ARDS Flashcards
ARDS
outcome determined by:
caused by range of conditions
outcome determined by underlying cause of ARDS
lung condition leading to low O2 in blood
ARDS can be life threatening as organs need O2 rich blood to work well
ARDs causes
direct and indirect
direct Covid-19 (17%-41%(Villar et al 2020) Pneumonia Aspiration of gastric contents Inhalation injury Pulmonary contusion Pulmonary vasculitis Drowning
Indirect Non pulmonary sepsis Major trauma Pancreatitis Severe burns Drug overdose
ARDS
pathophysiology
Acute inflammation affecting the lung’s gas exchange surface (the alveolar-capillary membrane).
Increased permeability of the membrane associated with the recruitment of acute inflammatory mediators into the airspace manifests as high permeability pulmonary oedema.
The resulting acute inflammatory exudate inactivates surfactant leading to collapse and consolidation of distal airspaces with progressive loss of the lung’s gas exchange surface area.
This would be compensated for by hypoxic pulmonary vasoconstriction, if the inflammatory process did not also effectively paralyse the lung’s means of controlling vascular tone, thereby allowing deoxygenated blood to cross unventilated lung units on its way to the left heart. The combination of these two processes causes profound hypoxaemia.
pathophysiology
later stages
occurrence of alveolar epithelia type 2 cell repaiir with production of extracellular matrix proteins - collagen
pro inflammatory and profibrotic responses - persistent / uncontrolled during mechanical ventilation leading to pulmonary fibrosis
time frame not always exact
diagnosis / clinical presentation
timing - in 1 week a known clinical insult of new/ worsening respiratory symptoms
chest images - bilateral opacities - not fully explained by effusions, lobar/ lung collapse or nodules
origins of oedema - respiratory failure not fully explained by cardiac failure or fluid overload
need objective assessment to exclude hydrostatic oedema if no risk factor present.
oxygenation
mild
200< PaO2 / FiO2 = 300
with PEEP or CPAP >/+ 5cm H2O
moderate
100/+ 5cm H2O
severe
PaO2 / FiO2 = 100 with PEEP >/= 5cm H2O
ARDS prevention
- no treatment known to improve outcome
Minimise the negative contribution of iatrogenic factors: fluid overload, ventilator-associated lung injury (VALI) from mechanical ventilation, transfusion of blood products and hospital acquired infection.
Need to heighten awareness of the diagnosis, particularly outside ICU, to prevent progression of the syndrome. .
Lung Injury Prediction Score
A LIPS of 4 – 7 has been suggested as the point of considering patients at high risks of ARDS
prevention
Concerns about the ability to identify patients at risk of ARDS
Patients post oesphagectomy have high risk of developing ARDS (up to 20%)
Suggestion to characterise patients early in their clinical course, before they develop ARDS (CXR, RR)
management
identify and treat
support adequate O2 delivery and tissue oxygenation ventilation positioning reduce MR control fever / anxiety / pain increase oxygen delivery fluid balance support (CVP <4mmHg) or PAWP <8mmHg decrease pulmonary oedema
nutritional support
enteral feeding and glucose control
prevent and treat complications VAP DVT
GI stress ulcer
prophylaxis
treatment
low TV: 6mL/kg predicted body weight
increase to 8mL/ kg if pt is double triggering or if insp pressure decreases below PEEP
high PEEP can be applied to patients with ARDS with moderate to severe ARDS.
this needs to be monitored carefully to prevent lung injury
physiotherapy treatment
Aims: (i) remove any excess secretions (not generally an issue) (ii) improve of gas exchange (iii) prevent/treatment of atelectasis
Therapies/techniques/modalities: MHI/VHI; suctioning (minimal, if needed requires humidification); positioning; manual techniques
Precautions: high PEEP; infection
prognosis
LV and spirometry normal after 6 months after ICU discharge
significant functional disability in many patients
impaired pulmonary function is not primary cause of pot ICU disability
older age group study
higher rates of restrictive lung disease
NM dysfunction rather than parenchymal abnormalities.
comparing imaging abnormalities and PFT abnormalities to help diagnosis true fibrotic changes
