Chronic Obstructive Pulmonary Disease
nonpharm recommendations in COPD
(1) smoking cessation, (2) reduction of other risk factors (eg, exposure to open cooking fires), (3) vaccinations, (4) oxygen therapy, and (5) pulmonary rehabilitation Age-appropriate pneumococcal vaccination should be offered to all patients with COPD. Pneumococcal polysaccharide vaccination (PPSV23, Pneumovax) is advised for patients under age 65 years; PPSV23 and pneumococcal conjugate vaccine (PCV13, Prevnar) are advised for patients age 65 years and older ● An annual influenza vaccine should be given to all patients, particularly those with COPD [10-13]. In a randomized trial of 125 patients with COPD, vaccination reduced the incidence of influenza by 76 percent, regardless of the severity of underlying COPD [10]. The influenza vaccination itself does not increase the risk of acute exacerbation
Differential diagnosis for COPD symptoms After diagnosing COPD it is important to consider what?
After confirming the presence of COPD, the next step is to consider the cause. For the majority of patients, the etiology is longterm cigarette smoking. However, it is important to review with the patient whether underlying asthma, workplace exposures, indoor use of biomass fuel, a prior history of tuberculosis, or familial predisposition is contributory, because mitigation of ongoing exposures may reduce disease progression. In areas of high prevalence of alpha-1 antitrypsin (AAT) deficiency, it is appropriate to screen all patients with COPD by obtaining an AAT serum level and AAT genotyping DIFFERENTIAL DIAGNOSIS — Among patients who present in mid or later life with dyspnea, cough, and sputum production, the differential diagnosis is broad (eg, heart failure, COPD, interstitial lung disease, thromboembolic disease) (table 3). Typically, the finding of persistent airflow limitation on pulmonary function testing and the absence of radiographic features of heart failure or interstitial lung disease direct the clinician to a narrower differential of COPD, chronic obstructive asthma, bronchiectasis, tuberculosis, constrictive bronchiolitis, and diffuse panbronchiolitis [8]. Importantly, these conditions can commonly occur together, for example, patients with asthma may develop COPD and patients with COPD may have concurrent bronchiectasis.
Airway changes in COPD -name the airway changes -name some cells that can be seen in chornic bronchitis vs asthma
Airways - Airways abnormalities in COPD include chronic inflammation, increased numbers of goblet cells, mucus gland hyperplasia, fibrosis, narrowing and reduction in the number of small airways, and airway collapse due to the loss of tethering caused by alveolar wall destruction in emphysema [17]. Among patients with chronic bronchitis who have mucus hypersecretion, an increased number of goblet cells and enlarged submucosal glands are typically seen. Chronic inflammation in chronic bronchitis and emphysema is characterized by the presence of CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages (picture 1) in the airways [39-43]. comparison, the bronchial inflammation of asthma is characterized by the presence of CD4+ T-lymphocytes, eosinophils, and increased interleukin (IL)-4 and IL-5 While these paradigms are helpful conceptually, they are not diagnostic and overlaps exist. For example, there may be a set of asthmatic patients who progress to develop COPD.
COPD complication testing
As a main focus of COPD management is on symptom control, it is essential to assess for complicating diseases that may contribute to symptoms, such as coronary heart disease, heart failure, arrhythmias, bronchiectasis, or interstitial lung disease. This evaluation may entail such tests as a chest radiograph, high resolution computed tomography (for bronchiectasis or interstitial lung disease), electrocardiogram (ECG), ambulatory ECG monitoring, transthoracic echocardiography, dobutamine stress echocardiography, and N-terminal pro-brain natriuretic peptide (NT pro-BNP)
Asthma -definition
Asthma — The Global Initiative for Asthma (GINA) gives the following definition of asthma: "Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread, but variable, airflow obstruction within the lung that is often reversible either spontaneously or with treatment [
Asthma COPD overlap
Asthma-COPD overlap — Consistent with the idea that significant overlap exists among the different types of COPD, many individuals have bronchial inflammation with features of both asthma and chronic bronchitis/emphysema [8,28-30]. Similarly, the nature of the bronchial inflammation varies widely even among individuals with a single type of COPD. In recognition of this overlap, GOLD and GINA issued a consensus statement on Asthma, COPD, and Asthma-COPD Overlap Syndrome (ACOS, also referred to as asthma-COPD overlap [ACO]) [31], which describes the overlap as "characterized by persistent airflow limitation with several features usually associated with asthma and several features usually associated with COPD. ACOS is therefore identified in clinical practice by the features that it shares with both asthma and COPD." Further study of this overlap will be needed to determine with certainty how treatment algorithms should be tailored to these patients [29]. As an example, a subgroup of patients with sputum eosinophilia may experience lung function improvement with anti-interleukin-5 or anti-IL-5 receptor monoclonal antibodies that deplete blood and sputum eosinophils [32,33]. Further Patients with asthma whose airflow obstruction is completely reversible are not considered to have COPD (subset nine in the figure).
COPD definition
COPD — The Global Initiative for Chronic Obstructive Lung Disease (GOLD), a project initiated by the National Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization (WHO), defines COPD as follows [8]: -"COPD is a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases. The chronic airflow limitation that characterizes COPD is caused by a mixture of small airways disease (eg, obstructive bronchiolitis) and parenchymal destruction (emphysema), the relative contributions of which vary from person to person. Chronic inflammation causes structural changes, small airways narrowing, and destruction of lung parenchyma. A loss of small airways may contribute to airflow limitation and mucociliary dysfunction, a characteristic feature of the disease."
Chronic bronchitis -definition?
Chronic bronchitis — Chronic bronchitis is defined as a chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough (eg, bronchiectasis) have been excluded [8]. It may precede or follow development of airflow limitation [8,10,11]. This definition has been used in many studies, despite the arbitrarily selected symptom duration. Symptoms of chronic bronchitis may develop in cigarette smokers as early as 36 years of age and have been associated with a higher frequency of exacerbation events, even in the absence of airflow obstruction [12]. Current and former smokers have increased airway mucin concentration (MUC5AC and MUC5B), compared with never smokers; those with symptoms of chronic bronchitis also have higher concentrations than those of similar GOLD stage without symptoms
Pulmonary Rehab -when should pulmonary rehab be suggested? Oxygen therapy -should be given for who?
Comprehensive pulmonary rehabilitation has been shown to improve exercise capacity, improve quality of life, decrease dyspnea, and decrease health care utilization. In addition, it may reduce mortality. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest participation in pulmonary rehabilitation for symptomatic patients who are in GOLD COPD categories B, C, or D Oxygen therapy — Many patients with stable severe COPD (especially GOLD Stage IV disease) have chronic hypoxemia. Long-term oxygen therapy (LTOT) should be prescribed for patients with chronic, severe hypoxemia at rest (arterial oxygen tension [PaO ] ≤55 mmHg or pulse oxygen saturation [SpO ] ≤88 percent), as LTOT has been shown to improve survival and quality of life in these patients [6,41,148]. The benefits, indications, and prescription of supplemental oxygen are discussed in detail elsewhere.
Diagnosis criteria When should you repeat spirometry
DIAGNOSIS — The presence of symptoms compatible with COPD (eg, dyspnea at rest or on exertion, cough with or without sputum production, progressive limitation of activity) are suggestive of the diagnosis, especially if there is a history of exposure to triggers of COPD (eg, tobacco smoke, occupational dust, indoor biomass smoke), a family history of chronic lung disease, or presence of associated comorbidities (table 4). The diagnosis of COPD is confirmed by the following [94]: Spirometry demonstrating airflow limitation (ie, a forced expiratory volume in one second/forced vital capacity [FEV /FVC] ratio less than 0.7 or less than the lower limit of normal [LLN] PLUS an FEV less than 80 percent of predicted) that is incompletely reversible after the administration of an inhaled bronchodilator (table 2A-B). (See 'Pulmonary function tests' above.) ● Absence of an alternative explanation for the symptoms and airflow limitation (table 3) [8]. The differential diagnosis of COPD is discussed below. (See 'Differential diagnosis' below and "Approach to the patient with dyspnea".) ● The Global Initiative for COPD (GOLD) guidelines suggest repeating spirometry on a separate occasion to demonstrate persistence of airflow limitation (FEV /FVC <0.7 or less than the LLN) for patients with an initial FEV /FVC between 0.6 and 0.8 [8,95,96].
COPD physical exam findings -early in the diesease -as disease severity progresses -end stage COPD -is nail clubbing a common finding in COPD
Early in the disease, the physical examination may be normal, or may show only prolonged expiration or wheezes on forced exhalation. As the severity of the airway obstruction increases, physical examination may reveal hyperinflation (eg, increased resonance to percussion), decreased breath sounds, wheezes, crackles at the lung bases, and/or distant heart sounds [63]. Features of severe disease include an increased anteroposterior diameter of the chest ("barrel-shaped" chest) and a depressed diaphragm with limited movement based on chest percussion. ● Patients with end-stage COPD may adopt positions that relieve dyspnea, such as leaning forward with arms outstretchedand weight supported on the palms or elbows. This posture may be evident during the examination or may be suggested by the presence of callouses or swollen bursae on the extensor surfaces of forearms. Other physical examination findings include use of the accessory respiratory muscles of the neck and shoulder girdle, expiration through pursed lips paradoxical retraction of the lower interspaces during inspiration (ie, Hoover's sign) [64,65], cyanosis, asterixis due to severe hypercapnia, and an enlarged, tender liver due to right heart failure. Neck vein distention may also be observed because of increased intrathoracic pressure, especially during expiration. ● Yellow stains on the fingers due to nicotine and tar from burning tobacco are a clue to ongoing and heavy cigarette smoking [66]. ● Clubbing of the digits is not typical in COPD (even with associated hypoxemia) and suggests comorbidities such as lung cancer, interstitial lung disease, or bronchiectasis.
Emphysema -definition -subtypes
Emphysema — Emphysema is a pathological term that describes some of the structural changes sometimes associated with COPD. These changes include abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis (ie, there is no fibrosis visible to the naked eye) [14]. Exclusion of obvious fibrosis was intended to distinguish the alveolar destruction due to emphysema from that due to the interstitial pneumonias. However, many studies have found increased collagen in the lungs of patients with mild COPD, indicating that fibrosis can be a component of emphysema [15,16]. While emphysema can exist in individuals who do not have airflow obstruction, it is more common among patients who have moderate or severe airflow obstruction [8,17-19]. The various subtypes of emphysema (eg, proximal acinar, panacinar, distal acinar) are described below.
COPD evaluation -when is work up for COPD appropriate? -how should someone be worked up? -is it recommended to screen for COPD in asymptmatic adults?
Evaluation for COPD is appropriate in adults who report dyspnea, chronic cough, chronic sputum production or have had a gradual decline in level of peak activity, particularly if they have a history of exposure to risk factors for the disease (eg, cigarette smoking, indoor biomass smoke) [8,51]. All patients are evaluated with spirometry and selected patients have laboratory testing and imaging studies. There is no evidence to support the benefit of population based screening of asymptomatic adults for COPD [67], but the Global Initiative for Chronic Obstructive Lung Disease (GOLD) does advocate active case finding among at risk individuals.
Category A COPD Treatment
For all patients with COPD, we recommend that a shortacting bronchodilator be used as-needed for relief of intermittent increases in dyspnea [6]. If patients have minimally symptomatic COPD and are at low risk of exacerbation (ie, modified Medical Research Council [mMRC] grade 0 to 1 or COPD Assessment Test [CAT] score <10; and 0 to 1 exacerbation per year), this is usually the only medication needed A regularly scheduled long-acting bronchodilator should be added if symptoms are inadequately controlled with short-acting bronchodilator therapy or if the patient is at greater risk for poor outcomes (eg, frequent exacerbations, more severe disease) Combination therapy increased the mean peak forced expiratory volume in one second (FEV ) more than either agent alone, but did not alter the frequency of exacerbations. A similar study reported that combination therapy decreased the frequency of exacerbation compared to albuterol, but not ipratropium [40].
Category B COPD -what is the treatment
For patients who are more symptomatic, but at low risk of exacerbation based on their past history of exacerbations (ie, modified Medical Research Council [mMRC] grade ≥2 or COPD Assessment Test [CAT] score ≥10; 0 to 1 exacerbation per year), we recommend regular use of a long-acting bronchodilator, in addition to a short-acting bronchodilator (beta agonist or antimuscarinic agent) prescribed for as-needed relief of intermittent increases in dyspnea (table 1) [6,41]. Long acting bronchodilators have been shown to be superior to short acting bronchodilators taken on a regular basis. Either a long-acting beta agonist (LABA) or a long-acting muscarinic agent (LAMA, also known as long-acting anticholinergic agent) is acceptable for patients with category B COPD. Initial selection between a LAMA or LABA is often based on patient specific needs, comorbidities, and side effects. The efficacy and safety of LABAs and LAMAs have been compared in meta-analyses and randomized trials most of the research has involved tiotropium as the LAMA. Overall efficacy and safety appear comparable in terms of symptom control. Individual patients may prefer one or the other. Both LAMAs and LABAs reduce exacerbations, but LAMAs have a greater effect. For patients taking a LAMA, we prescribe a short-acting beta agonist (SABA) for rescue use; for those taking a LABA, we prescribe a short-acting muscarinic agent (SAMA) or a combination SAMA-SABA for rescue use.
Category D COPD -therapy options -name the LABA/ICS combos -name the triple therapy
For patients with a higher symptom burden (ie, modified Medical Research Council [mMRC] grade ≥2 or COPD Assessment Test [CAT] score ≥10) and a high risk of exacerbation (ie, ≥2 exacerbations per year with one or more leading to hospitalization), we recommend regular treatment with a long-acting beta agonist-long-acting muscarinic agent (LABA-LAMA) combination, rather than a single long-acting bronchodilator or a LABA-inhaled glucocorticoid combination, based on the benefits of LABA-LAMA combination therapy noted above. If the patient has persistent symptoms or additional exacerbations, we suggest triple therapy with a LAMA, LABA, and inhaled glucocorticoid (inhaled GC). (Trelegy- fluticasone, umeclinidium, Vilanterol) ICS/LABA combos: Advair (fluticasone/salmeterol) Symbicort (budesonide/formoterol) Breo (fluticasone, vilanterol)
Category C COPD -initial therapy for grade C? -is LABA/LAMA or LABA/ICS preferred ?
For the uncommon patients who are minimally symptomatic on a day-to-day basis (ie, modified Medical Research Council [mMRC] grade 0 to 1 or COPS Assessment Test [CAT] score <10), but are at high risk of an exacerbation due to their history of exacerbations in the past year (ie, ≥2 exacerbations per year with one or more leading to hospitalization), we suggest initial treatment with a longacting muscarinic agent (LAMA) due to the reduced exacerbation rate associated with LAMAs For patients who have further COPD exacerbations despite regular use of a LAMA, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest regular treatment with one of these choices: -Both a LAMA and a long-acting beta agonist (LABA) -Both a LABA and an inhaled glucocorticoid (ICS) -Less preferred options include regular use of short-acting beta-agonist and/or short-acting muscarinic agent; a phosphodiesteras-4 inhibitor, or theophylline For patients with COPD GOLD group C whose disease is not well-controlled with a single long-acting bronchodilator (table 1), current guidelines prefer use of a LABA-LAMA combination over an ICS-LABA combination due to evidence of improved lung function, better control of mild exacerbations, and fewer episodes of pneumonia, although improvement in symptoms was variable. However, LABA-inhaled glucocorticoid combinations have demonstrated reductions in mortality and exacerbations, compared with single bronchodilator therapy.
Imaging in COPD -what imaging modalities coud be used? -when would you order a CXR -When would you order a CT
Imaging — Chest radiography and computed tomography (CT) are typically performed in patients with COPD when the cause of dyspnea or sputum production is unclear and during acute exacerbations to exclude complicating processes (eg, pneumonia, pneumothorax, heart failure). Imaging is not required to diagnose COPD. However, in patients with severe COPD, CT scanning identifies individuals with predominantly upper lobe disease who may be candidates for lung volume reduction surgery. Chest radiography — The main reasons to obtain a chest radiograph when evaluating a patient for COPD are to exclude alternative diagnoses, evaluate for comorbidities (eg, lung cancer with airway obstruction, bronchiectasis, pleural disease, interstitial lung disease, heart failure), or to look for complications of COPD (eg, pneumonia, pneumothorax) that might be suggested by a change in symptoms. Plain chest radiographs have a poor sensitivity for detecting COPD. As an example, only about half of patients with COPD of moderate severity are identified as having COPD by a plain chest radiograph (ie, sensitivity of 50 percent). Computed tomography — CT has greater sensitivity and specificity than standard chest radiography for the detection of emphysema.However, CT scanning is not needed for the routine diagnosis of COPD. Usually, it is performed when a change in symptoms suggests a complication of COPD (eg, pneumonia, pneumothorax, giant bullae), an alternate diagnosis (eg, thromboembolic disease) is suspected, lung cancer screening is indicated, or a patient is being considered for lung volume reduction surgery or lung transplantation
What do we do with patients with Category B COPD who do not get symptomatic relief on either a LAMA or LABA alone?
In patients with GOLD COPD category B whose symptoms are not well-controlled with a single long-acting bronchodilator (see 'Assessing disease pattern and severity' above), we suggest adding a second long-acting bronchodilator from the alternate bronchodilator class (eg, a LAMA or a LABA bronchodilator), rather than an inhaled glucocorticoid Tiotropium-olodaterol (inspiolotol) Umeclidinium-vilanterol (Anoro) Glycopyrronium-indacaterol (Ultibro)
Inhaled Glucocorticoids -these are used with what? -should they be used alone? -what do they not help with? what do they help with? -Name some ICS
Inhaled glucocorticoids are typically used in combination with a long-acting bronchodilator for patients in GOLD categories C and D, who have repeated exacerbations with or without persistent symptoms, despite regular use of a long-acting bronchodilator. The addition of an inhaled glucocorticoid may be warranted at the same time that a long-acting inhaled bronchodilator is initiated, if there are signs of inflammation or an asthmatic component to the COPD [107]. Inhaled glucocorticoids are continued in patients whose symptoms, frequency of exacerbations, and/or lung function improve within one month. The available data, which are presented in detail separately, suggest that inhaled glucocorticoids decrease exacerbations and modestly slow the progression of respiratory symptoms, but appear to have little impact on lung function and mortality. In COPD, inhaled glucocorticoids are used as part of a combined regimen, but should NOT be used as sole therapy for COPD Fluticasone (Flovent) Budesonide (Pulmicort) Mometaonse Beclamethasone
Long acting beta agonists -what are the drug names -what is the major side effect?
LABAs include salmeterol, formoterol, arformoterol, indacaterol, vilanterol, and olodaterol; all are beta-2 selective. Arformoterol is only available as a solution for nebulization; vilanterol is only available as a component of a combination product. Serevent (salmeterol) Onbreze (indacaterol) Major side effect concern is cardiac arrhythmia
Lung parenchyma -what is the lung parenchyma? in which disease is it most affected? -how do you determine the subtype of emphysema -what is the most common etiologies of proximal acinar, panacinar, and distal acinar emphysema
Lung parenchyma - Emphysema affects the structures distal to the terminal bronchiole, consisting of the respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli, known collectively as the acinus. These structures in combination with their associated capillaries and interstitium form the lung parenchyma. The part of the acinus that is affected by permanent dilation or destruction determines the subtype of emphysema. ● Proximal acinar (also known as centrilobular) emphysema refers to abnormal dilation or destruction of the respiratory bronchiole, the central portion of the acinus. It is commonly associated with cigarette smoking, but can also be seen in coal workers' pneumoconiosis. • Panacinar emphysema refers to enlargement or destruction of all parts of the acinus. Diffuse panacinar emphysema is most commonly associated with alpha-1 antitrypsin deficiency, although it can be seen in combination with proximal emphysema in smokers. • In distal acinar (also known as paraseptal) emphysema, the alveolar ducts are predominantly affected. Distal acinar emphysema may occur alone or in combination with proximal acinar and panacinar emphysema. When it occurs alone, the usual association is spontaneous pneumothorax in a young adult.
Monitoring -what things can be used to monitor COPD?
MONITORING — Routine monitoring of symptoms (eg, breathlessness, cough, sputum, activity limitations, sleep disturbance), as-needed medication use, exacerbations, airflow limitation, and oxygenation is needed to ascertain whether an adequate response to therapy has been achieved and whether complications or comorbidities have developed [6]. Optimal intervals for assessment have not been determined. In our practice, we see most patients at three to six month intervals to assess symptoms and oximetry; we obtain spirometry annually or sooner, if symptoms worsen. When monitoring symptoms, it is helpful to record specific parameters, such as the modified Medical Research Council (mMRC) dyspnea scale (table 7) or COPD Assessment Test (CAT) [25] for breathlessness, daily quantity of sputum produced, and frequency of rescue inhaler use. Arterial blood gases (ABGs) and pulse oximetry are the only reliable methods of detecting hypoxemia in patients with COPD because most patients have few if any symptoms that can specifically be related to decreased oxygenation. As pulse oximetry can overestimate oxygen saturation in COPD, ABGs are appropriate when the pulse oxygen saturation (SpO ) is <92 percent [6,151]. ABG analysis is also helpful in assessing the presence and severity of hypercapnia, which can complicate oxygen therapy. (See "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure".)
PFTs -what is the purpose?
Pulmonary function tests (PFTs), particularly spirometry, are the cornerstone of the diagnostic evaluation of patients with suspected COPD [69]. In addition, PFTs are used to determine the severity of the airflow limitation, assess the response to medications, and follow disease progression.
Laboratory studies -are any blood lab studies diagnostic of COPD? -what lab studies can be used to rule out other diseases or comorbidities
No laboratory test is diagnostic for COPD, but certain tests are sometimes obtained to exclude other causes of dyspnea and comorbid diseases. Assessment for anemia is an important step in the evaluation of dyspnea. Measurement of plasma brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) concentrations is useful as a component of the evaluation of suspected heart failure (HF). Blood glucose, urea nitrogen, creatinine, electrolytes, calcium, phosphorus, and thyroid stimulating hormone may be appropriate depending on the degree of clinical suspicion for an alternate diagnosis
Interelationship between the subtypes of COPD -are people who have asthma who have completely reversible airflow obstruction considered to have COPD? -What about asthma patients who is not fully reversible -when are patients with chronic bronchitis and emphysema considered to have COPD
Patients with asthma whose airflow obstruction is completely reversible are not considered to have COPD (subset nine in the figure). ● Patients with asthma whose airflow obstruction does not remit completely are considered to have COPD (subsets six, seven, and eight in the figure). The etiology and pathogenesis of the COPD in such patients may be different from that of patients with chronic bronchitis or emphysema. ● Chronic bronchitis and emphysema with airflow obstruction commonly occur together (subset five in the figure) [24]. Some of these patients may also have asthma (subset eight in the figure). ● Individuals with asthma may develop a chronic productive cough, either spontaneously or due to exposure (eg, cigarette smoke, allergen). Such patients are often referred to as having asthmatic bronchitis, although this terminology has not been officially endorsed in clinical practice guidelines (subset six in the figure). ● Persons with chronic bronchitis, emphysema, or both are not considered to have COPD unless they have airflow obstruction (subsets one, two, and eleven in the figure) [25,26]. ● Patients with airflow obstruction due to diseases that have a known etiology or a specific pathology (eg, cystic fibrosis, bronchiectasis, obliterative bronchiolitis) are not considered to have COPD (subset 10 in the figure). However, these exclusions are loosely defined [27].
Pulse OX -assess what? -when is supplemental oxygen not needed? -Pulse ox does not provide information about what?
Pulse oximetry is a noninvasive, easily performed test that assesses blood oxygen saturation. It has reduced the number of patients who require arterial blood gases (ABGs), as supplemental oxygen is not needed when the pulse oxygen saturation (SpO ) is >88 percent. However, pulse oximetry does not provide information about alveolar ventilation or hypercapnia (PaCO >45mmHg), and assessment of oxygenation by pulse oximetry may be inaccurate in the setting of an acute exacerbation of COPD [83].
Radiographic features of COPD
Rapidly tapering vascular shadows, increased radiolucency of the lung, a flat diaphragm, and a long, narrow heart shadow on a frontal radiograph (image 1). ● A flat diaphragmatic contour and an increased retrosternal airspace on a lateral radiograph (image 2). These findings are due to hyperinflation. ● Bullae, defined as radiolucent areas larger than one centimeter in diameter and surrounded by arcuate hairline shadows. They are due to locally severe disease, and may or may not be accompanied by widespread emphysema (image 3). ● When advanced COPD leads to pulmonary hypertension and cor pulmonale, prominent hilar vascular shadows and encroachment of the heart shadow on the retrosternal space may be seen [84,85]. The cardiac enlargement may become evident only by comparison with previous chest radiographs. (See "Classification and prognosis of pulmonary hypertension in adults".)
COPD screening -is it recommended in asymptomatic adults? -is mild assymptomatic airflow obstruction treated?
SCREENING — Routine screening spirometry is generally not indicated for adults who have none of the features suggestive of COPD (eg, no dyspnea, cough, sputum production or progressive decline in activity), as asymptomatic mild airflow obstruction does not require treatment [51,101]. Asymptomatic and nonsmoking subjects with mild airflow obstruction, but no history of asthma, do not have the same progressive decline in lung function that is observed among individuals who have a similar degree of airflow obstruction and are symptomatic or continue to smoke [102]. On the other hand, waiting for patients to report symptoms may miss a large number of patients who have COPD, as 20 percent of individuals with severe airway obstruction due to smoking or asthma will not report symptoms. Decrements in forced expiratory volume in one second (FEV ), even within the normal range, are associated with increased risk of acute cardiac events independent of age, gender, and smoking history [57]. Thus, performance of spirometry seems reasonable whenever COPD is a diagnostic consideration. The diagnosis of COPD may alter management of concurrent conditions and may affect the approach to exercise. Exclusion of COPD can often contribute to clinical management as much as its diagnosis by leading to alternative diagnoses.
Short acting Beta Agnosits -name the drugs -name the side effects Short acting Anticholinergics -name the drugs Combo -name the drug and what is in it
Short acting Beta agonists: -albuterol (proair) -salbutamol (Ventolin) Side effects: tremor and reflex tachycardia due, in part, to peripheral arterial dilation. Short acting anticholinergics -ipratropium (Atrovent) COMBO -salbutamol and ipratropium (combivent)
Short acting Broncho dilators -what are the options? how long do they usually last? -is combination therapy preferred?
Short-acting beta agonists and short-acting anticholinergics can be used alone or in combination for relief of intermittent symptoms of COPD. All of the short-acting bronchodilators improve symptoms and lung function. The advantage of short-acting beta agonists is their rapid onset of action; the disadvantage for patients with more frequent symptoms is the short duration of action, about four to six hours. Combination therapy is often preferred because the combination of a short-acting beta agonist plus a short-acting anticholinergic achieves a greater bronchodilator response than either one alone [33]. However, monotherapy with either agent is acceptable.
Smoke exposure and COPD -what is the most important risk factor in the development of COPD -in the absence of enviornemtnal exposures will a smoking history of 10-15 years be sufficient to cause COPD? What amount of pack years is linked to COPD? -what other important risk factors are there for COPD -what % of COPD is caused by smoking? what % is caused by other exposures?
Smoking and inhalational exposure history — The most important risk factor for chronic obstructive pulmonary disease (COPD) is cigarette smoking. Other exposures including passive smoke and biomass fuel use also play roles [8,47,48]. The amount and duration of smoking contribute to disease severity. Thus, a key step in the evaluation of patients with suspected COPD is to ascertain the number of pack years smoked (packs of cigarettes per day multiplied by the number of years), as the majority (about 80 percent) of patients with COPD in the United States have a history of cigarette smoking [49,50]. A smoking history should include the age of starting and the age of quitting, as patients may underestimate the number of years they smoked. With enough smoking, almost all smokers will develop measurably reduced lung function [6]. While studies have shown an overall "dose-response curve" for smoking and lung function, some individuals develop severe disease with fewer pack years and others have minimal to no symptoms despite many pack years [6]. The exact threshold for the duration/intensity of cigarette smoking that will result in COPD varies from one individual to another. In the absence of a genetic/environmental/occupational predisposition, smoking less than 10 to 15 pack years of cigarettes is unlikely to result in COPD. On the other hand, the single best variable for predicting which adults will have airflow obstruction on spirometry is a history of more than 40 pack years of smoking (positive likelihood ratio [LR], 12 [95% CI, 2.7-50]) [51,52] The chronologically taken environmental/occupational history may disclose other important risk factors for COPD, such as exposure to fumes or organic or inorganic dusts. These exposures help to explain the 20 percent of patients with COPD (defined by lung function alone) and the 20 percent of patients who die from COPD who never smoked [50,53,54]. A history of asthma should also be sought, as COPD is often misdiagnosed as asthma. In addition, asthma may progress to fixed airflow limitation and COPD [53].
Staging COPD -what system is used and what attributes of disease go into staging? -what are the stages?
Staging of COPD involves FEV1, severity of symptoms, risk of exacerbations, and the presence of comorbidities. Staging is done using the GOLD system Group A: Low risk, less symptoms: 0 to 1 exacerbation per year and no prior hospitalization for exacerbation; and CAT score <10 or mMRC grade 0 to 1. ● Group B: Low risk, more symptoms: 0 to 1 exacerbation per year and no prior hospitalization for exacerbation; and CAT score ≥10 or mMRC grade ≥2. ● Group C: High risk, less symptoms: ≥2 exacerbations per year or ≥1 hospitalization for exacerbation; and CAT score <10 or mMRC grade 0 to 1. ● Group D: High risk, more symptoms: ≥2 exacerbations per year or ≥1 hospitalization for exacerbation; and CAT score ≥10 or mMRC grade ≥2.
Testing for alpha 1 antitrypsin -should be done in who? -what level is suggestive of deficiency
Testing for alpha-1 antitrypsin (AAT) deficiency should be obtained in all symptomatic adults with persistent airflow obstruction on spirometry. Especially suggestive subsets include the presence of emphysema in a young individual (eg,age ≤45 years), emphysema in a nonsmoker or minimal smoker, emphysema characterized by predominantly basilar changes on the chest radiograph, or a family history of emphysema [68]. However, AAT deficiency may be present in a patient with otherwise "typical" COPD. A serum level of AAT below 11 micromol/L (~57 mg/dL by nephelometry) in combination with a severe deficient genotype is diagnostic.
long acting muscarinic antagonist -drug names -side effects
The LAMAs (also known as long-acting anticholinergic medications) include tiotropium, aclidinium, umeclidinium Spireva (tiotropium) major side effect concern is cardiac arrhythmia
ABGs -indications for measuring ABGs? -what can ABGs show?
The indications for measuring ABGs (eg, PaO , PaCO , and acidity [pH]), which must be considered in the clinical context, include the following: Low FEV (eg, <50 percent predicted) Low oxygen saturation by pulse oximetry (eg, <92 percent) ● Depressed level of consciousness ● Acute exacerbation of COPD Assessment for hypercapnia in at risk patients 30 to 60 minutes after initiation of supplemental oxygen In patients with mild to moderate COPD, arterial blood gases usually reveal mild or moderate hypoxemia without hypercapnia. As the disease progresses, the hypoxemia becomes more severe and hypercapnia may develop. Hypercapnia becomes progressively more likely when the FEV approaches or falls below one liter. Blood gas abnormalities worsen during acute exacerbations and may also worsen during exercise and sleep. The compensatory responses to acute and chronic respiratory acidosis are shown in the figure and discussed separately
COPD symptoms -three common symptoms -less common symptoms -what about weight in COPD -comorbid diseases in COPD
The three cardinal symptoms of COPD are dyspnea, chronic cough, and sputum production and the most common early symptom is exertional dyspnea. Less common symptoms include wheezing and chest tightness (table 2A). However, any of these symptoms may develop independently and with variable intensity. Approximately 62 percent of patients with moderate to severe COPD report variability in symptoms (eg, dyspnea, cough, sputum, wheezing, or chest tightness) over the course of the day or week-to-week; morning is typically the worst time of day [56]. Patients with COPD may experience weight gain (due to activity limitations), weight loss (possibly due to dyspnea while eating), limitation of activity (including sexual), cough syncope, or feelings of depression or anxiety. Weight loss generally reflects more advanced disease and is associated with a worse prognosis. However, the majority of COPD patients are overweight or obese. Comorbid diseases that may accompany COPD include lung cancer, bronchiectasis, cardiovascular disease, osteoporosis, metabolic syndrome, skeletal muscle weakness, anxiety, depression, and cognitive dysfunction. Patients may also report a family history of COPD or other chronic respiratory illness [8,57-62].
Spirometry -how is spirometry performed? what is used for bronchodilation? -what are the most important things to measure for COPD -what determines if airflow obstruction is present? -what determines severity? -an FEV1/FVC ration of less than what is indicative of COPD?
When evaluating a patient for possible COPD, spirometry is performed pre and post bronchodilator administration (eg, inhalation of albuterol 400 mcg) to determine whether airflow limitation is present and whether it is partially or fully reversible. Airflow limitation that is irreversible or only partially reversible with bronchodilator is the characteristic physiologic feature of COPD. Screening spirometry is not currently recommended. In contrast, spirometry should be performed in patients with suggestive symptoms The most important values measured during spirometry are the forced expiratory volume in one second (FEV ) and the forced vital capacity (FVC). The postbronchodilator ratio of FEV /FVC determines whether airflow limitation is present [8]; the postbronchodilator percent predicted value for FEV determines the severity of airflow limitation as shown in the table Airflow limitation is indicated by a postbronchodilatory FEV1/FVC ration less than .7
