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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We discuss assessment, monitoring, medical stabilization, and when to consider transplant of the patient with acute liver failure. We are joined by Dr. Sergio Navarrete, anesthesiologist and intensivist with fellowship training in transplant anesthesia.



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Takeaway lessons




* Transaminases rising into the many hundreds or thousands (especially with pre-existing liver disease), or a MELD in the low teens (from baseline normal) should raise concern for a concerning degree of liver injury, usually due to shock liver, congestion, or infection. This should also prompt consideration for transplant evaluation, and usually a phone call to your transplant center.



* Reversible causes, such as acetaminophen toxicity or portal vein thrombosis, must be ruled out.



* Optimization of perfusion should include not only the left-sided systemic circulation, but also the right-sided system and venous congestion; congestive hepatopathy (from volume overload or RV failure) can absolutely cause severe liver injury. Echo, potentially with tools like VEXUS scoring, can be a great help here.



* N-acetylcysteine has a clear indication for treating acetaminophen poisoning, but not much data for other causes of liver failure. However, many clinicians believe it may provide some benefit, and there is probably no harm—other than administering a fair amount of volume.



* Hypoglycemia and hypothermia are both relatively late and ominous findings in the ALF patient (put them on a dextrose infusion and hourly glucose checks). Transaminase levels reflect hepatocyte injury but not liver function. Synthetic function as measured by INR or fibrinogen are helpful. Bilirubin is usually too slow and non-specific to be actionable. Trend this stuff every 6 hours or so.



* Mental status is a key monitoring tool as a marker of cerebral edema. The clinical exam, ammonia level, potentially serial CT scans, and maybe invasive ICP monitoring (Sergio prefers a bolt over EVD) may all be needed in high-risk cases.



* The highest risk patients for cerebral edema are those with truly acute/hyperacute liver failure. Trend ammonia, which has some correlation with herniation risk, but the neuro exam is more useful. Neurosonography could be used as well.



* Lactulose should be used, and in extremis hyperosmolar therapy considered, although data for this is less clear than in other neurologic emergencies.



* Liver ischemia and death will reliably cause a systemic inflammatory state with resulting distributive shock; this can persist even after transplant, due to persistent elements of the dying liver. Treat this like any SIRS/distributive shock state.



* Bleeding and clotting can both occur; numbers usually suggest coagulopathy, but hemostatic rebalancing is often present, at least until something perturbs the balance (e.g. a procedure). Labs like the INR are a marker of disease severity, not bleeding risk. Fibrinogen is a little better, but TEG is probably the most useful marker of bleeding status, as many of these people are actually hypercoagulable.



* Some would use CRRT relatively early in a liver failure patient; Sergio would not. However, he would consider it in the volume overloaded patient to manage congestion (if diuresis proved inadequate).



* Liver-specific extracorporeal organ support us...

We talk about the nitty-gritty details of a well-run cardiac arrest, with Scott Weingart of Emcrit (@emcrit), ED intensivist.



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Takeaway lessons




* In any sudden loss of pulse/consciousness, particularly in a known cardiac patient, the presumption should be for a shockable arrhythmia and rapid defibrillation should be prioritized above all else.



* Anterior-posterior pad placement may or may not be superior, but tends to be logistically helpful, as it allows rolling the patient a single time then never again; a second set of pads can be added for double sequential defibrillation without moving them, and a mechanical compression device can be applied at the same time as the pads.



* The primary or highest-trained provider should not be the sole “code runner,” but ideally offering high-level leadership, thinking about reversible causes and judgment calls, and performing procedures, while another leader (often a nurse) runs the standard activities of ACLS such as timing, coordinating rhythm checks, assigning jobs, quality assurance, and directing the room. That frees your cognitive bandwidth by handling all your logistics, and they can act as the one-stop-shop for passing needs and issues up and down the chain.



* IOs are probably the go-to for immediate access, if no IVs are present. But Scott likes to always place central access, usually femoral. He does ECPR, so the access may be needed, and even if not, it maintains the skill for next time. He also likes an arterial line, so it’s easy to place venous alongside it. He would generally not place it fully sterile (gowns, drapes, etc), but will use sterile gloves and prep the skin, assuming that any femoral line placed in the ED is going to be replaced within 24 hours.



* Scott loves an arterial line. It eliminates the “pulse check,” allowing instant confirmation of pulsatility, while also allowing a very sophisticated assessment of coronary perfusion.



* A diastolic BP above 35–40 mmHg, measured from the arterial line during cardiac arrest, suggests adequate coronary perfusion. This must be measured manually, as the automated number will falsely measure the wrong spot in the waveform during the “suction” of chest recoil (see link below); the true point of measurement is just before the upstroke of systole begins. If you’re above this DBP, just skip epinephrine, which will probably merely be toxic (ie promoting arrhythmias).



* A low DBP should be used as a general marker of poor perfusion, and prompt other changes. Try modifying the point of compressions on the chest to avoid obstructing the LVOT (TEE is even better for this, but not available most places). Swap out compressors to ensure the most vigorous compressions, even if they still “look okay” or claim to be. Look for a reversible cause, such as hemorrhage or obstruction. Finally, if it’s truly just vasoplegia, consider other moves, such as adding vasopressin/steroids (an evidence-based practice) or high-dose epinephrine (5 mg epinephrine).



* ETCO2 should be used in all arrests, to confirm airways, prognosticate, and provide a marker of perfusion much like the arterial DBP.



* Scott thinks we should stick to 30:20 mask ventilation when an airway is not in place; breat...

We talk about the phenomenon of airway closure during mechanical ventilation, with Thomas Piraino, RRT, FCSRT, FAARC, adjunct lecturer for the Department of Anesthesia at McMaster University, editor of The Centre of Excellence in Mechanical Ventilation Blog, and a member of the editorial board of Respiratory Care.



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Takeaway lessons




* Airway closure occurs when airways, probably smaller ones (ie bronchioles) completely collapse at some point during expiration, causing flow to cease.



* This creates a false understanding of the “PEEP,” which may actually be higher than the set PEEP (effectively an autoPEEP), and hence an incorrect understanding of the driving pressure and compliance. (This autoPEEP may or may not be effective, as at higher FiO2s, this trapped volume may rapidly absorp, causing absorption atelectasis.)



* It may cause lung injury at the airway level from cyclic opening/closing, separate from more-discussed alveolar injury.



* ARDS, pulmonary edema, and obesity are all risk factors. Post-cardiac arrest is a particularly common substrate. Obstructive diseases like asthma/COPD can probably see this as well, although the recent discourse has focused on the hypoxic conditions; the phenotype is probably different, caused by intrathoracic pressure, not by air-fluid interfaces and surfactant issues.



* Probably 40% of at-risk patients may see this phenomenon occur. Its presence and the pressure where it occurs may be labile and dependent on the clinical condition. It should probably be checked at least daily in such patients.



* It may cause hypercarbia by terminating expiration early, leading to air trapping. Prolonging the expiratory time will not help, as flow has ceased.



* Plateau pressure may be elevated. Expiratory holds will not reveal this, however. A visible inflection point in continuous-flow VC breaths that has a different height (higher) than the gap between the peak and plateau pressure may be a rough suggestion of this as well.



* Plateau pressures will be accurate, as the airways should be open at peak inspiration (or no breath would be delivered). Thus, increasing PEEP and seeing no change in plateau pressure may be a sign of airway closure, although it can also be due to alveolar recruitment.



* Active patient effort during exhalation may worsen this phenomenon, particularly in the obstructive patient, due to increasing intrathoracic pressure.



* The best test is a slow-flow inflation curve. Draeger and Hamilton should have this built in (Hamilton does this incrementally, not continuously, which may make it a little harder to identify the exact inflection point). It can be done manually as such (patient must be passive):

* Set VC mode



* Square wave flow



* Flow 5L/min



* Rate 5/min



* PEEP 5 (or higher if needed for oxygenation)



* Freeze the screen and inspect the pressure scalar during inspiration. The upramp should be steady and continuous. If there is a change in slope or inflection point, this suggests a change in compliance, probably due to airway opening. Use the vent to measure pressure at this point.



* A clever time to do this might be shortly after intubation,

Our approach to common problems and troubleshooting:




* Difficulty feeding guidewires



* No flash on arterial lines



* Pneumothorax during subclavian lines



* Difficulty inserting ET tubes during hyperangulated laryngoscopy



* No response to vasopressors



* High gastric residuals during tube feeds




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We chat about the post-op transition of care from the OR to the ICU, including questions to ask, workflows, and pitfalls.



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Bryan’s textbook: Concepts in Surgical Critical Care



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We talk about diagnosis, treatment, and subsequent care of the patient with bacterial meningitis, with Emory neurointensivist Casey Albin, MD (@caseyalbin).



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Takeaway lessons




* Many septic patients have altered mental status, but suspicion should be raised for CNS infection when there is also: headache, photophobia, vomiting, or any possibility of seizure activity.



* Meningitis and encephalitis are separate entities usually involving different organisms, different imaging findings, and with different prognostic implications and downstream complications. However, at the early diagnostic stage, they can be largely lumped together.



* Empiric antimicrobials must consider CNS penetration. Piperacillin/tazobactam (ie Zosyn) has very little. Ceftriaxone is better. Cefepime is fine, although the prospect of cefepime neurotoxicity may make neurologists leery; ceftazidime is fine too. Add vancomycin (not necessarily for MRSA but for resistant Strep pneumo), acyclovir (for HSV), and a liberal approach to adding ampicillin for Listenia for anybody older, immunocompromised, or in the midst of an outbreak.



* Dexamethasone has been shown to reduce hearing loss after Strep pneumo meningitis. If suspicion for meningitis is strong early, it’s reasonable to give early (before or concurrent with antibiotics). It’s probably not worth giving >24 hours later.



* The main benefit of lumbar puncture is to allow stopping or narrowing antimicrobials without treating with the entire empiric cocktail for a full two weeks. (There is also the chance of identifying a resistance organism.)



* Ideally, LP is done before antimicrobials. However, if non-culture-based diagnostics are available such as PCR panels, successful diagnosis can often occur even after antibiotic administration. It’s worth doing the LP even if late and no PCR is available, as the signature of protein, glucose, etc will often still be useful. (At least, up front in a patient who might have CNS infection, avoid creating new obstacles like loading them with anticoagulation, antiplatelets, low molecular weight heparin, etc.)



* Most patients will already have a CT head performed before LP is considered, making the question of whether this is necessary (to assess risk of downward herniation) fairly moot. However, if not, it should probably be done prior to LP in anyone with an altered level of consciousness.



* Order from all CSF: Gram stain and culture, cell counts (first and last tubes), glucose, protein, and HSV PCR. (VZV generally does not cause clinical meningitis per se, usually causing a meningitis vasculitis, e.g. in someone with small-vessel strokes.) If available, order PCR arrays too, although some centers may not run it unless the CSF WBC count is elevated (e.g. >5). In a patient with any immunocompromise, test for cryptococcus as well. Other immunosuppressed testing is case-specific.



* Always measure opening pressure. This is not accurate in a patient sitting up. While technically possible to puncture a patient sitting up, then rotate them with assistance to lay flat, it’s not easy or elegant. In a sick patient, just do the LP laying down.



* Remember that opening pressure is measured at the bedside in centimeters of water, but should be converted to millimeters of mercury to be...

We chat with Nick Ghionni, pulm/crit attending at MedStar Baltimore Hospital, about identifying and combating cognitive biases in our clinical decision-making.



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