41y/M CP

Eden said:
Okay so now im more confident in my inital diagonsis. This guy is in cardiogenic shock due to lmca lesion.
What i would do
Asa o2 heparin put the pads on him and hang a pressor (in my case dopamine ). full throttle to closest stemi center

Bleeding, ascending aortic dissection and such can also cause these kind of changes in the ecg. But with the patient symptoms and this specific ecg, which is very imperssive and like stcemt said it nails every point for lmca lesion, It seems to me that this is the most probable dx.
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OK...food for thought...if his ascending aorta were dissecting, it could very well involve the root vessels. So your diagnosis of a left main lesion would be correct, but the treatment would be significantly different. A 41 year old having such severe left main disease would more than likely have a very strong family history (like his dad dying from the same thing at about the same age) and I'd want to tease that out as best as I could.
 
@E tank if we have the potential for an ascending aortic dissection...then we ought to be really cautious about doing anything on the coagulation inhibition spectrum, right? So is it conceivable that we might elect to do nothing other than O2, ECG, pain management, and a fluid bolus?
 
E tank said:
OK...food for thought...if his ascending aorta were dissecting, it could very well involve the root vessels. So your diagnosis of a left main lesion would be correct, but the treatment would be significantly different. A 41 year old having such severe left main disease would more than likely have a very strong family history (like his dad dying from the same thing at about the same age) and I'd want to tease that out as best as I could.
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Yes I agree, I would expect him to have relevant family history. But he does have the rest relevant risk factors.

Had an aortic dissection present itself as rca occlusion. These are definitely tricky.
I would measure bp on both hands too.
Minimal intervention approach to this case might not be wrong too.
 
EpiEMS said:
@E tank if we have the potential for an ascending aortic dissection...then we ought to be really cautious about doing anything on the coagulation inhibition spectrum, right? So is it conceivable that we might elect to do nothing other than O2, ECG, pain management, and a fluid bolus?
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So, at the risk of chasing zebras, if we are including an ascending dissection that is involving the coronaries, the only difference in treatment here would be where you brought the patient. That said, you wouldn't pass a hospital with a cath lab and drive 30 minutes to the heart center either.

Good thought about the anticoagulation therapy. Functionally speaking, an aspirin won't hurt someone like this. Even heparin would not be the end of the world. What really complicates surgical repair is when someone gives the patient something like Plavix. That is a real hassle when it comes to intraoperative bleeding.

I'd be very tolerant of a MAP of about 65 with a guy like this and hold off on inotropic support unless it fell below 60. I'd give fluid if I could instead.
 
I was actually about to ask you @E tank about the risk of with holding in this case. It seems like asa has more benefit if it is a LMCA occlusion vs harm if this was an aortic dissection. That answers my question.
 
@E tank, thanks! That makes sense. (Interestingly enough, we don't carry anything beyond aspirin - even on our ALS units - as far as I can tell, for anticoagulation).
 
A 41yr old with aortic stenosis? That should set off some bells as to a specific valvular pathology and an associated condition....
 
FLdoc2011 said:
A 41yr old with aortic stenosis? That should set off some bells as to a specific valvular pathology and an associated condition....
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So this was indeed a pt with severe cardiac ischemia secondary to untreated aortic stenosis. The pt was found to have clean coronary arteries and a PAWP of 42mmHg. The aortic valve was stented open by balloon valvuloplasty and is scheduled to have a valve replacement in the coming days. Hope you all enjoyed, loved seeing the comments and thought process, a lot of great ideas and considerations. As far as what this Pt's pre-hospital Tx actually consisted of was treated and transported to the closest hospital with Cath capabilities and en route received O2 15LPM NRB, 2x IV with 150mL of LR for BP. ASA was with held due to concerns of the surgery and delivered to the receiving hospital without further complications.
 
This was a good one. Guess I have to go look up the pathology FLdoc was talking about now.
 
Good case and patho. This is the type of patient you start vaspressors on then arrest... afterload kills.
 
Chase said:
Good case and patho. This is the type of patient you start vaspressors on then arrest... afterload kills.
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You would really think that, but it's counter intuitive...something like phenylephrine or vasopressin would actually help this guy. If you think about it, his afterload is already off the chart as it is because of the stenotic valve. This causes a wide pressure gradient between the left ventricle and the aortic root where the coronary arteries come off.

Basically, all of the pressure stays in the ventricle and there is little left over to push blood down the RCA and LMCA. When you add a pressor, you increase the pressure in the aortic root from the other side of the heart and restore pressure head to the coronaries.

What is a killer for a guy like this is a faster heart rate, so epinephrine is not a good choice for hemodynamic management at all.

The absolute quickest way to kill this guy? Nitroglycerin.
 
I get rate control and optimizing filling time but does normalizing the gradient really gain that much forward flow? You still likely have a poorly functioning LV that can't overcome Increased SVR.
 
E tank said:
The absolute quickest way to kill this guy? Nitroglycerin.
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In some places, EMTs and AEMTs who don't have ECG monitoring capabilities may administer EMS nitro (not patient carried nitro). This patient likely wouldn't be a candidate (as far as I can tell), given his hypotensive state, but if he were normotensive...how would we know not to administer nitroglycerin? Does it have something to do with reducing afterload through vasodilation?

(Probably a dumb question, just want to make sure I'm following here.)
 
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Chase said:
I get rate control and optimizing filling time but does normalizing the gradient really gain that much forward flow? You still likely have a poorly functioning LV that can't overcome Increased SVR.
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You won't increase the SVR any more than his stenotic valve does. There is no net increased work put on the LV. In fact the LV function should improve with the greater coronary artery flow.
 
EpiEMS said:
In some places, EMTs and AEMTs who don't have ECG monitoring capabilities may administer EMS nitro (not patient carried nitro). This patient likely wouldn't be a candidate (as far as I can tell), given his hypotensive state, but if he were normotensive...how would we know not to administer nitroglycerin? Does it have something to do with reducing afterload through vasodilation?

(Probably a dumb question, just want to make sure I'm following here.)
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Obviously, I'm not familiar with local protocol, but if someone gives a history of aortic stenosis that you would say is a candidate for NTG, I'd recommend running that by someone first.

The problem is that the NTG will unload the right heart by increasing venous capacitance at the periphery. That just causes the amount of blood ending up in the LV (read: the coronary arteries) to fall. With severe AS, existing impaired coronary flow falls even more. That causes the vicious cycle of pump failure causing more pump failure.
 
@E tank
Thanks for the explanation - appreciate it!
 
In this case, I'd hold the aspirin and nitro (as E tank explained) and go with fluid, O2 and a pressor PRN. Although we do carry heparin, this guy's recent kidney surgery would keep me away from it; the last thing he needs is to blow any clots we might need.
 
FLMedic311 said:
SO you are dispatched to a 41y M pt and on arrival of a fairly clean appearing home you find the pt just past the front door, sitting on the floor half in the jacket/shoe closet. He is clearly pale cool and diaphoretic. He is a/o x4 and complains of chest and side pain. The pt sts that 4 days ago he got home from surgery where half of one of his kidneys was removed. As to why his best explanation is that it was damaged. Initial vitals are P-102 irregular, R-38 and shallow, SPO2- 91%RA, BP-90/48 BGL-112.. Feel free to ask for any additional info and of course here is your first 12 lead..
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I think recent surgery with s/s of cardiac chest pain w/ high resp rate and Pulmonary Embolism comes to mind. Load and go to facility that has thrombolytic therapy.

Looks like possible ST depression?

Either way, it doesn't look good. Give O2 via CPAP, place in a semi-fowler position if tolerated with feet raised. Be prepared for CPR and chest compressions.
 
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