02 in COPD Patients?

[VentMedic]

Wow, lol-ing at the O2 allergy. Now as far as the risk of respiratory depression with elevated O2 levels and hypoxic drive, what is the reason it can take 1 or more hours for that to take effect? Does it take that long for the ABGs to shift, is hypoxic drive slower to react to a change in ABGs (I personally think that is less likely, as it wouldn't be much of a respiratory drive without the ability to compensate for minute by minute changes like that), or is it something else? Or is it something very basic that I am going to slap myself in the face for not thinking about?

Here is the link to Jeff's page.

http://home.pacbell.net/whitnack/

Whether you agree with all of the literature he sites or not, it does offer an indepth explanation to the various receptors. The powerpoint at the bottom of the page is decent also.

[firedoc5]

An O2 concentrator, depending on make, model and maintenance, may not deliver anywhere near what a flow meter from an O2 tank delivers.

People get hung up on memorizing numbers for O2 delivered for "2 L/min NC" as it to be 28%. That number all depends on the minute volume of the patient. The number 28% is derived from a normal Joe Public breathing at a text book normal rate with a normal tidal volume in no respiratory distress. That is why I find the arguments of "2 or 4 L/min?" so ridiculous in that it shows little understanding of respiratory basics 101 and the equipment.

If a person says they can't breathe...give O2.

If they are blue, give O2.

If the SpO2 is low and you have every reason to believe it is in the ball park give O2.

If they are symptomatic with any signs of increased work of breathing, give O2.

If they are talking to you, they are still ventilating.

The BVM is your friend because if you "knock out their drive" with an extra liter of O2 in the few minutes you are with them, they were going down anyway.

You must take into consideration V/Q mismatching and shunting along with all of the disease processes that are causing a low SpO2 and difficulty breathing. The dx of COPD always skew some from doing an adequate assessment to treat the real problem(s).

A dx of COPD does not mean they are even a CO2 retainer. Less than 5% are. I see that everyday. I may draw 20 ABGs on 20 different "COPD" pts on any given day and see only one that fits the criteria of being a CO2 retainer.

They hypoxic drive has been debated for almost 30 years. Do a literature search or check out the name Jeff Whitnack who has done the search for you on his website.

The only patient for which O2 is used with extreme caution or not used at all (16% may even be used instead) is on an infant with a ductal dependent cardiac anomaly or CHD.

DITTO

In our area we have coal mines. A lot of "black lungers", including the owner of the ambulance service I worked for before getting on the FD. Because of that we were instructed on COPD and SOB's more than what you would in an average EMS system.

And for some reason, we had a lot asthma pt.s it seemed like, including myself. If it wasn't for my Combivent inhaler I wouldn't have had the career I did.

We were all too familiar with knocking out someone's resp. drive, to bag and/ or intubate.

[VentMedic]

[DITTO

In our area we have coal mines. A lot of "black lungers", including the owner of the ambulance service I worked for before getting on the FD. Because of that we were instructed on COPD and SOB's more than what you would in an average EMS system.

And for some reason, we had a lot asthma pt.s it seemed like, including myself. If it wasn't for my Combivent inhaler I wouldn't have had the career I did.

Coal Workers' Pneumoconiosis is a fribrotic and inflammatory process which tend to make it more of a restrictive disease unless there is a smoking or asthma hx that can present as obstructive.

Glad you mentioned Combivent. It was on my list of things to do today for checking to see if it got its stay of execution for at least another year or until 2010.

[Richard B the EMT]

Is quiet short of breath most of the time but he needs to use accessory muscles on excretion.

Uh, on excretion? I hope that we have a really bizarre typo error, here, but could you mean on inspiration, meaning taking a breath, as opposed to someone relieving themselves of fecal matter?

[mobey]

Uh, on excretion? I hope that we have a really bizarre typo error, here, but could you mean on inspiration, meaning taking a breath, as opposed to someone relieving themselves of fecal matter?

Or exertion

[AnthonyM83]

The only patient for which O2 is used with extreme caution or not used at all (16% may even be used instead) is on an infant with a ductal dependent cardiac anomaly or CHD.

Does anyone have any literature saying how quickly they can be affected by O2 in the EMS setting. That and paraquat poisoning (sorry to steer it to these topics)....I can't get any straight info on TIME tables.

[CAPMEDIC-EMWFR]

Here is the link to Jeff's page.

http://home.pacbell.net/whitnack/

Whether you agree with all of the literature he sites or not, it does offer an indepth explanation to the various receptors. The powerpoint at the bottom of the page is decent also.

Thank you, exactly what I was looking for!

[VentMedic]

Does anyone have any literature saying how quickly they can be affected by O2 in the EMS setting. That and paraquat poisoning (sorry to steer it to these topics)....I can't get any straight info on TIME tables.

In the EMS setting? See previous posts.

Every patient is different and it will vary from disease process to process. There is no recipe that says a patient will stop breathing at 1 hour after you give O2. It will also vary as to the active disease process which may be the cause of a patient to fatique which many mistaken for "knocking out the hypoxic drive". If a patient has a bad PNA, other infection or whatever, they will be HYPOXIC and no matter how hard you try with some patients, with even the best technology, they stay hypoxic until they die or get better. Pts with "COPD exacerbations" often have an underlying cause.

The other thing to remember is not all COPDers are CO2 retainers and not all CO2 retainers are COPDers. I get more concerned about those that have a chronic hypoventilcation syndrome or hypoventilation caused by a neuromuscular or CNS disease than I do about the 3 pack a day or 100 pack year cigarette smoker. If you want a fansinating read try Ondine's curse which is congenital central hypoventilation syndrome or CCHS.

[tniuqs]

ED RN: "Any allergies?"

Me/partner: "Oxygen!"

ED RN: *priceless facial expression*

Me: "Don't look at me, your doctor wrote it!"

I had a patient inform me that Dimenhydrinate (marketed under brand names Dramamine, Gravol, and Vertirosan) an antiemetic.

Well apperantly it made him nauseated and puke .... talk about having to turn away and have ones partner step in because your laughing so hard your eyes water.

I think Ventmedic has answered all the major queries, I must agree Hypoxia will kill far faster than acid/base imbalances and in passing COPD is a generalization for a group of pulmonary disorders a "triade"

So ever hear of a drug called Bleomyacin ?

Before one jumps and down laughing at how smart you are, too hard. There are meds out there in the real world that we as EMS providers are really not informed and not covered in most EMS textbooks and where we got this limiting of O2 therapy of a concern fpr Hypoxic Drive (a rarity)

It makes me shake my head with this ongoing misinformation ..... an allergy to O2 not likely, severe side effects or contraindications to oxygen therapy oh yes !

Respiratory failure and pulmonary fibrosis as a late side-effect after chemotherapy-induced by oxygen administration:

Grahmann PR, Brauer M, Hüter L, Sayer H, Neumann R, Braun RK.

Friedrich-Schiller-Universität Jena, Klinik für Innere Medizin I, Kardiologie, Angiologie, Intensivmedizin, Pneumologie und Allergologie/Immunologie. pr.grahmann@med.uni-jena.de

Pulmonary fibrosis (PF) may develop following successful chemotherapy for malignancy, even if such therapy is not combined with radiotherapy. Bleomycin, which is known to induce acute pneumonitis and lung fibrosis, is especially associated with chemotherapy-induced PF, and bleomycin-induced pulmonary fibrosis can occur more than five years after such therapy. Additionally, supplemental oxygen therapy can trigger the onset of pneumonitis and lethal PF in patients who have previously received bleomycin therapy. Careful assessment of lung function via spiroergometry and arterial blood gas analysis during exercise are required if the administration of supplemental oxygen is considered. Two case reports reveal the potential lethal risk of oxygen for patients who have been treated with bleomycin: (1) a patient with successfully resected and treated basal tongue carcinoma and (2) a patient in remission after being treated for non-Hodgkin lymphoma. Single and double lung transplantation is the only therapeutic option for patients with severe, oxygen-induced PF and should be included as an indication for lung transplantation. Early recognition of pulmonary diffusion abnormalities and establishing a risk profile, as well as consequent monitoring of pulmonary function, may help to avoid or at least reduce the risk of PF induced by oxygen therapy when administered to patients who have previously been given bleomycin.

A couple of other links ... but please remember these are quite a rare.

http://www.ncbi.nlm.nih.gov/pubmed/1704473

http://ctec.uwa.edu.au/anaesthesiawa/bleomycin.pdf

cheers

[akroeze]

I had a patient inform me that Dimenhydrinate (marketed under brand names Dramamine, Gravol, and Vertirosan) an antiemetic.

Well apperantly it made him nauseated and puke .... talk about having to turn away and have ones partner step in because your laughing so hard your eyes water.

I don't know why this is so funny. Some people DO have an adverse reaction to Gravol. My moter for one.