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Year 2 - BRS > 5.6 - Respiratory failure > Flashcards

5.6 - Respiratory failure Flashcards

1
Q

What is the predominant feature of respiratory failure?

A

Shortness of breath

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2
Q

What is the definition of respiratory failure?

A

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

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3
Q

What are the components of the respiratory system?

A
  • nervous system - CNS/brainstem, peripheral nervous system, neuromuscular junction
  • respiratory muscle - diaphragm & thoracic muscles, extra-thoracic muscles
  • pulmonary - airway disease, alveolar-capillary, circulation
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4
Q

Which areas of the world is respiratory failure more prevalent in?

A
  • North America, Europe
  • SE and S Asia is less common
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5
Q

What are some epidemiological statistics for chronic respiratory disease?

A
  • 3rd leading cause of death
  • 39.8% rise from 1990
  • EU 380m euros annually
  • accounts for inpatient care, lost productivity
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6
Q

What is the biggest risk factor for men and women for chronic respiratory disease?

A
  • men - smoking
  • women - household air pollution from solid fuels
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7
Q

What are the risk factors for chronic respiratory failure? (6)

A
  • COPD
  • pollution
  • recurrent pneumonia
  • cystic fibrosis
  • pulmonary fibrosis
  • neuromuscular diseases
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8
Q

What are the risk factors for acute respiratory failure? (5)

A
  • infection - viral / bacterial
  • aspiration (drop in consciousness = aspiration of gastric contents into lungs which causes response from lungs)
  • trauma
  • pancreatitis
  • transfusion
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9
Q

How can we classify respiratory failure?

A
  • acute
  • chronic
  • acute on chronic
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10
Q

What diseases come under acute respiratory failure?

A
  • pulmonary - infection, aspiration, primary graft dysfunction following lung transplant
  • extra-pulmonary - trauma, pancreatitis, sepsis
  • neuromuscular - myasthenia / GBS
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11
Q

What diseases come under chronic respiratory failure?

A
  • pulmonary/airways - COPD, lung fibrosis, cystic fibrosis, lobectomy
  • musculoskeletal - muscular dystophy
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12
Q

What diseases come under acute on chronic respiratory failure?

A
  • infective exacerbation - COPD, CF
  • myasthenic crises
  • post-operative
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13
Q

How does acute respiratory distress syndrome (ARDS) present?

A
  • heterogenous disease presentation
  • can present as CF, pulmonary hypertension, pneumonia, COPD exacerbation
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14
Q

What is the prevalence and mortality of acute respiratory distress syndrome?

A
  • prevalence 6-7 per 100k in the UK
  • 30-40% mortality (severity and increased age increase mortality)
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15
Q

What are the diagnostic criteria for ARDS, and how can we classify acute respiratory distress syndrome (ARDS)?

A
  • Berlin definition
  • timing - within 1 week of a known clinical insult or new or worsening respiratory symptoms
  • chest imaging - bilateral opacities (not fully explained by effusions, lobar/lung collapse, or nodules)
  • origin of oedema - respiratory failure not fully explained by cardiac failure or fluid overload, need objective assessment (e.g. echocardiography) to exclude hydrostatic oedema if no risk factor present
  • oxygenation - ARDS classified as mild, moderate or severe
    • mild: 200mmHg<PaO2/FIO2<300mmHg, with PEEP or CPAP>5cmH2O
    • moderate: 100mmHg<PaO2/FIO2<200mmHg, with PEEP or CPAP>5cmH2O
    • severe: PaO2/FIO2 <100mmHg with PEEP >5cmH2O
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16
Q

How does ventilation change as you go from the top of the lung to the bottom?

A
  • pleural pressure goes from more negative (-8cmH2O) to less negative (-2 cmH2O)
  • transmural pressure gradient decreases
  • alveoli become smaller and more compliant
  • ventilation increases
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17
Q

How does perfusion change as you go from the top of the lung to the bottom?

A
  • intravascular pressure increase (gravity effect)
  • more recruitment of blood vessels
  • resistance to flow decreases
  • flow rate and perfusion increases
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18
Q

How is oxygen loaded at lungs?

A
  • RBCs on venous end are 75% saturated and have a venous oxygen of 5.3kPa
  • concentration gradient between alveoli and vessel = O2 enters blood
  • at arterial end, RBCs 100% saturated and venous oxygen is 13.5kPa
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19
Q

What is pulmonary transit time?

A
  • the time that the RBCs are within range for gas exchange for oxygen is 0.75s
  • hence around 12-15 breaths per minute
  • could theoretically happen in 0.25s hence when ill, breathing rate increases
  • CO2 is more soluble than O2 so moves into alveoli quicker
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20
Q

How does alveolar pressure (PA), arterial pressure (Pa) and venous pressure (Pv) change as you go down the lung?

A
  • zone 1: PA > Pa > Pv
  • zone 2: Pa > PA > Pv
  • zone 3: Pa > Pv > PA
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21
Q

Describe the graph of perfusion and ventilation from base to apex.

A
  • base - more blood going past exchange surface than can participate in gas exchange - wasted perfusion (V/Q<1)
  • apex - little blood and air - wasted ventilation as moving gases into parts of lung that are not getting blood supply (V/Q>1)
  • optimum - where lines cross (in between zone 2 and 3) - correct amount of perfusion for correct amount of ventilation (V/Q=1)
  • lung diseases distort this relationship
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22
Q

What is compliance?

A
  • the tendency to distort under pressure
  • delta V / delta P
  • condom has higher compliance than balloon
  • volume expansion of lung at pressure you apply
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23
Q

What is elastance?

A
  • the tendency to recoil to its original volume
  • delta P / delta V
  • balloon has higher elastance than condom
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24
Q

Why does max inspiratory and expiratory effort plateau?

A

Takes a lot of effort from muscles of airways to hold in/squeeze out the last bit of air

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25
Q

What is tidal volume?

A

Volume of air going in and out with each breath

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26
Q

What is inspiratory reserve volume?

A

Extra volume of air that you can get into lung on top of tidal volume

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27
Q

What is expiratory reserve volume?

A

The volume of air that you can empty past your tidal volume

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28
Q

What is residual volume?

A

Volume of air left in lungs - cannot fully empty air as lungs hold their structure to prevent collapse via surfactants etc

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29
Q

What is vital capacity?

A

Difference between max and min air in lungs (IRV + TV + ERV)

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30
Q

What is functional residual capacity?

A
  • everything below default position of lung capacity (bottom of tidal volume) - if you take in a deep breath then die, lungs will not empty fully as that takes muscle effort, but to baseline level due to elastic recoil
  • ERV + residual volume
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31
Q

What is inspiratory capacity?

A
  • everything above baseline value (bottom of tidal volume)
  • IRV + tidal volume
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32
Q

What are volumes?

A

Discrete sections of the graph and do not overlap

33
Q

What are capacities?

A

Sum of two or more volumes

34
Q

What is minute ventilation (L/min)?

A
  • gas entering and leaving the lungs
  • volume of expired air per minute
  • minute ventilation (L/min) = tidal volume (L) x breathing frequency (breaths/min)
  • typically 0.5 x 12 = 6 L/min
35
Q

What is alveolar ventilation (L/min)?

A
  • gas entering and leaving the alveoli
  • volume of air reaching respiratory zone (alveoli) per minute
  • alveolar ventilation (L/min) = [tidal volume (L) - dead space (L)] x breathing frequency (breaths/min)
  • typically (0.5-0.15) x 12 = 4.2 L/min
36
Q

How can we classify respiratory failure physiologically?

A
  • type I or hypoxemic respiratory failure
  • type II or hypercapnic respiratory failure
  • type III or perioperative respiratory failure
  • type IV respiratory failure (shock)
37
Q

What is type I (hypoxemic) respiratory failure?

A
  • failure of oxygen exchange
  • PaO2 < 60 at sea level
  • increased shunt fraction (QS/QT) - more blood transported through lungs without taking part in exchange
  • due to alveolar flooding
  • hypoxemia refractory to supplemental oxygen
38
Q

What are the causes of type I respiratory failure? (6)

A
  • collapse of airways/lobe
  • aspiration
  • pulmonary fibrosis
  • pulmonary oedema
  • pulmonary embolism
  • pulmonary hypertension

More airway/lung related

39
Q

What is type II (hypercapnic) respiratory failure?

A
  • failure to exchange or remove CO2
  • PaCO2 > 45 (and hypoxaemic)
  • decreased alveolar minute ventilation
  • dead space ventilation
40
Q

What are the causes of type II respiratory failure? (5)

A
  • nervous system issues
  • neuromuscular issues
  • muscle failure
  • airway obstruction
  • chest wall deformity
41
Q

What is type III (perioperative) respiratory failure?

A
  • increased atelectasis (collapse of lung/lobe) due to low functional residual capacity (FRC) with abnormal abdominal wall mechanics
  • hypoxaemia or hypercapnia
42
Q

How do you prevent type III respiratory failure? (5)

A
  • anaesthetic or operative technique
  • posture
  • incentive spirometry
  • analgesia
  • attempts to lower intra-abdominal pressure
43
Q

What is type IV respiratory failure (shock)?

A
  • describes patients who are intubated and ventilated during shock (septic/cardiogenic/neurologic)
  • optimise ventilation to improve gas exchange and unload the respiratory muscles, lowering oxygen consumption
  • ventilation increases thoracic pressure which affects heart - reduces LV afterload, increases RV pre and afterload
44
Q

What is the main thing we look at in history of patient presenting with acute respiratory failure?

A

Origin of shortness of breath

45
Q

What are some causes of shortness of breath in ARDS? (5)

A
  • lower respiratory tract infection - viral, bacterial
  • aspiration
  • trauma - transfusion
  • pulmonary vascular disease - pulmonary embolus, haemoptysis
  • extrapulmonary - pancreatitis, new medications
46
Q

What are some pulmonary (lung) causes of ARDS? (6)

A
  • infection
  • aspiration
  • trauma
  • burns - inhalation of hot gas/ash
  • surgery
  • drug toxicity
47
Q

What are some extrapulmonary causes of ARDS? (8)

A
  • infection
  • trauma
  • pancreatitis
  • transfusion
  • surgery
  • drug toxicity
  • burns
  • bone marrow transplant
48
Q

What drives the mechanism of acute lung injury? (5)

A
  • the lung
  • leucocytes
  • inflammation
  • infection
  • immune response
49
Q

What is the overall mechanism of acute lung injury (ARDS)?

A
  • alveolar macrophages are activated by inflammation/infection and release IL6, IL8, TNF-alpha
  • causes alveolar protein-rich oedema build up in lung
  • inactivation of surfactant = alveolus less efficient at expanding
  • migration of neutrophils into interstitium (cause damage by secreting proteases etc) before entering site of inflammation/infection in alveolus
  • leads to build up of more oedema in interstitium - increases distance between capillary and alveolus
  • greater distance for gas exchange to occur –> less efficient
50
Q

What happens to pulmonary transit time in acute lung injury?

A
  • alveoli damaged and inflamed
  • increased distance the gas has to travel between alveoli and capillary
  • pulmonary transit time increases
  • IL6/IL8/TNF causes fluid leak from capillary
51
Q

What in vivo evidence do we have for acute lung injury? (5)

A
  • TNF signalling implicated in vivo and in vitro (reduced injury by blocking TNFR-1 signalling pathway)
  • leukocyte activation and migration - macrophage activation (alveolar), neutrophil lung migration
  • DAMP release (HMGB-1 and RAGE)
  • cytokine release (IL-6, IL-8, IL-1B, IFN-y)
  • cell death (necrosis in lung biopsies and apoptotic mediators e.g. FAS, FAS-I and BCI-2)
52
Q

What pharmacological therapies have already been tried for ARDS? (7)

A
  • steroids
  • salbutamol
  • surfactant
  • N-Acetylcysteine
  • neutrophil esterase inhibitor
  • GM-CSF
  • statins
53
Q

What therapies are being trialled for ARDS? (3)

A
  • mesenchymal stem cells (ex-vivo benefit)
  • keratinocyte growth factor (repair factor)
  • steroids
54
Q

What kind of position when lying in bed helps patients with ARDS?

A

Proning - place patients on stomach

55
Q

What did the HARP-2 ARDS study identify?

A

Identified hyper and hypo inflammatory endotypes

56
Q

What can we split therapeutic management of ARDS into? (3)

A
  • treating underlying disease
  • respiratory support
  • multiple organ support
57
Q

What does treating underlying disease to manage ARDS include? (5)

A
  • inhaled therapies - bronchodilators, pulmonary vasodilators
  • steroids
  • antibiotics
  • anti-virals
  • drugs - pyridostigmine, plasma exchange, IViG, rituximab
58
Q

What does respiratory support to manage ARDS include? (7)

A
  • physiotherapy
  • oxygen
  • nebulisers
  • high flow oxygen
  • non-invasive ventilation
  • mechanical ventilation
  • extra-corporeal support e.g. ECMO (most severe treatment)
59
Q

What does multiple organ support to manage ARDS include? (3)

A
  • cardiovascular support - fluids, vasopressors (AVP, NA), inotropes, pulmonary vasodilators
  • renal support - haemofiltration, haemodialysis
  • immune therapies - plasma exchange, convalescent plasma
60
Q

What is the progression of respiratory support for ARDS?

A
  • conservative fluid management + low volume ventilation
  • increasing PEEP (positive end expiratory pressure)
  • prone positioning + neuromuscular blockade
  • inhaled pulmonary vasodilators
  • extracorporeal membrane oxygenation
61
Q

What are the four sequelae of ARDS?

A
  • poor gas exchange –> inadequate oxygenation, poor perfusion, hypercapnia
  • infection –> sepsis
  • inflammation –> inflammatory response
  • systemic effects
62
Q

What are ARDS specific interventions? (5)

A
  • respiratory support
  • intubation and ventilation
  • ARDS necessitates mechanical intervention
  • types of ventilation
  • procedures to support ventilation
63
Q

What are the types of ventilation? (4)

A
  • volume controlled
  • pressure controlled
  • assisted breathing modes
  • advanced ventilatory modes
64
Q

How is the pressure-volume loop different in ARDS to a normal patient?

A

Shifted down and right - more pressure used at top to get very little volume increase

65
Q

How is compliance of the lung changed in ARDS?

A

Markedly reduced in injured lung

66
Q

What is the upper inflection point (UIP)?

A

Above this pressure, additional alveolar recruitment requires disproportionate increases in applied airway pressure

67
Q

What is the lower inflection point (LIP)?

A
  • can be thought of as the minimum baseline pressure (PEEP) needed for optimal alveolar recruitment
  • anything below this and the lung may collapse
  • try and keep lung open with PEEP (but not too much pressure which can cause damage)
68
Q

What are some pitfalls of ventilation?

A
  • COPD/asthma patients have air trapped in lungs (cannot fully exhale on ventilator) = increased pressure in lung
  • control of CO2 hard as minute ventilation hard to get right
  • alveolar recruitment hard to get right via positive end expiratory pressure (PEEP) - these patients have intrinsic level of PEEP as chests always open
  • V/Q mismatch - ventilation without gas-exchange and vice-versa
  • ventilator-induced lung injury due to high driving pressure
69
Q

What imaging is used for ARDS patients? (2)

A
  • lung recruitment CT
  • lung ultrasound
70
Q

How does a lung recruitment CT work?

A

Use high pressure ventilatory strategy but with low driving pressure strategy to see if we can open up lung (but not too much pressure as this can over-expand lung –> reduced perfusion –> damage)

71
Q

What is a lung ultrasound used for?

A

To get an expanded lung to see consolidation (pathology instead of normal air)/fluid

72
Q

What system do we use for escalation of ARDS therapy?

A
  • Murray score
  • parameters scored from 0-4 then averaged:
    • PaO2/FIO2 (on 100% oxygen)
    • CXR
    • PEEP
    • compliance
73
Q

How do you interpret Murray score (ARDS)?

A
  • 0 = normal
  • 1-2.5 = mild
  • 2.5 = severe
  • 3+ = ECMO
74
Q

What is the national ECMO approach?

A
  • 5 national centres
  • telephone or online referral with Murray score >3 and pH < 7.2
  • consultant case review
  • transfer of imaging
  • advice
  • retrieval
  • transfer
  • ongoing management
75
Q

What are the inclusion criteria for ECMO? (2)

A
  • severe respiratory failure of non-cardiac cause (Murray score >3)
  • positive pressure ventilation is not appropriate e.g. significant tracheal injury
76
Q

What are the exclusion criteria for ECMO? (3)

A
  • contraindication to continuation of active treatment
  • significant comorbidity that would lead to dependency to ECMO support with no good chance of recovery
  • significant life-limiting comorbidity
77
Q

What are the most important criteria for being put on ECMO? (2)

A
  • patient must have a reversible disease process
  • ECMO should be unlikely to lead to prolonged disability
78
Q

How does ECMO (extra-corporeal membrane oxygenation) work?

A
  • cannula –> IVC (via femoral vein) OR jugular vein
  • blood is drawn –> tubing –> centrifugal pump –> oxygenator + artificial membrane
  • gas flows over the membrane and blood flows through oxygenator below –> allows removal of CO2 and input of O2
  • oxygenated blood passes back to patient
79
Q

What are some issues with ECMO? (8)

A
  • time to access
  • referral system - geographical inequity
  • consideration of referral (doctors may not know what ECMO is)
  • obtaining access - IJV, subclavian, femoral (hard in sick patients)
  • circuit
  • haemodynamics
  • clotting/bleeding
  • expensive

Year 2 - BRS (84 decks)

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