EM:RAP and Non-ACS Cardiovascular (February 2019)
AIR: https://www.aliemu.com/courses/cardiovascular-2019/
EM:RAP for Asynchronous Learning! For credit, first, listen to the entire podcast. Your participation in the discussion board here is your attestation that you have listened and engaged with the content in a meaningful way.
https://www.emrap.org/episode/emrap20192/acuteflaccid/
When you have finished listening to the podcast, answer the following questions:
- Please list three things you learned from this podcast that you were not aware of before.
- Are there any areas of your practice that you would change after listening to this podcast? If so, what would you do differently?
- What topics mentioned in this podcast is considered too “bleeding edge” (ex. too new, lacks enough evidence, not ready for prime time). Are there any practices mentioned in this podcast that you would consider to not be applicable to our practice setting here at BMC?
3 comments
1. I was not aware that thyroid antibodies can cause chronic hives. This condition sounds awful. In patients with migratory raised lesions and no clear trigger for their presentation I may in the future consider obtaining TFTs along with TRAB antibodies as part of my work-up. I had not previously heard of employing pH strips for obtaining a rough estimate of a patients plasma pH. I had also never previously considered using the etCO2 nasal prongs as a method for evaluating a patients acid/base status. This makes total sense and a great way to work around a problem (unable to obtain labs due to a rural medical work environment of otherwise). I don’t think that I was ever taught that the addition of epi to a local anesthetic worked to keep that medication local. I had always previously believed that it was to promote vaso-smooth muscle contraction and, thereby, control bleeding at the site of a wound. I always believed that when evaluating a patient for abdominal compartment syndrome you would have to initially paralyze the patient ahead of a measurement. While the section on this phenomenon states that some patients may not need to be paralyzed ahead of measuring a pressure within the bladder, in reality, I imagine that this would be hard to achieve without a hefty dose of rocuronium.
2. I really enjoyed the two-part series on the hypotensive post-cardiac arrest patient. I have on several occasions used both epi and nor epi gtts to provide inotropy in addition to chronotropy but have worried that this may be too much of a good thing. Listening to the Crit Care/ED doc explain why epi is frequently the best choice in patients who have achieved ROSC is reassuring. In the future, I would likely feel more confident dropping the NorEpi from the treatment while relying solely on Epi as my go to pressor. It was helpful to listen to the sections on LAST and on intra-articular injections. I can never remember the maximum doses per kg for bupivacaine but hopefully this segment will have scared me enough to look it up each time. Intra-articular blocks are not commonly done in our department for various reasons but I like the idea of using a combo of 1% lido/0.25% bupivacaine and 80mg kenolog for the management of a painful knee when you know that the patient has not had an injection in the last 3-4 months. As long as you can ensure an aseptic technique, this can be a very satisfying result for both patient and provider.
3. I found the rural medicine section on managing a patient in DKA without the aid of a lab super interesting. I suppose when you are up against a rock and a hard place: give some IVNS, some K and check EKGs is the best you can do. I personally would be nervous about not having a value for K while managing this patient. While this would never happen in a hospital I would accept a job at – or at BMC, Knowledge of these tricks is helpful when considering what is actually going on, in terms of physiology ,in these patients
Please list three things you learned from this podcast that you were not aware of before.
I don’t have any experience working with hypotensive post-cardiac arrest patients therefore these sections contained a lot of information I was not aware of before. This section was very helpful, these are the notes that I took on this section and on the May 2018 EMRAP section on the same topic:
Epinephrine
o Use in pts w/ PEs.
o Do not use Epi: (1) when the arrest was due to refractory V tach or V fib or (2) if the pt is profoundly/persistently acidotic post-arrest (pH my max dose of lidocaine w/ epi is 280mg. Therefore the max amount for that pt would be 28mL (in other words about 3 10cc syringes!!!).
•Finally, knowing what physical exam signs to keep an eye out for was very helpful. Knowing that the toxicity has a biphasic presentation was super helpful: perioral numbness or metallic taste, confusion and seizure being the first symptoms then cardiovascular collapse (as bradycardia, asystole, tachycardia, heart blocks and ventricular fibrillation/tachycardia) being the subsequent ones.
•Treatment: Intralipid!!! (100ccs)
Are there any areas of your practice that you would change after listening to this podcast? If so, what would you do differently?
I will definitely return to the section on abdominal compartment syndrome when I start my next ICU rotation. This section reminded of the importance of a good abdominal exam and a broad differential when my very sick patients are not getting better despite standard interventions. After listening to this section I will definitely have a higher index of suspicion for patients with ascites and patients/p trauma w/ severe low blood pressure + fluid resuscitation.
What topics mentioned in this podcast is considered too “bleeding edge” (ex. too new, lacks enough evidence, not ready for prime time). Are there any practices mentioned in this podcast that you would consider to not be applicable to our practice setting here at BMC?
Fortunately at BMC we have the capability to order the necessary labs for out DKA patients. I nevertheless enjoyed reading about the physical exam signs that we should keep tract of when assessing our DKA patients.
Nowadays when I take care of DKA patients I depend a lot on my lab results to guide the care I provide. I enjoyed this section because it reminded of the importance of the physical exam. I really enjoyed reviewing the signs that should make me think for hyperglycemia (polyuria, polydipsia, blurry vision and fatigue) dehydration (decreased skin turgor, dry armpits, dry oral mucosa, a low JVP, tachycardia, and hypotension) and for ketoacidosis (Kussmaul breathing, confusion, acetone smell on breath). It was great seeing all the pieces come together. Even though the details of this section don’t apply to BMC I still plan want to lean more on my physical exam when taking care of my DKA patients.
3 things I learned and how they will change practice:
1. Epinephrine seems like a natural choice on post-ROSC hypotension given you’ve likely already given rounds of bolus epi that may have contributed to the patient’s improvement. This podcast was helpful in reinforcing that epi’s greater beta agonism to provide ionotropy may give it an advantage over the premixed levophed at BMC. Further, I did not know that vasopressin was better in significant acidosis and given many of these patient’s have substantial metabolic derangements including acidosis, this is a pressor I’ve not once used that I will definitely consider adding earlier as an adjunct to levophed/epi. Finally, multiple bicarb bolus to combat acidosis must be met with increased MV as the H+ converts it to CO2 readily.
2. That medicolegal brief is terrifying. 38yo M with infiltrate on CXR with chest pain, decision made not to pursue troponin despite ?J point elevation on EKG (not specifically described in the podcast). Seems reasonable in a <40yo M without risk factors with a known explanation for his pain. Finally, he had no acute event for months after, so the initial "emergency" was likely not ACS given he had no decompensation. Regardless, the failure of establishing follow up for his chest pain, recognizing ?EKG changes, or sending a troponin on initial visit resulted in a lost malpractice suit. Often as a resident it feels like we are sending too many labs with most of our bloodwork panning out normal, and amongst younger patient's without risk factors, it is far to easy to anchor on the more common diagnosis. My takeaway is exertional chest pain is always worrisome and likely warrants troponin (this is the "typical" worrying presentation of young chest pain that might actually be cardiac)
3. Bupivicaine is dangerous. We don't use it often at BMC but the knowledge that it is far more lipophilic and more likely to cause LAST is important. Further, we often consider bupivicaine for nerve blocks and larger territories of pain control (ex. fascia iliaca block), which inherently involve more exposure to vasculature which even if not injected into, can passively absorb large amounts of anesthetic. I did not know the simplified dosing of intralipid, 100mL for everyone to make it easier. Repeat q3min to effect. However, this does not supersede typical treatment, so benzos are still first line for seizure and ACLS for any arrhythmia/arrest.
Too cutting edge for BMC:
Intraarticular injections for pain, specifically the knee, are not routinely used at BMC (concern for overuse, promoting patient's presenting for non-emergent taps/injections, the time it takes to perform them, concern for seeding the joint). However, there is a lot of data to support their use when performed appropriately. We do not frequently provide opiates for these patients, but this might allow us better patient satisfaction without giving in to opiates. Risk of septic joint per the podcast is surprisingly high (1/200 per ortho, 1/2600 per rheum). 1/200 seems unacceptable. If this comes in to use, it is good to know that the septic joint typically becomes symptomatic in 3-4 days (not in the earlier period when their may be a "post-injection flare" of symptoms which is normal).