Chronic obstructive pulmonary disease Flashcards
Definition
Chronic
Progressive
Irreversible
Airway obstruction
Chronic bronchitis
Emphysema
Diagnosis of chronic bronchitis
Clinical
3 months. most days, two consecutive years of sputum production and cough
Diagnosis of emphysema
Histological diagnosis
Enlarged airway spaces distal to terminal bronchioles with destruction of alveolar walls
Epidemiology
> 65
10-20% of all >40
Pathophysiology
Chronic inflammation
narrowing and remodelling of airways, increased number of goblet cells, enlargement of mucus-secreting glands of the central airways, and, finally, subsequent vascular bed changes leading to pulmonary hypertension
Decreased elastic recoil, fibrotic changes in lung parenchyma, and luminal obstruction of airways by secretions all contribute to increased airways resistance. Expiratory flow limitation promotes hyperinflation
Comparing pink puffers and blue bloaters
Pink puffers->+alveolar ventilation, normal 02, normal/low CO2. Breathless, not cyanosed. May progress to type 1 respiratory failure
Blue bloaters->-ve ventilation, hypoxemic and hypercapnic. Not breathless, cyanosed. May progress to cor pulmonale
Main symptoms
Breathless
Cough
Sputum
Wheeze
Signs
Tachypnoeic Cyanosed Use of accessory muscles Pursed lipped breathing Tracheal tug Plethoric
Reduced chest wall expansion
Hyper-resonant
-ve air entry
Quiet breath sounds
Evidence of cor-pulmonale->distended neck veins, hepatojugular reflux, loud P2, edema
Complications
Acute exacerbation Typer 1 respiratory failure Cor pulmonale Pneumothorax Polycythemia Lung cancer
Investigations and findings
Spirometry->FEV1/FVC ratio PaCO2 >50 mmHg and/or PaO2 of Flattened diaphragm, hyperinflation, large central pulmonary arteries, -ve vascular markings, bullae
FBC->+HCT, possible +WCC
ECG->RA and RV hypertrophy
Pulmonary function tests
Severity of COPD->mild, moderate, severe
Mild: FEV1 50-80% predicted
Moderate: FEV1 30-49% predicted
Severe: FEV1
Consultation checklist
SMOKES Smoking cessation Medications Oxygen Komorbidities->cardiac, sleep apnea, osteoporosis, depression, asthma
Pharmacotherapy options
short-acting β2-agonists (salbutamol, terbutaline) short acting anticholinergic drugs (ipratropium bromide) long-acting β2-agonists (eformoterol, salmeterol); long-acting anticholinergic drugs (tiotropium); and corticosteroids.
Management of mild
SABA before exercise->Salbutamol 200mcg as needed
1-2 puffs/4-6 hours
Patient education->disease progress, symptoms of exacerbation
Influenza/Pneumococcal
Smoking cessation
Advice: Avoid pollution Cool dry areas Avoid cold/flu Optimise diet and lifestyle
Management of moderate
Regular combined LABA (salmeterol) + anticholinergic (tiotropium), +SA dilator Salbutamol 200mcg as needed 1-2 puffs/4-6 hours Terbutaline 500mcg as needed Ipratropium 42 mcg Atrovent 1-2 puffs 4 X daily
Advice: Avoid pollution Cool dry areas Avoid cold/flu Optimise diet and lifestyle Education Smoking cessation Pulmonary rehab
Management of severe
Regular LABA + anticholinergic + SABA + regular inhaled corticosteroid
budesonide+eformoterol=
Symbicort 400/12
twice daily
fluticasone propionate+salmeterol
500/50 twice daily
Seretide
Advice: Warn risk of osteoporosis Rinse mouth out MDI-->use a spacer Avoid pollution Cool dry areas Avoid cold/flu Optimise diet and lifestyle Education Smoking cessation Self management plan Pulmonary rehab
Self management plan
Should have dose of steroids and antibiotics at home
If breathless–>adjust bronchoD dose
If sputum +–>start antibiotics
If breathless affects activities–>use inhaled corticosteroids
Advice to give to recognise acute exacerbation
increasing dyspnoea including use of accessory muscles at rest reduced effort tolerance tachypnoea (>25 breaths/min) increased fatigue increased cough and sputum increased wheezing
When is inpatient management appropriate
rapid rate of onset of
acute exacerbation with
increased dyspnoea, cough or sputum
inability to cope at home
inability to walk between rooms when previously mobile
severe breathlessness → inability to eat or sleep
inadequate response to ambulatory treatment
altered mental status suggestive of hypercapnia
significant comorbidity (e.g. cardiac disease)
new arrhythmia
cyanosis
Followup requirements for mild/moderate
12 monthly Smoking status Symptom control Pulmonary rehabilitation Complications of medications Effects of treatment Inhaler techniques Action plan
Followup requirements for severe
6 monthly Smoking status Symptom control Pulmonary rehabilitation Complications of medications Effects of treatment Inhaler techniques Action plan
EOL discussion Presence of cor pulmonale, heart failure, psychiatric Long term oxygen Nutrition Surgery Measure ABG
Management of acute COPD exacerbation
ABC
Assess patient->vitals, GCS, RR
Controlled oxygen therapy->24-28% depending on BAG
Nebulised salbutamol 5mg / 4h and iproatropium 600ug
Steroids->IV hydrocortison and oral prednisilone
Antibiotics->use if evidence of infection
Physiotherapy
If no response->repeat nebulised, nasal intermittent positive pressure ventilation if RR >30, ph
Guide to non-invasive ventilation
Patients should be considered for NIV with acute acidotic exacerbations
(pH 6.0 kPa).
Use a full fitting face mask.
Start NIV at EPAP þ 4 cm and IPAP þ10 cm Increase IPAP by 2 over the
next 1 hour to maximum of þ20 cm or whatever is best tolerated.
Set ventilator to timed.
Aim for 1–2 L O2 with sats 85–90%.
Repeat ABGs after 1 hour
If ABGs worsen, consider for ITU and invasive ventilation
Is sputum culture generally recommended
Sputum culture+in 50% but most consistently colonised with Haemo, Klebsiella, Strep–>so culture not recommended unless suggestive bacterial multiples
recently
Purpose of antibiotic use
Hasten recovery rather than eliminate
Choice of antibiotics
amoxycillin 500 mg orally,
8-hourly for 5 days
OR
doxycycline 200 mg orally, for the first dose,
then 100 mg daily for a total treatment duration of 5 days.
How is reversibility defined
+in FEV1 of >12% or 200ml
When is oxygen therapy indicated
hypoxemia (PaO2 ≤55 mm Hg or SaO2 ≤88% at rest) or where the PaO2 is less
than or equal to 60 mm Hg and there is polycythemia, pulmonary hypertension,
or peripheral edema suggesting heart failure. Oxygen therapy is the only
intervention that has been shown to decrease mortality and must be worn
for at least 15 h/d.
Benefit of smoking cessation
By quitting, his current pulmonary function will be unchanged, but the rate of pulmonary function decline will slow
By the time symptoms of COPD develop, how much as lung function reduced by
50%
When do patients lose their hypoxic drive
When they lose their hypoxia
How is +pCO2 followed clinically
Drowsiness
Vasodilation
Bounding pulses
Asterixis
How is alveolar ventilation monitored
pCO2
How long is the course of steroids following acute exacerbation
Taper over 2 weeks
Does the absence of crepitations exclude cardiogenic pulmonary congestion
No.
Those with low tidal volumes may not have prominent
crepitations or wheeze, due to the low
volumes of gas reaching the alveoli and low air
flows.
Letter to GP following D/C
What has happened Steroid tapering Need to pulmonary function tests Optimise lung function Smoking cessation Pulmonary rehab Other lifestyle modifications
