Critical Care Scenarios

Brandon Oto, PA-C, FCCM and Bryan Boling, DNP, ACNP, FCCM
Critical Care Scenarios

Join us as we talk through clinical cases in the ICU setting, illustrating important points of diagnosis, treatment, and management of the critically ill patient, all in a casual, "talk through" verbal scenario format.

  1. 22 JAN

    Episode 84: Acute liver failure with Sergio Navarrete

    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. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your merch here! 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...

    57 min
  2. 8 JAN

    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. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your merch here! 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...

    1h 10m
  3. 25/12/2024

    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. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your merch here! 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,

    1h 14m

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Join us as we talk through clinical cases in the ICU setting, illustrating important points of diagnosis, treatment, and management of the critically ill patient, all in a casual, "talk through" verbal scenario format.

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