Respiratory: COPD II Flashcards
Describe what is meant by the term cor pulmonale [2]
RIght-sided heart failure caused by respiratory disease:
- The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) limits the right ventricle pumping blood into the pulmonary arteries.
- This causes back-pressure into the right atrium, vena cava and systemic venous system.
What are the most common causes of cor pulmonale? [5]
COPD (the most common cause)
Pulmonary embolism
Interstitial lung disease
Cystic fibrosis
Primary pulmonary hypertension
State 5 symptoms of cor pulmonale
- Often asymptomatic
- peripheral oedema
- SOB
- syncope
- chest pain
State 6 examination findings of cor pulmonale [6]
- Hypoxia
- Cyanosis
- Raised JVP
- Peripheral oedema
- Loud second heart sound
- systolic parasternal heave
- Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
Describe how you treat cor pulmonale? [1]
Which drugs are not recommended? [3]
Loop diuretics for oedema
LTOT
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE
Oxygen therapy
What are O2 saturation targets for COPD? [1]
88-92%
Explain the physiological reasons of what can happen to CO2 levels when treated with oxygen in COPD patients? [2]
Many patients retain CO2 when treated with oxygen (oxygen induced hypercapnia)
Due to:
Increased V/Q mismatch (most important)
- COPD ptx optimise gas exchange by hypoxic vasoconstriction leading to altered Va/Q ratios
- Excessive oxygen administration overcomes this, leading to increased blood flow to poorly ventilated alveoli, and thus increased Va/Q mismatch and increased physiological deadspace
The Haldane effect:
- deoxygenated Hb binds CO2 with greater affinity than oxygenated Hb
- Thus: oxygen induces a rightward shift of the CO2 dissociation curve (Haldane effect)
When should you assess patients for LTOT in COPD patients? [5]
How often do you assess ABGs when deciding LTOT? [2]
- very severe airflow obstruction: FEV1 < 30% predicted
- cyanosis
- polycythaemia
- peripheral oedema
- raised jugular venous pressure
- oxygen saturations less than or equal to 92% on room air
Assessment is done by measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.
What pO2 level is LTOT therapy given to COPD without any other factors? [1]
What pO2 levels [1] and other conditions [3] mean that LTOT is given to COPD factors?
Offer LTOT to patients with a pO2 of < 7.3 kPa
OR
To those with a pO2 of 7.3 - 8 kPa and one of the following:
* secondary polycythaemia
* peripheral oedema
* pulmonary hypertension
What’s the rule with LTOT and smoking in COPD patients? [1]
do not offer LTOT to people who continue to smoke despite being offered smoking cessation advice and treatment, and referral to specialist stop smoking services (fire risks)
Which of the following is not an indication for long-term oxygen therapy (LTOT) in patients with stable chronic obstructive pulmonary disease (COPD)?
PaO2 = 7.3-8.0 kPa with secondary polycythaemia
PaO2 = 7.3-8.0 kPa with anaemia
PaO2 = 7.3-8.0 kPa with pulmonary hypertension
PaO2 < 7.3 kPa
PaO2 = 7.3-8.0 kPa with peripheral oedema
PaO2 = 7.3-8.0 kPa with anaemia
NICE recommends that LTOT should be considered in patients with stable COPD who do not smoke and are on optimal medical therapy in the following circumstances:
PaO2 < 7.3 kPa
PaO2 7.3-8.0 kPa with secondary polycythaemia
PaO2 7.3-8.0 kPa with peripheral oedema
PaO2 7.3-8.0 kPa with pulmonary hypertension (eg. loud P2, RVH on ECG)
What indicates COPD patients to start LTOT? [1]
LTOT if 2 measurements of pO2 < 7.3 kPa
A patient presents with COPD. They are currently on a SAMA but are having worsening symptoms. They show no signs of asthmatic involvement / eosinophilic involvement.
What is the next step in their treatment? [1]
COPD: Discontinue SAMA (switch to SABA) if commencing LAMA
