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1. Choose a spokesperson

2. All students in the group are to work on all of the following questions/sections included in the Padlet

3. You can use diagrams/images other visual resources to explain each respiratory condition.

4. When we come back to the whole class, the spokesperson will feedback the groups findings, with the teams support

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ARDS - Acute Respiratory Distress Syndrome
Acute widespread inflammation that ends with destruction and damage of diffuse alveoli.
Can be direct injury (ie. pneumonia, pulmonary sepsis, COVID) or indirect injury (sepsis non pulmonary source, trauma, burns, TRALI)

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2. Is it obstructive or restrictive? Why?

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2. Is it obstructive or restrictive? Why?

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Restrictive

Decreased lung compliance from diffuse fibrosis

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3. How does the condition effect lung compliance and/or airway resistance?

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3. How does the condition effect lung compliance and/or airway resistance?

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Decreases lung compliance.
Three phases:

1. Oedematous phase: migration of neutrophils into the alveoli, releasing variety of substances ie. Proteases, gelatinases A and B and reactive nitrogen that damage the alveoli. Further damage occurs by alveolar macrophages and release of proinflammatory cytokines that amplify inflammatory response. Significant V/Q mismatch ( intrapulmonary shunt) evolves causing hypoxemia.

2. Proliferative phase: begins after 1-2 weeks, fibrosis and remodelling occurs. Reduced alveolar ventilation and pulmonary compliance and V/Q mismatch. Reduced compliance (stiff lungs) causes further atelectasis in mechanically ventilated pt as alveoli are damaged by increased volume and /or pressure on inspiration.

3. Fibrotic phase: the final phase where alveoli become fibrotic and the lung is left with emphysema - like alterations.

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4. Explain the role of V/Q mismatch in this condition.

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4. Explain the role of V/Q mismatch in this condition.

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V/Q mismatch (low V/Q ratio)- minimal alveolar ventilation with normal perfusion. Increased atelectasis/fibrotic tissues leads to intrapulmonary shunting.

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6. What type of respiratory failure would this condition lead to?

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6. What type of respiratory failure would this condition lead to?

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Mild/moderate - T1RF
Severe - T2RF

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5. How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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5. How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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Ventilation is reduced by the exudate/oedema and decreased surfactant function, causes the alveolar to collapse leading to impaired diffusion of O2 across the alveolar-capillary membrane.
Low PaO2 due to increased A-a gradient

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Starts as a respiratory alkolosis - patient hyperventilating, as the disease progresses it will become a respiratory acidosis.

Respiratory Acidosis:
Mild/ Mod ARDS - T1RF: Low PaO2, normal PaCO2, Low pH
Severe ARDS - T2RF: becomes hypercapnic with high PaCO2

Could be a mixed acidosis depending on cause of initial insult

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8. What are the typical clinical manifestations/ patient assessment data? (relate these to pathophysiology concepts already described)

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8. What are the typical clinical manifestations/ patient assessment data? (relate these to pathophysiology concepts already described)

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Increased WOB -  V/Q mismatch (low)
Tachypneoa
Crackles - increased pulmonary oedema due to destruction of the pulmonary epithelium.
Decreased SpO2/ decreased PaO2 - exudate, alveoli collapse, fibrosis
Cough - clear the airway from debris
CXR - 'white out' appearance
Fatigue - prolonged increased WOB and potential for pulmonary HTN
Hypercapnia on ABG
Low p/f ratio

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9. OPTIONAL: Important vocabulary (include list of key vocabulary referenced; if you do not know the term(s), look up and add a definition for the word(s))

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9. OPTIONAL: Important vocabulary (include list of key vocabulary referenced; if you do not know the term(s), look up and add a definition for the word(s))