Flash Pulmonary Edema

[usafmedic45]

the not so happy venacava, causing the hypotension with CPAP

You have the basic idea, although it's not the vena cava necessarily. The issue is more with compression of the right ventricle in situations where the intraventricular pressure is reduced or, more accurately, the pressure gradient (atrial to ventricular) is not sufficient to ensure adequate ventricular filling during atrial systole.

 

[EMS Patient Care Advocate]

Was there any peripheral edema? JVD? Heart tones? Who called 911 did they see what happened?

the man was, VERY LARGE, was there pitting edema, no. JVD- Pt is VERY LARGE, unable to assess for JVD- maybe not with such a low BP though? Heart tones, I didnt assess.

 

[EMS Patient Care Advocate]

You have the basic idea, although it's not the vena cava necessarily. The issue is more with compression of the right ventricle in situations where the intraventricular pressure is reduced or, more accurately, the pressure gradient (atrial to ventricular) is not sufficient to ensure adequate ventricular filling during atrial systole.

I like it!! Good stuff. So is it by increasing pressure on vena cava the pressure gradient is reduced atrial to ventricular? The pressure prevents the natural "kick" of respiration on the vena cava that assist with RVFP?

 

[usafmedic45]

I like it!! Good stuff. So is it by increasing pressure on vena cava the pressure gradient is reduced atrial to ventricular? The pressure prevents the natural "kick" of respiration on the vena cava that assist with RVFP?

No, there's not really an effect of pressure on the SVC (and the IVC is located so posterior that it's not effected that much) but pressure on the right ventricle and the right atria. The "loss of kick" is mostly an issue in things like atrial fib where there is an actual dysfunction of the heart. Mostly, it's an issue once you get into pressures above 10-15 cmH2O (it varies with a lot of factors, including cardiac rhythm, blood pressure, cardiac contractility, pulmonary compliance, etc) because of more or less direct compression of the right ventricle and atria which, you will recall have much thinner and more compliant walls than on the left side.

There's no real practical respiratory role in cardiac filling pressures until you get into some very abnormal situations (like severe air trapping, etc) and mostly it becomes a negative issue. There are some effects but the physiology is complicated and the effect is negligible enough in healthy average persons to not be a factor for this discussion lest I just confuse everyone involved.

 

[EMS Patient Care Advocate]

No, there's not really an effect of pressure on the SVC (and the IVC is located so posterior that it's not effected that much) but pressure on the right ventricle and the right atria. The "loss of kick" is mostly an issue in things like atrial fib where there is an actual dysfunction of the heart. Mostly, it's an issue once you get into pressures above 10-15 cmH2O (it varies with a lot of factors, including cardiac rhythm, blood pressure, cardiac contractility, pulmonary compliance, etc) because of more or less direct compression of the right ventricle and atria which, you will recall have much thinner and more compliant walls than on the left side.

There's no real practical respiratory role in cardiac filling pressures until you get into some very abnormal situations (like severe air trapping, etc) and mostly it becomes a negative issue. There are some effects but the physiology is complicated and the effect is negligible enough in healthy average persons to not be a factor for this discussion lest I just confuse everyone involved.

Thank you. All my previous instruction has focused on the vena cava. Makes wonderful sense, I have lots to look up and review!

 

[ArcticKat]

Yes when I say pink frothy I dont mean he could spit it up. I mean pink frothy was FLOWING from his mouth. Quite a site to be honest

Agreed. it was the Asystole part that was new, not the Hypoxemia. I would likely have done the same thing in your position. I've actually had that happen to me a few years ago before we could CPAP. Flashover is not a pretty thing and I remember every second of it.

 

[04_edge]

We actually had a conversation at work yesterday about something very similar to this case.

To me, it seems counter productive to use dopamine in a pt with acute pulmonary edema considering the point of using NTG(Which i would not have used on this pt either) is to vasodilate and allow that fluid to shift back out of the alveoli. This pt was obviously in a profound hypoxic state and(without knowing the dose of dopamine you gave) would increase cardiac workload requiring more O2 that wasnt there.

If it were me, i would have initiated RSI right off the bat, depending on the pt's current LoC, and hauled *** to the nearest facility. But im still a newb, so feel free to correct me if im wrong about my thought process with this.

 

[Smash]

We actually had a conversation at work yesterday about something very similar to this case.

To me, it seems counter productive to use dopamine in a pt with acute pulmonary edema considering the point of using NTG(Which i would not have used on this pt either) is to vasodilate and allow that fluid to shift back out of the alveoli. This pt was obviously in a profound hypoxic state and(without knowing the dose of dopamine you gave) would increase cardiac workload requiring more O2 that wasnt there.

If it were me, i would have initiated RSI right off the bat, depending on the pt's current LoC, and hauled *** to the nearest facility. But im still a newb, so feel free to correct me if im wrong about my thought process with this.

In a normal situation, you are right. This patient is well beyond pulmonary edema though. Pulmonary edema is a problem of inappropriate vascular response in the setting of an impaired left ventricle. i.e. too much afterload, too much preload and a heart that can't pump as hard as it should. So basically, too much blood pressure, hence the aggressive use of nitrates to increase venous pooling, decrease preload, decrease LVEDP and so on and so forth.

So typically we see patients with a relative hypertension with acute, sympathetically mediated cardiogenic pulmonary edema.

I like to keep things pretty simple (because I'm pretty simple) so I look at it like this: (assuming no pneumonia or COPD history) Rales and hypertension = pulmonary edema. Rales and hypotension = cardiogenic shock.

Ok, so that is maybe oversimplifying things, but you can hopefully see where I am coming from. Now this patient is clearly someone with frank cardiogenic shock, so he needs something to get that heart kicking along a bit harder by increasing contractility primarily.

Dopamine in this setting is not inappropriate for this reason, but having said that, there is no evidence that the use of pressors/inotropes in cardiogenic shock do anything to improve outcome. There is also no evidence that any particular drug is better or worse that any other.

At best, they are a temporising measure to get someone to hospital where hopefully it turns out they have had an infarct, and can be revascularised.

Have a look at some of the studies Judith Hochman has published on this matter. She and her colleagues have published extensively on cardiogenic shock, pulmonary edema and pressors.

As for RSI: that would be dangerous and terrifying in this situation. Not that intubation isn't warranted, I just don't know that RSI is necessarily the way to go about it. I would go for an awake (or semi-awake as the case may be) intubation, preferably using ketamine to maintain some cardiac output (although ketamine can be a negative inotrope, so this might be a bit scary as well)

 

[medicsb]

At best, they are a temporising measure to get someone to hospital where hopefully it turns out they have had an infarct, and can be revascularised.

Double emphasizing the temporary use of a pressor. A patient in cardiogenic shock is most likely going to need a balloon pump, even if revascularized, which may not be successful (e.g. performed too late). In that case, the patient could be looking at a spot on a heart transplant list and maybe an LVAD in the mean time.

No matter what, this patient is up the creek with a turd for a paddle.

 

[04_edge]

So i guess in this situation, dopamine is the lesser of two evils basically?

I guess my way of thinking is that the pt's current condition is probably caused by an MI. So now you have to deal with that and the respiratory failure its causing. Giving the dopamine would increase C.O., but would increase its oxygen demands( which i can only imagine what this pt's spo2 is, i would assume in the 50's if not lower), potentially worsening the infarct, and possibly making the P.E. even worse, which i dont even know thats possible with what the OP is describing?

I guess in a case like this, you just run the dopamine and hope for a positive change?

Id fully understand if p.e. wasnt nearly as profound and this pt's 02 sats werent in the crapper.

 

[usalsfyre]

If your a stud of a clinician (using typical EMS drugs) you'll run dopamine around 5-8 mcgs for as much inotropic affect as you can get out of it and then slowly put IV NTG on board to drop your afterload. Dobutamine MAY be used here as well, it's got some amount of afterload reduction as well. The real issue is all of this increases MvO2, so it's damaging the same heart tissue it's stimulating meaning your only hoping to buy time. Like was mentioned above, what they really need is an IABP or possibly a LVAD and transplant.

 

[Smash]

If your a stud of a clinician (using typical EMS drugs) you'll run dopamine around 5-8 mcgs for as much inotropic affect as you can get out of it and then slowly put IV NTG on board to drop your afterload. Dobutamine MAY be used here as well, it's got some amount of afterload reduction as well. The real issue is all of this increases MvO2, so it's damaging the same heart tissue it's stimulating meaning your only hoping to buy time. Like was mentioned above, what they really need is an IABP or possibly a LVAD and transplant.

 

[EMS Patient Care Advocate]

Im loving this thread.
I think 02 demand was addressed in this thread at one point. Also we discussed inotropy for cardiogenic shock. Im sure the ACLS eppi didnt do his case ANY favors either.
Simple or not I love that " rales/hypertension: rales/hypotension" something kinda clicked when I read this.

 

[Enzo]

Would furosemide have helped?

 

[medicsb]

Would furosemide have helped?

Furosemide is not an inotrope, so no.

 

[ArcticKat]

Would furosemide have helped?

A common side effect is hypotension, so not likely.

 

[usafmedic45]

Would furosemide have helped?

Depends on what your goal with it is.....


Ooops....should have read the responses already up before starting to comment.

 

[Enzo]

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

 

[18G]

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.

 

[medicsb]

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.

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.