Lightning rounds 52: Echo tips with Michael Lanspa

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Takeaway lessons

  1. 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.
  2. 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).
  3. 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).
  4. In general, tracking the VTI alone using a similar technique will yield more consistent results than attempting a full cardiac output calculation.
  5. 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.
  6. s’ tends to “see” better with a poor view than TAPSE, as tissue doppler is more sensitive than M-mode.
  7. With more severe TR, the doppler gradient tends to underestimate the RVSP, as the pressure equilibrates faster during systole.
  8. 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.
  9. 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).
  10. 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.
  11. 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.

Episode 89: Thrombectomy for stroke, with Justin Fraser

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Buy your merch here!

Takeaway lessons

  1. 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.
  2. 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.
  3. The main current question is the utility of thrombectomy in “medium vessel occlusions,” such as M2 and more distal vessels.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. Post-procedure blood pressure targets are controversial. Fraser targets SBP <160 for 24 hours to limit reperfusion hemorrhage.
  9. 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.
  10. 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. Smaller centers also need a link to a larger center that can support them for scheduling gaps and complications.

Resources

Society of Neurointerventional Surgery

Get Ahead of Stroke

Episode 87: Maternal-fetal monitoring with Stephanie Martin

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Buy your merch here!

Takeaway lessons

  1. 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.
  2. 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.
  3. If a fetus will not be delivered early, there may be no role for fetal monitoring.
  4. 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.
  5. 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.
  6. Maternal sedation leads to fetal sedation, which can make interpreting the heart rate more difficult.
  7. Uterine contractions rarely turn into labor, but they provide a natural stress test to the fetus.
  8. 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.
  9. 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.
  10. 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.)
  11. There is relatively little role for ultrasound or other tools for fetal monitoring; the gold standard is fetal heart rate monitoring.
  12. Paroxysms of vital sign changes (tachycardia, hypertension, etc) in a pregnant woman could be a subtle marker of contractions.
  13. With regards to ionizing radiation, generally, do whatever test you would do in a non-pregnant woman. Birth defects are generally established by the end of the first trimester, so in a viable pregnancy, it should not be a concern at all. While appropriate attention should be paid to avoiding needless radiation, if an important diagnosis needs to be made, do the x-ray or CT scan (or even fluoroscopy, likely the highest risk).
  14. In the post-partum patient, the longer it’s been since birth, the less likely a maternal illness is pregnancy-related. In the first week, assume it’s pregnancy related. In the first six weeks, consider it, especially hypertension complications. Cardiac problems (e.g. peripartum cardiomyopathy) can occur even later, especially as the diagnosis may be delayed. A common presentation is post-partum “asthma,” actually pulmonary edema, as the fluid bolus of delivery overloads a cardiomyopathic heart. The most hypercoagulable period in pregnancy is actually the first six weeks post-partum, so VTE is an important concern.

Episode 86: EEGs in the ICU with Carolina Maciel

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Buy your merch here!

Takeaway lessons

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. Carolina hates fosphenytoin due to the cardiotoxic effects. Lacosamide is quite benign.
  10. The ictal-interictal spectrum is an electrical finding (not meeting the arbitrary definition of unequivocal status epilepticus) that may be important or not; you must consider the patient. If there is a clinical alteration in mental status that may be due to the activity, you should challenge them with a loading dose of a fast-acting, minimally sedating anti-seizure medicine and see if it helps their EEG and clinical status. Carolina dislikes benzos for this (sedating), thinks levetiracetam is only okay (too slow to reach peak brain concentration, ~90 minutes); brivaracetam (5 mins) and valproic acid (5-10 mins) are good.

References

Training modules for ACNS 2021 ICU EEG terminology

ACNSNomenclature2021_Condensed_2020_08-22ForPublicCommentDownload
ACNSNomenclature2021_ReferenceChart_2020_0725ForPublicCommentDownload

Lightning rounds 51: Hemodynamic interfaces with Philippe Rola

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.)

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Buy your merch here!

Episode 88: ICU Liberation SCCM Congress 2025

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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

Lightning rounds 50: Mastering PA catheter placement with Matt Siuba

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Buy your merch here!

Takeaway points

  1. 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).
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. If a balloon does not self-deflate, replace the catheter; the balloon is not reliable.
  7. 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.
  8. 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.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. Once you get an RV tracing, run! The faster you get through, the less likely you’ll have trouble. Most people who think they’re coiled in the RV are really coiled in the RA. The main exception is when the tip is pointed into the apex, and further advancement is just squishing you into that blind cul-de-sac. The other possibility is that you coiled in the RA, then the tip entered the RV; this usually manifests as difficulty wedging or reliably entering the PA, with all your slack in the RA. The only way out of these is to drop balloon and retract (to perhaps 35–45 cm), ideally not exiting the RV, but enough to change direction and readvance.
  14. There should be a clear diastolic step-up as you enter the PA, with a change in diastolic shape (downsloping, not upsloping); there may or may not be a dicrotic notch.
  15. Once you enter the PA, slow down. Advance a centimeter at a time. Wedge will usually occur around 50–51 cm; if you reach 55 cm without wedge, something has gone wrong.
  16. Occasionally, the balloon size is inappropriate for the PA branch you’re in. Try deflating the balloon, then reinflate; you may find that it wedges before fully inflating (probably the catheter moved forward once you deflated it). You may also be in the wrong branch; come back to the main PA (around 45-50 cm), reinflate and readvance.
  17. As you wedge, the pressure drop will be massive and obvious in pre-capillary/PAH disease; it may be less notable when PA pressures are elevated due to left heart disease. (Rarely the wedge may even be higher than the PA diastolic.) However, the waveform should significantly change.
  18. If unsure if you’re fully wedged, drop balloon and readvance, see if it changes. When in doubt, draw a blood gas from the tip. The specimen should be arterial in oxygenation (eg SaO2 >92%). It is usually not needed to draw a simultaneous ABG peripherally to compare, and two simultaneous gasses may be easily mixed up in the lab. A “wedge gas” will have some resistance to aspirating the blood.
  19. Once wedged and deflated, you can leave the catheter, or withdraw a little. If quite deep, maybe withdraw; the CXR will help guide you. The catheter will usually advance itself somewhat as it softens in the body, so if left quite deep it may auto-wedge later. If left too proximal, though, especially with high PA pressures, it may flop out of the PA. It is often necessary to leave a catheter in a spot where it needs to be floated forward a couple centimeters each time you want to rewedge, which is fine.
  20. Once left in the body for a while (~30 minutes), it is nearly impossible to readvance into the PA (if it escapes) due to increased catheter floppiness.
  21. Daily CXRs are still the standard in patients with a Swan to monitor for tip migration.
  22. All measurements are ideally taken at end expiration, but for bedside purposes, this is often not too important; the mean monitor number may be adequate.
  23. The best way to avoid PA injury during wedging is to check your tip position and ensure it’s not too deep or auto-wedged before you inflate. Remember that you don’t need a full syringe to wedge everyone; once you wedge, stop inflating. Use good communication with your team during insertion, to ensure the balloon is down and the catheter position locked when you leave it.
  24. An overwedged waveform will show continuously rising pressures, often very high (either it’s too deep or turned into the wall). Deflate and retract. If your wedge keeps rising as you measure it, you’re probably overwedging.
  25. A TTE view of the RV base/RVOT view (parasternal or subcostal – latter may even be better) might be helpful for guidance in the absence of fluoroscopy, as you’ll see the tricuspid valve, RV, and pulmonic valve.
  26. Tricuspid valve issues are the most important relative contraindications for a Swan without guidance, particularly an artificial valve or tricuspid endocarditis.
  27. If you don’t need to monitor PA pressures/wedge, probably remove the Swan; you can leave the sheath if you think you might want to measure later. Retracting it to an RA position will probably not leave the possibility of refloating later, as it will be all floppy by then; just remove it and float a new one later if needed.

References

Insertion video

Wedge distance

How measurement technique affects diagnosis

Thermo in TR review

POCUS for PAC placement

Lightning rounds 49: The Vortex approach with Nicholas Chrimes

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Buy your merch here!

References

  1. The Vortex website

Episode 85: Tracheostomy basics with Vinciya Pandian

Podcast: Play in new window | Download

Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS

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.

Learn more at the Intensive Care Academy!

Find us on Patreon here!

Buy your merch here!