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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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