Episode 83: Cardiac arrest with Scott Weingart

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

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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).
  7. 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).
  8. ETCO2 should be used in all arrests, to confirm airways, prognosticate, and provide a marker of perfusion much like the arterial DBP.
  9. Scott thinks we should stick to 30:20 mask ventilation when an airway is not in place; breaths don’t really go in during compressions, and bagging during the upstroke is very tough. But he prefers to just insert a supraglottic airway quickly and use that, a skill anyone attending cardiac arrests should have. If using the BVM, you should use capnography to confirm breaths are actually going in.
  10. Intubation should be done with video if available. Hyperangulated or regular geometry are both fine. Use a bougie if you have regular geometry (and are good with it). There should never be an intentional pause in compressions for the airway, however; just intubate during compressions, not so hard with video and a bougie. Position the patient optimally, just as in any situation; don’t rush.
  11. Never perform “pulse checks,” only rhythm checks. If the rhythm is non-perfusing, resume compressions. If it’s organized and potentially perfusing, only then check for a pulse (or preferably your arterial line).
  12. POCUS is essential: look for pericardial effusions, a dilated RV (although this is usually present), signs of hemorrhage, and pneumothorax. Maybe even more importantly, use it for pulse checks rather than your fingers. Scott will start with this, and if a “sonographic pulse” (visual pulsatility of the vessel) is found, he’ll then apply his fingers to see if it’s strong enough to feel. At this moment in time, he thinks palpability is a reasonable cutoff for when to call flow PEA vs hypotension.
  13. Once he’s ruled out reversible causes, he tries not to look at the heart with ultrasound, since it tends to detract from compressions (without TEE); sonographic pulse implies organized cardiac activity. An arterial line obviates all of this, although it’s not clear what BP is adequate; Scott still uses a DBP 35-40 but would accept a MAP of 40 as a reason to defer compressions, if rapid efforts are undertaken to increase it.
  14. Scott always likes mechanical compression devices when available (he likes the Lucas), which ensures good quality, provides a backboard, and reduces the energy in the room, even if it doesn’t improve outcomes. Buy one for your hospital’s code team and bring it to the arrests. If not available, he likes a backboard.
  15. The impedence threshold device (ITD), potentially in combination with active compression-decompression devices, is interesting but the initial promising data has not been replicated; he would not consider this ready for use.
  16. Heads-up CPR is also interesting but not yet proven.
  17. When defibrillating, always max out the current on the machine. It creates no meaningful injury and maximizes your chance of conversion.
  18. When a shockable rhythm is seen, he resumes compressions while charging, and in fact often performs hands-on defibrillation (shocking during compressions, using some kind of standoff between hands and chest, such as a towel, or even just gloves); mechanical compressions make this easiest.
  19. Pre-charging before the rhythm check is wise, and the nurse code leader can coordinate this; do it every time.
  20. Amiodarone or lidocaine are equally reasonable first line antiarrhythmics. If they’ve had one and you’re still in electrical storm, try the other.
  21. If storm persists, these are excellent ECPR cases. Otherwise, you can try esmolol (bolus 500 mcg, usually no drip), then double sequential defibrillation.
  22. DSD: don’t let pads touch; shock as simultaneously as possible (used to be intentionally separated, but some data now suggests closer together is better). There is a very small but real risk of damaging defibrillators doing this (and the damage may actually not be obvious, i.e. the machine will still pass a later self-check).
  23. How long to go? Depends on baseline functional status, rhythms seen, and other factors. Past 40 minutes of low-flow time, arrest is probably not survivable without ECPR (for which the cutoff is probably 90 minutes), unless there has been stuttering flow (intermittent ROSC), which tends to reset that timer. ETCO2 persistently <10 is very poor. No cardiac motion seen on echo in PEA is poor.
  24. One exception might be if your interventional cardiologists are willing to cath intra-arrest during mechanical compressions; in that case you might go longer to bridge to this.
  25. In a young or baseline well patient, Scott would almost never stop before 40–45 minutes.
  26. Scott always runs a norepinephrine drip at 50 mcg during the arrest, making it easy to transition to the drip after ROSC and avoiding any delays.
  27. After ROSC, a STEMI or high-risk patient should go to the cath lab. Everyone else should have a pan-CT, including head, chest, abdomen/pelvis. This ideally is gated/timed to triple rule out PE, coronary occlusion, and aortic dissection. It also identifies important post-CPR trauma.
  28. In 2025, Scott’s take on TTM is reactive: place an invasive temp probe (esophageal or Foley, not rectal, which is too slow and inaccurate) and monitor for fever; if it occurs, then cool actively to normothermia. There are probably some patients who benefit from more cooling, but nobody knows who (longer downtimes?). This method is as good and cheaper than empirically applying a cooling device to maintain normothermia before fever occurs, and that might cause problems, such as if it aggressively cools for a trivially increased temperature and induces shivering. Put the cooling device at the bedside without opening the pads if you really want to be ready.
  29. If having trouble inserting your floppy esophageal temp probe, use an esophageal stethoscope from the OR, or use a split 8.0 ET tube to introduce a lubricated probe into the esophagus.
  30. For out-of-unit codes, it’s all the more important to have a nurse code leader. A code team should bring the specialized equipment (maybe make a cart) to the bedside, such as mechanical compression devices, ultrasound, capnography, etc.

Resources

  1. PO Berve at Emcrit on correctly measuring arterial line diastolic BP during cardiac arrest
  2. Emcrit on ultrasound in cardiac arrest
  3. Cardiopulmonary Resuscitation Quality: Improving Cardiac Resuscitation Outcomes Both Inside and Outside the Hospital: A Consensus Statement From the American Heart Association

Lightning rounds 48: Complete airway closure with Thomas Piraino

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

  1. Airway closure occurs when airways, probably smaller ones (ie bronchioles) completely collapse at some point during expiration, causing flow to cease.
  2. 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.)
  3. It may cause lung injury at the airway level from cyclic opening/closing, separate from more-discussed alveolar injury.
  4. 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.
  5. 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.
  6. It may cause hypercarbia by terminating expiration early, leading to air trapping. Prolonging the expiratory time will not help, as flow has ceased.
  7. 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.
  8. 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.
  9. Active patient effort during exhalation may worsen this phenomenon, particularly in the obstructive patient, due to increasing intrathoracic pressure.
  10. 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, while patients are deeply sedated and paralyzed.
  11. That this inflection represents airway opening can be proven by measuring the compliance up to that point (volume delivered vs pressure), which will usually be <3 cmH2O/ml, roughly the compliance of the ventilator circuit.
  12. Inflection can occur from alveolar recruitment as well, but this is usually a less abrupt, steady change in slope. If present, it will occur above the airway closing pressure inflection.
  13. In general, set the vent PEEP at the same level as the measured closing pressure. This will normalize your understanding of the driving pressure and probably limit cyclic collapse and lung injury. It may also facilitate expiration and hence ventilation.

Links

  1. RT Maven R/I calculator
  2. Center for Excellence in Mechanical Ventilation

Episode 82: When it goes wrong

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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Lightning rounds 47: Post-op care transitions

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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Episode 81: Bacterial meningitis with Casey Albin

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

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.)
  6. 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.)
  7. 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.
  8. 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.
  9. 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.
  10. Remember that opening pressure is measured at the bedside in centimeters of water, but should be converted to millimeters of mercury to be clinically applicable.
  11. Draw at least 20 cc of CSF in all cases. If opening pressure is high (and CT not concerning), fill the four tubes (~36 cc) and measure the closing pressure. Few patients are harmed by draining <40 cc. Draining >40-50 can create some risk for herniation or hemorrhage (eg small subdural hemorrhage) and should not be done thoughtlessly.
  12. Meaningfully elevated CSF protein should not just be “high,” but should exceed the patient’s age.
  13. Any meningitis patient with an altered mental status should at least have a spot EEG, and possibly long-term EEG depending on the findings.
  14. Any meningitis patient with a high opening pressure on LP, who is sufficiently obtunded to be intubated, should be considered for invasive ICP monitoring (e.g. EVD), if available. Otherwise, close monitoring for ICP crisis with neuro and pupil checks and serial CT scans.
  15. Treating high ICP in meningitis with EVD or lumbar drain is often appropriate.
  16. Any neurologic deterioration after antibiotics and other initial care is very likely either seizure or ICP crisis. These are fixable patients; diagnose and treat these complications aggressively.
  17. Transcranial doppler may be a useful non-invasive screen for elevated ICP, by revealing a high-resistance waveform (high pulsatility index) as ICP increases.

Resources

Lightning rounds 46: Nick Ghionni on combating cognitive bias

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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Episode 80: Implementing the A-F bundle with Kali Dayton

We discuss the practical barriers to implementing the A-F ICU liberation bundle, with Kali Dayton, ACNP-BC (@daytonicu), host of the Walking Home from the ICU podcast, and consultant to ICUs working on these issues.

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Lightning rounds 45: Noelia Bischoff on transitioning nursing roles

We chat with Noelia Bischoff, recently off orientation in the medical ICU at Johns Hopkins as a nurse practitioner, about the transition from her role as a bedside ICU nurse.

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Episode 79: Transfusion reactions with Joe Chaffin

We discuss transfusion reactions, risks, and management, including infection, consent, TRALI, TACO, and hemolytic reactions—with Dr. Joe Chaffin (@bloodbankguy), the “Blood Bank Guy” and transfusion medicine specialist.

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Takeaway lessons

  1. The risk of transfusion-related infection (HIV, hepatitis B, and hepatitis C) is around 1 in 3 million.
  2. Acute hemolytic transfusion reactions (usually due to clerical errors or unit mix-ups) occur about 1 in every 75 or 76 thousand transfusions. Mortality is only one per million or so, however.
  3. Simple febrile transfusion reactions occur about 1/100-300 transfusions.
  4. Transfusion is always slightly immunosuppressing, perhaps increasing risk of post-op infection, cancer recurrence, etc. This effect is real, but small and not easily quantified.
  5. Urticarial reactions (hives) seem trivial to clinicians, but can be very frightening to patients, even causing them to refuse future transfusions.
  6. 80% of hemolytic reactions initially present with only fever, perhaps some chills. There is no way to differentiate from non-hemolytic febrile reaction at this stage. While the odds favor a non-hemolytic reaction, if you presume this and continue your transfusions, you are relying on luck, and you will eventually be wrong, which would be an indefensible medical error.
  7. Once a hemolytic reaction is obvious, you waited too long. The main determinant of mortality after hemolytic transfusion reaction is the volume of blood transfused.
  8. Typical workup for a febrile, possible hemolytic reaction is to confirm the labels and clerical match, then return the blood to the blood bank, where they will check patient blood for hemolysis, direct Coomb’s, and usually repeating the ABO/Rh testing. This can cause a delay in transfusion and maybe loss of the unit of blood; by typical regulations, once blood is removed from the blood bank or portable cooler, it must be transfused within 4 hours or wasted.
  9. The hallmark of ABO mismatch is severe intravascular hemolysis. Most other hemolytic reactions yield extravascular hemolysis, e.g. in the spleen. Cytokine storm will be be seen. Compared to the myoglobin released in rhabdomyolysis, the free hemoglobin released in intravascular hemolysis is not quite as nephrotoxic (the resulting AKI may be more related to shock than from direct toxicity).
  10. Hemolysis is only destructive to the transfused blood, so anemia per se generally does not develop. One exception can occur in sickle cell patients, where transfusion can induce a “hyperhemolysis” phenomenon where native red cells are also hemolyzed.
  11. Mortality from acute hemolytic reactions is fairly low in previously healthy patients. Patients already critically ill may not do as well.
  12. TRALI is mostly diagnosed by consensus criteria. “Definitive” TRALI (there is no longer a less definite category) is defined as:
    • No evidence of lung injury prior to transfusion
    • Onset within 6 hours after end of transfusion
    • P/F ratio <300 or SaO2 <92% on room air
    • Radiographic evidence of bilateral infiltrates with no evidence of left atrial dysfunction
  13. The challenge when hypoxia occurs after transfusion is usually to distinguish TRALI from TACO. The latter is mere volume overload; the former occurs when pre-existing inflammation primes neutrophils for activation in the lungs, whereupon factors in the transfused blood causes neutrophil activation as a second hit. The most common of these triggers is incompatible anti-HLA antibodies in the transfused blood.
  14. TRALI is largely a clinical diagnosis. However, if a case of possible TRALI is reported, the donor will be investigated and potentially screened for anti-HLA antibodies (something usually not done without a suspicious case). Other products from that donor will also be recalled from the bank. Report your possible TRALI cases!
  15. Now that female donors with previous pregnancies are excluded from donating plasma (without HLA screening), the old truism that plasma-rich products (e.g. FFP or platelets) are the highest risk for inducing TRALI is no longer true; the most common precipitant is PRBCs. Any product can induce TRALI, however, including HLA antibody-negative products.

Lightning rounds 44: Post-intubation sedation roundup

Experts in critical care share their approach to post-intubation sedation.

Contributors:

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