Episode 61: ECPR with Scott Weingart

We chat with Scott Weingart of Emcrit about the use of crash VA ECMO for the cardiac arrest patient.

Check out the REANIMATE course here!

Listen to the ED ECMO podcast on ECPR here

Find us on Patreon here!

Buy your merch here!

Takeaway lessons

  1. ECPR candidacy may account for age, comorbidities, and code duration. Physiologic age is probably more important than chronological age. No-flow time without CPR should be very brief (witnessed is best), but low-flow time (with CPR) can actually be very long and still have good outcomes with ECPR. New systems should probably have stricter inclusion criteria, as numerous poor outcomes can endanger a fledgling program.
  2. The cause of arrest is usually not as important, partly because it’s often not known so early. ECPR can be a bridge to diagnosis and prognosis.
  3. One team should run the ACLS arrest while another handles the ECMO cannulation; it’s not possible to effectively do both. The cannulator should have their own ultrasound machine, and can function alone, although at least one skilled assistant is helpful. Mechanical CPR devices help by reducing energy in the room and reducing movement of the lower body; if not present, assign someone to manually stabilize the pelvis.
  4. Cannulation can be done by various services as long as they’re immediately available. Whoever it is should be comfortable using ultrasound. Cutdowns are probably not the preferred technique except in niche cases. A second service like CT surgery can arrive after a short delay to do the dilation and cannula placement if the in-department provider like EM or CCM can get initial access with smaller devices.
  5. Get ready by setting up equipment, position the ultrasound, and get sterile. As the patient arrives, have someone strip the clothes, expose the femoral region, and prep it, then get started with venous and arterial access.
  6. Vein vs artery cannot be distinguished without ultrasound, and can be difficult even with it. Don’t use anatomic location – use appearance. Arteries are thicker walled and small in cardiac arrest. TEE with a bicaval view to see your wire can be a huge help.
  7. The femoral artery should be accessed between the ligament and the bifurcation. Too high means RP bleeding risk; too low means potential for vessel damage. Similar for the venous access, although it’s more forgiving.
  8. Initially, place wires and then some kind of sheath, dilator, or line that will accept a larger, stiffer wire (Scott uses the Amplatz Superstiff). Going directly from needle to stiff wire is challenging and higher risk for vessel damage. This also means if you end up not proceeding to ECMO, you can just use the smaller sheaths for venous and arterial access.
  9. Even when a pulse returns, it’s often safer to proceed to ECMO in good candidates with a long arrest time. Supporting them through the next few days when they’re high risk of re-arrest, reperfusion injury, and other complications is likely to be safer than letting their heart do the work.
  10. Dilation for ECMO is similar to other dilation, just less forgiving. Follow the same consistent angle as the needlestick, constantly rack your wire, and consider dilating to a somewhat smaller cannula than in other VA ECMO situations, which is often tolerated post-arrest. Arterial cannulae of 17fr (women) to 19fr (men) or even smaller can achieve adequate flows, with venous cannulae of 19-23 Fr or even smaller.
  11. Goal: 5 minutes from first needlestick to active bypass.
  12. Ideally, one cannula per leg, but you can place both in the same side if needed. Certainly use the same side if using a cutdown.
  13. Venous cannula for the arrest patient should have the tip in the SVC (i.e. traversing the RA, not stopping before it). Use TEE to visualize this, or measure externally from groin to right nipple.
  14. Pumps can be pre-primed and sit waiting for 30-60 days in most cases; check manufacturer guidelines. Nurses can handle the pump with some extra training, at least for initial set-up, then transition care after 15 minutes or so to a perfusionist or ECMO-trained respiratory therapist.
  15. Pan-CT everyone. In fact, pan-CT all your cardiac arrests, as traumatic bleeding is common. Maybe do a coronary artery CT as well.
  16. Initial settings: 100% oxygen and titrate down quickly. Flow can be somewhat low compared to normal VA ECMO, allowing the native heart to keep some output and allowing smaller cannulas. Traditionally set sweep gas at roughly similar to bloodflow, but this tends to cause dramatic, rapid initial drops in PCO2, which may be harmful to a vulnerable brain; instead, start at a low sweep and gradually titrate it up.
  17. Do NOT prognosticate cardiac function early; recovery may happen late, and early withdrawal falsely affects your outcome figures from ECPR cases. The best numbers can only be achieved when the ECPR team continues to “own” the patient during their initial ICU course and doesn’t allow early withdrawal of ECMO.
  18. Neuroprognostication, conversely, tends to be easier; patients often stratify relatively early into clear good and bad outcomes. It should be established early on that families may want to pursue life support and that’s fine, but the team determines how long to continue ECMO, and it won’t be continued indefinitely.
  19. Economics: ECPR pump runs are short (<1 week usually), and reimbursement is all up front, so it actually pays well compared to many ECMO types, like long VV courses.
  20. The future: ideally, EMS would recognize good ECMO candidates and divert patients to ECPR centers. In rural areas, ED teams would be able to cannulate and start initially on ECMO, then transfer to larger referral centers.

TIRBO #35: Vent double-triggering

Understanding the causes of doubled vent breaths, including premature/short cycling and reverse triggering, plus a basic approach to managing them.

Lightning rounds #27: Our favorite FOAM

Bryan and Brandon share their favorite podcasts, blogs, social media, and other online channels for medical education.

Podcasts

Blogs/websites

Twitter accounts

So, with Twitter, we could post all day and still leave a bunch of people out. Here are a few…the best way to find good Twitter followers is to start with these and see who THEY follow and interact with. Then see who THEY follow…repeat.

  • @IMcrit
  • @rbarbosa91
  • @caseyalbin
  • @critconcepts
  • @CritCareNotes
  • @emily_fri
  • @Dr_Oubre
  • @VLSorrellImages
  • @NephroPOCUS

TIRBO #34: What makes it a central line?

Reflections on the definition of a central line, whether it’s arbitrary, and the clinical implications of making the distinction.

Episode 59: Takotsubo cardiomyopathy with Vincent Sorrell

We look at stress (Takotsubo) cardiomyopathy in the setting of critical illness, with Dr. Vincent Sorrell. Dr. Sorrell is a cardiologist at the University of Kentucky, where he helped develop the Advanced Cardiovascular Imaging Program, and is current Acting Chief of both the Division of Cardiovascular Medicine and the Gill Heart and Vascular Institute.

Find us on Patreon here!

Buy your merch here!

Takeaway lessons

  1. If considering ACS in any post-menopausal woman, you should also consider stress cardiomyopathy. Echo is the test of choice.
  2. While hypokinesis classically occurs at the apex in TCM, almost any distribution can occur; 10% or more will have atypical distributions, particular outside the traditional demographics (older women), such as the critically ill. Of course, atypical anatomical distributions can also occur in ACS due to distinct anatomy.
  3. Recurrence of TCM may occur with a different distribution. Recurrence occurs in up to 40% in the first four years. Withdrawal of beta blocker therapy may precipitate this, which may be a reason to select other therapies (e.g. ACE inhibition).
  4. In general, TCM is a diagnosis of exclusion after ruling out ACS. The ECG pattern is non-specific, but STE in V1 or lead I is unusual in TCM. ACS usually causes more troponin elevation than TCM, and matches the degree of EF reduction. Persistent troponin elevation in a patient without intervention may suggest a missed ACS instead of TCM, but you should generally not wait that long.
  5. The InterTAK score may give some guidance. Dr. Sorrell is working on echo criteria.
  6. Cardiac CT may also be a helpful non-invasive tool.
  7. Contraindications to stenting (e.g. bleeding) could also suggest utility in a non-invasive approach.
  8. When addressing hemodynamics, always ask whether outflow tract obstruction is present or absent; this will be a critical decision-point.
  9. Without obstruction, treat patients as usual. Vasopressors should not be viewed as potentially worsening the condition, and early beta blockers probably have no role.
  10. Anticoagulate as soon as it’s safe, when there are large wall motion abnormalities; this is similar to WMA from other causes. Apical ballooning is probably somewhat riskier than other distributions due to the flow patterns.
  11. The natural history of TCM involves recovery in most within 2 weeks, although the course during that period can vary widely. Almost all recover within a couple months.
  12. Outpatient care focuses on ACE inhibition, diuresis if needed, anticoagulation when appropriate, with a gradually decreasing emphasis on beta blockers. Aspirin and statins are not usually needed if there is no concomitant ACS.
  13. Hormone replacement may have a role.
  14. RV involvement can occur atypically. It can help point to TCM, since this would be an unusual anatomic distribution for ACS.

Episode 58: Toxic alcohols with Jerry Snow

We look at evaluating the patient with encephalopathy and unexplained anion gap, including the workup and treatment of toxic alcohol poisoning, with guest Dr. Jerry Snow (@ToxicSnowEM), medical toxicologist and director of the toxicology fellowship at Banner University Medical Center in Phoenix.

Find us on Patreon here!

Buy your merch here!

Click here to claim your free CME credit!

Takeaway lessons

  1. A toxicologic exposure should be suspected, even without a clear story, based on the prehospital scene. EMS or family reports of chemicals, pill bottles, etc should be elicited. Prescribed medications should be questioned, as well as any other meds that could be available to the patient, such as older meds, current and older meds prescribed to family members, and supplements.
  2. Physical exam maneuvers high-yield for tox diagnosis include the pupillary exam, skin exam (diaphoretic vs dry), and examination of muscle tone and deep tendon reflexes.
  3. Laboratory clues of tox diagnoses include an elevated anion gap in the absence of common causes (lactate, ketones, uremia), as most of the remaining causes of a gap are toxins.
  4. Elevated osmolal gaps should also be investigated, although considered an insensitive test for most toxins. A serum chemistry, as well as salicylate and acetaminophen levels, should be sent routinely. An ECG should be checked for findings like interval prolongation and morphology changes.
  5. “Normal” osmolality varies too much for a low osm gap to be useful, but a clearly elevated gap is diagnostically helpful, particularly when its presence/absence is compared with the presence/absence of an anion gap.
  6. The most common source of methanol ingestion in the US is windshield wiper fluid; it’s also present in poorly-distilled homemade moonshine, hand sanitizer, model car fuel, food-warmer fuel, lacquer and paint thinner, and many others. For ethylene glycol, the most common US source is automotive antifreeze. In both cases, these are usually intentional ingestions.
  7. Toxic alcohol levels, namely methanol and ethylene glycol levels, are send-out tests in most centers and result too slowly to be useful in the early stages. You will need to treat empirically based on suspicion and perhaps based on osmolar gap.
  8. Urine tox screens rarely change management, and may lead to missed diagnoses due to anchoring. Many substances are not tested, and positive tests (e.g. for opioids or benzodiazepines)—even for substances that may explain the clinical picture—can be false positives. Even true positives do not rule out the presence of another medical or even a second toxicologic cause. Correlate cautiously with the clinical picture (e.g. opioid toxicity may not explain encephalopathy in a patient with normal pupils and hyperventilation), or simply don’t send it to begin with.
  9. Acute iron overdose can cause anion gap acidosis, GI symptoms including bleeding, and shock and an overal critically ill presentation.
  10. Ethanol has fallen out of favor for treatment of toxic alcohols, although it does work; it is logistically challenging, requiring frequent lab checks to ensure therapeutic levels, central venous access, and other fuss; complications are much higher than with fomepizole. It’s good for low-resource settings that may not have the more expensive fomepizole, however, and co-ingestion of ethanol with toxic alcohols provides some fortuitous initial protection until the ethanol level falls.
  11. Ethylene glycol and methanol are not themselves toxic, but as the parent alcohols are metabolized, they turn into toxic acids. The goal of fomepizole or ethanol is therefore to block this conversion (by alcohol dehydrogenase). This also means that if checked early after ingestion, osmolar gap will be high, but anion gap is low, as only the parent compounds are active osmoles. As metabolism continues, osmolar gap falls, but the anion gap increases. One upside of treatment with hemodialysis is that it clears both the parent alcohol and the toxic metabolites, so it’s helpful even in late presentations.
  12. Toxic alcohols may confuse testing for lactate. Some methods, mainly used on blood gas analyzers that report lactate, can be fooled by glycolate—a metabolite of ethylene glycol—and report a falsely elevated lactate. The same sample tested in the lab using another method may show a lower lactate. This “lactate gap” can be diagnostically useful if understood.
  13. A normal fomepizole course is two days, dosed every twelve hours, but monitoring should be done of either methanol/ethylene glycol levels (if lab turnaround is fast), or monitoring the pH, anion gap, and osm gap for response. If not resolved, a longer treatment course may be needed, and dose may need to be increased, as it induces its own metabolism.
  14. Hemodialysis may be used in the sickest patients, as a rescue, if pH is severely deranged, or if there is severe kidney injury, since renal clearance is needed to clear ethylene glycol. Fomepizole should usually still be given to temporize until treatment is completed, and may need to be dosed more frequently during dialysis as it is a dialyzable compound. A single prolonged HD session (eg 8 hours) is often adequate, and HD is superior to CRRT.
  15. Thiamine and pyridoxine (vitamin B6) can be given to help shunt toxic alcohols to benign metabolites, although evidence for this is fairly poor. Other supportive care is as routine.
  16. If acute toxicity is survived, ethylene glycol patients usually do well, although they occasionally have calcium crystal deposition in nerves and develop cranial nerve palsies or peripheral neuropathy. Methanol patients tend to do worse, sometimes developing permanent blindness and CNS pathology like delayed intracranial hemorrhage or Parkinsonism.
  17. Every hospital in the US has a poison control center available to them as a resource, which includes an on-call medical toxicologist who can discuss cases if needed. They are available even to review med lists and assist with diagnostic mysteries. The most common error in tox cases is the failure to consider a tox diagnosis!