Cpap

[systemet]

Hi, I've been out of the field for a little bit. It looks like a lot of the services in the area I want to work in are using CPAP. I'm wondering if anyone has any experiences they can share or any good resources for me to learn more about it?

- I understand that it's primarily used in CHF, at pressures up to 10cmH20. How does a cautious (sensible) provider start with CPAP? Do you begin at 2.5 cmH20, wait a few minutes, check the blood pressure, WOB, SpO2, ETCO2, lung sounds, etc. then go to 5cm H20, and so on?

- How rapid is the effect? If I put a relatively sick (but still conscious) CHFer on CPAP, is it going to take 20 minutes to know if I need to increase the pressure?

- If they go hypotensive, presumably the smartest thing is to back off on the CPAP and consider the need for intubation? Or is it better to reach for the dopamine?

- hypotensive CHF, but following commands? Dope to CPAP / nitrates? Where does it fall in the list of priorities?

- Other airway disorders? Asthma, COPD, talc lung etc. I here lower pressures with CPAP here?

- Other than hypotension / pneumothoraces, anything major to watch for?

- Do you just use an inline ETCO2 device to record from the mask while doing CPAP? Because I imagine the NC adaptor would interfere with the mask seal.

Thanks for the help.

 

[jjesusfreak01]

- I understand that it's primarily used in CHF, at pressures up to 10cmH20. How does a cautious (sensible) provider start with CPAP? Do you begin at 2.5 cmH20, wait a few minutes, check the blood pressure, WOB, SpO2, ETCO2, lung sounds, etc. then go to 5cm H20, and so on?

Turn the dial doohickey until the guagey thing is in the green area.

- How rapid is the effect? If I put a relatively sick (but still conscious) CHFer on CPAP, is it going to take 20 minutes to know if I need to increase the pressure?

Very very fast...

- Do you just use an inline ETCO2 device to record from the mask while doing CPAP? Because I imagine the NC adaptor would interfere with the mask seal.

We use NC adapters, and they don't seem to cause a problem with the mask seal.

 

[systemet]

Turn the dial doohickey until the guagey thing is in the green area.


Very very fast...


We use NC adapters, and they don't seem to cause a problem with the mask seal.

Thanks for the rapid feedback.

Any problems you've run across?

 

[usalsfyre]

Hi, I've been out of the field for a little bit. It looks like a lot of the services in the area I want to work in are using CPAP. I'm wondering if anyone has any experiences they can share or any good resources for me to learn more about it?

- I understand that it's primarily used in CHF, at pressures up to 10cmH20. How does a cautious (sensible) provider start with CPAP? Do you begin at 2.5 cmH20, wait a few minutes, check the blood pressure, WOB, SpO2, ETCO2, lung sounds, etc. then go to 5cm H20, and so on?

Really pretty useful in any situation with a high work of breathing refractory to other treatment modalities, Journey and usafmedic will be a lot more helpful in describing those situations. Standard thought around her us start at 5cm and titrate up to till the work of breathing improves.

- How rapid is the effect? If I put a relatively sick (but still conscious) CHFer on CPAP, is it going to take 20 minutes to know if I need to increase the pressure?

Generally you should be titrated up to your max pressure inside a few minutes. If after 5 minutes or so you don't see improvement, your probably looking at intubation and mechanical ventilation.

- If they go hypotensive, presumably the smartest thing is to back off on the CPAP and consider the need for intubation? Or is it better to reach for the dopamine?

Intubation will make the hypotension worse if anything. It's all positive pressure in the chest, whether introduced through spontaneous respiration or mechanical ventilation. Treat with fluid first (fill the tank) then pressors.

- hypotensive CHF, but following commands? Dope to CPAP / nitrates? Where does it fall in the list of priorities?

"Hypotensive CHF" is really cardiogenic shock. What's usually needed is increasing initropy and loosening the vascular bed. Dobutamine does both these, but most services don't have access to it. Follow your local protocol, because my workaround would likely get some people fired.

- Other airway disorders? Asthma, COPD, talc lung etc. I here lower pressures with CPAP here?

Short answer, depends, you may not use it at all. Again, hopefully the experts will chime in here.

- Other than hypotension / pneumothoraces, anything major to watch for?

Vomit. Increased work of breathing in obstructive/restrictive lung disease.

- Do you just use an inline ETCO2 device to record from the mask while doing CPAP? Because I imagine the NC adaptor would interfere with the mask seal.

Thanks for the help.

The NC adapter has never prevented me obtaining a seal. Just keep the KY handy for facial hair.

 

[18G]

CPAP is an awesome modality that works pretty quick at stabilizing and turning patients around. Now of course, there are the sick, sick patients where CPAP is not enough and they will still need to end up being intubated. But the great news is the majority who receive CPAP do not need intubated.

You will see results from CPAP within a few minutes and will know if it is enough to turn your patient around. The pressure to start CPAP at is usually defined in an EMS systems protocols. The general rule is to start at 5cmH20 and do not exceed 10cmH2O. If you start at 5 and see your patient still has a really increased WOB, SpO2 still not improving that much, you can titrate up to 10cmH20 but no higher unless MC orders higher. 2.5cmH2O won't be enough to do anything in an acute illness like PE, asthma/COPD. People have a physiological PEEP of 2-3cmH2O so 5 is the starting point.

Above 10cmH2O there starts to be concern with barotrauma (ie pneumothorax). Also your disease processes like asthma and COPD where there is auto-PEEP (air trapping) taking place you don't want to be going overboard with the CPAP pressure. 5cmH2O is usually enough to help these patients pre-hospital.

As far as priority, CPAP is the priority in severe resp distress. It is an airway modality so if you have a patient with a severely increased WOB, CPAP right away.

You can use a NC line filter... it doesnt interfere with the seal.

Hope this info aided u in better understanding.

 

[Aidey]

- Do you just use an inline ETCO2 device to record from the mask while doing CPAP? Because I imagine the NC adaptor would interfere with the mask seal.

Thanks for the help.

Unless the inline device is specifically designed for CPAPs it won't work. After the patient exhales it is instantly mixed with oxygen, rendering any reading useless. I've never had a problem getting a seal with the NC EtCo2 sensor, however it has been hit or miss if it gets a good reading or not.

 

[systemet]

Unless the inline device is specifically designed for CPAPs it won't work. After the patient exhales it is instantly mixed with oxygen, rendering any reading useless. I've never had a problem getting a seal with the NC EtCo2 sensor, however it has been hit or miss if it gets a good reading or not.

Ha ha. Yeah I'm an idiot! Thanks!

I should have thought of that!

Thank you everyone for all the great help and advice.

usalfyre --- how much fluid are you comfortable giving in this situation? I'd be worried that this would worsen the problem

 

[usalsfyre]

usalafyre --- how much fluid are you comfortable giving in this situation? I'd be worried that this would worsen the problem

Small bolus, 5-10mls a kilo.

Your trying to accomplish two things, decrease systemic vascular resistance(SVR) and stimulate inotropy via Starling's law.

Quick pathophys lesson, despite what I, probably you and most other paramedics educated in the not-too-distant past decompensated heart failure and resultant shock is usually NOT about fluid overload. Simplified, the ventricles inability to clear the pulmonary system causes increased hydrostatic pressure in the lungs, meaning fluid is able to third space into the alveoli. Meanwhile the decreased ventricular output means the vascular system begins to constrict to compensate via various mechanisms (hint for self study, the RAA system is very important in the treatment of CHF). This is why you initially see sky high pressures. The compensation though, leads to higher demand on the myocardium, worsening output, which leads to more vasoconstriction, and so on and so forth. Eventually no amount of compensation can make up for the failing left ventricle, leading to hypotension. Please keep in mind this is massively simplified.

Pharmacologically, it's far more effective to to treat the increased SVR and decreased inotropy than fluid overload. What your hoping to do with fluid is "fill the tank" thereby decreasing SVR and using Starling's law to increase inotropy. This is unlikely to help, but it's worth an initial try. As far as other agents, the strong beta effects of dobutamine make it "the"choice for this, however it's not commonly available and you have to confirm it's classic heart failure and not say, aortic stenosis causing the hypotension. My plan in this case, not having dobutamine is moderate dose dopamine (5-10mcg) used in conjunction with HIGH dose IV nitro (at some point after around 30mcg/min it begins to affect afterload as well). It's not however something every medical director will support, nor is it something everyone has enough experience at titrating meds to do.

CPAP fits into all this by increasing the surface area available for gas exchange and helping to recruit alveoli lost to surfactant washout.

That's my grossly oversimplified CHF/cardiogenic shock rundown. Maybe overkill for what you were asking, but a little background is important in understanding how the tool helps.

 

[18G]

+1 to the above.

 

[systemet]

Quick pathophys lesson, despite what I, probably you and most other paramedics educated in the not-too-distant past decompensated heart failure and resultant shock is usually NOT about fluid overload.

I've read in a few places that many acute CHF patients are actually dehydrated, or at the least, normovolemic. I understand that this, and the common misdiagnosis of pneumonia +/- early ARDS with CHF, and the initial hypotensive effect, are reasons why prehospital lasix has been virtually abandoned.

Simplified, the ventricles inability to clear the pulmonary system causes increased hydrostatic pressure in the lungs, meaning fluid is able to third space into the alveoli.

And this makes sense, and is in line with what I'd learned previously. This is all Starling's law of the capillary.

Meanwhile the decreased ventricular output means the vascular system begins to constrict to compensate via various mechanisms (hint for self study, the RAA system is very important in the treatment of CHF).

Ok. So low RPP, lots of AT-I production, gets converted elsewhere to AT-II, vasoconstriction / HTN, and aldosterone release. So whereas before the idea was aldosterone causing fluid retention is the primary problem, now the thought is AT-II (and obviously, other mediators) is/are causing vasoconstriction / afterload problems?

This is why you initially see sky high pressures. The compensation though, leads to higher demand on the myocardium, worsening output, which leads to more vasoconstriction, and so on and so forth. Eventually no amount of compensation can make up for the failing left ventricle, leading to hypotension. Please keep in mind this is massively simplified.

Cool. Anywhere you'd recommend to read a little more. I'm beginning to realise that my understanding of HTN / CHF needs to improve.

Pharmacologically, it's far more effective to to treat the increased SVR and decreased inotropy than fluid overload. What your hoping to do with fluid is "fill the tank" thereby decreasing SVR and using Starling's law to increase inotropy.

I get that if I can increase renal perfusion, I get less AT-II, less vasoconstriction, less afterload, better EF, less preload, decreased mVO2.

But by adding fluid, aren't I also increasing CVP / venous return, helping the RV push more fluid into the pulmonary circulation, and pushing the LV further to the right on the Frank-Starling curve and worsening the original problem?

This is unlikely to help, but it's worth an initial try. As far as other agents, the strong beta effects of dobutamine make it "the"choice for this, however it's not commonly available and you have to confirm it's classic heart failure and not say, aortic stenosis causing the hypotension. My plan in this case, not having dobutamine is moderate dose dopamine (5-10mcg) used in conjunction with HIGH dose IV nitro (at some point after around 30mcg/min it begins to affect afterload as well). It's not however something every medical director will support, nor is it something everyone has enough experience at titrating meds to do.

How does that work for you without invasive monitoring? How do you r/o Ao stenosis? Is this by cardiac auscultation/hx?

I was a fairly good medic, but I think I'd be a little uncomfortable with that. Perhaps you've had a greater exposure to critical patients than me.

CPAP fits into all this by increasing the surface area available for gas exchange and helping to recruit alveoli lost to surfactant washout.

That's my grossly oversimplified CHF/cardiogenic shock rundown. Maybe overkill for what you were asking, but a little background is important in understanding how the tool helps.

Absolutely. I would love to hear more, and would greatly appreciate any literature suggestions you have.

Thanks for an incredibly helpful post.

 

[usalsfyre]

Ok. So low RPP, lots of AT-I production, gets converted elsewhere to AT-II, vasoconstriction / HTN, and aldosterone release. So whereas before the idea was aldosterone causing fluid retention is the primary problem, now the thought is AT-II (and obviously, other mediators) is/are causing vasoconstriction / afterload problems?

Yep, and why you see ACE inhibitors are now big in decompensated heart failure management.

Cool. Anywhere you'd recommend to read a little more. I'm beginning to realise that my understanding of HTN / CHF needs to improve.

Any critical nursing or physician level textbook. Online www.ccmtutoirals.com has great info pertaining to shock in a more general manner than say CHF specifically.

I get that if I can increase renal perfusion, I get less AT-II, less vasoconstriction, less afterload, better EF, less preload, decreased mVO2.

But by adding fluid, aren't I also increasing CVP / venous return, helping the RV push more fluid into the pulmonary circulation, and pushing the LV further to the right on the Frank-Starling curve and worsening the original problem?

What your hoping is that the LV isn't already off the Frank-Starling chart. It's a bandaid fix if it works at all, and will simply bridge to better therapy. Your also betting the CPAP will help keep the alveolar space somewhat clear while the body responds to increased systemic perfusion. The other important point to remember is that a pressor to a hypovolemic patient will worsen MvO2 way more than fluid so it makes sense to bolus. It's gonna work, or it's not gonna work, hence the very conservative amount, one time. If it makes the patient worse shut it down, even if you don't get the full amount in.

How does that work for you without invasive monitoring? How do you r/o Ao stenosis? Is this by cardiac auscultation/hx?

I was a fairly good medic, but I think I'd be a little uncomfortable with that. Perhaps you've had a greater exposure to critical patients than me.

I wouldn't say I was "comfortable" with it. This is a last ditch kinda thing, and involves lots of hands on the patient. Your looking at titrating to skin signs, mentation, pulses, heart rate, ect. Up on the dopamine till you have a B/P, then up on the NTG till you don't then back up on the dopamine...you get the idea. The goal is to end up with a conscious patient with reasonable pulses and skin signs that don't make you think the SVR is ungodly high, and hopefully you can measure U/O. Invasive monitors just give you concrete numbers to things you can guesstimate off of other vital signs/patient condition. There's actually a trend away from things like PA catheters for this reason. I'm lucky, I had one job in which I got to titrate a lot of meds, so I'm sorta comfortable doing it. It's not for everyone though. Treat to the best of your ability.

Ruling out stenosis is gonna be a function of history mainly, auscultation secondarily.

Absolutely. I would love to hear more, and would greatly appreciate any literature suggestions you have.

Thanks for an incredibly helpful post.

Like I said, look outside the paramedic realm. I've used ASTNAs book and "Critical Care Nursing; A Holistic Approach" extensively, combined with college level A&P text. One day I'm gonna break down and buy Harrison's my kids just keep doing these annoying things like outgrowing clothes . This site is actually a really good resource itself, I learn something new just about daily from it.

No problem, glad all my rambling was useful.