Lecture 9b - Acute Trauma: ARDS - acute respiratory distress syndrome Flashcards
What changes occur as a result of #rib or flail segment
- 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
What are some examples of blunt trauma to the lungs/rib cage
rib #
flail segment
sternal fracture
pulmonary contusion - bruising of lung
What are the effects of a pulmonary contusion
activation of coagulation cascade
- impaired lung function
- decreased co2 movement - decrease in Cl, incr resp load
- decrease 02 movement - decreased SA
Physio managment for rib#, pulmonary contusion
pain management
- if intubated - MHI for gas, Suction for secretion
- if spontaneously breathing - DBE for gas, huff/cough
positioning
mobs
What is the definition of ARDS/Acute lung injury (ALI)
clinical syndrome characterized by non-cardiogenic pulmonary edema with bilateral disuse alveolar damage
results from endothelial injury/inflammation and increased microvascular permeability
What are the characteristics of ARDS
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
what is the BERLIN definition criteria for ARDS
Mild - 200-300mmHg paO2/Fio2
Moderate: 100-200
Severe: <100
What are the causes of ARDS (direct lung insult)
pneumonia aspiration of gastric contents lung contusion near drowning inhalation of toxic gas fat embolus
What are the causes of ARDS (indirect lung insult)
sepsis non thoracic trauma multiple transfusions pancreatitis cardiopulmonary bypass severe burns drug overdose
ARDS pathogenesis 3 phases? and key features
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
ARDS pathophysiology for o2 and co2 movement
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
ARDS medical management
mechanical vent
prone lying
management of underlying insult
Risks of ventilation with ARDS
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
Why do you place a patient with ARDS in prone lying
- alveolar recruitment and reinflation of dorsal (posterior) lung
- improves v/q mismatch
- improves oxygenation
Physio managment of ARDS
position
suction
MHI
exercises/early mob