CPAP discussion

[croaker260]

Why is CPAP contraindicated in folks with hx of asthma? Just curious.

There is a fear of pneuomothorax secondary to air trapping in COPD and Asthma. This rarely happens, if ever. Now, this is different than the very real concern of pneomo's when the same patient is intubated, or in trauma.

Now, I would add more, but chbare has already done an excellent job especially about stinting open the lower airways and aveoli.

Edited January 15, 2012 by croaker260

[tniuqs]

To fully understand my position please understand this: I transport my patients to a small rural clinic with a few on-call GP's. There is very very little real EBM or even target based medicine go on out here.

Given we are in flu season full force, I have had quite a few of the following patients:

Elderly, Cardiac history, cough for a week or more, febrile, weakness, wheezy/crackly lungs.

Specifically I am talking the critically ill ones here. grey, Sp02 in 70/80's but not hypotensive.

For the most part I diagnose them in pulmonary edema with underlying chest infection.

As of late I have been treating with ventolin, and Nitro and having good results. The problem I am having is as soon as I get to the freaking clinic all treatment stops while the doc's start lasix therapy. There is just not enough time to clear up the edema with Nitro prior to transfer of care.

To be honest I would like to put these people on CPAP, however I have always stayed away from CPAP in suspected pneumonia patients.

Thoughts?

Many .. will have to read all 3 pages so get the gist of this thread, but what device are you using to deliver CPAP ?

Oh ya: try to resist the temptation to derail this thread into a SIRS/SEPSIS thread at least for the first page.

[mobey]

Many .. will have to read all 3 pages so get the gist of this thread, but what device are you using to deliver CPAP ?

Looking forward to that!

Boussignac CPAP. Don't kill the messenger! It is all AHS will let us use.

[tniuqs]

After digesting some of the posts:

Lets discuss this NON INVASIVE part first .. any positive pressure ventilation is invasive to a degree, invasive your reversing all pulmonary mechanics and can affect Right Ventricular Output, just think of a dam in the lungs between the right and left side of the heart .. hence one can drop LV output and drop BP like a stone with higher levels of CPAP / PEEP, in fact in ACLS PEA or relative hypovolemic states can directly be attributed to Dynamic Hyper Inflation. Point being monitor BP as you increase CPAP always.. and look to ETCO2 and Sats .

(ps some patients have not read the pulmonary mechanics books )

1- A most excellent slide presentation BUT I would STRONGLY disagree with the European study, CPAP does increase WOB i.e. forced expiration and increased assessory muscle usage .. try one on for yourself in fact.

2- Yes BI LEVEL support does increase mean airway pressure but not WOB it decreases it with upper level support augmenting / supporting the inspiratory flow, but that's entirely the point (oxygenation is dependant on mean airway pressure) Dr. Neal Finer.

3- CPAP and BILEVEL, NIPPV are used in any modern day ER .. asthma, COPD, CHF, TALC LUNG +++ to stray off the tube.

The problem exists that it can be very clinician dependent in success rate and early application as opposed to late decreases "chewing on the ETT" and as a sidebar "cost efficacy" in ICU and decreased mortality morbidity.

OMG I said PEEP "splint's" terminal airways open mechanically in ICU once in front my Respirologist and 4 residents and got a new one ripped .. apparently the real definition: CPAP / PEEP matches intrinsic PEEP, some COPDers / CHFers (of which its a 50/50 deal as most COPD/CHF are the same critters, its not a matter one is a dog and one is a cat.

4- A big fat fail for AHS in choice of devices on 4 counts, a- the Boussniac is not approved for in-hospital use, b- It uses a huge amount of O2 (controversy in high vs low O2 delivery). c- inconsistent Fi02 this dependant on the Minute Volume of the Patient, d- serious lack of education during inception of a completely new therapy.

5-The one that a friend @ AAA allowed me to bench test does not deliver what it claimed to do .. goggle that POS and look at the Israeli studies a mixed bag of justifications ... you just cant replace a Visions CPAP, PB 840 or an LTV with 50 dollar device.

6- Curiously the ACoP did not have "in attendance a representative" at the AHS meeting of regulatory bodies when the topic of transport ventilation and CPAP was discussed ... WTF over ?

7- The Booooosniac it doest work like a jet turbine engine LMFAO its called the venturi effect, ok enough slamming AHS for their bean counter purchasing department follys.

8- Real CPAPok, better yet BI Level Support IMHO which is an available mode(s) on many new transport ventilators, (and education, sorry dust, my bad ?) this should be the choice for any EMS if they actually wanted to improve the system overall, then you get a bigger bang for the buck OR "buy once, cry once"

[Doczilla]

A few things looking at this thread.

Mobey, I would not diagnose someone like you describe with "pulmonary edema and overlying chest infection". If they are febrile and short of breath and have crackles and/or wheezes on exam, my working diagnosis is pneumonia. I would not give this patient NTG (or lasix), as that would be asking for trouble. Bronchodilators, antibiotics, and fluids. Not to say it doesn't happen, but the diagnosis of pneumonia AND CHF is reached only after x-ray, labs, and observing response to therapy.

CPAP is fine for patients with pneumonia. Because these patients tend to be volume depleted, they have decreased preload already, and could therefore develop hypotension with the CPAP. That's fine, since we can treat that with IV fluids to increase preload. This is why NTG would also be dangerous in these patients. The CPAP will decrease work of breathing and increase alveolar recruitment and increase oxygenation.

There is quite a bit of literature on CPAP in the prehospital and in-hospital setting, which shows clear benefit in CHF, some benefit in pneumonia and mixed causes of respiratory failure, and modest benefit in COPD.

FHubble MW, Richards ME, Jarvis R, Millikan T, Young D. Effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema. Prehospital Emergency Care. 2006 Oct-Dec;10(4):430-9.

FPark M, Sangean MC, Volpe Mde S, Feltrim MI, Nozawa E, Leite PF, Passos Amato MB, Lorenzi-Filho G. Randomized, prospective trial of oxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema. Crit Care Med. 2004 Dec;32 (12):2407-15.

FRam FS, Picot J, Lightowler J: Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2004; CD004104

FBrochard L, Mancebo J, Wysocki M, et al: Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med 1995 Sep 28; 333(13): 817-22

FKeenan SP, Sinuff T, Cook DJ: Does noninvasive positive pressure ventilation improve outcome in acute hypoxemic respiratory failure? A systematic review. Crit Care Med 2004 Dec; 32(12): 2516-23

FDelclaux C, L'Her E, Alberti C, Mancebo J, Abroug F, Conti G, Guerin C, Schortgen F, Lefort Y, Antonelli M, Lepage E, Lemaire F, Brochard L. Treatment of acute hypoxemic nonhypercapnic respiratory insufficiency with continuous positive airway pressure delivered by a face mask: A randomized controlled trial. JAMA. 2000 Nov 8;284(18):2352-60.

FCollins S, Mielniczuk L, Whittingham H, et al: The use of noninvasive ventilation in emergency department patients with acute cardiogenic pulmonary edema: A systematic review. Annals of Emergency Medicine. 48(3):260-269, 2006

FHonrubia T, Garcia Lopez FJ, Franco N: Noninvasive vs conventional mechanical ventilation in acute respiratory failure: a multicenter, randomized controlled trial. Chest 2005 Dec; 128(6): 3916-24

FKeenan SP, Sinuff T, Cook DJ: Does noninvasive positive pressure ventilation improve outcome in acute hypoxemic respiratory failure? A systematic review. Crit Care Med 2004 Dec; 32(12): 2516-23

FMasip J, Roque M, Sanchez B: Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA 2005 Dec 28; 294(24): 3124-30

FKallio T, Kuisma M, et al. The use of prehospital continuous positive airway pressure treatment in presumed acute severe pulmonary edema. Prehosp Emerg Care 7:209-213, 2003.

FKosowsky J, Storrow A, Carleton S. Continuous and bilevel positive airway pressure in the treatment of acute cardiogenic pulmonary edema. Am J Emerg Med 18:91-95, 2000.

Dallas has been using CPAP for a while now, and have approximately 1000 CPAP uses per year. They estimate that they prevent approximately 300 intubations per year altogether. Calculating the cost difference between an intubated patient and a nonintubated patient, which is about $100,000, they estimate that they save the healthcare system $30M per year.

In our system in Ohio at least, most of the patients getting CPAP are non-payers, so it's a significant savings if they can avoid being tubed.

There is some literature calling into question the use of lasix in the prehospital environment. Acute CHF can be a difficult diagnosis to make without ancillary studies.

Of 144 patients given lasix by EMS, 42% did not have CHF, 17% had pneumonia, dehydration, or sepsis. Of the 9 patients who died without CHF, 7 got lasix. So by giving it, we are only potentially helping 58% of patients, and outright harming 17%. This has led several systems to pull lasix altogether.

Jaronik J, Mikkelson P, Fales W, Overton DT. Evaluation of prehospital use of furosemide in patients with respiratory distress. Prehosp Emerg Care. 2006 Apr-Jun;10(2):194-7.

'zilla

[mobey]

Thank you Squint for yet another great post regarding pulmonary physiology and the effects we have on it at the Paramedic level without going "over my head".

Doczilla: That is quite possibly one of the most informative posts I have seen in a long time. Reminds me of the 'ol City, and I think posts like that have been lacking here over the past few years.

Back to the thread:

I have been taking into consideration these pt's have a hypovolemia, as I do with all patients who have been tachypnic for any amount of time.

I will admit right now that I do have a very hard time distinguishing pure pneumonia, and pneumonia with CHF exacurbation in the setting of a Heart failure patient whom is febrile with crackles/wheezes. Clearly I would not be using NTG on a pure pneumonia patient on purpose.

I fully understand I was missing a link in my thinking, and I will spell it out so no one else misses it.

History of "unwell" with cough/fever/SOB presenting with crackles/wheezes = Presumed pneumonia

Pneumonia = Volume depletion

Volume depletion= decreased preaload & therefore afterload (unless some other vascular issue is causing constriction)

Decreased preload/afterload = No CHF exacubation.

One of my biggest concerns in CPAP use in pneumonia is clearing secretions and (for lack of better words) "Solidifying" inflammitory exudate or pus causing further complications. is this a real issue? or just something I made up?

Squint, you may be pleased to know that whether i intubate or apply CPAP, I always give a fluid bolus of some size as I have effectively removed the "bellows pump" from the right heart.