Scenario

[MediMike]

Alright, I had that rarest of creatures the other night, a non-intubated patient who could talk, also one of the sicker I've run across recently. Details changed to protect identity of course.

70yo female w/ hx HLD, PAD, CAD s/p 3vCABG 2 weeks earlier (discharged to home 10 days ago) brought in by EMS after being found slumped over and lethargic by family.

In ED patient complaining of dyspnea. Labs notable for AKI w/ Scr 2.5, noted to be 1.48 on clinic visit 1 week prior and 0.7 on discharge, K is 5.1, AST/ALT 300 & 227, INR 1.3. BNP 256, troponin 0.05, glucose 227

BP per EMS 90/68, unobtainable by cuff in ED, arterial line placed by ED physician showing 70/40. Bedside echo done by MD shows depressed LV function, pulmonary edema throughout lung fields. CXR clear, no PTX. He starts her on dobutamine and quickly ratchets it up to 15mcg/kg/min, pressure continues dropping, shows up to you on 30mcg/min of NE and 5mcg/min of epi with a pressure of 84/50, no central access.  Patient is grey and vomiting.

What do you want to know and what do you want to do? (I'm starting a 5 night stretch so I'll try to keep up)

[LT_Oneal_PAC]

@MediMike

i assume that is a troponin I HS? If so it’s elevated, but could just be a trop leak as it’s not significant at the current time. I see no remarks on a EKG. 

I would like the rest of the vitals. If HR amenable I prefer epi for the ED management and keeping it simple during resuscitation. Dobutamine can activate B2 and cause further BP drop. 

what was the IVC like? JVD? Do we think the patient is Fluid tolerant? Fill the tank but continue pressors. Either way I would be hesistant to initiate diuresis as this patient may be preload dependent.

that INR is troubling along with the elevated LFT. Do we have any prior LFT? A dose of vit K could assist, but I’ll admit this is me practicing how I was taught and not my knowledge of the scientific evidence.

the big picture here appears to be cardiogenic shock with multiple end organ damage. If febrile pan-culture. 

from an CCM perspective need to treat hyperglycemia. SSI, but low dose or half of what they typically use (initially) due to AKI that may become significantly worse in this scenario. Start CVL. I would consider Milrinone. Trend the troponin. Stat formal echo, but we need our own RUSH US exam to confirm ED findings. Bipap if says are dropping. Cards consult. Surprised this came back to the medical ICU, which is where I believe you work? Tell cards it’s their patient.

This could be a lot of things post CABG, but a slim down version will look like

Dressler, graft failure, valvulopathy, acute MI, arrhythmia, pulmonary hypertension, sternal infection.

Consider non-occlusional mesenteric ischemia with vomiting, especially if abdominal pain is present, since it seems all the other organs are dying. The gut can handle 75% reduction in flow for 12 hours, but sounds like this has been going on for a while.

[MediMike]

7 hours ago, LT_Oneal_PAC said:

@MediMike

i assume that is a troponin I HS? If so it’s elevated, but could just be a trop leak as it’s not significant at the current time. I see no remarks on a EKG. 

I would like the rest of the vitals. If HR amenable I prefer epi for the ED management and keeping it simple during resuscitation. Dobutamine can activate B2 and cause further BP drop. 

what was the IVC like? JVD? Do we think the patient is Fluid tolerant? Fill the tank but continue pressors. Either way I would be hesistant to initiate diuresis as this patient may be preload dependent.

that INR is troubling along with the elevated LFT. Do we have any prior LFT? A dose of vit K could assist, but I’ll admit this is me practicing how I was taught and not my knowledge of the scientific evidence.

the big picture here appears to be cardiogenic shock with multiple end organ damage. If febrile pan-culture. 

from an CCM perspective need to treat hyperglycemia. SSI, but low dose or half of what they typically use (initially) due to AKI that may become significantly worse in this scenario. Start CVL. I would consider Milrinone. Trend the troponin. Stat formal echo, but we need our own RUSH US exam to confirm ED findings. Bipap if says are dropping. Cards consult. Surprised this came back to the medical ICU, which is where I believe you work? Tell cards it’s their patient.

This could be a lot of things post CABG, but a slim down version will look like

Dressler, graft failure, valvulopathy, acute MI, arrhythmia, pulmonary hypertension, sternal infection.

Consider non-occlusional mesenteric ischemia with vomiting, especially if abdominal pain is present, since it seems all the other organs are dying. The gut can handle 75% reduction in flow for 12 hours, but sounds like this has been going on for a while.

Sounds good! You drop the dobutamine down to 5mcg/kg/min and the pressure goes from 80/40 to 64/38.  No significant JVD noted.  12 lead showed nonspecific T wave abnormalities, late R wave transition (V5), nothing else jumping out at you.

Vitals:

HR 122 (sinus)

BP 64/38

RR 24

SpO2 100%

Temp 37.2C

Prior LFTs are wnl, no benefit in VitK unless you've got a bleeding concern, wouldn't worry about it at that level anyways.  Is there some association with renal function and insulin that I've never been aware of?

Milrinone will actually have a greater drop in afterload than dobutamine in most cases, especially in the setting of an AKI where it can accumulate. 

Next trop is 0.12.  You give a liter of LR and the BP transiently increases to 94/60 then trends back down. Work of breathing is fine although he is now requiring intermittent epi boluses (200mcg push gets you up to 120 systolic for a couple minutes)

Patient is now glazed over, occasionally vomiting but responsive still.

Your SonoSite from 1992 doesn't have enough crystals to get a good view, sonographer is coming in from whatever mansion they live in.

Cardiology says "we'll comment when the formal echo is done"

CT Surgery says "Are we 30 days post-op yet?"

[LT_Oneal_PAC]

@MediMike

whoa cowboy! Never said I wanted it turned down.  I though you were fluent in IM mental masturbation speak.
But it does tell us more likely a pump issue.

is that 100% on RA? I like to be trusting, but we have a ED that says pulmonary edema, yet a CXR is clear, as well as severe LV dysfxn but no other signs of failure like JVD, edema, elevated BNP? Just feeling like I need confirmation or I need to explore other  causes. Could this be a vena cava thrombus, acute bleed, metabolic issue? Trying not to anchor on this being related to just being pure HF related to prior cabg.
 

you’re breaking my balls here with your busted US  

What has been his symptoms in the preceding few days? What are his meds? Any new medications? Could he have mixed any up? Could he have popped several isosorbide? 

what does the rest of the exam look like? Is the belly tender or distended? Is there edema? Asymmetrical pulses? Bilious, coffee ground, or bloody emesis?

I would assume the ED had done these and you would have noted them if abnormal, but I’ll ask:

CBC, lactic, ABG. 

so am I understanding we are currently on dobutamine, NE, and epi? Our MAP before was 61mmHg, so let’s undo what we did and up the dobutamine. 

If we think he could survive it, some droperidol and an NGT might help alleviate some of his suffering. He’ll definitely need close monitoring to ensure he doesn’t need airway protection. 

In chronic or significant acute (like doubling Cr) we typically in the ED reduce insulin by half when using it to treat hyperkalemia. I’ve also personally seen many patients sent to the ED by FM for hypoglycemia because of worsening CKD, not huge jumps either, when there is no change in insulin dosing of insulin dependent diabetics.

I’ve never used milrinone at the provider level. Ran the pumps as an ICU RN, but no ED I’ve been in has had it and didn’t rotate through CVICU. Good note on it being Renally eliminated and the greater afterload reduction. 
 

well, that is an acute MI level troponin where I am. Now, I hate cards at my local university. Toxic residency that everyone hates. I once waited 2 hours and talked to 4 cards fellows before someone would come see my patient having an RV infarct in the ICU, who ended up dying with an RVAD, and another time a person was having a STEMI in the ED and the person said “my shift doesn’t start for 15 minutes, call the other guy.” So I’m very pushy with cards. “This patient is 2 weeks post op from a CABG. This is a STAT page. You can comment to me informally now, wait for the echo, but I’ll be documenting the times you were notified and the time I received recommendations.”
 

Listen, I’m just the dumb ED guy. 

 

[ChrisPAinED]

Pulmonary Edema with a clear chest x ray? Haven't seen that before, ain't saying it's impossible but just saying haven't ever seen it. 

Also be careful with fluids for BP if pulmonary Edema is noted. 

If troponin is starting to trend up may need to get a cardiologist on the line to see the patient for there input. 

Also a 100% O2 with pulmonary Edema? Is this on RA or do you have them on oxygen? If you have them on oxygen might be good to present that with vitals. 

 

 

[LT_Oneal_PAC]

@ChrisPAinED

US is far more sensitive than CXR for edema. 

https://pubmed.ncbi.nlm.nih.gov/29400365/#:~:text=Results%3A The overall sensitivity of,CI%3A 97%-99%).

https://pubmed.ncbi.nlm.nih.gov/29400365/#:~:text=Results%3A The overall sensitivity of,CI%3A 97%-99%).

it’s also far more sensitive for pneumothorax, but one could make an argument if it is so small you can’t see it on a upright CXR, is it big enough to care about it?

You need to be careful with fluids, but in the preload dependent it can be helpful and 250cc-500cc blouses aren’t killing anyone. 
 

But I do agree, something seems to not add up here. 
 

 

[MediMike]

8 hours ago, LT_Oneal_PAC said:

whoa cowboy! Never said I wanted it turned down.  I though you were fluent in IM mental masturbation speak.
But it does tell us more likely a pump issue.

is that 100% on RA? I like to be trusting, but we have a ED that says pulmonary edema, yet a CXR is clear, as well as severe LV dysfxn but no other signs of failure like JVD, edema, elevated BNP? Just feeling like I need confirmation or I need to explore other  causes. Could this be a vena cava thrombus, acute bleed, metabolic issue? Trying not to anchor on this being related to just being pure HF related to prior cabg.
 

you’re breaking my balls here with your busted US  

What has been his symptoms in the preceding few days? What are his meds? Any new medications? Could he have mixed any up? Could he have popped several isosorbide? 

what does the rest of the exam look like? Is the belly tender or distended? Is there edema? Asymmetrical pulses? Bilious, coffee ground, or bloody emesis?

I would assume the ED had done these and you would have noted them if abnormal, but I’ll ask:

CBC, lactic, ABG. 

so am I understanding we are currently on dobutamine, NE, and epi? Our MAP before was 61mmHg, so let’s undo what we did and up the dobutamine. 

If we think he could survive it, some droperidol and an NGT might help alleviate some of his suffering. He’ll definitely need close monitoring to ensure he doesn’t need airway protection. 

In chronic or significant acute (like doubling Cr) we typically in the ED reduce insulin by half when using it to treat hyperkalemia. I’ve also personally seen many patients sent to the ED by FM for hypoglycemia because of worsening CKD, not huge jumps either, when there is no change in insulin dosing of insulin dependent diabetics

While I can MM with the best of them I remain a medic at heart and just take action sometimes Alright, you put the dobutamine back up and your BP... doesn't change. (You've gone down the same path I did for whatever it's worth)

Remain in: Levo 30, dob 15, epi 5 > Pressure back in the low 60s, your guy is in/out of alertness.

No new meds, no symptoms (supposedly) up until today. Abdo is SNT, no edema, vomit is vomity looking without blood.

H/H 13/40 (unchanged from prior)

Lactate 12.5

ABG 7.22/30/256/100% on 10lpm NRB

And what's this?! You find, hidden at the bottom the op note that they wanted to put another graft to his distal RCA but the vessels were too small, formal TTE shows LV 55%-60%, RV with severely reduced function and dilation. No valve issues, no tamponade, IVC 2.4cm

Next step? Plans for the pressure? Your lovely nursing staff has been kindly pushing those 200mcg boluses to keep him awake and a quasi-normal color for the past 30min or so, starting to have intermittent ectopy (you know the kind, just enough to make you pucker then feel real good when it stops) 

[LT_Oneal_PAC]

1 hour ago, MediMike said:

While I can MM with the best of them I remain a medic at heart and just take action sometimes Alright, you put the dobutamine back up and your BP... doesn't change. (You've gone down the same path I did for whatever it's worth)

Remain in: Levo 30, dob 15, epi 5 > Pressure back in the low 60s, your guy is in/out of alertness.

No new meds, no symptoms (supposedly) up until today. Abdo is SNT, no edema, vomit is vomity looking without blood.

H/H 13/40 (unchanged from prior)

Lactate 12.5

ABG 7.22/30/256/100% on 10lpm NRB

And what's this?! You find, hidden at the bottom the op note that they wanted to put another graft to his distal RCA but the vessels were too small, formal TTE shows LV 55%-60%, RV with severely reduced function and dilation. No valve issues, no tamponade, IVC 2.4cm

Next step? Plans for the pressure? Your lovely nursing staff has been kindly pushing those 200mcg boluses to keep him awake and a quasi-normal color for the past 30min or so, starting to have intermittent ectopy (you know the kind, just enough to make you pucker then feel real good when it stops) 

So he is having an RV infarct with failure and end organ damage. Had a similar situation on MICU as a resident, the one who no one would come to see.
 

Honestly, I’m meeting my limit of management. Make sure his lytes are straightened out to prevent arrhythmia, I’d keep some pads on, titrate epi to life (dosing is a guideline at this point) and flog the last few myocytes to get the hell to work, start nitric oxide for RV afterload reduction, place central line/swan to start telling you to diurese or bolus, start measuring Central venous blood gas, tell CT surgery and cards dude is dying and may need an RVAD/crash ECMO and pray for a successful punt.

[polarbebe]

4 hours ago, MediMike said:

Lactate 12.5

ABG 7.22/30/256/100% on 10lpm NRB

And what's this?! You find, hidden at the bottom the op note that they wanted to put another graft to his distal RCA but the vessels were too small, formal TTE shows LV 55%-60%, RV with severely reduced function and dilation.

Thank you for sharing this case.  
 

RV failure. 
 

Anytime I have a patient with suspected or elevated pulmonary artery systolic pressures my first vasopressor of choice is vasopressin.  It doesn’t cause pulmonary vasoconstriction. 
 

As a last ditch effort can consider RV after load reduction with iloprost, epoprostanol or inhaled nitro.

 

Careful with the fluids because of the intraventicular dependence, with the right ventricular overloaded (in diseases such as massive PE) pushing into the left ventricular decreasing the LV preload and also possibly causing some LV outflow tract obstruction.   I would probably gently diurese and start with small doses. 

 

Although the CVP has fallen out of favor, there is some utility…. Particularly in RV failure, I would trend (not look at a single value) the CVP as a surrogate of the pressure at the cavoatrial junction.  In addition, measuring the CVSpO2 before and after any adjustments in either the dobumatine or milirinone.  Also trending the CVP after adjustments of the inotrope.

If on a ventilator also know that PEEP adds to RV after load.  

 

If the patient is not intubated… I have seen these patients crash and code peri-intubation.  Very preload dependent.  I have read some people start pressors before intubation when the patients really drop their blood pressure.

 

 

 

Edited April 13, 2022 by polarbebe

[MediMike]

Thanks for all the replies, I've got to say for a dumb ED guy @LT_Oneal_PAC you seem to have a similar thought process as me. 

Patient came upstairs, I did the same thing with dropping the dobutamine thinking we were vasodilating without having enough cardiac reserve to recruit and make up for it in stroke volume, BP dropped and bounced around for a bit.  Formal echo showed RV dysfunction as mentioned and pressures continued to tank as I worked on central access, had to abandon the IJ and get the fem as they were vomiting and thrashing a bit. 

Ended up on dobut 12.5mcg/kg/min, NE 30, epi of 40mcg/min just to keep a pressure in the 80s.  Gave a single liter with a transient response so threw another at her and seemed to perk her up a bit, maintaining a SBP in the low 100s and a MAP of 60.  The picture just didn't add up to an RV infarct with a minimally raised trop, but neither did a PE with the same trop and a BNP in that range.  Formal read on the TTE came back with an RV systolic pressure of 84 clenching the idea that I didn't have a damn clue what was going on.  Sudden onset of pHTN doesn't make sense outside of a PE but nothing else added up with no hypoxemia and other biomarkers looking fine...but what else could it be?  Called my collaborating doc and pushed for giving tPA, the patient was getting quasi regular 200mcgs of epi to maintain perfusion and were clearly going to die without some intervention.  (Called their kids and put the phone up for them as I didn't think they were going to make it). 

Got her to the point where I corraled the nursing staff and had a powwow that if we didn't get this gal down to the CT scanner they were going to die in front of us, the group of bada$$e$ agreed to run her down.  I had pharmacy with them at the bedside with tPA ready to go, as the images came in there were bilateral proximal PEs.  Hung the tPA and within 40 minutes the pressors were coming down like crazy. Never seen such a dramatic result in my life.  Was great to finally chalk up a win in the unit, happens so rarely!

@polarbebe great input on RV failure! I also avoid any alpha agonists when I'm able to in the setting of pHTN/RV failure.  I will always put those folks on pressors if I'm forced to intubate, induction itself kills them let alone the addition of PPV.

 

[LT_Oneal_PAC]

great case. You really threw me off the scent. In the ED if I had seen RV dilation I would immediately thought PE and looked for McConnel or D sign, but reports of LV failure, CABG, your op note, and pulmonary edema  you got me to commit the mortal sin of anchor bias!! A topic in which I preach a lot about to my students.
 

I shall now go perform seppuku to restore my honor.

[MediMike]

4 minutes ago, LT_Oneal_PAC said:

great case. You really threw me off the scent. In the ED if I had seen RV dilation I would immediately thought PE and looked for McConnel or D sign, but reports of LV failure, CABG, your op note, and pulmonary edema  you got me to commit the mortal sin of anchor bias!! A topic in which I preach a lot about to my students.
 

I shall now go perform seppuku to restore my honor.

Why'd you have to go and steal my thunder? Next post was going to be the risks of anchor bias and selection bias!

So easy to take the information presented and let it shape your entire work up and treatment plan. Once the formal echo came in and completely contradicted the EDP's it took me a bit to frame shift away from "heart no good". And I'm not gonna lie, when he told me pulmonary edema on POCUS and I saw the clean CXR a small part of me thought "Hmmm... didn't some strange dude on the internet tell me something about this?"

Always keep your mind open when developing a diagnostic and treatment plan!

Edit: Not intended to throw you off btw, this is exactly what I went through

Edited April 13, 2022 by MediMike

[ChrisPAinED]

27 minutes ago, LT_Oneal_PAC said:

great case. You really threw me off the scent. In the ED if I had seen RV dilation I would immediately thought PE and looked for McConnel or D sign, but reports of LV failure, CABG, your op note, and pulmonary edema  you got me to commit the mortal sin of anchor bias!! A topic in which I preach a lot about to my students.
 

I shall now go perform seppuku to restore my honor.

Lol same. RV enlargement is the biggest massive PE ED warning. I agree time to restore honor lol

[LT_Oneal_PAC]

7 hours ago, MediMike said:

Why'd you have to go and steal my thunder? Next post was going to be the risks of anchor bias and selection bias!

So easy to take the information presented and let it shape your entire work up and treatment plan. Once the formal echo came in and completely contradicted the EDP's it took me a bit to frame shift away from "heart no good". And I'm not gonna lie, when he told me pulmonary edema on POCUS and I saw the clean CXR a small part of me thought "Hmmm... didn't some strange dude on the internet tell me something about this?"

Always keep your mind open when developing a diagnostic and treatment plan!

Edit: Not intended to throw you off btw, this is exactly what I went through

Hey, I had to make up for my error! It was a great case!

definitely US is more sensitive for pulmonary edema than CXR, but like pneumothorax, they are probably both equally sensitive for severe disease. It’s best for those COPD versus CHF “I’m short of breath” but without vital sign changes.

Sounds like someone in the ED needs some remediation on their US though. Sounds like they can’t tell the RV from the LV