Module 3 Respiratory Disorders: COPD
GOLD group C treatment
SABA or SAMA (rescue) + LAMA Preferred bronchodilator: LAMA If symptoms persist: LAMA + LABA (preferred) LABA + ICS (less preferred - risk of PNE)
SABA ADR
Tachycardia, tremor, hypokalemia
FNP when to think COPD?
Dyspnea - progressive, persistent, worse w/exercise Chronic Cough Chronic sputum Hx of exposure risk factors Family Hx of COPD
When are antibiotics used in COPD
(1) to treat an acute exacerbation, (2) to treat acute bronchitis, and (3) to prevent acute exacerbations of chronic bronchitis (prophylactic antibiotics).
SABA dosing
1-2 puffs Q4-6hrs PRN
What is COPD?
1. Airway and/or alveolar abnormalities typically caused by significant exposure to noxious particles or gases 2. Persistent airflow limitation that is not fully reversible 3. Progressive w/ periodic exacerbations
Goal of COPD Management
1. Reduce symptoms 2. Reduce exacerbation risk
SAMA dosing
2 puffs Q6hrs PRN (slower onset, longer duration)
PDE4-i dosing
500mcg daily
CAT (COPD Assessment Test) Score
8 items, 0-5 Likert scale, score from 0 to 40 (10 is threshold for significant symptoms)
COPD FEV1/FVC ratio
< 70% or 0.70
Explain the concept of asthma-COPD overlap syndrome
ACOS is not a single disease state, no longer acceptable term Differentiation b/w asthma and COPD can be difficult, use spirometry and clinical presentation to determine how to treat
Complications of COPD
Acute bronchitis, pneumonia, pulmonary thromboembolism, atrial dysrhythmias (such as atrial fibrillation, atrial flutter, and multifocal atrial tachycardia), and concomitant left ventricular failure may worsen otherwise stable COPD. Pulmonary hypertension, cor pulmonale, and chronic respiratory failure are common in advanced COPD. Spontaneous pneumothorax occurs in a small fraction of patients with emphysema. Hemoptysis may result from chronic bronchitis or may signal bronchogenic carcinoma.
In what stages does hypoxemia occur in COPD? Early Advanced
Advanced
Signs & Symptoms COPD
Age 50 to 60 at onset Asymptomatic in early disease Dyspnea Chronic Cough Chronic Sputum Production Exacerbations
List the three clinical characteristics that should trigger spirometry testing for COPD
Age >= 40 years Chronic cough/dyspnea Known exposure to risk factors (tobacco, occupational hazards, etc.)
General Considerations
Airflow obstruction is caused by chronic bronchitis, emphysema, or both. Obstruction is progressive and may be accompanied by airway hyperreactivity, which is partially reversible.
Pathophysiology of emphysema
Alveolar and parenchymal damage
ICS dosing
BID or daily
LABA dosing
BID or daily (nebulizer, DPI)
SABA MOA
Beta-2 receptor agonist, promotes bronchodilation
LABA MOA
Beta-2 receptor agonist, promotes bronchodilation for ~12 hrs
LAMA MOA
Blocks M3 receptor, reduces bronchoconstriction, no mucus change
SAMA MOA
Blocks M3 receptor, reduces bronchoconstriction, no mucus change
Importance of vaccinations in COPD
Flu vaccine decr. hospitalization/death in COPD pts by 50% Pneumococcal vaccine suggested for: all over 65, all ages 19-65: -smokers/COPD (CDC) -COPD w/ FEV1 <40% (GOLD)
GOLD definition of COPD
COPD is characterized by airflow limitation that is not fully reversible; the limitation is progressive and associated w/ an abnormal inflammatory response to noxious particles
Terms falling out of favor
Chronic Bronchitis Emphysema
CXR of COPD shows
Chronic Bronchitis - nonspecific peribronchial and perivascular markings Emphysema - not reliable, how hyperinflation with flattening of the diaphragm or peripheral arterial deficiency in 50% of cases - Need CT to Diagnosis
#1 Cause of COPD in North America
Cigarette smoking is the most important cause; 80% of patients have tobacco smoke exposure.
LAMA dosing
Daily (DPI, breath-activated MDI)
Importance of smoking cessation in COPD
Decreases velocity of change when compared with smokers; benefits present regardless of stage of COPD
What is the differential diagnosis of chronic obstructive pulmonary disease?
Differential Diagnosis Asthma Bronchiectasis, which features recurrent pneumonia and hemoptysis, with distinct radiographic findings Bronchopulmonary mycosis Central airflow obstruction Severe α1-antiprotease deficiency Cystic fibrosis, which is usually first seen in children and young adults
Explain why patients with COPD will have air trapping and how this can lead to feelings of dyspnea
Distal bronchioles with alveolar attachments (which maintain airway patency) having build-up of scar tissue. Air gets trapped d/t collapse of alveoli during expiration (leads to thoracic hyperinflation and diaphragmatic flattening) Results in less room for inspired air and increased work to breathe, causing dyspnea
Prevention of COPD
Don't smoke Avoid inhaled toxins
What are the essentials of diagnosis and general considerations regarding chronic obstructive pulmonary disease?
Essentials of Diagnosis History of cigarette smoking Chronic cough, dyspnea, and sputum production Rhonchi, decreased intensity of breath sounds, and prolonged expiration on physical examination Airflow limitation on PFT = NOT REVERSIBLE
Importance of Pulmonary rehab in COPD
Exercise training to decr. dyspnea, incr. quality of life, and improve ADLs; no effect on spirometry
Define the spirometry parameters that confirms the diagnosis of COPD
FEV1/FVC < 70%
A 72-year-old man with chronic obstructive pulmonary disease (COPD) presents to the emergency department with progressively worsening shortness of breath. Using 2 L/min of oxygen at home, he is usually able to walk around the house without limitation. Over the past 4 days, however, he has had increasing dyspnea on exertion and increased cough productive of thick green sputum. He has not had chest pain or worsening of his chronic mild ankle edema. He has smoked two packs of cigarettes daily for the past 50 years. Previous pulmonary function tests (PFTs) demonstrated a decreased forced expiratory volume in 1 second (FEV1) and FEV1/FVC (forced vital capacity) ratio. Physical examination shows tachycardia, tachypnea, and decreased breath sounds with diffuse wheezing bilaterally. Arterial blood gas (ABG) analysis shows acidemia from a partially compensated respiratory acidosis. He is placed on noninvasive positive-pressure ventilation with marked improvement of his acidemia. How do you think through his problem?
How to think through: This patient with COPD presents in respiratory distress. Already on oxygen at home, he has little pulmonary reserve. What test best assesses the severity of his pulmonary status? (ABGs.) His ABGs show acute respiratory acidosis, and noninvasive positive-pressure ventilation is initiated. In addition to ventilatory support, what are the treatment priorities? (Corticosteroid, inhaled β-agonist, inhaled anticholinergic agents.) What clinical developments would necessitate transition to endotracheal intubation? (Altered mental status, failure to decrease PaCO2.) When the patient has recovered to baseline, what therapies decrease COPD exacerbations? (Smoking cessation, inhaled corticosteroids, influenza and pneumococcal vaccinations.) What other therapy decreases the mortality rate? (Home oxygen.)
Outline the mechanism behind chronic respiratory acidosis with metabolic compensation in patients with COPD
Inability to fully expel air results in build-up of CO2 in the respiratory system Long-standing respiratory acidosis causes metabolic compensation Kidneys produce excess serum HCO3 to offset respiratory acidosis
COPD exacerbations usually caused by
Increased sputum purulence accompanied by dyspnea or an increase in the quantity of sputum are thought to benefit the most from antibiotic therapy
Pathophysiology of chronic bronchitits
Inflammation and remodeling of airways with excessive mucus production
Pathophysiology of COPD
Inhaled Irritants Inflammatory Cascade Tissue Damage Structural Changes & Parenchymal destruction to lung tissue Increase in mucus secreting cells Damage to mucociliary transport system Decrease mucus clearance Airway remodeling Airflow obstructions - inability to exhale quickly Decreases FEV1/FVC
What are the laboratory and imaging findings in chronic obstructive pulmonary disease?
Laboratory Tests Sputum examination may reveal pathogens, although cultures correlate poorly with exacerbations. Electrocardiography shows sinus tachycardia, abnormalities consistent with cor pulmonale in severe disease, or supraventricular tachycardias and ventricular irritability. ABGs are unnecessary unless hypoxemia or hypercapnia is suspected and may show a compensated respiratory acidosis with worsening academia during exacerbations. Spirometry shows reduced FEV1 and FEV1/FVC ratio in late disease, reduced FVC in severe disease, and increased total lung capacity (TLC) and residual volume (RV) from air trapping. Obtaining an α1-antiprotease level may reveal a deficiency in young patients with emphysema. Imaging Studies Radiographs in patients with chronic bronchitis may show nonspecific peribronchial and perivascular markings. Plain radiographs are insensitive for emphysema; they may show hyperinflation with a flattened diaphragm or peripheral arterial deficiency. In advanced disease, radiographs that show enlarged central pulmonary arteries may indicate pulmonary hypertension. Computed tomography (CT) of the chest is more sensitive and specific for the diagnosis of emphysema. Doppler echocardiography estimates pulmonary artery pressure.
Importance of oxygen therapy in COPD
Low-flow on nasal cannula; only tx to reduce mortality in COPD - given if SpO2 < 88% or PaO2 < 55 mmHg
Blue Boater - Bronchitis predominant
Major complaint: Cough & mucopurulent sputum Frequent chest infections Pt's appear overweight Age when appears is 30's to 40's Lungs: rhonchi & wheezing
Pink Puffer - Emphysema predominant
Major complaint: dyspnea Cough: rare Pts are appear thin and frail Lungs: no adventitious sounds
What are the treatments for chronic obstructive pulmonary disease?
Medications Supplemental oxygen in hypoxemic patients increases survival and reduces hospitalizations. Bronchodilators offer improvement in symptoms, exercise tolerance, and overall health. Ipratropium bromide and short-acting β2-agonists (eg, albuterol) are used, often in combination. Long-acting β2-agonists (formoterol, salmeterol, indacaterol, arformoterol, vilanterol) and anticholinergics (tiotropium, aclidinium, and umeclidinium) are also beneficial. Corticosteroids are often used for exacerbations; they are generally not effective in outpatients. Antibiotics slightly improve outcomes when used to treat acute exacerbations of chronic obstructive pulmonary disease and when used to prevent acute exacerbations of chronic bronchitis. Preventative use of azithromycin or moxifloxacin can reduce the frequency of exacerbations in patients with frequent exacerbations despite optimal medical therapy. Opioids and sedative-hypnotic drugs can manage severe and refractory dyspnea. Surgery Lung transplantation greatly improves pulmonary function and exercise tolerance. Lung volume reduction surgery in highly selected patients results in modest improvements. Bullectomy is used for palliation of dyspnea in patients with severe bullous emphysema. Therapeutic Procedures Smoking cessation is the single most important goal and includes both behavioral and pharmacologic interventions. Noninvasive positive-pressure ventilation in exacerbation reduces the need for intubation, shortens intensive care unit lengths of stay, and may reduce the risk of health care-associated infections.
COPD class 1
Mild FEV1 predicted > 80%
LAMA ADR
Minimal systemic absorption, dry mouth
SAMA ADR
Minimal systemic absorption, dry mouth
COPD class 2
Moderate FEV1 predicted 50-80%
The late stages of COPD are characterized by:
Pneumonia, pulmonary hypertension, cor pulmonale, and chronic respiratory failure
GOLD group A treatment
Preferred: SABA or SAMA (rescue) No preferred bronchodilator Alternative: LABA or LAMA SABA + SAMA combination
GOLD group B treatment
Preferred: SABA or SAMA (rescue) + LABA or LAMA No preferred bronchodilator If symptoms persist: LABA + LAMA
When to start oxygen in COPD
Pts with resting PaO2 < 56 mmHG - only therapy with evidence of improvement in the natural history of COPD.
ICS MOA
Reduces mucus production, proteolytic enzymes, prostaglandin production
GOLD group D treatment
SABA or SAMA (rescue) + LABA + LAMA Preferred Bronchodilator: LABA + LAMA If symptoms persist: LABA + LAMA + ICS Continued refractory Symptoms: LABA + LAMA + ICS + -Roflumilast -Macrolide (azythromycin) (also consider stopping ICS)
Definitive Diagnosis
SPIROMETRY •Post-bronchodilator FEV1/FVC < 0.70 •Use age related normal values to avoid over-diagnosis in elderly
A 72-year-old man with chronic obstructive pulmonary disease (COPD) presents to the emergency department with progressively worsening shortness of breath. Using 2 L/min of oxygen at home, he is usually able to walk around the house without limitation. Over the past 4 days, however, he has had increasing dyspnea on exertion and increased cough productive of thick green sputum. He has not had chest pain or worsening of his chronic mild ankle edema. He has smoked two packs of cigarettes daily for the past 50 years. Previous pulmonary function tests (PFTs) demonstrated a decreased forced expiratory volume in 1 second (FEV1) and FEV1/FVC (forced vital capacity) ratio. Physical examination shows tachycardia, tachypnea, and decreased breath sounds with diffuse wheezing bilaterally. Arterial blood gas (ABG) analysis shows acidemia from a partially compensated respiratory acidosis. He is placed on noninvasive positive-pressure ventilation with marked improvement of his acidemia. What are the salient features of this patient's problem?
Salient features: Worsening dyspnea; change in cough and sputum; home oxygen use; 100 pack-year smoking history; obstructive pattern on spirometry; wheezing and respiratory distress; lower extremity edema; acidemia with partially compensated respiratory acidosis; improvement on noninvasive positive-pressure ventilation
COPD class 3
Severe FEV1 predicted 30-50%
When to admit to hospital?
Severe symptoms or acute worsening that fails to respond to outpatient management. • Acute or worsening hypoxemia, hypercapnia, peripheral edema, or change in mental status. • Inadequate home care, or inability to sleep or maintain nutrition/hydration due to symptoms. • The presence of high-risk comorbid conditions.
most common etiology of COPD
Smoking (90% of COPD patients smoke, but only 15% of smokers develop COPD)
Other COPD staging scale
St. George's Repiratory Questionnaire (SGRQ)
What are the symptoms and signs of chronic obstructive pulmonary disease?
Symptoms and Signs Presentation usually at 40 to 50 years of age with cough, sputum production, and shortness of breath. Dyspnea initially occurs only with heavy exertion, progressing to symptoms at rest in severe disease. Exacerbation of symptoms is beyond normal day-to-day variation, often including increased dyspnea, an increased frequency or severity of cough, increased sputum volume, or a change in sputum character. Infections (viral more commonly than bacterial) precede exacerbations in most patients. Late-stage COPD characterized by hypoxemia, pneumonia, pulmonary hypertension, cor pulmonale, and respiratory failure. Clinical findings may be absent early. Patients are often dichotomized as "pink puffers" or "blue bloaters" depending on whether emphysema or chronic bronchitis predominates.
LABA ADR
Tachycardia, tremor, hypokalemia
What is the GOLD initiative?
The Global Initiative for Chronic Obstructive Lung Disease
ICS ADR
Thrush, dysphonia, decreased height, increased fracture risk
COPD class 4
Very Severe FEV1 predicted < 30%
PDE4-i ADR
Weight loss, anorexia, diarrhea, anxiety, depression, other neuropsychiatric SE
FNP when to think COPD?
cough, dyspnea, and sputum production.
List the three cardinal symptoms of COPD exacerbations
Worsening dyspnea Increased sputum volume Increased sputum purulence Abx indicated if: -3 cardinal signs present -2 cardinal signs if sputum purulence is one
PDE4-i MOA
cGMP is not broken down by PDE4, bronchodilation, anti-inflammation
Chronic Bronchitis
characterized by excessive mucous secretions with productive cough for 3 months or more in at least two consecutive years.
Human alpha-1-antitrypsin is available for replacement therapy in emphysema
congenital deficiency
Most common cause of COPD exacerbations is
infection - more frequently viral enviromental factors
Emphysema
is abnormal enlargement of air spaces distal to terminal bronchiole with destruction of bronchial walls without fibrosis.
Phosphodiesterase 4 inhibitor - Roflumilast
reduce exacerbation frequency in patients who have moderate or severe COPD
COPD Assessment Tools
•Modified British Medical Research Council (mMRC) Questionnaire - Measures breathlessness •COPD Assessment Test (CAT) - Measures comprehensive assessment of symptoms
