Respiratory topics Flashcards
1
Q
What are the physiological responses to NHFO2?
A
- PEEP effect
- Dead space washout provides ventilatory support leading to reduced resp rate and WOB
- High flow rates usually exceed peak insp flows during AHRF (30-40L) preventing dilution with inhaled gas with room air.
2
Q
What are the physiological responses to NIV?
A
- CPAP/ or PEEP/PS
- Up to 100% O2
- Improves oxygenation
- Decreases resp effort 5. Minimises lung injury
3
Q
What defines life-threatening haemoptysis?
A
No definitive criteria
- > 100mls/hr
- > 500mls/24 hours
4
Q
What factors predict poor outcome in life-threatening haemoptysis?
A
- Rapid rate of bleeding
- Aspiration into contralateral lung
- Need for OLV
- Multilobar opacities
- Mechanical ventilation
- Involvement of pulmonary artery
- Cancer
- Aspergillosis
- Chronic alcoholism
5
Q
What are the general categories of aetiology of haemoptysis?
A
- Intrinsic pulmonary parenchymal disease
- Medications and toxins
- Collagen vascula diseases involving the lung
- Cardiovascular diseases
- Bleeding disorders
6
Q
What intrinsic pulmonary parenchymal diseases cause haemoptysis?
A
- Bronchiectasis - sarcoid, CF, TB, non-TB mycobacteria, fungus
- Infection - TB, fungal, necrotising pneumonia, mycetoma, lung abscess, parasitic infection
- Pulmonary malignancy
- Pulmonary vascular - AV malformations, subepithelial bronchial artery, aortic aneurysm with erosion, PE, iatrogenic injuries, PA injury from PAFC, aorto-bronchial fistula from aotic graft or stent, biopsy complications
- Pulmonary trauma - penetrating chest injury, blunt force chest injury
7
Q
What medications and toxins are a/w haemoptysis?
A
- cocaine
- bevacizumab
- anticoagulants
- antiplatelets
- nitrogen dioxide
8
Q
What collagen vascular diseases cause haemoptysis?
A
- SLE
- Granulomatatosis with polyangitis or other vasculidities
- Anti-glomerular basement membrane disease
- Idiopathic haemosiderosis
- Amyloidosis
- Behcet’s disease
9
Q
What cardiovascular diseases can cause haemoptysis?
A
- pulmonary oedema
- mitral stenosis
- tricuspid endocarditis
- congenital heart disease
10
Q
What happens to bronchial blood vessels in infection and inflammation?
A
- It causes bronchial arteries to become dilated and tortuous which increase the risk of bleeding.
- The vascular anastomosis between the bronchial arteries and pulmonary vessels becomes more prominent - leading to greater blood flow through dilated bronchial arteries.
- Angiogenic growth factors promote new, collateral vessels which are thin walled and prone to rupture.
11
Q
What are the diagnostic options for life-threatening haemoptysis?
A
- CXR - may identify site of bleeding (50%) or cause (35%)
- Ct scan - may not allow localisation in pre-existing lung disease or contamination of non-bleeding segments. May not be practical in an unstable patient. Can diagnose extrapleural causes and help plan IR.
- Bronch - can localise source, clear the airway and allow some topical treatments
12
Q
Describe the initial stabilisation of a patient with life-threatening haemoptysis
A
- Airway control
- Volume resuscitation
- Correction of coagulopathy
- Can be bleeding side down to prevent contamination of non-bleeding lung
- Single lung ventilation may be useful to protect non-bleeding lung
- TXA mauy be helpful
- DLT not recommended and needs expertise and narrow lumens prone to clotting.
13
Q
What are the complications of IR to bronchial arteries?
A
- chest pain and dysphagia, both self limiting
- groin haematoma, dissection, artery perforation, cortical blindness, bronchial stenosis, necrosis, broncho-oesophageal fistula, pulmonary infarction, ischaemic colitis, spinal artery embolisation (in 5% the spinal artery originates form bronchial artery)
14
Q
What is the role of surgery in managing life-threatening haemoptysis?
A
- needed in chest trauma, iatrogenic PA rupture or resecatble lung tumour.
- Otherwise mortality is high if done as an emergency - better to wait at least 48 hours if able
- Useful in TB and aspergilloma after the acute phase, due to high risk of rebleeding.
15
Q
What is the pathophysiology of a PE?
A
- Blood clots are usually embolic from the deep lower limb veins
- Clot obstructs blood flow and increases pressures proximal to clot and reduces from distal to it
- Increased PA pressures result in vasoconstriction and release of tissue mediators including serotonin and thromboxane A2
- R sided afterload increases, leading to higher myocardial O2 consumption and increased filling pressures. Acute RV failure in some. Cardiac ischaemia occurs
- ## Systemic hypoxaemia is mediated by mismatch between perfusion and ventilation and areas of atelectasis in ischaemic areas due to decreased surfactant production
