COPD Flashcards
define chronic bronchitis
productive cough for at least 3 months per year for 2 consecutive years that cannot be explained by an alternative diagnosis
define emphysema
permanent dilatation of pulmonary air spaces distal to the terminal bronchioles that is cuased by the destruction of the alveolar walls and pulmonary capillaries required for gas exchange
endogneous risk factors
lung growth and development abnormalities - recurrent pulmonary infections, premature birth
a1-antitrypsin deficiency
airway hyperresponsiveness
antibody deficiency syndrome eg. IgA deficiency
primary ciliary dyskinesia
presenting findings of COPD
chronic cough with expectoration especially in the morning
dyspnea and tachypnoea
pursed lip breathing
prolonged expiratory phase
end expiratory wheezing
crackles
muffled breath sounds
cyanosis
tachycardia
features of advanced COPD
congested neck veins
baarrel chest
use of accessory respiratory muscles due to diaphraagmatic dysfunction
hyperresonant lungs
decreased breath sounds
right heart failure and cor pulmonale
weight loss and cachexia
cor pulmonale
pulmonary heart disease
altered structure or impaired functioning of the right ventricle caused by a primary disorder of the respiratory system
pink puffers
emphysema predominating
noncyanotic
cachectic
pursed lip breathing
mild cough
blue bloater
chronic bronchitis predominating
productive cough
overweight
peripheral oedema
a1-antitrypsin deficiency
deficiency of a protease inhibitor
presents with panacinar emphysema and cirrhosis
age of onset usually younger
often also have hepatic signs and symptoms related to hepatitis or cirrhosis
centrilobular/centriacinar emphysema
most common type
seen in smokers
destruction of respiratory bronchiole (central portion of acinus) sparing distal alveoli
usually affects upper lobes
panlobular/panacinar emphysema
rarer type
associated with a1-antitrypsin deficiency
characterised by destruction of entire acinus (respiratory bronchiole and alveoli)
usually affects the lower lobes
initial tests for COPD
spirometry - FEV1/FVC ratio <0.7 after bronchodilator inhalation confirms the diagnosis
serum AAT level
what finding on spirometry is diagnostic of COPD
FEV1/FVC ratio of less than 0.7
restrictive lung disease
eg. pulmonary fibrosis
inability to inflate fully
obstructive lung disease
eg. bronchial asthma, COPD
difficulty exhaling air
assessment for respiratory failure
pulse oximetry: obtain in patients with signs of respiratory distress or signs of right heart failure
measure aat rest and on ambient air or usually oxygen prescription
ABG: obtain in patients with SO2 < 92% and/or acute illness
ABG findings of COPD
may show hypoxemic resp failure (low PO2) with or without hypercapnic respiratory failure
(high PCO2)
chronic hypercapnia due to CO2 trpping is common in patients with severe COPD
imaging
not required for diagnosis
signs of pulmonary hyperinlfation
- increased anteroposterior diameter (barrel chest)
- pushed down and flattened diaphragm
- horizontal ribs and widened intercostal spaces
- hyperlucency of lung tissue
- long and narrow heart shadow
signs of bullous emphysema: parenchymal bullae or pulmonary blebs
lifestyle modifications for COPD
counsel on smoking cessation eg. varenicline, buproprion, nicotine replacement therapy, lozenges, transdermal patch, gum
encourage physcal activity to recduce the risk of acute exacerbations
educate on indoor air pollution, work related pollution
recommend vaccinations
pulmonary rehabilitation for symptomatic patients
mild COPD
60-80% predicted FEV1 post bronchodilator
breathless on moderate exertion, few symptoms or effects on ADLs
moderate COPD
40-59% predicted FEV1 increasing dyspneoa, breathless on the flat, increasing limitation of ADLs
severe COPD
<40% predicted FEV1
dyspnoea on minimal exertion, ADLs severely curtailed
pharmacotherapy for COPD
symptomatic bronchodilator: short acting bronchodilator SABA salbutamol and/or ipratropium used when needed
regular bronchodilator: long acting beta-2 agonist LABA added when frequent deterioration in symptoms prompts additional medication use
regular bronchodilators that can be added in more severe disease
long acting anticholinergic tiotropium once daily
and then
fluticason propionate with salmeterol xinafoate
oral medications for COPD
oral slow release theophylline
may be useful after trial of short and long acting bronchodilator or where no inhlater use is possible
SABA
A class of bronchodilating medications with a short duration of action (< 6 hours). These medications also have a quick onset of action (1-5 minutes). Used to treat acute exacerbations of asthma and COPD. Usually administered via a nebulizer or metered-dose inhaler.
LABA
A class of bronchodilating medications with a long duration of action (≥ 12 hours). Onset of action is variable (quick for formoterol, longer for salmeterol). Used for long-term control of symptoms of asthma and COPD. Usually administered via a nebulizer or metered-dosed inhaler.
LAMA
A class of muscarinic antagonists that have a long duration of action (typically ≥ 12 hours). Used for maintenance therapy for asthma and chronic obstructive pulmonary disease. Examples include tiotropium, aclidinium, umeclidinium, and glycopyrrolate.
SAMA
A class of muscarinic antagonists with an onset of action of 10-15 minutes and a short duration of action (4-6 hours). Used to treat acute exacerbations of asthma and COPD. Examples include ipratropium and aclidinium.
ICS
inhaled corticosteroid eg. fluticasone
other drugs for COPD
palliative pharmacotherapy for dyspnoea eg. opiates
mathyxanthines eg. theophylline, not recommended in australia
LTOT
long term oxygen therapy
PaO2 < 55 mmHg or SaO2 < 88% at rest despite optimal medication
or pulmonary hypertension, CHF, polycythaemia
target O2 saturation >90%
continous oxygen therapy for > 15 hours/day
reevaluate after 60-90 days with ABG or pulse oximetry
ventilatory support
continuous positive airway pressure is useful in patients with COPD and pbstructive sleep apnoea
long term noninvasive positive pressure ventilation may be considered in select patients with severe chronic hypercapnia
surgical management
surgical bullectomy - in severe emphysema with hyperinflation and large bullae
lung volume reduction - for severe emphysema and hyperinflation without large bullae
lung transplantation
complications of COPD
chronic respiratory failure
acute exaacerbation of COPD
cor pulmonale
secondary spontaneous pneumothorax due to rupture of bullae (especially in bullous emphysema)
stepwise drug management of COPD
multidisciplinary care team for COPD
GP
respiratory physician for advanced COPD
practice nurse for spirometry testing, inhaler education
pulmonary rehabilitation
physiotherapist for exercise training including airway clearance techniques
occupational therapist
speech therapist for swallowing difficulty
pharmacist
use of SABA therapy for COPD
does not reduce the rate of decline
for as required therapy, use
salbutamol MDI with spacer or
terbutaline DPI
use of LABA when SABA is not sufficient
LABA/LAMA plus SABA
for LABA: indacaterol DPI (only LABA available on the PBS as monotherapy for COPD)
for LAMA: tiotropium DPI
use if long acting bronchodilator dual therapy when monotherapy is not sufficient
check inhaler technique first and other causes of breathlessness
fixed dose combination inhalers are avilable for dual therpy
if dual therapy is insufficient
add an ICS, fixed done combination inhalers available
be aware that this increases the risk of pneumonia
consider referral to a respiratory physician
role of SAMA in COPD
ipratropium is not usually used for symptom relief in COPD
contraindicated in patients using a LAMA, is more expensive than SABA, and may increase risk of cardiovascular events
cor pulmonale
right ventricular hypertrophy nd dilation secondary to lung disease
should be considered in a patient who has COPD and any of the following:
- peripheral oedema
- raised JVP
- a systolic parasternal heave
- a loud pulmonary secondary heart sound
pulmonary rehabilitation
effective intervention if the patient is motivated to reduce frequency of hospitalisations and exacerbations
involves exercise training, education, behaviour modification, outcome assessment
