Respiratory Failure from Acute Obstructive Lung Disease


Acute Asthma

Continue Reading

Acute Exacerbation of Chronic Obstructive Pulmonary Disease

Acute on Chronic Respiratory Failure

Asthma Exacerbation

Status Asthmaticus

Ventilatory Failure

Related Conditions




Bronchopulmonary Dysplasia

Chronic Obstructive Pulmonary Disease

Crack Lung

Cystic Fibrosis



Inhalation Injury

Injection Drug Use

Occupational Lung Disease

Reactive Airways Disease



1. Description of the problem

Respiratory failure from acute obstructive lung disease is a common critical care encounter. This form of ventilatory failure is most typically the result of an exacerbation of asthma or chronic obstructive pulmonary disease (COPD), chronic medical conditions with high prevalence. Less commonly, it can result from exacerbations of less prevalent lung diseases or an acute injury to the airway as occurs with an inhalation injury. Acute obstructive lung disease causes an increase in the resistance to airflow during exhalation and, depending on the disorder, inhalation.

The obstruction of expiratory airflow increases the work of breathing required to ensure maintenance of adequate ventilation. Expiration, normally a passive recoiling of the elastic lungs, may require the use of respiratory muscles to drive airflow past the obstruction. As expiratory flow is limited and gas is trapped in the lungs (dynamic hyperinflation), increased lung volumes increase the load on respiratory muscles during inspiration as well. Inability to sustain the increased work of breathing can result in respiratory failure.

Respiratory failure from acute obstructive disease can itself be life-threatening, leading to respiratory arrest without prompt recognition, treatment and supportive care. This condition can also pose a threat to other organ systems, namely via circulatory collapse from dynamic hyperinflation of the lungs. Additionally, respiratory failure in the setting of obstructive lung disease may be the result of another underlying process that worsens obstruction and/or increases the load on the respiratory system, such as pneumonia. These conditions require diagnosis and treatment concurrent with management of the acute obstructive lung disease.

Clinical features


  • Cough

  • Sputum production

  • Dyspnea

  • Wheezing

  • Chest tightness

  • Fatigue (from increased work of breathing and sleep disturbance)


  • Tachypnea

  • Tachycardia

  • Hypertension

  • Hypotension

  • Hypoxemia (mild, responsive to oxygen supplementation)

  • Increased work of breathing

  • Conversational dyspnea

  • Somnolence

  • Use of accessory muscles of respiration

  • Paradoxical breathing

  • Diminished airflow

  • Wheezing

Assess need for and provide adequate ventilatory support

The patient with acute obstructive lung disease is at risk of rapid clinical deterioration and respiratory arrest. Early recognition of distress and initiation of ventilatory support is essential. Bedside assessment revealing hypoxemia, severe distress (eg, tachypnea > 30), greatly increased work of breathing (eg, accessory muscle use, climbing pulsus paradoxus), or patient fatigue (eg, somnolence, falling pulsus paradoxus) are signs that positive-pressure ventilatory support is likely to be beneficial.

  • Support the circulation. Air trapping resulting from expiratory flow obstruction (intrinsic positive end-expiratory pressure – PEEP) increases intrathoracic pressures and impedes venous return to the heart. Positive-pressure ventilation can greatly exacerbate this hyperinflation and may lead to cardiovascular collapse. Resuscitation to ensure adequate circulating volume and allowing adequate time for full exhalation (minimizing intrinsic PEEP) decreases this risk.

  • Bronchodilation. Concurrent with supportive care, relief of the expiratory flow limitation is essential. Inhaled beta-agonists and corticosteroids are the primary therapies, but other therapies may be added for more severe obstruction.

  • Identify and treat triggers. Acute obstructive disease most often occurs in patients with chronic underlying airway disease (asthma, COPD). However, triggers for acute worsening (eg, pneumonia, medications) that have specific therapies should be investigated and treated if present.

  • Avoid, identify, and treat complications. Respiratory failure and the critical care it requires places patients at risk for complications. Cardiac events, acute kidney injury, delirium, and secondary infection are some of the more common complications.

2. Emergency Management

Assess need for and provide ventilatory support

The following signs may be suggestive of pending respiratory failure, and positive-pressure ventilation should be considered:

  • worsening hypoxemia

  • acute hypercarbia

  • severe tachypnea (respiratory rate > 30)

  • use of accessory muscles of breathing

  • dyspnea precluding speech

  • patient-declared fatigue

  • somnolence and/or delirium

Non-invasive positive-pressure ventilation is considered the standard of care for patients with an acute exacerbation of COPD, and should be used when no contraindications are present. Despite less robust data supporting the use of non-invasive positive pressure ventilation (NIPPV) in asthma, this therapy is commonly used in practice. Both continuous and bi-level positive airway pressure support have been utilized successfully.

Endotracheal intubation should be considered if contraindications to non-invasive ventilation (including hemodynamic instability or arrest, severe encephalopathy, anatomical facial anomalies, and inability to protect the airway from secretions) are not present. Additionally, the transition to invasive ventilation should be made if non-invasive ventilation fails to improve the clinical factors described above in a relatively short period of time (30 minutes or less).

Regardless of the mode of ventilation, the clinician should avoid overventilation. High respiratory rates and/or tidal volumes increase the risk of hyperinflation and may cause life-threatening alkalosis as the carbon dioxide is rapidly lowered in a patient with a chronic compensatory metabolic alkalosis.

Support the circulation

Patients suffering from an acute obstructive lung disease have often been ill for days to weeks, and whole body depletion of salt and water is common. Paired with positive-pressure ventilation that exacerbated lung hyperinflation, patients are at risk for diminished venous return and cardiovascular collapse due to low cardiac output. Keys to early management include:

  • establishment of intravenous access

  • resuscitation with intravenous fluids (normal saline) to ensure adequate urine output

Patients with severe disease placed on positive-pressure ventilation may require large volumes of resuscitation fluid (> 5 liters) to ensure adequate perfusion.


Many patients with acute obstructive lung disease will improve quickly with bronchodilator therapy. For this reason, early initiation of this therapy targeting the underlying disease is imperative.

The complexity of care for patients with respiratory failure from obstructive lung disease necessitates a systematic approach. This will help ensure that goals of therapy are met and that alternate or complicating processes are identified and treated. Patients should be re-assessed frequently, and a non-affirmatory answer to a question below likely requires adjustment of the management plan:

  • Is the patient’s ability to oxygenate and ventilate adequate?

    Is the patient protecting his/her airway?

    Is oxygen saturation > 92%?

    Is respiratory rate acceptable?

    Is the work of breathing sustainable?

  • Is the patient’s circulation adequate?

    Does the patient have adequate circulating volume?

    Does therapy minimize air-trapping and hyperinflation?

    Does the patient have adequate perfusion?

  • Is therapy for obstructive lung disease adequate?

    Have beta-agonists been administered in adequate doses?

    Have corticosteroids been administered?

    Has the patient improved on therapy?

    Have other therapies used in severe cases been considered?

  • Is there an underlying cause and is it being treated?

    Is treatable infection being treated?

    Have exacerbating exposures/ingestions/medications been stopped?

  • Is this obstructive lung disease?

    Are there sufficient data to support this diagnosis?

    Are all the data consistent with this diagnosis?

    Have other disease processes been considered?

  • Is the patient being treated in a manner that will minimize and help recognize known complications?

    Is urine output adequate?

    Are measured airway pressures acceptable?

    Are sedatives and analgesics adequately titrated to my goals?

    Is the patient on appropriate prophylactic therapy?

3. Diagnosis


A compelling medical history typically makes acute obstructive lung disease a leading candidate for the cause of respiratory failure. Acute onset of symptoms consistent with obstructive lung disease, particularly in a patient with a past history of asthma or COPD, should raise clinical suspicion.

Exposure to a common exacerbant or severe inhalation exposure also increases the likelihood of acute obstructive lung disease.

Physical examination

Examination helps the physician both confirm the presence of airflow obstruction (wheezing, diminished airflow) and assess the severity of respiratory distress (vital sign abnormalities, use of accessory muscle, mental state).

Diagnostic testing

For the patient presenting with impending respiratory failure, history and examination are often sufficient for diagnosis. Less severe presentations may benefit from an objective measure of airflow to confirm the suspected diagnosis. Peak flow measurements showing a decrease of > 20% from baseline suggest acute obstruction (with decrease of > 50% suggestive of severe exacerbation) in patients with asthma. This test is not nearly as sensitive in patients with COPD, who may develop respiratory failure with much smaller incremental change from baseline.

Arterial blood gas perturbations may reflect the severity of the patient’s condition as well. Patients with classic asthma physiology tend to have normal arterial pCO2 at baseline and develop a mild respiratory alkalosis (decrease in pCO2) in the early phase of an exacerbation. Elevated or even normal pCO2 levels may indicate respiratory muscle fatigue and impending respiratory failure. Patients with COPD may have elevated baseline arterial pCO2, which must be considered when interpreting the blood gas in the acute setting.

It should be noted that a normal blood gas DOES NOT indicate that the patient does not need support or that the patient is not at risk for respiratory failure. Clinical observation and assessment indicating impending respiratory failure almost always precede perturbations in the blood gas (which report that failure has already occurred). Physical examination suggesting that respiratory failure is imminent should be acted upon without awaiting results of the arterial blood gas.

A chest X-ray is almost always performed in this clinical setting. This test may support the diagnosis (large lung volumes, flattened diaphragms), but much of its utility is in evaluating for an etiology of exacerbation (eg, pneumonia), alternative diagnoses (eg, congestive heart failure), or the complications of severe obstructive lung disease (eg, pneumothorax).

The patient’s history and physical examination are often sufficient to make the diagnosis, and objective testing (peak flow, spirometry and arterial blood gas) serves only to confirm the diagnosis or determine the severity of the physiologic abnormalities.

Several other disease processes can present with acute onset of worsening shortness of breath with cough and wheeze, and evaluation for these alternative diagnoses is important.

Congestive heart failure

Elevated cardiac filling pressures can lead to airway edema and alveolar flooding (pulmonary edema), which can present very similarly to acute obstructive lung disease (dyspnea and wheezing). It is appropriate to evaluate patients at risk for cardiovascular disease for congestive heart failure or myocardial ischemia.

Upper airway obstruction

Obstruction of the large upper airway (oropharynx, trachea) or abnormal movement of the vocal cords can mimic the obstruction of medium to small airways characteristic of obstructive lung disease. Clues to this diagnosis include high-pitched inspiratory sounds heard anteriorly over the neck (stridor). If the patient requires intubation, the endotracheal tube often bypasses the upper airway lesion and eliminates the physiologic obstruction completely, helping differentiate upper airway obstruction from obstructive lung disease. Ideally upper airway obstruction as a cause of obstructive lung disease is identified before intubation is required.

Chronic lung diseases

Chronic lung diseases such as organizing pneumonia, interstitial pneumonias, or bronchiolitis may present acutely and should be considered, although the degree of actually obstruction is variable and often minimal in these disorders.

Pulmonary embolism

Respiratory failure due to thromboembolic disease may present similarly to acute obstructive lung disease. Some data support a high incidence of pulmonary embolism in acute exacerbation of COPD specifically, but the literature is inconclusive.

Confirmatory tests

The patient’s history and physical examination are often sufficient to make the diagnosis, and objective testing (peak flow, spirometry, arterial blood gas) serves only to confirm the diagnosis or determine the severity of the physiologic abnormalities.

Cardiac evaluation is appropriate in patients at risk and should be done early in the patient presentation. In addition to history and physical examination, a chest X-ray, electrocardiogram, cardiac enzymes, and echocardiography are commonly performed tests.

Failure to respond to treatment should prompt consideration of alternative diagnoses and additional diagnostic testing, including imaging and/or visualization of the upper airway as well as high-resolution imaging of the chest.

4. Specific Treatment

First-line and other therapies

Respiratory supportive care

  • Oxygen as needed (first line)

  • Positive-pressure ventilation (as needed)

    Non-invasive positive pressure ventilation (first line for COPD, less experience in use for asthma)

    Intubation and mechanical ventilation (as needed)

    ▪ Goal of ventilation is to rest the respiratory muscles to allow time for the underlying disease process to be reversed.

    ▪ Increase expiratory time and avoid lung hyperinflation.

    ▪ Reducing gas trapping avoids impeded venous return (with cardiovascular collapse when extreme) and risk of pneumothorax.

    ▪ Low respiratory rate helps achieve longer expiratory time.

    ▪ High inspiratory flow rate with square wave form (for assist control ventilation)

    ▪ Tidal volumes of 5 to 7 ml/kg of ideal body weight

    ▪ Permissive hypercapnea (maintaining acceptable serum pH) to achieve above goals

Circulatory supportive care

  • Intravenous fluids as needed (first line)

    Titrated to maintain adequate urine output

    Volume requirement may be large (> 5 liters), particularly for patients receiving positive-pressure ventilation.

  • Vasoactive medications (second line, adjuvant)

Bronchodilation (smooth muscle)

  • Albuterol (first line)

  • Ipratropium bromide (second line, adjuvant)

  • Magnesium sulfate (second line, adjuvant)

Bronchodilation (inflammation)

  • Corticosteroids (first line)

Other therapies

  • Heliox (second line)

Drugs and dosages


  • 2.5 mg nebulized every 20 minutes (or less frequently) OR

  • 10 mg nebulization over one hour OR

  • 4-8 puffs from metered-dose inhaler through spacer every 20 minutes (or less frequently)

Ipratropium bromide:

  • 500 mcg nebulized every 20 minutes (or less frequently, up to 3 doses) OR

  • 8 puffs from metered-dose inhaler through spacer every 20 minutes (or less frequently)

Magnesium sulfate:

  • 2 grams IV over 20 minutes


  • For patients with more severe disease: Methylprednisolone 60-125 mg IV push every 6 to 12 hours for the first few days

  • Prednisone 40-60 mg po OR

  • Equivalent

Refractory cases

Most patients with acute obstructive lung disease will demonstrate improvement with initial therapy with inhaled bronchodilators. Patients requiring high levels of care initially or rapid escalation of care likely have:

  • Severe obstructive lung disease that will take additional time to improve

  • A pathologic process other than or in addition to obstructive lung disease (pneumonia, CHF)

  • Developed respiratory muscle fatigue or end-organ dysfunction that requires support after improvement in the obstructive lung disease

Patients who fail to respond to initial therapy should be evaluated for alternative causes of respiratory distress or an additional process that is driving the acute obstruction (pneumonia, medication).

Patients in respiratory failure have a load on the respiratory system that exceeds their ability to perform the work of breathing. Exacerbations of both asthma and COPD have often started days to weeks prior to seeking medical attention. This prolonged depletion of respiratory reserve may require a prolonged recovery and duration of ventilatory support (days) even if the obstruction is rapidly relieved.

Some patients have truly difficult-to-treat obstructive lung disease. These patients may require:

  • Deep sedation and possibly paralysis to achieve goals of ventilation

  • Use of adjuvant bronchodilators (ipratropium, magnesium sulfate)

  • Use of heliox to improve airflow and aid distal delivery of bronchodilator medications

  • Prolonged period of support to allow improvement of obstructive lung disease (accordingly, may require tracheostomy)

5. Disease monitoring, follow-up and disposition

Expected response to treatment

The vast majority of patients with acute obstructive lung disease will demonstrate improvement with inhaled bronchodilators and will continue to improve over subsequent days. The mortality rate from asthma is low but not rare, which is unfortunate given the preventable and treatable nature of asthma. Mortality for a given COPD exacerbation is greater than asthma but also quite low. However, the disease prevalence of COPD is high and the exacerbations are frequent, and COPD is the fourth leading cause of death in the United States.

Incorrect diagnosis

Failure to respond to treatment should prompt consideration of alternative diagnoses and additional diagnostic testing, including imaging and/or visualization of the upper airway, high-resolution imaging of the chest, evaluation for pulmonary embolism, and evaluation for cardiac pathology.


Many exacerbations of obstructive lung disease are avoidable, and all patients admitted to the hospital should undergo counseling prior to discharge to minimize recurrent exacerbations. These should include discharge planning to ensure:

  • Continued abstinence from smoking or engagement with a smoking cessation plan

  • Identification of triggers and teaching regarding trigger avoidance

  • Education regarding discharge medications

  • Appropriate technique during use of all inhaled medications

  • Immunization against respiratory pathogens (S. pneumoniae and influenza)

  • Recognition of worsening symptoms

  • Understanding of a plan should symptoms worsen

  • Appropriate ambulatory follow-up for management of chronic disease

Ambulatory follow-up should confirm or assess for:

  • Full recovery from acute exacerbation

  • Review of symptoms and signs of obstructive lung disease

  • Titration of controller therapy

  • Appropriate technique of all inhaled medications

  • Immunization against respiratory pathogens (S. pneumoniae and influenza)

  • Recognition of worsening symptoms

  • Understanding of a plan should symptoms worsen


Obstructive lung disease is present when expiratory airflow is limited by increased airways resistance, often with associated decreased lung elastic recoil as in emphysema. The prototype of the former mechanism is asthma, where airway inflammation and smooth muscle hypertrophy decrease airway caliber, while the latter is characterized by emphysematous destruction of lung parenchyma. Individual patients may demonstrate one or both of these mechanisms.

The airway hyper-reactivity characterized by asthma is reversible, and thus respiratory distress from acute obstructive lung disease of this sort is often the result of acute airway narrowing and significant change in the physiologic properties of the respiratory system. This is in contrast to respiratory failure from COPD/emphysema, where the physiologic change (increased obstruction or increased load on the system) is small but sufficient to overwhelm an individual with poor pulmonary reserve, resulting in respiratory failure.


  • Obstructive lung disease has a high prevalence in the population, and exacerbations are common. For this reason the clinical and financial burden of acute respiratory failure from obstructive lung disease is large.

  • Asthma affects over 22 million people in the United States, leading to 14.7 million outpatient visits, 1.8 million emergency department visits, almost 500,000 hospital admissions, and approximately 4000 deaths annually.

  • Almost 15 million people in the United States carry a diagnosis of COPD (including chronic bronchitis and emphysema), which almost certainly understates the true prevalence. COPD is estimated to be responsible for over 125,000 deaths annually in the United States.


Admission to the hospital with asthma is associated with a favorable prognosis, with approximately 0.5% mortality. However, progression to respiratory failure requiring intubation and mechanical ventilation, which occurs in about 4% of admissions, increases the mortality to almost 7%, underscoring the importance of early recognition and treatment of acute asthma exacerbation.

Admission for an acute exacerbation of COPD carries a mortality of about 2 to 5%, a rate that increases to over 25% for patients requiring intubation and mechanical ventilation.

Special considerations for nursing and allied health professionals.


What's the evidence?


“Asthma Prevalence, Health Care Use, and Mortality: United States, 2003-2005”. Available from . (A valuable review of recent data detailing asthma epidemiology in the US.)

“Chronic Obstructive Pulmonary Disease (COPD) FastStats”. Dec. 17, 2010. (Current epidemiologic information concerning COPD.)

“Deaths from Chronic Obstructive Pulmonary Disease”. MMWR Weekly. vol. 57. 2008. pp. 1229-32. (Epidemiologic information concerning mortality in COPD in the US.)


Krishnan, V, Diette, GB, Rand, CS. “Mortality in Patients Hospitalized for Asthma Exacerbations in the United States”. American Journal of Respiratory and Critical Care Medicine. vol. 174. 2006. pp. 633-8. (Epidemiology of the hospitalized patient with COPD.)

Stein, BD, Charbeneau, JT, Lee, TA. “Hospitalizations for Acute Exacerbations of Chronic Obstructive Pulmonary Disease: How You Count Matters”. COPD: Journal of Chronic Obstructive Pulmonary Disease. vol. 7. 2010. pp. 167-71. (Discusses pitfalls in determining adverse effects and requirement for hospitalization in patients with COPD.)

Tabak, YP, Sun, X, Johannes, RS. “Mortality and Need for Mechanical Ventilation in Acute Exacerbations of Chronic Obstructive Pulmonary Disease: Development and Validation of a Simple Risk Score”. Archives of Internal Medicine. vol. 169. 2009. pp. 1595-602. (Points to the increased risk of death in the most severely ill patients with COPD who have progressed to respiratory failure.)