Falling O2 sats.....on CPAP?

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.
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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.
 
needsleep said:
Now I don't have that confidence in it. Also, this was my first time ever seeing it used.
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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.
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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.
 
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.
 
@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.
 
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.
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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?
 
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.
 
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.
 
RocketMedic said:
I dunno how deep you went into CHF, but here's the Cliff Notes EMT-B version:
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This is a great (very intuitive) explanation. I may have to steal this...
 
Feel free
 
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.
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I would've liked your post had you used a Dodge Cummins instead of a FORD ;)
 
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.
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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!
 
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?
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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.
 
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?
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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.
 
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.
 
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.
 
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?
 
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.
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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?
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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?
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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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