COPD.15 Avoid using hypnotics to manage sleep problems related to COPD; instead, focus on minimizing sleep disturbance by limiting cough and dyspnea.
Antipsychotics and nicotine metabolism
Multiple studies have focused on the interplay among nicotine, dopamine, and antipsychotic agents. Nicotine receptors are present in the ventral tegmental dopaminergic cell bodies, which induce the release of dopamine and other neurotransmitters when stimulated. Smoking has been noted to increase in patients administered haloperidol (a dopamine antagonist) and to decrease with administration of bromocriptine (a dopamine agonist).16 This suggests that psychiatric patients might smoke to overcome the dopamine blockade caused by most typical antipsychotics, therefore alleviating their negative and extrapyramidal side effects.17