Respiratory topics Flashcards
What are the physiological responses to NHFO2?
- 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.
What are the physiological responses to NIV?
- CPAP/ or PEEP/PS
- Up to 100% O2
- Improves oxygenation
- Decreases resp effort 5. Minimises lung injury
What defines life-threatening haemoptysis?
No definitive criteria
- > 100mls/hr
- > 500mls/24 hours
What factors predict poor outcome in life-threatening haemoptysis?
- Rapid rate of bleeding
- Aspiration into contralateral lung
- Need for OLV
- Multilobar opacities
- Mechanical ventilation
- Involvement of pulmonary artery
- Cancer
- Aspergillosis
- Chronic alcoholism
What are the general categories of aetiology of haemoptysis?
- Intrinsic pulmonary parenchymal disease
- Medications and toxins
- Collagen vascula diseases involving the lung
- Cardiovascular diseases
- Bleeding disorders
What intrinsic pulmonary parenchymal diseases cause haemoptysis?
- 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
What medications and toxins are a/w haemoptysis?
- cocaine
- bevacizumab
- anticoagulants
- antiplatelets
- nitrogen dioxide
What collagen vascular diseases cause haemoptysis?
- SLE
- Granulomatatosis with polyangitis or other vasculidities
- Anti-glomerular basement membrane disease
- Idiopathic haemosiderosis
- Amyloidosis
- Behcet’s disease
What cardiovascular diseases can cause haemoptysis?
- pulmonary oedema
- mitral stenosis
- tricuspid endocarditis
- congenital heart disease
What happens to bronchial blood vessels in infection and inflammation?
- 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.
What are the diagnostic options for life-threatening haemoptysis?
- 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
Describe the initial stabilisation of a patient with life-threatening haemoptysis
- 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.
What are the complications of IR to bronchial arteries?
- 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)
What is the role of surgery in managing life-threatening haemoptysis?
- 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.
What is the pathophysiology of a PE?
- 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
How do you assess the severity of a PE?
ESC 2019 guidelines which include heamodynamics, sPESI score, RVD and raised troponin
What is the simplified PESI score?
Used for risk stratification in PE. A score of 1 or more indicates high risk. It includes:
- age > 80
- cancer history
- chronic cardiopulmonary disease
- heart rate > 109
- SBP < 100
- O2 sats < 90%
What are the hall mark features of a high-risk PE?
- Haemodynamic instability
- sPESI of 1+
- Evidence of RVD
- Elevated troponin
What are the hall mark features of an intermediate-high risk PE?
- No HD instability
- sPESI of 1+
- RVD
- Rasied trop
What are the hallmark features of an intermediate-low risk PE?
- No HD instability
- sPESI of 1+
- 1 or none or RVD or raised trop
What is first line treatment of a high-risk PE?
Thrombolysis
When should IR intervention be considered in PEs?
- High-risk and CI to thrombolysis
- High-risk and failure to respond to thrombolysis
- Intermediate-high risk and deteriorating despite anti-coagulation
What are the absolute CIs to thrombolysis?
- Allergy
- Ischaemic stroke within 3 months
- Thromophilia
- Brain or spinal surgery in preceeding 3 months
- Head trauma in past 3 months
- History of intracranial haemorrhage
- Current active bleeding
- Structural intracranial disease
What are the relative CIs to thrombolysis?
- History of major bleeding (non-IC)
- Recent surgery or invasive procedure
- Pregnancy
- Older age (esp over 75years)
What is successful weaning?
Extubated and no need for reintubation within 48 hours
What are the 3 types of weaning and their definitions?
- Simple
- Difficult - needs up to 3 SBTs or less that 1 week to wean
- Prolonged - needs 4+ SBTs or more that a week to wean
What are the causes of weaning failure?
- Airway and lung dysfunction
- Weaning-induced cardiac dysfunction
- Cognitive dysfunction
- Endocrine and metabolic dysfunction
- Diaphragm dysfunction
- Nutrition
Discuss airway and lung dysfunction in failure to wean
- Either increased airway resistance or decreased lung compliance
What causes of airway resistance may prevent weaning?
- ETT
- Tracheal injury
- Tracheomalacia
- Granulation tissue
- Laryngeal oedema
- Asthma and COPD
Discuss intrinsic PEEP in weaning
Increased airway resistance is a/w development of PEEPi
May develop due to increased flow resistance, expiratory flow limitation, high rr and loss of elastic recoil
Pulmonary hyperinflation resulting from PEEPi places the diaphragm in a suboptimal position and thus impairs its ability to generate negative pressure
PEEPi is a/w patient-vent asynchrony and ineffective triggering
What causes reduced lung compliance?
Pulmonary oedema
Pleural fluid
Ascites
Increased abdo pressure
Obesity
Pneumonia
Interstitial lung disease
Alveolar oedema
How do you calculate the compliance of the respiratory system?
= Vt / Pplat - PEEPtotal
What is normal static lung compliance?
200mls/cmH2O is normal
What is the static compliance of patients needing intubation?
60mls/cmH2O or lower
What interventions may be helpful to diagnose or manage airway and lung dysfunction as a cause of weaning failure?
- Bronchodilators
- Calculating PEEPi (In those with small airways disease applied PEEP should = PEEPi)
- Diagnostic bronch (diagnose potential causes of airway resistance)
- Diuretics - reduce lung oedema
- Thoracocentesis and paracentesis
What are the risk factors for laryngeal oedema a/w intubation?
- Traumatic intubation
- I+V > 6 days
- Large ETT
- Female
- Reintubation after unplanned extubation
What is the pathophysiology of weaning-induced cardiac dysfunction?
Reduced intrathoracic pressure, activation of the adrenergic system, hypoxaemia, hypercarbia and increased work of breathing are all consequences of unsuccessful weaning and may lead to an acute increase in LVEDP and cardiogenic oedema
What interventions may be helpful if you’re suspecting cardiac dysfunction as a cause of weaning failure?
- ECG during SBT- ischaemia
- TTE to look for diastolic dysfunction
- BNP - biomarker of volume status and cardiac failure
- Pulmonary artery wedge (occulusion) pressure. If increases during SBT it indicates a CVS dysfunction contributing to severe imbalance between O2 delivery and O2 consumption
- Check Hb / plasma protein before and after SBT. If they increase by >5% this reflects volume contraction induced by pulmonary oedema
- Diuretics can reduce LVEDV which can cause a marked decrease in LVEDP
- Nitrates - decrease LV afterload and improve myocardial O2 delivery via vasodilatation
What interventions may be helpful in cognitive dysfunction being a cause for failure to wean?
- Delirium screening
- Reorientation
- Early mobilisation
- Decrease noise and light at night
- Anxiolytics
What metabolic and endocrine dysfunction can lead to weaning failure?
- Low K+ / PO4 / Mg can all lead to weaning failure
- Adrenal insufficiency
- Hypothyroidism
- Uncontrolled BMs
What is the usual process of weaning?
2-step strategy
1. Assess readiness
2. SBT
How do you assess readiness to wean?
- Cause for resp failure reversed?
- P/F > 150 or sats > 90% on FiO2 of 40% or less
- pH > 7.25
- Haemodynamic stability
- Initiate inspiratory effort
- Hb > 70
- Core temp <38.1
- Awake and alert or easily rousable
What is the rapid shallow breathing index?
f/Vt
If < 105 its more likely a/w successful extubation.
However using it as a tool prolonged time to extubation in one study
How do you complete a SBT?
- Assessment of parameters predicting weaning success
- T-piece or
- PS 5-8 / PEEP 5 FiO2 0.40 or lower (+ATC)
A tolerance of 30-120 mins should prompt consideration for extubation
If pt fails then correct the reversible and try again in 24 hours.
What are the SBT failure criteria?
- RR > 35
- Increased accessory muscle use
- Sats < 92% on >40%
- hr > 140
- SBP > 180
- Signs of hypoperfusion (cyanosis / mottling)
- Depressed mental status or agitation
Who is at increased risk for ICU associated weakness?
- Female
- Mulitple organ dysfunction
- Duration of MV
- Steroids
- Duration of vasopressors
- ICULOS
- Increased blood sugars
- Decreased albumin
- Neurological failure
- NMBA infusion increases risk after 48 hours (ok for short-term use)
What is a recruitment maneouvre?
Transient increase in transpulmonary pressure above values used during MV with the aim of opening unstable distal airways +/or collapsed alveoli
What pressures are needed to open collapsed alveoli?
> 35-40cmH20
How do you assess lung recruitability on the Hamilton ventilator?
Use the PV tool
Pstart = 5cmH2O
Ptop = 40cmH2O
EndPEEP = 5cmH2O
Ramp speed = 2cmH2O/s
Tpause = 0
T maneouvre = 35s
When prompted whether to change PEEP at end = no
What are the preconditions for assessing lung recruitability?
- Deep sedation +/- NMB with no spont resp effort
- Monitor haemodynamics
- ETT cuff above Ptop - occurs automatically if using intellicuff
- Minimum 5 breaths between RMs
What are the indications for a RM?
Early in the management of mod-severe ARDS
As part of an open lung strategy
If O2 is impaired after an intervention
What are the CIs to a RM?
- Air leaks
- Pregnancy
- Emphysena
- HD instability
- Intracranial hypertension
- Pts who can’t tolerate high intra-pulmonary pressures e.g. RHF
After a low-flow PV curve has been generated how do you assess lung recruitability?
Calculate the normalised maximum distance =
Max delta volume between ins and exp limbs / max volume
What NMD is considered to have high potential for recruitment?
> 40%
What should you do in patients that are hypoxic with low potential for recruitment?
Consider
- keeping PEEP < 10
- Prone
- ECMO
How to perform a recruitment maneouvre on the Hamilton ventilator?
- Consider reducing FiO2 to target sats 92% to help assess effectiveness
Settings:
Pstart - current PEEP
Ptop = 40cmH2O
End PEEP = 15chH2O (or higher if current PEEP > 15)
Ramp speed = 5cmH2O
Tpause = 10s
Tmaneouvre = 20s
How to assess effectiveness of a RM?
- Vol and Ptop was > 2mls/Kg IBW
- Sats > 97% within 5 mins
Both should occur for it to have been effective
How do you assess the volume increase at Ptop?
- Use Paw/V + Paw/dV graph option
Loot at volume at top of insp and exp limbs
What is the sequence for performing a RM via the Hamilton?
- Assess recruitability
- First RM
- Second RM
- Decremental PEEP titration to assess optimal PEEP for 3rd RM
- 3rd and final RM
What is decremental PEEP titration?
- Sats at 92% before starting
- Decrease PEEP every 3 mins after the 2nd RM
- As soon as sats reduce by 2% go back to the PEEP before and use this as the optimal PEEP value for the 3rd RM
What is a parapneumonic effusion?
Pleural fluid collection secondary to pneumonia and pleural inflammatory response
How are parapneumonic effusions categorised?
- Uncomplicated - free-flowing inflammatory sterile effusion
- Complicated - bacterial invasion and more severe inflmmatory response
- Empyema - purulent material within the pleural cavity
How common is empyema in patients hospitalised with pnuemonia?
5-10%
What is the most common bug in empyema?
strep pnuemoniae
What determines the normal volume of pleural fluid?
Production and absorption depends on the hydrostatic and oncotic pressure gradients across the 2 pleural layers and the pleural space. It’s principally mediated by the parietal pleural since it has higher hydrostatic pressures (fluid production) and the lymphatic stomata responsible for fluid resorption
What is the usual volume of pleural fluid?
0.26mls/kg
Why do parapnuemonic effusions occur?
They arise when the inflammatory reaction to pulmonary infeciton spreads across the visceral pleura into the pleural space, evoking fluid exudate rich in neutrophils and proteins through increased capillary permeability mediated by interleukin-8 and TNF-alpha
How does a parapnuemonic effusion progress to an empyema?
It’s a continuum involving 3 phases - exudative, fibrinopurulent and organised.
As infectious and inflammatory phases progress, fibrin clots and fibrin membrane deposition in the pleural cavity ensues within 5-10days leading to fluid loculations.
Bacterial invasion may then induce empyema characterised by frank ;us, pneumatoceles and pleural thickening or septations on imaging.
What are the characteristics of simple parapneumonic fluid?
- clear
- free flowing on imaging
- pH > 7.2
- glucose > 3.3
- LDH u/l < 1000
- No growth
- drainage usually not needed
What are the features of complicated parapneumonic pleural fluid?
- clear or turbid
- septations and loculations on imaging
- pH < 7.2
- gluc < 3.3
- LDH > 1000
- no bacterial growth
- may or may not need draining
What are the features of empyema in pleural fluid?
- purulen
- septations, loculations, pleural thickening and split pleura sign on CT
- pH < 7.2
- gluc < 3.3
- LDH > 1000
- +ve fluid culture
- needs abx and drainage
Which antibiotics don’t adequately penetrate the pleura?
Aminoglycosides
How long should abx continue in empyema?
Optimal duration unknown
2-6 weeks.
What is intrapleural enzymatic therapy?
e.g. tPA, DNAse
Breaks down loculations, decreases viscosity and helps drainage
May decrease LOS and need for surgery
Optimal dosing unknown
4.1% risk of intrapleural haemorrhage
When should surgery be explored for empyems?
When there is ongoing sepsis despite chest drain and antibiotics
What scoring system can predict outcome in parapnuemonic effusion
RAPID score
Describe mucus
- Made up of water, proteins, lipids, carbs and electrolytes
- Acts as a physical and immunological barrier to pathogens
- Aids air humidification
- Is a selectively permeable barrier for gas exchange and nutrient absorption
Why do ICU patients get mucus accumulation and airway plugging?
- Infection, inflammation, airway dehydration, decreased cough reflexes, supra-normal oxygenation and mechanical stress all lead to changes in mucus characteristic and increased mechanical impedence to mucociliary clearance
