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EDIC academy > ARDS (2) > Flashcards

ARDS (2) Flashcards

1
Q

Characteristics of ARDS on histological examination?

A
  • Diffused alveolar damage
  • Oedema
  • Cell necrosis
  • Fibrosis
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2
Q

What was the initial definition of ARDS?

A
  • Acute onset hypoxia
  • PaO2 to FiO2 ration < 200mmHg
  • Bilateral infiltrates on CXR
  • PAWP < 18mmHg or cardiogen pul oedema
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3
Q

What is the current Berlin definition of ARDS?

A
  • Acute onset ARDS within 7 days of insult
  • Degree of hypoxia based on PaO2/FiO2
  • PEEP of at least 5
  • Absence of fluid overload or CCF
  • Infiltrates on CXR & CT
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4
Q

Classification of ARDS based on degree of hypoxaemia (PaO2/FiO2 ratio)?

A
  • Mild - 201 and 300
  • Moderate - 101 and 200
  • Severe - <100 mmHg
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5
Q

Characteristics of ARDS?

A
  • Precipitated by underlying factors
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6
Q

Distinguishing between types of ARDS?

A
  • Pulmonary
  • Extra-pulmonary
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7
Q

What is pulmonary ARDS?

A

Direct insult to the lung affecting pulmonary epithelium

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8
Q

What is extra-pulmonary ARDS?

A

Indirect lung injury caused by inflammatory mediators acting on vascular endothelium

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9
Q

What are the causes of pulmonary ARDS?

A
  • Pneumonia (Main cause)
  • Aspiration pneumonitis
  • Inhalation injury
  • Pulmonary contusion
  • Pulmonary vasculitis
  • Near drowning
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10
Q

What are the causes of extra-pulmonary ARDS?

A
  • Non-pulmonary sepsis
  • Non-cardiogenic shock
  • Pancreatitis
  • Major trauma
  • TRALI
  • Burns
  • Drug overdose
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11
Q

What are the mimics of ARDS?

A
  • Vasculitis (Alveolar haemorrhage)
  • Drug induced
  • Eosinophilic pneumonia
  • Interstitial pneumonia
  • Lung mets (Cancer)
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12
Q

What are the phases of ARDS pathophysiology?

A
  • Exudative
  • Proliferative
  • Fibrosis
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13
Q

Features of the exudative phase of ARDS?

A
  • Capillary congestion
  • Alveolar oedema
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14
Q

Features of the proliferative phase of ARDS?

A
  • Proliferation of alveolar Type-2 cells
  • Proliferation of fibroblasts
  • This phase can lead to resolution or formation of fibrosis
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15
Q

What are the intrapulmonary causes of hypoxaemia in ARDS?

A
  • Shunt
  • Dead space
  • Impairment of gas diffusion
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16
Q

What are the mechanisms contributing to hypoxaemia in ARDS?

A
  • Epithelial damage and increased shunt
  • Endothelial damage and increased dead space
  • Interstitial damage and impaired diffusion
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17
Q

Explain the mechanism of epithelial damage and increased shunt?

A
  • Primary cause of hypoxaemia in ARDS
  • Loss of lung volume - Surfactant deficiency
  • Alveolar oedema
  • Lung collapse
  • Intraplulmonary shunt
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18
Q

Explain the mechanism of Endothelial damage and increased dead space ?

A
  • Abnormalities in pulmonary blood flow
  • The lung region is usually well ventilated
  • Surrogate for dead space is ventilatory ratio
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19
Q

Explain the mechanism of Interstitial damage and impaired gas diffusion?

A
  • Interstitial oedema
  • Hyaline membrane
  • Fibrosis - Thickened alveolar-capillary memebrane
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20
Q

What are the components of ventilator induced lung injury ? (VILI)

A
  • Volutrauma
  • Barotrauma
  • Atelectrauma
  • Biotrauma
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21
Q

Risk factors of VILI?

A
  • High end-inspiratory lung volume
22
Q

What is volutrauma?

A

This is high end-inspiratory lung volume

23
Q

Factors promoting volutrauma?

A
  • Lung strain
24
Q

What is lung strain?

A

This is the ratio of VT to end-expiratory lung volume. Excess in strain results from high VT or high PEEP which brings the end-expiratory lung volume closer to TLC

25
Q

What are the risk factors for barotrauma?

A
  • Lung hyper-inflation
26
Q

What is atelectrauma?

A

This is due to the repeat opening and closing of the small airway over the breathing cycle at low tidal volumes.

27
Q

Factors promoting atelectrauma?

A
  • Surfactant deficiency
  • Alveolar instability
  • Oedema
  • Increased permeability
  • Inflammation
  • Structural damage
  • Fibrin accumulation
  • Fibrosis
28
Q

How can atelectrauma be be prevented?

A
  • Application of high PEEP
29
Q

What is biotrauma?

A
  • Release of inflammatory mediators
  • Oxygen toxicity
30
Q

What are the major determinants of VILI and in-hospital mortality ?

A
  • Driving pressure (Plateau pressure - PEEP)
  • Mechanical power
31
Q

Phenotype of Covid-19?

A
  • Type L
32
Q

Characteristics of L-type covid-19?

A
  • Low elastance (i.e high compliance)
  • Low ventilation/perfusion ratio
  • Low lung weight
  • Low recruitability
33
Q

Characteristics of type-H ARDS sub-phenotype?

A
  • High elastance (Low compliance)
  • High right to left shunt
  • High lung weight
  • High recruitability
34
Q

What is the ventilatory strategy for the L-type phenotype?

A
  • High VT 8-9ml/kg
  • Low PEEP
35
Q

What is the ventilatory strategy for the H-type phenotype?

A
  • Low VT
  • High PEEP
  • Prone ventilation
36
Q

What is compliance ? How is it calculated

A
  • Tidal volume divided by driving pressures
  • Combination of lung/chest wall compliance
  • Chest wall compliance > lung compliance
37
Q

What is the average value of the respiratory system compliance?

A

30ml/cmH2O or less

38
Q

Factors increasing respiratory system resistance?

A
  • Low lung volumes
39
Q

Methods of measuring chest wall compliance?

A
  • Oesophageal pressure
40
Q

What is the influence of compliance on plateau pressure and driving pressure

A
  • Relevant in intra-abdominal pathology
41
Q

What are the methods of oxygenating patients ?

A
  • CPAP
  • HFNC
  • NIV
42
Q

What is the ROX index?

A
  • Ratio between sats & FiO2
  • High respiratory rate
  • Predicts therapy failure in pts on HFNC
43
Q

What is the HACOR scale?

A

Predicts NIV failure by evaluating;
- HR
- Acidosis
- GCS
- RR

44
Q

What is the driving pressure?

A
  • VT / Compliance
  • > 15cmH2O is high risk for mortality
45
Q

What is the volume of oxygen and flow rate that can be delivered during ECMO?

A
  • 400ml O2/min
  • Flow 6L/min
46
Q

Characteristics of the Extracorporeal CO2 removal?

A
  • CO2 clearance 150-200ml/min
  • Veno-venous blood flow (1-2L/min)
47
Q

What are the characteristics of the High Frequency Oscillatory Ventilation?

A
  • 900 cycles/min
48
Q

What are the advantages of iNO in ARDS ?

A
  • Selectively dilates pulmonary vessels
  • Improves oxygenation (preserved HPV)
  • Reduction of PVR
49
Q

What are the components of the total peak pressure? This can be separated in VCV

A
  • Resistive (Peak pressure - Plateau pressure)
  • Elastic (plateau pressure)
50
Q

What is End-Expiratory Lung Volume ?

A
  • Amount of aerated lung at the end of exp
  • Evaluates collapse or over-distention
  • Assessment of the effect of PEEP
  • Its underestimated by bedside
  • Circuit leaks can compromise measurement
51
Q

What is acute cor-pulmonale?

A
  • Increased RV afterload
  • Complication of ARDS
  • Increased HPV & compression pul capillaries
  • Increased PVR
  • Dilated RV & septal dyskinesia

EDIC academy (20 decks)

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