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ARDS Flashcards

1
Q

What is respiratory failure?

A

Syndrome of inadequate gas exchange due to dysfunction in 1 or more components of the respiratory system

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2
Q

What are the components of the respiratory system that could contribute to respiratory failure?

A
  1. nervous system (CNS/brainstem, PNS, neuro-muscular junction)
  2. respiratory muscles (diaphragm & thoracic muscles, extra-thoracic muscles)
  3. pulmonary (airway disease, alveolar-capillary, circulation)
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3
Q

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

A

For men smoking. For women household air pollution from solid fuels

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4
Q

How do people present with ARDS, what is mortality from ARDS and what increases it?

A

Heterogenous presentation (present differently). Mortality 30-40%. Severity and age increase mortality.

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5
Q

What are the ARDS berlin criteria?

A
  1. timing - within 1 week of known clinical insult or new/worsening respiratory symptoms
  2. imaging shows bilateral opacities not fully explained by effusions, lung collapse or nodules
  3. origin - respiratory failure not fully explained by cardiac failure or fluid overload (need objective assessment eg ECHO to exclude hydrostatic oedema if no risk factor present)
  4. oxygenation: mild P/F ratio 200-300mmHg with PEEP or CPAP >5cmH20. moderate: P/F ratio 100-200 mmHg. Severe P/F ratio <100
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6
Q

what are acute causes of respiratory failure?

A
  1. pulmonary - infection, aspiration, primary graft dysfunction after lung transplant
  2. extra-pulmonary: trauma, pancreatitis, sepsis
  3. neuro-muscular: myasthenia gravis / GBS
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7
Q

What are chronic causes of respiratory failure?

A
  1. pulmonary: COPD, lung fibrosis, CF, lobectomy

2. neuromuscular: muscular dystrophy

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8
Q

What are acute on chronic causes of respiratory failure?

A

Infective exacerbation of COPD/CF, myasthenia gravis crisis, post-operative

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9
Q

What is type I respiratory failure? What are potential causes? What is seen?

A
  • Hypoxaemic respiratory failure PaO2 <60. failure of oxygen exchange.
  • Causes: collapse of lobe, aspiration, pulmonary oedema, fibrosis, pulmonary embolism, pulmonary hypertension.
  • There is increased shunt fraction (QS/QT) - amount of blood pumped by heart not completely oxygenated due to alveolar flooding in heart failure patients.
  • Hypoxaemia refractory to supplemental oxygen
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10
Q

What is type II respiratory failure? What are potential causes? What is seen?

A
  • Hypercapnic PaCO2 >45. failure to remove/exchange CO2. decreased alveolar minute ventilation, dead space ventilation.
  • Due to nervous system, neuromuscular diseases (weak muscles cant drive good tidal volumes) or airway obstructive diseases like COPD or chest wall deformities (severe scoliosis) and ageing (thorax cant open as efficiently) leading to hypoventilation
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11
Q

What is type III respiratory failure? What are causes? What is seen?

A
  • Peri-operative.
  • Increased atelectasis due to low functional residual capacity FRC (can cause lung collapse) with abnormal abdominal wall mechanics (can be due to collapse of airways).
  • Can have hypoxaemia or hypercapnea.
  • Prevent by good positioning when extubating, anaesthetic or operative technique, incentive spirometry, analgesia, attempt to lower intra-abdominal pressure.
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12
Q

What is type IV respiratory failure? What happens? what is impact on ventilation on heart?

A
  • In those who are intubated/ventilated during shock (septic/cardiogenic/neurologic).
  • Poor perfusion of lung, cant transfer oxygen, get peripheral pooling of blood and need intubation (positive pressure).
  • Optimise ventilation to improve gas exchange & unload respiratory muscles lowering their oxygen consumption.
  • Good for LV because reduces afterload (amount of work it needs to do). Bad for RV because increased pre-load (increased pressure in thorax so much harder to fill with blood and contractility affected)
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13
Q

What are acute risk factors for respiratory failure?

A

Infection (viral, bacterial), aspiration, trauma, pancreatitis, transfusion

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14
Q

What are chronic risk factors for respiratory failure?

A

COPD, pollution, recurrent pneumonia, CF, pulmonary fibrosis, neuro-muscular diseases

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15
Q

What are pulmonary and extra-pulmonary causes of acute respiratory failure?

A
  1. pulmonary: aspiration, trauma, burns - inhalation, surgery, drug toxicity, infection
  2. extra-pulmonary: trauma, pancreatitis, burns, transfusion, surgery, BM transplant, drug toxicity, infection
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16
Q

What is the pathophysiology of an acute lung injury in ARDS?

A
  • Lung injury to interstitium causes resident macrophages & type 2 pneumocytes to release cytokines IL-6, IL-7, TNF-a.
  • the inflammation makes capillaries leaky and we get protein rich pulmonary oedema and alveolar fluid build up.
  • Damage to type 2 pneumocytes so inactivation/degradation of surfactant causes less efficient expanding.
  • Migration of neutrophils causes damage, secrete proteases that damage and cause build up of fluid.
  • More oedema, more diffusion distance, less efficient gas exchange.
  • Systemic infection can cause bactaraemia
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17
Q

What is in vivo evidence of molecules in ARDS? What is implicated?

A
  • TNF signalling is implicated (KO animal TNFR-1 causes reduced injury).
  • Alveolar macrophage activation & neutrophil lung migration.
  • DAMP (damage associated molecular patterns) release HMGB-1 and RAGE.
  • Cytokines released are IL-6, IL-8, IL-1B, IFN-γ.
  • Cell death shown by necrosis in lung biopsies and apoptotic mediators -FAS, FAS-I, BCI-2
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18
Q

What pharmacological interventions have been trialled and have had success?

A

Steroids, surfactant (more promising in kids), N-acetylcysteine (reduces viscosity of secretions so easier to ventilate), neutrophil esterase inhibitor, salbutamol (no real response), statins

19
Q

What therapies are we trialling and why?

A

Mesenchymal stem cells (ex-vivo benefit), keratinocyte growth factor (to reduce fibrotic response), micro-vesicles, high dose VItC, thiamine, steroids, ECCOO2R (not really efficient for oxygenation)

20
Q

What types of endo-types have been identified in ARDS?

A

Hyper and hypo-inflammatory endotypes.

21
Q

What is upregulated in hyper-inflammatory endotype?

A

Epithelial and vascular DAMPS upregulated in inflammatory endotype

22
Q

How can vascular DAMPS be used to discriminate between 2 diseases?

A

Discriminate between influenza & and COVID ARDS ECMO cohorts.

23
Q

Why is it important to identify driving mechanism in ARDS?

A

it is heterogenous

24
Q

What are the 3 keys to therapeutic intervention of ARDS?

A
  1. treat underlying disease 2. respiratory support 3. multiple organ support
25
Q

How do you treat the underlying cause in ARDS? What drugs can be used?

A

If underlying neuromuscular disease (pyridostigmine or steroids), if vasculitic (steroids, plasma exchange), bronchodilators, pulmonary vasodilators, steroids, antibiotics, anti-virals, IVIG, rituximab

26
Q

How do you offer respiratory support in ARDS? What can be given?

A

Physiotherapy, oxygen, nebulisers (salbutamol, ipatropium bromide, hypertonic saline/mucocysteine to loosen up secretions), high flow oxygen (nasal cannulae/face masks up to 70L & 100% oxygen if airway patent), mechanical ventilation (intubation), for facial trauma/epistaxis non-invasive ventilation with tight fitted mask or air stent to open alveoli & let in oxygen in Type I or add booster assistant breath support to clear CO2, ECMO (extra-corpeal support)

27
Q

Why not give liberal oxygen to COPD patients or with chronic type II respiratory failure?

A

Supplemental O2 removes a copd patient’s hypoxic respiratory drive causing hypoventilation which causes higher carbon dioxide levels, apnea and respiratory failure

28
Q

How do you offer multiple organ support in ARDS?

A
  • CV: fluids, vasopressors, inotropes, pulmonary vasodilators.
  • Renal: hemofiltration, haemodialysis.
  • Immune: plasma exchange, convalescent plasma
29
Q

How does ARDS lead to other things (sequalae)?

A

Poor gas exchange, infection (sepsis), inflammation, systemic effects (stress on liver, CV, renal system can cause multi-organ dysfunction)

30
Q

What is positive pressure ventilation? How does it work? What types exist?

A
  • Blows air into lungs with positive pressure.
  • Peak pressure to drive into lung & underlying base pressure to keep airways open.
  • Too much pressure can be damaging.
  • Types: volume controlled, pressure controlled, assistant breathing modes (to drive pressure using sensor) , advanced ventilatory modes
31
Q

Why is compliance reduced in lung injury?

A

Amount of lung that opens for amount of pressure used reduced because lung much thicker.

32
Q

What is upper inflection point and lower inflection point?

A
  • Upper inflection point UIP - above this pressure additional alveolar recruitment requires too much pressure to point it would damage lung.
  • Lower inflection point LIP - minimum baseline pressure PEEP needed for optimal alveolar recruitment. If you drop below this you get lung collapse
33
Q

How do you manage ventilation in patients with COPD and why? What can be the consequences of too low or too high pressures?

A
  • COPD have normally high CO2 and don’t exhale completely. On ventilator hard to manage because airways constricted so hard to get pressure right.
  • Air stays in lung (trapping) so increased lung pressure cant efficiently ventilate.
    1. set time for exhalation to be long enough for gas to leave lung
    2. don’t use too much pressure to drive air in because we wont be able to get air out
    3. because they have intrinsic level of peak (chest held open) if we use lower pressure have to work much harder - tires muscles, trapping of air makes chest fuller. SO keep driving pressure (difference between peak and static pressure) to reduce ventilator induced lung injury
34
Q

How can a lung recruitment CT be used? What can it show?

A
  • Lung recruitment CT to see if we can open up lung, see if it is recruitable by increasing distension of lung to see if can get some alveolar units to ventilate patients.
  • Too high pressure can over-distend lung trapping more gas in chest and reducing perfusion and causing RV dysfunction.
35
Q

How can a lung ultrasound be used? What can it show?

A

See how well expanded lung is - bedside - can see fluid in lung. Doesn’t pick up as much as CT but can pick up fluid (can drain)

36
Q

How do you guide escalation of therapy in ARDS? What are the parameters?

A

Murray score (average score of 4 parameters):

  1. PF ratio
  2. CXR (1 point per quadrant infiltrated)
  3. PEEP
  4. compliance.

0=normal, 1-2.5 moderate, 2.5 severe, 3 ECMO

37
Q

What is the P/F ratio? What indicates ards?

A

P/F ratio is PaO2/FiO2.

-assesses severity of hypoxameia - less than 300 indicates ARDS

38
Q

What are ECMO inclusion criteria?

A
  1. Severe respiratory failure (non cardiac cause),
  2. murray score 3 or more,
  3. positive pressure ventilation not appropriate (eg trachael injury)
39
Q

What are ECMO exclusion criteria?

A
  1. Contraindication to continuation of active treatment,
  2. significant co-morbidity (depend on ECMO support/no prospect of recovery),
  3. significant life-limiting comorbidity (better for those with reversible disease & not prolonged disability)
40
Q

What else needs to be considered when choosing ecmo?

A

Aetiology - eg patients with flu recover well

41
Q

How is ECMO done?

A
  • Pass large cannula usually via groin (femoral vein) sit it bellow right atrium, withdraw blood with tubing - run it across artificial membrane that oxygenated and removes Co2 from blood and pass it through patient.
  • Either femoral-femoral axis or femoral-jugular axis
42
Q

How efficient is ECMO?

A

Good survival rate 79%. Case selection important

43
Q

What are issues with ECMO?

A

Time to access, referral system has geographical inequity, referral consideration, expensive, technical requires expertise, perfusionists in short supply, need blood thinning (heparin/anticoagulant) because increased risk of clotting/bleeding

BRS (81 decks)

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