Thursday Teaching Sessions

Pulmonary and Critical Care

February 20th 2014

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Asthma

Patients with asthma have increased nonspecific airway responsiveness that results in increased sensitivity to inhaled bronchoconstrictive agents (such as methacholine) and airway obstruction that is typically reversible. When patients with asthma are exposed to relevant allergens, they develop an early-phase response that manifests 15 to 30 minutes after the exposure and resolves in 1 to 2 hours. Roughly half of patients develop a late-phase response 3 to 8 hours following the exposure.

Epidemiology and Natural HistoryAsthma is one of the most common diseases, affecting 5% of the adult population in the United States.Between 70% and 90% of patients with asthma have allergies demonstrated with skin testing and confirmed by relevant history.Although airway obstruction in asthma is reversible, there is a greater decline in lung function over time among patients with asthma compared with healthy controls. This decline is more prominent in patients who smoke.

Clinical EvaluationSpirometry should be performed in patients with suspected asthma to confirm airway obstruction and reversibility. Patients with suspected asthma who have normal spirometry should undergo a bronchial challenge test to assess for airway hyperresponsiveness; a negative test generally excludes asthma.

The majority of patients with asthma have a personal and family history of allergies, and their exposure to relevant allergens often provokes asthma symptoms. Other triggers include viral upper respiratory tract infections, cold air, stress, and exercise. Asthma is generally worse at night. Most patients report increased asthma symptoms at night or in the early morning at least once a month. On initial evaluation of patients who are suspected of having asthma, spirometry should be performed to confirm the diagnosis with demonstrated airway obstruction (low FEV1/FVC ratio) and reversibility (12% or greater improvement in FEV1 after administration of bronchodilators)

Asthma Syndromes Occupational Asthma Reactive Airways Dysfunction Syndrome Virus-Induced Asthma Cough-Variant Asthma Gastroesophageal Reflux Disease and Asthma Allergic Bronchopulmonary Aspergillosis Exercise-Induced Bronchospasm Vocal Cord Dysfunction Aspirin-Sensitive Asthma

Occupational AsthmaExposure to irritants, allergens, and sensitizing chemicals can be an important contributor to the development or worsening of asthma. Therefore, any patient with asthma should be asked about work-related exposures, keeping in mind that some exposures may be in the home environment. Patients with occupational asthma report feeling better when away from the offending environment, such as on weekends or vacations; however, symptoms may still occur even when away from the work environment because of underlying airway hyperresponsiveness.

Avoidance of exposure to the offending agent (by changing jobs, changing the work environment, or using protective equipment) is recommended. Patients with occupational asthma can show improvement in lung function, symptoms, and airway hyperresponsiveness over time and can return to normal if they have no further exposure to the offending agent.

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Reactive Airways Dysfunction SyndromeReactive airways dysfunction syndrome (RADS) is a distinct type of occupational asthma that results from a single accidental exposure to high levels of irritant vapors, gases, or fumes such as chlorine gas, bleach, or ammonia. This exposure leads to significant airway injury with persistent airway inflammation, dysfunction, and hyperresponsiveness. Patients with RADS typically do not have a history of asthma and do not have “allergic sensitization” to the offending irritant prior to the accidental exposure.

Virus-Induced AsthmaInfections with respiratory viruses such as rhinovirus, respiratory syncytial virus, and influenza virus are associated with asthma exacerbations.Patients with viral respiratory tract infections typically have increased airway responsiveness that lasts 4 to 6 weeks following the infection, leading to increased asthma symptoms.

Cough-Variant AsthmaCough-variant asthma is present in patients who have cough as their main symptom. The cough is typically dry and is sometimes the only symptom of asthma. The diagnosis is confirmed with spirometry that demonstrates airway obstruction with improvement following inhaled bronchodilator administration or with bronchial challenge testing that demonstrates airway hyperresponsiveness.

Gastroesophageal Reflux Disease and AsthmaPatients with asthma often have associated GERD that can contribute to symptoms (typically cough) or increased frequency of exacerbations. It is important to recognize that many patients with GERD can be asymptomatic; therefore, GERD should be considered in patients who have asthma that is difficult to control

Allergic Bronchopulmonary AspergillosisThis ubiquitous fungus colonizes abnormal airways in patients with asthma or cystic fibrosis, with subsequent development of specific immune responses that can lead to pulmonary inflammation, bronchiectasis, and fibrosis. The diagnosis of ABPA is confirmed by demonstrating elevated serum levels of IgE (total and specific Aspergillus IgE), a positive skin test to A. fumigatus, and eosinophilia. High-resolution chest CT scan demonstrates proximal bronchiectasis, often with mucus occluding airways or leading to atelectasis. Achieving disease control in these patients requires systemic corticosteroids in addition to inhaled corticosteroids and bronchodilator rescue therapy. Once disease is under control, systemic corticosteroids can be tapered off, as guided by evaluation of symptoms, pulmonary function testing, levels of circulating eosinophils, chest radiograph, and IgE levels. Left untreated, ABPA can result in progressive pulmonary fibrosis and loss of lung function.

Exercise-Induced BronchospasmBronchial obstruction in exercise-induced bronchoconstriction peaks 5 to 10 minutes after cessation of exercise and resolves within 30 minutes; symptoms are at their worst not during exercise but immediately following cessation of exercise.

Treatment with short-acting β2-agonists given 15 minutes before exercise prevents EIB in most patients. The protection lasts up to 3 hours, allowing most patients to engage fully in desired physical activity. Leukotriene-modifying drugs can also be used to prevent EIB; however, they are not as effective as inhaled β2-agonists. Nonpharmacologic approaches to prevent EIB include gradual warmup before intense exercise, using a mask over the nose and mouth during cold weather, and avoidance of high-intensity intermittent exercise.

Vocal Cord Dysfunction

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When patients with asthma present with prominent wheezing that is more notable during inspiration (stridor), vocal cord dysfunction (VCD) should be suspected. Typically, patients with VCD have abrupt onset of symptoms that are felt in the neck, but these symptoms are often difficult to distinguish from symptoms of typical asthma. Clinical evaluation of VCD demonstrates monophonic wheezing that is loudest over the neck, as opposed to polyphonic wheezing over the chest as is seen in patients with asthma. Abrupt onset and termination of the episode is characteristic of VCD and is atypical for asthma. Further confirmation can be obtained with laryngoscopy, which shows marked adduction of the vocal cords with severe airway narrowing. Flow-volume loops show inspiratory flow cutoff and preserved expiratory flow, in contrast to what is seen in asthma. Treatment of VCD includes patient education, behavior modification, and speech therapy. GERD, which is often present in patients with VCD, may also need to be treated. During acute attacks, inhaled helium-oxygen mixture and/or continuous positive airway pressure can relieve acute symptoms of VCD.

Aspirin-Sensitive AsthmaA small percentage of adults with asthma are aspirin sensitive. A subset of these patients has severe asthma, aspirin sensitivity, and nasal polyps (Samter triad). Aspirin sensitivity should be considered in patients with difficult-to-control disease and should be confirmed based on history and aspirin challenge. Patients who must use aspirin should be referred for desensitization. Once patients are desensitized and taking aspirin regularly, aspirin sensitivity remains quiescent; however, it could become symptomatic again if there is a hiatus in aspirin use. Other NSAID medications may also provoke asthma symptoms in these patients and should be avoided

ManagementDespite the availability of widely disseminated guidelines, management of many patients with asthma remains less than optimal.Effective management of asthma requires a multifaceted approach that includes patient education, agreement on goals of therapy in partnership with patients, and providing asthma action plans that guide patients in self-management of this chronic illness. The goals of asthma management are to (1) maintain a normal functional status; (2) preserve normal lung function; (3) reduce the need for rescue albuterol to less than twice weekly; (4) reduce symptom flares that require more intensive therapy; and (5) decrease the side effects of treatment. Asthma is classified as intermittent or persistent; persistent asthma is further classified as mild, moderate, or severe

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These different categories are associated with a stepwise approach to asthma management aimed at reducing impairment and risk

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PharmacotherapyPatients with asthma should be instructed on the use of inhalation devices at the initial clinic visit, and their technique should be reviewed at subsequent visits.Short-acting β2-agonists are the most effective bronchodilator medications available and have a rapid onset of action.Long-acting β2-agonists should be added to other asthma medications only after inhaled corticosteroid therapy has been optimized.Inhaled corticosteroids are the mainstay controller therapy for asthma.Regular use of inhaled corticosteroids can result in systemic side effects; patients should be evaluated at regular intervals for appropriateness of stepping down therapy to the lowest inhaled corticosteroid dose consistent with adequate asthma control.

Management of Asthma ExacerbationsIncreasing short-acting β2-agonists and consideration of a short course of systemic corticosteroids is recommended to initiate treatment of exacerbation at home. If symptoms do not respond to these measures, the patient should be evaluated in a clinical setting.

Spirometry and/or peak expiratory flow rate (PEFR) measurement is recommended. Patients with moderate (PEFR 40%-69% of predicted or personal best) or severe (PEFR <40%) exacerbations should be treated with frequent short-acting β2-agonists and systemic corticosteroids. In patients with severe exacerbations, bronchodilator medications (short-acting β2-agonists and ipratropium) should be given by nebulization, whereas in mild attacks an MDI with a holding chamber can be used. The intravenous route is preferred for corticosteroids in severe attacks, whereas the oral route is used in milder cases. Most patients should receive 5 to 7 days of oral corticosteroids (40 mg/d of prednisone) to ensure resolution and reduce chances for recurrence. Pulse oximetry should be monitored, and supplemental oxygen should be given to maintain saturation above 92%. Follow-up pulmonary function tests should be obtained in 1 hour; patients without significant improvement should be considered for hospitalization and patients with a good response (PEFR >70%) that is sustained for 1 hour can be discharged.

Asthma and PregnancyAsthma is one of the most common medical problems that complicates pregnancy; better asthma control is likely to reduce the risk to both mother and fetus.During pregnancy, one third of patients have improvement in asthma control, another third have worsening asthma, and another third have no change.Short-acting β2-agonists (albuterol) are recommended for quick relief of asthma symptoms during pregnancy, while inhaled corticosteroids are the mainstay controller medications. Among corticosteroids, budesonide has the most safety data available during gestation and is recommended for use in pregnant patients; however, patients who are already doing well on other inhaled corticosteroids can continue them after they become pregnant because there has been no evidence of harm from the use of these medications. The preferred second-line therapy is long-acting β2-agonists.Alternative drugs that can be used during pregnancy include leukotriene receptor antagonists and theophylline. Although systemic corticosteroids have been linked to a small risk of congenital abnormalities, their use is recommended in patients with acute severe asthma. Left untreated, acute asthma exacerbations can have serious morbidity for the mother and outcome of pregnancy.

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Chronic Obstructive Pulmonary Disease

Risk FactorsRisk factors for COPD include exposure to tobacco smoke (including second-hand smoke), dust and chemicals (vapors, irritants, fumes), outdoor air pollution, and environmental (biomass) smoke, as well as genetic factors such as α1-anti-trypsin deficiency

Risk for COPD is dose related. The age when the patient started to smoke, total pack-years smoked, and current smoking status are predictive of COPD mortality. Smoking cessation is the single most clinically effective and cost-effective way to prevent COPD, slow progression of established disease, and improve survival.

Extrapulmonary Effects and Comorbid ConditionsWeight loss, muscle wasting, and weakness are common in severe COPD as a result of deconditioning and malnutrition. In the presence of chronic inflammation and smoking-related toxins, comorbid conditions further complicate disease management and significantly affect COPD morbidity and mortality.

Assessment and ClassificationA clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough, intermittent wheezing, sputum production, decreased exercise tolerance, a history of significant exposure to tobacco smoke, and/or a history of other risk factors for the disease.

Spirometry is essential for the diagnosis of COPD, although testing for airflow limitation should not be performed in asymptomatic individuals as a screening intervention. When indicated, diagnostic spirometry should be performed after administration of an inhaled bronchodilator because this will improve the accuracy of the study results.

Guidelines from both the American College of Physicians (ACP) and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) define airflow obstruction as a postbronchodilator FEV1/FVC ratio less than 70%. The GOLD guidelines further classify COPD based on the level of airflow obstruction assessed by spirometry

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Another means of assessing disease severity is the BODE (BMI, Obstruction, Dyspnea, Exercise) Index, which is a composite disease marker that takes into account the systemic nature of COPD. The index incorporates spirometry, MMRC scores, and other parameters and is useful in evaluating the risk for hospitalization and estimating the long-term prognosis for patients with COPD. A higher score is associated with worse outcomes. Pulmonologists also may use BODE scores in the assessment of patients for lung transplantation. Patients with a BODE index score of 7 or higher will have a 4-year survival rate of 20% or lower.

Ongoing MonitoringMonitoring to adjust COPD therapy should focus on doses of medications, adherence to the regimen, inhaler technique, effectiveness of symptom control, and the side effects of treatment. Periodic spirometry should be performed to track a patient's lung function.

Exacerbation frequency and severity should be assessed with patient history and evaluation of symptoms.

ReferralInternists may consider referral to a pulmonary specialist in the presence of disease onset before 40 years of age, a rapidly progressive course of disease, severe COPD despite optimal treatment, need for oxygen therapy, onset of a comorbid condition, diagnostic uncertainty, symptoms disproportionate to the severity of airway obstruction, confirmed or suspected α1-antitrypsin deficiency, a request for a second opinion, possibility for lung transplantation or lung volume reduction surgery, very severe disease requiring elective surgery that may impair respiratory function, or frequent exacerbations and persistent symptoms despite adequate treatment

ManagementThe components of a COPD management plan are (1) identification and reduction of risk factors, (2) assessment and monitoring of disease progression, (3) managing stable COPD, and (4) managing exacerbations.

The frequency of exacerbations increases as the severity of COPD increases. Patients who experience frequent exacerbations are also likely to have more symptoms, worsened health status, faster disease progression, and an increased risk of death. To maximize outcomes, treatment regimens must be sustained for the long term and reassessed periodically to monitor for efficacy and side effects.

Pharmacologic TherapyInhaled medications are central to the management of COPD; if a patient is not responding to therapy, adherence should be verified and inhaler technique should be assessed before therapy is adjusted.

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COPD treatment consists of initiating monotherapy with a long-acting bronchodilator (including long-acting β2-agonists or long-acting anticholinergic agents) in symptomatic patients with an FEV1 less than 60% of predicted.

Inhaled corticosteroids should not be used alone for maintenance or rescue therapy in COPD.

Therapy with different combinations of long-acting β2-agonists, long-acting anticholinergic agents, and inhaled corticosteroids is frequently used in patients with symptomatic COPD not controlled on monotherapy; the optimal combination of medications and their safety and efficacy have not yet been established.

Pneumococcal vaccination and annual influenza vaccination are recommended for all patients with COPD.

Antibiotic AgentsAntibiotic therapy is most beneficial in treating infectious exacerbations of COPD that are characterized by increases in dyspnea, sputum volume, and sputum purulence. Antibiotic therapy also is indicated in patients with severe exacerbations of COPD who require mechanical ventilation, whether invasive or noninvasive. Although the inciting factor of an exacerbation may be unknown, a fluoroquinolone such as levofloxacin or the combination of a third-generation cephalosporin plus a macrolide antibiotic will usually cover the most common bacterial pathogens (Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis as well as causes of “atypical” pneumonia). Even when the cause of the exacerbation is viral, patients with COPD are often colonized with bacteria. Antibiotics in this setting have been demonstrated to improve air flow, reduce mortality, and reduce treatment failure, especially in patients experiencing more severe exacerbations. A number of meta-analyses and systematic reviews support the use of antibiotic treatment for acute exacerbations of COPD.

Nonpharmacologic TherapySmoking cessation and oxygen therapy are the only interventions demonstrated to reduce COPD risk and positively affect decline in pulmonary function; smoking cessation is the most important goal in the management of COPD in patients who smoke, and it should be addressed at every visit.

Pulmonary rehabilitation (consisting of education, nutritional counseling, exercise training, assessment, and follow-up) can be considered for all symptomatic patients with COPD who have an FEV1 less than 50% of predicted.

Oxygen therapy is a major component of treatment for patients with very severe COPD and is indicated for patients who have hypoxemia (arterial PO2 ≤55 mm Hg [7.3 kPa] or arterial oxygen saturation ≤88%).

Managing Exacerbations of COPDTreatment of COPD exacerbations may involve additions or adjustments to bronchodilator therapy, inhaled or systemic corticosteroid therapy, initiation of antibiotic treatment, possibly mechanical ventilation, or hospitalization in severe exacerbations.

Home ManagementHome care is increasingly common for the treatment of mild-to-moderate exacerbations of COPD as well as for patients with end-stage disease.

Hospital ManagementRisk of death from an exacerbation of COPD closely correlates with development of respiratory acidosis, the presence of significant comorbidities, and requirement for ventilatory support. Patients with COPD exacerbations should be hospitalized in the presence of underlying severe COPD, advanced patient age,

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significant comorbidities, marked increase in intensity of symptoms, newly occurring arrhythmias, diagnostic uncertainty, insufficient home support, onset of new physical signs, or failure to respond adequately to initial medical management. Admission of patients with severe exacerbations to intermediate or special respiratory care units may be appropriate if personnel, skills, and equipment exist to successfully identify and manage acute respiratory failure. Some patients may require direct admission to the intensive care unit

Hospital Discharge and Follow-upAfter hospitalization for an acute exacerbation of COPD, patients should be discharged when they no longer require short-acting inhaled β2-agonist therapy more frequently than every 4 hours, are clinically stable and have demonstrated stable arterial blood gas levels for 12 to 24 hours, and can understand the correct use of medications (either personally or through a caretaker).

After hospitalization for a COPD exacerbation, early follow-up is important to reduce hospital readmission rates.

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Pulmonary Nodule Evaluation

A pulmonary nodule is defined as a focal, nodular opacity that is up to 3 cm in diameter, is surrounded by normal lung, and is not associated with lymphadenopathy. Lesions larger than 3 cm are considered lung masses; the high likelihood of a malignancy in masses reduces the consideration of differential processes. Pulmonary nodules may be single or multiple.

Assessment of Risk for MalignancyThe likelihood of malignancy of a pulmonary nodule is based on the size, surface characteristics, patient age, smoking history, and history of prior malignancy. Nodule size is often the most important feature in predicting malignancy. A smooth border is an indication a nodule is more likely benign; a spiculated border indicates a high likelihood of malignancy. Risk from smoking increases with earlier age at onset of smoking, duration of smoking, and number of cigarettes smoked per day. Risk for lung cancer increases with age, and the age-specific lung cancer incidence rates for both women and men are highest after age 70 years. Lung cancers are less frequent in persons younger than 45 years. A history of another malignancy increases the likelihood that a pulmonary nodule is malignant. Metastasis to the lung is common.

ManagementNo follow-up is necessary for pulmonary nodules that are smaller than 4 mm in never-smokers with no other known risk factors for malignancy (history of a first-degree relative with lung cancer or significant radon or asbestos exposure).Examination of previous chest imaging studies is critical in pulmonary nodule evaluation and may show that a nodule is stable, growing, or shrinking over time.

The Fleischner Society for Thoracic Imaging and Diagnosis recommendations for follow-up of various nodule sizes are.

Solid nodules that remain stable in size for 2 years on chest radiograph or CT scan are considered benign, and no further follow-up is indicated; this is known as the 2-year stability rule.

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Respiratory FailureAdmission to the intensive care unit (ICU) for respiratory insufficiency is prompted by three basic conditions: (1) hypoxemic respiratory failure; (2) ventilatory, or hypercapnic, respiratory failure; and (3) impaired upper airway.

Hypoxemic Respiratory FailurePositive end-expiratory pressure is the first-line approach to correcting shunt-associated hypoxemia in patients with acute respiratory distress syndrome, but it is less applicable in the setting of focal disease.

The diagnosis of acute respiratory distress syndrome (ARDS) is predominantly made on clinical grounds, and pulmonary artery catheters infrequently play a role in the diagnosis or management of ARDS.

Atelectasis is an important cause of hypoxemia in surgical and mechanically ventilated patients.

Acute hypoxemic respiratory failure is characterized by an abrupt, severe decline in oxyhemoglobin saturation that does not readily correct with supplemental oxygen. Generally, the ambient air arterial PO2 is 60 mm Hg (8.0 kPa) or less and the arterial PO2/FIO2 is 200 mm Hg (26.6 kPa) or less; the arterial PCO2 is typically normal or reduced. Rather, hypoxemia is reversed by application of positive end-expiratory pressure (PEEP) to the lung, which opens up, or “recruits,” flooded or collapsed alveoli.

Acute Respiratory Distress SyndromeThe Berlin criteria for the diagnosis of ARDS include: (1) acute onset within 1 week of an apparent clinical insult or development and progression of respiratory symptoms; (2) bilateral opacities on chest imaging not explained by other pulmonary pathology (such as pleural effusions, lung collapse, or nodules); (3) respiratory failure not explained by heart failure or volume overload. Mild ARDS is defined by an arterial PO2/FIO2 ratio between 201 and 300 mm Hg (26.7 and 39.9 kPa). In moderate ARDS, the ratio is between 101 and 200 mm Hg (13.4 and 26.6 kPa), and Severe ARDS is defined by a ratio of 100 mm Hg (13.3 kPa) or less. All three categories require that measurement of the arterial PO2/FIO2 ratio be performed with a PEEP level of at least 5 cm H2O, which may be delivered noninvasively with CPAP in the mild ARDS group.

More than 60 disorders can precipitate ARDS by direct or indirect injury to the lung, but severe sepsis from pneumonia or nonpulmonary sources constitutes the majority of cases. Deaths are primarily caused by the underlying precipitant of lung injury or subsequent nosocomial infections rather than directly by lung injury.

Non–Ventilator-Related ManagementMechanical ventilation is the primary supportive treatment in ARDS. Many other therapies have been tried in ARDS, and most have shown an improvement in oxygenation but not survival. Many therapies (inhaled vasodilators, prone positioning, occasionally corticosteroids) are still used in the minority of patients with life-threatening hypoxemia despite aggressive ventilator support even though there is no proven survival benefit.

Heart FailurePatients with left ventricular systolic dysfunction are prone to acute cardiogenic pulmonary edema, but the ejection fraction is normal in approximately half of patients admitted for heart failure. Diastolic dysfunction, myocardial ischemia, hypertension, valve disease, and a variety of tachyarrhythmias are important considerations in the absence of systolic failure. Regardless of the underlying cause, left-sided heart failure can produce bilateral pulmonary infiltrates that are radiographically indistinguishable from ARDS. Unlike ARDS, cardiogenic edema can rapidly improve with aggressive medical management, and therefore early differentiation of the two disorders is important. Echocardiography is the primary means

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of diagnosing systolic and diastolic failure and valve disease. Evaluation for myocardial ischemia includes measuring troponin levels and review of electrocardiograms for ischemic changes.

Electrocardiograms are also used to evaluate arrhythmias. B-type natriuretic peptide levels can be useful in distinguishing cardiogenic from noncardiogenic edema in ambiguous cases, but they do not reliably diagnose or exclude heart failure when evaluated in isolation.

AtelectasisChest physiotherapy, incentive spirometry, early mobilization, and continuous positive airway pressure (CPAP) are commonly used in the perioperative period to prevent respiratory complications. Atelectasis is also common in patients receiving invasive mechanical ventilation. Supine position, absence of intermittent larger sigh breaths, and low tidal volumes predispose patients to bibasilar atelectasis. Mucus plugging and right-mainstem intubation can precipitate lobar collapse.

PneumoniaLung consolidation due to pneumonia creates a physiologic shunt similar to cardiogenic and ARDS-related edema. Pneumonia is the most common trigger for ARDS among nonhospitalized patients, and differentiating bilateral pneumonia from pneumonia that has evolved into ARDS can be difficult. Positioning the patient in the lateral decubitus position with the “good” lung dependent is a temporizing measure that may reduce intrapulmonary shunt.

Ventilatory (Hypercapnic) Respiratory FailureVentilatory respiratory failure stems from inadequate alveolar ventilation relative to CO2 production. Causes of decreased alveolar ventilation fall into one of three basic categories: (1) decreased respiratory drive, as seen with sedating drugs; (2) respiratory muscle weakness or excessive mechanical work of breathing, as seen in neuromuscular disease and severe kyphoscoliosis; and (3) lung diseases in which much of the inhaled gas does not participate in gas exchange. For instance, patients with COPD and severe ARDS have increased dead space, or “wasted” ventilation, resulting from ongoing ventilation of lung units that have injured capillary beds.

Ventilatory respiratory failure is characterized by hypoventilation and hypercapnia caused by excess mechanical load, decreased respiratory drive, respiratory muscle weakness, increased dead-space ventilation, and neuromuscular weakness.

Management of critically ill patients with neuromuscular weakness should consist of early identification and treatment of ventilatory failure, minimizing aspiration risk, and assisting with airway clearance.

Increased work of breathing due to high airway resistance and air trapping, combined with increased ventilatory demands, may lead to ventilatory failure in patients with obstructive lung disease.

The need for large amounts of supplemental oxygen in patients with exacerbations of COPD or asthma should prompt consideration of alternative diagnoses.

Patients with acute upper airway obstruction should be closely monitored and there should be a low threshold for intubation given the difficulty of endotracheal tube placement in this population.

Patients with a severe asthma exacerbation that does not respond to 1 hour of aggressive bronchodilator therapy are candidates for admission to the intensive care unit.A slightly elevated, or even normal, arterial PCO2 in a patient with an asthma exacerbation may indicate impending respiratory arrest.

Noninvasive Mechanical Ventilation

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Noninvasive positive pressure ventilation (NPPV) consists of delivery of positive airway pressure breaths without the use of an endotracheal tube or tracheostomy. NPPV settings include an inspiratory positive airway pressure (IPAP) and an end-expiratory positive airway pressure (EPAP).

IndicationsObstructive Lung DiseaseNoninvasive positive pressure ventilation is the standard of care for managing moderate to severe COPD exacerbations.Cardiogenic Pulmonary EdemaSeveral randomized trials indicate that NPPV and CPAP improve dyspnea and gas exchange in patients with respiratory failure due to acute cardiogenic pulmonary edema. Immunocompromised PatientsThere is a strong rationale for avoiding intubation in immunocompromised patients given their increased risk of nosocomial infections, including ventilator-associated pneumonia. Following ExtubationNPPV can be used in various ways to facilitate weaning from invasive mechanical ventilation. Taken together, the evidence suggests that the use of NPPV in patients in whom a trial of extubation has failed should be limited primarily to those with chronic lung disease and hypercapnia.Other Populations with Hypoxemic Respiratory FailureCPAP reduces the need for intubation in patients with hypoxemic respiratory failure complicating abdominal surgery as well as following lung resection, presumably by reducing atelectasis.

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