Flash Pulmonary Edema

[Smash]

It's basically the first thing the doctors here give when they hear the words, pulmonary edema.

That's unfortunate for the patients.

 

[ArcticKat]

It's basically the first thing the doctors here give when they hear the words, pulmonary edema.

Pulmonary Edema, yes, Flashover with associated hypotension, no.

 

[18G]

Fluid bolus would most likely hasten his arrest. He has all the preload in the world. His LVEDP is likely through the roof. That ventricle can't stretch anymore than it already has. I'd say if his BP were to come up, I'd assess for resolution of the pulmonary edema, NTG would only be worth trying if you can give it very carefully via an IV pump (can't control the dose too much with NTG paste, spray, or tabs). You don't want this guy to be normotensive, you want enough inotropy to improve cardiac output to reduce the pulmonary edema. If he improves at 80, 90 or whatever systolic, keep it there. Don't tax the heart any more than absolutely necessary.

How do we know this patient did not suffer a massive inferior wall MI? Right side involvement? A little extra volume may help. Sounds like patient condition and deterioration rate did not allow for a 12-lead.

I do agree with the nitro comment. We don't have IV NTG as an option, however. And with the shock state transdermal NTG probably won't work too well.

I am curious to know if the patient had a PMH of renal failure.

 

[medicsb]

How do we know this patient did not suffer a massive inferior wall MI? Right side involvement?

RVMI doesn't typically produce pulmonary edema. When it does it is due to LV dysfunction. Fluid won't help in that situation.

 

[Handsome Robb]

What about RVMI secondary to Cor Pulmonale? Cor Pulmonale is very capable of producing pulmonary edema. Fluid could help in that situation if I'm not mistaken due to increased ventricular filling but then again I'm a noob and a half.

 

[EMS Patient Care Advocate]

How do we know this patient did not suffer a massive inferior wall MI? Right side involvement? A little extra volume may help. Sounds like patient condition and deterioration rate did not allow for a 12-lead.

I do agree with the nitro comment. We don't have IV NTG as an option, however. And with the shock state transdermal NTG probably won't work too well.

I am curious to know if the patient had a PMH of renal failure.

no renal failiers in Hx. obese but otherwise healthy male

 

[EMS Patient Care Advocate]

Sounds like you did everything you could have with the patient in cardiogenic shock. With the dopamine, I would have titrated starting at 5 and going up and not started at a high dose though.

The patient was behind the 8-ball when you got there it sounds like. Patient prob had a massive MI leading to the shock. Pre-hospital all you can do is maintain patient positioning, intubate, and run dopamine until pressure comes up. Then you can go for some SL or NTG paste. I agree with the other person who suggested a small fluid bolus like 250cc to increase preload, the stretch of the heart, and hopefully increase contractility.

One other thing to consider in a case like this if time permitted would be to insert an NG tube (should anyway) and give aspirin if patient complained of chest pain (prior to arresting of course ) and wasn't able to take PO.

I have personally never heard of any cases where intubation resulted in vfib. In fact, I have read a study where this thinking was proved to be wrong.

I really am so glad to have covered so much about dopamine for this case. This patient died by the time dopamine was actually administered, quickly D/C dopamine and ACLS protocols initiated for PEA.
Starting at a higher end dosing and trying for inotropic with pressor effects was my goal in mind also suggested by my supervising doc at the time. Doesnt make it right- I like a poster comment about more middle range 8-10mcg/min because the pressor action is not needed for this patient. I was thinking at the time I needed to have increased inotropy and needed to narrow vasculature- this silly newbie learned a lot in this thread.

 

[EMS Patient Care Advocate]

I really am so glad to have covered so much about dopamine for this case. This patient died by the time dopamine was actually administered, quickly D/C dopamine and ACLS protocols initiated for PEA.
Starting at a higher end dosing and trying for inotropic with pressor effects was my goal in mind also suggested by my supervising doc at the time. Doesnt make it right- I like a poster comment about more middle range 8-10mcg/min because the pressor action is not needed for this patient. I was thinking at the time I needed to have increased inotropy and needed to narrow vasculature- this silly newbie learned a lot in this thread.

And on that note Im sure eppi did not increase his chances for survival any in this situation. Maybe CPR only would have been better

 

[18G]

RVMI doesn't typically produce pulmonary edema. When it does it is due to LV dysfunction. Fluid won't help in that situation.

I agree and am aware right sided involvement MI results in systemic backup of blood more so than pulmonary. However, that is not always the case and biventricular involvement is present often.

A small fluid bolus is reasonable to help increase CO in CHF sometimes. Just saying.

 

[jjesusfreak01]

And on that note Im sure eppi did not increase his chances for survival any in this situation. Maybe CPR only would have been better

Cardiogenic shock leading to respiratory failure precipitating cardiac arrest...

I don't think it really would have mattered, no point in moving deoxygenated blood around the body in circles. You had no chance without a miracle to clear out the lungs.

 

[FFEMT427]

Cardiogenic shock leading to respiratory failure precipitating cardiac arrest...

I don't think it really would have mattered, no point in moving deoxygenated blood around the body in circles. You had no chance without a miracle to clear out the lungs.

I agree this patient was at a point were you were being forced to race the clock. It would be nice to have a 12-15 lead which would have been easy.....if you had 10 hands so you could intubate....start a line.....hang a dope drip......get your 12 lead....load your patient.....and drive to the hospital. But thats the way it is. There may have been other things that could have been done but at this patients level of acuteness its hard to say what the outcome would have been. Have you gotten a follow up see if they did an autopsy maybe try to get info on whether the patient had a Left sided heart failure secondary to right sided heart failure. In any case even with the pulmonary edema I would have tried a small fluid challenge and reassessed (seeing as how me as an armchair quarterback I have 10 hands lol)

 

[ekgpress]

Arrive to find overweight male with pink frothy sputum, EMTs on scene are trying to lie him down on a backboard. I immidiately stopped this. Patients Vitals were a systolic of less than 80, RR and everything else is also in the dumps. So CPAP is out, Nitro is out. The only two pressors available you your box at this time is eppi or dopamine. What would you do?
I assisted ventilations with BVM, started high dose dopamine, about 5 minutes later the patient codes and pressors arent a problem as you are now pushing code doses of eppi and d/c the dopamine. He coded while trying to place an ETT tube prior to transport. We arrived at ED withn 2 min of code, pt did not survive. This was my first patient EVER that died during the course of my care. Any suggestions? I stumped docs with this one. Flash PE/CHF is usually paired with hypertension. Dopamine is not great but its not a bad option to if you have nothing else. I had to defend my use of dopamine on this call.

Hypotension with chest pain or heart failure is a "bad sign" - especially if not due to something you can "fix" (like a tachyarrhythmia or immediately post-intubation). I'd be interested in what this patient's 12-lead ECG showed - since pulmonary edema with hypotension not due to new-onset rapid A Fib may be the result of cardiogenic shock from a large acute MI - in which case it is highly unlikely that anything you do will save the patient ... NO need to "defend" your use of dopamine - it was completely indicated. Bottom Line: Hypotension with pulmonary edema not due to a "fixable cause" is a bad sign, almost regardless of what you do ...

 

[ekgpress]

Hypotension in a Patient with Pulmonary Edema

Hypotension with chest pain or heart failure is a "bad sign" - especially if not due to something you can "fix" (like a tachyarrhythmia or immediately post-intubation). I'd be interested in what this patient's 12-lead ECG showed - since pulmonary edema with hypotension not due to new-onset rapid A Fib may be the result of cardiogenic shock from a large acute MI - in which case it is highly unlikely that anything you do will save the patient ... NO need to "defend" your use of dopamine - it was completely indicated. Bottom Line: Hypotension with pulmonary edema not due to a "fixable cause" is a bad sign, almost regardless of what you do ...