Lecture 9b - Acute Trauma: ARDS - acute respiratory distress syndrome Flashcards

1
Q

What changes occur as a result of #rib or flail segment

A
  • pain
  • decreased movement of ribs
  • decreased gas mvmnt = decreased paO2
  • decreased gas mvmnt = increase paCO2 - increased -load, decreased pump efficiency
  • decreased secretion movement - decrease cough effectiveness, decreased lung vols = decreased EFR
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2
Q

What are some examples of blunt trauma to the lungs/rib cage

A

rib #
flail segment
sternal fracture
pulmonary contusion - bruising of lung

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3
Q

What are the effects of a pulmonary contusion

A

activation of coagulation cascade

  • impaired lung function
  • decreased co2 movement - decrease in Cl, incr resp load
  • decrease 02 movement - decreased SA
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4
Q

Physio managment for rib#, pulmonary contusion

A

pain management
- if intubated - MHI for gas, Suction for secretion
- if spontaneously breathing - DBE for gas, huff/cough
positioning
mobs

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5
Q

What is the definition of ARDS/Acute lung injury (ALI)

A

clinical syndrome characterized by non-cardiogenic pulmonary edema with bilateral disuse alveolar damage

results from endothelial injury/inflammation and increased microvascular permeability

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6
Q

What are the characteristics of ARDS

A

acute hypoxaemic resp failure (within a week)
new bilateral diffuse infiltrates on CXR consistent with pulmonary edema
no clinical evidence of heart failure, fluid overload, or chronic lung disease

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7
Q

what is the BERLIN definition criteria for ARDS

A

Mild - 200-300mmHg paO2/Fio2
Moderate: 100-200
Severe: <100

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8
Q

What are the causes of ARDS (direct lung insult)

A
pneumonia 
aspiration of gastric contents
lung contusion
near drowning 
inhalation of toxic gas
fat embolus
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9
Q

What are the causes of ARDS (indirect lung insult)

A
sepsis 
non thoracic trauma 
multiple transfusions 
pancreatitis 
cardiopulmonary bypass
severe burns
drug overdose
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10
Q

ARDS pathogenesis 3 phases? and key features

A

1) Exudative phase - fluid accumulation - damage to alveolar capillary barrier (leaky), inflammatory infiltrates, surfactant dysfunction
2) Proliferative phase - thickening of endo,epithelium and insterstitial space
Fibrotic Phase - interstitial fibrosis, vascular occlusion

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11
Q

ARDS pathophysiology for o2 and co2 movement

A

o2 - decrease SA - caused by fluid filled alveoli and perfusion of non-ventilated alveoli, pulmonary vasoconstriction/microvascular occlusion

co2- increased resp load - decreased CL- pulmonary oedema and patchy infiltrated. decreased CL b/c of fibrosis in later stage, increase Raw = oedema, emphysematous type changes in later stage

decreased pump efficiency - increased RR and Ve –> resp mm fatigue, increased alveolar dead space

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12
Q

ARDS medical management

A

mechanical vent
prone lying
management of underlying insult

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13
Q

Risks of ventilation with ARDS

A

Barotrauma -high airway pressures
volutrauma - high lung volumes –> regional overinflation

inflammation occurs in response to mechanical ventilatory forces. the combo of these 2 traumas exacerbate the diffuse alveolar damage associated with the syndrome

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14
Q

Why do you place a patient with ARDS in prone lying

A
  • alveolar recruitment and reinflation of dorsal (posterior) lung
  • improves v/q mismatch
  • improves oxygenation
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15
Q

Physio managment of ARDS

A

position
suction
MHI
exercises/early mob

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