5.6 - Respiratory failure Flashcards
1
Q
What is the predominant feature of respiratory failure?
A
Shortness of breath
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
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
4
Q
Which areas of the world is respiratory failure more prevalent in?
A
- North America, Europe
- SE and S Asia is less common
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
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
7
Q
What are the risk factors for chronic respiratory failure? (6)
A
- COPD
- pollution
- recurrent pneumonia
- cystic fibrosis
- pulmonary fibrosis
- neuromuscular diseases
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
9
Q
How can we classify respiratory failure?
A
- acute
- chronic
- acute on chronic
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
11
Q
What diseases come under chronic respiratory failure?
A
- pulmonary/airways - COPD, lung fibrosis, cystic fibrosis, lobectomy
- musculoskeletal - muscular dystophy
12
Q
What diseases come under acute on chronic respiratory failure?
A
- infective exacerbation - COPD, CF
- myasthenic crises
- post-operative
13
Q
How does acute respiratory distress syndrome (ARDS) present?
A
- heterogenous disease presentation
- can present as CF, pulmonary hypertension, pneumonia, COPD exacerbation
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)
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
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
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
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
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
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
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
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
23
Q
What is elastance?
A
- the tendency to recoil to its original volume
- delta P / delta V
- balloon has higher elastance than condom
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
25
What is tidal volume?
Volume of air going in and out with each breath
26
What is inspiratory reserve volume?
Extra volume of air that you can get into lung on top of tidal volume
27
What is expiratory reserve volume?
The volume of air that you can empty past your tidal volume
28
What is residual volume?
Volume of air left in lungs - cannot fully empty air as lungs hold their structure to prevent collapse via surfactants etc
29
What is vital capacity?
Difference between max and min air in lungs (IRV + TV + ERV)
30
What is functional residual capacity?
- 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
31
What is inspiratory capacity?
- everything above baseline value (bottom of tidal volume)
- IRV + tidal volume
32
What are volumes?
Discrete sections of the graph and do not overlap
33
What are capacities?
Sum of two or more volumes
34
What is minute ventilation (L/min)?
- 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
What is alveolar ventilation (L/min)?
- 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
How can we classify respiratory failure physiologically?
- type I or hypoxemic respiratory failure
- type II or hypercapnic respiratory failure
- type III or perioperative respiratory failure
- type IV respiratory failure (shock)
37
What is type I (hypoxemic) respiratory failure?
- 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
What are the causes of type I respiratory failure? (6)
- collapse of airways/lobe
- aspiration
- **pulmonary fibrosis**
- pulmonary oedema
- pulmonary embolism
- pulmonary hypertension
## Footnote
More airway/lung related
39
What is type II (hypercapnic) respiratory failure?
- failure to exchange or remove CO2
- PaCO2 > 45 (and hypoxaemic)
- decreased alveolar minute ventilation
- dead space ventilation
40
What are the causes of type II respiratory failure? (5)
- **nervous system issues**
- neuromuscular issues
- muscle failure
- airway obstruction
- chest wall deformity
41
What is type III (perioperative) respiratory failure?
- increased atelectasis (collapse of lung/lobe) due to low functional residual capacity (FRC) with abnormal abdominal wall mechanics
- hypoxaemia or hypercapnia
42
How do you prevent type III respiratory failure? (5)
- anaesthetic or operative technique
- posture
- incentive spirometry
- analgesia
- attempts to lower intra-abdominal pressure
43
What is type IV respiratory failure (shock)?
- 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
What is the main thing we look at in history of patient presenting with acute respiratory failure?
Origin of shortness of breath
45
What are some causes of shortness of breath in ARDS? (5)
- lower respiratory tract infection - viral, bacterial
- aspiration
- trauma - transfusion
- pulmonary vascular disease - pulmonary embolus, haemoptysis
- extrapulmonary - pancreatitis, new medications
46
What are some pulmonary (lung) causes of ARDS? (6)
- **infection**
- aspiration
- trauma
- burns - inhalation of hot gas/ash
- surgery
- drug toxicity
47
What are some extrapulmonary causes of ARDS? (8)
- **infection**
- trauma
- pancreatitis
- transfusion
- surgery
- drug toxicity
- burns
- bone marrow transplant
48
What drives the mechanism of acute lung injury? (5)
- the lung
- leucocytes
- inflammation
- infection
- immune response
49
What is the overall mechanism of acute lung injury (ARDS)?
- 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
What happens to pulmonary transit time in acute lung injury?
- 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
What in vivo evidence do we have for acute lung injury? (5)
- 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
What pharmacological therapies have already been tried for ARDS? (7)
- steroids
- salbutamol
- surfactant
- N-Acetylcysteine
- neutrophil esterase inhibitor
- GM-CSF
- statins
53
What therapies are being trialled for ARDS? (3)
- mesenchymal stem cells (ex-vivo benefit)
- keratinocyte growth factor (repair factor)
- steroids
54
What kind of position when lying in bed helps patients with ARDS?
Proning - place patients on stomach
55
What did the HARP-2 ARDS study identify?
Identified hyper and hypo inflammatory endotypes
56
What can we split therapeutic management of ARDS into? (3)
- treating underlying disease
- respiratory support
- multiple organ support
57
What does treating underlying disease to manage ARDS include? (5)
- inhaled therapies - bronchodilators, pulmonary vasodilators
- steroids
- antibiotics
- anti-virals
- drugs - pyridostigmine, plasma exchange, IViG, rituximab
58
What does respiratory support to manage ARDS include? (7)
- physiotherapy
- oxygen
- nebulisers
- high flow oxygen
- non-invasive ventilation
- mechanical ventilation
- extra-corporeal support e.g. ECMO (most severe treatment)
59
What does multiple organ support to manage ARDS include? (3)
- cardiovascular support - fluids, vasopressors (AVP, NA), inotropes, pulmonary vasodilators
- renal support - haemofiltration, haemodialysis
- immune therapies - plasma exchange, convalescent plasma
60
What is the progression of respiratory support for ARDS?
- conservative fluid management + low volume ventilation
- increasing PEEP (positive end expiratory pressure)
- prone positioning + neuromuscular blockade
- inhaled pulmonary vasodilators
- extracorporeal membrane oxygenation
61
What are the four sequelae of ARDS?
- poor gas exchange --> inadequate oxygenation, poor perfusion, hypercapnia
- infection --> sepsis
- inflammation --> inflammatory response
- systemic effects
62
What are ARDS specific interventions? (5)
- respiratory support
- intubation and ventilation
- ARDS necessitates mechanical intervention
- types of ventilation
- procedures to support ventilation
63
What are the types of ventilation? (4)
- volume controlled
- pressure controlled
- assisted breathing modes
- advanced ventilatory modes
64
How is the pressure-volume loop different in ARDS to a normal patient?
Shifted down and right - more pressure used at top to get very little volume increase
65
How is compliance of the lung changed in ARDS?
Markedly reduced in injured lung
66
What is the upper inflection point (UIP)?
Above this pressure, additional alveolar recruitment requires disproportionate increases in applied airway pressure
67
What is the lower inflection point (LIP)?
- 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
What are some pitfalls of ventilation?
- 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
What imaging is used for ARDS patients? (2)
- lung recruitment CT
- lung ultrasound
70
How does a lung recruitment CT work?
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
What is a lung ultrasound used for?
To get an expanded lung to see consolidation (pathology instead of normal air)/fluid
72
What system do we use for escalation of ARDS therapy?
- Murray score
- parameters scored from 0-4 then averaged:
- PaO2/FIO2 (on 100% oxygen)
- CXR
- PEEP
- compliance
73
How do you interpret Murray score (ARDS)?
- 0 = normal
- 1-2.5 = mild
- 2.5 = severe
- 3+ = ECMO
74
What is the national ECMO approach?
- 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
What are the inclusion criteria for ECMO? (2)
- severe respiratory failure of non-cardiac cause (Murray score >3)
- positive pressure ventilation is not appropriate e.g. significant tracheal injury
76
What are the exclusion criteria for ECMO? (3)
- 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
What are the most important criteria for being put on ECMO? (2)
- patient must have a reversible disease process
- ECMO should be unlikely to lead to prolonged disability
78
How does ECMO (extra-corporeal membrane oxygenation) work?
- 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
What are some issues with ECMO? (8)
- 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
