Acute Respiratory Distress Syndrome “acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue…[with] hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space, and decreased lung compliance.” ARDSnet, NEJM, 2000.
Acute Respiratory Distress Syndrome Within 7 days of a trigger PaO2/FiO 2 <300 (40kPa) Bilateral CXR changes Not solely due to cardiac failure
Lung protective ventilation 6ml/kg IBW RR up to 35 to achieve desired MV Plateau pressure less than 30cmH 2 O I:E ratio Permissive hypercapnia Paralysis High PEEP?
Fixing the broken patient Is there… Patient-ventilator asynchrony? Fixable contributory problems i.e. effusions, pneumothorax, bronchospasm? Actually a problem? Consider… Recruitment Paralysis I:E ratio PEEP Fluid status And then consider…
Proning Improves Distribution of ventilation and perfusion Recruitment Secretion clearance Problems Tube/line displacement Pressure injury Facial oedema Early and for prolonged periods = improved mortality? Guerin, NEJM, 2013
High Frequency Oscillatory Ventilation RR 60-3000bpm TV < dead space Convection, molecular diffusion, streaming, Pendelluft & cardiogenic mixing Now predominantly discredited OSCAR & OSCILLATE, NEJM, 2013
Extra Corporeal Membrane Oxygenation Made famous by H1N1 Severe, reversible, respiratory failure where conventional methods are failing Early rather than late Venovenous vs venoarterial Evidence in adults not (IMO!) conclusive CESAR, Lancet, 2009
Summary Types of airway & what to do if they fall out ARDS Ventilatory strategy Proning, HFOV and ECMO