COPD Flashcards
What are the major types of COPD?
Chronic Obstructive Pulmonary Disease (COPD) is a progressive, irreversible airway obstruction due to chronic bronchitis or emphysema.
What define the two major types of COPD?
- Chronic Bronchitis: Productive cough for at least 3 months over 2 consecutive years.
- Emphysema: Alveolar destruction due to excess protease activity.
What is the primary cause of COPD?
Cigarette smoking is the most common cause of COPD.
What are the major risk factors for COPD?
- Smoking or secondhand smoke
- Genetics, such as Alpha-1 antitrypsin deficiency
- Environmental/occupational exposure
- Air pollution
- Chronic poorly controlled asthma
What is the most common cause of COPD?
Smoking.
What is the key pathophysiologic process in emphysema?
Destruction of alveolar walls due to excess protease activity, leading to air trapping and loss of elastic recoil.
What is the difference between centrilobular and panlobular emphysema?
Centrilobular: Seen in smokers, affects upper lobes.
Panlobular: Seen in alpha-1 antitrypsin deficiency, affects lower lobes.
What are the symptoms of COPD?
Dyspnea, chronic cough, sputum production, wheezing, and chest tightness.
A 62-year-old man presents to the emergency department due to three days of shortness of breath and difficulty lying flat. The patient has not seen a physician in twenty years and takes no medications. The patient smokes one pack of cigarettes per day. Temperature is 37.4 °C (99.3 °F), pulse is 90/min, blood pressure is 136/84, respiratory rate is 20/min, and oxygen saturation (SpO) is 90% on room air. Cardiac auscultation reveals normal S1 and S2. Pulmonary auscultation reveals rales at both lung bases and faint wheezes in bilateral mid-lung fields. There is mild non-pitting edema in both feet. Electrocardiogram shows normal sinus rhythm with voltage criteria of left ventricular hypertrophy.
Serum electrolytes and kidney function are normal. Chest x-ray shows mild pulmonary congestion. What diagnostic tests should be ordered next?
This patient with dyspnea, orthopnea, and hypoxemia has faint wheezes, basilar rales, and pedal edema on examination. ECG findings of left ventricular hypertrophy and chest x-ray finding of pulmonary congestion point towards congestive heart failure (CHF) as the cause of dyspnea. The next step in diagnosing this patient would be to check brain natriuretic peptide (BNP) which has a high sensitivity and high negative predictive value for diagnosing CHF. Dyspnea is a very common presenting symptom for patients. Hemodynamic and respiratory stability should be assessed immediately in all patients with dyspnea. Once stability is ensured, life-threatening diagnoses (e.g., cardiac tamponade, cardiogenic shock, massive pulmonary embolism, myocardial infarction) should be ruled out. Exacerbation of COPD and CHF make up a large portion of older adult patients presenting with dyspnea, and it may be challenging to differentiate between the two. While orthopnea and paroxysmal nocturnal dyspnea are much more common in CHF, patients with COPD and severe mucus buildup can also develop orthopnea. Wheezing is much more common in COPD but can also occur in CHF due to fluid compressing the airways (cardiac wheezing). Chest imaging often shows pulmonary edema and/or pulmonary congestion in CHF exacerbation, but right-sided heart failure may have clear lungs on auscultation and imaging. Serum BNP or proBNP are peptides that are released in response to ventricular stretch in the heart, mostly from cardiac-driven volume overload. Other factors besides CHF that increase BNP levels include kidney failure, older age, sepsis, medical therapy with an angiotensin receptor-neprilysin inhibitor (ARNI), and female sex. BNP levels are typically reduced in patients with an elevated BMI. A high BNP level can help diagnose CHF, and a low BNP level can help rule it out. Many diagnoses that cause dyspnea have overlapping symptoms and presentations. A strong understanding of the laboratory and imaging findings seen with each diagnosis is crucial. Serum brain natriuretic peptide has a high sensitivity and high negative predictive value for acute heart failure and can be used as part of the diagnostic workup for suspected CHF.
A 73-year-old man presents to the emergency department for evaluation of three days of shortness of breath and a new cough. The patient has a history of difficulty controlling hypertension and takes multiple antihypertensives.
Previously, the patient was active and could walk up two to three flights of stairs before stopping to catch his breath, but now he can only walk up three steps before stopping. The patient has a significant smoking history. Temperature is 37.1 °C (98.8 °F), pulse is 96/min, respiratory rate is 18/min, blood pressure is 146/84 mmHg, and Sp02 is 98% on room air. On physical examination, the patient is not in acute distress. On lung exam, crackles are heard at both lung bases. There is mild pedal edema bilaterally. Transthoracic echocardiogram performed four months ago show preserved ejection fraction. What test should be performed initially to help determine the underlying cause of this patient’s presentation?
This patient with a significant smoking history and difficult-to-control hypertension presents with new shortness of breath and an acute cough. Given the finding of pulmonary crackles on auscultation and mild peripheral edema, the presentation is suggestive of congestive heart failure (CHF). However, new onset chronic obstructive pulmonary disease (COPD) cannot be ruled out in this patient. A serum proBNP level can be performed initially to help differentiate between CHF and other etiologies. A significantly elevated serum proBNP level is indicative of CHF. Acute cough can be due to several cardiopulmonary pathologies and generally refers to a cough present for less than 3 weeks. If the history and physical examination do not reveal an obvious cause of the cough, the next step is to obtain a chest radiograph. For patients with a normal chest radiograph, consider pulmonary embolism, viral bronchitis, gastrosophageal reflux disease, medication side effects, and exacerbation of COPD. For patients with an abnormal chest radiograph, consider bacterial pneumonia, bronchiectasis exacerbation in a patient with known bronchiectasis, and congestive heart failure (CHF). In some cases, such as in patients with both COPD and CHF, it can be difficult to discern between primary cardiac or primary pulmonary etiology. While a transthoracic echocardiogram should be performed, it may take several hours before it is performed and interpreted and often does not change management. Serum proBNP measurement is an appropriate initial test to help narrow down the differential diagnosis. This test is comparatively inexpensive, and results return quickly. While proBNP measurements alone are not necessarily diagnostic, an acutely elevated level suggests cardiac etiology rather than pulmonary etiology.
What are the classic physical exam findings for chronic bronchitis?
Prolonged expiration, wheezing, coarse crackles, cyanosis (‘blue bloaters’).
What are the classic physical exam findings for emphysema?
Decreased breath sounds, hyperinflation, barrel chest, pursed lip breathing (‘pink puffers’).
What imaging findings are seen in COPD on chest X-ray or CT scan?
Hyperinflation, increased lung translucency, flattened diaphragm, and subpleural blebs.
What is the gold standard for diagnosing COPD?
Pulmonary Function Tests (PFTs).
What is the hallmark of COPD on PFTs?
- FEV1/FVC ratio <0.7
- Decreased FEV1
- Increased total lung capacity (TLC)
- Increased residual volume (RV)
- Decreased DLCO in emphysema
What is the disease course in COPD that causes the alteration in PFTs?
Early in the disease course, loss of elastin tethering fibers leads to abnormal expiratory collapse of the distal airways. Expiratory flow is reduced, leading to poor lung emptying. This is measured as a markedly increased residual volume (RV), known as air trapping. With continued elastin loss, lung tissue becomes abnormally compliant (ie, distensible, “loose and baggy” alveoli); destruction of the interalveolar septal walls results in alveolar enlargement. These conditions lead to an increased total lung capacity (TLC), known as lung hyperinflation. Air trapping limits the lung’s ability to expire air, decreasing expiratory reserve volume (ERV). Lung hyperinflation flattens the diaphragm, impairing its ability to descend and draw air into the lungs during inspiration. This leads to reduced inspiratory reserve volume (IRV). The reduced IRV and ERV (ie, decreased air movement during both inspiration and expiration) manifests as a decrease in forced vital capacity (the total volume of air that can be forcefully exhaled after a maximal inspiration).
What is the GOLD classification for COPD severity?
- Mild (FEV1 ≥80%)
- Moderate (FEV1 50-79%)
- Severe (FEV1 30-49%)
- Very severe (FEV1 <30%)
What is the stepwise treatment for COPD according to GOLD stages?
- Mild (FEV1 ≥80%): SABA (Albuterol)
- Moderate (50-79%): SAMA or LAMA (Ipratropium, Tiotropium)
- Severe (30-49%): Add Inhaled Corticosteroids (ICS)
- Very Severe (<30%): Add Home Oxygen Therapy
What is the mMRC dyspnea scale?
0: shortness of breath with strenuous activity
1: shortness of breath with heels or brisk walk
2: walk slower than others of the same age at a slower pace
3: takes a break after 100 yard walk
4: shortness of breath while dressing and can’t leave the house due to symptoms
0-1 with one exacerbation is class A so give LAMA with as needed SABA
2 or more with one exacerbation is class B so give LAMA+LABA with as needed SABA
2 or more exacerbations or 1 hospitalization is class E so give LAMA+LABA with as needed SABA with ICS
What is the role of SABAs and LABAs in COPD?
SABAs (Albuterol) for acute relief, LABAs (Salmeterol, Formoterol) for maintenance therapy.
What is the role of SAMAs and LAMAs in COPD?
SAMAs (Ipratropium) and LAMAs (Tiotropium, Aclidinium) provide long-term bronchodilation by blocking muscarinic receptors.
Which LAMA can be used as the initial treatment in patients with COPD?
Tiotropium
When should inhaled corticosteroids (ICS) be added in COPD treatment?
For patients with frequent exacerbations (GOLD Stage 3 or 4).
What is Roflumilast and when is it used?
A phosphodiesterase-4 inhibitor used in severe COPD with chronic bronchitis to reduce exacerbations.
When is home oxygen therapy indicated in COPD?
When FEV1 is less than 30% or If PaO2 <55 mmHg or SpO2 <88% (or <60 mmHg or SpO2 <92% if the patient also has polycythemia, CHF, or pulmonary hypertension).
What defines a COPD exacerbation?
An acute worsening of symptoms with increased cough, sputum production, or dyspnea.
What are common triggers of COPD exacerbation?
- Respiratory infections (most commonly Haemophilus influenzae)
- Environmental irritants
- Noncompliance with treatment
- Cardiac events
How is COPD exacerbation managed?
- Oxygen therapy: Maintain SpO2 88-92%
- Bronchodilators: SABA (Albuterol) + SAMA (Ipratropium)
- Systemic corticosteroids: Prednisone (5-7 days)
- Noninvasive positive pressure ventilation (NIPPV) if needed
A 62-year-old woman presents to the primary care clinic because of five days of persistent shortness of breath and a frequent cough productive of yellow sputum. She has a history of chronic obstructive pulmonary disease (COPD) and normally has an intermittent cough productive of clear sputum. She needed to use her albuterol inhaler several times this week without significant relief. The patient is usually highly active and has not had any recent prolonged immobility. Her grandson visited her last week, and he had an upper respiratory infection. Current medications include albuterol and inhaled fluticasone-umeclidinium-vilanterol. Temperature is 37.1 °C (98.8 °F), pulse is 89/min, respiratory rate is 22/min, blood pressure is 136/82 mmHg, and oxygen saturation is 92% on room air. On physical examination, the patient appears fatigued. There are significant wheezes auscultated in all lung fields with a prolonged expiratory phase. There is no peripheral edema. A chest radiograph shows no acute changes. Which of the following additional tests should be performed next? A) No further testing is needed, B) Negative inspiratory force, C) Transthoracic echocardiogram, D) Computed tomography (CT) of the chest, E) Forced expiratory volume.
This patient with chronic obstructive pulmonary disease (COPD) and recent exposure to a patient with a respiratory virus presents with dyspnea, and a change in the character and frequency of sputum production suggestive of COPD exacerbation. Significant wheezing and prolonged expiration on heard on pulmonary auscultation, and the chest radiograph is normal supporting the diagnosis of COPD exacerbation. In cases with classic clinical findings of COPD exacerbation, no further testing is warranted, and treatment can be initiated. Acute cough can occur due to many cardiopulmonary pathologies and generally refers to a cough present for less than 3 weeks. The first step in the evaluation is typically ordering a chest radiograph. For patients with a normal chest radiograph, consider pulmonary embolism, viral bronchitis, gastrosophageal reflux disease, medication side effect, and exacerbation of chronic obstructive pulmonary disease (COPD). COPD exacerbations are a frequent reason for patients to present to the primary care clinic, pulmonology clinic, cardiology clinic, urgent care facility, and emergency department. A chest radiograph can be helpful to rule out other etiologies such as bacterial pneumonia or congestive heart failure, but further testing is usually not necessary. Patients with known COPD who present with worsening dyspnea and a change in their typical sputum can be diagnosed with a COPD exacerbation and do not require spirometric testing or additional imaging and can be treated presumptively. Patients with known COPD presenting with worsening dyspnea and a change in the character and frequency of sputum may need a chest radiograph to rule out other conditions, but additional testing is not necessary if the X-ray is negative, and the clinical picture is consistent with COPD exacerbation.
When should noninvasive positive pressure ventilation (NIPPV) be used in COPD exacerbation?
If pH <7.35 or CO2 >45 mmHg with respiratory distress. Noninvasive positive pressure ventilation is a type of ventilatory support delivered by a noninvasive method, like facemask, that improves alveolar ventilation, enhancing oxygenation, and alleviating respiratory muscle fatigue. It is indicated for the management of COPD exacerbations with evidence of respiratory acidosis and hypercapnia. Contraindications to NIPP V include medical instability (e.g. cardiorespiratory arrest, pH <7.10, ARDS, organ failure), inability to protect the airways, and airway mechanical issues (e.g. facial trauma or surgery, upper airway obstruction). Acute COPD exacerbations can be caused by a variety of factors such as infections, environmental exposures, or nonadherence to medications. The primary goal of acute management of a patient with unstable COPD is to reverse hypoxemia, provide relief from respiratory distress, and address the underlying cause of the exacerbation. AFTER addressing airway, oxygenation, and improving hypercapnia with NIPPV, COPD exacerbation can be further managed with with short-acting bronchodilators, such as beta-agonists and anticholinergics, and systemic corticosteroids. Empiric antibiotics should be administered to patients who have symptoms consistent with an infection (e.g. increased cough severity or frequency, increased volume of or change in character of sputum, increased dyspnea) or are on mechanical ventilation.
What is the role of magnesium sulfate in COPD exacerbation?
Used in severe exacerbations as a bronchodilator to reduce airway resistance.
When are antibiotics indicated in COPD exacerbation?
If 2 of 3 symptoms are present: increased dyspnea, sputum volume, or sputum purulence.
What antibiotics are used for uncomplicated COPD exacerbation?
Azithromycin or 2nd/3rd gen cephalosporins (Cefpodoxime, Cefuroxime). Azithromycin has been shown to reduce neutrophil-mediated airway inflammation.
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Complicated COPD exacerbation includes age greater than 65, and FEV1 less than 50%, or more than two exacerbations in a year.
What antibiotics are used for complicated COPD exacerbation (FEV1 <50%, >2 exacerbations/yr)?
Levofloxacin or Cefepime to cover Pseudomonas.
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Complicated COPD exacerbation includes age greater than 65, and FEV1 less than 50%, or more than two exacerbations in a year.
How does DLCO change in COPD?
DLCO is decreased in emphysema due to alveolar destruction but remains normal in chronic bronchitis.
How does DLCO differ in other lung diseases?
Decreased: Emphysema, pulmonary fibrosis, pulmonary hypertension.
Normal: Chronic bronchitis, asthma.
Increased: Polycythemia vera, pulmonary hemorrhage.
What is the best initial treatment for mild COPD?
Short-acting bronchodilator (SABA or SAMA).
Which COPD phenotype has decreased DLCO?
Emphysema.
Which COPD phenotype has normal DLCO?
Chronic bronchitis.
What is the most important intervention to improve COPD survival?
Smoking cessation. The other therapy that lowers mortality is home oxygen.
How does smoking cessation improve a patient’s FEV1?
In healthy persons who never smoke, lung function peaks at approximately age 30. Afterward, there is a gradual decline in forced expiratory volume in 1 second (FEV,) of approximately 25 mL/year. In the average person who smokes tobacco, the rate of lung function declines approximately 3 times faster. Cigarette smoke contains numerous toxins (eg, formaldehyde, acrolein) that provoke inflammatory proteolytic damage to the airways and alveoli. These changes are responsible for airway inflammation and narrowing (chronic bronchitis: increase airway resistance) and alveolar septal destruction (emphysema: decrease elastic recoil pressure). Together these conditions lead to expiratory flow limitation, typically measured as a reduction in FEV1. Once lost, lung function is not recoverable. However, smoking cessation can markedly slow the decline in FEV1. Within a year of complete abstinence, a successful quitter’s rate of FEV, decline returns to that of normally aging nonsmokers. Therefore, after a patient quits smoking, the slope of the FEV1 decline curve will decrease, but no function will be regained.
Is the FEV1/FVC ratio a predictor for patient mortality in COPD?
No, Low FEV,/FVC ratio (ie, ≤0.7) defines obstructive lung disease but is uncorrelated with mortality. The ratio remains relatively constant as lung disease progresses because FEV, and FVC both fall concomitantly. Individually, low FEV, is a crude predictor of mortality and is merely one element of the BODE composite index.
Why is a lower BMI associated with an elevated risk of mortality for patients with COPD?
Low BMI (eg, ≤21 mg/kg3) predicts higher mortality in COPD, possibly because it indicates pulmonary cachexia (eg, insufficient caloric intake to sustain the work of breathing).
Is frequent systemic corticosteroid use (eg, for treatment of recurrent acute exacerbations) is associated with a higher risk of mortality in COPD?
Frequent systemic corticosteroid use (eg, for treatment of recurrent acute exacerbations) is associated with a higher risk of morbidity (eg, osteoporosis) and hospitalization, but not mortality.
What are the best predictors for patient mortality in COPD?
FEV, only loosely correlates with survival. Of far greater significance is functional status: how patients adapt to their diminished lung function. A key indicator of functional status is how dyspnea and fatigue, the most debilitating symptoms of COPD, impact a patient’s daily life. This patient has disabling dyspnea that interferes with his ability to leave home, socialize (eg, volunteer), and perform self-care (eg, difficulty with bathing). These functional domains integrate the physical and psychosocial impacts of the disease, and limitation of daily activities is the strongest predictor of mortality.
Incorporating functional status, multidimensional risk indices have been developed to forecast survival in COPD. The BODE index (low BMI, very severe Obstruction [FEV1 ≤ 35%], disabling Dyspnea, and low Exercise capacity) is the most widely used instrument. In aggregate, these 4 factors are superior to any individual measure. COPD is a multisystem condition with extrapulmonary intersections, and progressive respiratory failure accounts for only 30% of deaths. The majority of deaths are attributed to other highly prevalent comorbidities in patients with COPD (eg, cardiovascular disease, lung cancer). Thus comorbid coronary artery disease, abdominal aortic aneurysm, and atrial fibrillation elevate the risk of death independent of the BODE index and functional impairment.
What is the underlying causes for these pulmonary findings in a patient with COPD?
In a patient with COPD, atelectasis can cause decreased breath sounds and hemithorax pacification with tracheal deviation toward the opacified side. In patients with COPD, this is most commonly due to obstruction of the mainstem bronchus and most commonly occurs due to mucus plugging in patients with chronic obstructive pulmonary disease. This can also be seen in patients with bronchietasis, or due to malignant obstruction by a centrally located lung cancer (eg, squamous cell lung cancer). Distal to the obstruction, air becomes trapped in the alveoli and gradually gets absorbed into the bloodstream, with ensuing large-volume alveolar collapse and pulling of the trachea toward the affected side. Other mediastinal structures (eg, heart, esophagus, great vessels) may also shift in the same direction. The loss of radiolucent air, combined with shifting of organs into the hemithorax, appears as a completely opacified hemithorax on chest x-ray.
In contrast, space-occupying pathology such as large pleural effusion or tension pneumothorax (ie, air accumulation in the pleural space) forces tracheal deviation away from the affected side.
