VirginiaEMT
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Has anyone here ever witnessed high-flow 02 knocking out a person's hypoxic drive?
HYPOXIC DRIVE, real of urban legend?
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DrankTheKoolaid
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Urban legend
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No,
I have had my share of partners and RNs upset with me though claiming I was "killing" the pt.
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DrankTheKoolaid
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While that is true Ven, that was not his question. He asked if anyone has seen it.
While that is true Ven, that was not his question. He asked if anyone has seen it.
A lack of understanding the relationship between two different concepts, hypoxic drive and rising CO2, is more the problem. Hypercapnia and the delivery of oxygen, including the correct device, is usually the issue. The hypoxic drive has its place but rarely in emergent situations. The hypoxic drive theory which is so often misquoted came about before sophisticated diagnostic equipment validated more reasonable theories.
Very few COPD patients are CO2 retainers to where this is a concern on a daily basis. Patients with hypoventilatory diseases may be more of a concern. But, understanding PaCO2 and its relationship to increased or decreased ventilatory effort is the issue. Correcting or supporting PaCO2 with early identification of the problem is most of the battle. This is one of the reasons CPAP/BiPAP has been around for a long time in the hospitals as well as home care.
High flow is also not a problem and TRUE high flow is recommended to meet inspiratory demands of the patient. True high flow can deliver as little as 24% oxygen but at very high liter flows. Low flow devices such as a nonrebreather mask can become part of the problem with increased work of breathing and inadequate inspriatory flow regardless of what is taught about the bag. At high inspiratory demand per the patient, the FiO2 value is diluted by air mixed from outside of the mask so the EMT textbook value is not delivered. Most EMS protocols are written using a nonrebreather since that device will ensure an FiO2 greater than 25% will be delivered. With nasal cannulas, the FiO2 could be very, very low even at 6 liters. None these devices are truly effective in distress.
High FiO2 becomes a problem if the PaO2 is also very high. Some COPD patients are not able to increase their PaO2 to a high level even with an FiO2 of 1.0 being delivered by a true high flow device or a ventilator. SpO2 often clouds the judgement for correct decision making when they do not understand the relationship between carrying compacity, shifts in the oxyheomglobin curve or saturation points vs PaO2, disease processes, A-a gradient, V/Q mismatching and hyperoxygenation.
This article explains most of the concepts behind oxygen and hypercapnia.
http://cmbi.bjmu.edu.cn/uptodate/cr...se of oxygen in patients with hypercapnia.htm
That being said, I have seen hypercapnia cause patients to cease to breathe.
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I mentioned in another thread, I was personally skeptical about this in med school.
So, I spent 2 weeks on a pulmonology ward and asked specifically about it.
I was educated and shown these people.
It is not as dramatic as EMS providers make it out to be and truthfully requires diagnositcs not available to EMS in most places so it will not change EMS treatment.
I suspect somebody had one of these patients once upon a time and just like the stories of people walking around with spinal injuries, when way way out of control about it and things went viral.
For example, I have seen 2 cases of M.E.L.A.S. in my career. But it doesn't mean I go around suspecting it in every ped I see.
Pulmonology has the answers... Ask them.
You should not need any special diagnostic equipment to recognize a decrease in ventilatory effort. The treatment is the same regardless of the cause. You assist ventilations. If the patient needs oxygen, you should be competent enough to recognize this and educated enough to anticipate any changes in respiratory effort by either disease process or fatique.
The hypoxic ventilatory drive for EMS and nursing education is usually only mentioned as it related to COPD which is where the controverey has arisen. But, some don't learn the difference between the "theory" of the hypoxic drive and what it actually is and how it pertains to disease processes which include more than just COPD.
Anyone who has long term chronic hypoxemia can have a blunted hypoxic ventilatory drive. Those who live in high altitiudes should know this.
People with congenital heart disease, inherited anomalies to the CNS and even elite athletes can have a decreased hypoxic ventilatory drive.
There are more physicians than just Pulmonologists who know about hypoxic ventilatory drive. Two weeks on a pulmonary ward may only give you a very limited view of it.
The hypoxic ventilatory drive for EMS and nursing education is usually only mentioned as it related to COPD which is where the controverey has arisen. But, some don't learn the difference between the "theory" of the hypoxic drive and what it actually is and how it pertains to disease processes which include more than just COPD.
Anyone who has long term chronic hypoxemia can have a blunted hypoxic ventilatory drive. Those who live in high altitiudes should know this.
People with congenital heart disease, inherited anomalies to the CNS and even elite athletes can have a decreased hypoxic ventilatory drive.
There are more physicians than just Pulmonologists who know about hypoxic ventilatory drive. Two weeks on a pulmonary ward may only give you a very limited view of it.
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MSDeltaFlt
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Now that I have silenced yet another ventmedic personality with the ignore list...
The treatment of various causes of retention is usually done by the respective specialty.
I asked pulmo about hypoxic drive in COPD and they were kind enough to help me. (Imagine that, going to the experts on a given disease)
One ofthe first questions I asked was how to distinguish it clinicaly from CHF.
The answer? They were admitted to cardio and then transferred to us asthe primary cause was determined to be COPD.
Imagine treating COPD on a pulmonary ward instead of cardiac...?
I would also assume that if CHF was the principle cause, cardio would have kept the patients. They have toold like esophageal echo and everyone seems to like ABGs. (neither of which I have ever seen on a an EMS unit)
Another of my outstanding questions was"what if a person has both?"
The answer: "Admit to one and consult the other."
One of the things I really like about intensive medicine is that it is all systems simultaneously. But the ventilation is rather a simple part of it. Probably why the US has ancillary staff do it.
The treatment of various causes of retention is usually done by the respective specialty.
I asked pulmo about hypoxic drive in COPD and they were kind enough to help me. (Imagine that, going to the experts on a given disease)
One ofthe first questions I asked was how to distinguish it clinicaly from CHF.
The answer? They were admitted to cardio and then transferred to us asthe primary cause was determined to be COPD.
Imagine treating COPD on a pulmonary ward instead of cardiac...?
I would also assume that if CHF was the principle cause, cardio would have kept the patients. They have toold like esophageal echo and everyone seems to like ABGs. (neither of which I have ever seen on a an EMS unit)
Another of my outstanding questions was"what if a person has both?"
The answer: "Admit to one and consult the other."
One of the things I really like about intensive medicine is that it is all systems simultaneously. But the ventilation is rather a simple part of it. Probably why the US has ancillary staff do it.
I think you need to listen more closely to the pulmonologist to gain a better understanding of the hypoxic ventilatory drive.
Yes, you can find iSTATs on a few EMS units if they also do CCT but proving hypercapia proves what? You should be able to recognize the effects of hypercapnia or decreased ventilatory effort without waiting for ABG results.
I do suggest the OP do a little research beyond just the COPD and "theory" aspect. The science behind the hypoxic drive is fascinating and does relate to many things besides just COPD. Altitude medicine is a great topic also in relation to it and so is sports medicine.
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Pickwickian Syndrome and Obesity Hypoventilation syndrome are definitely things to look up also. One thing can lead to another which causes another and cascades into a very complex broken system whch the body tries to compensate for.
Fixed that for you. Not sure what I would do if some specialist (medical or surgical) ever actually admitted their own patient.
They don't?
Here, EM is not a specialty, technically the EDs are split and ortho runs the surgical ED with various surgeons covering. Anesthesia runs the medical side, but on any given day it could be any nonsurgical physician.
They admit patients to their service all the time...Particularly if it is an interesting case.
mycrofft
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Never seen it personally, but had a couple patients as a nursing student who were moved off my ward and it was brought up.
The short time EMS should be handling such a pt (other than an overland transfer from like Cherry County NE to Omaha Methodist) should not furnish the time necessary for this to rear its ugly head.
The short time EMS should be handling such a pt (other than an overland transfer from like Cherry County NE to Omaha Methodist) should not furnish the time necessary for this to rear its ugly head.
Non-ICU players either get admitted to medicine or gen. surg and any sub-specialist will simply consult (way less work this way). ICU is a little different. If it is a closed unit an intensivist will admit/manage, if it is open unit god knows who will admit and every sub-specialist under the sun will consult.
According to this there is a subset of COPD pts with CO2 retention who do have hypoxic drive.
It further goes on to say say a trial of higher concentration oxygen needs to be tiatred to a specfic o2 range.
Then it states several times about the myth of hypoxic drive being a myth even after suggesting the pt be weaned to a more appropriate oxygen level. based on PO2. (which sounds remarkably like needing special equipment to determine, like an ABG)
"The truth is that less than 25 percent of chronic CO2 retainers use the hypoxic drive to breathe, (4) and it's not as significant as once believed. Of patients who present to hospitals in respiratory distress, half will have reversible CO2 retention, and half will be chronic CO2 retainers. (5)"
I don't think anyone suggests these patientswill suddenly stop breathing and instantly die.
This kind of thing is exactly why physicins do not do not accept nonphysician opinion.
Perhaps these ancillary providers might challenge physicians after finishing medical school?
There is probably a good reason why these providers are not found in great quantity outside North America.
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I guess your opinion also applies to why EMS should not be involved in research and should never ask questions of why things are done the same way over and over even with other EBM out there.
The blog was written from several references who are doctors. You should have noticed this at the end of the artile. Many are now available on line to read. Mr. Whitnack has also presented his collection of data at conferences for Physicians. At these conferences questions can be asked and the information can be disputed in discussion or more medical articles and blogs if so desired.
But, at least the references have been provided by the author for the reader to make their own informed decisions rather than just restating something they heard from an aquaintance who is a doctor at some unknown unit.
This issue here is knowing the difference between acute, stable and chronic. Knowledge of basic physiological response to hypoxia within the body and the various regulatory responses will also provide a good base to understanding and anticipating the body's response.
References: (found at the end of the blog)
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I have experienced it a couple of times across my 20 year career where the patient required high FiO2 delivery to maintain acceptable sat levels, yet became drowsy and incoherent upon reaching SpO2 levels of 98+%. When I lowered the FiO2 to maintain 88-92%, their level of consciousness improved to the level where they were coherent and alert (this was in a hospital where I treated these patients over many hours or days).
The mechanism is often misunderstood and at no time have seen an awake patient stop breathing from hyperoxic delivery. It takes time for the PCO2 to build, but it's not from apnea. There are other physiological effects at work, but the end result is to maintain proper blood oxygenation without going overboard (and, yes, you might have to deliver true 100% oxygen just to achieve SpO2 levels of 90%).
I have seen far too many times, the opposite situation where anyone that smoked half a cigarette when they were 12 were kept hypoxic "just in case".
The mechanism is often misunderstood and at no time have seen an awake patient stop breathing from hyperoxic delivery. It takes time for the PCO2 to build, but it's not from apnea. There are other physiological effects at work, but the end result is to maintain proper blood oxygenation without going overboard (and, yes, you might have to deliver true 100% oxygen just to achieve SpO2 levels of 90%).
I have seen far too many times, the opposite situation where anyone that smoked half a cigarette when they were 12 were kept hypoxic "just in case".