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1B Cardiorespiratory > 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 systems can respiratory failure act on?

A
  1. nervous system
    1. CNS/Brainstem
    2. peripheral nervous system
    3. neuro-muscular junction
  2. respiratory muscle
    1. diaphragm and thoracic muscle
    2. extra-thoracic muscles
  3. pulmonary
    1. airway disease
    2. alveolar- capillary circulation
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3
Q

what are the risk factors for respiratory failure?

A

males: smoking biggest risk factor
women: household air pollution from solid fuels

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4
Q

how is ARDS classified?

A

4 criteria used to classify ARDS

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5
Q

what is the trend with Acute respiratory distress syndrome over time?

A

increased severity with age

increased mortality

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6
Q

what is the classification of ARDS physiologically?

A
  1. type I or hypoxemic
  2. type II or hypercapnic
  3. type III
  4. type IV
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7
Q

what occurs in type 1 respiratory failure?

A
  1. PaO2<60 at sea level
  2. Failure of oxygen exchange
  3. Increase shunt fraction
  4. Frequently Due to alveolar flooding
  5. Hypoxemia refractory to supplemental oxygen
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8
Q

what happens in type II respiratory failure?

A
  1. PaCO2>45
  2. Failure to exchange or remove CO2
  3. Decreased alveolar minute ventilation
  4. Dead space ventilation
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9
Q

what happens in type III respiratory failure?

A
  1. Perioperative respiratory failure
  2. Increased atelectasis due to low functional residual capacity (FRC) with abnormal abdominal wall mechanics
  3. Hypoxaemia or hypercapnoea
  4. Prevention: anesthetic or operative technique, posture, incentive spirometry, analgesia, attempts to lower intra- abdominal pressure
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10
Q

what happens in type IV respiratory failure?

A
  1. Shock
  2. Type IV describes patients who are intubated and ventilated during shock (Septic/cardiogenic/neurologic)
  3. Optimise ventilation improve gas exchange and to unload the respiratory muscles, lowering their oxygen consumption
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11
Q

what are the ventilatory effects of respiratory failure?

A

reduced afterload (good for LV)

increased pre-load (bad for RV)

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12
Q

what are the chronic risk factors for respiratory failure?

A

COPD

pollution

recurrent pneumonia

cystic fibrosis

pulmonary fibrosis

neuro-muscular diseases

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13
Q

what are the acute risk factors for respiratory failure?

A

infection (viral and bacterial)

aspiration

trauma

pancreatitis

transfusion

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14
Q

how do pulmonary causes cause ARF?

A
  • aspiration
  • trauma
  • burns: inhilation
  • surgery
  • drug toxicicity
  • infection

affect alveolus and airways to alveolus

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15
Q

how do extra-pulmonary causes cause ARDS?

A
  • trauma
  • pancreatitis
  • burns
  • transfusion
  • surgery
  • BM transplant
  • drug toxicity
  • infection

systemic disease causing cytokine release and activation of neutrophils/macrophages in vascular supply

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16
Q

what is the mechanism of acute lung injury?

A
  1. inflammation:
    • Release further cytokines
      • IL6, IL8
      • TNF-alpha and IL8
      • Causes alveolar fluid build-up/ protein rich oedema in lung`
      • Cause degradation or inactivation of surfactant so alveolus less efficient as expanding
  2. Immune response
    • Tracheal migration of leukocytes ( neutrophils) into interstitium causing damage before getting to site of response due to chemokines
    • Secrete proteases and inflammatory mediators -> fluid build up + damage
  3. Increased distance between alveolus and capillary due to leukocytes and odema
    • Greater distance for gas exchange -> less efficient
17
Q

what is the leukocyte response and inflammatory response in acute lung injury govered by?

A

infection

systemic (bacteraemia)

directly in airways or higher up in airways

18
Q

what overall concepts is acute lung injury response governed by?

A

infection

inflammation

immune response

the interplay between these 3

19
Q

what is the in vivo evidence of the infection, inflammation, and immune response in respiratory failure?

A
  • TNF signalling implicated in vivo and in vitro
    • Reduced injury in TNFR-1
  • Leucocyte activation and migration
    • Macrophage activation: alveolar
    • Neutrophil lung migration
  • DAMP release
    • HMGB-1 and rage
  • Cytokine release
    • IL-6, 8
    • IL-1B
    • IFN-gamma
  • Cell death
    • Necrosis in lung biopsies
    • Apoptotic mediators
      • FAS, FAS-Ligand, BCI-1
20
Q

what are the 3 aspects to be treated in ARDS?

A

treat underlying disease

respiratory support

multiple organ support

21
Q

what are the therapeutic interventions to treat underlying disease?

A
  • inhaled therapies
    • bronchodilators
    • pulmonary vasodilators
  • steroids
  • antibiotics
  • anti-virals
  • drugs
    • pyridostigmine
    • plasma exchange
    • IViG
    • rituximab
22
Q

what are the therapeutic interventions for respiratory support?

A

physiotherapy

oxygen

nebulizers

high flow oxygen

non-invasive ventilation

mechanical ventilation

extra-corporeal support

23
Q

what are the therapeutic interventions for multiple organ support

A
  • cardiovascular support
    • fluids
    • vasopressors
    • inotropes
    • pulmonary vasodilators
  • renal support
    • haemofiltration
    • hemodynamics
  • immune therapies
    • plasma exchange
    • convalescent plasma
24
Q

what are the consequences of ARDS?

A
  • Poor gas exchange
    • Inadequate oxygenation
    • Poor perfusion
    • Hypercapnoea
  • Infection
    • Sepsis
  • Inflammation
    • Inflammatory response
  • Systemic effects
25
Q

what are the ARDS specific intervention?

A
  • Respiratory support
  • Intubation and ventilation
  • ARDS necessitates mechanical intervention
  • Types of ventilation
    • Volume controlled
    • Pressure controlled
    • Assisted breathing modes
    • Advanced ventilatory modes
  • Procedures to support ventilation -> pronation
26
Q

what is the normal pressure-volume loop and how is it affected by ARDS?

A
27
Q

what are the pitfalls of ventilation in asthma and COPD?

A
  • In asthma and COPD there can be air trapping (not full air exhalation)
  • This can cause an increased pressure
  • Causing ventilator induce lung injury
  • Harder to manage CO2 and minute ventilation and causes V/Q mismatch as ventilation without gas exchange vice- versa
28
Q

how can you determine the ventilation levels?

A

imaging and guiding therapy

  • Lung recruitment: CT
    • Determine pressure to put ventilation at as shows alveolar recruitment at different pressure levels
  • Lung ultrasound
    • Evaluate how well expanded someone’s lung is and any fluid that is present
29
Q

what is used the guide the escalation of therapy?

A
  • Uses Murray score
    • Measures PF ratio
    • Chest X-Ray
    • PEEP
    • Lung compliance
    • Score >3 -> ECMO or pH <7.2
30
Q

what are the ECMO inclusion criteria?

A
  • Severe respiratory failure
    • Non cardiac cause (Murray lung injury score 3.0 or above)
  • Positive pressure ventilation is not appropriate
    • E.g significant tracheal injury
31
Q

what are the ECMO exclusion criteria?

A
  • Contraindication to continuation of active treatment
    • Significant co-morbidity -> dependent to ECMO support
    • Significant life limiting to co morbidity
32
Q

overall what does ECMO treatment require?

A
  1. Reversible disease process
  2. Unlikely to lead to prolonged disability
33
Q

how does ECMO work?

A
  • Pass canula in IVC below right atrium
    • Canula can be placed through internal jugular, subclavian, femoral
  • Withdraw blood into pump and through artificial membrane
  • This causes removal CO2 and oxygenation
  • Blood passes back into RA
34
Q

what are the issues with ECMO?

A
  1. Time to access
  2. Referral system- geographical inequity
  3. Consideration of referral
  4. Technical
    1. Obtaining access
    2. Haemodynamics
    3. Clotting/bleeding
  5. Costs
35
Q

what are the benefits of ECMO?

A
  1. Increased survival
    1. Improve oxygen delivery
    2. Improve CO2 removal
    3. Rest ling and prevent ventilator-associated lung injury
    4. Resolve respiratory acidosis
    5. Reduce multiple organ dysfunction arising from hypoxaemia and hypercarbia

1B Cardiorespiratory (15 decks)

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