# Flash Pulmonary Edema



## EMS Patient Care Advocate

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.


----------



## fast65

Wow, tough situation. Why were they trying to backboard him?

I would have immediately started assisting ventilations while getting ready to RSI him (although I know you don't have that option). Make sure to keep up with suctioning the tube and depending on the transport time I would have set the vent up with a little PEEP, probably around 5 cmH2O. I would have hung dopamine after securing the airway and then beat cheeks to the hospital.


----------



## EMS Patient Care Advocate

the only reason they were laying him on a board is because they didnt know better. I also dont have a vent but tried PPV and would have used a peep valve if available. Yes no es bueno.


----------



## fast65

EMS Patient Care Advocate said:


> the only reason they were laying him on a board is because they didnt know better. I also dont have a vent but tried PPV and would have used a peep valve if available. Yes no es bueno.



That makes no sense, didn't they have any sort of common sense?

Yeah, sorry, I guess it sounds like I would have only used a PEEP valve with the vent. But, it sounds like you did everything that you could for this patient, nothing else I can really think of.


----------



## EMS Patient Care Advocate

fast65 said:


> That makes no sense, didn't they have any sort of common sense?
> 
> Yeah, sorry, I guess it sounds like I would have only used a PEEP valve with the vent. But, it sounds like you did everything that you could for this patient, nothing else I can really think of.



what is your thoughts behind PEEP with vent being ok but not with BVM? (all vents should have 5mmh20 baseline I understand anyways). a BVM with PPV and a PEEP valve set at 5mmH2o would expect different results? 
Thank you for the input.


----------



## fast65

EMS Patient Care Advocate said:


> what is your thoughts behind PEEP with vent being ok but not with BVM? (all vents should have 5mmh20 baseline I understand anyways). a BVM with PPV and a PEEP valve set at 5mmH2o would expect different results?
> Thank you for the input.



Oh, I didn't mean to imply that I wouldn't do it with the BVM, I would, I just worded it weird


----------



## ArcticKat

The act of intubating may have initiated a vagal response and put him into VFib.


----------



## EMS Patient Care Advocate

i would have taken VF over asytole. Neither is good but im just sayin


----------



## fast65

ArcticKat said:


> The act of intubating may have initiated a vagal response and put him into VFib.



Perhaps, but I'm thinking that the hypoxemia is a more likely cause of cardiac arrest in this patient. However, I wouldn't be surprised if it was a combination of the two.

What rhythm did he go into? Asytole?


----------



## EMS Patient Care Advocate

fast65 said:


> Perhaps, but I'm thinking that the hypoxemia is a more likely cause of cardiac arrest in this patient. However, I wouldn't be surprised if it was a combination of the two.
> 
> What rhythm did he go into? Asytole?



Unfortunately yes, lost pulses, quick PEA to asytole, this patient had no lungs left. Post chest x ray there was NO lung space not occupied by fluid. Prolly caused himself to tamponade. 
My VF vs asytole comment is more against the argument of what ifs. There is no what if, this patient needed intubation or he was going to die. And he died anyway. There is risk in EVERYTHING! But I’m confident the risk vs gain in this scenario without even hesitation warrants an advanced airway specifically ETT, IMHO.


----------



## Voodoo1

May I ask why you used dopamine and not epi? I'm asking strictly as a student. What is the desired response from using dopamine vs. epi in this case?


----------



## medicsb

What dose of dopamie did you start at?  Usually a inotropic dose would be indicated and not a pressor (high) dose?

Sounds like profound cardiogenic shock from a massive MI.  He probably would have died no matter what you or anyone did.


----------



## CAOX3

So there was no reasoning behind them attempting to board him?

Were they assisting ventilations?


----------



## EMS Patient Care Advocate

Voodoo1 said:


> May I ask why you used dopamine and not epi? I'm asking strictly as a student. What is the desired response from using dopamine vs. epi in this case?



 My reasoning was spillover affect. Meaning eppi will cause unwanted effects for this patient. Increased heart rate was undesirable. At high doses dopamine is alpha 1, mid to high dose is beta1 and alpha 1 primary. So my thinking was I get more squeeze (taking into consideration increased cardiac 02 demand) and vasoconstriction. With eppi I would have gotten vaso-constriction, increased heart rate and so on. This was my thinking at the time anyways


----------



## EMS Patient Care Advocate

medicsb said:


> What dose of dopamie did you start at?  Usually a inotropic dose would be indicated and not a pressor (high) dose?
> 
> Sounds like profound cardiogenic shock from a massive MI.  He probably would have died no matter what you or anyone did.



I started high dose, yes for vaso-constriction. Levophed would have been the better option, and based on this call and upcoming sepsis protocols we now have it. I argue that I would prefer the vasoconstriction over increased cardiac workload (increasing squeeze-inotropic) on a non functioning heart for this patient. But either way- death was likely not avoidable.


----------



## EMS Patient Care Advocate

CAOX3 said:


> So there was no reasoning behind them attempting to board him?
> 
> Were they assisting ventilations?



No to both. I think they intended to move him using the backboard not thinking that laying him down would drown him more, he was using his last few ounces of life to fight them and sit up. There was a "medic" on scene that had called me as an intercept because that service didnt have paramedic drugs. That was one of the most dangerous medics i have met in a while.


----------



## medicsb

EMS Patient Care Advocate said:


> I started high dose, yes for vaso-constriction. Levophed would have been the better option, and based on this call and upcoming sepsis protocols we now have it. I argue that I would prefer the vasoconstriction over increased cardiac workload (increasing squeeze-inotropic) on a non functioning heart for this patient. But either way- death was likely not avoidable.



Cardiogenic shock is not a problem with the container, but with the pump.  Alpha-1 effects can be crucial for septic shock as the hypotension is secondary to vaso-/veno- dilation and third-spacing due to various mediators of inflammation.   

With cardiogenic shock, the goal is to improve cardiac output.  Ideally, dobutamine would be the ideal drug of choice (mostly beta 1).  Going straight to a high dose of dopamine actually providesa a double wallop on the heart instead of just one.  It increases inotropy (which IS needed), but also increases SVR, which isn't needed so much, if at all.  (The beta effect of dopamine persists at high doses, though the alpha will predominate.) Both will increase myocardial oxygen demand.  There really is no way to increase CO in cases of cardiogenic shock in the prehospital setting without increasing myocardial O2 demand.    For cardiogenic shock (and CHF in general), less SVR is better as it can directly hinder cardiac output.  

Something to ponder is the relationship of BP, cardiac output, and systemic vascular resistance:  MAP = CO x SVR  or  CO = MAP/SVR


----------



## EMS Patient Care Advocate

medicsb said:


> Cardiogenic shock is not a problem with the container, but with the pump.  Alpha-1 effects can be crucial for septic shock as the hypotension is secondary to vaso-/veno- dilation and third-spacing due to various mediators of inflammation.
> 
> With cardiogenic shock, the goal is to improve cardiac output.  Ideally, dobutamine would be the ideal drug of choice (mostly beta 1).  Going straight to a high dose of dopamine actually providesa a double wallop on the heart instead of just one.  It increases inotropy (which IS needed), but also increases SVR, which isn't needed so much, if at all.  (The beta effect of dopamine persists at high doses, though the alpha will predominate.) Both will increase myocardial oxygen demand.  There really is no way to increase CO in cases of cardiogenic shock in the prehospital setting without increasing myocardial O2 demand.    For cardiogenic shock (and CHF in general), less SVR is better as it can directly hinder cardiac output.
> 
> Something to ponder is the relationship of BP, cardiac output, and systemic vascular resistance:  MAP = CO x SVR  or  CO = MAP/SVR



OOPs, that makes a heck of a lot of sence. Pump not container how careless of me. Thank you!


----------



## EMS Patient Care Advocate

Im so frustrated I got that confused in my head when I responded to you earlier.


----------



## EMS Patient Care Advocate

medicsb said:


> Cardiogenic shock is not a problem with the container, but with the pump.  Alpha-1 effects can be crucial for septic shock as the hypotension is secondary to vaso-/veno- dilation and third-spacing due to various mediators of inflammation.
> 
> With cardiogenic shock, the goal is to improve cardiac output.  Ideally, dobutamine would be the ideal drug of choice (mostly beta 1).  Going straight to a high dose of dopamine actually providesa a double wallop on the heart instead of just one.  It increases inotropy (which IS needed), but also increases SVR, which isn't needed so much, if at all.  (The beta effect of dopamine persists at high doses, though the alpha will predominate.) Both will increase myocardial oxygen demand.  There really is no way to increase CO in cases of cardiogenic shock in the prehospital setting without increasing myocardial O2 demand.    For cardiogenic shock (and CHF in general), less SVR is better as it can directly hinder cardiac output.
> 
> Something to ponder is the relationship of BP, cardiac output, and systemic vascular resistance:  MAP = CO x SVR  or  CO = MAP/SVR



Reducing SVR is why we treat with Nitro in CHF I would think, I made a mistake earlier for some reason- i do know this lol. Unfortunatly I did not have a usable blood pressure, so why not try to increase SVR some while also increasing inotropy-more bang for my buck, my origional stated goal? Isnt that part of titrating to effect? I have limited experience actually using dopamine. Im going to sponge information off you if its ok


----------



## EMS Patient Care Advocate

or based on the equations that would be counterproductive? I need to study up on MAP big time, useful stuff.


----------



## ArcticKat

fast65 said:


> Perhaps, but I'm thinking that the hypoxemia is a more likely cause of cardiac arrest in this patient. However, I wouldn't be surprised if it was a combination of the two.
> 
> What rhythm did he go into? Asytole?



Agreed, given the new information and quick Asystole, I'd say the Hypoxemia played a big part.


----------



## EMS Patient Care Advocate

ArcticKat said:


> Agreed, given the new information and quick Asystole, I'd say the Hypoxemia played a big part.



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


----------



## medicsb

EMS Patient Care Advocate said:


> Reducing SVR is why we treat with Nitro in CHF I would think, I made a mistake earlier for some reason- i do know this lol. Unfortunatly I did not have a usable blood pressure, so why not try to increase SVR some while also increasing inotropy-more bang for my buck, my origional stated goal? Isnt that part of titrating to effect? I have limited experience actually using dopamine. Im going to sponge information off you if its ok



The equation can take a bit to wrap your head around, because most people equate MAP (BP) with SVR when they are actually different.  (Also, I should mention that for simplicity, I've left out CVP - for completeness the full eqn is CO = (MAP-CVP)/SVR)  

With the patient you had, it is possible that the patient is not vasodilated and is already vasoconstricted to some degree due to endogenous catecholamines.  However, it is possible that should there be enough metabolic byproducts and/or inflammatory mediators floating around, that vasodilation has begun to occur or is occuring (particularly if this was slowly evolving).  Anyhow it still comes down to the fact that the pump is the biggest problem and it is worth taking a step wise approach to improve cardiac function and tissue perfusion.  You don't want to over tax the heart anymore than you need to, so if you can improve hemodynamics with inotropes alone, then good, if it doesn't work then move on to stimulating vasoconstriction.  

Anyhow, with CHF where shock is not present, there are multiple mechanism producing the cardiovascular effects observed.  Ultimately the goal of NTG is to reduce preload, though it does affect SVR, so it can allow CO to increase as long as preload is not decreased too much (CO does rely on preload).


----------



## medicsb

EMS Patient Care Advocate said:


> 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



It'll probably be a long time before you see a case like that again.  I don't think I ever did.

Though, I once pronounced a man who had pink frothy sputum that had been flowing down his chest.  It started and killed him at the wheel of his car.  We would have coded him had bystanders not waited 20 minutes to call 911.  (His car rolled to a stop in the middle of a parking lot.)


----------



## EMS Patient Care Advocate

medicsb said:


> It'll probably be a long time before you see a case like that again.  I don't think I ever did.
> 
> Though, I once pronounced a man who had pink frothy sputum that had been flowing down his chest.  It started and killed him at the wheel of his car.  We would have coded him had bystanders not waited 20 minutes to call 911.  (His car rolled to a stop in the middle of a parking lot.)



Yes I think I intentionally failed to mention this was one of my first paramedic intercepts withen a few months of receiving my card. You have been so helpful. Please keep feeding it to me. I dont know how this site works yet but Id love to link up. Your brain is power.


----------



## EMS Patient Care Advocate

medicsb said:


> The equation can take a bit to wrap your head around, because most people equate MAP (BP) with SVR when they are actually different.  (Also, I should mention that for simplicity, I've left out CVP - for completeness the full eqn is CO = (MAP-CVP)/SVR)
> 
> With the patient you had, it is possible that the patient is not vasodilated and is already vasoconstricted to some degree due to endogenous catecholamines.  However, it is possible that should there be enough metabolic byproducts and/or inflammatory mediators floating around, that vasodilation has begun to occur or is occuring (particularly if this was slowly evolving).  Anyhow it still comes down to the fact that the pump is the biggest problem and it is worth taking a step wise approach to improve cardiac function and tissue perfusion.  You don't want to over tax the heart anymore than you need to, so if you can improve hemodynamics with inotropes alone, then good, if it doesn't work then move on to stimulating vasoconstriction.
> 
> Anyhow, with CHF where shock is not present, there are multiple mechanism producing the cardiovascular effects observed.  Ultimately the goal of NTG is to reduce preload, though it does affect SVR, so it can allow CO to increase as long as preload is not decreased too much (CO does rely on preload).



Ill be re-reading this a few times, back to the books! Thank You for your help and time


----------



## usafmedic45

> 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.



Why is CPAP out?  Define "in the dumps".



> I also dont have a vent but tried PPV and *would have used a peep valve if available.* Yes no es bueno.



Do you see the irony of these two conflicting statements?  I'm guessing no, so I bolded the parts in question to make it easier for you.


----------



## EMS Patient Care Advocate

usafmedic45 said:


> Why is CPAP out?  Define "in the dumps".
> 
> 
> 
> Do you see the irony of these two conflicting statements?  I'm guessing no, so I bolded the parts in question to make it easier for you.



Well I am trying to learn so Id be thankful if you stopped being a punk. And Ill gladly address your questions. In my training someone who has little to no respiratory drive contraindicates CPAP- what else would you like to know was in the dumps to change your decision?

Just so you know, they do make a cute little device that goes on the end of a BVM called a peep valve. They are expensive, provide PEEP with pressure bagging- im sorry you dont know how to do this, Id be happy to show you the device and how to use it on the BVM to provide PEEP. Is it perfect, nope. Is it a product that might work, yup.


----------



## Scott33

*The F word*

Just going to throw this out there. Would anyone have considered a fluid challenge?


----------



## Scott33

EMS Patient Care Advocate said:


> Well I am trying to learn so Id be thankful if you stopped being a punk.
> 
> Just so you know, they do make a cute little device that goes on the end of a BVM called a peep valve. They are expensive, provide PEEP with pressure bagging- im sorry you dont know how to do this, Id be happy to show you the device and how to use it on the BVM to provide PEEP



...And so endeth the adult discussion.


----------



## fast65

Scott33 said:


> Just going to throw this out there. Would anyone have considered a fluid challenge?



Wouldn't that make things worse? How large of a fluid challenge were you thinking?


----------



## EMS Patient Care Advocate

fast65 said:


> Wouldn't that make things worse? How large of a fluid challenge were you thinking?



Well how to you know if the patient has third spaced all his fluid and is empty in the vasculature warrenting fluid. I dont think the Pulmonary Edema patient is automatically assumed to have an overload of fluid in the veins?


----------



## EMS Patient Care Advocate

Scott33 said:


> ...And so endeth the adult discussion.



He is attacking me on another thread as well for some reason my lack of education and willingness to learn makes him mad.


----------



## fast65

EMS Patient Care Advocate said:


> Well how to you know if the patient has third spaced all his fluid and is empty in the vasculature warrenting fluid. I dont think the Pulmonary Edema patient is automatically assumed to have an overload of fluid in the veins?


This is true, I had not really considered that


----------



## usafmedic45

> someone who has little to no respiratory drive contraindicates CPAP- what else would you like to know was in the dumps to change your decision?



Just wanted to know which end of "in the dumps" you were at because some will refer to someone who is struggling to but not achieving good volumes as "in the dumps".  Pardon me for asking for clarification and trying to make a teaching point out of something that confuses a lot of EMS providers (PEEP vs. CPAP)



> Just so you know, they do make a cute little device that goes on the end of a BVM called a peep valve. They are expensive, provide PEEP with pressure bagging- im sorry you dont know how to do this, Id be happy to show you the device and how to use it on the BVM to provide PEEP. Is it perfect, nope. Is it a product that might work, yup.



Actually it works quite well if you have a closed airway circuit (read as: a tubed patient).  It doesn't do so great if you're just using a mask seal.



> Well I am trying to learn so Id be thankful if you stopped being a punk.



I'm trying to teach, so I would appreciate that out of you.


----------



## EMS Patient Care Advocate

usafmedic45 said:


> Just wanted to know which end of "in the dumps" you were at because some will refer to someone who is struggling to but not achieving good volumes as "in the dumps".  Pardon me for asking for clarification and trying to make a teaching point out of something that confuses a lot of EMS providers (PEEP vs. CPAP)
> 
> 
> 
> Actually it works quite well if you have a closed airway circuit (read as: a tubed patient).  It doesn't do so great if you're just using a mask seal.
> 
> 
> 
> I'm trying to teach, so I would appreciate that out of you.



I commend all my teachers and their time. You dont call your students a moron, EVER. No clarification needed. Thats where you lost me


----------



## usafmedic45

> for some reason my lack of education and willingness to learn makes him mad



LOL Who's mad?  I don't know anything about your level of education and I applaud your supposed willingness to learn but being hostile to those who are instructors of the things you are trying to learn doesn't really lend itself to the belief that one is really interested in anything but having himself or herself patted on the back and told that his way of thinking was the best one out there.



> He is attacking me on another thread



No, I questioned your decision making.  Ask anyone here....if I was attacking you personally, I'd already be wearing your spine as a necklace.  Learn the difference between someone attacking you and someone being critical of your choices.  There is a significant difference and being able to separate the two is very helpful if one wishes to last long in any career field.


----------



## EMS Patient Care Advocate

EMS Patient Care Advocate said:


> I commend all my teachers and their time. You dont call your students a moron, EVER. No clarification needed. Thats where you lost me



This patient was two minutes from hospital. Treatments rendered while moving patient to ambulance, at hospital by time I had a scope in my hand. Perhaps I would have intubated sooner but he had a gag reflex.


----------



## usafmedic45

> You dont call your students a moron, EVER



I called_ your decision_ moronic, not you.  We all have our moments where we make bad calls.  See my post immediately proceeding this one for a lesson about this....


----------



## EMS Patient Care Advocate

usafmedic45 said:


> LOL Who's mad?  I don't know anything about your level of education and I applaud your supposed willingness to learn but being hostile to those who are instructors of the things you are trying to learn doesn't really lend itself to the belief that one is really interested in anything but having himself or herself patted on the back and told that his way of thinking was the best one out there.
> 
> 
> 
> No, I questioned your decision making.  Ask anyone here....if I was attacking you personally, I'd already be wearing your spine as a necklace.  Learn the difference between someone attacking you and someone being critical of your choices.  There is a significant difference and being able to separate the two is very helpful if one wishes to last long in any career field.



and we all have our opinions. I exposed myself, and my decisions to have people be critical of me. It was your approach I didnt care for, dont read into it more than that.


----------



## fast65

usafmedic45 said:


> Pardon me for asking for clarification and trying to make a teaching point out of something that confuses a lot of EMS providers (PEEP vs. CPAP)



Would you go further into this?


----------



## usafmedic45

> Would you go further into this?



The five cent explanation.....from a physiological standpoint, PEEP and CPAP are the same thing.  The only difference is that in PEEP, the patient is receiving at least some of their breaths from a mechanical source.  In CPAP, the patient is breathing entirely on their own.  If you want more detail, I can provide it.


----------



## usafmedic45

> I exposed myself, and my decisions to have people be critical of me. It was your approach I didnt care for, dont read into it more than that.



If you want people to be critical of you, then you should expect them to be critical of you.  Sugarcoating stuff or blowing sunshine and rainbows up someone's *** doesn't fix the problem nearly as succinctly as just getting down to the point.


----------



## Handsome Robb

fast65 said:


> Would you go further into this?



seconded. I think I understand what your getting at USAF but I'm not sure.


Both are providing positive end expiratory pressure (PEEP) one manually through a BVM + PEEP valve whereas CPAP or BiPAP for that matter are controlled by a regulator and use "self" sealing masks. BiPAP is more complicated than CPAP seeing as the pressure is alternated between an inspiratory pressure and an expiratory pressure that is selected by the provider. Like USAF pointed out BVM+PEEP valve work in closed circuits better than just with a mask due to difficulty maintaining an adequate mask-to-face seal.

The only difference I see is for BiPAP or CPAP requires the pt to be breathing spontaneously, but couldn't the increase in FiO2 along with the pressure pushing the edema back into the vascular space which increases oxygenation and will help correct the hypoxia which in turn will cause an increase in RR.

Let the lynching begin


----------



## fast65

usafmedic45 said:


> The five cent explanation.....from a physiological standpoint, PEEP and CPAP are the same thing.  The only difference is that in PEEP, the patient is receiving at least some of their breaths from a mechanical source.  In CPAP, the patient is breathing entirely on their own.  If you want more detail, I can provide it.



Alright, that makes sense, but I would still love some more detail if you have time.


----------



## usafmedic45

> Like USAF pointed out BVM+PEEP valve work in closed circuits better than just with a mask due to difficulty maintaining an adequate mask-to-face seal.



Actually the bigger issue, especially with higher PEEP settings in the hands of a person skilled with a BVM, is with gastric insufflation.


----------



## Handsome Robb

fast65 said:


> Alright, that makes sense, but I would still love some more detail if you have time.



I'm gonna keep quoting because I'm agreeing :rofl:


----------



## usafmedic45

fast65 said:


> Alright, that makes sense, but I would still love some more detail if you have time.



http://www.ccmtutorials.com/rs/mv/page14.htm  This is a good introduction and be sure to follow the link at the bottom of the page....any further questions, let me know.


----------



## Scott33

fast65 said:


> Wouldn't that make things worse?



CHF can be caused by a number of things - we commonly assume it is a systolic problem ("failure of the pump", another classroom mantra) and I am sure 9/10 times it will be. However heart failure can also be due to diastolic dysfunction where ventricular filling pressures and / or volume is inadequate, and the root cause of the patient's symptoms. What would we expect the BP to show in a situation like this? This is where a fluid bolus _could_ increase preload and raise CO. 

If you have an obvious case of CHF, but with an abnormally low BP, it may point more to a filling problem more than a pumping problem.


----------



## fast65

I'll take a look at that link, thanks usaf! And thanks Scott for that little bit of info as well.


----------



## EMS Patient Care Advocate

NVRob said:


> seconded. I think I understand what your getting at USAF but I'm not sure.
> 
> 
> Both are providing positive end expiratory pressure (PEEP) one manually through a BVM + PEEP valve whereas CPAP or BiPAP for that matter are controlled by a regulator and use "self" sealing masks. BiPAP is more complicated than CPAP seeing as the pressure is alternated between an inspiratory pressure and an expiratory pressure that is selected by the provider. Like USAF pointed out BVM+PEEP valve work in closed circuits better than just with a mask due to difficulty maintaining an adequate mask-to-face seal.
> 
> The only difference I see is for BiPAP or CPAP requires the pt to be breathing spontaneously, but couldn't the increase in FiO2 along with the pressure pushing the edema back into the vascular space which increases oxygenation and will help correct the hypoxia which in turn will cause an increase in RR.
> 
> Let the lynching begin


dont forget about the fact it cannot be used with hypotension. I think.


----------



## usafmedic45

> dont forget about the fact it cannot be used with hypotension. I think.



As long as you watch the patient and are able to tailor the settings to the patient's condition you should be fine.  CPAP has much less of a relative contraindication with hypotension than you would see with BiPAP.  Any ventilatory mode is going to have a potential issue with worsening hypotension especially in cases where the ventricular filling "kick" has been lost.

The other thing to keep in mind is that you need to remember that CPAP, BiPAP and any other ventilatory measure is simply an adjunctive treatment.  It's not the magic bullet that a lot of EMS providers like to believe it is when it comes to CHF and pulmonary edema.  It buys you time to fix the underlying problem.


----------



## Handsome Robb

EMS Patient Care Advocate said:


> dont forget about the fact it cannot be used with hypotension. I think.



If the hypotension is secondary to hypovolemia specifically blood loss, not pulmonary edema. I'm guessing due to the possible vagal reflex? However if I'm understanding it correctly, used with volume replacement it is just a relative contraindication, not absolute. Risk vs. Reward.

If it I am wrong, it's happened before, then PEEP would be contraindicated as well.


----------



## EMS Patient Care Advocate

usafmedic45 said:


> As long as you watch the patient and are able to tailor the settings to the patient's condition you should be fine.  CPAP has much less of a relative contraindication with hypotension than you would see with BiPAP.  Any ventilatory mode is going to have a potential issue with worsening hypotension especially in cases where the ventricular filling "kick" has been lost.
> 
> The other thing to keep in mind is that you need to remember that CPAP, BiPAP and any other ventilatory measure is simply an adjunctive treatment.  It's not the magic bullet that a lot of EMS providers like to believe it is when it comes to CHF and pulmonary edema.  It buys you time to fix the underlying problem.



Any suggestions for when you have flash edema with severe hypotension? Less than 80 systolic?


----------



## sdennislee

I agree in theory with OP, that sometimes the response provided by usafmedic45 can seem harsh, having said that, I have never failed to learn something from his posts. I tend to appreciate to the point critiques and advice. I can see where if you are the one receiving the critique it could be painful, but assume you will learn and remember and after all isn't that the point.


----------



## EMS Patient Care Advocate

NVRob said:


> If the hypotension is secondary to hypovolemia specifically blood loss, not pulmonary edema. I'm guessing due to the possible vagal reflex? However if I'm understanding it correctly, used with volume replacement it is just a relative contraindication, not absolute. Risk vs. Reward.
> 
> If it I am wrong, it's happened before, then PEEP would be contraindicated as well.



I believe its more to do with intrathoactic pressures and the not so happy venacava, causing the hypotension with CPAP.


----------



## usafmedic45

> I'm guessing due to the possible vagal reflex?



Nope.  It's due to compression of the right side of the heart as a result of the increased intrathoracic pressure associated with CPAP/PEEP.  



> However if I'm understanding it correctly, used with volume replacement it is just a relative contraindication, not absolute. Risk vs. Reward.



Pretty much. 



> If the hypotension is secondary to hypovolemia specifically blood loss, not pulmonary edema.


Anything that reduces ventricular filling will do it.  It's even something of a problem when you have higher pressures in folks with atrial fibrillation.


----------



## Handsome Robb

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


----------



## EMS Patient Care Advocate

sdennislee said:


> I agree in theory with OP, that sometimes the response provided by usafmedic45 can seem harsh, having said that, I have never failed to learn something from his posts. I tend to appreciate to the point critiques and advice. I can see where if you are the one receiving the critique it could be painful, but assume you will learn and remember and after all isn't that the point.



Great advice!


----------



## 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

NVRob said:


> 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

usafmedic45 said:


> 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

usafmedic45 said:


> 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

EMS Patient Care Advocate said:


> 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

04_edge said:


> 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

Smash said:


> 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

usalsfyre said:


> 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

Enzo said:


> Would furosemide have helped?



Furosemide is not an inotrope, so no.


----------



## ArcticKat

Enzo said:


> Would furosemide have helped?



A common side effect is hypotension, so not likely.


----------



## usafmedic45

Enzo said:


> 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

18G said:


> 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.


----------



## Smash

Enzo said:


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



That's unfortunate for the patients.


----------



## ArcticKat

Enzo said:


> 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

medicsb said:


> 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

18G said:


> 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

18G said:


> 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

18G said:


> 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

EMS Patient Care Advocate said:


> 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

medicsb said:


> 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

EMS Patient Care Advocate said:


> 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

jjesusfreak01 said:


> 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

EMS Patient Care Advocate said:


> 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 ...


----------

