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Couple other items I forgot:

Nitrates are fantastic. Venodilation>>arteriodilation but this lady will benefit from both.

Be careful with furosemide. When patients aren't actually volume overloaded it can tank their pressures and hypokalemia and worsen an AKI...But it also has some rapid venodilatory effects via prostaglandin pathways which is pretty cool.

Opiates (morphine in particular) are also an option but again, be wary as it can knock out some respiratory drive, plus if someone starts puking on NIPPV you're gonna have a bad time.

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On 9/9/2021 at 12:17 PM, LT_Oneal_PAC said:

We still seem to be hinging on PE, and I'm not saying that's wrong. While she is at risk, if you develop a PE, where is the obstruction? Where does it cause fluid to back into? Does it lead to pulmonary edema? what is making you believe there is heart strain from a PE? How does heart strain manifest in imaging and lab work? What part of the heart is strained? If you believe she is having heart strain, do you want to thrombolyse her with tPa? What are some indications to give thrombolytics? 

A PE would be located in an artery in the lung. This would cause fluid to back into the right ventricle. So you would see right ventricle strain, correct? ECG might show some strain with RAD, RBBB, and T wave inversion in V1. No RV was seen on POCUS, though. Did we get a BUN, although won't distinguish b/t right and left heart strain. An indication for thrombolytics would be a massive PE, which she doesn't seem to meet from the risk stratification I found on EMCrit. She does have high-risk PESI score, so she'll probably need anticoagulation at some point. 

Acute on chronic mitral regurgitation is a excellent Ddx. Why is it all of the sudden worse? Look back at the vitals. What emergent diagnosis causes sudden fluid in the lung? It can also cause acute kidney injury, acute heart failure, confusion, seizures, end organ damage.

Can we add hypertensive emergency to the ddx. BP was 210/124 on initial presentation. Hoping we got some repeat BPs - they any better? Also if thinking PE, especially massive, it would more likely lead to hypotension. Nitro would be a good choice to tx, or clevidipine with her AKI. Want to make sure you don't decrease the BP by >25%. 

While we've got her on BiPAP and supporting her respirations, can we work to get her BP down? Just curious, how quickly can you expect to see clinical improvement with tx of hypertensive emergency? Don't feel comfortable r/o PE, but it doesn't seem like she'll need thrombolytics right now. I appreciate you all mentioning that she is not stable right now for a CTA (things students forget about). She's obviously not going home, so could we add an anticoagulant before transferring and they could get the CT when she is more stable? Also, is it too early to be thinking about deposition? She needs ICU care, which our small facility has. Does the interventionist feel comfortable or is she going to need to be shipped (which is going to be a ton of fun with COVID pts filling up all the beds). 

 

 

 

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22 minutes ago, Sacarroll10 said:

 

 

 

Hypertensive emergency! Ding ding! We can determine this pretty quickly. Patient comes in, can’t breath. IV, O2, monitors. Simultaneously grab cardiac probe and look at heart and lungs. No RV strain, no LV dysfunction or wall motion abnormality, B lines present. If she has PE, unlikely to need thrombolysis. B lines, JVD, history suggest likely either CHF exacerbation and unlikely PE as the cause, as PE does not cause fluid in the lungs. It backs up the RV. The normal EF suggests she has HFpEF. All this combined with the vitals and acute onset (as opposed to a more insidious onset in volume overload) that the hypertension is our primary issue leading to FLASH pulmonary edema. I wouldn’t hesitate to start some NTG.

Now if I was really concerned for PE, I wouldn’t start NTG. Some would get a CTA here “just to be safe” and I firmly stand by not being a Monday morning quarterback, but would encourage students to follow the evidence. The burden of evidence is to do the test, rather than thinking you need evidence to not do a test. It’s all Bayesian statistics. What is the pre-test probability of a positive test. For me, I’m this patient, it’s less than 2%. Maybe an easier thing to say from a standpoint of experience. 

NTG is our bestest friend here. Normally it’s garbage in HTN emergency, but this is one of its few indications. With its primarily venodilation, we rapidly expand the tank, sucking out the fluids from the lungs. Combined with bipap (or cpap)pushing it out, you would have this lady tip top before the admitting service calls you back.

now she is a little tachycardic. I would not fault someone for also giving some metoprolol, as NTG can lead to reflex tachycardia.

while typically this person would go to an ICU, I would 100% admit this lady to me (I’m also the Hospitalist) and put her on the floor. Larger centers won’t take any infusions like this and certainly not bipap. Though I suspect she’ll need neither in about 6 hours with some good inpatient management and all will be good.

 

@MediMikebrought up a good question: what do we do if she doesn’t tolerate the bipap?

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2 hours ago, ohiovolffemtp said:

If the patient won't tolerate the BiPAP, 1st try a small dose of ativan, e.g. 0.5 mg iv.  If that doesn't work,  try sub-dissasociative doses of ketamine.

Great work. You're going to do wonderful on your rotations 😂

Some type of anxiolysis may be necessary. Be careful with ketamine and patients who have a HTN emergency as it can result in more HTN and tachycardia. Benzos are an option in some patients, or if you're lucky enough to have dexmedetomidine that is my preference.

Nicely done all. If there are any questions about this case please shout them out!

 

 

 

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28 minutes ago, MediMike said:

Great work. You're going to do wonderful on your rotations 😂

Some type of anxiolysis may be necessary. Be careful with ketamine and patients who have a HTN emergency as it can result in more HTN and tachycardia. Benzos are an option in some patients, or if you're lucky enough to have dexmedetomidine that is my preference.

Nicely done all. If there are any questions about this case please shout them out!

 

 

 

Is this an actual case? If so, do you think the mitral regurgitation caused the appearance of r>L lung pulmonary edema? I’ve seen a lot of reports of primarily or even unilateral pulmonary edema if certain leaflets were affected in MR. 

Were you saying westermark sign on the CXR as an indicator of PE? Little less fluffy in the bottom left, but then again I thought maybe it was due to the above. 
 

Would dobutamine ever be something you would use here? Obviously the nitro is best in flash pulmonary edema, but in hypertensive emergency with acute heart failure, could it Improve forward flow and dobut can also lower blood pressure? We can often oversimplify in the ED (norepi is often the go to for every shock type except anaphylactic shock where we use epi) but I like to be more nuanced. I haven’t used dobut since I was a heart transplant nurse.

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12 hours ago, LT_Oneal_PAC said:

Is this an actual case? If so, do you think the mitral regurgitation caused the appearance of r>L lung pulmonary edema? I’ve seen a lot of reports of primarily or even unilateral pulmonary edema if certain leaflets were affected in MR. 

Were you saying westermark sign on the CXR as an indicator of PE? Little less fluffy in the bottom left, but then again I thought maybe it was due to the above. 
 

Would dobutamine ever be something you would use here? Obviously the nitro is best in flash pulmonary edema, but in hypertensive emergency with acute heart failure, could it Improve forward flow and dobut can also lower blood pressure? We can often oversimplify in the ED (norepi is often the go to for every shock type except anaphylactic shock where we use epi) but I like to be more nuanced. I haven’t used dobut since I was a heart transplant nurse.

It's a conglomerate of multiple patients I've seen. The acute pulmonary edema d/t MR was a classic patient I'd see in the CCU. You are spot-on with the R>L being seen with posterior leaflet issues, the jet ends up directed into the PV in just the right fashion. Crazy.

I wasn't trying to imply anything at all on the CXR, it's just pure edema to my read. The stupid sign I was referring to was S1Q3T3 which one if the posters picked up on super quick. We teach it as being pathognomonic when in fact the specificity is crap and can show up with any kind of RV strain (COPD, pHTN, ARDS etc)

For treatment I prefer nitroprusside as it has a greater arteriodilatory effect, can run into problem with lack of familiarity among staff when trying to give it, NTG works too! Main goal is afterload reduction to improve forward flow.

When I think about MR I break it down into primary and secondary causes, primary is related to the leaflet or valve itself while secondary is due to structural changes of the LV or LA. In my experience primary is well managed with afterload reduction via meds or worst case a balloon pump. Secondary MR, particularly those involving a dilated LV will often have a low EF to begin with and will require both afterload reduction and inotropes.

The beta 2 action of dobutamine isn't all that pronounced in my experience unless you've reached the maximal B1 augmentation of the myocardium and keep pushing.

I miss the CCU sometimes 🙂

 

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@MediMike

my bad, I didn’t reread it. I thought you asked something about the CXR and not the ekg. Interestingly we were taught it was very specific as well, but I have lost faith in that since I’ve seen it several times with no PE found.

I remember in heart transplant seeing a lot of hypotension from dobut, but then again those were the sickest of the sick so I was probably seeing correlation and not causation. Thanks!

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For our students I think there are several teaching points, many of which aren't really taught in PA school:

  • Stabilization/resuscitation of patients not only can, but must, occur before diagnosis, and often before even full assessment.  It does not matter whether this patient's lungs are full of fluid because of flash pulmonary edema, acute exacerbation of chronic congestive heart failure, or other reasons.   They need pressure support to push the fluid out of their alveoli.  This extends to other interventions for breathing, blood pressure support, altered mental status, etc.
  • During this phase of patient care good enough quick is way more important than best slower.  Nitroprusside is great, but requires an IV, which this patient may or may not have.  SL nitro or transdermal nitro paste may not be as fast, until you consider the time to get the IV, get the drip ready, etc.  You may need to start with the quick and transfer to the better later.  More broadly, PO and IM may be 1st step, if IV access is going to be slow.
  • Symptomatic management doesn't require definitive or necessarily even probable diagnosis as a pre req.  Fever gets antipyretics, nausea gets antiemetics, pain (if likely to be real) gets analgesics.  It doesn't matter if the fever is from cellulitis, pneumonia, UTI, etc; if the nausea is from gastroenteritis, head injury, etc; same for pain.
  • This thought process for resuscitation/stabilization/symptom management goes for all types and locations of practice, whether primary care, urgent care, emergency medicine, in-patient medicine, etc.  The tools available to you will change and you will need to know them.  Your only option may be to punt, even if it's calling 911.
  • Even with the same type of practice, say EM, approaches will vary based on local capabilities.  For example, the Lt. reaches for ultrasound because he's calling his rad tech in from home.  My rad tech is at worst 30 yards away and will get me a stat portable chest before my ultrasound machine even boots up.  We're both in critical access hospitals.  We don't have exactly the same meds, in house labs, etc. available to us.  Some of the tools: meds, labs, imaging that Mike the hospitalist/ICU guy has I'll never have at my sites.

Biggest point:  PA school teaches this flow:

Patient shows up and gives symptoms/chief complaint  => history & physical => differential diagnosis => work-up: imaging, test, etc. => diagnosis => treatment plan.

Actual medicine:

Patient shows up and gives symptoms/chief complaint  =>  Initial assessment => resuscitation/stabilization/symptom management => history & physical => differential diagnosis => work-up: imaging, test, etc. => diagnosis(es) => treatment plan => patient response => loop back to differential diagnosis; repeat until patient better, transferred to other care, or deceased.

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