# Falling O2 sats.....on CPAP?



## needsleep (Dec 4, 2017)

I've been practicing EMS for only 5 months, so forgive me if this is a dumb question. My medic and I responded to a DIB call. 65 Y/O M Pt with PMH of CHF, Type 2 DM, and Renal failure. Pt is tripoding upon our arrival and appears very anxious. We get him on the rig and give him 3 rpm nasal canula while we prepare a 2.5 mg albuterol treatment. Sats go from 83 to 94. Pt begins to lean forward and starts saying , "I can't breathe! I can't breathe!" Sats begin dropping. At 79% we put Pt on CPAP. Pt begins sweating and sats DROP to 70%! 
After "thereupetic touch" and breathing coaching, he gets to 82% by the time we get to the ER.

Question: in school we were taught CPAP is the end-all be-all solution for DIB for CHF/COPD. I always thought it was the ace card you always had in your deck if things got sketchy. Now I don't have that confidence in it. Also, this was my first time ever seeing it used.

Any theories on the pathophys. behind this?


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## Gurby (Dec 4, 2017)

What if it wasn't CHF or COPD?

What were the lung sounds?  BP and HR?  ETCO2?

CPAP is sweet but it definitely isn't the end-all be-all solution to anything.  It's just something else to try before intubation...


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## TXmed (Dec 4, 2017)

In airway & respirstory emergencies there is NO end all be all. 

What did your breath sounds reveal ? Do you think it was bronchoconstriction or pulmonary edema? Or did you go to a treatment without a field diagnosis? There is other pathologies ie PE that will play out like this. If he wasnt accepting cpap you could try versed/ativan/ valium at a very low, anti-anxiety dose. Always be planning your next move.


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## NomadicMedic (Dec 4, 2017)

An SpO2 reading is nice, but it’s only half of the picture. What was the patient’s end tidal CO2? What did the waveform look like? Was there actually a good plethora with the pulse ox? Respiratory rate? Lung sounds? Why did you use albuterol? You didn’t mention anything in the PHX about COPD or any reactive airway issue. What time of day was it? 

Lots of unanswered questions, but this smells like a PE.


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## needsleep (Dec 4, 2017)

Also, forgot to add HTN to PMH.

Upon loading into the truck:
BP: 250/110
P: 105 
RR: a lot and shallow
BGL: 195
Breath sounds: bilateral, muffled uppers w/ bilateral rales and "wet" lowers. Again, I'm so new, it sounded to me like someone blowing bubbles through a straw into a glass of Coke. 

As far as EtCo2, the only way we have to monitor this is via the attachment/connector piece between the airway tube and BVM which then goes in to the monitor. Forgive my inexperience and ignorance, but how would that have factored into this specific case? PT was obviously going to be very acidotic, but would that change the direction of immediate treatment? I would imagine it would still just be high flow oxygen to clear those "drowning" alveoli. 

Thank you to all for such quick, thorough replies! Im learning so much.


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## NomadicMedic (Dec 4, 2017)

Well, from your description, it’s CHF. This patient needs NTG and CPAP, not albuterol.


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## DrParasite (Dec 4, 2017)

needsleep said:


> BP: 250/110
> [snip]
> Breath sounds: bilateral, muffled uppers w/ bilateral rales and "wet" lowers. Again, I'm so new, it sounded to me like someone blowing bubbles through a straw into a glass of Coke.


In my experience,  super high BP + bilateral rales (with the occasional "I can't breath") = flash pulmonary edema.  Solution?  CPAP, and Nitro.  

ETO2 would be nice, especially if you have those nasal canulas that do ETO2.  

Why are you giving Albuterol?


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## needsleep (Dec 4, 2017)

Would EtCo2 readings change treatment choices? Anyway to construct my own NC type EtCo2 detector, via combining the top half of a NC and the bottom half of the EtCo2 connector piece hose that inputs into the monitor?

To no surprise, my medic called the hospital a few hours later and the Pt's RN said that upon arrival his EtCo2 was in the 70s. They said they "gave him 2 bottles of NTG" and that he was "maxed out" on BiPAP. 


As far as albuterol, I'm not sure. My medic just grabbed it and administered. My (limited) understanding is why not?


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## DrParasite (Dec 4, 2017)

needsleep said:


> Would EtCo2 readings change treatment choices? Anyway to construct my own NC type EtCo2 detector, via combining the top half of a NC and the bottom half of the EtCo2 connector piece hose that inputs into the monitor?


This was what I was referring to.  And sometimes ETCO2 can change a treatment path





needsleep said:


> As far as albuterol, I'm not sure. My medic just grabbed it and administered. My (limited) understanding is why not?


I'm only a dumb firefirefighter, but even I know "Why not" is a horrible reason to do something, especially if administering that medication can have unwelcome side effects on your sick patient.

Your an AEMT; didn't they cover why you give albuterol in class?  I'm pretty sure rales and hypertension are not indicators to give it.  Does your medical director give you different protocols to follow?  Isn't albuterol within your AEMT scope?  so shouldn't you know when you should and should not give it?


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## needsleep (Dec 4, 2017)

Absolutely agreed. When I said "why not" I meant that in a "why would it not be a treatment option" context. I would never just think "why not?" when administering any medication. My medic initiated that treatment.

With all of that said, I am aware that there is no contraindication to albuterol....except hypersensitivity to albuterol, which Pt did not mention.


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## NomadicMedic (Dec 4, 2017)

Albuterol is indicated for bronchoconstriction, which would be indicated by expiratory wheeze and a shark fin morphology of the end tidal waveform. 

Pulmonary edema may have a wheezing component, but you’d be more likely to hear crackles in the bases if the patient was sitting up. The treatment for this is always CPAP and NTG. It’ll also present with a non obstructive end tidal waveform. So yes, capnography can help guide the treatment. And you can’t roll your own, you need to purchase the nasal capnography cannula. They fit under a CPAP mask and together with SpO2, it can give you a much better sense of the patient’s respiration, not just ventilation. 

However, this case is basic clinical correlation. The signs all scream pulmonary edema, not anything reactive that would be treated with Albuterol. That should be QIed as a protocol violation and the medic should get a little refresher on reactive airways vs CHF.


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## VFlutter (Dec 4, 2017)

Agree with everyone else that it sounds like pulmonary edema. Albuterol probably didn’t help the situation.

Do you remember the CPAP settings? Probably wasn’t aggressive enough given the situation. And given that he was also hypercapnic Bipap would have been better if you have it.


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## DrParasite (Dec 4, 2017)

Skipping the reply from @NomadicMedic (which is 100% correct btw)


needsleep said:


> Absolutely agreed. When I said "why not" I meant that in a "why would it not be a treatment option" context. I would never just think "why not?" when administering any medication. My medic initiated that treatment.


I think the better question is, why would it be a treatment option?


needsleep said:


> With all of that said, I am aware that there is no contraindication to albuterol....except hypersensitivity to albuterol, which Pt did not mention.


While you might be right, there is no contraindication to using it, the better question is what indications were there to use it?  I will agree with you that there was no reason you couldn't give the medication, but is there a reason you should have given albuterol?  You're an AEMT, isn't albuterol in your scope of practice? if your medic had told you to give the albuterol, would you have?

I know I'm not as educated as you, the AEMT, but based on the situation you described, it appears your medic gave the incorrect medication for this patient, and should probably get flagged by QA/QI


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## medichopeful (Dec 4, 2017)

NomadicMedic said:


> Well, from your description, it’s CHF. This patient needs NTG and CPAP, not albuterol.



And probably a tube.


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## NomadicMedic (Dec 4, 2017)

medichopeful said:


> And probably a tube.



Nope. These folks usually turn around with agressive CPAP and NTG administration.


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## medichopeful (Dec 4, 2017)

NomadicMedic said:


> Nope. These folks usually turn around with agressive CPAP and NTG administration.



Agreed that many (probably even most) do.  But one of the OP's posts stated:



needsleep said:


> To no surprise, my medic called the hospital a few hours later and the Pt's RN said that upon arrival his EtCo2 was in the 70s. They said they "gave him 2 bottles of NTG" and that he was "maxed out" on BiPAP.



If that information is true, I see a tube in his future unless he makes a miraculous turn-around (or the information isn't correct).


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## VFlutter (Dec 4, 2017)

https://emcrit.org/emcrit/scape/

Important to note the difference between a “SCAPE” patient vs CHF exacerbation with Pulmonary Edema. The former really requires aggressive intervention, usually outside the comfort zone of most providers.


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## TXmed (Dec 4, 2017)

Sometimes CPAP needs more time to work. On SCAPE patients its really gonna push your comfort zone for how long to try cpap and how much nitro to push. But youll learn to be more patient the more experience you get. On some cpap msaks youncan attach the inline etco2 between the mask and the tubing. 

If its night/dawn, slightly cool with fog mist in the air. Most likely CHF, these conditions are ripe for pulmonary edema/copd.


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## E tank (Dec 4, 2017)

Chase said:


> https://emcrit.org/emcrit/scape/
> 
> Important to note the difference between a “SCAPE” patient vs CHF exacerbation with Pulmonary Edema. The former really requires aggressive intervention, usually outside the comfort zone of most providers.



Pretty interesting stuff...in my clinical setting, the NTG doses he's talking about would be lethal for a bunch of reasons. I've never heard of this strategy and I notice the post is about 8 years old. 

Anyone else aware of this kind of NTG use these days?


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## VFlutter (Dec 4, 2017)

E tank said:


> Pretty interesting stuff...in my clinical setting, the NTG doses he's talking about would be lethal for a bunch of reasons. I've never heard of this strategy and I notice the post is about 8 years old. With the advent of nitric oxide and something called Flolan, it isn't something that is commonly practiced where I am at all (at least I'm not aware of it).
> 
> Anyone else aware of this kind of NTG use these days?



Those dosages are used exclusively for the hypersympathetic flash pulmonary edema patients with significant hypertension. Usually those whom have diastolic dysfunction but no other significant cardiac conditions.

Inhaled or IV Flolan? I’ve used inhaled for ARDS V/Q mismatch and intravenous or intra PA for significant PAH. Never used it specially for APE. It seems like selectively reducing pulmonary pressures without addressing the excessive systemic afterload first wouldn’t be the most effective strategy tho.


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## E tank (Dec 4, 2017)

Chase said:


> Those dosages are used exclusively for the hypersympathetic flash pulmonary edema patients with significant hypertension. Usually those whom have diastolic dysfunction but no other significant cardiac conditions.
> 
> Inhaled or IV Flolan? I’ve used inhaled for ARDS V/Q mismatch and intravenous or intra PA for significant PAH. Never used it specially for APE. It seems like selectively reducing pulmonary pressures without addressing the excessive systemic afterload first wouldn’t be the most effective strategy tho.



You got me before I edited my post! I edited that because the settings that we use flolan or NO for flash pulmonary edema in the CT surgery setting are kind of removed from what we're talking about here so I deleted that part of my post for simplicity's sake. Didn't really apply but where in theory a huge slug of NTG would help in those situations, the dose would otherwise kill the patient. 

But to your point, you are, of course correct, the dose is so high though, I was wondering with the common possibility of acei/arb being so high these days, I was curious as to whether or not this was used more commonly. Those medications could potentially present a more than anticipated fall in CO and MAP with such a big hit of NTG. 

 Like I said, I'm unfamiliar with it.


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## StCEMT (Dec 4, 2017)

needsleep said:


> Now I don't have that confidence in it. Also, this was my first time ever seeing it used.



You've seen it used once. Not a great deal of times having used it. It may not always make a huge difference, but you will see a noticeable improvement quite quickly with plenty of people. 



NomadicMedic said:


> Nope. These folks usually turn around with agressive CPAP and NTG administration.


I've found some hospitals here tend to pull the trigger quickly on tubes. Brought in something similar last week with improvements in O2 sat and work of breathing, but they still decided to intubate. I think BiPAP was worth a shot and could have been beneficial since there were signs of improvement and it was right there with us, but they opted to do otherwise. Thought for sure it would have been a perfect example of CPAP doing what it does best, or at least delaying intubation enough to definitively rule out alternative treatment plans.


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## TXmed (Dec 4, 2017)

Intubating a CHF patient is difficult due to anatomjc issues but mainly physiological issues as pre-ox and FRC are barely existant. On top of that extubating them is also fairly complicated. Pressure is what they need and it is easy to give it to them with NIPV (in most cases, not all) CHF patients should PROVE to me they need a tube.

@E tank i believe there is some studies posted on RebelEM podcast. High dose IV nitro as a start is begining to show some good promise.


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## Summit (Dec 4, 2017)

Chase said:


> https://emcrit.org/emcrit/scape/
> 
> Important to note the difference between a “SCAPE” patient vs CHF exacerbation with Pulmonary Edema. The former really requires aggressive intervention, usually outside the comfort zone of most providers.


Linked article was worth the read
http://www.ijccm.org/article.asp?is...0;issue=12;spage=719;epage=723;aulast=Agrawal


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## TXmed (Dec 4, 2017)

@Summit great article


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## TXmed (Dec 4, 2017)

@needsleep i do beleive CHF and asthma realted emergencies is where medics can seperate themselves and really make a difference. I know some of these guys throw out somethings that may or may not apply to your practice but the more you understand the physiology of both the better you can help your patient. Sounds like a good experience building call.


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## needsleep (Dec 4, 2017)

TXmed said:


> @needsleep i do beleive CHF and asthma realted emergencies is where medics can seperate themselves and really make a difference. I know some of these guys throw out somethings that may or may not apply to your practice but the more you understand the physiology of both the better you can help your patient. Sounds like a good experience building call.




Absolutely! I love learning and have read all of the studies on the links provided. I cannot get enough of EM. I want to be the best clinician I can. 

so for future reference, SL NTG would have been a much more beneficial and appropriate form of treatment alongside the CPAP?


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## RocketMedic (Dec 4, 2017)

With that pressure and presentation, yes.

I dunno how deep you went into CHF, but here's the Cliff Notes EMT-B version:

A heart can pump X hard. People with chronically-high blood pressure, extra size, etc. work their hearts hard, and generally somewhat faster than 'normal'. This means that their hearts are basically getting their Beast Mode on and gettin' swoll. Great, right?

Well, sorta. Big Strong Hearts need a lot of blood, and get big...but Big Strong Hearts generally tend to develop in people who are Big but not Strong. This means that those hearts tend to develop in the old, the sedentary, the obese, etc. This affects blood supply to that big heart and continues to increase the workload on that heart. On the one hand, these people need the Big Heart to push enough blood to live. On the other hand, that Big Heart takes a lot to keep going, and cardiac circulation does not scale up well. We're basically taking a Turbocharged 2-liter I4 and trying to move an F350 with it. Sure, it _works_ on most days, but it doesn't have the functional reserve of the 6.7 diesel we wish we had. Obviously, this 'motor swap' is going to leave us reliant on higher RPM (rates), increased fuel burn (increased cardiac oxygen/glucose demand / circulation. Remember Starling's Law? Big floppy hearts can't squeeze as well as normally-sized ones.

So, anyways, CHF. One fine day, let's say something stresses our Big Heart. Might be additional physiological demands like unusual exercise, a missed medication, or it could be a fairly minor change in blood/oxygen supply to the heart. It could even be simple bad luck. All of a sudden, we're taking that high-revvin' Focus motor and expecting it to haul lumber up the Rockies. Blood starts backing up because the heart literally can't pump it clear against the _back pressure (_*diastolic pressure*) of the heart. We can see this in two different ways: first, we're likely going to see _symptoms_  and signs of cardiac insufficiency, and second, we're going to see that blood/fluid start to pool. Think of pushing that full-size pickup- you might get a little progress and not die, but good luck handling anything else!

CHF may involve the right side, left side or both sides of the heart. In right-sided heart failure, the right ventricle isn't pumping blood hard enough to push it through the pulmonary vasculature, which means that the blood that should have gone through the lungs is actually backing up through the right side of the heart and back into the body. Some blood is still getting through, just a lot less than we'd like to see. In this case, we'd classically see edema _below_ the heart, with engorged legs, abdomen, scrotum, etc. This is because immobilized blood is leaking plasma/fluid (_thirdspacing) _out into the body. A _lot_ of people live with this problem.

Let's say one of two things happens: either something happens to decrease the effectiveness of the left side of the heart's pump or the right side becomes too weak to pump blood through the lungs effectively. All of a sudden, that blood that _was_ going through the pulmonary vasculature starts to sit there, and it starts to leak fluid into that amazingly empty air (osmosis in action) on the other side of the alveoli. This edema is primarily composed of water. Now we've got left-sided heart failure, and we're going to see a panic response from your body.

First, your body is going to see this and say "whoa, heart. Don't suck!". Enter adrenaline releases, pain, dyspnea and Ominous Doom. Your blood pressure is going to climb because your body is fighting the lack of perfusion the only way it knows- beat harder and faster. This doesn't work well because the Big Floppy Heart doesn't fill as quickly, beat as efficiently or squeeze as hard as the Normal Heart, so it isn't squeezing like your body anticipates, and as the diastolic pressure rises, so does the amount of force required to overcome that back pressure and create a useful pulse pushing blood forward. Your patient, with a BP 250/110, is literally squeezing his heart twice as hard as normal to clear the doubled back pressure in his arteries. Kinda like our 2.0-liter motor in a logging truck up the Rockies, this isn't sustainable.


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## RocketMedic (Dec 4, 2017)

So, on to treatment. We need to make the heartbeat more effective, but we're not putting in LVADs or time travelling in our ambulances, so we need to cheat a little. First, we need to look at what our vitals are telling us- is the heart effectively pushing fluid in some form? If they're hypertensive, the answer is yes- so we want to _lower_ the back pressure on the heart, with the intent of allowing it to relax and work less hard. We're changing that diesel pickup we're pushing across the lot for a reasonably-sized compact sedan. We are _not_ trying to change the heartbeat itself. Nitroglycerin, lasix, etc. 

If, on the other hand, the heartbeat is _inadequate (_hypotensive + slow, way too fast, etc), we need to change the heartbeat itself. These folks are the ones in cardiogenic shock, and where we start getting schwifty with pressors, electricity, antiarrhythmics, etc. These are the CHF-ers who get converted out of A-fib RVR, placed on dopamine, etc. 

So where does CPAP fit into this? Well, we want those lungs to open up, and CPAP/BiPap are great tools to push wet lungs open. Oxygen is a necessity to live, and we can far more effectively exchange it when our lungs inflate. Not all CHF needs CPAP, but it certainly helps open wet, editimous lungs.


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## EpiEMS (Dec 4, 2017)

RocketMedic said:


> I dunno how deep you went into CHF, but here's the Cliff Notes EMT-B version:



This is a great (very intuitive) explanation. I may have to steal this...


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## RocketMedic (Dec 4, 2017)

Feel free


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## CALEMT (Dec 4, 2017)

RocketMedic said:


> We're basically taking a Turbocharged 2-liter I4 and trying to move an F350 with it. Sure, it _works_ on most days, but it doesn't have the functional reserve of the 6.7 diesel we wish we had.



I would've liked your post had you used a Dodge Cummins instead of a FORD


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## RocketMedic (Dec 4, 2017)

CALEMT said:


> I would've liked your post had you used a Dodge Cummins instead of a FORD


Cummins don't fail. Those are the hearts that beat forever.


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## needsleep (Dec 4, 2017)

RocketMedic said:


> So, on to treatment. We need to make the heartbeat more effective, but we're not putting in LVADs or time travelling in our ambulances, so we need to cheat a little. First, we need to look at what our vitals are telling us- is the heart effectively pushing fluid in some form? If they're hypertensive, the answer is yes- so we want to _lower_ the back pressure on the heart, with the intent of allowing it to relax and work less hard. We're changing that diesel pickup we're pushing across the lot for a reasonably-sized compact sedan. We are _not_ trying to change the heartbeat itself. Nitroglycerin, lasix, etc.
> 
> If, on the other hand, the heartbeat is _inadequate (_hypotensive + slow, way too fast, etc), we need to change the heartbeat itself. These folks are the ones in cardiogenic shock, and where we start getting schwifty with pressors, electricity, antiarrhythmics, etc. These are the CHF-ers who get converted out of A-fib RVR, placed on dopamine, etc.
> 
> So where does CPAP fit into this? Well, we want those lungs to open up, and CPAP/BiPap are great tools to push wet lungs open. Oxygen is a necessity to live, and we can far more effectively exchange it when our lungs inflate. Not all CHF needs CPAP, but it certainly helps open wet, editimous lungs.




I understand the need for the heart to relax and not “red line” itself, but isn’t that a necessity to get th fluid out of the lungs? If nitro alone is given to relieve the oxygen demands on the heart, how does that improve the overall outcome of the Pt? Wouldn’t that equate to more fluid retention in the lungs? 


Btw, thank you so much for that BP explanation. All of these responses are beyond appreciated!


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## CALEMT (Dec 4, 2017)

needsleep said:


> but isn’t that a necessity to get th fluid out of the lungs? If nitro alone is given to relieve the oxygen demands on the heart, how does that improve the overall outcome of the Pt? Wouldn’t that equate to more fluid retention in the lungs?



That isn't really the primary function of NTG in this case. You want the vasodilation that the NTG causes in the pulmonary vessels. That combined with CPAP will move the fluid out of the lungs. You can go more in depth, but that is pretty must the gist of it.


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## VFlutter (Dec 4, 2017)

I understand the need for the heart to relax and not “red line” itself, but isn’t that a necessity to get th fluid out of the lungs? If nitro alone is given to relieve the oxygen demands on the heart, how does that improve the overall outcome of the Pt? Wouldn’t that equate to more fluid retention in the lungs?
[/QUOTE]

The fluid is backing up into the lungs because the forward flow out of the heart is impaired by the increased resistance. Step on a hose and the pressure behind your foot increases. The nitro opens the hose back up. 

If you want some terms to look up and become farmiliar with..

As Systemic Vascular Resistance (SVR) increases so does Left Ventricular End Diastolic Pressure (LVEDP) which increases pressure Left Atrial Pressure (LAP) which we measure as Pulmonary Artery Wedge Pressure (PAOP/PAWP). Once PAWP reaches a certain point the pulmonary vasculature attempts to compensate by becoming more permeable and leaks fluid out of the vessels resulting in pulmonary edema. So you can see it’s a snowball effect that all starts with SVR or blood pressure. Fix that with Nitro and everything else down the line improves. CPAP buys you time by increasing pressure in the lungs and keeping fluid in the vessels.


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## Colt45 (Dec 4, 2017)

There has been some amazing topics in here to read through. I do want to add that although albuterol doesn't necessarily  have any contrainications- it is synergistic with other sympathomimetics. For this case that wouldn't be a big deal. But worth understanding.


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## needsleep (Dec 5, 2017)

So, is it safe to say that in any hypertensive crisis NTG could be administered? In school and in my text it says the indications are for stable and unstable angina.


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## needsleep (Dec 5, 2017)

Another question: once NTG vasoldilates the pulmonary vasculature allowing more “space” for the accumulating blood, how does the pulmonary edema get back into the vessels? Would lasix be a candidate for treatment even without peripheral edema?


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## DrParasite (Dec 5, 2017)

needsleep said:


> So, is it safe to say that in any hypertensive crisis NTG could be administered? In school and in my text it says the indications are for stable and unstable angina.


As a general rule, prehospitally, we don't treat HTN, with NTG, because the HTN is often a sign, not the underlying condition

Although, BLS in NC can administer NTG for difficulty breathing for patients with suspected flash pulmonary edema / CHF, provided they have a prescription for it from their doctor.


needsleep said:


> Another question: once NTG vasoldilates the pulmonary vasculature allowing more “space” for the accumulating blood, how does the pulmonary edema get back into the vessels?


 I want to say via diffusion, but I would need to look up the exact way.


needsleep said:


> Would lasix be a candidate for treatment even without peripheral edema?


We used to use Lasix on the ambulance back in the day.... we stopped doing it because it dehydrated our already sick patients, causing additional issues.


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## VFlutter (Dec 5, 2017)

For these patients in particular volume overload is not the issue, they are actually hypovolemic usually, it is that the fluid is in the wrong place so Lasix is not really helpful and may worsen the situation (RAAS).


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## Carlos Danger (Dec 5, 2017)

needsleep said:


> So, is it safe to say that in any hypertensive crisis NTG could be administered? In school and in my text it says the indications are for stable and unstable angina.



Current thinking is that rapid reductions in blood pressure are generally a bad thing. It is probably even true that the higher the BP, the more important it is to lower it in a slow, controlled fashion. Unless there is evidence of end-organ damage resulting from the hypertension, even very high BP should be lowered over a period of hours or even days, usually using PO meds.



needsleep said:


> Another question: once NTG vasoldilates the pulmonary vasculature allowing more “space” for the accumulating blood, how does the pulmonary edema get back into the vessels? Would lasix be a candidate for treatment even without peripheral edema?



The fluid that was pushed into the alveoli by the high pulmonary pressure will simply be reabsorbed into the tissues. CPAP will speed that process up by increasing pressure within the alveoli, which causes a "driving pressure" across the alveolar-cappilary membrane. Read about Starling Forces. You should be able to find some videos on YouTube that illustrate the concepts well, and there's plenty of more in-depth reading available on the topic if you are so inclined.

Lasix is just a diuretic. It causes the kidneys to filter more water from the blood than they otherwise would. If the cause of the high pulmonary pressure is due to (or even partly due to) intravascular fluid overload, then using lasix to get rid of some of that excess intravascular volume can be helpful. But usually, the primary problem isn't fluid volume, it is a weak heart. Using lasix in those cases has been shown unhelpful and even harmful. Also, lasix's contribution is very slow compared to NTG and CPAP.


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## ThadeusJ (Dec 6, 2017)

There are two schools of thought about the effects of CPAP on lung fluid: 1) that it physically pushes the fluid back into the capillaries using Starliing Forces, and 2) that as it recruits the alveoli, the fluid is spread out and redistributed, but still exists in the lung.  I prefer the latter explanation as I have read studies that showed that the net fluid volume in the lung was the same before and after CPAP.  I also see it as asking whether a faucet leaks faster or slower based on the atmospheric pressure (Starling Forces would say that it leaks less with increasing atmospheric pressure).  Both theories have merit however the net result is that CPAP recruits collapsed airways and keeps them open.

One thing you have to keep in mind is that there is no set pressure that will work its magic on CHF.  While you want to deliver the lowest amount of pressure that will do the job, I have worked on patients that required incrementally higher pressures until an effect was experienced.  This was a particular patient in a hospital who was hypotensive but needed increased ventilation.  We had the benefit of serial ABG's to determine the most effective pressure.  As we slowly increased the pressures to 12.5 cmH2O,  we saw the effects of lung recruitment as the chest sounds cleared and SpO2 levels skyrocketed (they were hovering around 84% through all of this).  I don't expect this to be mirrored in the field, but was used for illustration purposes.

I have attached a copy of a lung when pressure is applied.  If you start at the top left corner and move in a clockwise pattern, you can see how it reacts to increasing inflation pressures through inhalation (see scale along the bottom).  Once inflated, you can see how it stays inflated as the pressures lower to levels even below the inflation levels (if that makes sense).  This is one reason why you don't want to keep removing the mask for meds or suction once you start CPAP - you keep interfering with the constant pressure aspect of the therapy.


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## alsmcq (Dec 6, 2017)

needsleep said:


> I've been practicing EMS for only 5 months, so forgive me if this is a dumb question. My medic and I responded to a DIB call. 65 Y/O M Pt with PMH of CHF, Type 2 DM, and Renal failure. Pt is tripoding upon our arrival and appears very anxious. We get him on the rig and give him 3 rpm nasal canula while we prepare a 2.5 mg albuterol treatment. Sats go from 83 to 94. Pt begins to lean forward and starts saying , "I can't breathe! I can't breathe!" Sats begin dropping. At 79% we put Pt on CPAP. Pt begins sweating and sats DROP to 70%!
> After "thereupetic touch" and breathing coaching, he gets to 82% by the time we get to the ER.
> 
> Question: in school we were taught CPAP is the end-all be-all solution for DIB for CHF/COPD. I always thought it was the ace card you always had in your deck if things got sketchy. Now I don't have that confidence in it. Also, this was my first time ever seeing it used.
> ...



Next time, go simple if you do not have too many resources:
1) A couple of ampules of furosemide (40 mg) intramuscular will make the patient to pee and BP will come down.
2) GTN spray or tablet sublingual.
3) In the acute episode, start BIPAP, IPAP 15, EPAP 5 and adjust to tidal volumes of around 500 ml.  Titrate until the patient is comfortable.
4) Morphine 2mg sc will help the patient to keep calm and adapted to the NIV.


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## NomadicMedic (Dec 6, 2017)

alsmcq said:


> Next time, go simple if you do not have too many resources:
> 1) A couple of ampules of furosemide (40 mg) intramuscular will make the patient to pee and BP will come down.
> 2) GTN spray or tablet sublingual.
> 3) In the acute episode, start BIPAP, IPAP 15, EPAP 5 and adjust to tidal volumes of around 500 ml.  Titrate until the patient is comfortable.
> 4) Morphine 2mg sc will help the patient to keep calm and adapted to the NIV.




I’m guessing you’re not in the states.


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## needsleep (Dec 7, 2017)

Remi said:


> The fluid that was pushed into the alveoli by the high pulmonary pressure will simply be reabsorbed into the tissues. CPAP will speed that process up by increasing pressure within the alveoli, which causes a "driving pressure" across the alveolar-cappilary membrane.



Got it! That made it click.




ThadeusJ said:


> One thing you have to keep in mind is that there is no set pressure that will work its magic on CHF. While you want to deliver the lowest amount of pressure that will do the job, I have worked on patients that required incrementally higher pressures until an effect was experienced. This was a particular patient in a hospital who was hypotensive but needed increased ventilation. We had the benefit of serial ABG's to determine the most effective pressure. As we slowly increased the pressures to 12.5 cmH2O, we saw the effects of lung recruitment as the chest sounds cleared and SpO2 levels skyrocketed (they were hovering around 84% through all of this). I don't expect this to be mirrored in the field, but was used for illustration purposes.



I thoroughly appreciated this response and accompanying picture. Extremely informational! Thank you!




Chase said:


> For these patients in particular volume overload is not the issue, they are actually hypovolemic usually, it is that the fluid is in the wrong place so Lasix is not really helpful and may worsen the situation (RAAS).



How is this proven? (I imagine nothing we can do to know this pre-hospital)


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## RocketMedic (Dec 7, 2017)

I'm not at all a supporter of morphine or versed in these cases. We want more and better breathing, not "let's get high". I've found its safer to adjust breathing to comfort (to include bvm) than drugging folks into tolerance


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## VFlutter (Dec 7, 2017)

RocketMedic said:


> I'm not at all a supporter of morphine or versed in these cases. We want more and better breathing, not "let's get high". I've found its safer to adjust breathing to comfort (to include bvm) than drugging folks into tolerance



Agreed however Morphine is extremely effective at treating dyspnea and make these patients much more comfortable. Low dose Morphine works wonders for COPD/PF patients. Don’t have to knock them out but a little goes a long way to making the situation more tolerable


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## VFlutter (Dec 7, 2017)

needsleep said:


> How is this proven? (I imagine nothing we can do to know this pre-hospital)



Clinical assessment and history. But most people do not carry Lasix prehospital anyway.


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## Carlos Danger (Dec 7, 2017)

RocketMedic said:


> I'm not at all a supporter of morphine or versed in these cases. We want more and better breathing, not "let's get high". I've found its safer to adjust breathing to comfort (to include bvm) than drugging folks into tolerance



Morphine actually works great in these cases. It treats sensations of air hunger very effectively, which reduces anxiety and improves breathing and compliance.


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## E tank (Dec 7, 2017)

ThadeusJ said:


> There are two schools of thought about the effects of CPAP on lung fluid: 1) that it physically pushes the fluid back into the capillaries using Starliing Forces, and 2) that as it recruits the alveoli, the fluid is spread out and redistributed, but still exists in the lung.



Probably elements of both are present.


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## needsleep (Dec 14, 2017)

Curious, what would the SpO2 level look like for someone who became unconscious due to a respiratory emergency? 
For instance, in this example the patient broke out in a sweat and appeared to really be tanking around 70%. Would he remain conscious if it hit 60%? 50%?


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## Colt45 (Dec 14, 2017)

needsleep said:


> Curious, what would the SpO2 level look like for someone who became unconscious due to a respiratory emergency?
> For instance, in this example the patient broke out in a sweat and appeared to really be tanking around 70%. Would he remain conscious if it hit 60%? 50%?



I've taken care of COPD patients whose normal spo2 is in the mid to high 80's. I don' think it' ever safe to assume an exact number when it comes to someone still being conscious or not with anything in medicine. Some people will surprise you. I think the best answer to your question is he would  "most likely" not be conscious. But not always.


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## ThadeusJ (Dec 14, 2017)

To understand SpO2 levels better, take a look at the oxyhemoglobin dissociation curve where you can see that the lower it goes, the faster it drops (like falling off a cliff).  In my young and carefree days, I was able to hold my breath until I got the SpO2 down into the 70's, but that was for a microsecond and I have seen people walking around with SpO2 levels in the 80's (and an ABG-verified PCO2 level around 140 mmHg).

Remember that its relatively easy to fix an oxygen problem, but most respiratory emergencies are CO2 problems. Also, many oximeters aren't all that accurate below normal ranges. You get what you pay for.


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## VFlutter (Dec 14, 2017)

I’ve seen pulmonary fibrosis patients awake in the 50’s. Pretty anxious tho.


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## dumbenoughtostay (Dec 15, 2017)

VFlutter said:


> Agreed however Morphine is extremely effective at treating dyspnea and make these patients much more comfortable. Low dose Morphine works wonders for COPD/PF patients. Don’t have to knock them out but a little goes a long way to making the situation more tolerable




Concerning morphine working wonders, you may want to consider this:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821770/ for patients in CHF.  I don't know if it applies to COPD/PF.  

Pay particular attention to the section on morphine.  Another example of a good idea with what seemed to be sound reasoning taught and retaught until it is accepted as truth, yet in the long run...may be an independent predictor for death.  Perhaps they looked better for us, but the cost was they look worse later.


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## VFlutter (Dec 15, 2017)

dumbenoughtostay said:


> Concerning morphine working wonders, you may want to consider this:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821770/ for patients in CHF.  I don't know if it applies to COPD/PF.
> 
> Pay particular attention to the section on morphine.  Another example of a good idea with what seemed to be sound reasoning taught and retaught until it is accepted as truth, yet in the long run...may be an independent predictor for death.  Perhaps they looked better for us, but the cost was they look worse later.



Ya high dose Morphine should be not be used as a first line treatment in ADHF like was traditionally done in the past. Nothing wrong with giving 1-2mg of IV morphine after they have been appropriately treated with NTG and NPPV.


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## Carlos Danger (Dec 16, 2017)

dumbenoughtostay said:


> Concerning morphine working wonders, you may want to consider this:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821770/ for patients in CHF.  I don't know if it applies to COPD/PF.
> 
> Pay particular attention to the section on morphine.  Another example of a good idea with what seemed to be sound reasoning taught and retaught until it is accepted as truth, yet in the long run...may be an independent predictor for death.  Perhaps they looked better for us, but the cost was they look worse later.



Well we aren’t talking about using morphine to “manage” HF; merely giving small doses for its anxiolytic effect. Lots of drugs treat anxiety but morphine seems to be uniquely effective at treating the sensation of air hunger that these folks experience.

Two of the articles cited in that piece were quite old (1987 and 1999) so without having read them I would bet that they are referring to the time when morphine was one of the first drugs you reached for in suspected CHF. The idea was essentially to use morphine’s histaminergic effects as a vasodilator, but it never worked well. Folks ended up getting pretty large doses and it turns out that large doses of a respiratory depressant isn’t such a good idea for folks in HF.

As an aside, one of the reasons why morphine gets a bad rap in general is because people don’t understand it and give too much of it too quickly. How many protocols have you seen that call for dosing every 5 minutes? Well, considering that 5 minutes is the earliest that you’ll start to see the peaks effects of morphine, and that those peak effects can take up to 20 minutes to show themselves completely, you can see how giving it every 5 minutes can cause problems. If you dose it every 5 minutes, then you can conceivably have given three additional doses before you even see the full effects of the first dose on the respiratory drive. When people get into trouble with morphine, I think this is very often why.


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## E tank (Dec 16, 2017)

Remi said:


> ....When people get into trouble with morphine, I think this is very often why.




Most especially in the elderly, critically ill.  A modest dose of any CNS depressant that would be absolutely reasonable in a well, perhaps post operative 75 year old could cause respiratory failure in the same patient if very sick.


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## Tigger (Dec 19, 2017)

RocketMedic said:


> I'm not at all a supporter of morphine or versed in these cases. We want more and better breathing, not "let's get high". I've found its safer to adjust breathing to comfort (to include bvm) than drugging folks into tolerance


When I give benzo's to CPAP patients, I try to use tiny doses to achieve some sort of anxiolytic effect. 1-2mg of Valium is often perfect get people to accept the mask, which is really the first step.


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## Avickmedic (Dec 20, 2017)

NomadicMedic said:


> Well, from your description, it’s CHF. This patient needs NTG and CPAP, not albuterol.


THANK YOU! I thought this was obvious off the bat.


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