unmodifiable risk factors for COPD
age
being female
emphysema in base of lungs is probably caused by
Alpha-1 Antitrypsin Deficiency
emphysema in apex of lungs is likely caused by
smoking
how does Alpha-1 Antitrypsin Deficiency cause COPD
eventually causes elastase to be produced
destroying alveoli elastic capacity
spirometry can be used to diagnose
airway obstruction
stage 1 COPD FEV1 value
80%
diagnosis is only done by symptoms at this point
stage 2 COPD FEV1 value
50–79%
stage 3 COPD FEV1 value
30-49%
stage 4 COPD FEV1 value
less than 30%
residual volume and total lung capacity in COPD
RV increased
TLC increased
RV/TLC MORE THAN 30%
some general clinical features of COPD
Cyanosis Pursed lip breathing Use of accessory muscles Wheeze Peripheral oedema
how is COPD diagnosed
AND Airflow obstruction confirmed by post-bronchodilator spirometry
signs of sever COPD exacerbation
Breathless (RR>25/min) Accessory muscle use at rest Purse lip breathing Fluid retention Cyanosis (Sats<92% o/a) Confusion FLAPPING TREMOUR tripod postition
primary care management of exacerbations
secondary care management of severe exacerbation
Oxygen
Nebulised bronchodilator (2 & anti-muscarinic) Oral/IV corticosteroid
+/-antibiotic
type 1 vs type 2 respiratory failure
* Type 2: ↓ pO2and ↑ pCO2 (ventilatory failure)
whats Secondary polycythaemia
Body produces ↑ erythropoietin in response to low O2
•↑ Haemoglobin, ↑ Haematocrit
•↑ bloody viscosity
COPD – Non- Pharmacological Management
Short acting Bronchodilators
–SABA (eg- Salbutamol)
–SAMA (eg- Ipratropium)
Long acting bronchodilators
–LAMA (Long acting anti – muscarinic agents, eg-Umeclidinium, Tioptropium etc)
–LABA (Long acting B2agonist, eg- Salmeterol)
High dose inhaled corticosteroids (ICS) and LABA–
Relvar (Fluticasone/vilanterol)
Fostair MDI
when is long term O2 use used
PaO2 <7.3kPa
Or PaO7.3-8kPa if polycythaemia nocturnal hypoxia peripheral oedema pulmonary hypertension
when to admit to hospital
–Tachypneoa
–Low Oxygen saturation (< 90-92%)
–Hypotension etc