Respiratory Failure Flashcards
(33 cards)
What is respiratory failure?
Syndrome of inadequate gas exchange due to dysfunction of one or more components of the respiratory system
What can dysfunction during respiratory failure?
Nervous system: CNS/Brainstem, PNS and neuromuscular junction
Respiratory muscle: Diaphragm and thoracic muscles as well as extra-thoracic muscle
Pulmonary: Airway disease, alveolar-capillary, circulation
Describe the epidemiology of chronic RDS
Chronic respiratory disease 3rd leading cause of death* (2017) 39.8% rise from 1990
Males: Smoking biggest risk factor
Women: Household air pollution from solid fuels
Costs: EU 380m Euro’s annually (2019) care for chronic respiratory disorders
Accounts for: Inpatient care, lost productivity
Despite extensive costs: limited granular data
Describe the Berlin definition of ARDS
- Timing - within a week of a known clinical insult or new or worsening respiratory symptoms
- Chest imaging - if bilateral opacities seen which are not explained by effusion/lobar or lung collapse/nodules
- Origin of oedema - not fully explained by cardiac failure or fluid overload. If no risk factor, ECG needed to cross out hydrostatic oedema.
- Oxygenation - determines if mild, moderate or severe
What causes lead to acute respiratory distress syndrome?
Pulmonary: Infection, aspiration, Primary graft dysfunction (Lung Tx)
Extra-pulmonary: Trauma, pancreatitis, sepsis,
Neuro-muscular: Myasthenia/GBS
What causes lead to chronic respiratory distress syndrome?
Pulmonary/Airways: COPD, Lung fibrosis, CF, lobectomy
Musculoskeletal: Muscular dystrophy
What causes lead to acute on chronic RDS?
Infective exacerbation
COPD, CF
Myasthenic crises
Post operative
What is type 1 respiratory distress syndrome?
Hypoxemia due to failure of oxygen exchange. Characterised by: Increased shunt fraction (QS/QT), Due to alveolar flooding, Hypoxemia refractory to supplemental oxygen
What can cause type 1 respiratory distress syndrome?
Collapse, Aspiration (gastric contents), Pulmonary oedema, Fibrosis, Pulmonary embolism, Pulmonary hypertension
What is type 2 respiratory distress syndrome?
Hypercapnia due to failure to exchange or remove carbon dioxide. Characterised by: Decreased alveolar minute ventilation (V A ), Dead space ventilation
What can cause type 2 respiratory distress syndrome?
Lack of nervous system involvement, neuromuscular causes, muscle failure, airway obstruction or chest wall deformation.
What is type 3 respiratory distress syndrome?
Perioperative respiratory failure. Increased atelectasis due to low functional residual capacity (FRC) with abnormal abdominal wall mechanics. Hypoxaemia or hypercapnoea can occur.
How can type 3 respiratory distress syndrome be prevented?
Anesthetic or operative technique, posture,
incentive spirometry, analgesia, attempts to lower intra- abdominal pressure
What is type 4 respiratory distress syndrome?
Describes patients who are intubated and ventilated. Occurs during shock (Septic/cardiogenic/neurologic). Treated by optimising ventilation to improve gas exchange and to unload the respiratory muscles, lowering their oxygen consumption. However, ventilatory effects on left and right of heart are different - Reduced afterload (good for LV) Increased pre-load (bad for RV)
What are risk factors for chronic respiratory distress syndrome?
COPD Pollution Recurrent pneumonia Cystic fibrosis Pulmonary fibrosis Neuro-muscular diseases
What are risk factors for acute respiratory distress syndrome?
Infection - Viral, Bacterial Aspiration Trauma Pancreatitis Transfusion
How is history for acute respiratory failure assessed?
Origin of shortness of breath can be:
- Lower respiratory tract infection - viral/bacterial
- Aspiration
- Trauma
- Pulmonary vascular disease - pulmonary embolus, haemoptysis
- Extrapulmonary: pancreatitis, new medications
PATEL
Describe how acute lung injury leads to ARDS
- Injury leads to damage of the interstitium
- Macrophages are activated by an infection/inflammation, release cytokines (IL-6,8 and TNF-alpha).
- In response to this inflammatory state, get a fluid build-up/protein-rich oedema forming within the alveolus. Degardation of surfactant can occur making alveolus less efficient at expanding.
- Migration of leucocytes into interstitium occurs where they cause a degree of damage before reaching site of interest.
- Therefore, damage and fluid build-up occurs in all these tissues increasing the distance between the alveolus and the capillary, making gas exchange more difficult.
What is in vivo evidence of respiratory distress syndrome?
- TNF signalling implicated in vivo and in vitro
- Leucocyte activation and migration - alveolar macrophage activation and neutrophil lung migration
- DAMP release: HMGB-1 and RAGE
- Cytokine release IL-6,8,IL-1B, IFN-y
- Cell death - necrosis and apoptotic mediators: FAS, FAS-l, BCl-2
What pharmacological interventions are available?
Steroids, salbutamol. surfactant, N-Acetylcysteine, Neutrophil esterase inhibtitor, GM-CSF, Statins
What pharmacological interventions are being trialled?
Mesenchymal stem cells, keratinocyte growth factor, microvesicles, (High dose Vitamin C, thiamine, steroids), ECCO2R (Echo-corporeal removal of CO2)
What biological processes underlie ARDS?
Pulmonary vascular endothelial inflammatory response seen – as cause known to be COVID, cases comparable. Angiogenesis also observed. Radiological evidence of poor perfusion also noted.
What is IL-18?
IL-18 is a necro-inflammatory mediator constitutively expressed in the airway
What is IL-18’s role?
Circulating IL-18 is increased in COVID ARDS, hyper-inflammatory and ECMO ARDS cohorts.
1. Initiates pro-inflammatory NF-kB signalling, and is pivotal to T cell differentiation and IFN-γ production.
2. Induces airway hyperresponsiveness and macrophage activation, common features associated to ARDS.
3. IL-18 and IFN-γ are enhanced in COVID and non-COVID ECMO cohorts, in keeping with viral infection.
4 The IFN-γ response is protective in early defence against IAV & SARS but prolongs damaging IFN-γ cytokine responses and diminished antibacterial protection.
