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 parts of the nervous system are in the respiratory system?

A
  • CNS/Brainstem
  • Peripheral nervous system
  • Neuro-muscular junction (e.g. myasthenia gravis)
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3
Q

What parts of the respiratory muscle are in the respiratory system?

A

•Diaphragm & thoracic muscles
•Extra-thoracic muscles
e.g. msucular underlying disease

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4
Q

What parts of the pulmonary are in the respiratory system?

A
  • Airway disease
  • Alveolar-capillary e.g. fibrosis or vascular disease
  • Circulation e.g. pulmonary hypertension
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5
Q

Why is chronic respiratory disease important?

A

Chronic respiratory disease 3rd leading cause of death* (2017) 39.8% rise from 1990

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6
Q

What is the biggest risk factor for males and females for chronic respiratory disease?

A
  • Males: Smoking biggest risk factor

- Women: Household air pollution from solid fuels

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7
Q

How expensive is it to treat chronic respiratory disease?

A
  • 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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8
Q

How has chronic respiratory disease change from 1990 to 2017?

A

From 1990 to 2017, the prevalence, mortality, and DALY rates per 100k dropped by 14·3%, 42·6%, and 38·2%,

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9
Q

Why is acute respiratory disease hard to monitor?

A
  • Present in different ways and different times
  • Heterogenous disease, down to pneumonia or COPD or cystic fibrosis or pulmonary hypertension
  • So look at acute respiratory distress syndrome (ARDS)
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10
Q

How common is ARDS?

A

-Prevalence: 6-7 per 100,000 = 6-700 people/yr in UK
-30 to 40% Mortality (ALIEN/Esteban)
35, 40 and 46% (Severity dependent. Bellani)
-Severity and advance age
-> increase mortality

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11
Q

How do you classify ARDS?

A
  1. Timing
  2. Chest imaging
  3. Origin of oedema
  4. Oxygenation / PF ratio
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12
Q

What is needed to classify acute?

A
  1. Pulmonary: Infection, aspiration, Primary graft dysfunction (Lung Tx)
  2. Extra-pulmonary: Trauma, pancreatitis, sepsis,
    - Neuro-muscular: Myasthenia/GBS
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13
Q

What is needed to classify chronic?

A
  1. Pulmonary/Airways: COPD, Lung fibrosis, CF, lobectomy

2. Musculoskeletal: Muscular dystrophy

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14
Q

What is needed to classify acute and chronic?

A
  1. Infective exacerbation: COPD, CF
  2. Myasthenic crises
    3 Post operative
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15
Q

What is Type 1 respiratory failure?

A
  1. Failure of oxygen exchange
  2. Increased shunt fraction (Q S /QT )
  3. Due to alveolar flooding (usually heart failure)
  4. Hypoxemia refractory to supplemental oxygen
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16
Q

What is another word for Type 1 respiratory failure?

A

Hypoxemic (PaO2 <60 at sea level)

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17
Q

Why might you have Type 1 respiratory failure?

A
  1. Collapse (of lobe)
  2. Aspiration
  3. Pulmonary oedema
  4. Fibrosis
  5. Pulmonary embolism
  6. Pulmonary hypertension
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18
Q

What is Type 2 respiratory failure?

A

-Failure to
exchange or remove carbon dioxide
-Decreased alveolar minute ventilation (V A )
-Dead space ventilation

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19
Q

What is another word for Type 2 respiratory failure?

A

Hypercapnic (PaCO2 >45)

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20
Q

Why might you have Type 2 respiratory failure?

A
  1. Nervous system disease
  2. Neuromuscular disease
  3. Muscle failure
  4. Airway obstruction e.g. COPD
  5. Chest wall deformity
    - Muscle weak so cannot drive adequate tidal volumes or respiratory rates as very tired or muscle fatigue or progressive weakness
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21
Q

What is type 3 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
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22
Q

How do you prevent type 3 respiratory failure?

A

Prevention:

  1. anesthetic or operative technique
  2. posture
  3. incentive spirometry
  4. analgesia
  5. attempts to lower intra- abdominal pressure
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23
Q

What is type 4 respiratory failure?

A
  • Shock
  • patients who are intubated and ventilated
  • During shock (Septic/cardiogenic/neurologic)
  • gas doesn’t meet blood, poor perfusion of lungs
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24
Q

How do you get positive pressure ventilation?

A

using ventilator

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25
Q

How does ventilation affect the heart?

A
  • Push air into chest get positive pressure
    1. Good for LV as reduces afterload so stress on heart muscle reduced, so work heart muscle has to do is reduced as pressure differential between LV and thorax is lower
    2. Bad for RV as increased pre-load
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26
Q

What are the chronic risk factors?

A
  • COPD
  • Pollution
  • Recurrent pneumonia
  • Cystic fibrosis
  • Pulmonary fibrosis
  • Neuro-muscular diseases
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27
Q

What are acute risk factors?

A
•Infection
-Viral
-Bacterial
•Aspiration
•Trauma
•Pancreatitis
•Transfusion
28
Q

What could be the origin of shortness of breath in acute respiratory failure?

A
  1. Lower respiratory tract infection
  2. Aspiration of gastric contents
  3. Trauma
  4. Pulmonary vascular disease
  5. Extra pulmonary: pancreatitis, new medications
29
Q

What could cause a lower respiratory tract infection?

A
  1. Viral

2. Bacterial

30
Q

What could result from trauma?

A

transfusion (if large volume loss)

31
Q

What could be a result from pulmonary vascular disease?

A
  1. Pulmonary embolus

2. Haemoptysis

32
Q

What are the pulmonary causes of ARDS?

A
  1. Aspiration
  2. Trauma
  3. Burns: inhalation/gas/ash
  4. Surgery
  5. Drug toxicity
    - Infection
33
Q

What are the extra-pulmonary causes of ARDS?

A
  1. Trauma
  2. Pancreatitis
  3. Burns: extrathoracic and acute inflammatory response
  4. Transfusion
  5. Surgery
  6. BM transplant
  7. Drug toxicity
    - Infection
34
Q

What do pulmonary causes affect?

A

alveolus or airway

35
Q

What do extra-pulmonary causes affect?

A

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

36
Q

What is the response in acute lung injury?

A
  1. Injury that leads of damage of the instutium
  2. Alveolar macrophages and type II pnemocytes
  3. When macrophages activated by infection will release cytokines TNF-alpha, IL-6, IL-8
  4. Alveolar fluid build up lead to inactivation or degradation surfactant so lung/alveolus less efficient at expanding
  5. When inflammation in alveolus often get tracking or migration of leukocytes out of blood vessels such as neutrophils squeezing though into the instituium
  6. can cause a degree of damage before they get to site of interest due to chemokines
  7. they secrete proteases or other inflammatory mediators which can cause damage and build up of fluid in some of tissues which then get more oedema so increase distance between alveolar and capillary so less efficient
37
Q

What are two ways looking to reduce alveolar lung injury?

A
  1. Block TNF-1 signalling pathway to reduce alveolar lung injury
  2. Block macrophage activation (alveolar) and neutrophil lung migration
38
Q

What is some of the ways to predict systemic damage?

A

-Looking at DAMPs (HMGB-1 and RAGE) to see how response
-Looking at cytokine release (IL-6,8 and IL1B and IFN-gamma)
-Different types of cell death
(Package up these (apoptosis) DAMPS and Cytokine so not induce these systemic effects to organs) compared to necrosis

39
Q

What are therapies tries in pharmacological interventions?

A
  1. Steroids
  2. Salbutamol
  3. Surfactant
  4. N-acetylcysteine
  5. Neutrophil esterase imhibitor
  6. GM-CSF
  7. Statins
40
Q

What are some trialling pharmacological interventions?

A
  1. Mesenchymal stem cellsL ex-vivo benefit
  2. Keratinocyte growth factor: repair factor
  3. Microvesicles
  4. High dose Vitamin C, thiamine, steroids… (may help for sepsis ut not really???)
  5. ECCO2R
41
Q

How can you treat underlying disease?

A
  1. Inhaled therapies
  2. Steroids
  3. Antibiotics
  4. Anti-virals
  5. Drugs
42
Q

What inhaled therapies are used to treat the underlying disease?

A
  • Bronchodilators

- Pulmonary vasodilators

43
Q

What drugs are used to treat the underlying disease?

A
  1. Pyridostigmine (underlying muscular disease)
  2. Plasma exchange
  3. IViG
  4. Rituximab
44
Q

What type of respiratory support is used?

A
  1. Physiotherapy
  2. Oxygen
  3. Nebulisers
  4. High flow oxygen
  5. Non-invasive ventilation
  6. Mechanical ventilation
  7. Extra-corporeal support
45
Q

What is some cardiovascular support?

A
  • Fluids
  • Vasopressors
  • Inotropes
  • Pulmonary vasodilators
46
Q

What is some renal support?

A
  • Haemofiltration

- Haemodialysis

47
Q

What are the immune therapies?

A
  • Plasma exchange

- Convalescent plasma

48
Q

What does poor gas exchange lead to?

A
  1. Inadequate oxygenation
  2. Poor perfusion
  3. Hypercapnoea
    - Lots of organs systemic effects
    - Infection: sepsis
    - Inflammation and inflammatory response
49
Q

What happens when you ventilate someone?

A
  • Use positive pressure and blow air into lungs
  • Set the volume
  • Set the pressure
  • aim 6ml/kg at tidal volume
  • turn up and down inspiratory pressure and positive end inspiratory pressure
  • Peak pressure: pressure that drives into the lung and underlying base pressure to keep airway open
  • Proning ca support ventiltion
50
Q

What are different types of ventilation?

A
  1. Volume controlled
  2. Pressure controlled
  3. Assisted breathing modes (patient drives pressure)
  4. Advanced ventilatory modes
51
Q

When can ventilation be hard to manage?

A

If COPD or normally high CO2 or barrel chest don’t completely exhale in normal life so on ventilation hard to manage as airways are constricted and tight and hard to get pressure right and push air into lung

52
Q

What is the danger of the extremes of pressure?

A
  • Traping air and building up the amount of air left in the lung and ultimately leads to increase pressure
  • so can efficiently ventilate patient so set time for exhalation of breath to be long enough so most of this gas can leave the lung and can’t use too much pressure to drive into lung
  • These patients have intrinsic level of PEEP as chests always help open so always have open pressure so if you use lower pressure then they have work much harder which can tire out muscles
53
Q

What can happen with ventilating people with asthma or COPD?

A

can get trapping of air within the lung which leads to breath stacking and the chest getting fuller and fuller so harder to manage their CO2

54
Q

How do you minimise ventilator induced injury?

A

By keeping driving pressure (difference between PEEP and plateau pressure)

55
Q

What imaging do you use to manage ARDS?

A
  1. Lung recruitment: CT - to see if can open up lung (to see which areas are recruitable) (can find other things wrong)
  2. Lung USS - to evaluate how well expanded (bedside and no radiation)
56
Q

What does the murray score involve?

A
  1. PF ratio
  2. CXR
  3. PEEP
  4. lung compliance
    (average score of all 4 parameters)
57
Q

What is 0 on murray?

A

normal

58
Q

What is 1-2.5 murray?

A

mild

59
Q

What is 2.5 murray?

A

severe

60
Q

What is 3 murray?

A

ECMO

61
Q

What is the inclusion criteria for ECMO?

A

• severe respiratory failure
-non-cardiac cause (i.e. Murray Lung Injury score 3.0 or above)
• Positive pressure ventilation is not appropriate (e.g. significant tracheal injury).
•REVERSIBLE DISEASE PROCESS
•UNLIKELY TO LEAD TO PROLONGED DISABILLITY

62
Q

What is the exclusion criteria for ECMO?

A
  • Contraindication to continuation of active treatment;
  • Significant co-morbidity -> dependency to ECMO support
  • Significant life limiting co-morbidity
63
Q

How does ECMO work?

A
  1. Very invasive
  2. Pass large cannula up through groin and femoral vein and in IVC below the RA and withdraw blood into pump
  3. Runs blood across an artificial membrane and gas flowed over top layer of membrane 4. This allows for removal of carbon dioxide and input of oxygen and that oxygenated red blood then passes straight back into the patient
  4. Bi femoral access or femoral and jugular access
64
Q

What are issues with ECMO?

A
  1. time to access
  2. referral system: geographical inequity
  3. Consideration of referral
  4. Costs
65
Q

What are the technical issues of ECMO?

A
  1. Obtaining access: internal jugular/subclavian/ femoral
  2. Circuit
  3. Haemodynamics
  4. Clotting/bleeding