COPD patients

Ediron

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I know there might be a question in my final exam about COPD patients and oxygen. I wanted to clarify it.

So do COPD patients get oxygen via a nasual cannula? NRB? and how many liters per min?

If they are inadequately breathing do we still provide these patients with artificial ventiliation? even if this causes cardiac arrest?
 
In EMS you treat the patient. You treat a COPD patient in EMS no differently than any other patient. O2 via nasal cannula (1-4 LPM) and NRB (10-15 LPM) may be administered based on your protocols.

If the patient breathing is inadequate, you would assist ventilation with a BVM or tube.
 
Never withold oxygen from someone who could potentially benefit from it.

The idea of knocking out a COPDers breathing ability is largely not true as the hypoxic drive only exist in a very small percentage of COPDers and you typically won't know till it's too late.



COPD pts tend to sat in the low 90s, so your goal to providing oxygen to them is aimed at keeping it in tge low 90s. Don't aim for the usual 98-100%.

If protocols allow, try using the pts venturi mask to fine tune it to them.


Provide enough oxygen to maintain adequate oxygenation. I know that sounds vague, but that's the best answer.
 
For an EMT-B test: Always provide all patients with high flow oxygen and be prepared to assist ventilations.

Real clinical answer: Titrate oxygen to keep sat above 90 until the patient can have an ABG done in the hospital. Read up on the oxyhemoglobin disassociation curve. Be prepared to assist ventilations should the patient go into resp failure. COPD patients may also benefit from prehospital administration of bronchodilators and CPAP.
 
You guys all answered my question.
thanx everyone
 
The idea of knocking out a COPDers breathing ability is largely not true as the hypoxic drive only exist in a very small percentage of COPDers and you typically won't know till it's too late.

I don't understand why the real reason to be careful with O2 and COPDers is so difficult for people to understand. It is NOT the hypoxic drive thing which has been disproved ad nauseum.


The problem is acidosis people. COPDers cannot blow off CO2. The more O2 you provide, the higher the partial pressure of carbon dioxide in the system which translates to higher acidosis. You put hurricane force O2 on these people and you can really cause them serious harm. SPO2 in these patients at the best of times is only in the low 90s. If you try and force the sat up higher, you are not helping.
 
I don't understand why the real reason to be careful with O2 and COPDers is so difficult for people to understand. It is NOT the hypoxic drive thing which has been disproved ad nauseum.


The problem is acidosis people. COPDers cannot blow off CO2. The more O2 you provide, the higher the partial pressure of carbon dioxide in the system which translates to higher acidosis. You put hurricane force O2 on these people and you can really cause them serious harm. SPO2 in these patients at the best of times is only in the low 90s. If you try and force the sat up higher, you are not helping.

Not quite. More O2 will increase the PaO2 but only if there is not a significant V/Q mismatch to where the A-a gradient is extremely wide. 100% O2 does not alway raise the PaO2 significantly in sick patients. Thus, it is the PaO2 and not the FiO2 that might raise concern for those few patients which might depend on the hypoxic drive. COPD patients buffer themselves to withstand high PaCO2 and for them to lose that ability to compensate, there are other serious issues going on and respiratory failure may be inevitable.

Some EMT(P)s are often baffled to find we are getting ready for intubation on a patient shortly after arrival that has an SpO2 of >92% on a NRBM but has an A-a gradient of > 400 mmHg. Also, it depends on how close to the curve on the oxyhemoglobin dissociation curve the SpO2 is as there is a very steep drop off between "ok" and really, really bad. Work of breathing is another issue. If the patient is struggling, knocking them out may eventually come either by respiratory failure or with meds for an RSI.

Now, in modern day, medicine has been leaning toward two other theories as explanation with the most popular being V/Q mismatch secondary to reversal of pulmonary vasoconstriction. This can give rise to the PaCO2.

Good articles:


http://www.idasrc.org/1

http://home.pacbell.net/whitnack/The_Death_of_the_Hypoxic_Drive_Theory.htm
 
As usual, good work Vent. The first link is not working but the second was very good. I do remember getting a patient in distress, with O2 sats around 78%. I applied 15lpm via non-rebreather. ED RN was very concerned. "How long are you going to give that much O2?" she asked me. I said "until I can get these sats to an acceptable level and I see some improvement in her work of breathing" I answered.

ABGs were drawn at that point, and patient had PCO2 of 68. O2 was immediately turned down and 20 minutes later, a repeat ABG was drawn.

I felt really really bad, because I figured it was my treatment that resulted in the high PCO2 and the need for an additional painful procedure (and it hurt) on the patient.

I am going to give very serious consideration to RT education. My meat grinder 911 transport job is starting to wear thin and I hate not knowing what I need to know to really help. You have been a real inspiration and I am thinking more and more of following in your footsteps.
(although you can always deny it was your fault.. ;) )
 
Don't beat yourself up Kaisu, hypoxia needs treating, it won't fix your pco2, but that is less important for us pre hospital folks than po2. No one should have an spo2 in the 70's on supplemental o2, so I would say you did fine.

As for following in Vent's footsteps, good on you. She is passionate about what she does and having a greater understanding of respiratory patho can only make you a better clinician.
 
As usual, good work Vent. The first link is not working but the second was very good. I do remember getting a patient in distress, with O2 sats around 78%. I applied 15lpm via non-rebreather. ED RN was very concerned. "How long are you going to give that much O2?" she asked me. I said "until I can get these sats to an acceptable level and I see some improvement in her work of breathing" I answered.

ABGs were drawn at that point, and patient had PCO2 of 68. O2 was immediately turned down and 20 minutes later, a repeat ABG was drawn.

I felt really really bad, because I figured it was my treatment that resulted in the high PCO2 and the need for an additional painful procedure (and it hurt) on the patient.

For some patients, if it is purely a high CO2 problem from something like hypoventilation I can get them to respond after using a BVM for a few minutes. This is especially true for patients with chronic hypoventilation syndrome or conditions such as MS, MD and ALS that sometimes forget to use their BiPAP when sleeping. However, if there is a condition that is impairing gas exchange with V/Q mismatching or where the patient is fatiqued, they may need a ventilator to assist. Also, if the patient is acidotic due to other metabolic conditions to where they no longer can buffer their "normal PaCO2", mechanical ventilation may also be a necessity. If a COPD patient tells me "I'm tired" and that they have been fighting to breathe for a couple of days, I know their rising PaCO2 will probably happen regardless of what intervention I do especially with the O2. And yes, the O2 may cause increased PaCO2 as explained by the reversal of pulmonary vasoconstriction but usually the COPD patient is able to compensate very well if they are not fatiqued. Patients tell me they run their O2 on the highest level on their home O2 concentrators althougth that may only be 5 or 6 liters and giving the equivalent of 3 depending on the machine and maintenance. But even in the hospital I will find them blasting the wall O2 because they are enjoying what extra PaO2 can do. Also, in pulmonary rehab or physical therapy, we'll titrate the O2 up to keep the SpO2 at a decent level.


I am going to give very serious consideration to RT education. My meat grinder 911 transport job is starting to wear thin and I hate not knowing what I need to know to really help. You have been a real inspiration and I am thinking more and more of following in your footsteps.
(although you can always deny it was your fault.. ;) )

As you've probably read my posts before, doing a specialty healthcare takes passion. I loved to intubate when starting out as a Paramedic and was well respected in the field for being really good at it although, most Paramedics from the 70s and 80s were quite good and very seious about what they did. I paid attention to the airway people in the hospitals and on CCTs regardless of their title (RRT, MD, RN, NP) and realized I had much to learn. I also felt helpless when field treatments didn't break an asthma attack as the text book made it seem like such an easy treatment. Even with an ETI in place I learned how difficult an airway can be to manage with some disease processes. When I started learning more about hemodynamics I get another look at CHF and pulmonary hypertension. Also, when I first started EMS in 1978, saving 26 week gestation babies was still quite a challenge. By the time I finished my RT in the mid 80s, saving 23 weekers was becoming a reality. The technology and meds to support their cardiopulmonary systems was absolutely fascinating. In RT school I also found out how much I had to learn about intubation even though I was so incredibly awesome at it in the field.

Now it is an incredible experience and challenge to be a part of an ICU team that tries everything possible to save patients with severe ARDS such as in trauma and now H1N1. The asthmatic patient is another extremely challenging patient once they end up on a ventilator. It is really a good (and sometimes frustrating) feeling when the team looks at you when a difficult patient is not responding to all the therapy being given and ask "is there something else?" or "are we missing something?" Occasionally we might take a run at something totally unconventional and see a turn around. But of course, the RN will also have to be well versed in what will be happening when we switch modes and may have to titrate 6 different drips quickly.

The other aspects is the teaching. Again, you have to be passionate to get across your message sometimes. We have seen better compliance with the pulmonary patients now that we have RRTs who are Asthma and COPD educators working in the ED. Too often a patient is just handed an inhaler and a piece of paper with generic instructions. Now they get a few minutes of RT (billable) time to personalize their instructions.

Rehab is another great specialty and it can be either in Pulmonary Rehab to improve the quality of life for patients with chronic lung problems or in Acute Rehab to get patients with TBIs or SCIs back into their life even if it will not be the same one they knew.

Nurses can of course specialize but often their other duties take precedence over the detailed work of the specialty. So again, I advise anyone who is considering another career to find something that they can be passionate about. I advise all who do routine transfers to various hospital and outpatient services to pay attention and interact with the professionals there. I have known several EMTs and Paramedics who became Physical Therapists with a doctorate degree. They happened to see the workout area and what patients with incredible disabilities were able to do which made their own routine at Gold's look wimpy. There are many professions out there that can compliment the Paramedic and one does not have to always give up one to become the other. After 30 years in EMS I may still have another 20 as an RRT.

Kaisu, you have also seen some of the impressive posts on the other forum from an RN who went back to school for RT. I think RT school will compliment what he does as an RN even if he doesn't work as an RT. His posts show that he has gotten the grasp of now knowing how much more there is to any area of medicine just as yours have over the past couple of years.
 
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