The Elective Rotation: A Critical Care Hospital Pharmacy Podcast

The Elective Rotation: A Critical Care Hospital Pharmacy Podcast

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The Elective Rotation: A Critical Care Hospital Pharmacy Podcast episodes

  • 19: When and how to write a pharmacy progress note - Critical Care Pharmacy Podcast









    In this episode I’ll share the decision making process I use to decide when and how to write a pharmacy progress note.
    When to write a pharmacy progress note?
    Not all communication is appropriate for a progress note.  There are 3 main ways that I communicate with other members of the medical team. They are:
    -Verbal communication (in person or on the phone)
    -Sticky notes (or other communication not part of the medical record)
    -Progress notes
    Verbal communication
    If a recommendation can’t wait until the next time the chart is read, or I am responding to a provider’s request for help, I will have an in person or telephone conversation with the provider. In person conversations are always preferred, and I will not hesitate to go wherever the provider is in the hospital if possible.
    Sticky notes
    I often use sticky notes in the morning before ICU rounds. I am mindful that much of a pharmacist’s job involves advising providers to change what they have already ordered.
    While I’ll never phrase things this way to a provider, on a very basic level I am saying “Don't do that, do this instead.” To maintain positive relationships with providers I try to minimize the amount of time I am providing recommendations in a public forum like ICU rounds. Sticky notes help with this - here is an example:
    A patient originally admitted for GI bleed went to the OR for a perforated bowel. All of their orders were rewritten post-op by the surgical physician assistant. I was seeing the patient in the morning, before the ICU attending. I noted the following issues:
    1. The patient had been switched from a PPI to famotidine, but they had a GI bleed earlier in the admission.
    2. The patient was intubated but did not have an order for oral care with chlorhexidine.
    3. The patient was septic with a perforated bowel but was on levofloxacin (30%+ resistance to e coli) and metronidazole.  To find out what I would have recommended in place of levofloxacin check out episode 8 about empiric antibiotic section in the ICU.
    I knew ICU rounds would start in an hour or so, but rather than bringing these points up on rounds I left a sticky note on the patient’s flow sheet (which the physician always reviews) similar to this one:






    When we rounded later in the morning, I noticed all of my recommendations had been implemented, and I didn’t need to say a thing.
    When appropriate, I prefer this sticky note method because it makes the provider look good, and that helps me build my relationship with them.
    Progress notes
    When it comes to documentation of pharmacy services, I write progress notes in response to a formal consult (pain management, antibiotic monitoring, medication reconciliation, etc…) and whenever there is something I need to communicate to the entire medical team. If there is a grossly ridiculous issue going on, I make sure to call about it rather than write: “Would consider changing synthroid 10 mg po daily to 100 mcg po daily”. It is courteous and helps develop a working-relati...
    12 min
  • 18: Sedation of the acutely agitated patient when intubation is prohibited - A Critical Care Pharmacy Podcast









    In this episode the methods I am going to discuss in this episode are not first line or even second line therapies for controlling acute agitation.  I use them rarely - as in a few times per year or less.  But in some difficult situations they are like having an Ace up your sleeve!
    Almost all acutely agitated patients can be treated with benzodiazepines and/or antipsychotics. If doses escalate to the point of respiratory failure, the patient is sedated further, intubated and is then awakened later after the period of acute agitation is over.
    But occasionally patients do not respond to benzodiazepines or antipsychotics. Other times, patients may have conditions that make benzodiazepines or antipsychotics relatively contraindicated, may have advanced heart or lung disease and might never wean from the ventilator, or have an advanced directive that prohibits intubation.
    Here are three strategies that can be used in these circumstances:
    -Valproic acid
    -High dose dexmedetomidine infusion
    -Ketamine
    Valproic acid
    About two years ago an intensivist I work with (also named Joe by the way) suggested using a loading dose of 15mg/kg valproic acid to control acute agitated delirium in an ICU patient. I could not find much evidence, but other therapies had not been very effective for the patient and we gave it a try. The patient in question had a history of various mental health diagnoses, and the addition of valproic acid seemed to control the agitation over the next few days.
    Ever since then I’ve been keeping an eye out for the use of valproic acid in acute agitation. I was very happy when in May 2015 a randomized, double blind trial directly comparing valproic acid to haloperidol for acute agitation was published. The trial was published in the journal of International Clinical Psychopharmacology and compared valproic acid 20mg/kg IV vs haloperidol 5mg IM in 80 patients in an emergency department with acute agitation. Agitation was measured at baseline and 30 min after the first injection using 3 different scales: the Agitation–Calmness Evaluation Scale (ACES), the Positive and Negative Syndrome Scale-Excited Component subscale, and the Agitated Behavior Scale.
    No significant differences were observed between groups after 30 min for the agitation scales. More patients in the haloperidol group experienced intense sedation (36%) and extrapyramidal symptoms (8%) compared with the valproate group (2.5% for intense sedation, no patient for extrapyramidal symptoms). The findings suggest that in an emergency setting, IV valproic acid is as effective as haloperidol in reducing agitation, with a better safety profile.
    Since the publication of this article I have had the opportunity to use v...
    11 min
  • 17: When to IV push alteplase for massive PE - A Critical Care Pharmacy Podcast









    In this episode I’ll cover when, why, and how to give alteplase for massive pulmonary embolism (PE).  I’ll also touch on bleeding risk and whether to stop or continue the heparin infusion while you give the alteplase.
    First, let’s define massive PE.  Massive pulmonary embolism is present when a patient has an acute PE and hypotension, profound bradycardia, or cardiac arrest.
    When to give alteplase
    There is broad agreement among experts to administer alteplase in the setting of massive PE. It makes good sense considering the pathophysiology - the clot has to go for oxygenation to return. Anti-thrombotics like heparin and enoxaparin aren’t going to do a thing to the existing clot - they will just prevent the clot from getting bigger.
    The specific CHEST guideline statement is: In patients with acute PE associated with hypotension (systolic BP , 90 mm Hg) who do not have a high bleeding risk, we suggest systemically administered thrombolytic therapy over no such therapy (Grade 2C) .
    Why is alteplase given in massive PE
    The hope is that mortality will be decreased by lysing the clot. In the 2012 CHEST guidelines, the authors note that there is only a trend pointing towards a mortality benefit with lytic therapy. Since the publication of those guidelines there has been a meta-analysis which does point to an association with lower all-cause mortality with lytic therapy. However the wide range of patient groups and treatments in this meta-analysis leaves many unanswered questions. Even though the available evidence is less than ideal, I doubt further trials will compare lytic therapy to placebo in massive PE given the clear pathophysiology and rationale for lytics. As the CHEST guidelines state: Patients with the most severe presentations who have the highest risk of dying from an acute PE have the most to gain from thrombolysis.
    Plenty of “soft endpoints” are improved after alteplase is given for massive PE. Clot lysis is accelerated and there is early hemo...
    14 min
  • 17: When to IV push alteplase for massive PE
    Show notes at pharmacyjoe.com/episode17. In this episode I ll cover when, why, and how to give alteplase for massive pulmonary embolism (PE). I ll also touch on bleeding risk and whether to stop or continue the heparin infusion while you give the alteplase.
    14 min
  • 16: How to use ketamine in the critical care setting - A Critical Care Pharmacy Podcast









    In this episode I’ll highlight the key points that set ketamine apart from other sedatives & analgesics, and discuss how to use ketamine in the critical care setting.
    There is a lot of buzz around the use of ketamine in the critical care setting, and for good reason.  But a lot of providers are unfamiliar with and hesitant to use the drug.  
    What is ketamine?
    Ketamine is a noncompetitive NMDA receptor antagonist that produces analgesia and dissociative anesthesia.
    What makes ketamine different from other sedatives & analgesics used in critical care?
    Ketamine’s analgesic effect is dose-dependent in the same manner as opioid analgesics. Give a little bit more ketamine, get a little more pain relief.
    What sets ketamine apart is how it produces anesthesia / amnesia. Ketamine causes a dissociation of the cortex and limbic systems, with the result that the patient cannot perceive the surrounding environment.  The key difference between ketamine and other agents such as etomidate, midazolam and propofol is that this dissociative state does not exist on a continuum.  It is either on or off.  I think of it like pregnancy - just like you can’t be “a little bit pregnant”, you can’t be “a little bit dissociated”.
    When using it as a sedative, it is critical to keep in mind this on/off nature of ketamine.
    What effects does ketamine produce besides analgesia and dissociative anesthesia?
    Respiratory:
    Ketamine does not suppress respirations, unless it is given too rapidly IV push (give over 1 minute, complications when given <30 seconds).
    Rarely ketamine may cause laryngeal spasms.
    Ketamine increases airway secretions.
    Ketamine causes bronchodialation.
    Cardiovasular:
    Ketamine causes the release of endogenous catecholamines. This means in most patients ketamine has a neutral to positive effect on the cardiovascular system. Expect at most a few points increase on the systolic BP and HR. However if the patient is catecholamine depleted (such as in prolonged severe illness) ketamine may paradoxically cause hemodynamic collapse.
    Neurological:
    An emergence phenomenon may occur as the ketamine wears off. This is more common in adult patients. The patient may experience vivid dreams and be extremely agitated. IV midazolam can be used to treat or prevent this effect.
    When used at sub-anesthetic doses some patients report feeling “weird” and this feeling can cause anxiety.
    Ketamine carries a warning for use in the setting of elevated intracranial pressure (ICP).  There is evidence that suggests any effects on ICP are not of consequence to the patient and the authors of
    17 min
  • 15: Pharmacist assisted intubation - Critical Care Pharmacy Podcast









    If one of us is not already at the bedside, pharmacists at my institution are frequently called by critical care providers to assist with intubation procedures in critically ill patients.
    In this episode I'll review the pharmacists' role and expectations during intubation of critically ill patients.
    We’ll cover the following scenarios in this episode:
    1. Crash airway
    2. Rapid sequence intubation
    3. Delayed sequence intubation
    4. Difficult airway predicted
    5. Awake airway
    6. Failed airway
    I treat these scenarios similar to code blue and rapid response calls in that I am focused on:
    1. Identifying and predicting patient and provider needs
    2. Preparing in advance to meet those needs
    Crash airway
    A crash airway exists when the patient is in cardiac or respiratory arrest or is otherwise near death.
    Endotracheal intubation is attempted without medications.
    If the patient is not relaxed, a single dose of a paralytic (usually succinylcholine) may be given.  Use 2mg/kg for this indication (go big or go home dosing strategy).
    Rapid sequence intubation (RSI)
    RSI is established as the best way to ensure airway placement success in the absence of a difficult airway.
    RSI is described as occurring in 7 phases:
    1. Preparation
    2. Preoxygenation
    3. Pretreatment
    4. Paralysis with induction
    5. Positioning
    6. Placement
    7. Post intubation
    Preparation
    In this phase the first thing I do is identify the provider’s preference for medications, and I will make suggestions on what to use if I see a reason to do so.
    A general rule of thumb I use is to obtain double the amount of medication the physician says they want.  Nothing is worse than having to run to the med room to get more induction agent after the procedure has started.
    I use tape to label the syringes as it is always in my pocket or on the unit.
    Preoxygenation
    Preoxygenation is critical to maximize the “safe apnea time” for the patient. This is the time the provider has to place the airway after the patient stops breathing and before their O2 saturation drops to dangerous levels. This may be 8 minutes for a healthy adult, or less than 4 minutes for a critically ill or obese adult.
    In this phase there is not much for the pharmacist to do so I continue with preparing / labeling if needed.  If I have time, I lay several blank pieces of tape out on a table so that I have labels ready to go if additional drugs are called for.
    Pretreatment
    16 min

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