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ARDS is an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue
Causes
Direct

pneumonia (46%)

aspiration of gastric contents (29%)

lung contusion (34%)

fat embolism

near drowning

inhalational injury (toxic gases etc)

reperfusion injury

Indirect

non-pulmonary sepsis (25%)

multiple trauma (41%)

massive transfusion (34%)

pancreatitis (25%)

cardiopulmonary bypass

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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, as compliance is decreased by the damage and swelling caused to lung tissue from the influx of inflammatory response

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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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Compliance is decreased by the damage and swelling caused to lung tissue and alveolar capillary from the influx of pro inflammatory mediators (cytokeines, protein, and cells), also resulting in the damage of alveolar type 2 cells, and loss of surfactant leading to alveolar collapse, and stiff lung tissue

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Dyspnoea, hypoxaemia with poor response to FiO2 supplementation. Hyperventilation due to decreased lung compliance and respiratory alkalosis.
Decreased tissue perfusion causing a metabolic acidosis & organ dysfunction. Leading to increased WOB, decreased Tv and hypoventilation, leading to T2RF (hypercapnoea) & respiratory acidosis with worsening hypoxaemia. & right oxyhaemogolbin curve shift. Hypercapneoic vasodoliation, inflammatory response and organ dysfuntion leads to shock.

Pt assessment:
Increased WOB, dyspneoa (accessory muscle use)
chest pain, wheeze, Haemoptosis, Cyanosis, High PIPs, Decreased air entry. Crackles. Decreased UO
Febrile
Low BP, with compensatory tachycardia
Due to organ dysunction - deranged LFTs, and U&E
Decreased GCS & RAS due to hypercapneoa, hypoxia, potentially ureamia,
CXR - diffuse opacity from oedema, atelectasis

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The inflammatory response causes neutrophil infiltration and pro-inflammatroy cytokins leading to tissues oedema impairing gas exchange due to increased thickness of the alveolar membrane, inhibiting O2 diffusion (Increased A-a gradient)
Neutrophil containing pulmonary exudate also interfere with surfactant  function leading to alveoli collapse and therefore decreases surface tension/ compliance.
Alveolar infiltrates and collapse results decreased ventilation resulting in shunting, and low V/Q

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5. How is oxygenation and ventilation affected? 

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5. How is oxygenation and ventilation affected? 

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Flooding to the alveoli from the inflammatory response, fluids, proteins and cells causing shunting, a low V/Q mismatch (decreased alveloar ventilation), reducing O2 diffusion, and thus reducing PaO2 & SpO2. In addition with the destruction of Type 2 alveolar cells, surfactant is reduced resulting in alveolar collapse

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By definition, arterial blood gas (ABG) analysis shows hypoxemia, which is often initially accompanied by acute respiratory alkalosis, and an elevated alveolar-arterial oxygen gradient. This can later turn into a hypercapneoic resp acisosis Metabolic acidosis from hypoxemia is unusual and, if present, is more likely to be due to the precipitating etiology (eg, sepsis) or associated organ injury (eg, acute kidney injury).
If develop shock - High lactate

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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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Type 1 and turns into a T2RF
Initially the patient is only hypoxic. However, due to decreased tissue perfusion this changes to a metabolic acidosis wich increases WOB & RR, as pt tires RR is not longer able to compensate for decreased Tv (due to decreased compliance), in addition to worsening gas exchange, the patient also develops a T2RF (hypercapneoa).