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Cardiorespiratory 2 > Respiratory Failure > Flashcards

Respiratory Failure Flashcards

1
Q

What is respiratory failure?

A

Syndrome of inadequate gas exchange due to dysfunction of one or more components of the respiratory system

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2
Q

What can dysfunction during respiratory failure?

A

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

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3
Q

Describe the epidemiology of chronic RDS

A

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

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4
Q

Describe the Berlin definition of ARDS

A
  1. Timing - within a week of a known clinical insult or new or worsening respiratory symptoms
  2. Chest imaging - if bilateral opacities seen which are not explained by effusion/lobar or lung collapse/nodules
  3. Origin of oedema - not fully explained by cardiac failure or fluid overload. If no risk factor, ECG needed to cross out hydrostatic oedema.
  4. Oxygenation - determines if mild, moderate or severe
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5
Q

What causes lead to acute respiratory distress syndrome?

A

Pulmonary: Infection, aspiration, Primary graft dysfunction (Lung Tx)
Extra-pulmonary: Trauma, pancreatitis, sepsis,
Neuro-muscular: Myasthenia/GBS

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6
Q

What causes lead to chronic respiratory distress syndrome?

A

Pulmonary/Airways: COPD, Lung fibrosis, CF, lobectomy

Musculoskeletal: Muscular dystrophy

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7
Q

What causes lead to acute on chronic RDS?

A

Infective exacerbation
COPD, CF
Myasthenic crises
Post operative

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8
Q

What is type 1 respiratory distress syndrome?

A

Hypoxemia due to failure of oxygen exchange. Characterised by: Increased shunt fraction (QS/QT), Due to alveolar flooding, Hypoxemia refractory to supplemental oxygen

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9
Q

What can cause type 1 respiratory distress syndrome?

A

Collapse, Aspiration (gastric contents), Pulmonary oedema, Fibrosis, Pulmonary embolism, Pulmonary hypertension

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10
Q

What is type 2 respiratory distress syndrome?

A

Hypercapnia due to failure to exchange or remove carbon dioxide. Characterised by: Decreased alveolar minute ventilation (V A ), Dead space ventilation

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11
Q

What can cause type 2 respiratory distress syndrome?

A

Lack of nervous system involvement, neuromuscular causes, muscle failure, airway obstruction or chest wall deformation.

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12
Q

What is type 3 respiratory distress syndrome?

A

Perioperative respiratory failure. Increased atelectasis due to low functional residual capacity (FRC) with abnormal abdominal wall mechanics. Hypoxaemia or hypercapnoea can occur.

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13
Q

How can type 3 respiratory distress syndrome be prevented?

A

Anesthetic or operative technique, posture,

incentive spirometry, analgesia, attempts to lower intra- abdominal pressure

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14
Q

What is type 4 respiratory distress syndrome?

A

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)

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15
Q

What are risk factors for chronic respiratory distress syndrome?

A 
COPD
Pollution
Recurrent pneumonia
Cystic fibrosis
Pulmonary fibrosis
Neuro-muscular diseases
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16
Q

What are risk factors for acute respiratory distress syndrome?

A 
Infection - Viral, Bacterial
Aspiration
Trauma
Pancreatitis
Transfusion
17
Q

How is history for acute respiratory failure assessed?

A

Origin of shortness of breath can be:

  1. Lower respiratory tract infection - viral/bacterial
  2. Aspiration
  3. Trauma
  4. Pulmonary vascular disease - pulmonary embolus, haemoptysis
  5. Extrapulmonary: pancreatitis, new medications

PATEL

18
Q

Describe how acute lung injury leads to ARDS

A
  1. Injury leads to damage of the interstitium
  2. Macrophages are activated by an infection/inflammation, release cytokines (IL-6,8 and TNF-alpha).
  3. 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.
  4. Migration of leucocytes into interstitium occurs where they cause a degree of damage before reaching site of interest.
  5. 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.
19
Q

What is in vivo evidence of respiratory distress syndrome?

A
  1. TNF signalling implicated in vivo and in vitro
  2. Leucocyte activation and migration - alveolar macrophage activation and neutrophil lung migration
  3. DAMP release: HMGB-1 and RAGE
  4. Cytokine release IL-6,8,IL-1B, IFN-y
  5. Cell death - necrosis and apoptotic mediators: FAS, FAS-l, BCl-2
20
Q

What pharmacological interventions are available?

A

Steroids, salbutamol. surfactant, N-Acetylcysteine, Neutrophil esterase inhibtitor, GM-CSF, Statins

21
Q

What pharmacological interventions are being trialled?

A

Mesenchymal stem cells, keratinocyte growth factor, microvesicles, (High dose Vitamin C, thiamine, steroids), ECCO2R (Echo-corporeal removal of CO2)

22
Q

What biological processes underlie ARDS?

A

Pulmonary vascular endothelial inflammatory response seen – as cause known to be COVID, cases comparable. Angiogenesis also observed. Radiological evidence of poor perfusion also noted.

23
Q

What is IL-18?

A

IL-18 is a necro-inflammatory mediator constitutively expressed in the airway

24
Q

What is IL-18’s role?

A

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.

25
Q

What treatments are provided to treat underlying disease?

A

Inhaled therapies - Bronchodilators, Pulmonary vasodilators
Steroids
Antibiotics
Anti-virals
Drugs - Pyridostigmine, Plasma exchange, IViG, Rituximab

26
Q

What respiratory support is provided in ARDS?

A 
Physiotherapy
Oxygen
Nebulisers
High flow oxygen
Non invasive ventilation
Mechanical ventilation
Extra-corporeal support
27
Q

What multiple organ support is offered during ARDS?

A

Cardiovascular support - Fluids, Vasopressors, Inotropes, Pulmonary vasodilators
Renal support - Haemofiltration, Haemodialysis
Immune therapies - Plasma exchange, Convalescent plasma

28
Q

Describe sequelae of ARDS

A

Poor gas exchange -> Inadequate oxygenation, Poor perfusion, Hypercapnoea
Infection - Sepsis
Inflammation - Inflammatory response
Systemic effects

29
Q

What types of ventilation is offered for ARDS?

A

Volume controlled
Pressure controlled
Assisted breathing modes
Advanced ventilatory modes

30
Q

Describe 3 important points on a flow-volume loop

A

Compliance - markedly reduced in injured lung as compared to normal lung
Upper inflection point - Above this pressure, additional alveolar recruitment requires disproportionate increases in applied airway pressure
Lower inflection point - Can be thought of as minimal baseline pressure (PEEP) needed for optimal alveolar requirement.

31
Q

What imaging techniques are used?

A

CT and ultrasound

32
Q

What guides escalation?

A 
Murray score calculated - takes PaO2/FlO2, CXR, PEEP, Compliance
0 = normal
1-2.5 Mild
2.5 Severe
3  ECMO
33
Q

Describe the National ARDS approach

A

There are 5 national centres

  1. If Murray score >3, or pH<7.2, telephone/online referral
  2. Consultant case review occurs
  3. Transfer of imaging
  4. Advice
  5. Retrieval
  6. Transfer
  7. Ongoing management

Cardiorespiratory 2 (13 decks)

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