Brandon and Bryan mock up a goals of care discussion for a critically ill patient, and reflect on the right and wrong ways to execute this complex procedure.



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Resources



Center to Advance Palliative Care



The Conversation Project

We chat about neuromuscular blockade, monitoring, and reversal in the ICU, including why sugammadex isn’t more widely used, with Sara J Hyland, PharmD, BCCCP, FCCP, researcher and clinical pharmacist in perioperative and emergency medicine.



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Takeaway lessons




* Aminosteroids (rocuronium, vecuronium) can be reversed by neostigmine + glycopyrrolate (the latter to mitigate peripheral cholinergic effects of neo), or sugammadex. Benzylisoquinoliniums (e.g. cisatracurium) can only be reversed by the neostigmine option.



* Neostigmine is an acetylcholinesterase inhibitor; in other words, it doesn’t directly antagonize the effect of the paralytic, it simply helps boost the supply of ACH at the neuromuscular junction to overcome it. This means its reversal effect is indirect and imperfect.



* Neo is completely ineffective when blockade is deep. In fact, it can have a paradoxical effect of prolonging paralysis when used in these situations. It should really only be used when the train-of-four is 4 twitches. It is also slower acting than sugammadex, and even given with glyco, has inevitable risk of cholinergic toxicity (e.g. bradycardia).



* Neo + glycopyrrolate costs around $30 for a dose, versus around $150-200 for a sugammadex approach. (This does not take into consideration broader system costs from a less effective and less efficient reversal method.) Overall cost with sporadic ICU use will always pale in comparison to high-volume perioperative use, though.



* Sugammadex is a direct binder of the rocuronium/vecuronium molecule, and can attract even already-bound compound from its receptor; hence, it can function at any level of blockade (even very deep).



* A large number of our patients who appear to have cleared their paralysis (seeming clinically “strong,” TOF 4) still have a significant continuing effect of neuromuscular blockade. This may contribute to failures of extubation and other complications. In one ICU study of random ICU patients, >40% had active neuromuscular blockade to a degree that would have precluded extubation by anesthesia standards.



* As a result, the international, guideline-directed gold standard for reversal of neuromuscular blockade is now using quantitative, objective neuromuscular monitoring (before and after reversal agents) to confirm resolution to a >90% TOF ratio.



* What’s that? Normal train-of-four devices (qualitative peripheral nerve stimulators) are inadequate; 4 out of 4 twitches may be present despite 70% of nicotinic ACH receptors still blocked. Better devices (with accelerometers, myometers, EMG, etc) can measure the actual twitch strength and compare the ratio of first to last twitch—i.e. does it fade or maintain strength? The fourth twitch should be >90% the strength of the first before extubation. (All four twitches must be present to even attempt this technique; other techniques can be used at levels of blockade deeper than this.)



* Although sugammadex will be effective at any degree of block, it is dosed differently at different levels, so pre-drug assessment is still important. (It may also reveal the option of using neostigmine, if desired.) Post-drug assessment is then needed to confirm adequate response.



* “Recurarization,” or recurrence of paralysis after reversal, is a known phenomenon. It is rare after sugammadex, and tends to occur when it was underdosed; the immediate effect may be good but the paralytic may outlast the reversal.

We chat with Leeah Sloan, PA-C, co-chair of the Critical Care APP Steering Committee for the American College of CHEST Physicians (CHEST), about the newly available CHEST critical care certification for APPs.



The Vandalia CAMC Charleston APP critical care fellowship




* CHEST APP Critical Care Certification



* Essential Critical Care Concepts for APPs 



* CHEST SEEK® Critical Care Medicine for Advanced Practice Providers 



* CHEST Medcast 




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Melissa Bridges, director of PA fellowships at Atrium Health and president of the Association of Post-graduate PA Programs (APPAP), chats with us (Bryan is president of APGAP, the Association of Post Graduate APRN programs) about PA/NP residencies/fellowships in critical care.



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Andrew Schulman, medical musician, former ICU patient, and president of the Medical Musician Initiative, tells us how music can help the critically ill.



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From constipation to hepatorenal syndrome. Fan favorite Elliot Tapper (@ebtapper, @ebtapper), gastroenterologist, transplant hepatologist, academic chief of hepatology, and director of the cirrhosis program at the University of Michigan, returns to answer a grab-bag of GI questions.



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Takeaway lessons




* Constipation may be an “afterload” problem (outlet obstruction, usually identified by a stool ball), best treated by manual disimpaction or a lubricating suppository or enema; a “preload” problem (osmotic diuretics; often polyethylene glycol a good place to start); or a contractility problem (motility agents like senna or bisacodyl; these work where they touch, so give orally for proximal impaction, rectally for distal issues).



* Ondansetron is a good first line anti-emetic. Olanzapine has good evidence for chemo-based nausea, prochlorperazine is also good. QTc should always be considered with these prolonging meds but torsades is really a rare effect from anti-emetics. Sniffing an isopropyl alcohol swab can also be effective in the short term, and has been equivalent to IV ondansetron (superior to oral) in studies.



* Ultrasound is the most important tool to ensure a safe location for paracentesis, but the right lower quadrant is usually a good place to start (no spleen here).



* A very acute CBD obstruction may lead to fulminant cholangitis, but maybe not much ductal dilation, because it hasn’t had time to dilate. (One out of five cases of ALT >1000 may be from hyperacute CBD obstruction.) Dilation should not be considered essential to diagnose cholangitis; empiric ERCP can be appropriate. (In the non-shocked patient, EUS to confirm obstruction before doing sphincterotomy may be useful intraprocedurally.)



* In less obvious cases, MRCP can be useful, especially in a more stable patient, or when the diagnosis (or benefit of drainage) is less clear.



* When stenting or drainage of the CBD directly is not possible, sometimes it can be accessed retrograde from the gallbladder – or sometimes draining the gallbladder may indirectly decompress the CBD. Most of the time this is not the first line approach.



* Actually just doing a cholecystectomy first line may be the right option more often than not, if you can find an accepting surgeon.



* Percutaneous chole tubes can sometimes cause downstream problems, particularly when patients



* Cirrhotics get AKI for reasons other than hepatorenal syndrome… a lot. ATN is at least four times as common as HRS. Check the urine for casts, etc, but ultimately you can never be sure of the diagnosis up front, so time and response to treatment are always key diagnostic tools.



* Blindly fluid challenging HRS up front is usually needed. But if you truly believe they’re euvolemic or even fluid overloaded, it’s appropriate to treat those is usual. Otherwise, challenge with fluid (albumin is not a magical choice, use anything).



* Octreotide is not the treatment of choice for HRS in the ICU; use norepinephrine and titrate up until you see an increase in urine output (or it doesn’t work). Terlipressin works too but is pricey and more appropriate for outside the ICU.



* Pumping lactulose into an ileus, or any gas- and volume-promoting agent, tends to worsen bloating without much help. You don’t want constipation to exacerbate the problem,

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We chat with Dr. Michael Lanspa, intensivist and director of the Intermountain Critical Care Echocardiography Core Lab, about common pitfalls among bedside POCUS users and tricks for doing it better.







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Takeaway lessons




* It’s a fallacy to think that any quantitative method of EF evaluation is truly objective; cardiologists eyeball the EF and adjust their calculation if it seems wrong.



* EF is always loading sensitive, and will not reflect stroke volume accurately if the chamber is small or large. The eyeball/gestalt method is usually harder with non-symmetric contraction (i.e. RWMA).



* LVOT VTI is often compromised by an off-axis angle of insonation (within 15 degrees will introduce negligible inaccuracy), and a poor signal (the VTI should ideally be hollowed out).



* In general, tracking the VTI alone using a similar technique will yield more consistent results than attempting a full cardiac output calculation.



* TAPSE fails when the free wall contracts more or less than the longitudinal contraction. This is common in PAH, where the free wall may be more impacted than the longitudinal function. The converse may occur in the LV in hypovolemia, where radial contraction may appear hyperdynamic but longitudinal shortening remains diminished.



* s’ tends to “see” better with a poor view than TAPSE, as tissue doppler is more sensitive than M-mode.



* With more severe TR, the doppler gradient tends to underestimate the RVSP, as the pressure equilibrates faster during systole.



* A sniff test during IVC ultrasound is part of the standard echo method of estimating CVP. It is not well-proven to approximate volume responsiveness.



* Remember that when dynamic LVOT obstruction occurs, LVOT VTI may be extremely high, but the stroke volume is not elevated — it’s balanced out by the reduction in effective orifice size (i.e. the LVOT diameter is not the diameter of the jet, which has been narrowed).



* In general, eyeball assessment of regurgitation using color doppler and B-mode is probably all that’s needed for POCUS; attempting additional quantification is rarely high-yield.



* Assessing aortic stenosis is generally an unreasonable ask for bedside POCUS users. The easiest tool is probably to get the best possible 2d view of the valve and eyeball its opening; a reasonable visualized valve excursion is probably not consistent with severe stenosis. Beyond that, obtain a full study.

We explore the world of thrombectomy for acute ischemic stroke with Justin F. Fraser (@doctorjfred), MD, FAANS, FAHA, Professor and Vice-Chair of Neurological Surgery and Director of Cerebrovascular Surgery and Neuro-interventional Radiology at University of Kentucky, where he specializes in cerebrovascular, endovascular, skull base, and endoscopic transsphenoidal surgery.



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Takeaway lessons




* In the opinion of Dr. Fraser, thrombectomy for qualifying patients with acute ischemic stroke is the current standard of care. Patients in non-thrombectomy centers should be transferred. Failure to do so is potentially negligent.



* Dr. Fraser feels there are few true contraindications to thrombectomy (as long as the patient’s goals are concordant), and the current indications should probably be most strokes <24 hours with a large vessel occlusion on CTA – i.e. ICA (including with a tandem extracranial carotid occlusion), MCA, ACA, or basilar. He no longer feels most cases need perfusion imaging as even large or older infarcts seem to benefit.



* The main current question is the utility of thrombectomy in “medium vessel occlusions,” such as M2 and more distal vessels.



* Radial artery access is growing in popularity, similar to its growth in cardiovascular interventions, now that devices have shrunk enough to fit. The right wrist is preferred.



* In general, qualifying patients should still receive systemic thrombolytics as soon as possible prior to performing thrombectomy, at least with the state of the evidence in 2025. This also helps manage any particles that embolize into more distal vessels during aspiration of a larger thrombus.



* Generally, thrombectomy is merely a process of aspirating an embolus. However, if thrombosis also involved an intracranial atherosclerotic narrowing, there may still be unstable stenosis afterwards, so about a third of cases also require stent placement. (Carotid occlusions are a different story and usually need stenting, just as with elective endarterectomies.) When stents are placed for this reason or for a carotid lesion, dual antiplatelet inhibition is usually needed; this may be started during the procedure with an intra-arterial agent if DAPT is not already on board.



* Thrombectomy can be performed under local anesthesia only, or under deeper sedation; the practice for Dr. Fraser’s group is to put everybody under general anesthesia. Anesthesia’s efforts are performed simultaneously to the interventional prep and should not delay it.



* Post-procedure blood pressure targets are controversial. Fraser targets SBP <160 for 24 hours to limit reperfusion hemorrhage.



* Post-procedure MRI is usually appropriate to delineate infarct size and to appreciate the degree of edema, potentially requiring decompressive craniectomy (large hemispheric or cerebellar stroke). If MRI is delayed, CT is appropriate, perhaps dual-energy CT to differentiate hemorrhage from contrast staining.



* Expanding thrombectomy to more patients in smaller hospitals requires more trained neurointerventionalists, but this is not a completely simple matter, as it must be balanced against adequate volume to maintain proficiency for the proceduralists and their teams.

We learn about the basics of fetal monitoring in the critically ill pregnant woman and how to integrate them into our ICU workflows, with Stephanie Martin, MFM obstetrician and host of the Critical Care Obstetrics podcast and teacher at the Critical Care Obstretrics Academy.







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Takeaway lessons




* A fetus is considered potentially viable at 23-24 weeks gestational age, with 22-23 weeks being occasionally viable in specific circumstances and highly specialized centers. “Potentially viable” does not mean guaranteed survival, as fetal mortality is still quite high. In other words, at 23 weeks and above, intervention to promote fetal survival make sense. Every additional day of gestation improves outcomes.



* A conversation should occur preemptively between the mother, ICU, and obstetric teams to clarify what options will be considered—in some circumstances, early delivery (via C-section) is not desired due to the risk to the mother, and should not be assumed to be the contingency in all viable pregnancies. On the flip side, delivery of a non-viable fetus could still be appropriate for the mother’s health, such as in uterine infection or hemorrhage.



* If a fetus will not be delivered early, there may be no role for fetal monitoring.



* Fetal monitoring is therefore relevant at viable gestational ages. However, it is also more difficult for early pregnancies; the monitors can easily wander off a tiny fetus, and the strips are harder to interpret.



* Fetal monitors essentially monitor 1. Fetal heartrate (via Doppler), and 2. Uterine contraction. Heartrate is monitored primarily to determine variability, i.e. how much the rate changes from its average baseline in response to stimulus, particularly uterine contraction (which causes fetal stress of sorts). Poor variability with markers like late decelerations can be a sign of fetal acidosis and ischemia, particularly to the brain, which can increase the risk of fetal demise or birth defects such as cerebral palsy. Prematurity creates particular vulnerability to this.



* Maternal sedation leads to fetal sedation, which can make interpreting the heart rate more difficult.



* Uterine contractions rarely turn into labor, but they provide a natural stress test to the fetus.



* Much of the interpretation of “fetal distress” comes down to the context—for instance, maternal acidemia will always cause fetal acidemia, but in a rapidly reversible setting such as DKA, the best solution may simply be resuscitating the mother.



* Fetal distress is often an early marker of shock and other systemic stress, as uterine perfusion is sacrificed fairly early by the body in favor of other organs. This often manifests as uterine contractions.



* Any pregnant woman with a gravid uterus up to the umbilicus, or >20 weeks, who is critically ill, should not lie supine; the uterus will compress the great vessels and may cause shock. Elevate the head of the bed or tilt them laterally at all times. (During CPR, assign someone to manually displace the uterus to the left, as tilting the entire patient is challenging.)



* There is relatively little role for ultrasound or other tool...

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We discuss the basics of EEG in the ICU, including when to do it, selecting the appropriate study, and the basics of bedside interpretation, with Carolina B Maciel, MD, MSCR, FAAN, triple boarded in neurology, neurocritical care, and critical care EEG.



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Takeaway lessons




* There is little to no role for a very short (<2 hour) EEG in the critically ill patient, who generally has “less of everything”; to determine the presence of seizure activity or other electrical disease, more data is usually necessary.



* Long-term or continuous EEG is usually defined as >12 hours. 2-12 is a middle ground (both clinically and for billing purposes). In most ICU cases, a “middle” study of a few hours can be done, then the findings used to inform the need for a longer study; validated scores exist for this, such as 2HELPS2B.



* Don’t forget the non-seizure diagnoses that can be made/supported from EEG, such as brain death, cefepime-induced encephalopathy, sudden clinical changes due to osmotic shifts, etc. In reality, EEG readers, particularly in the community, may or may not be making great efforts to appreciate these things. You will get better reads if you communicate your questions to the reader, and consulting neurologists/neurointensivists may be able to glean more from a non-specific EEG report as well. Critical care EEG folks like Carolina may be the most helpful, but there are very few training programs for this.



* Basic filters on the EEG include the high and low pass filters (should be LFF of 1 hz, HFF ~7–8 hz), and potentially a notch filter for 60 hz (in the US) or 50 hz (in Europe) to filter out AC electrical noise.



* Dark vertical lines on the strip occur every 1 second. With normal scale there should be about 3 centimeters (around your thumb’s length) between them.



* Odd numbered leads are on the left side of the head. Even numbers are on the right. Z-numbered leads are in the sagittal midline.



* Do you see intermittent bursts of something pointy, like it will hurt to sit on? These may be muscular artifact, which can be hard to distinguish (look at the patient to see if they’re moving/twitching), but if not, this may be an epileptic discharge; similar to a PVC, or someone coughing in the symphony audience, it’s an inappropriate interruption in brain activity. This may be focal or global (all leads), and focal may be higher risk. They may be repetitive, occurring somewhat regular intervals, which are also more concerning. Ultimately, the concern is always whether they are going to evolve/organize into full seizures, so if no evolution ever occurs, that is also more reassuring.



* When to treat epileptogenic discharges on EEG is always a judgment call and must be put in context of the patient. More abundant discharges with a more malignant appearance are more concerning, but the clinical correlation matters too; EEG findings with no clinical correlate are less worrisome. Convulsive seizures are a medical emergency (especially with continuous tonicity), but non-convulsive electrical activity, even non-convulsive status, usually has room and time to weigh the risks versus the benefits of therapy. Talk to experts and make a thoughtful decision.



* Carolina hates fosphenytoin due to the cardiotoxi...

Philippe Rola, intensivist, master of the VEXUS scan, and founder of the Hospitalist and Resuscitationist conference, shares his recent model of four hemodynamic interfaces to describe the entire circulatory system.



Register for the H&R conference (May 22-23 2025) here with the discount code provided in the show. (No, we’re not sponsored, just a cool event.)







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A roundup from members of the SCCM’s ICU Liberation committee, recorded at SCCM Congress 2025.



Included:




* Heidi Engel



* Kali Dayton



* Kristina Betters



* Stacey Williams



* Jessica Anderson



* Jenna Domann



* Sergio Zanotti



* Erika Setliff



* Brian Peach

We learn the vanishing art of placing the PA (Swan-Ganz) catheter, with intensivist and friend of the podcast Matt Siuba (@msiuba).



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Takeaway points




* Good sheath placement: ensure your skin nick is in the same hole as your dilator; use patient, steady pressure, especially as the “shoulder” (where the dilator meets the sheath) reaches the skin; insert the dilator completely into the sheath so you can see if it shifts, and dilate using both hands (one near the tip, one at the back holding the sheath and wire).



* The right IJ is best (try to leave this open when placing non-positional lines like a triple lumen), left subclavian next best, third choice left IJ or right subclavian. Femoral placement is very tough without fluoroscopy; it requires two turns (into the RV, then out into the PA) and can be challenging to escape the RV. A brachial vein in the arm can occasionally be used as well.



* Floating out of the left IJ is often obstructed by bumping into the innominate-SVC junction. Instilling just 0.5-1 cc of air in the balloon is often enough to float around this turn. This occurs less from the left subclavian or brachials, but if it does occur, the same maneuver may help.



* Remember to place the contamination sleeve (Swandom) before inserting the Swan! Once you’re in, it’s too late; you’ll need to remove it and refloat. You don’t need to seal it, just get it around the catheter.



* Flush each lumen before inserting and cap each one, except the distal/PA port. Connect that to your transducer and flick it to test transduction. Check the balloon; rarely, but sometimes, they will fail. Remember to always inflate the balloon using the included volume-limited syringe, and allow it to passively deflate from its elasticity.



* If a balloon does not self-deflate, replace the catheter; the balloon is not reliable.



* Once you reach 15 cm, inflate the balloon. By 15-20 cm, you should be in the RA; measure your RA pressure (overall mean is fine for ICU purposes). If the waveform is not distinct with clear components, flush the catheter; it may be damped by clots.



* Tricuspid pathology (TR, stenosis) can make a Swan challenging, but not as often as people think. And the harder the Swan, often, the more important the data.



* If you reach 30 cm without an RV tracing (except in some very large or very end-stage PH patients), you have probably gone astray, either coiled in the RA or gone through to the IVC.



* Once in the RA, make a quarter rotation counter-clockwise (assuming you started with the tip curved medially). This will help orient the tip towards the tricuspid valve. If it’s not getting through, drop the balloon, come back to 20, readvance, repeat as needed.



* If still not going, sometimes the tip has looped back into the RA while the middle of the catheter has “elbowed” through the tricuspid into the RV. If this happened, retract the catheter, and the tip may flop through as you come back. You’ll know this as the RV waveform will appear during retraction; inflate the balloon then and drive forward fast.



* If you can’t get through a regurgitant valve, a faster/more aggressive advancement through the tricuspid valve may help. You need to launch through before it kicks you out.

We learn about the Vortex approach to airway management, as well as airway algorithms and mental models in general, with Vortex creator and anesthesiologist Dr. Nicholas Chrimes, anaesthetist and cofounder of the Safe Airway Society.



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References




* The Vortex website

We discuss the basics of evaluation for tracheostomy placement, periprocedural care, and post-procedure complications with Vinciya Pandian, PhD, ACNP, FCCM, tracheostomy nurse practitioner and researcher.



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