Chronic Obstructive Pulmonary Disease (COPD) Flashcards
In what groups is COPD more common?
women - slightly
smokers
lower socioeconomic status
rural settings
What percentage of COPD cases are NOT associated with smoking?
25%
How much money do Americans spend on COPD? 2010? 2020?
$32 billion in 2010
estimated $49 billion in 2020
Chronic Obstructive Pulmonary Disease
persistent respiratory symptoms AND measurable obstructive airflow limitation
by definition NOT completely reversible
common, preventable, and treatable, but not curable
characterized by emphysema, chronic bronchitis, and sometimes asthma
What is the irreversible pathophysiology of COPD?
fibrosis and narrowing of the airways
loss of elastic recoil due to alveolar destruction
destruction of alveolar support that maintains patency of small airways
What is the reversible pathophysiology of COPD?
inflammatory cells, mucus, and plasma exudate in bronchi
smooth muscle contraction in peripheral and central airways
What affects will COPD have on Pulmonary Vasculature? Which lab finding will indicate this?
Vascular intimal hyperplasia – thickening of alveolar-capillary barrier due to inflammation, mucus, and exudate
Chronic hypoxic vasoconstriction can lead to smooth muscle hypertrophy/hyperplasia
Alveolar destruction leads to loss of adjacent capillaries
Lab: low diffusion capacity (DLCO): measures CO and quantifies gas diffusion across alveolar-capillary membrane
Chronic Bronchitis
productive cough for more than 3 months in duration in each of two successive years
may occur in absence of airflow obstruction
due to airway thickening and decreased mucociliary activity
Emphysema
abnormal and permanent enlargement of and damage to the walls of the alveoli without obvious fibrosis
can exists without airflow obstruction, but is more common among patients who have moderate or severe airflow obstruction
Asthma
chronic airway inflammation and airway hyperresponsiveness
recurrent episodes of wheezing, breathlessness, chest tightness, and coughing; particularly at night or in the early morning
episodes are reversible either spontaneously or with treatment; COPD is NOT reversible
reactive airway – greater than 12 percent improvement in FEV1 with bronchodilator
In order to diagnose COPD, the patient must have….
measurable airflow obstruction that is not completely reversible
people with chronic bronchitis, emphysema, or both are not considered to have COPD unless they have measurable airflow obstruction
patients with airflow obstruction due to diseases that have a known etiology or a specific pathology are NOT considered to have COPD
Risks
cigarette smoking - leading cause; 38% of COPD patients are current smokers and 37% are former smokers
long-term exposure to other irritants - air pollution, chemical fumes, cooking fumes, dusts
alpha-1 antitrypsin deficiency (AATD)
Apha-1 Antitrypsin Deficiency (AATD)
hereditary deficiency or absence of the alpha-1 anti-trypsin protein in the blood
produced by the liver, protects elastin in the lungs from inflammation and inhaled irritants
low AAT occurs because the AAT is abnormal and cannot be released from the liver
Low alpha-1 antitrypsin in the blood leads to….
High alpha-1 antitrypsin leads to….
low - lung disease (emphysema)
high - liver disease (cirrhosis)
What types of patients should you suspect have alpha-1 antitrypsin deficiency?
suspect alpha-1 antitrypsin deficiency in patients with cirrhosis or lung disease, especially if it is more serious than expected or in those younger than 40
DNA Genotype as follow-up: MM normal, MS or MZ carriers, ZZ or SZ have AATD
Symptoms
constant coughing – smoker’s cough
shortness of breath while doing everyday activities
inability to breathe easily or take a deep breath
excess mucus production – coughed up as sputum
wheezing
What test is required for diagnosing COPD?
spirometry
Exam Findings or Sings
odor of tobacco
coughing
increased work of breathing or pursed-lip breathing, especially during minimal activity
prolonged expiration
wheezing or forced expiration (whistle) - sometimes airways are too tight to even produce a whistle
hyperinflation - increased resonance or percussion, diminished breath sounds, distant heart sounds, increased AP diameter (barrel chest), and depressed diaphragm
yellow/brown nicotine and tar stains on fingers
cachexia - loss of weight, muscle atrophy, fatigue, weakness, and significant loss of appetite
What will the FEV1/FVC be?
less than 70% after bronchodilators
What will the total lung capacity be?
normal or increased
What will the residual volume be?
normal or increased
What method is used for determining COPD severity?
GOLD Staging
severity of functional impairment based on FEV1 doesn’t always correlate well
air trapping (RV and TLC) and reduction of DLCO may be more accurate reflectors of impact on daily functioning
GOLD Classification for COPD - first confirm …..
FEV1/FVC <70% and not reversible by bronchodilators
GOLD Classification - Mild COPD
mild airflow limitation
FEV1 > 80% predicted
with or without chronic symptoms
GOLD Classification - Moderate COPD
worsening airflow limitation
50% < FEV1 < 80%,
SOB on exertion
GOLD Classification - Severe COPD
further worsening airflow limitation
30% < FEV1 < 50%
greater SOB, reduced exercise capacity, repeat exacerbations, which impact quality of life
GOLD Classification - Very Severe
severe airflow limitation
FEV1 < 30% or FEV1 <50% with chronic respiratory failure
quality of life impaired, exacerbations might be life-threatening
Common Chest X-ray findings in patients with COPD
retrosternal airspace
bulla - hyperlucency > 1cm with arcuate shadow
barrel chest
hyperlucency
hyperinflation - flat diaphragm
Chest CT in those with COPD
mostly to assess for emphysema and to rule out bronchiectasis & others
focal lucencies scattered in lungs
often predominates in upper zones of each lobe
may reveal large bullae or blebs
associated loss of vasculature in areas of emphysema
Therapy Goals
prevent decline in pulmonary function
prevent exacerbations
maximize physical function/wellness
decrease mortality and increase longevity
Pharmacologic Treatments
bronchodilators
steroids
combination of long-acting bronchodilators and steroid formulations
phosphodiesterase-4 inhibitor (roflumilast)
oxygen
chronic macrolide therapy in selected individuals with frequent exacerbations
consider treatment for asthma/atopic/allergic component as well
Non-Pharmacologic Treatment
smoking cessation – never too late
education, self-management
pulmonary rehab
nutrition
vaccination
end of life and palliative care
treatment of hypoxemia (oxygen)
treatment of hypercapnia, or elevated CO2, (biPAP or other NIV)
Surgical Procedures for COPD
Lung volume reduction surgery: considered in pts with upper-lobe emphysema
Bronchoscopic lung volume reduction: for advanced emphysema
Bullectomy: open lung or VATS resection of large bullae
Lung transplant: high post-op mortality
Not common
Acute Exacerbations of COPD - Definition
o worsening of respiratory symptoms (dyspnea, cough, and/or sputum production) over the course of hours to days that is outside of usual day-to-day variability
Acute Exacerbations of COPD - Goal
reduce frequency and reduce severity
Acute Exacerbations of COPD - Prevention
smoking cessation
hang hygiene
immunizations
avoidance of triggers
Acute Exacerbations of COPD - Hospitalization
severe symptoms: worsening of resting dyspnea, high respirations, hypoxia, confusion, drowsiness
acute respiratory failure: respirations greater than 30, increased work of breathing, either hypoxic or hypercapnic
onset of new physical signs (cyanosis, peripheral edema)
failure of exacerbation to respond to initial medical management
presence of serious comorbidities (heart failure, EKG changes, high troponin)
insufficient home support
more aggressive antibiotics and steroids early
When are antibiotics recommended for Acute Exacerbations of COPD?
Increased dyspnea
Increased sputum volume
Increased sputum purulence
OR
If patient requires mechanical ventilation for AECOPD (either invasive or noninvasive)
Really relies on sputum; color of sputum doesn’t matter, unless it is a change
Other Acute Exacerbations of COPD Treatment
parenteral steroids
short acting bronchodilators + - short acting anticholinergics
continued maintenance therapy
respiratory therapy
Indications for Noninvasive Mechanical Ventilation
At least one of the following:
Resp acidosis: PaCO2>45mmHg AND pH <7.35
Severe dyspnea with clinical signs of respiratory fatigue
Persistent hypoxemia despite supplemental oxygen therapy
Indications for Invasive Mechanical Respiration
Unable to tolerate NIV or NIV failure
S/p resp or cardiac arrest
Diminished consciousness, psychomotor agitation uncontrolled by sedation
Massive aspiration
Persistent inability to remove resp secretions
Severe hemodynamic instability without response to fluids & pressors
Severe ventricular or supraventricular arrhythmias
Life-threatening hypoxemia in pts unable to tolerate NIV
When to Refer
A1AT deficiency or known FH of AATD
Restrictive pattern on PFTs
Any finding that seems worse than you expect (eg severe ↓DLCO in someone with mild obstruction)
Rapid progression of symptoms
Frequent exacerbations despite whatever you’re doing for them
Pulmonary nodules (esp if multiple – malignancy until proven otherwise)
Adenopathy noted on imaging
Whenever you are considering the use of less common treatments
