Bronchitis

Acute Bronchitis

Acute bronchitis is an inflammatory condition of the tracheobronchial tree that is especially familiar to primary care physicians. Acute tracheobronchitis is part of a continuum that includes:

• Nasopharyngeal infection
• Bronchitis
• Bronchiolitis
• Pneumonitis.

Symptomatically, these processes may be indistinguishable. Acute tracheobronchitis implies site-specific airway inflammation between the glottis and the bronchioles. In the United Kingdom, 25% of all primary care visits are related to respiratory disease, and more than half of these are due to upper and lower respiratory tract infections. In Europe, >80% of all lower respiratory tract infections are treated with antibiotics. Most physicians do not differentiate acute bronchitis, acute exacerbation of chronic bronchitis (AECB), community-acquired pneumonia (CAP), and viral respiratory tract infections. The pattern of antibiotic prescribing for these infections varies from country to country, but there is no clear rationale for the antimicrobial choices.

The disorder affects approximately 5% of adults annually, with a higher incidence observed during the winter and fall than in the summer and spring. In the United States, physicians report that acute bronchitis is the ninth most common illness among outpatients. The mean annual attack rate in the United States for acute bronchitis is approximately 87 cases/100,000 persons per week, peaking in winter at approximately 150 cases/100,000 persons per week. Acute bronchitis accounts for an estimated 12 million physician visits per year, with an annual cost of $200 million to $300 million for physician visits and prescriptions. In a national survey sampling of >1,500 practicing physicians in the United States, 66% of patients with the diagnosis of bronchitis were treated with antibiotics. Risk factors for increased antimicrobial prescribing were female sex and rural practice location, while Black race was associated with a lower prescribing rate.

Etiology

The syndrome of acute bronchitis is most often associated with respiratory viruses, including common cold viruses (i.e., rhinovirus, coronavirus) in addition to more virulent agents, such as influenza and adenovirus. Other viral causes of acute bronchitis include measles, respiratory syncytial virus (RSV), SARS-CoV-2, parainfluenza virus, metapneumovirus, and herpes simplex virus. A small proportion of cases of acute bronchitis are of nonviral etiology. M pneumoniae, B pertussis and C pneumoniae are recognized bacterial causes of acute bronchitis. The etiologic role of S pneumoniae and
H influenzae in acute bronchitis is not clear as these bacteria may represent resident flora of the upper respiratory tract of normal individuals. Acute tracheobronchitis may also be a consequence of the inhalation of irritating, toxic substances as a result of air pollution or occupational exposures, including ammonia, chlorine, sulfur dioxide, nitrogen dioxide and ozone. The recent worldwide SARS-CoV-2/COVID-19 pandemic has upended conception of acute bronchitis; this pathogen must now always be considered in the differential diagnosis of upper airway symptoms.

Pathogenesis

During acute bronchial infection, the mucous membrane of the tracheobronchial tree is hyperemic and edematous. Increased bronchial secretion is also a common feature. While extensive destruction of the respiratory epithelium is seen in infection with influenza, other viral agents, such as rhinovirus, cause minimal epithelial injury. Impaired mucociliary function is seen in all infections, even in those without overt mucosal damage. Prospective studies frequently fail to isolate a specific pathogen. One explanation may be the delay in seeking medical care after the onset of symptoms, which may bring the patient to medical attention beyond the period of viral shedding. Determination of a causative agent is further complicated in subjects with chronic lung disease who may have tracheobronchial colonization by potentially pathogenic bacteria, including H influenzae, S pneumoniae and M catarrhalis. A rise in serum antibody titers to bacteria associated with acute bronchitic symptoms suggests that bacteria may play a causative role, although analysis of antibody coating of bacteria in sputum is not helpful.

It is also possible that severity of attacks of acute bronchitis may be increased by exposure to cigarette smoke and air pollutants. These substances, in association with recurrent acute bronchial infection, may result in permanent injury to the bronchial tree. Increased airway reactivity and airway resistance, usually manifested as a bothersome cough, may persist for 6 to 8 weeks. The elevated airway resistance observed after a bronchial infection is largely reversible with β-sympathomimetic and anticholinergic bronchodilators.

Clinical Presentation

Cough is uniformly found in acute bronchitis, and it may be productive of mucoid or purulent sputum. The cough may be accompanied by variable amounts of hemoptysis or retrosternal pain that is often described as of a burning quality. It is usually accentuated on inspiration. Generally, the temperature is only minimally to moderately elevated. Physical examination often shows harsh breath sounds, rhonchi and variable amounts of expiratory wheezing. Occasionally there are focal areas of diminished breath sounds, which suggest that inspissated mucus has caused atelectasis. Atelectasis may be relieved by the use of humidifiers, bronchodilators, vigorous coughing and, if needed, tracheal suction. Sometimes there is diffuse diminution of air intake or inspiratory stridor. These findings indicate obstruction of major bronchi or the trachea. Most viral acute tracheobronchitis runs a benign, self-limited course. However, herpes simplex type 1 has been associated with severe febrile tracheobronchitis and respiratory failure in normal immunocompetent adults.

Diagnosis

Bronchitis may be suspected in patients with an acute respiratory tract infection associated with cough. Bronchitis is a diagnosis of exclusion since many other diseases of the lower respiratory tract can also cause coughing. A complete history should include information on exposure to toxic substances and cigarette use, epidemiologic considerations and vaccination history. A complete physical examination is essential to exclude other causes of cough, including cardiovascular and parenchymal lung disease.

Routine bacterial cultures of expectorated sputum are not helpful because of the sampling problem of contamination by nasopharyngeal flora. Occasionally, the nature of sputum may provide some diagnostic clues. For instance, except for adenovirus infections, the sputum in viral infections almost always shows a marked predominance of mononuclear cells on Gram’s or Wright’s stain. In contrast, in bacterial infections, the sputum shows a predominance of PMN leukocytes. Mycoplasma infections are usually associated with mononuclear cells, but there might be a predominant PMN cell population. Culture methods and a microimmunofluorescence test have been developed for the laboratory diagnosis of
C pneumoniae. The use of an IgM-specific conjugate helps detect current infection. Patients in whom cough persists beyond the expected duration of the acute illness should undergo further diagnostic examination, including chest radiography, sputum cytology and/or bronchoscopy to exclude other diseases of the tracheobronchial tree and lungs.

Treatment

In most cases of acute bronchitis, only symptomatic treatment is needed. However, patients with underlying chronic cardiopulmonary disease who contract influenza or other severe forms of bronchitis may develop serious symptoms requiring hospitalization, oxygen therapy and ventilatory assistance due to progression to overt pneumonia. Cough suppressants, adequate hydration to prevent drying of bronchial secretions, and symptomatic treatment of mild fever and malaise associated with some influenza syndromes are the cornerstones of treatment of acute bronchitis in otherwise healthy individuals. If broncho­spastic symptoms are dominant, there may be a role for inhaled broncho­dilators. Antiviral agents may be useful if started early in patients with suspected influenza. Indications for antiviral treatment of COVID-19 are discussed in Community-Acquired Pneumonia.

The value of antibiotics in the treatment of otherwise healthy individuals with acute bronchitis has not been established and the use of these agents is not recommended as a general practice. This uncertainty stems from conflicting results of clinical trials, which may be explained based on variations in type of antibiotics, dosage schedule, duration of follow-up, the season of the year (reflecting prevalence of different pathogens), and lack of a placebo-controlled design in many of these studies. A Cochrane Review of nine randomized, controlled trials of antibiotic agents showed a significant but minor reduction in the duration of cough (0.6 days). There was a nonsignificant reduction in the number of days of feeling ill and a nonsignificant increase in adverse events attributed to antibiotics (relative risk of adverse events, 1.22; 95% CI, 0.94 to 1.58). The role of procalcitonin in differentiating viral from bacterial bronchitis is equivocal.

Acute bronchitis caused by M pneumoniae infection should be treated with macrolide antibiotics or tetracycline; B pertussis infection, with macrolides; and C pneumoniae infection, with tetracyclines. During epidemics known to be due to influenza virus, treatment with antivirals active against the virus recommended in patients with suspected influenza if the illness is <48 hours in duration or if symptoms are progressive even if outside the 48 hour window. Anti-influenza agents () decrease the duration of symptoms and result in an earlier return to normal activity (by 0.5 day) among patients with infections caused by susceptible viruses.

Acute Exacerbations of COPD

Chronic obstructive pulmonary disease (COPD) has some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. COPD afflicts almost 16 million Americans, with significant numbers undiagnosed, and is the sixth leading cause of death in the United States. The global prevalence of COPD based on spirometry is 10% in individuals over age 40. In the United States in 2020, the combined direct and indirect costs of COPD were $49 billion. COPD is a progressive disease characterized by reduced expiratory airflow that is relatively stable over several months of observation. Chronic bronchitis is defined clinically as excessive cough, productive of sputum on most days, for at least 3 months during at least 2 consecutive years.

The major risk factor for chronic bronchitis is cigarette smoking, and cumulative smoking history is most closely related to symptom development. For reasons that are unclear, only 10-20% of chronic heavy smokers develop clinically significant COPD. Familial factors and exposure to dusty environments also play a role, although to a much lesser extent than cigarette smoking. From the Lung Health Study, airways (methacholine) reactivity, after cigarette smoking, is the most important determinant of decline in forced expiratory volume in 1 second (FEV₁). The prognosis of COPD is affected most when lung function, as reflected by the FEV₁, falls below 50% of predicted values. When the FEV₁ falls below 1 L, the 5-year survival is approximately 50%. Once patients reach very low levels of FEV₁, other markers such as level of dyspnea, exercise capacity, BMI, health status, anemia, hypoxemia, comorbidities, and hyperinflation are also significant predictors of prognosis. The average severe COPD patient has more than one exacerbations and demonstrates an often significant decline in quality of life.

Role of Bacterial Infection

An acute exacerbation of COPD (AECOPD) is usually defined as respiratory decompensation requiring an adjustment of baseline medications or introduction of new medications such as antibiotics and/or corticosteroids. The role of bacterial infection in AECOPD is controversial. Many patients are treated with antibiotics, but the role of antibiotics has been questioned. Several observations have been made in support of bacteria playing an important role. For example, an increased number of bacteria and neutrophils in sputum during exacerbations have been demonstrated. The appearance of an acute antibody response in serum to these bacteria and an increase in inflammatory mediators in purulent sputum suggest a causal relationship. At least 50% of patients have bacteria in high concentrations in their lower airways during exacerbations. However, the linkage between bacterial infection and symptoms is complicated by a high spontaneous remission rate; this can be expected since bacterial exacerbations are usually limited to the bronchial mucosa. The appearance of purulent sputum appears to be the best single clinical predictor of the presence of potential bacterial pathogens in respiratory secretions.

In a landmark study, Anthonisen and coworkers (1987) demonstrated that patients could be stratified according to symptoms in order to predict a response to antimicrobial therapy. Among patients with at least two of the following symptoms—increased dyspnea, sputum volume and sputum purulence—broad-spectrum antibiotics (amoxicillin, trimethoprim/sulfamethoxazole (TMP/SMX), or doxycycline) led to improved clinical outcomes, fewer therapeutic failures and a more rapid rate of lung function recovery compared with placebo. Overall, the length of illness was 2 days shorter for the antibiotic-treated group compared with the group receiving placebo. If patients presented with all three symptoms (type I exacerbation), the benefit in outcome for antibiotic-treated patients was the greatest, while there was no difference if the patient had only one symptom (type III exacerbation). A meta-analysis of nine randomized, placebo-controlled trials of patients treated with antibiotics for AECOPD concluded that a small but statistically significant clinical and physiologic improvement could be expected in antibiotic-treated patients (Table 13-1). A beneficial impact of antibiotics was demonstrated in studies that included the largest number of patients. While this improvement is small, it may be clinically relevant, particularly in patients with limited respiratory reserve.

Other studies have confirmed these observations and a re-analysis of the original data suggest that the greatest benefit is seen among patients with the worst baseline lung function (Table 13-1). Nouria and colleagues demonstrated that a fluoroquinolone, compared with placebo, administered to patients with acute respiratory failure associated with an AECOPD was associated with a significant reduction in mortality and length of hospital stay. Another meta-analysis suggested antibiotics reduced the risk of short-term mortality by 77% and decreased the risk of treatment failure by 53% and the risk of sputum purulence by 44%, with a small increase in the risk of diarrhea. These data suggest that bacterial infection plays a role in a significant proportion in patients experiencing an AECOPD, especially those with more severe disease and the use of risk stratification according to the Anthonisen criteria permits the selection of those patients most likely to benefit from antimicrobial therapy. These data for the most part precede the more widespread use of macrolide antibiotics for prophylaxis of exacerbation.

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Bacterial Pathogens

Bacterial pathogens can be isolated from sputum in 50% to 60% of patients with an AECOPD, with H influenzae being the most commonly isolated organism from sputum (Table 13-2). H parainfluenzae, S pneumoniae and M catarrhalis are also found frequently. Studies utilizing bronchoscopy with PSB technique whereby lower respiratory tract samples are not contaminated with oropharyngeal flora have confirmed the important role of bacterial pathogens. Organisms identified using these techniques are similar to those found in sputum (H influenzae, H parainfluenzae, S pneumoniae, M catarrhalis), but quantitative cultures indicate a greater number of organisms.

Sethi and colleagues demonstrated that the risk of an exacerbation is doubled if a patient becomes colonized with a new strain of a respiratory pathogen. The ability to type strains of organisms has allowed a careful reassessment of the role of bacteria and explains earlier observations that bacteria were isolated in equal numbers of patients when they were well or during an exacerbation. While the organism was of the same species (e.g.,
H influenzae), the acquisition of a new strain of H influenzae significantly increased the risk of new symptoms consistent with an exacerbation.

Exacerbations can be caused by endogenous or exogenous reinfection with H influenzae. Persistently infected patients keep the same H influenzae strain for longer periods, and antibiotic therapy may not be effective in eradicating H influenzae. Sethi and coworkers have also shown that an identical strain of H influenzae can be found in a patient in respiratory samples taken months apart while intervening cultures are negative. However, using advanced techniques, such as polymerase chain reaction, DNA from the identical infecting strain can be seen in respiratory secretions even when cultures are negative. These data suggest that in some patients, the organisms persist, perhaps in an intracellular location. The persistence of the organism may be harmful as colonization of the airways is associated with an airway inflammatory response that may lead to progressive loss of lung function and impaired quality of life. There is an association between bacterial colonization and increased markers of inflammation in sputum and with the frequency of exacerbations.

Among patients with reasonably well-preserved lung function, gram-positive organisms, such as pneumococcus and simple gram-negative organisms (e.g.,
H influenzae and M catarrhalis) are frequently isolated from respiratory secretions. However, with declining lung function, there is an increasing prevalence of enteric gram-negative organisms and P aeruginosa.
H parainfluenzae has been isolated in patients with AECOPD. Its role is uncertain because the systemic antibody response to this organism is not as brisk as that seen with other respiratory pathogens, such as H influenzae or M catarrhalis. β-lactamase-mediated amoxicillin resistance is seen in H influenzae strains and in most M catarrhalis strains. Macrolide resistance in S pneumoniae is frequently identified in multiple surveillance studies.

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Pathogenesis of Bronchial Infections

Cigarette smoking is a common cause of chronic bronchitis. The mucociliary system forms a primary defense mechanism of the respiratory tract against all inhaled particles, including bacteria. Viral infection and cigarette smoke frequently damage ciliated epithelium, which, in turn, impairs mucociliary clearance. Long-term cigarette smoking leads to a change from pseudostratified, ciliated columnar epithelium to squamous epithelium with its attendant loss of cilia and attenuation of mucociliary clearance. Loss of ciliated epithelium also occurs during viral and bacterial infections and contributes to impaired muco­ciliary clearance. Delayed mucociliary clearance affords bacteria the opportunity to multiply and attach, first to mucus and then to mucosal surfaces. Organisms, such as H influenzae, produce substances that:

• Impair ciliary function
• Stimulate production of mucus
• Destroy local immunoglobulins
• Impair phagocytic function
• Damage the tracheobronchial epithelium.

H influenzae synthesizes histamine and releases an uncharacterized factor that impairs human neutrophil function. When these bacteria loiter in the airways, a host inflammatory response is stimulated. With the movement of large numbers of neutrophils and their subsequent release of proteinases and toxic oxygen radicals, production of mucus and epithelial surface damage may be enhanced. Progressive airway damage may occur from the products of the bacteria themselves or from the host response to these bacteria. Local host defense may be further impaired, leading to an ever greater chance of bacterial colonization and thus to further damage. This process has been termed the “vicious circle hypothesis” (Figure 2-1) and may account for the insidious progression of airway disease.

Risk Stratification

Acute respiratory failure may develop in patients with significant compromise of lung function as a consequence of an acute exacerbation. Identification of these patients and application of an aggressive therapeutic approach from the outset may avoid this important complication. If respiratory failure develops, mechanical ventilation is required in 20% to 60% of patients, especially when other associated comorbid illnesses are present. However, with current treatment standards this outcome has become distinctly rare.

Patient age and severity of airway obstruction in those with COPD have been identified as the major determinants of survival of patients followed for 3 years after discharge from hospital. Other factors linked to survival are performance status and use of oral corticosteroids.

Following institution of antibiotic therapy for an AECOPD, factors predicting failure of initial antimicrobial therapy (return to the prescribing physician for more treatment) include coexistent cardiopulmonary diseases and the number of previous exacerbations. The need for hospitalization is best predicted by the presence of significant cardiopulmonary disease. The presence of cardiovascular comorbidity and more than four exacerbations in the previous year has a sensitivity of 70% and specificity of 37% in predicting return to the prescribing physician for further treatment. Advanced age, significant impairment of lung function, poor performance status, comorbid conditions, long duration of chronic bronchitis and a history of previous frequent exacerbations requiring systemic corticosteroid medications characterize a high-risk group of patients.

Since the cost of failure of treatment of these patients is high, an aggressive approach to treatment of this high-risk group might improve outcome. Routine antimicrobial therapy fails in 13% to 25% or more of exacerbations. Therapeutic failure leads to increased cost of care due to extra physician visits, further diagnostic tests and repeated courses of antibiotics. It may also lead to more hospitalizations and prolonged absence from work. Stratification of patients into risk categories may allow the physician to select targeted antimicrobial therapy to prevent some of these consequences. This approach has become increasingly more important due to increasing rates of resistance to standard antimicrobial therapy.

Canadian guidelines have divided patients into four groups (Table 13-3). Group 0 patients have tracheobronchitis that is usually viral in origin. Since there is no underlying lung disease in this group, the illness is usually self-limited and runs a benign course.

Group 1 patients (uncomplicated) have simple chronic bronchitis, are younger, have only mild-to-moderate impairment of lung function (FEV₁ >50% predicted value), and have fewer than four exacerbations per year. There is no significant cardiopulmonary comorbidity. In this group of patients, typical pathogens, including H influenzae, S pneumoniae and M catarrhalis, are present, although viral infection often precedes bacterial superinfection. Treatment with a b-lactam or any other first-line agent (tetracycline, macrolide, TMP/SMX) is usually successful and the prognosis is excellent. More potent drugs should be reserved for treatment failures. Among this group of patients, placebo-controlled trials are still necessary to confirm the efficacy of antibiotics.

Group 2 patients are older, may have poor underlying lung function (FEV₁ <50% predicted) or only moderate impairment of lung function but significant comorbidity (diabetes mellitus, HF, chronic renal disease, chronic liver disease, etc.) and/or experience four or more exacerbations per year. H influenzae, S pneumoniae and M catarrhalis continue to be the predominant organisms. In patients with more advanced lung disease, gram-negative organisms, such as K pneumoniae or even P aeruginosa, should be considered. In this group of patients, initial treatment failure has major implications for the patient and the health care system,
including increased time lost from work and/or hospital­ization. Treatment with medications directed toward more difficult to treat and/or resistant organisms, such as a respiratory fluoroquinolone (levofloxacin, moxifloxacin, delafloxacin) or amoxicillin-clavulanate, perform better than amoxicillin alone or other first-line antibiotics.

Group 3 patients suffer from chronic bronchial suppuration with frequent exacerbations characterized by increased sputum production, increased sputum purulence, cough and worsening dyspnea. Many of these patients will have evidence of bronchiectasis if subjected to HRCT scanning. These individuals tend to have a chronic progressive course, and an aggressive therapeutic approach should be offered. Besides the usual respiratory organisms, other gram-negative organisms, including Enterobacteriaceae and Pseudomonas spp, should be considered as potential pathogens. Sputum cultures may be helpful in identifying these organisms. High-dose ciprofloxacin and levofloxacin are the only oral agents with reliable activity against these organisms and should be considered the agent of choice when they are identified.

Three studies examining the role of respiratory fluoroquinolones in this disorder have demonstrated superior clinical outcomes compared with standard first-line therapy. In the Gemifloxacin Long-term Outcomes in Bronchitis Exacerbations (GLOBE) study, gemifloxacin was associated with fewer exacerbations within 6 months of treatment of the original exacerbation compared with patients treated with clarithromycin. Moxifloxacin in a randomized, blinded trial, demonstrated fewer treatment failures and a prolongation of the infection-free interval compared with a basket of first-line agents (amoxicillin, clarithromycin, or cefuroxime). Levofloxacin given as 750 mg once daily for 5 days was comparable to amoxicillin/clavulanate given for 10 days but levofloxacin-treated patients recovered faster. These studies tend to support the recommendation that more severe patients should be treated aggressively with potent, broad-spectrum antibiotics to prevent treatment failures and recurrent exacerbations.

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Nonantimicrobial Treatment

Treatment of AECOPD falls into two general approaches of prophylactic and symptomatic therapies.

Preventive Measures

Smoking cessation has been identified as a major cornerstone of management of patients with chronic bronchitis. The Lung Health Study confirmed that smoking cessation reduces the rate of decline of FEV₁ and is the only intervention that has been demonstrated to alter the natural history of the disease. The benefit of smoking cessation is seen even among patients >60 years of age. Chronic sputum production often clears within 4 weeks of stopping smoking. Nicotine replacement therapy, including with e-cigarettes, is an effective approach to smoking cessation along with pharmacotherapy, although counseling by a physician has been shown to be important as well.

Annual influenza vaccination reduces morbidity and mortality of influenza in the elderly by 50%. This beneficial effect is felt to be the result of prevention of airway epithelial damage predisposing to subsequent bacterial infection caused by the virus. The beneficial effect of pneumococcal vaccine in patients with COPD has not been firmly established. The vaccine provides partial protection against bacteremic pneumococcal pneumonia but not against bronchitis. However, current recommendations are that patients with COPD receive a pneumococcal vaccine at least once in their life and consideration be given to repeating the vaccine especially in high-risk patients or those that have reduced or declining pneumococcal antibody levels. Respiratory syncytial virus (RSV) vaccination is now available for patients over 60 years old who have comorbid illnesses that place them at higher risk for the impact of RSV infection. Additional effective prevention of exacerbations has been achieved through the use of three times weekly macrolide antibiotic therapy.

Symptomatic Therapy

Generally, a combination of inhaled anticholinergic with inhaled b-agonist is used in the treatment of acute exacerbations of COPD. The method of delivery of inhaled bronchodilators has not been shown to influence clinically significant outcomes. The long-term administration of inhaled anticholinergics does not alter the prognosis of COPD. The addition of inhaled corticosteroids is useful in preventing exacerbations when circulating or sputum eosinophils are elevated. Oxygen therapy to maintain arterial oxygen saturation >90% may be required. Pulmonary rehabilitation programs have been demonstrated to improve quality of life for patients with COPD and are generally recommended.

Retrospective reviews of patients presenting to the emergency department with AECOPD show a clear benefit in the group treated with corticosteroids. Faster improvement of pulmonary function tests utilizing parenteral corticosteroids during acute exacerbations of COPD has been reported. The results of the Systemic Corticosteroids in COPD Exacerbation (SCCOPE) clinical trial confirm this observation and the investigators also report that treatment failures and length of hospital stay are reduced. Short-term use of corticosteroids has been generally advocated in acute exacerbations, although it is only recently that this has been supported by randomized clinical trials. A short course (2 weeks) of prednisone results in a more rapid improvement in FEV1, reduced rate of deterioration and shortened hospital stay; it also prevents relapses. The optimal dose and duration are unclear, but no benefit was noted with an 8-week course compared with 2 weeks. A 2014 Cochrane review of 16 studies (and more than 1700 patients) on the use of systemic corticosteroids in AECOPD found that systemic corticosteroids significantly improved several outcomes, including decreasing treatment failure, decreasing relapse after treatment, and improving lung function, symptoms of breathlessness and blood gases.

Noninvasive mechanical ventilation should be considered for patients with an AECOPD demonstrating hypercapnic respiratory failure despite initial therapy with bronchodilators. Outcomes are improved if this therapy is delivered in units that provide adequate cardiopulmonary monitoring in the intensive care unit. Noninvasive mechanical ventilation is not helpful in patients with milder exacerbations (pH >7.35) or in those with very severe exacerbations (pH <7.20), somnolence, or excessive secretions. For patients who demonstrate progressive deterioration despite aggressive medical measures, intubation and mechanical ventilation may be lifesaving.