COPD Flashcards
p pulmonale (elevation) or p mitrale ( biphasic prolonging)
p pulmonale due to right atrial enlargement seen in pulmonary hypertension and COPD
list some of the ECG changes seen in COPD
Prominent P wave in inferior leads
The most likely underlying condition is COPD. The following ECG changes may therefore be seen:
Right axis deviation
Prominent P waves in inferior leads
Inverted P waves in high lateral leads (I, aVL)
Low voltage QRS
Delayed R/S transition in leads V1-V6
P pulmonale
Right ventricular strain pattern
RBBB
Multifocal atrial tachycardia
bronchitis features - cough
Chronic productive cough for at least 3 months in at least 2 consecutive years without other identifiable cause
Abnormal irreversible enlargement of the airspaces distal to the terminal bronchioles, due to destruction of their walls.
In a normal lung, α1-antitrypsin is responsible for inhibiting excessive activity of neutrophil elastase. However, in emphysema, the normal balance of proteases and antiproteases is lost. The stimulated neutrophils release free radicals that inhibit the activity of α1-antitrypsin.
This results in loss of elastic recoil and subsequently airway collapse during expiration and air trapping.
what are the types of emphysema
Centriacinar - The proximal part of the airways such as the respiratory bronchioles, mainly the upper lobes - mainly caused by Cigarette smoking
Panacinar- The entire acini from respiratory bronchioles to alveolar duct and alveoli, mainly the lower lobes. caused by - α1-antitrypsin deficiency
Distal acinar- The distal part of the airways, mainly the paraseptal region casued by - Fibrosis, atelectasis
features of emphysema
Carbon dioxide retention
Pursed lip breathing
Exertional dyspnoea
Use of accessory muscles in breathing
Barrel chest (hyperexpanded chest)
Hyperresonant chest on percussion
Sits forward in a hunched-over position
what might you see on a CXR of COPD
Hyperinflated chest (>6 anterior ribs)
Bullae
Decreased peripheral vascular markings
Flattened hemidiaphragms
MX acute exacerbation
ABCDE
patent airway
O2 sats 88-92%
Give nebulisers Salbutamol, Ipratropium
Steroids: oral Prednisolone or IV Hydrocortisone (if severe)
Abx if sign of infection
No improve ITU input will be required and they may need to be started on non-invasive ventilation such as BiPAP. Further deterioration is an indication for invasive ventilation.
when can you get long term oxygen therapy
Long Term Oxygen Therapy (LTOT): A trial showed that maintaining oxygen above 8kPa for at least 15 hours a day improved mortality rates.
NICE guidelines state that LTOT can be prescribed for patients who:
Have a PaO2 <7.3kPa on two readings more than 3 weeks apart, and are non-smokers (but not absolutely contraindicated in smokers).
Or have a PaO2 of 7.3-8kPa alongside one of the following: nocturnal hypoxia, polycythaemia, peripheral oedema and pulmonary hypertension.
LTOT can also be prescribed for patients with terminal illness.
so basically Pa02 below 7.3 if not smoke and between that and 7.8 with a symtpom
pulmonary hypertension is defined as pulmonary artery pressure above what
25mmHg
A 65 year old male patient is reviewed in the respiratory clinic.
He was diagnosed with COPD 10 years ago and use to smoke 10 cigarettes per day but has given up for the last 2 years. He reports worsening breathlessness and marked restriction on his activities of daily living despite maximal medical therapy with combination fluticasone, salmeterol, and tiotropium. He has engaged poorly with pulmonary rehabilitation.
Arterial blood gas reveals a PaO2 of 8.5 kPa and PaCO2 of 7 kPa. CT scan reveals upper lobe predominant emphysema, but no large bullae. His FEV1 is 40% predicted.
Which of the following management options is most suitable in this patient?
long volume reduction surgery
This is the correct answer. Patients with severe COPD who remain breathless despite maximal medical therapy should be considered for lung volume reduction surgery if they meet the criteria of: upper lobe predominant emphysema, FEV1 >20% predicted, PaCO2 below 7.3 kPa, and TlCO above 20% predicted
A 58-year-old-man with a known diagnosis of chronic obstructive pulmonary disease (COPD) presents to the emergency department with worsening breathlessness and purulent sputum production. His respiratory rate is 26 and his oxygen saturations 85%.
The admitting doctor suspects an infective exacerbation of his COPD and takes an arterial blood gas (ABG) which shows a pH 7.32, pO2 7 kPa, pCO2 7.5 kPa, bicarbonate 45 mmol/l.
What is the correct interpretation of the ABG results?
Acute on chronic respiratory acidosis
The pH is <7.35, confirming that this is an acidosis, and the raised pCO2 suggests that this is of a respiratory origin. The raised bicarbonate (HCO3) shows that there is metabolic compensation. However, such high levels, which takes time to develop, indicate long-term compensation for chronic respiratory acidosis due to his underlying COPD
A 70 year old male patient presents to the emergency department with shortness of breath and cough productive of sputum.
He has a 50 pack year history. On physical examination he is hyper-expanded and there is asterixis. The respiratory rate is 24/minute, and the oxygen saturations are 85% on room air.
Which of the following is the most appropriate oxygen therapy for this patient?
15 L/min via non-rebreathe mask
In the setting of an acutely breathless patient with no confirmed diagnosis of COPD, it is important to treat the hypoxia using a 15L non-rebreathe mask at first. This may then be adjusted once an ABG is performed and if there is evidence of type 2 respiratory failure.
get difficult expiration and excessive mucus production
after non-rebrethe mask and ABG back what way of giving oxygen next
respiration, into a hypoxic drive for respiration. This means if they are over-oxygenated this can prompt respiratory arrest as they lose their hypoxia that was previous driving respiration - to reduce this risk it is always best to use a controlled method of oxygen delivery such as a Venturi mask in COPD patients.
A 75-year-old gentleman with a background of severe COPD requiring home oxygen and nebulisers is admitted with shortness of breath, wheeze and a productive cough. He is started on 6L/minute of oxygen via a simple face mask. His oxygen saturations rise from 79% to 96%. This appears to calm the patient and his work of breathing decreases substantially. An arterial blood gas is subsequently performed which shows:
pH 7.268 (7.35-7.45)
PaO2 10.9kPa (>10.6kPa)
PaCO2 9.6kPa (4.7-6kPa)
Base excess +13mmol/L
HCO3 35mmol/L (23-30mmol/L)
What is the most appropriate initial management for this patient?
28% oxygen via Venturi mask
This patient has severe COPD and is a chronic CO2 retainer as shown by the raised HCO3 and base excess on his arterial blood gas. His target oxygen saturations should be 88-92%. By over-oxygenating him and achieving saturations of 96%, he is losing his hypoxic drive and is hypoventilating. This is shown by his reduced work of breathing and looking calmer, which is in fact a decreasing level of consciousness due to CO2 narcosis. He should be switched onto 28% oxygen via a Venturi mask with an aim of achieving target oxygen saturations of 88-92%
cause of ARDS
sepsis
