Josh Farkas MD 💊

I just updated the IBCC chapter on pulmonary vasodilators, here are new pearls I learned 🤯 🫁 The dosing of inhaled pulmonary vasodilators is a little different for ARDS versus for treatment of RV failure. In ARDS, you're shooting for selective vasodilation of the best-ventilated alveoli to maximize V-Q matching, so you want a mid-range dose (too high and you start vasodilating the worse-ventilated alveoli). In RV failure you're trying to vasodilate every alveoli as much as possible to bring down the pulmonary vascular resistance, so go high. 🫁 Nebulized milrinone causes selective pulmonary vasodilation for ~20-30 minutes, then gets systemically absorbed. One dose of nebulized milrinone in the OR is great, but scheduling milrinone nebs q4hr doesn't make pharmacological sense (it doesn't achieve consistent pulmonary vasodilation and there are risks of systemic accumulation in renal failure). IMHO milrinone nebs don't have much role in ICU. If you want to give milrinone just give it IV. 🫁 There's a gradually escalating amount of evidence supporting combined simultaneous use of inhaled epoprostenol and inhaled NO to treat RV failure. See the article by Andre Denault below. This may be a good option for RV failure before escalating to an Impella RP Flex. It's pretty easy to trial a patient on inhaled pulmonary vasodilators - if they work great, if they don't work you haven't lost much. #1/2, link in next post.

Fresh IBCC chapter: APRV guide 😁 My first APRV guide came out in 2017. I updated it during COVID in 2020. I just completely overhauled it again. Two APRV guides were published recently (one by @TheEMNerd in 2022 and one by Nieman et al. 2026). Both guides focus on how to get patients initiated on APRV. My APRV guide is consistent with them. There is a general consensus about how to get APRV started. Currently, the most challenging & controversial aspect is how to wean *off* APRV. Much less is written about this. I've described two possible approaches based on the best data that we have (Zhou et al. RCT) and basic vent weaning principles. But this remains murky. Some approaches to weaning off APRV involve a gradual removal of ventilator support, without spontaneous breathing trials. This strategy isn't consistent with modern techniques of ventilator liberation (i.e., providing comfortable non-fatiguing support with intermittent spontaneous breathing trials). APRV is a great rescue modality currently. However, for APRV to demonstrate benefit in clinical trials, proper attention is needed to rapid APRV weaning. Inadequately aggressive weaning strategies will destroy the ability of APRV to improve ventilator-free days & ICU length-of-stay. I'd love to hear about folks' experience in terms of APRV weaning. The role of APRV in ARDS remains controversial. It was hotly debated during COVID in a partisan fashion without any real conclusion. Hopefully further RCTs will clarify its precise use. This is tough because outcomes depend on how APRV is set (not simply the binary presence/absence of APRV). Aside from ARDS, APRV is pretty fabulous for mucus plugging and atelectasis. Physiologically, its ability to produce biased airflow that promotes secretion clearance is simply unparalleled (slow inspiration & fast expiration clears secretions out of the airway). So regardless of where we land with APRV for ARDS, I do think that there will always be some use for APRV in critically ill patients. So this guide will hopefully be evergreen. (#1/2, link next)

Fresh IBCC chapter: Airway clearance techniques! This topic is pretty murky due to an absence of much evidence or review articles. It's tempting to just ignore the entire topic, but there IS physiology and some data behind this, so we should try to understand it. (Unintentional pun with "IS" = incentive spirometry, a technique which sadly doesn't really work. I mean maybe it would work if people truly used it a bajillion times like they're supposed to, but in reality it sits on the bedside table and achieves nothing.) Lemme know if you have any post-publication peer review. The chapter isn't exhaustive. There are dozens of techniques out there so I've focused on techniques that I've seen to be helpful. (The goal of IBCC is always to be pragmatic & realistic, not exhaustive.) (#1/2)

Wake up babe, there are now THREE types of delayed sequence intubation (DSI) Following the PREOXI trial, BiPAP preoxygenation has become standard in many ICUs. BiPAP allows patients to remain well recruited and oxygenated, even if they aren't awake and breathing hard. This opens up the door to a variety of types of delayed-sequence intubation. These techniques involve the same exact materials as a standard intubation, and similar medications. They represent ways to slow down the intubation process and proceed in a more stepwise fashion. This can be helpful for the physiologically challenging airway. [1] DSI-Oxygenation 🫁 Classic & most common type of DSI (what most people refer to when they say "DSI"). 🫁 This is fundamentally sedation to allow the patient to tolerate preoxygenation 🫁 Used for patients who are too agitated or anxious to tolerate BiPAP preoxygenation [2] DSI-Sedation 💉 Patient is placed on BiPAP and receives titrated doses of sedation to gradually promote unconsciousness. 💉 This is useful for patients who are hemodynamically tenuous, for two reasons. First, it minimizes the sedative dose to what you actually need (often very little, for sicker patients). Second, it allows you to observe how the patient responds to some sedation and positive-pressure ventilation. 💉 Sometimes BiPAP plus sedation will elicit severe hypotension! You have time to resuscitate the patient further before proceeding to paralysis and positive-pressure ventilation (which could make things worse). 💉 This could also be used for a patient with a history of being very difficult-to-sedate, because it allows you to be confident that the patient is unconscious prior to paralysis. [3] DSI-NPV (DSI to facilitate Negative Pressure Ventilation 🫀This is most often used for patients who are at the highest risk of hemodynamic collapse following positive pressure ventilation (e.g., severe PE, tamponade, refractory cardiogenic shock). It could also be useful in severe DKA (to maximize spontaneous minute ventilation post intubation). The goal is to preserve negative-pressure ventilation, which may improve hemodynamics and pCO2. 🫀You start out with DSI-Sedation as discussed above: initiate BiPAP and titrate sedatives to the point of unconsciousness. Follow hemodynamics and resuscitate further as needed. 🫀Then push rocuronium, intubate, then immediately give sugammadex to reverse the rocuronium. You end up with an intubated patient who is spontaneously breathing with negative pressure ventilation (e.g., on 5 cm of CPAP). 🫀This is one type of Hemodynamically Neutral Intubation as described by Weingart (the goal is intubation without perturbing hemodynamics). DSI-NPV is technically easier than an awake intubation. Unless you're insanely great at awake intubation, DSI-NPV will be easier and less likely to go sideways. #1/2, links in the next post.