Falling O2 sats.....on CPAP?

[VFlutter]

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).

 

[Carlos Danger]

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.

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.

 

[ThadeusJ]

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.

 

[alsmcq]

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?

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.

 

[NomadicMedic]

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.

 

[needsleep]

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.

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!

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)

 

[RocketMedic]

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

 

[VFlutter]

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

 

[VFlutter]

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.

 

[Carlos Danger]

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.

 

[E tank]

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.

 

[needsleep]

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%?

 

[Colt45]

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.

 

[ThadeusJ]

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.

 

[VFlutter]

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

 

[dumbenoughtostay]

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.

 

[VFlutter]

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.

 

[Carlos Danger]

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.

 

[E tank]

....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.

 

[Tigger]

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.