Septal infarct > Flash Pulmonary edema > Code

mrhunt

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67yo M, A&0X4 GCS15 presents with Syncopal episode and Pinkish blood stain On pillow with 911 called by family.

Initial BP is 80 over 40 systolic and 12 lead comes back with ST elevations in V1 & V2 with recripocral changes and Septal infarct confirmed by ER physician over phone consult. Pt initially Satting about 94% RA, Chest pain 4/10, constant, non-radiating, substernal. Skins Extremely pale, Limbs cold to touch and developing diaphoresis. Pt symptomatic with Dizziness, weakness and shortness of breath.

Denies nausea, vomiting abdominal, back pain. Denies any medical history, Meds or allergies, Drug or etoh use / abuse.

pt unable to be flown out and stemi Facility 80 Mins by ground.
Enroute Dual large bore IV's started with liter of NS hung Bolus with lungs re-assesed every 250ml and remain clear.324 ASA given PO , Nitro Withheld due to Hypotension. No pain meds given as contraindicated by Hypotension. Pt Develops near syncopal episode with Drop in BP to 50/20, Brady to 50's and Drop in SP02 to 80's.....

placed flat with legs elevated, NRB @ 15LPM.... Symptoms clear and BP begins to rise...

- Serial 12 leads show Evolving Stemi tombstoning and Deep ST depression almost globally.....Also begins to show Widespread interventricular Conduction Defects / delays and a widening QRS.

After approx 900ML Pt develops increasing shortness of breath on NRB and Becomes tachy, BP now 111/ 78, States cannot catch breath......Extremely anxious. SP02 Worsing to 80's and Resp Rate 30's with Now bilateral Rhonci / Rales. Pt is placed on CPAP With little to No improvement in symptoms. Pt is foaming at mouth and nose after being on CPAP and Suctioned as necessary. Nitro is still withheld due to Pt anxiety / non-compliance..... Pt States Breathing is WORSE on Cpap and Cannot tolerate and removes mask and placed back on NRB....

approx 10 mins out Pt codes, ACLS Protocols followed to best of my abilities with 2 rounds epi given. OPA in place and CPR started immediately. 12 lead captured during pulse check shows a PEA rthym. Hospital Immediately intubates, Bloody foamy sputum in tube immediately. Dr confirms Major Septal infarct........





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Sooooooo........This guy seemed to be in left heart failure from the start As well as A Septal infarct that was clearly affecting his conduction system....

Our protocls Go against dopamine Unless IV fluids are refractory (which they were not)

Fluid was NECESSARY due to extreme hypotension and symptomatic.....and was trying to do permissive hypotension as well.....But it seems clear i sorta fluid overloaded this guy.....

on the other hand, if i DIDNT give him fluid i had no chance of starting CPAP or hopes of ever giving him nitro which is what he badly needed...

So did he crash cause Flash pulmonary edema? or A major septal infarct that Stopped his heart? A bit of both? We'll never know?

What could i have done better? differently?
 

Gurby

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Thanks for sharing, good case. I look forward to hearing discussion about this from the more experienced people here.
I'm not sure if there is a good answer. It seems like there was a high probability of him crashing before making it to hospital unless you had a cath lab in the back of the truck.

What was his heartrate when you first got there and the BP was 80/40?

Textbook answer for treatment of cardiogenic shock is pressors and inotropes. Maybe could have started out with a 250mL bolus instead of 1L and seen where that got you, though I'm not sure what your protocols look like.

I think when the BP dropped to 50/20 you could have considered calling up medical control for advice / permission to give dopamine (though if you're alone in the back of the truck I understand that's easier said than done), or maybe just given it because at this point you could say he's refractory to fluids.

Once the BP came up to 111/78 you (I think) correctly reconsidered nitro, but it sounds like patient couldn't tolerate the tab under his tongue due to SOB and you don't have the spray? Maybe could have tried nitro paste?
At this point if he's not tolerating CPAP it sounds like he needs to be intubated, but if you're by yourself in the back of a moving truck without a ton of experience under your belt, it's probably better to just leave him on the NRB and pray. Make sure you sit him up at this point and don't keep him in trendelenburg.

Fluid was NECESSARY due to extreme hypotension and symptomatic.....and was trying to do permissive hypotension as well.....But it seems clear i sorta fluid overloaded this guy.....

on the other hand, if i DIDNT give him fluid i had no chance of starting CPAP or hopes of ever giving him nitro which is what he badly needed...
Raising the BP using fluids in a patient with cardiogenic pulmonary edema, just to be able to use nitro/cpap, feels counterproductive to me.


Those are my armchair quarterback thoughts. Again I think there's a good chance the patient doesn't make it either way... But I look forward to hearing what other people think.
 

E tank

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Our protocls Go against dopamine Unless IV fluids are refractory (which they were not)
Here's your problem, in my opinion. If this guy had presented in the hospital, he might have rec'd a little fluid but the mainstay of therapy (before the CCL) would have been an inopressor and probably not dopamine, but that would be better than fluid.

The guy's blood pressure is falling because of ischemic impairment of his contractility. You can temporarily raise the cardiac output and BP in someone like this by adding volume to the system (by improving coronary blood flow and contractility), but in a decompensating heart, you see where that gets you. You see improvement until you push him too far right in his Starling curve. That you needed to improve coronary flow was evident. How the protocols dictate that you do it in this situation is dicey...again, just my opinion.

So, I don't agree with your protocol, especially because it doesn't seem to have an end point for giving volume. Seems like a set up for this happening. If you'd need a little volume to buy some time before you set up an epi or dopamine drip, stopping at or before 400-500 ml would be OK. But not using volume until it didn't work.

But a really good case, thanks for sharing.
 
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mrhunt

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We give 250ml boluses up to one liter. Checking lungs every 250. He did have a brief drop in b.p but overall trends showed a positive b.p reaction to fluids until 900 had gone in....
 

E tank

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We give 250ml boluses up to one liter. Checking lungs every 250. He did have a brief drop in b.p but overall trends showed a positive b.p reaction to fluids until 900 had gone in....
Yeah...calling for up to a liter of fluid in a situation like this needs to be revisited by the medical director.
 

GMCmedic

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I think you did pretty good here considering protocol limitations. Typically 250ml gives a reasonably pressure in most patients, in a patient like this, that is probably my threshold for pressors, certainly stopping at 500ml.
 
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mrhunt

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I mean,lung sounds were fine until after full amount had gone in or I would have stopped It sooner!
 
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mrhunt

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Soooo protocols states start with initial 250ml bolus, and " consider additional fluid bolus " if no still below 90 which it was.

It states if no below 80 systolic which it WASNT except for one brief point to consider dopamine.

Soooooo it isn't exactly clear on exact max for shock/ hypoperfusion protocol.

Was trying to maintain 90 systolic, it went at end to like 112 systolic so not CRAZY high.

I documented everything. I dunno if imma get in trouble for this or fluid overload....I feel like I'm still within protocols however...
 

E tank

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Soooo protocols states start with initial 250ml bolus, and " consider additional fluid bolus " if no still below 90 which it was.

It states if no below 80 systolic which it WASNT except for one brief point to consider dopamine.

Soooooo it isn't exactly clear on exact max for shock/ hypoperfusion protocol.

Was trying to maintain 90 systolic, it went at end to like 112 systolic so not CRAZY high.

I documented everything. I dunno if imma get in trouble for this or fluid overload....I feel like I'm still within protocols however...
Don't get wrapped around the axle over this. Sounds like there is a lot of play in your protocol.

Are lung sounds given as one of the end points for stopping volume? By the time you hear fluid in the lungs, you're already at least one bolus in too many. If so, the protocol is basically asking you to make the condition worse to escalate to an inotrope.

There should be a clear time interval between boluses as well, like between 5 and 10 minutes. And once the target pressure is reached, you stop.

Say your first bolus got the guy to a systolic of 100 and 8 minutes later the pressure was 80 again. The patient has demonstrated that volume is not the answer regardless of what his lungs sound like. That's when he's saying he wants an inotrope.
 

GMCmedic

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I mean,lung sounds were fine until after full amount had gone in or I would have stopped It sooner!
If my comment came off as sounding like what you did was wrong, I apologize. Just because I choose to treat a different way, doesnt make me right, I wasnt there in the moment. As Etank said, by the time you hear evidence of fluid in the lungs, youre behind.
 
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mrhunt

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No need to apologise, I didn't take it that way at all man. Your good ☺

There IS alot of play in our protocols, we have ALOT of freedom which is nice until something like this happens then it's like fuuujjck.
 

VFlutter

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Agree with E Tank, if you are waiting until you can auscultate crackles as a stopping point for fluids then you are probably going too far

Remember in Cardiogenic Shock the problem is decreased cardiac output. Pressure does not equal perfusion. SBP is afterload that the failing heart has to pump against. It isn't unexpected that the patient de-compensated and developed pulmonary edema with a SBP of 110. At that point Nitro was probably indicated as well as an inotrope.

Sounds like he was late in the game with an acute MI or an acute MI ontop of prior congestive heart failure. Either way these patients are pretty difficult to manage pre-hospitality or even in hospital.
 
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mrhunt

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Lesson from now on.... 500ml bags for everyone regardless to avoid fluid overload in future.

Also with his hemoptysis I was initially questioning if this was possibly a volume issue as well as a pump problem ontop of that.
 

silver

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Our protocls Go against dopamine Unless IV fluids are refractory (which they were not)
In your protocol, what defines refractoriness?

(Unfortunately you are stuck by your protocols, and that being said reperfusion is what would would change mortality in the end anyway so don't sweat it.)

In hypotension, its important to remember the goal of giving boluses in your treatment algorithm is to test fluid responsiveness. If they are not responsive, time to start vasopressors/inotropes to try to normalize perfusion. With 250ccs in adults over 10-15 mins, you should see an improvement in hemodynamics and certainly by 500cc you will either see an improvement or not. Even in hypovolemic shock if you aren't getting any fluid responsiveness, its time to start pressors (you can always retest later to help get them off pressors). In a patient who we pretty much know has cardiogenic shock (STEMI + cool/pale limbs), my threshold to test fluid responsiveness would be way below 1L and closer to 250cc (or maybe 250 x 2). If along the way they had a drop in BP to 50/20 and HR to 50 I would probably deem them refractory and start dopamine, and if they weren't bradycardic, levo.
 

Tigger

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Bradycardia and profound hypotension at 50/20 would be an indicator of a critically ill patient in need of inotropes or pacing. To me a fluid bolus was probably not needed. Fluids aren't how you want to treat this patient anyway, so does it matter whether or not the hypotension is "refractory?" You've identified the LV failure in this patient and fluid is not likely to help as this is not a volume issue and increasing preload is not likely to be helpful. The hemoptysis is probably an indicator of heart failure and not a bleeding issue here (though it's confusing that the lung sounds are clear, who knows?).

Trendelenburg is probably not going to help and may make patient worse, good old semi-fowler's might be just fine and help preserve the patient's respiratory drive.

Don't worry about getting a 12 lead during a pulse check, that's probably a longer pause than needed during a rhythm check.

I wouldn't say 500 bags for everyone, some patients will benefit from a liter or more, this patient probably not.

Generally speaking, I think it's better to be more concerned with whether your treatments are helping the patient rather than "staying in protocol." No clinical protocols mandate you do something bad for your patients.
 
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mrhunt

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So to clarify, my monitor was doing automatic 12 leads every 15 mins. It just so happened to capture during a pulse check which was really neat and amazing timing actually.

Pts pulse rate was actually 90s to 130s, and only dropped to 50 with the extremely low BP for a very brief period that coincided with a significant electrical conduction delay globally (and evidence of impending arrest apparently).... Pacing was never needed or necessary. Sorry for the confusion.

Trendelenburg actually did help the pt during this episode and then he was out back to semi Fowler's position for rest of transport (until resp issues started)

But yeah I completely agree that I overdid it on fluids and that wasn't the issue. I don't think that's what caused him to arrest, but it def didn't help him.
 
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mrhunt

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Pt stated hasn't gone to Dr in a long time so no diagnosis on existing issues.

He clearly should have been going to catch a multitude of serious impending Hart issues.
 

Peak

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The all out ED/ICU treatment would probably include RSI and ventilation, norepi, and dobutamine. Perhaps a nitro drip if the patient becomes hypertensive on their own and still has pulmonary edema, if hypertensive without edema consider a beta blocker (metoprolol vs labetalol); I doubt at hypertension would be anything more than a transient pressure regardless though and it will probably turn into collapse in a few moments. Pacing is preferred over epi, epi increases oxygen demand on the heart and is arrhythmogenic. Dopamine is a bit of a mixed bag, it's a pretty dirty drug and a lot of studies showing poor outcomes compared to other drugs in the unit; if it is your only pressor it is better than nothing. Consider fairly aggressive vent pressures to push fluid back into the vascular bed.

This patient probably needs a cath lab immediately for any kind of chance at survival. I would expect possible balloon dilation, pacing wires, impella, or a balloon pump if he survives cath lab. That being said I'm not sure many cardiologists would take him. He'd start having to make a pretty rapid turn around to not die on the cath lab table.

If you have never dissected a heart I would highly recommend it. I think in most programs we think of the septum as this wall between the RV and LV that doesn't do a whole lot. In reality the septum is essentially the right wall of the left ventricle and is a huge part of the squeeze in your left ventricle. As that fails you loose a lot of LV ejection resulting in left sided heart failure and LV dilation.

Giving fluids will give you preload to the right side of the heart, but this patient already has too much preload to the left side hence the fluid getting pushed from the pulmonary capillary bed into the alveoli and giving you his 'pink frothy foam' that we associate with left sided heart failure. His low BP is from poor LV function plus any systemic after load issues, not from preload which would be addressed with IV fluids.

If he is to survive he needs his LV ejection fixed. We can optimize ejection with inotropes, appropriate LV afterload with pressors, and his respiratory status with appropriate ventilatory strategies. He is going to need surgical or PCI management to survive; and any delays such as living far away from a chest pain center are going to lower that.
 

Summit

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Ywhat peak sakd

I was thinking dobutamine and maybe milrenone. A little fluid will help support that, but the problem is not low preload in this patient until we vasoldilate. He needs contractility which is being impaired by ischemia really afffting the left side. Dropping after load supports the forward flow with impaired contractility.
 

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