Podcast: Play in new window
See Part 1 for pathophysiology
Things What Known Be Worky
–First and Foremost, treat the underlying condition.
–ALL these patients need to be on THE BREATHY MACHINES: vents. Anything else will kill them. This is by definition a ventilator disease. (You MAY be able to get away with CPAP / BiPAP, maybe?)
–Low tidal volumes (4-6 mL/kg IBW) with high RRs to maintain minute volume (oxygen delivered per minute). These patients are really prone to overinflation injuries because their lungs become stiff with that fibrosis, so low TV is really important.
–PEEP is your friend! He wants to come to the party! Sure, he can be rowdy and break your furniture, but let him come! He’s here to stay. Why? He stents open some of those shut-off alveoli. BUT, a PEEP too low can actually derecruit the alveoli you’re recruiting on your inspiration, and if you recruit and then derecruit, it’s actually HARDER to open the airway.
–BUT: high PEEP Increases pulmonary shunting in PFOs! Be. Careful. Also, high pressures can cause pneumothorax and hypotension due to increased intrathoracic pressure (reduces venous return).
–Paralytics: Improved P:F, decreased mortality. More to the point this allows us to override their ventilations entirely, increases vent compliance, reduces bucking.
–Fluids? Fluids BAD! Treat sepsis aggressively in the first 48 hours, but 48 hours is the tipping point with ARDS. Be restrictive! Be strict! Because of capillary leakage, excess fluid is going to wind up in the lungs! Reduced fluid doesn’t have a proven mortality benefit BUT increased number of ventilator-free days during admission.
–Pressors >> Fluids! If their BP drops, give pressors. If they need transfusions, give transfusions.
–ECMO. Yep, put ‘em on V/V ECMO and your problems are more or less over though not completely. Reduced mortality is a wonderful thing. You’re not going to take them off the vent completely, but you are buying the lungs time to heal and recuperate and hopefully to let that inflammation start to subside before you wean them back onto the vent.
Things What Maybe Might Work Ish And/Or Hurt?
–Proning: LIE EM ON THEIR FACE! This actually recruits large portions of the lungs that are normally dependent (eg filled with fluid). Data is unclear; no mortality benefit evident; improves P:F ratios; use as a rescue tool for severe ARDS and worsening failure. Last-ditch effort.
–SYSTEMIC vasodilators — Prostaglandins, sildenafils – DECREASE oxygenation and INCREASE MORTALITY, maybe, depending on who you read.
–INHALED vasodilators…. say, INO? Interesting stuff. Might improve oxygenation just a smidge, but doesn’t lower Pulm. Artery pressures the way you’d think it would. In other words? No really good data yet on INO.
–Systemic Corticosteroids: Who knows?? Mixed data, no mortality benefit. Maybe that has to do with mixed causes.
–High-Flow Oscillatory Vents? Resp rates 300-900/min? Useful? WHO KNOWS?! Data isn’t clear! Lastest study from Britain says NO mortality benefit.
–Liquid Ventilation / Partial Liquid Ventilation: Still in early phases of work. The idea is to fill the lungs with an oxygenating fluid, perfluorocarbons (PFCs) , just like in The Abyss. That should, theoretically, cause better ventilation in dependent areas of the lungs, give better oxygenation across the capillaries, etc. Research is ongoing. So far no big trials, some results in porcine models.
–Continuous External Negative Pressure Ventilation (CENPV) – tank ventilators, AKA the modern man’s Iron Lung. NEGATIVE pressures -33 on inspiration to -15 cmH2O at exhalation (basically, it’s counterPEEP, or NEEP). Needs a lot of research but has some serious benefits in reduced airway, transpulmonary, and intraabdominal pressures. Also case reports of this type of tx being done with CENPV with a traditional vent on the outside providing pressure support. That sounds counterintuitive to me, but I’m just a PIG!