1B respiratory failure Flashcards
What is the predominant feature of respiratory failure?
Shortness of breath
Define respiratory failure
Syndrome of inadequate gas exchange due to dysfunction of ≥1 components of respiratory system
What are the parts of the resp system?
-
Nervous system
- CNS/brainstem
- Peripheral nervous system
- Neuromuscular junction
-
Respiratory muscle
- Diaphragm and thoracic muscles
- Extrathoracic muscles
-
Pulmonary
- Airway disease
- Alveolar capillary
- Circulation
Which areas of the world is resp disease more prevalent in?
- North America, Europe
- SE and S Asia we don’t see as much
What is the biggest risk factor for men and then women for chronic resp disease?
- 3rd leading cause of death
- Men- smoking biggest risk factors
- Women- household air pollution from solid fuels
How does acute respiratory failure present and what diseases is part of it?
- Heterogenous disease presentation
- Can present as CF, pulmonary hypertension, pneumonia, COPD exacerbation (Acute Respiratory Distress Syndrome: ARDS)
What is mortality from ARDS?
30-40%
What does severity and increased age increase in ARDS?
Increases mortality
How do we classify ARDS?
Berlin definition
How can we classify respiratory failure?
- Acute
- Pulmonary
- Extra-pulmonary
- Neuromuscular/myasthenia/GBS
- Chronic
- Pulmonary/airways
- Musculoskeletal
- Acute on chronic
- Infective exacerbation
- Myasthenic crises
- Post operative
What diseases come under acute pulmonary?
- infection
- aspiration
- primary graft dysfunction following lung transplant
What diseases come under acute extra-pulmonary?
- Trauma
- Pancreatitis
- Sepsis
What diseases come under chronic pulmonary/airways?
- COPD
- Lung fibrosis
- CF
- Lobectomy
What diseases come under chronic musculoskeletal?
Muscular dystrophy
What diseases come under acute on chronic infective exacerbation?
- COPD
- CF
- myasthenic crises
- post-operative
How can we classify respiratory failure physiologically?
- Type 1/ Hypoxemic resp failure
- Type 2/ Hypercapnic resp failure
- Type 3/ Perioperative failure
- Type 4/ Shock
What is Type 1/ Hypoxemic resp failure?
- Failure of oxygen exchange
- PaO2 <60 at sea level
- Increased shunt fraction (QS/QT)
- Hypoxemia refractory to supplemental oxygen
What does increased shunt fraction (QS/QT) mean?
More blood transported through lungs without taking part in gas exchange
Why does increased shunt fraction happen?
Due to alveolar flooding in heart/CVD failure patients
What are causes of hypoxemic resp failure?
- Collapse of lobe
- Aspiration
- Fibrosis
- Pulmonary oedema
- Pulmonary embolism
- Pulmonary hypertension
What does Type 2/ hypercapnic resp failure mean?
- Failure to exchange or remove CO2
- Decreased alveolar minute ventilation
- Dead space ventilation
What causes of Type 2/ hypercapnic resp failure are there?
- Nervous system issues
- Neuromuscular issues
- Muscle failure- muscles too tired to maintain tidal volume
- Airway obstruction
- Chest wall deformity
What is the caveat of O2 therapy in type 2 resp failure patients and how does it affect target O2 sats?
- Patients with chronic hypercapnic resp failure shouldn’t be given liberal O2 as it can exacerbate resp failure
- This is because it doesn’t maintain hypoxic drive to breathe (hypoxia stimulates breathing in COPD) so patients become more hypoxic
- This means O2 sats in these patients is 88-92%
What does Type 3/Perioperative failure mean?
- Increased atelectasis (collapse of entire lung or lobe) due to low functional residual capacity (FRC) with abnormal abdominal wall mechanics
- You can have hypoxemia or hypercapnia
How is type 3/perioperative failure prevented?
- Anaesthetic or operative technique
- Posture
- Incentive spirometry
- Analgesia
- Attempts to lower intraabdominal pressure
What does type 4 resp failure/aka shock mean?
Happens in intubated and ventilated patients during shock. Poor perfusion of the lung so gas can’t come into blood.
What rarely happens when neurologic shock happens?
- Patients become vasoplegic (low systemic vascular resistance → low bp despite normal/raised cardiac output)
- Peripheral pooling of blood and not much central return of blood to pulmonary vasculature
- Get significant drop in pulmonary perfusion
What are the risk factors for chronic resp failure?
- COPD
- CF
- Pulmonary fibrosis
- Pollution
- Recurrent pneumonia
- Neuromuscular diseases
What are the risk factors for acute resp failure?
- Infection- viral or bacterial
- Aspiration- when someone’s conscious level drops, they aspirate gastric contents into lungs which causes response from lungs
- Trauma
- Pancreatic- inflammation
- Transfusion
What’s the main thing we look at in history of patient presenting with resp failure?
Origin of shortness of breath
What causes could there be of ARDS shortness of breath?
- Lower respiratory tract infection- viral or bacterial
- Aspiration
- Trauma- transfusion
- Pulmonary vascular disease- pulmonary embolus or haemoptysis
- Extrapulmonary- pancreatitis, new medications
What pulmonary (lung) causes of ARDS are there?
- Aspiration
- Trauma
- Infection
- Burns- inhalation of hot gas/ash
- Surgery
- Drug toxicity
What do pulmonary causes tend to affect in the body?
- Alveoli
- Airways down to alveoli
What extrapulmonary causes of ARDS are there?
- Trauma
- Infection
- Pancreatitis
- Burns
- Surgery
- Drug toxicity
- Transfusion
- Bone marrow transplant
What do extrapulmonary causes tend to affect in the body?
A systemic disease causing cytokine release and macrophage/neutrophil activation within vascular supply
What is the overall mechanism of acute lung injury?
- Alveolar macrophages get activated by inflammation/infection, release further cytokines → IL-6 and 8, TNF alpha
- In response to this we get alveolar protein rich oedema build up in lung
- Inactivation of surfactant means alveolus becomes less efficient at expanding
- You get migration of neutrophils into interstitium where they can cause some damage by secreting proteases etc before getting to the site of infection/inflammation in the alveolus
- Leads to build up of more oedema in interstitium- this increases distance between capillary and alveolus
- This means greater distance for gas exchange to occur → gas exchange becomes less efficient
What in vivo evidence do we have for acute lung injury?
- TNF signalling implicated- reduced injury of alveolar lung injury by blocking TNFR-1 signalling pathway with Ab or using TNFR-1 knockouts
- Macrophage activation occurs in alveolar space and neutrophil lung migration also occurs
- DAMP release (commonest for lung are HMGB-1 and RAGE)
- Cytokines are released e.g. IL-6, 8, IL-1B, IFN-gamma (this is important for viral response and T cell differentiation)
- Cell death- there is necrosis in lung biopsies, and also apoptotic mediators e.g. FAS, FAS-I and BCl-2
What therapies have been tried already for ARDS?
- Steroids
- Salbutamol
- Surfactant
- N-Acetylcysteine- reduces viscosity of secretions
- Neutrophil esterase inhibitor
- GM-CSF
- Statins
What therapies are being trialled for ARDS?
- Mesenchymal stem cells- good ex vivo benefit but pools of stem cells are highly variable
- Keratinocyte growth factor
- Repair factor
- Steroids
What can we split therapeutic intervention for ARDS into?
- Treating the underlying disease
- Respiratory support
- Multiple organ support
What does treating the underlying disease include?
- Inhaled therapies commonly- bronchodilators and maybe pulmonary vasodilators
- Commonly get antibiotics or anti-virals
- May get steroids
- Drugs:
- Pyridostigmine (for muscular failure)
- Plasma exchange (for vasculitis presentation)
- IViG
- Rituximab
What does respiratory support include?
- Physiotherapy
- Nebulisers- could be salbumatol or hypertonic saline to reduce mucous load- patients are too tired to cough up this mucous so we reduce it
- Oxygen- depending on patient e.g. type 2 resp failure shouldn’t be given liberal O2 since it could exacerbate it
- High flow oxygen- normally delivered through nasal cannulae
- Non invasive ventilation- can use single air pressure (commonly used for type 1 resp failure)
- Mechanical ventilation
- Extra-corporeal support (e.g. ECMO: extra corporeal membrane oxygenation)
What is extra-corporeal support?
- Take blood out of patient and pass it across a membrane and back into patient
- Oxygenates blood well and scrubs out CO2
What does multiple organ support include?
-
Cardiovascular support
- Fluids
- Vasopressors, e.g. vasopressin, noradrenaline
- Inotropes
- Pulmonary vasodilators e.g. nitric oxide
-
Renal support
- Haemofiltration
- Haemodialysis
-
Immune therapies
- Plasma exchange
- Convalescent plasma
What are the sequelae of ARDS?
- Poor gas exchange which leads to inadequate oxygenation, hypercapnia, poor perfusion
- Infection which leads to sepsis
- Inflammation leads to inflammatory response
What are the ARDS specific interventions?
- Respiratory support
- Intubation and ventilation
- ARDs necessitates mechanical intervention
- Types of intervention
- Volume controlled
- Pressure controlled
- Assisted breathing modes
- Advanced ventilatory modes
- Procedures to support ventilation
How does the pressure-volume loop change for ARDS from normal?
- ARDS lung is much stiffer so volume is reduced and more pressure is used at the top to get very little gain in volume increase
- Lung can drop below lower inflection point leading to lung collapse
- We try to keep end expiratory pressure so that lung remains open and that we open lung just enough- we don’t push it too hard with too much pressure that would cause damage and inflammation and oedema and alveoli will stop working
What are the pitfalls of ventilation?
- Minute ventilation
PaCO2 control - Alveolar recruitment
Positive end exspiratory pressure (PEEP) - V/Q mismatch
- Ventilation without gas exchange vice-versa
What imaging is used for ARDS patients?
- Lung recruitment CT
- Lung ultrasound
How does lung recruitment CT work?
Use high pressure ventilatory strategy but with low driving pressure strategy to see if we can open up lung
- Below, top left is consolidated lung- as we increased distending pressure in lung we can open up areas of lung
- In top right the lung is recruitable
- But when we get to too much pressure we overexpand lung and traps more gas in chest which reduces ability for perfusion and could cause right ventricular dysfunction and causing pressure trauma
What system do we use for escalation of ARDS therapy?
Murray score
What is the national ECMO approach?
- 5 national centres
- Telephone or online referral with Murray score >3 and pH < 7.2
- Consultant case review
- Transfer of imaging
- Advice, retrieval then transfer then ongoing management
What are the inclusion criteria for ECMO?
- Severe resp failure
- non cardiac cause i.e Murray score >3
- Where positive pressure ventilation is not appropriate e.g. significant tracheal injury
What are the exclusion criteria for ECMO? (who won’t get it)
- Contraindication to continuation of active treatment
- Significant comorbidity that would lead to dependency to ECMO support with no good chance of recovery
- Significant life limiting comorbidity
How is ECMO done?
- Patient gets a cannular put into femoral vein through groin and it goes into IVC below right atrium OR jugular vein and down into right atrium
- Blood is drawn and taken through tubing through a pump and runs across artificial membrane which flows gas over the membrane that allows for removal of CO2 and input of O2
- Oxygenated blood passes back into patient
What are the issues with ECMO?
- Time to access
- Referral system- geographical inequity
- Consideration of referral- doctors may not know what ECMO is
- High cost
- Invasive
- Circuits and haemodynamics need a perfusionist
- Clotting/bleeding
