Critical Care Scenarios

Brandon Oto, PA-C, FCCM and Bryan Boling, DNP, ACNP, FCCM
  • 4.5 (220)
  • 医学
  • 半月一更
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. 10月16日

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

    58 分钟

  2. 10月2日

    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. Check out the Intensive Care Academy here! Find us on Patreon here! Buy your merch here!

    39 分钟

  3. 9月18日

    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. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your merch here! Takeaway lessons * The risk of transfusion-related infection (HIV, hepatitis B, and hepatitis C) is around 1 in 3 million. * 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. * Simple febrile transfusion reactions occur about 1/100-300 transfusions. * 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. * Urticarial reactions (hives) seem trivial to clinicians, but can be very frightening to patients, even causing them to refuse future transfusions. * 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. * 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. * 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. * 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). * 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. * Mortality from acute hemolytic reactions is fairly low in previously healthy patients. Patients already critically ill may not do as well. * 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 n...

    56 分钟

  4. 9月4日

    Lightning rounds 44: Post-intubation sedation roundup

    Experts in critical care share their approach to post-intubation sedation. Contributors: * Jason Wieland * Casey Albin * Jace Mullen * Kali Dayton * Nick Ghionni * Emily Fridenmaker Check out the Intensive Care Academy here! Find us on Patreon here! Buy your merch here!

    32 分钟

  5. 8月21日

    Episode 78: Echoing the RV with Matt Siuba

    We talk the nitty-gritty of assessing the right heart using echocardiography, with our friend Matt Siuba (@msiuba), intensivist at the Cleveland Clinic and master of zentensivism. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your merch here! Takeaway lessons * RV echo starts with evaluating three things: size, squeeze, and septal kinetics. * Size should be 2/3 the LV * Squeeze can be assessed in a variety of ways * The septum should not be bowing into the LV. * Dilation is an early and somewhat compensatory finding, and can be used as a screening test (the “D-dimer of RV dysfunction”). Septal changes are probably later and more of a sign of dysfunction (i.e. not compensatory). * Evaluating the RV’s ejection fraction is impractical due to its complex shape (without 3D echo or cardiac MRI or other advanced tools). So methods like TAPSE that reduce it to its longitudinal function become a more practical surrogate. * TAPSE is not an isolated marker of RV contractility, but a marker of the overall RV-PA unit. However, this is probably a feature, not a failure. You don’t really want to know how the RV is contracting in the abstract, but how it’s contracting in its current loading conditions. So TAPSE will vary by afterload and preload, but not artifactually—i.e. if the loading conditions change and TAPSE improves, then contractility is better in the current conditions. * s’ is similar to TAPSE, and similarly limited (mainly evaluating longitudinal function). It assesses velocity, not movement, which theoretically may represent something different (maybe a better marker of function?), although that difference is not very well studied; some studies do suggest that s’ may be more sensitive to changes after adding an inotrope, but who knows if that means anything. The most common cause for a big discrepancy between TAPSE and s’ is probably technical error, not a clinical distinction. * RVSP can be useful as a marker of afterload, but says nothing about the cause of RVSP—high left sided pressures vs high PVR—and also incorporates the RV function, so separating all this out can be difficult. * TAPSE/PASP (or TAPSE/RVSP) ratio might be a somewhat more accurate marker of RV/PA coupling, but not really clear if it’s clinically better than using the TAPSE alone, which is already a fair marker of RV/PA coupling. By measuring more things, it also introduces more room for technical error (usually underestimating RVSP), such as the need to estimate the TV gradient and the CVP. More tricuspid regurgitation will also tend to reduce the ratio, without necessarily indicating better RV function. * CVP estimates derived from the IVC are very unreliable in the critically ill. Many chronic PH patients have chronically distended IVCs regardless of their RAP. Using a transduced CVP is probably better. You can also just trend the TV gradient as a marker of its own and ignore the CVP component. * Shortening of the PA acceleration time (PAAT or PVAT) is a useful marker of pulmonary afterload. Notching of the waveform usually indicates a very high afterload, much more likely to be caused by pulmonary factors than high left heart pressures.

    55 分钟

  6. 8月7日

    Lightning rounds 43: AI in medicine, with Nawar Shara

    We explore the fascinating world of artificial intelligence and its role in medicine, with Nawar Shara (@NawarShara), PhD, Chief of Research Data Science at Medstar Health Research Institute and cofounding director of the AI Collab between Medstar and Georgetown. Check out the Intensive Care Academy here! Find us on Patreon here! Buy your merch here!

    57 分钟

  7. 7月31日

    Special episode: The Intensive Care Academy

    We share our grand new project, the Intensive Care Academy, an online, video-based, subscriber-only educational platform. Check it out at icu101.com!

    22 分钟

  8. 7月24日

    Episode 77: Mastering APRV with Rory Spiegel

    We discuss the practicalities of using airway pressure release ventilation (APRV) with Dr. Rory Spiegel (@EMnerd_), emergency physician and intensivist at MedStar Washington Hospital Center (and EMNerd at Emcrit). Find us on Patreon here! Buy your merch here! Takeaway lessons * The most immediate benefit of APRV is to help restore lungs to FRC (functional residual capacity). While this can be achieved with PEEP, most people don’t use enough PEEP. APRV proves a higher mean airway pressure while also reducing sedation requirements, and provides a physiologically automatic titration of “PEEP” based on lung compliance. * Phigh can usually be set to equal the previous plateau pressure on a conventional mode (assuming reasonably appropriate settings there). This helps match higher Phigh to a more poorly compliant lung and vice versa. The release volume that results should be checked to give a sense of the effects; it should be more or less in the range of normal tidal volumes, although usually lower than your previous tidal volume on a conventional mode due to the intentional air trapping. (If it’s not lower, your Tlow may be set too long, allowing too much release.) * Thigh can range from 1.5 seconds to infinity. Longer T-high is better for recruitment, shorter is better for ventilation. When initially flipping to APRV, shorter Thigh is usually needed; try to match the patient’s minute ventilation (from the prior mode) fairly closely, although usually you’ll need to accept a small loss of ventilation. A too-long initial T-high is a common error; patients this sick usually cannot tolerate more acidosis. Usually an initial T-high of 2 seconds is about right. * Tlow should be set to terminate when the expiratory flow drops to 75% of the peak expiratory flow (so if the peak was 100 L/s, terminate Tlow when it drops to 75 L/s). This was about the point in pig models where alveolar derecruitment began to occur. Peak and end expiratory flow can be checked on most modern vents, although it may not be easy to find in the screens. Usually the right T-low is around 0.3–0.6 seconds. * Occasional patients may need a shorter T-low than this for optimal recruitment. But few need longer; Tlow should rarely be lengthened, even as patients recruit. Although the amount of air trapping will usually increase as the lung becomes more compliant (e.g. the same T-low duration will terminate expiration at 85% instead of 75% of peak expiratory flow), this is usually fine; this is when you’ll start weaning and stretching your Thigh. * Plow should be set to zero in almost all cases, allowing the fastest expiration (higher Plow reduces the driving pressure and substantially reduces expiratory flow). In a few vents (older Puritan Bennett, older Servos), the machine may attempt to synchronize with patient efforts by allowing the Tlow to “kick out” and extend, creating large release volumes and loss of desired air trapping. Increasing the Plow may provide some safety margin in this case, although switching from APRV altogether is probably the best solution. * As the patient recruits on APRV, release volume should gradually increase despite a fixed Phigh, as the lung recruits. The expiratory flow curve will flatten and the compliance will increase. Thus, release volumes are initially small—”lung protective” in conventional thinking—and later will increase. This increase should be allowed,

    1 小时 2 分钟
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关于

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.

信息

  • 创作者
    Brandon Oto, PA-C, FCCM and Bryan Boling, DNP, ACNP, FCCM
  • 活跃年份
    2019年 - 2024年
  • 单集
    188
  • 分级
    儿童适宜
  • 节目网站
    Critical Care Scenarios

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