12/12 ARDS - Sunderram Flashcards
ARDS
acute respiratory distress syndrome
- severe resp distress following sepsis, pneumonia, aspiration of gastric contents, major trauma
- systemic inflammatory response → pulmonary edema at low cap pressure (NOT due to high venous pressure! its due to cap leak!)
- pts present with
- progressive arterial hypoxemia (due to accumulation of fluid in lung)
- dyspnea (activation of stress/stretch? chemoreceptors)
- marked increase in work of breathing (bc lungs are v stiff, heavy, noncompliant
bilateral pulmonary infiltrates on CXR
ARDS pathogenesis
diffuse alveolar damage
how does it occur?
diffuse alveolar damage:
- acute inflammation
- edema
- hyaline membranes
- hemorrhage
pathogen
insult → inflammatory cells and cytokines → cap endothelial and alveolar epithelial injury
- incr permeability → protein rich interstitial and alveolar edema
- decr surfactant production and fx → atelectasis
neonatal respiratory distress syndrome
main reason is PREMATURITY leading to decr alveolar surfactant
key difference: endothelial and epithelial damage do occur, BUT they are a consequence of acidosis and vasoconstriction
phsio principles of ARDS
four things you see
- protein rich alveolar edema
- impairs alveolar ventilation
- inactivates surfactant
- decr lung compliance
- mismatched V/Q
- intrapulmonary shunt
trans-pulmo pressure volume curve is shifted down and to the right
- more pressure required to start inflation
- heterogeneous inflation: some parts of teh lung will be overinflated
ARDS pathology
all components of alveolus are diffusely involved (epithelium, endothelium, interstitial space)
- NOTE: diffuse alveolar damage does NOT necessarily involve lung diffusely
two main stages:
- early/exudative stage
- late/organizing stage
stages not necessarily progressive, process can stop at any time
acute/exudative phase
first week following onset:
- type I pneumocyte necrosis and sloughing of basement membrane
- congestion of alveolar caps, interstitial and alveolar edema, intra-alveolar hemorrhage
- hyaline membranes in region of alveolar ducts
- intracapillary neutrophil aggregates
- interstitial inflammation: lymphocytes, macrophages, plasma cells
- microvascular thromboemboli
end of first week:
- hyperplasia of type II pneumocytes which continutes throughout organizing phase
organizing phase
towards end of first week, start organizing phase:
- exudate within interstitium and alveolar spaces begins to organize → extensive proliferation of type 2 pneumocytes and fibroblasts along basement membranes of damaged alveolar septa
- fibroblasts and myofibroblasts proliferate within interstitium and migrate through breaks in basement membrane into intra-alveolar fibrinous exudate
- can end in either complete resolution, stable fibrosis, progressive fibrosis
- vascular thromboemboli common
- squamous metaplasia seen
repair and resolution
- type 2 pneumocytes regenerate into type 1 pneumocytes
- allows for restoration of normal alveolar gas exchange
- exudate transforms into granulation tissue that may be resporbed as lung returns to normal
fibrotic (chronic) phase
- patients survive 3-4wk on ventilator
- see extensive remodeling by dense fibrous tissue
- alveolar spaces and bronchioles my haphazardly enlarge, become surrounded by dense fibrosis
- progressive increase in intra-alveolar fibrosis and collagen
in fatal cases, fibrosis progresses for several weeks with extensive reconstruction of lung parenchyma and FINALLY, honeycomb lung
management of ARDS
risks of management with ventilation
mechanical ventilation is required BUT need to be careful not to cause ventilator-induced lung injury
- can happen due to extra-high tidal volume ventilation
- even physhiological levels of vent can worsen injury due to extreme heterogeneity of alveolar patency
- combo of fluid-filled/patent/collapsed alveoli
high pressure trauma: BAROTRAUMA, leading to
- pneumothorax
- pneumomediastinum
- subcutaneous emphysema
what happens?
- alveoli rupture at border of alveolar base/bronchovascular sheath
- air dissects along vascular sheaths towards mediastium, into hilum and mediastinal soft tissues
- mediastinal parietal pleura ruptures, pneumothorax develops
positive pressure vent can lead to
- end-inspiratory alveolar overdistention (volutrauma)
- incr wall stress/”stretch” → physical disruption of tissue, activation of stretch-response infl pathways, incr parenchymal infl/atelectasis/hypoxia/cytokine production
- end-expiratory alveolar derecruitment (atelectrauma)
- biochem injury/infl (biotrauma)
management strategies to avoid risks
lung protection strategy
- low tidal volume
- optimal end-exp pressure
- improves arterial oxygenation by redistributing lung water from alv to interstitial spaces
- recruits atelectatic alveoli → incr FRC
- recruitment maneuvers
- prone positioning
- reduction in shunt
- perfusion preferentially directed to dorsal lung regions
- gravitational pleural pressure gradient is more uniform
- regional V/Q ratio more uniform and better matched
