Jump to content

NRB & COPD your input please

Posted

Specializes in Med Surg/Tele/ER. Has 7 years experience.

I had a pt come in the other night severe resp. distress. We had little hx on the pt at the time except COPDer, and he could not talk (working to breathe). He was diaphoretic, rr 30+ guppy breathing, tachy,lethargic. Sats with good wave form 70%. Lungs sounded like crap. EMS had him on 4l nc.

RT was there took him off oxygen to get room air ABG, then back on 4l. During this sats dropping rapidly down to 60% and they were not coming up....rr increasing along with hr.

I wanted to put him on a NRB, another nurse said no he's a retainer.....waht are you thinking??? I was a little upset with this.....my response was so we let him code & then do something? My thinking if you need oxygen you need oxygen.... treat what you see in front of you. His ABG ph 7.2, PCO2 60, HCO3 30.

Just wondering how you all would respond to a pt like this?

btw...I posted this in pulmonary also to gain more feedback

I will attempt to explain this. I am sure someone else can do better than me. Ppl with COPD retain CO2. Their drive to breathe is oxygen whereas our drive to breathe is CO2. If you fix the oxygen problem then they will not have a drive to breathe anymore. That's why ppl with COPD, usually the MD writes to keep O2 sats 88-92%. That is usually normal for the pt.

Now to add to your question. If you put more oxygen on him just to get O2 sats 88-92% and no higher. Would that have been ok? Did this pt end up intubated?

Hope this helps a little until someone can explain it a little better. :)

crb613, BSN, RN

Specializes in Med Surg/Tele/ER. Has 7 years experience.

I agree to keep sats 88-92% would probally be normal....but 60%? I may be confused on this but it is my understanding that not all people with copd are retainers.....and no he was not intubated BIPAP was working when I left. Thanks for your reply.

Sorry all, this hypoxic drive theory is a scarecrow that nursing instructors use to frighten their students. If somebody needs oxygen, give them oxygen. With the ABG stated, this patient is in failure and will most likely require intubation.

highlandlass1592, BSN, RN

Specializes in Critical Care. Has 13 years experience.

That's correct, not all COPD'ers are retainers. You didn't state what the PO2 on the ABG was, but CO2 was very high and he was retaining. This might be the kind of patient you allow to have a higher CO2 level, which may be in the say 50's. Using Bipap is like using a recruitment manuever for an inutbated patient, opens the alveoli to get a better oxygen exchanged. (Positive pressure)

Now I don't know a NRB would be the way to go. Honestly, we have special flow meters at our facility where we can use what's called a "high flow" mask and I've found it works MUCH better than a NRB. This set up uses humidified oxygen with this special flow meter and mask; it actually delivers a higher oxygen concentration than a NRB...and as the oxygen is moist, can help a patient mobilize secretions. However, if a NRB is what you have, it's what you use. I definitely would NOT have left him on 4L via NC, could have tried a venti-mask if the Bipap wasn't an option.

What would have also been important would have been to figure out what was causing the lungs to sound "like crap". Fluid overload due to heart failure? Pneumonia? The hypoxia is the symptom, if possible you wanted to try to find the cause of the problem. On our telemetery floor, we can't initiate Bipap..per RT protocol, they have to go to ICU if no documented sleep study. The great thing in the ICU is they can do Bipap off the vent...same set-up as when someone's intubated, just has the Bipap mask attached instead of hooking up to an ET tube. That way, if the Bipap doesn't work, they just tube them and use the same vent. Gotta love these newer vents, so many more options!

So anyway, I hope this gives you some more ideas of options out that. As to your point that "were you supposed to wait for this guy to code?", absolutely you treat this pt. And honestly, if you did have to intubate this pt due to him not improving with other interventions, this is probably the type of pt who would code as soon as he was tubed...I've seen it happen a lot. You get the oxygen problem fixed, they are still acidotic as heck and then lose a pressure promptly followed by a pulse. So, I have a tendency to have the crash cart nearby. You're usually gonna need it. Hope some of this helps.

There is a lot more to the ABG then just a few numbers. What was the PaO2 and A-a gradient? What was the base deficit? Lactate? Anion gap? Those will give a clue about the events leading up to the present situation.

Most patients that fall into the category of "COPD" are not retainers. Either way, you treat hypoxia especially when a patient is this symptomatic. The hypoxic drive has been disputed for over 30 years and it is now thought to be the pulmonary vasoconstriction response to high FiO2 that causes the rise in PaCO2. If it is significant enough to cause an immediate need for intubation, then the patient was heading that way already. Long term use of a higher FiO2 can influence the patient's PaCO2 retention but in the ED, this will probably not be an issue.

BiPAP splints the airways and also promotes fluid redistribution for patient who may have a CHF component or for cor pulmonale. Cor Pulmonale itself is an interesting factor.

Now I don't know a NRB would be the way to go. Honestly, we have special flow meters at our facility where we can use what's called a "high flow" mask and I've found it works MUCH better than a NRB.

The reasoning behind this is that the NRB is not a high flow device. It is actually a low flow device because it limits the amount of flow a patient can receive. To be clasisified as a high flow device it must be able to meet both the patient's inspiratory flow demand and total minute volume. Patients in respiratory distress can require a minute volume of over 20 liters. The NRB mask is a device that is limiting with a set flow. A venturi device which is probably what the high flow system you are descibing is based, will enable a total flow of over 40 liters/minute and probably more. You may have seen some RTs rig up two aerosol flow devices in attempt to gain more flow and a consistent FiO2. If the patient can acheive and adequate flow for a stable FiO2, the FiO2 might be lowered.

Fluid overload due to heart failure? Pneumonia? The hypoxia is the symptom, if possible you wanted to try to find the cause of the problem. On our telemetery floor, we can't initiate Bipap..per RT protocol, they have to go to ICU if no documented sleep study.

BiPAP for sleep apnea and that for an acute situation are two different things. Even if the patient has a documented sleep study, when something acute arises, this patient needs more monitoring. The setting for their home sleep machine was designed for a normal night's sleep and not treating unknown situations. It is lucky your RTs have specifically spelled out their protocols because some places don't and then the RNs end up with a very hgh acuity patient.

Edited by GreyGull

There is a difference between a COPDer and COPDer who is in resp. distress. If they are hypoxic and in distress give them oxygen.

We tend to place our COPDers on a venti/venturi instead of a NRB.

SummitRN, BSN, RN

Specializes in ICU + Infection Prevention. Has 8 years experience.

Removing the hypoxic drive in a COPD pt by delivering high ppO2 is something that occurs CHRONICALLY in some COPD pts. It should never stop you from giving high flow O2 to an acutely hypoxic patient in order to stabilize them!

It should never stop you from giving high flow O2 to an acutely hypoxic patient in order to stabilize them!

Or at least a NRB mask or increasing the flow of the NC or whatever other low flow device you might be using if a high flow device is not available.

crb613, BSN, RN

Specializes in Med Surg/Tele/ER. Has 7 years experience.

Thanks to all....that is the way I was thinking. As to the rest of the ABG I dont remember...those were the numbers that stuck in my head, and he did have CHF. Thanks again!

casi, ASN, RN

Specializes in LTC. Has 3 years experience.

I'd say slap the NRB on him until RT can set up the bi-pap. Letting someone hang out with O2Sats of 70 probably isn't that helpful for the patient.

FlyingScot, RN

Specializes in Peds/Neo CCT,Flight, ER, Hem/Onc. Has 28 years experience.

There is a big difference between chronic CO2 retainers and COPDers with respiratory failure. When I looked at the ABG I saw respiratory acidosis and hypercarbia which indicates respiratory failure not chronic CO2 retention. Patients with chronic CO2 retention are usually not so severely acidotic. They may have slightly lower pH's and slightly increased HC03 (compensatory) but not down to 7.2. In addition they are not usually in severe respiratory distress. IMO an NRB would be an acceptable stopgap measure while equipment is being set up for more intense respiratory support. If I had a venti handy I would probably grab that first but only if I had it really handy. I wish nursing schools would stop teaching the "limit O2 with COPDers" crap. It really muddies up their emergency care.

canoehead, BSN, RN

Specializes in ER. Has 30 years experience.

I'd stat page RT, and a doc, and put on the NRB. If he loses conciousness and respiratory drive I can still bag him.

I have been waiting for a consult with a COPD pt and found he would get less responsive when I put the O2 on needed to keep sats above 90%, but he started having runs of vtach when I allowed the sats to go any lower. That was a long 15 minutes.

RT was there took him off oxygen to get room air ABG, then back on 4l. During this sats dropping rapidly down to 60% and they were not coming up....rr increasing along with hr.

I am going to elaborate a little more on this.

One of the few and probably the ONLY time you ever need a room air ABG is when you are qualifying someone for home oxygen near the end of their hospital stay after all other acute problems are resolved and that is only if the insurance insists that an SpO2 is not adequate. If a physician can not tell whether a patient is in distress by an assessment or by the A-a gradient from an ABG drawn after some type of treatment is done to alleviate the patient's distress......the rest of what I have to say is not suitable for print on a public forum. If the physician sees the patient is in distress, why the heck would he/she want to cause them more distress by removing the patient from O2 and doing a painful arterial sick?

Patients have great coping mechanisms...until they tire and crash. ABGs do not take into consideration the patient's appearance and if the patient's ABG came back normal, what was the physician going to do? Discharge him or declare he needs no O2 or assisted breathing? I've seen physicians delay treatment because of a "good ABG" only to have the patient code 10 minutes later and the sad thing with each situation was that the patient's initial presentation screamed "code". I've also heard "good ABG" results called to the physician without stressing the physical appearance. It is too bad this RT's time had to be spent inflicting more pain and increasing O2 demand on an already distressed cardiovascular system instead of providing relief to the patient by way of more O2 and/or BiPAP.

Besides home O2 qualification, another time which might call for a room air ABG would be for a shunt study done on some high risk surgical patient pre-op. But, the patients are not in acute respiratory distress when this is done since it is a lengthy process which requires full non distracted cooperation from the patient. Other situations might be for acid-base problems but the breathing part should be taken care of also. One more exception might be on a borderline 1 or 2 L NC to get a baseline CYA ABG in the ED for a discision to discharge but the patient is not struggling to breathe.

I wish nursing schools would stop teaching the "limit O2 with COPDers" crap. It really muddies up their emergency care.

A couple of the newer textbooks are now careful in their wording about this and do mention that just "2 L NC" is not always enough for emergent situations.

WonderRN

Specializes in ED. Has 5 years experience.

I know many have already weighed in on this issue, but I'll give my 2 cents....

NRB for all hypoxic patients regardless of history. They need oxygen first and foremost, you can fix the acidosis later. Many COPDers live at PaCO2 of 60 anyways.

I would have called for the BiPap stat and had intubation equipment readily available.

I agree that the whole NC only for COPDers is a VERY dangerous thing they are teaching. It does not apply to emergent situations.

No need to take the patient off of 02 for an ABG. NEVER have I seen this done.

Also would have like to know what the Pa02 was. I'm sure it was extremely low considering the Sp02 was in the toilet already.

ZippyGBR, BSN, RN

Specializes in Spinal Cord injuries, Emergency+EMS.

i will attempt to explain this. i am sure someone else can do better than me. someppl with copd retain co2. their drive to breathe is hypoxaemia whereasnormal drive to breathe is reduced blood ph from dissolved co2.

if you create an oxygen problemthrough poor monitoring and injudicious oxygen adminstration then they will not have a drive to breathe anymore. that's why ppl with copd, usually the md writes to keep o2 sats 88-92%. that is usually normal for the pt.

now to add to your question. if you put more oxygen on him just to get o2 sats 88-92% and no higher. would that have been ok? did this pt end up intubated?

hope this helps a little until someone can explain it a little better. :)

i've fixed some of the dangerous statements

the fact is that if someone's po2 is dangerously low they need oxygen hypoxaemia will kill before hypercapnia

someone in this much respiratory distress is going to be closely monitored and may well end up needing bipap or if clinically suitable intubation

also interpreting the blood gas also depends on base excess etc

you also need to consider how effectively the patient is breathing from an actual mechanical gas flow point of view and thinking aobut the psychological approaches to improving ventilation as well ( coaching, temperature, 'breeze' )

i'd also agree that the room air abg is only really relative in determining whether some one should have long term o2 therapy. in an emergency situation it makes very little difference and may well increase hypoxaemia.

Pixie.RN, MSN, RN, EMT-P

Specializes in EMS, ED, Trauma, CNE, CEN, CPEN, TCRN. Has 12 years experience.

No need to take the patient off of 02 for an ABG. NEVER have I seen this done.

Yep ... on the form we send to the lab with the ABG, we note what kind of O2 we have them on (NRB, NC, BiPAP, Vent + settings, etc.), and they adjust accordingly.

Yep ... on the form we send to the lab with the ABG, we note what kind of O2 we have them on (NRB, NC, BiPAP, Vent + settings, etc.), and they adjust accordingly.

If you work around intense pulmonary patients such as in the ED or ICU, you should be able to do a few simple pulmonary calculations yourself or at least understand what they mean. The only thing the lab will do, maybe, is print the A-a gradient, O2 content and hopefully give a measured rather than calculated SaO2. But, you should be familiar with what each means, an understanding of the Alveolar Air Equation and associate the A-a to V/Q mismatching.

If you understand the responses concerning V/Q mismatching, deadspace ventilation, pulmonary vasoconstriction and the Haldane Effect on profoundly hypoxic COPD patients, you won't be taken by surprise and will have more of an explanation why a patient's PaCO2 did rise from a physiological standpoint. The hypoxic drive is still valid but rarely is the situation with the COPD patient in acute respiratory failure because they ARE hypoxic. A NRB mask may give a quick change in the above mentioned factors other than the hypoxic drive and yes, a rise in PaCO2 may be expected. But, to just blame the hypoxic drive shows you are missing the big picture. The PaO2 may also not rise as quickly as the PaCO2. After a patient is placed on a ventilator, the first ABG may show a surprise by having a higher PaCO2 then even the pre-intubation ABG. Did the RT or Physician screw up on the ventilator settings? Probably not. That again goes back to an understanding of all the factors I mentioned in the first sentence of this paragraph.

Some hospitals have started using masks (OxyMask) that can be categorized as high flow and can be titrated from 1 liter up to 30 liters. These are ideal for walking up the patient's SpO2 according to patient AND health care provider's comfort level. They can also stay in place while NT suctioning or NGT placement is being done as well as drinking or taking meds and temp by mouth. You can even give a mouth piece neb with the mask left in place.

I also recommend quality CEUs to update yourself on the latest concepts that the textbooks did not provide a good foundation on or just gave a general "hypoxic drive" explanation.

One excellent seminar is from PESI.

Patient Crisis: Identify the Signs and Symptoms Before the Patient Crashes with Educator Carol Whiteside, MSN, PhD.

I also recommend taking an advanced ABG class. The very simplified course of "look at the pH" left out some very important components that must be considered.

This website gives you an idea about what I mean there is more to the story of ABGs.

http://www.thoracic.org/clinical/critical-care/clinical-education/abgs.php

A little side note: this formula is known as Winter's and is used to calculate normal PaCO2 for a patient so the ventilator settings don't take the PaCO2 down too low. If the PaCO2 is taken down to low and the body no longer compensates for the higher PaCO2, when the patient is extubated the PaCO2 rises quickly, pH falls and the extubation is written off as a "failure" when it may not be the patient who failed but rather those managing the ventilator.

PaCO2 = (1.5 x [HCO3-]) +8