ARDS (TU1) by Pauline Wong https://padlet.com/paulinewong1/izmx5kcc4mni5vaa NUR5923 Respiratory Pathophysiology en-us 2023-03-08 00:28:25 UTC 2023-06-05 02:05:25 UTC hello@padlet.com 1. Brief definition paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721385 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
]]> 2023-03-08 00:28:25 UTC https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721385 2. Is it obstructive or restrictive? Why? paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721386 Restrictive, as compliance is decreased by the damage and swelling caused to lung tissue from the influx of inflammatory response]]> 2023-03-08 00:28:25 UTC https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721386 3. How does the condition effect lung compliance and/or airway resistance? paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721387 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]]> 2023-03-08 00:28:25 UTC https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721387 4.How does this effect V/Q mismatch? paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721389 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


]]> 2023-03-08 00:28:25 UTC https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721389 5. How is oxygenation and ventilation affected? paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721391 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]]> 2023-03-08 00:28:25 UTC https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721391 6. What type of respiratory failure would this condition lead to? paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721392 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).]]> 2023-03-08 00:28:25 UTC https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721392 7. What are the typical ABGs and why? paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721394 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]]> 2023-03-08 00:28:25 UTC https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721394 8. Clinical manifestations paulinewong1 https://padlet.com/paulinewong1/izmx5kcc4mni5vaa/wish/2507721395 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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