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 failing parts of the nervous system that can cause respiratory failure?

A

1- The Nervous system- Central nervous system through disordered consciousness, peripheral nervous system e.g. the outflow of the cervical spinal cord, NMJ- e.g., Myasthenia gravis
2- The respiratory muscles- Injured or splinted, or weak
3- Pulmonary
The conducting airways and the tissue of the lung- Reactive airways disease, inspissation with secretions, pulmonary oedema, PEs

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3
Q

What are the failing respiratory muscles which can cause respiratory failure?

A
  • Diaphragm & thoracic muscles
  • Extra-thoracic muscles
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4
Q

What are the failing parts of the pulmonary system which can cause respiratory failure?

A
  • airway disease
  • alevolar-capillary
  • circulation
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5
Q

How has the epidemiology of chronic respiratory failure changed since the 1990s?

A

More prevelant, rise in 40%
Disproportionate effect on women across Russia and North America which has not improved

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6
Q

What is the biggest risk factor of chronic respiratory failure for men?

A

smoking

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7
Q

What is the biggest risk factor of chronic respiratory failure for women?

A

household air pollution from solid fuels

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8
Q

What is the prevalence of acute respiratory failure?

A
  • 6-700 people/year
  • 30-40% mortality
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9
Q

What are the risk factors for chronic respiratory failure?

A
  • COPD
  • Pollution
  • Recurrent pneumonia
  • Cystic fibrosis
  • Pulmonary fibrosis
  • Neuro-muscular diseases
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10
Q

What are the risk factors for acute respiratory failure?

A
  • viral or bacterial infection
  • aspiration
  • trauma
  • pancreatitis
  • transfusion
    -aspiratioon
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11
Q

What factors can increase the mortality of acute respiratory failure?

A
  • severity
  • age
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12
Q

Which dieseases can be classified as acute respiratory failure?

A
  • infection
  • aspiration
  • primary graft dysfunction
  • trauma
  • pancreatitis
  • sepsis
  • myasthenia/GBS
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13
Q

What possible diseases are classed as chronic respiratory failure?

A
  • COPD
  • Lung fibrosis
  • CF
  • lobectomy
  • muscular dystrophy
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14
Q

What are examples of acute on chronic respiratory failure?

A
  • Infective exacerbation (COPD, CF)
  • Myasthenic crises
  • Post-operative complications
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15
Q

Which area of the lung has greater ventilation and why?

A
  • bottom of lung
  • smaller transmural pressure
  • alveoli are smaller and more compliant
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16
Q

Which part of the lung has greater perfusion and why?

A
  • bottom of lung
  • higher intravascular pressure
  • more recruitment and less resistance
  • higher flow rate
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17
Q

Where will the bulk of gas exchange occur in the lungs?

A

Middle and bottom

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18
Q

What is compliance?

A

The tendency to distort under pressure

Compliance is the volume per unit pressure- ease of stretching

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19
Q

Describe the pressure in each zone in ventilation perfusion matching

A

Zone 1- Alveolar pressure is higher than arterial and venous
2- arterial pressure is higher than alveolar and venous
3- arterial and venous are higher than alveolar

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20
Q

What is elastance?

A

The tendency to recoil to its original volume

Elastance is the amount of pressure required to distend by a volume- resistance to being stretched
-The elastic recoil of the chest and lung tissue

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21
Q

What are the equations for minute ventilation and alveolar ventilation?

A

Minute ventilation is gas entering and leaving the lungs
tidal volume x breathing frequency

Alveolar ventilation is gas entering and leaving the alveoli
(tidal volume - dead space) x breathing frequency

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22
Q

What happens in type 1 (hypoxemic) respiratory failure?

A
PaO2 < 60
failure of oxygen exchange
- increased shunt fraction (QS/QT)
- due to alveolar flooding
- refractory to supplemental oxygen
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23
Q

What can cause type 1 respiratory failure?

A
  • collapse
  • aspiration
  • pulmonary oedema
  • fibrosis
  • pulmonary embolism
  • pulmonary hypertension
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24
Q

What happens in type 2 (hypercapnic) respiratory failure?

A

PaCO2 > 45
failure to exchange or remove carbon dioxide
- decreased alveolar minute ventilation
- dead space ventilation

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25
Q

What can cause type 2 respiratory failure?

A
  • CNS/PNS
  • muscle failure
  • airway obstruction
  • chest wall deformities
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26
Q

What happens in type 3 (perioperative) respiratory failure?

A
  • increased atelectasis (airway collapse) due to low functional residual capacity
  • abnormal abdominal wall mechanics (limiting chest movement)
  • hypoxaemia OR hypercapnia
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27
Q

How do you prevent type 3 respiratory failure?

A
  • anethetic or operative technique
  • posture
  • incentive spirometry
  • analgesia
  • efforts to lower intra-abdominal pressure
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28
Q

What happens in type 4 (shock) respiratory failure?

A

poor lung perfusion in patients that are intubated and ventilated during shock (septic, cardiogenic, nuerologic)

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29
Q

How do you prevent type 4 respiratory failure?

A

optimise ventilation to improve gas exchange and to unload the respiratory muscles, lowering oxygen consumption

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30
Q

What are the effects of ventilation on the heart?

A
reduced afterload (good for the LV)
increased preload (bad for the RV)
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31
Q

What are the 5 main origins of shortness of breath?

A
  • lower respiratory tract infections viral or bacterial
  • aspiration
  • trauma transfusion
  • pulmonary vascular disease
  • extrapulmonary: pancreatitis; new medications
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32
Q

What form of pulmonary vascular disease can cause shortness of breath?

A
  • pulmonary embolus
  • haemoptysis
33
Q

What is ARDS?

A

Acute respiratory distress syndrome

34
Q

What are the pulmonary causes of ARDS?

A

Pulmonary causes insult within the lung- most commonly infection triggering secondary responses which may impact other organ systems- aspiration
- trauma
- burns (inhalation)
- surgery
- drug toxicity
- infection

35
Q

What are the extra-pulmonary causes of ARDS?

A

Extra-pulmonary causes predominantly considered to be a secondary host response.
- trauma
- pancreatitis
- burns
- transfusion
- surgery
- BM transplant
- drug toxicity

36
Q

what do the pulmonary causes of ARDS tend to effect?

A

The alveoli

37
Q

what do the extra-pulmonary causes of ARDS tend to effect?

A
  • systemic
  • cytokine release
38
Q

How does acute lung injury happen?

A

Within the lung infection will lead to macrophage and neutrophil activation, triggering release of cytokines such as TNF and IL-6, IL-8 for example.

These result in activation of a cascade of inflammatory responses which are key to resolution of lung injury but may often become disruptive.

In additional to the biological consequences at the receptor level, these responses drive inflammation and alveolar fluid leak across the endothelium.

As the endothelium becomes oedematous this secondarily impairs gas exchange.

39
Q

Describe the link between inflammation and pulmonary transit time

A

As the alveolar-capillary units become damaged and leaky, the distance for gas exchange increases, thereby reducing efficiency of gas exchange.

Leading to reduced availability of oxygen globally and within the injured lung.
This may further exacerbate the inflammatory response

40
Q

What DAMP and cytokines are relased?

A

DAMP release: HMGB-1 and RAGE
Cytokine release IL-6,8,IL-1B, IFN-y

41
Q

What are apoptotic mediators of cell death?

A

FAS, FAS-l, BCl-2

42
Q

What forms of pharmacological interventions have been tried for ARDS?

A
  • steroids
  • salbutamol
  • surfactant (children)
  • N-Acetylcysteine
  • Nuetrophil esterase inhibitor
  • GM-CSF
  • Statins
43
Q

What forms of pharmacological interventions are being trialled for ARDS?

A
  • Mesenchymal stem cells
  • keratinocyte growth factor
  • microvesicles
  • high dose vitamin C, thiamine and steroids
  • ECCO2R
44
Q

Why is there limited evidence for treatment for ARDS?

A

because the disease is so heterogenous

45
Q

What is the key to treating ARDS?

A

that identification of the driving biological mechanism is key

46
Q

What are the three key aspects when managing ARDS?

A
  • treat the underlying disease
  • respiratory support
  • multiple organ support
47
Q

What options are available to treat the underlying cause?

A
  • inhaled therapies
    brochilators, pulmonary vasodilators
  • steroids
  • antibiotics
  • anti-virals (got cold/during flu season)
  • drugs
    pyridostigmine, plasma exchange, IViG, rituximab
48
Q

What forms of respiratory support is available for those with ARDS?

A
  • physiotherapy
  • oxygen
  • nebulisers (salbutamol, saline)
  • high flow oxygen
  • non-invasive ventilation
  • mechanical ventilation
  • extra-corporeal support (ECMO)
49
Q

What forms of cardiovascular support is available for those with ARDS?

A
  • fluids
  • vasopressers
  • inotropes
  • pulmonary vasodilators (NO)
50
Q

What forms of renal support is available for those with ARDS?

A
  • haemofiltration
  • haemodialysis
51
Q

What forms of immune support is available for those with ARDS?

A
  • plasma exchange
  • convalescent plasma
52
Q

What are the consequences of ARDS?

A
  • poor gas exchange
  • inadequate oxygenation/poor perfusion
  • hypercapnoea
  • sepsis (sick with underlying infection)
  • inflammation
  • systemic effects
53
Q

What are the types of ventilation?

A
  • volume-controlled
  • pressure-controlled (most common)
  • assisted breathing modes
  • advanced ventilatory modes
54
Q

What respiratory support is necessary with ARDS?

A

mechanical intervention (ventilation)

55
Q

What are is the change in compliance with ARDS?

A
  • reduced in the injured lung
  • reaches peak volume slower, and peak volume is lower than that of a normal lung
  • takes longer to accept changes in the volume and pressure
56
Q

What is the significance of the the upper inflection point with ARDS?

A

above that pressure, additional alveolar recruitment requires disproportionate increases in applied airway pressure

57
Q

What is the significance of the the lower inflection point with ARDS?

A

the minimum baseline pressure (PEEP) needed for optimal alveolar recruitment

58
Q

What are the negatives of ventilation?

A
  • PaCO2 control is difficult (Type II or high chest volume)
  • Positive end expiratory pressure due to poor emptying of the lung
  • V/Q mismatch
    ventilation w/o gas exchange
  • ventilator induced lung injury (reduced by decreasing driving pressure)
59
Q

What happens in a lung recruitment CT?

A
  • high pressure ventilator
  • low driving pressure
  • aim: open up the lung
60
Q

What does it mean when consolidation reduces during a lung recruitment CT?

A

there are recruitable alveoli present

61
Q

What is the risk of over distending the lung in a lung recruitment CT?

A
  • traps more gas
  • reduces perfusion
  • limit right ventricular function
  • damage via trauma
62
Q

What is ECMO?

A
  • extracorporeal membrane oxygenation
  • pumps and oxygenates a patient’s blood outside the body, allowing the heart and lungs to rest
63
Q

What are the guidelines used when trying to escalate treatment?

A

Murray score

  • PaO2
  • CXR
  • PEEP
  • Compliance
64
Q

What are the classifications of the Murray score?

A
0 = normal
1-2.5 = mild
>2.5 = severe
>3 = ECMO
65
Q

Where can ECMO occur?

A

5 national centres

66
Q

What can be done to reduce the Murray score?

A
  • proning

-

67
Q

What is the national ARDS approach?

A
  • telephone/online referral
  • consultant case review
  • imaging transfer
  • advice
  • retrieval
  • transfer
  • ongoing management
68
Q

What is the inclusion criteria for ECMO?

A
  • severe respiratory failure
  • non-cardiac cause (Murray score 3+)
  • positive pressure ventilation is not appropriate
69
Q

When may positive pressure ventilation not be appropriate?

A

eg: significant tracheal injury

70
Q

What is the exclusion criteria for ECMO?

A
  • contraindication to continuing treatment
  • significant co-morbidity (dependency to ECMO support)
  • significant life limiting co-morbidity
71
Q

What is the general requirement for ECMO?

A
  • reversible disease process
  • unlikely to lead to prolonged disability
72
Q

What happens in ECMO?

A
  • cannula from groin into the IVC
  • draw blood through a pump and artificial membrane
  • gas flow through oxygenator above allows for CO2 removal and supplementation of oxygen
  • re-enters via jugular vein/femoral vein into the right atrium
73
Q

What are the issues with ECMO?

A
  • time to access
  • referral system: geographical inequity
  • awareness of ECMO
  • obtaining access: (internal jugular, subclavian, femoral)
  • circuit
  • haemodynamics
  • clotting/bleeding (required)
  • expensive
  • infection of the cannula
  • epistaxis
  • haemolysis
  • haemoptysis
74
Q

Which criteria is used to classify ARDS?

A
  • timing
  • chest imaging
  • oedema origin
  • PF ratio
75
Q

What are the common causes to acute respiratory failure?

A
  • LRT infection
  • aspiration
  • trauma
  • pancreatitis
  • pulmonary vascular disease
  • TRALI
  • PE
76
Q

What are the 3 mechanisms of acute lung injury?

A
  • inflammation
  • infection
  • immune response
77
Q

What 2 imaging options are available for diagnosis and treatment of ARDS?

A
  • recruitment lung CT
  • lung USS
78
Q

What are the advantages of using ECMO?

A
  • improve oxygen delivery
  • improve carbon dioxide removal
  • rest lung
  • prevent ventilator associated lung injury
  • resolve respiratory acidosis
  • reduce multiple organ dysfunction arising from hypoxaemia and hypercapnoea