The greatest article about Albuterol ever written

Way before I started my fictitious quest for bronchodilator reform I met a really cool RT who had some brilliant RT wisdoms to share with me and my fellow RTs here at the RT Cave.

This was quite a few years ago, probably about the time I was realizing that Albuterol breathing treatments weren't really ordered for what they were indicated for.

Like most RTs, I loved my job, but often became frustrated that I had to wake someone up at 2:00 in the morning for a treatment he didn't need. Yet instead of venting our frustration, we develop that infamous RT Humor.

We thought it was cool the brilliant wisdoms this fellow RT had to share, particularly regarding the "wonder drug" Albuterol.

Perhaps you've read this before. If not, it's a great read. Click here to read the infamous: "Albuterol: Not Just for Bronchospasm Anymore."

New hope for those who want to quit smoking

We as RTs are constantly working with patients who smoke. In fact, if people ever did stop smoking we might simply be out of a job.

In fact, one of the ironies of the medical field, is we make a conscious effort to do thing to that we think will benefit other people but ultimately put ourselves out of work. It would be like Marborro heading an anti-smoking campaign.

We here at the RT Cave have this neat little pamphlet we give to our patients who want it, and it provides some awesome information about the dangers of smoking and how to quit. I'm sure your hospital does too.

In doing my daily search of blogs last weekend, I found my way to COPD News of the Day, where she reports that "kicking the habit may become easier for the nation’s 45 million smokers.

For the first time, researchers have identified patterns of genes that appear to influence how well individuals respond to specific smoking cessation treatments."

Anything that would make it easier for people to quit is good news, even if it extinguishes our jobs in the process.

I also found this article about how researchers have linked smoking with midlife memory loss. Yet another reason for people to quit, or to not start in the first place.

Help out a girl with a rare disease called chILD

We have a greater mission today, and that is to help out the cute little girl in the picture to the left.

Bob Sherman, my fellow RT blogger over at Respiratory Report, has written a couple posts about Julia Roberson, who has been stricken with a rare disease called Children's Interstitial Lung Disease (chILD).

She is involved in a fundraiser in an effort to raise money. Click here to learn more.

I've taken care of patients with interstitial lung diseases (ILD) before, but all of them were adult with idiopathic pulmonary fibrosis. This would be a disease that causes scarring in the distal air passages that causes the lungs to stiffen and decreases the lung's ability to exchange gases. Interstitial pneumonia is also considered a type of ILD.

One of my favorite all time patients was a 40-year-old lady with pulmonary fibrosis. Her and I used to have some really cool discussions, but only while she had her BiPAP on. She told me she hated that BiPAP, but that's what was needed to maintain an SpO2 level even in the mid 80s. That and lots of supplemental oxygen. And even with it on she remained dyspneic.

She told me one night, shortly before she died, that she so much wished that she would get better so she could help other people who had a disease that made it difficult to breath. She was thinking of other people even while she knew she was dying, and for that I respected and admired her greatly.

But there was nothing she could do to stop the disease process, as so little was known about it. Likewise, very little is known about chILD.

So what exactly is chILD? The cause is idiopathic, or of unknown origin. But there are some theories.

child Foundation reports that adult ILD is different than child ILD. It involves a series of diseases "that vary in their severity and in their long term outcomes. In simplest terms, all types of chILD decrease a child’s ability to supply oxygen to their body. If you suspect your child has chILD a pediatric pulmonologist with expertise in chILD should be consulted."

According to emedicine, and per the most recent research, the process is believed to be the result of "tissue injury with aberrant wound healing resulting in collagenous fibrosis." This ultimately leads to "structural remodeling (scarring) of the distal airspaces, leading to impaired gas exchange."

While the exact cause is questioned, it is theorized that the disease process is the result of "some type of lung injury to the distal air spaces caused by the adenovirus (RSV), or exposure to organic dust. This results in damage to the epithelial or endothelial layers and the associated basement membrane."

It is very rare for such a disease to inflict a child, but when it does the mean life expectancy has been just 47 months.

According to the chILD Foundation, after ruling out other diseases, a child would be considered to have this disease if he or she has three of the following:

• Fast breathing
• Use of accessory muscles
• Abnormal chest x-ray
• Need for supplemental oxygen
• Failure to gain weight
• Persistent crackles, wheezing or other abnormal sounds heard during auscultation
• Recurrent pneumonia
• Recurrent bronchiolitis
• Recurrent cough

A more definitive diagnosis would come from a lung biopsy.

So, very little is known about this disease, and there is no cure. Which is why more money is needed to research it.

The respiratory report writes that "Julia is going to participate in the Respiratory Health Association of Metropolitan Chicago’s 2008 Hike for Lung Health. She has set a fundraising goal and I want to help her reach that goal. If each person who reads this article would donate $10.00 to Julia’s effort along with $10.00 to chILD Foundation, you would be doing so much more than that for her and her family’s spirit. Continue reading →"

So, we here at the RT Cave urge you to open up your hearts and your wallets, and click on this link for more information about Julia Roberson and her rare illness. Or, click on one of the links above to help her out.

Asthma/COPDers should avoid pop & beer

One of the things I regret most about when I finished the RT program is my decision to burn all my notes. Little did I know some day I'd have a yearning for all those superfluous facts I incinerated.

My RT Student today reminded me of one of those fact I had all but forgotten. She said, "Did you know that pop and beer can be bad for COPD and asthma patients?"

"Yes I did," I told her, "But I had forgotten."

This is the kind of information we don't use on a regular basis here in the hospital setting, although should store somewhere in the crevices of our minds.  We should know why it may not a good idea for that COPD patient to have that Diet Coke or Sprite.

Being the good RT Blogger that I am, I had her dig through her notes for more information regarding this, and she made me a copy of her class notes for that day. I'm not sure who the teacher's source for this information was, so I'm just going to attribute this to general RT knowledge.

According to the information she provided me, here are some basic facts:

• The normal human body breathes to eliminate CO2, producing 200cc per minute that has to be eliminated at the same rate.


• One can of soda contains up to 1000cc of dissolved CO2, most of which is absorbed into the blood stream by the intestines.


• The Lungs are presented with the extra CO2 to eliminate by increased minute volume leading to increased respiratory effort.

A normal individual won't have a problem with this extra CO2, as the extra CO2 absorbed via the intestinal track will signal the central chemoreceptors to "immediately" increase the respiratory rate (click here to see why we breath).

However, for a patient who already has a compromised respiratory system, such as symptomatic asthmatics and chronic lung patients, this extra CO2 may cause problems.
Simply put, they may not have the lung capacity to increase their respiratory rate enough to blow of the extra CO2, and this may cause additional dyspnea and further aggravate respiratory failure.

Since it takes longer for them to normalize their CO2 level, that can of pop could actually "aggravate their acid base problems."
In short: "Carbonated beverages will increase the respiratory efforts in normal individuals; but symptomatic asthmatics and COPDers will need to exercise caution when consuming carbonated beverages."

Carbonated beverages can also cause excess gas and bloating, which may result in the diaphragm being pushed up against the lungs, further compromising them and making it even more difficult to breathe.

Beer is something that symptomatic asthmatics and COPDers might also want to consider avoiding because it also has a tendency to cause dehydration.
When your body is dry, your lungs become dry, and this may further exacerbate breathing difficulties.

This is just another example of how lung patients have to think about things that normal people simply take for granted.

High & low humidity both bad for asthma

I remember when I was a kid -- like say 10-years-old or so -- and having an asthma attack, and my dad taking me into a bathroom that was full of hot steam. Sometimes he'd have me sit in there for what seemed like a long, long time.

It never worked. In fact, every time I remember my dad doing this with me -- every time in the middle of the night -- I ended up in the emergency room anyway. I do remember feeling more refreshed when I walked out of the bathroom, but I was still short-of-breath.

I also have vague memories of a humidifier in my bedroom. My mom would set that up whether I was having a bout of asthma or not. Despite her efforts to set this up, it never seemed to do anything for my breathing. If asthma was going to occur, it was going to occur.

My parents did this because they were told by my pediatrician that humidity was good for breathing. It was common knowledge back then for doctors to recommend humidity for asthma.

I was discussing this with Jane Sage today, and she said she used to set up ice tents on asthma children routinely. She said scientists and doctors honestly believed they were doing something to help asthmatics.

It was a fallacy. We know that now. Steam works well for inflammation of the upper airway, or croup, but it does not work for asthma.

Many times a mom woke up because her child had a harsh barky cough, or croupy (stridor) expiration, and the child was working hard to breath as a result. A trip to the bathroom usually
worked wonders, and prevented many trips to the hospital. Steam can be soothing to the upper airway.

Cool mists work well for croup too, but not for asthma. If the mom of the croupy child decides to come to the hospital, and it's the middle of winter or a rainy day, the child is usually cured even before she arrives at the hospital.

And, if this croupy child did get admitted, he would be placed either in a cool mist tent or set up with a cool mist aerosol. Now we just use a cool mist aerosol in stead of the tent.

But this therapy seldom works for asthma. In fact, steam, or cool mist tents, or aerosols, have a tendency to make asthma worse. It makes the air thicker, and the patient has a more difficult time inhaling it in.

Still, I have asthma mom's and asthma dad's ask me on a regular basis if they should set up humidifiers for their asthma children, and each time I have to correct the old fallacy that humidity is good for asthma.

That in mind, allow me to introduce you to RT Cave Rule #19:

RT Cave Rule #19: Humidity or cool mists may work wonders for croup, but can make the air difficult to breath for asthmatics. In the hospital, cool mist therapy can be used for croup patients, but not for asthma.

And this is one of the reasons that dehumidifiers and air conditioners can be of benefit for asthmatics (and COPD patients) because they remove the humidity from the air and make it lighter and, thus, easier to breath.

This is my opinion of course. As you will read in a moment, there has been much scientific research on humidity and asthma.

According to Sue Hare and Joe Buchdahl, co-coordinators of the Atmosphere,Climate and Environment Information Programme (see article here, or related article here), areas on the planet that had a relative humidity lower than 50% had fewer "rates of asthma." This problem may be exacerbated in big cities, "because the urban 'heat island' effect caused by asphalt and concrete trapping heat at night."

The report also states that "for every 10% increase in indoor humidity was associated with a 2.7% increase in the prevalence of asthma."

While they may not have had access to these expensive studies, this is also one of the reasons why asthmatics, like Teddy Roosevelt for example, used to report finding relief moving to areas like Arizona where the air is dry all the time.

However, moving to Arizona is no longer recommended, as the increased levels of smog may offset the benefits of the dry air.

Now we have plenty of scientific evidence to support the claim that dry air is better for asthma.

Scientists, according to American Academy of Allergy, Asthma and Immunology (aaaai.org), have determined that high humidity levels have a tendency to be harboring grounds for fungus and molds that might bother asthmatics. Plus, when the humidity is greater than 50%, the amount of dust mites in the air is increased. For this reason alone, humidity is no longer recommended for asthmatics by pediatricians.

Likewise, if you have ever been in a hospital, you probably noticed how dry it is in these places. Noses get dry, hands get chapped and start to crack (especially in the winter months). The reason is because the humidity of hospitals is kept low as to not create a harboring ground for fungus, molds and dust mites.

That's also why the air is cranked up in the summer months too. Sure, you may be cold, but this is good for disease control, and great for asthmatics.

As per The American Lung association, "Air-conditioning can help. It allows windows and doors to stay closed. This keeps some pollen and mold spores outside. It also lowers indoor humidity. Low humidity helps to control mold and dust mites."

On the other hand, also according to aaaai.org, if the relative humidity is less than 15%, this may trigger an excessive cough for asthmatics. Thus, it is recommended for "asthmatic patients to aim for a 'happy medium' relative humidity in their homes, monitoring their home humidity regularly with a reliable gauge."

The Center for Disease Control and Prevention recommends humidity be set between 35% and 50%.

I suppose you could use a convenient humidity monitor (like this). (I am not endorsing this product, I just coincidentally found it while doing my research tonight. In fact, I didn't even know it existed until a few moments ago.)

Personally, I do not have an air conditioner at home, nor do I control my humidity, but often times in the dog days of summer I wish I could afford it.

Likewise, working in the nice cool, clean air environment of a hospital was one of the best incentives of me deciding to be an RT.

(Allergy Be Gone has an excellent related article. This is also where I got that cool picture from.)

A cure for aging on the horizon????

I walked into the ER to do an EKG on a patient who looked like he wasn't a day over 60. Then, as I was typing my information into my EKG machine, I had to do a double take when I typed in his age: 99.

I looked at the patient, at the age on the sheet, back at the patient. Wow!

Of course, we know by now that a patient who takes care of himself and does not smoke looks a heck of a lot younger than the patient who smokes and over eats -- which would include the majority of our patients.

Later in the night I had a patient who was 95, and full of secretions. She looked all of 90. She was way overweight, and her skin was paper thin. She was diagnosed with pneumonia and sepsis, and was admitted to the med/surg floor.

"And of course she was ordered on breathing treatments," I said to a co-worker, "That treatment sure is going to help that rhonchi."

My co-worker said, "I think when someone is over 95 we should just let them stay at home and let nature take its course. I don't want to sound inhumane or anything, but I certainly don't want to live that long."

That got me to thinking. The person I was talking to was 38, the same age as me. So, when she is 95, it will be the year 2065. By 2065, technology may have improved to the point where the average lifespan is 150. Thus, my co-worker might just have to eat her words.

So I said, "You better watch what you say."

That in mind, I reminded her of an article I read recently. That, by the year 2030, scientist will have a cure for aging. And, whatever age you are in 2030, you will be that age forever. If you are 30, you will be 30 forever. And if you are 60, of which I will be, you will be 60 forever -- barring a tragedy.

Of course if you are born after 2030, you will age until you are 20 or so, and then you will be 20 forever. How many women would love that. Guys might not, because they tend to appear wiser as they age. But who cares what guys want.

What the article mentioned is that every disease you will ever get in your lifetime is in your DNA the day you are born. And, during the course of your life, if those genes are triggered, you get the disease. If your genes are not triggered, you do not get the disease.

And, as we age, we increase the likelihood you will trigger these "disease" genes. So, if we can stop the aging process, we can prevent people from getting diseases, and they will live forever (barring a fluke, a new disease, or a trauma).

I'm talking about hereditary diseases here, not those acquired by other means, such as the flu, AIDS, colds, etc. But the idea here if we have genetic diseases, and aging, under control, so to would we have these diseases controlled as well.

Here's what I think about this. If I'm 60 when this is invented, I will be among the wisest looking people on the planet. In the year 3070 I will be able to tell my great,great, great, great grandchildren what life was like in the 1980s.

Not only will I look wiser, as I will actually be still only 60 while 90% of the rest of the people will look 20, I will be among the few alive with memories of the 1900s.

So, if this new gene is invented, would that mean that we asthmatics can smoke to our hearts content without worrying about developing COPD? Or cancer?

I suppose if this scenario did happen, I would have to find another career to work the rest of my millennium of a life, because there might not be a need for hospitals.

This might pose a dilemma for all the patients who are already chronically ill, extremely old, and near death. Or, will an equally brilliant discovery be able to reverse aging? Aha, wouldn't that be great. So there might be a chance for me looking 20 again after all, or all of us for that matter.

Of course there might be a need for RTs for a while, as doctors allow nature to take its course for these folks. Be a neat idea for a book anyway.

I suppose it might be sadder for some of us who already lost our parents to aging, so we'd be a rare breed to only have known our parents, or grand parents, a short time. If one of us loses a spouse before 2030, we would be a rare breed to have to go through forever alone.

And what about Heaven. Some of us might get tired of life at some point, say after 300 years, and want to go to Heaven.

So will there be a cap on life.

And what about world population? Right now there are so few people in the world that if you took every person, you could fit them all into the state of Texas. What would happen if nobody ever died? Of course politicians in Washington would be happy, because there'd be plenty of taxpayers.

On another note, it says right in the Bible that no person, after Noah and his family, will ever live past 120 years. So I suppose you'd have some philosophers debating the Bible.

If people lived forever, the Bible might actually be of more use, as Thomas Jefferson and James Madison once discussed, God is needed to maintain order in society. Or, to state it another way, fear of the Devil is needed to encourage kids to be good to one another.

Currently, we spend our entire lives acquiring knowledge and possessions, and by the time we are old enough to appreciate these things we start to age, and then nature takes its course.

After this discovery, all people will be able to keep their knowledge forever. Right now, we see a lot of times mistakes of the past are repeated, mainly because the people who experienced the mistakes of long ago are now deceased.

So, there is one thing I can say for sure: we'd be a wiser nation/world.

Since people no longer die, wisdom of our fathers will not be forgotten, because our fathers will still be alive to share that wisdom.

And that is the thought of the day.

An RT with a Segway would be COOL

It is said that an average RT walks 20 miles each 12 hour shift. There are some busy days that my feet are killing me by the time my shift is done. Sure, the excercise is good, but there comes a point when all that walking catches up with you.

I also think that I do not want to be doing this when I'm 60, as I see some of my elder co-workers are limping and ailing all the time. Is it because their bodies are superanuated? (That means: worn out from years of service.) Or just the normal aging process?

Still, when I first saw a Segway on TV a few years back, I thought: I definitely want one of those.

That would be so cool to drive a segway from room to room, floor to floor. Man, that would be awesome.

Now if I could just talk my RT Boss into buying me one.

A guideline is just a guideline

The Happy Hospitalist wrote a neat post about guidelines from a doctor's perspective. But he reminds us that while a guideline is a good tool, it is just a guideline.

We'll make this RT Cave Rule #15:

RT Cave Rule #15: A guideline is just a guideline. It is not a substitute for experience and common sense. For the most part, that guideline is just a tool.

I've written on this blog about how sometimes asthmatics require a bronchodilator more often than is recommended on guidelines.com. Sure the guideline states that if a rescue inhaler is needed more than 2-3 times a week, your asthma is not controlled. But just because someone uses his inhaler more often, does not always make for uncontrolled asthma.

Look at it this way. What if a person had bad asthma, and used his inhaler 10 or more times in a day. As time goes by he and his doctor eventually find a better medicine routine, and the patient makes a few changes in his life, that allows him to only need to use his MDI 2-3 times a day instead of 10.

This same person is active in the community, and stays physically active. You cannot tell me that this person has uncontrolled asthma.

In fact, this brings us to RT Cave Rule #16:

RT Cave Rule #16: If you have asthma and you do not miss work, and you do not miss school when you are a kid, and you are able to lead a relatively normal life, then your asthma is controlled. That's how we define asthma control. It's not based on how often you use your rescue inhaler.

The same is true of COPD:

RT Cave Rule #17: Whether someone has controlled COPD is not based on how many times a rescue inhaler is used, or how much oxygen the patient is on, but whether or not that patient can continue to be a productive member of society.

Ideally, however, you want your asthma and COPD patients to not need to use their rescue inhalers, but in the real world, many lung patients get short-of-breath when they wake up in the morning, and might need a few puffs. I don't see a problem with that.

I can use myself as an example here. I have asthma. I work out just about every day, and I jog (not walk) four times a week. And I rarely use my inhaler during the day. However, I do use it a few times during the night, most particularly first thing in the morning. And, most important, I have never missed one day of work due to my asthma. I'd consider my life as normal; my asthma stops me from doing nothing.

However, I have had a few people email me and tell me my asthma is not controlled because the asthma guidelines state that if you use your MDI more than twice a week, then your asthma is not controlled. That might be true of most asthmatics, but there are exceptions to every rule that doctors have to be prepared for.

The same can be said of COPD patients. If you measured COPD control based on how often a rescue inhaler is used, then there would be very few COPD patients who have control of their illness. As we learn in RT school, the goal with COPD patients is to help them remain productive members of society.

Sure, Mrs. Beady might need to use oxygen 24 hours a day, and may even go through an inhaler every month, but her disease does not stop her from performing the daily routines she has been doing her entire life. She is a productive member of society.

Another example of how guidelines are sometimes misused is with ACLS. We have some doctors here who go by ACLS as though it were the Bible.

The other day, for example, I was bagging this little-old-lady with one hand while holding the mask with the other. There was no problem. Air was going in easy.

Then Dr. Krane decided to hold the mask with her two large hands, and I let go and used two hands to bag the same tidal volume. Air started squirting out the edges of the mask: BLLLLLLLLPPPPPPPP.

I looked through the mask, and saw that poor little old ladies facial features all squeezed together. Air wasn't getting in.

"I think you better ease up a bit," I said.

She said, "ACLS recommends one person hold the mask, and one person bag." Yeah, but this lady was ventilating just fine until you grabbed the mask. Let go!

She did not. She had to live up to those ACLS guidelines to a tee, even if it was to the detriment to the patient. The patients sats dropped suddenly.

Now I was in a predicament, because I certainly didn't want to overrule a doctor when she was standing right next to me. Finally, she let go to grab the ETT, and I pumped in some nice easy breaths real fast, and our patient pinked up just fine.

Our doctors are also particular to doing three Q20 minutes treatments. Or, in Dr. Krane's case, Q1 hour treatments. One day I asked Dr. Krane why she does that, she said, "Because it's in the asthma guidelines."

That's fine and dandy, I thought. But what if that first treatment worked and a second wasn't needed. Do I still need to give a second treatment when that first one worked just fine? The patient's all shaky and jittery from the first, do we have to give a second?

According to her guidelines the answer is yes. According to my RT Cave rule, common sense says no.

This brings me to another RT cave rule #18:

RT Cave #18: While guidelines should always be considered, each patient and each patient situation should be assessed and treated individually. We cannot treat all patients the same, as most guidelines portray.

It all comes down to common sense. Guidelines are only as good as the paper they are written on. While they can be a great tool, common sense is the key.

What's a humble RT to say to a suicide attempt?

When I get called to ER to do an EKG, it's rare that I know anything about the patient before I go into the room. But it doesn't take long to figure things out.

All I knew from the point of entering the room was that she was a nice looking 23 YO female who had been crying lying on the ER bed of room three.

I pushed my machine to the back of the bed and provided my humble presentation. "Hi, I'm Rick from cardiopulmonary, I'm here to do an EKG. It's quick and painless"

"Why do I need that?" She asked without looking up at me.

"It's just to check out your heart?"

"I can tell you my heart is fine."

"Are you having chest pain?"

"No. My heart is fine."

Grasping at straws here, I said, "The doctor wants me to check out your heart. It's routine for what you came here for." I had no idea what she was here for, but I knew she did. To be honest, by this point I didn't' want to know.

"There's nothing wrong with my heart."

"I have to put stickers here, here and here," I said, pointing to areas on her chest where I would need to lift her shirt. "I can keep you covered." At this point I thought she might refuse at any moment.

"Yeah, I don't care if you see me. I don't care about anything anymore." I stared placing my stickers where I needed them, never exposing her out of respect for the young lady.

"You don't have to tell me. I don't care about anything!" She paused, then added, "I don't want to be here."

"I know what you mean." I said.

"You don't know what I mean."

Ah, how stupid. This is why I usually keep my mouth shut.

"My only regret," she continued, "was that I didn't take more. I knew I should have taken more."

What do you say to someone who tried to kill themselves. Knowing what to say is something beyond my scope of expertise, and is usually why I keep my mouth shut, do the job I'm ordered to do, and leave the room.

She's going to be admitted, I decided. And by law she was going to be kept back in the psyche unit for at least three days. And I'm certain the doctors will talk to her about this. But what if they can't talk her out of doing it again.

"Do you have children" I said.

"Yes, I have three."

"Won't your children be sad if their mommy wasn't here no more?" While she was preocupied in thought, I pushed the button on my machine.

"They live with their dad."

"Still, won't they miss you. Don't they love their mommy?"

"I don't care about anything anymore."

The nurse came back in as I was pealing my stickers off the patient. "As soon as Rick is done with you the police are going to come in and talk with you."

"I don't want to talk with them. I don't like police."

"They are really nice guys," the nurse said. "Remember, you promised me you would cooperate with all the good people who want to come in and help you."

"I don't want help," the patient said. When I go home I'm just going to do this again, and I will succeed this time."

On that note, I wheeled my machine out the door. This was another reminder to myself how well off I have it.

I always thought that if I was ever having suicide thoughts I wouldn't do it because I'd always be thinking about how much I would hurt the people who do love me, most particularly my kids. Man, could you imagine what that would do to kids.

But that's just me. However, as I am reminded from time to time, when you are really depressed, you don't think straight. And you do stupid things. You don't think that killing yourself is a permanent solution to a temporary problem.

However, my initial impression about this young lady is she was seeking attention. I will never know for sure. Either way, and even though she said otherwise, I hope that she thinks about what I said to her. I hope she doesn't do it again for her kids sakes if nothing else.

But what do I know.

The basics of oxygen therapy: part 2

(This is part 2 of an ongoing series, to view the rest click here)

There are a few exceptions to this rule I'm about to state, but for the most part, no patient admitted to the hospital should ever be ordered on a specific oxygen device at a specific FiO2 or a specific liter flow.

Personally, with the exception of the exceptions I will list in a moment, the amount of oxygen a patient receives should be based on the patients sat, otherwise known as the SpO2.

This is why I love it when doctors order oxygen per protocol, because both our oxygen and ventilator protocols call to maintain an SpO2 of 92% unless otherwise specified.

We must realize that as a patient ages, or a chronic illness progresses, his or her normal resting SpO2 drops. This is especially true as an aging person sleeps. If I had a dollar for every time I was called to an elderly person's bedside because his or her sat was 88-89% while the patient was sleeping, I'd be rich.

To me, that's an exception to my rule. I see no reason to provide supplemental oxygen to these patients, unless they show complications. The same thing is true with a chronic CO2 retainer. If he or she is maintaining an SpO2 of 88-90% and shows no complications, then leave that patient alone.

Three more exceptions: the anemic patient, carbon monoxide toxicity, and the cardiac patient. For these patients, you probably want to maintain an SpO2 of 98%. Otherwise, 92% should be the target SpO2.

That should be plenty of oxygen to maintain a PO2 of greater than 60, and thus prevent hypoxemia, or too low oxygen level to the blood supply which causes the heart to be overworked in normal patients.

So, basically, if a doctor orders a 40% ventimask because the patient's sat was 88% on 3LPM, you should question the order. What if the sat is 100% on 40%. Then why can't you decrease the oxygen to 30%, or even 28%, or even lower if that maintains the required SpO2?

Why keep someone on a nonrebreather for two days with a sat of 100%, when you could just as easily get by with a 50% ventimask to maintain the sat.

See what I mean. The RT should always have the opportunity to lower the oxygen to maintain that sat.

He should also have the opportunity to increase the oxygen should that be required. Now, if I had to increase oxygen from 2LPM to 4LPM no big deal. But if the oxygen now required is 50% instead of the 2LPM the patient was on, then I'd sure be calling the doctor so he knows that something is changing with this patient.

However, as it stands where I work, we can go down on oxygen without an order, but we cannot go up over the original order. But, if I had my way, I'd add the above paragraph into our protocol.

A ventimask should be ordered in only two situations: 1) if the nasal cannula just isn't quite cutting it, but a partial rebreather isn't needed 2) the patient has a normal SpO2, but has an irregular respiratory rate. A ventimask will guarantee that FiO2 of 24-50% regardless of the patients minute ventilation.

One rule of thumb for a ventimask: to maintain the desired FiO2, you have to dial in the recommended liter flow. It usually goes something like this: 24% and 26% = 3LPM, 28% and 30% = 6LPM, 35% = 9LPM, 40% = 12LPM, and 50% = 15LPM.

If you set the mask to 50% and you do not at least set the flow at 15, the patient will not be getting 50% FiO2, and he may be retaining CO2. We don't want that. However, it is okay to go over the recommended liter flow.

If a patient is so bad off that a ventimask isn't working, then order a non-rebreather (NRB). However, don't assume a NRB delivers 100% Fio2, because it doesn't. It only provides about 75% FiO2. So don't call it a 100% NRB. With both flaps on it would deliver 100%, but since by law one of the flaps has to be removed, it only delivers 75%.

If a patient still needs more oxygen on an NRB, then turn that flowmeter to flush. If that still don't work (and perhaps even if it does work) you may want to consider CPAP, BiPAP or the more invasive ventilator.

If that sat on 75%FiO2 is 96%, then take off the other flap and turn the NRB into a partial rebreather (PRB). Now you are giving the patient about 60% FiO2. But certainly don't keep it there if a 50% ventimask would suffice to maintain that 92% sat.

Why all this complicity about oxygen? Because oxygen is a drug, and it can cause complications. Not only that, but it costs money to have patients on oxygen when they don't need it.

And this includes post-operative patients. Let's not be putting patients on 2LPM just because they had surgery. If the sat is 92%, lets cut them off.

So, technically speaking, and with the exception of the exceptions stated above, liter flow and FiO2 really don't matter so long as you are maintaining the recommended SpO2.

Regardless, doctors often have exceptions of their own, and we RTs do what we are ordered to do. But that doesn't mean we can't question an order, or push for changes that might benefit the patient.

New Breakthrough in asthma, COPD research

It seems scientists are making some breakthroughs in the study of asthma and COPD.

Over at COPD Alert, someone posted about how researchers at Washington University School of Medicine in St. Louis linked asthma and COPD to a new type of immune response "that is activated in patients with COPD and severe asthma."

Click here for a link to the article.

Scientists say "their discovery could dramatically improve diagnosis and treatment of patients with chronic inflammatory lung disease...With this information, we can more precisely diagnose and monitor these types of diseases and then better target our treatment to specific abnormalities. That's a big step forward from simply monitoring breathing status."

Basically, this new theory proposes that asthma and COPD are basically a chronic immune response triggered by a respiratory viral infection.

While the cause of asthma has alluded scientists, this research may lead them in the direction of finding a cure.

The basics of oxygen therapy: Part 1

To view rest of series, click here.

As I've written before, I think I've spent more time debunking oxygen myths and educating about oxygen than anything else I have to teach regarding respiratory therapy stuff. And I'm not talking patients.

Don't get me wrong, I don't have a problem with this, nor am I implying that nurses are stupid. I think one of the big differences in RN school and RT school is that RN school covers a little about a lot, and RT school teaches a lot about a little.

Sure, oxygen therapy is covered in RN school, but only briefly. Which explains why we RTs have to explain the basics from time to time.

Respiratory Therapy Driven has good post today about some RT basics. A non-rebreather, for instance, is ideally supposed to deliver 100% FiO2, but because of the slim chance the oxygen gets shut off, the masks come with one one-way valve instead of two. Thus, the FiO2 obtained is only 75%. But try explaining that 100 times.

"Yep, chart 100% if you want," is what I usually tell them now. This gets to be a tricky thing to explain at three o-clock in the morning.

We have one old school doctor who orders a bubbler with every nasal cannula order, but our protocol states that one is not needed unless the flow is 4LPM or greater.

And like Djanvk wrote, all our post op patients are ordered up on 2-3LPM times 24 hours. What's the deal with that?

We estimate adult nasal cannula FiO2s based on the following formula:

1. 2LPM = 28%


2. 3LPM = 32%


3. 4LPM = 36%


4. 5LPM = 40%


5. 6LPM = 44%

However, don't dare put a nasal cannula on a three week old baby at 6LPM. That would be the equivalent of an adult sticking his head out the window while traveling 60MPH down the highway

We have a special flowmeter now that maxes out at 3LPM to prevent someone from accidentally (or purposefully) turning up the flow too high. Then we start at low as 1/4 LPM. Obviously, increasing to maintain a specified SpO2 (in my opinion 92%, but most of your docs like 94%.)

The reason I bring this up, and actually the reason for this blog post, is I'm curious to know what the estimated FiO2s would be for neonates and smaller children. It can't possibly be the same as for adults.

I have never found the answer on the Internet nor in any RT literature. I asked the question on Ventworld.com once, and no one there knew the answer either.

Maybe nobody cares but me

My guess is it would be something like this:

• 0.5LPM = 28%


• 1 LPM = 32%


• 1.5LPM = 36%


• 2 LPM = 40%


• 2.5LPM = 44%

Of course I'm just making these neo numbers up. Technically speaking it really doesn't matter what the FiO2 is, so long as you're maintaining a sat, but I'm still curious.

The hypoxic drive theory: Should be still taught

(This is part six of a six post series. To view entire series click here. )

I'm enthralled with this hypoxic drive theory, so I have to make one more post about it, and then I will probably never mention it again. But I can't help but to delve into this topic, to smell it, to read Jeff Whitnack's rantings with awe.

After all, I have been on a rampage myself on my own RT Cave blog about bronchodilator reform. I think doctor's and nurses have been inculcated with the idea that bronchodilators are indicated for everything pulmonary, when they are really only indicated for COPD and asthma.

So, I can hear Whitnack's frustration.

He writes, "When I bring up my arguments against the hypoxic drive, often I feel as if I am arguing religion and not science."

I feel the same way when I argue for bronchodilator reform. I often feel as though I'm blowing into the wind, and will never win. However, I cannot stop trying.

There is a reason I wanted to make this one last post about the hypoxic drive, and it has to do with this quote from Whitnack's RRT Page: "I have asked local RT instructors their opinion. One said, 'I don't believe in it (CO2 retainer/hypoxic drive theory), but I've got to teach it.'"

I discussed my opinion about the hypoxic drive theory being a fallacy with one of my RT students a few weeks ago. After I brought it up with her I wished I had not, because I decided I shouldn't confuse her, considering she would be taught the hypoxic drive theory in school, as I was by her same teachers.

However, she came back the next week, and she reported that she told her teachers about what I said.

She told me her teacher said this: "There is a lot of evidence against the hypoxic drive theory, and we are actually thinking about not teaching it anymore."

That is definite progress.

However, I would have one thing to say to this teacher, which may surprise you guys:

I would not stop teaching the hypoxic drive theory.

Are you shocked that I'm saying that?

Well, actually, you wouldn't be if you read my other blog. Because I believe that all theories should be taught in school, and that the students should be allowed to decide for themselves which is real and which is fallacy.

Because, after all, these are just theories. And, either way, there will still be doctors for years to come who are "brainwashed" into the idea that the CO2 retainer/ hypoxic drive theory is as real as the screen you are reading this on.

For no other reason, the hypoxic drive theory must be taught so new RTs aren't befuddled by a doctor's insistence that low oxygen levels are okay.

Overall, as per this slide show: (source unknown) "Health care providers need a clear understanding of the risk factors associated with oxygen induced hypercapnia... This knowledge needs to be applied in clinical practice to select patients to be identified at risk for oxygen induced hypercapnia instead of withholding treatment to all patients with the diagnosis of COPD"

Anyway, I hope my posts, coupled with Whitnacks, and other sources floating around or available for free on the Internet, will help make other RTs, RNs and doctors, and -- probably more important -- teachers aware that the hypoxic drive theory has been "debunked," and replaced with a greater concern, which is oxygen induced hypercapnia.

Wait!! There is one more thing that is more important than what we RT thinkers think: the patients. If we can show that it is okay to have a COPD patient on more than 2 LPM, then the person who benefits is the COPD patient.

I lied about one thing. I WILL definitely bring up this hypoxic drive theory again, as I have just recently been contacted by a COPD patient who personally does not believe in the theory. As soon as she gives me permission, I will write more. Her story is very inspirational.

Thus, more coming... (to view all articles on hypoxic drive, click here)

Further reading:  The Hypoxic Drive Theory:  A Hystory of the Myth

Happy Father's day to us RT dads

"They tend to follow what you do more than what you say," Father Wayne, Sunday, June 15, 2008.

Happy Father's day to all us dad's.

The Hypoxic Drive Theory: completely debunked

(This is part five of a six post series. To go to part one click here.)

I hope my readers understand by now that there is a hypoxic drive, but the hypoxic drive theory is not true. This is a distinction that is very important when providing adequate care for our COPD patients.

I mentioned this before on my blog, that only a small percentage of COPD patients are real chronic CO2 retainers. Thus, 70% of COPD patients can and should be given oxygen as they need it. And even the remaining 30% should get oxygen as they need it regardless of the hypoxic drive.

Read on I'll explain.

Here's one recent example. The COPD patient was in the emergency room for 8 hours on a 75% non-rebreather. His PO2 was only 70 on the mask. His CO2 was 45 (no big deal), and his HCO3 was 27. Usually, chronic retainers have a chronically elevated HCO3 level. So, upon the initial ABGs, I surmised the patient was not a retainer.

The patient was awake, alert and was still slightly labored, but his gases were improving. He was moved upstairs. The admitting doctor wrote this order: "Oxygen at 2.5 lpm and never higher."

I talked to the doctor and told him that the patient had been in the ER for eight hours and did not have any complications to the high oxygen level, but he said he didn't care. "We have to take care of our CO2 retainers," he said, and hung up.

This is what we call taking the hypoxic drive theory overboard.

Another patient who was an end stage COPD patient came into the hospital by ambulance with a 75% nonrebreather on. He had this mask on for about 45 minutes. The patient never showed any complications to the high oxygen.

If the hypoxic drive theory is true, then why didn't this patient stop breathing? Wasn't this oxygen supposed to knock out his drive to breathe.

One doctor even went as far as to tell this man was going to die with in the next two weeks, and more than likely because in order to maintain a PO2 of 50, he needed an FiO2 of 100%. According to the doctor, this man was going to die of hypoxemia (low blood oxygen) or we will simply knock out his drive to breath. This man was given a 10% chance of living.

Well, guess what? This man survived four days on 100% oxygen.

Ironically, he was eventually discharged to home on 2lpm, and the next time he came in with a similar problem, the doctor refused to allow us RTs to put his oxygen on anything higher than a 40% ventimask because "he's a chronic retainer. We don't want to knock out his drive to breathe."

Needless to say, I cringed.

Now, According Jeff Whitnack, RRT/RPFT in an online article he wrote called "The Death of the Hypoxic Drive Theory," the hypoxic drive accounts for approximately 10-15% of a person's drive to breathe. So that's a little lower than the 30% I estimated earlier. Some have it even lower.

"We all have it," he writes, "unless perhaps we've had bilateral carotid surgery. It becomes obliterated at a PaO2 about 170, and becomes a greater stimulus as the PaO2 drops below 70, and especially below 50."

But this is not what causes CO2 retainer's CO2 to go up when he or she is given high amounts of oxygen. There are other factors at play here, and they are called the Haldane Effect and V/Q mismatching. (I covered these in yesterday's post)

Let me sum this us: Yes, there is such a thing as the hypoxic drive. If you give a CO2 retainer too much oxygen, you will knock out his hypoxic drive. But the central chemoreceptors will still work enough to signal the brain to breathe. Thus, the hypoxic drive theory is debunked.

As you increase the oxygen of 90% of COPD patients their CO2 will go up. That's just common knowledge. But the CO2 does not go up because you knocked out their hypoxic drive. Their CO2 goes up due to V/Q mismatching about 70% of the time, and the haldane effect the other 30% of the time.

Likewise, COPD patients who are not labored and not fatigued will blow off that extra CO2 just like a normal person would. Thus, that extra oxygen will not knock out this stable COPD patient's drive to breath.

And, even if they don't blow off that CO2, it will not be a big deal. All COPD patients have their CO2 levels rise from time to time. It does not kill them. What kills them is lack of oxygen.

When you have a chronic CO2 retainer in the emergency room of whom is struggling to breathe, already has a high CO2 level, and has worn out, fatigued, respiratory muscles and no further capacity to blow off the excess CO2, then these patients are the ones you have to worry about knocking out their drive to breath when you increase their FiO2.

Thus, yes, a high level of oxygen given to a COPD patient can still knock out his drive to breath, can cause them to become lethargic, and can cause them to go into cardiopulmonary arrest, but only when the patient is already compromised, and still only to about 30% of Chronic retainers.

So, if a COPD patient comes into the hospital, is in respiratory distress, and requires more than a 40% FiO2 to maintain an appropriate SpO2, it is acceptable to give them the oxygen they need. It is mandatory to give them the oxygen they need.

However, Whitnack writes, if their CO2 goes up over 90, and they become lethargic, "one should not fear apnea and cardiopulmonary arrest when giving oxygen to a patient with an exacerbated obstructive lung disease and respiratory failure. Instead, one should be prepared to help the patient eliminate CO2 when deadspace increases. Providing assistance with the elimination of CO2 has been around since the beginning of critical care medicine. It is called mechanical ventilation."

Back when Whitnack wrote his article (I believe it was in 2000), I'm not sure if BiPAP was used regularly on COPD patients, but it is now. I find that as the CO2 rises and PO2 falls on COPD patients, a trial of BiPAP usually works well, if they can tolerate it. Most of the time when a patient is sick enough they tolerate it just fine. If not, a small dose of a sedative or xanax work well in this situation.

If the patient is not a DNR (Do Not Resuscitate) patient, and they do not tolerate the BiPAP, mechanical ventilation is always an option.

At the same time, however, whether we resort to BiPAP or mechanical ventilation or not, the patient should definitely get adequate oxygenation, even if that means 100% FiO2. (However, this should be titrated down as fast as possible while maintaining an appropriate SpO2).

Historically, according to Egan, an appropriate, acceptable, SpO2 is anything between 80-90%, or a PO2 of 50-60. However, if the patient does not show signs of oxygen toxicity, an SpO2 of 92% should be maintained.

In light of recent evidence, and understanding now that the hypoxic drive theory is not true, and that V/Q mismatching cause CO2 to rise in most of these situations, medical staff should feel comfortable adequately oxygenating a majority of COPD patients without worrying about their respiratory drive.

Whitnack quotes Dr. John Hoyt, "Debunking Myths of Chronic Obstructive Lung Disease," Critical Care Medicine, editorial Sept. 1997:

"The human body, particularly key organs such as the heart and brain, are not
all that forgiving of insufficient supplies of oxygen. Thus, medical decision-making—based on the mythology that oxygen causes apnea and cardiorespiratory arrest in patients with chronic obstructive pulmonary disease by turning off the oxygen respiratory drive—might take the path of with-holding or delivering inadequate doses of oxygen to meet the metabolic needs of the patient in respiratory failure. This mistake is generally fatal for the patient, and a treatment tragedy for the misinformed physician."

Thus, if a patient needs oxygen, he should be provided oxygen. If his drive to breathe diminishes, appropriate means to ventilate the patient should be sought.

And, as a final reminder, this issue pertains to the patient who is in respiratory distress, and not the CO2 retainer who is stabilized in his room, and "not the CO2 retainer whom is home and stable while eating and watching a ball game on TV."

Of course this is obvious, but I will state it again and again: "At all costs, we must first relieve the hypoximia. Ideally, we will do so without increasing hypercarbia needlessly. But it is bound to happen to a degree anyway. If the level of PaCO2 becomes a clinical problem, you local RCP should be there to assist ventilation, either in a non-invasive fashion or with a secure airway."

Or, in other words, "In the midst of this dilemma, we must remember that hypoxia kills, hypercarbia by itself does not."

(To view part six click here to advance to part one click here.)

A note to my readers: A disclaimer

I am the kind of person who loves to have all the facts on the table, whether I agree with them or not, and from there I like to make an educated decision. Of course, when it comes to respiratory therapy, I have my own personal experiences to consider too.

I would like people to consider this as they read this blog. From my own observation as an RT, I see many times a breathing treatment is ordered for reasons that I think are stupid. But that does not mean that I do not do the treatments when I am ordered to do them.

Likewise, while I have often had qualms with doctors leaving COPD patients on 2lpm when their sats are in the low 80s, I have to leave the oxygen on 2lpm if that is what the doctor has ordered. Doing otherwise would more or less cost me my job and my licence.

That said, I still like to keep up on the latest scientific research and theories. If nothing else, I can question the doctor to have him tell me to go stuff my opinion in a closet. That's fine. Or maybe we can slowly but surely educate people as to new theories.

I have succeeded here too. We here at the RT Cave have finally convinced our RT bosses that a protocol is needed, and we will in the near future start the process of obtaining one. This is one small step in the right direction.

However, as our director said, a protocol could backfire on us. It could make our workload go up. It could also make our workload go down and force the bosses to lay off RTs. Who knows.

But that is exactly why we do not endorse any one particular theory here at the RT Cave, we like to learn and to discuss. That's what this blog is about. We like to come up with new ideas. I like to come up with the latest information.

And then we can consider them, and even debate them in the arena of ideas, of which this blog is a part of.

And that is why I blog. I do not blog to convince you guys that I am right all the time. I am smart enough to know that many of you probably disagree with me a good portion of the time. That's fine.

Thus, when I write about the hypoxic drive theory, and set forth facts to support it and some to prove it is not true, I do so in an effort to educate myself first, and, as a result, I like to share what I learn on my blog, and you guys can maybe learn something too.

I also like to share my experiences. In my opinion, I may be right and I may be wrong. And when I'm wrong, some of you guys are quick to tell me. You are also quick to tell me when I write something that doesn't make sense. Cool.

The fact is, I've learned from your many comments and emails too. After all, I don't have an editor here to tell me when I don't make sense. I don't want one either, because then this would be a job and not just a hobby.

And while I try to be as factual in what I write as possible, and while I am always 100% honest and humble in my writings, I am just a blogger. I am a respiratory therapist with a brain, plenty of experience, a great education, a desire to learn, and a passion for writing.

But please understand that I am not a doctor and I am not a scientist and I am not a researcher and I have never participated in an experiment in my adult life, nor do I do them. I am, as my banner states, a humble RT.

Yes, and it doesn't help that I'm an asthmatic too, so I have an opinion on breathing therapies and medicines from that perspective too. In this way, I have plenty of empathy for my patients. And, as you have witnessed from some of my writings, that certain touch of stubbornness some of us develop.

I want you guys to take what I write about here and discuss it amongst yourselves, to enrich your knowledge base, and to further your studies. Or, you can use it as simple entertainment.

I never did put a disclaimer on this blog as other bloggers have. So, I suppose, I will make this my disclaimer.

The hypoxic drive theory: debunked

(This is part four of a six post series. To go to part one click here.)

All my fellow RTs have whitnessed it: the CO2 retainer who is breathing normal, is not in respiratory distress, has his oxygen turned up, and nothing bad happens. The patient does not stop breathing. Why is that?

It is because the hypoxic drive theory is not true. If it were, we'd have many more COPD patients dying each day.

What is really going on?1

The hypoixic drive is real, but it is not what causes CO2 to rise. There are essentially two different reasons why CO2 might rise in COPD retainers.

Reason #1: V/Q mismatching. Allow me to quote Jeff Whitnack from over at Jeff Whitnack's RT Page (actually, I believe he is paraphrasing a chapter by Robert Lodato in Martin Tobin's book, "Principles and Practices of Mechanical Ventilation," (pages838-9):

Imagine the worst ventilated alveoli. The local CO2 pressure there may be 100 or more. On room air the local O2 pressure will surely be less than 60 torr. At this level of local hypoxemia, the adjacent pulmonary vasculature will constrict. Blood will then be sent to the alveoli which is ventilating more effectively. Ventilation/ perfusion matching is enhanced. But if 100% O2 is given the O2 pressure will not drop below 60, the pulmonary vasculature will not constrict, and V/Q matching will not be optimized. Just as giving Nipride may drop the PaO2 as hypoxic pulmonary vasoconstriction is released, so giving 100% O2 may also raise the PaCO2. This also can happen to patients in an asthmatic crisis given 100% O2. It’s not that we knock out a hypoxic drive, so much as we drive in a hypercarbic potential. Then further compromise ventilation through increased V/Q mismatching.

For the patients I described at the top of this post, it is this -- V/Q mismatching -- that is causing the patient's CO2 to be high, and therefore it is actually safe to have this patient on 100% FiO2 without causing that patient to become lethargic or to die.

If we simply clung to the hypoxic drive theory, and didn't give these patients the oxygen they need to maintain a healthy heart and brain, they are more likely to die than if we given them oxygen.

Reason #2: The Haldane Effect:

Unsaturated hemoglobin carries CO2. A patient in crisis may arrive in the ER with an SpO2 on room air of 75%, the unmeasured mixed venous saturation may then in turn also be much lower than the 75% norm. All this unsaturated hemoglobin is then carrying an extra CO2 load. This is in the setting whereby the patient has an already elevated PaCO2, perhaps has an elevated Hgb (hemoglobin) after years of hypoxemia, and is “topped off” on their ability to ventilate. So for every rise in their SpO2 we are driving more CO2 into the plasma. If this were you or I, we would simply then ventilate this extra CO2 out via the lungs. But their lungs can’t and don’t, therefore the CO2 shows up in the “downstream” ABG.

This is why you will see a rising CO2 in many CO2 patients when they are placed on increased amounts of oxygen, and they can still talk to you. They are in no respiratory distress, yet the doctor is thinking, "Turn down the oxygen."

If the Haldane effect is causing a person's CO2 to be high, then we need to be on the lookout for impending respiratory failure, and have our BiPAP or ETT ready.

If a patient is on 100% Fio2 you should be concerned that the CO2 might go up, especially if his sat of 100%. What you should do here is back off on the oxygen until you have an SpO2 of 92%, which is where most of our doctors like to keep that sat per our oxygen protocol on non COPD patients.

So why do we make COPD patients suffer with a sat of 88%? It's because most of our doctors believe in the hypoxic drive theory.

Usually the patient will only become lethargic with excessive O2 therapy when he is already compromised, he is pooped out (fatigued), and he cannot blow off the excess CO2 because he has no more pulmonary capacity of which to increase his minute ventilation. It is these patients whose CO2 increases to greater than 90, and of whom are prone to pass out due to too high of a CO2.

And we have all seen this happen. It's about 30% of COPD patients.

So keep an eye on them. Have your airway box ready. But don't make them suffer with an SpO2 in the low 80s just because of the hypoxic drive theory.

Many times we have a patient on the vent and have to get them down to 88% SpO2 because "that's what they live with at home on 2lpm." So, why not send them home on 4lpm with an SpO2 of 92%? This is exactly what is recommended on this slide (source unknown):

• Give oxygen, maintain SpO2 >92%
• Close observation for changes in mental status
• Use of non-invasive CO2 monitoring
• Early use of non-invasive ventilation if needed

At least we could try them on 4lpm and do an ABG an hour or so later. If the CO2 doesn't go up and you have the PO2 you want, then by golly send the patient home on 4lpm. Likewise, if the CO2 does go up slightly, and the patient is still talking to you, then by golly send the patient home on 4lpm.

But you know what? We never do this study on patients. I've never done it once in my 10 year career as an RT. Why? Because doctors don't need to do this oxygen study, because they have already bought into the hypoxic drive theory.

But, as Whitnack writes, "if that same patient is at home and resting while watching the ball game on TV as their O2 accidentally gets turned up by 1 l/m -- well, they won't stop breathing and that's why I've never met an ambulance with such a patient on board."

Great point I say.

Consider this example he gives. I've seen it, and so have you more than likely:

Picture the COPDer whom arrives in the ER SOB with a RR 45 and initial PaO2 44, PaCO2 66, pH 7.35 on RA. So someone places them on 8 l/m simle mask and draws another ABG-- now they are PaO2 110, PaCO2 80, pH 7.25. The patient's RR is now 26 and the patient's respiratory effort is much less labored. Did we knock out that patient's drive to breathe? Or did we relieve the patient's hypoxemia sufficient that the patient could practice their own form of permissive hypercapnea? If we intubated the patient and considered his auto-peep, we may be happy with the latter ABGs also.

Which is also a reason why we should never panic and rush to intubate someone.

Why is it that we never hear about the COPD patient dying who is stable in his room, but accidentally has his oxygen increased from 2lpm to 5lpm? If the hypoxic drive were true, shouldn't that patient become lethargic, and maybe even go into cardiopulmonary arrest.

Instead, he's in his room watching the Detroit Tigers and munching on gram crackers.

Now we know why.

Click here for a neat slideshow regarding the hypoxic drive myth. Rather, it's now called Oxygen Induced Hypercapnia, not hypoxic drive.

(To view part five click here. To return to part one click here.)

The hypoxic drive theory: The CO2 retainer

(This is part three of a six post series. To go to part one click here.)

Today I would like to add to our discussion of why people breath. In particular, today's post will delve further into the topic of oxygen induced hypoventilation.

As we described earlier, the body will continually try to make sure that gases in the body are balanced in order to maintain a normal pH, and in this way maintain a certain level of homeostasis within the body.

Usually, increases and decreases in carbon dioxide levels detected by the central chemo receptors is what causes people to breath. When a person is in respiratory failure, and the carbon dioxide level is high, decreasing levels of oxygen as detected by the peripheral chemo receptors then takes over as the drive to breath.

Thus, if a person has a chronically high carbon dioxide level, and you give this person 100% oxygen, you knock out their drive to breath. This, my friends, is what we call the hypoxic drive theory. Actually, this is the gold standard of respiratory care. It is what helped to establish us as a profession.

According to Donald Egan's "Fundamentals of Respiratory Care," when a healthy person "breathes 100% oxygen, the peripheral chemo receptors remain essentially inactive. However, because blood oxygen levels are high, there is less reduced hemoglobin available to carry carbon dioxide. This causes a slight rise in (carbon dioxide) CO2, which in turn stimulates the medullary respiratory center (at the base of the brain)." This in turn causes a person to breath faster.

Now, if you have a patient who has a chronically low level of oxygen and high level of CO2, breathing high levels of oxygen (FiO2) can cause a person to slow down his breathing (per the theory). In essence, the "high blood O2 (oxygen) levels suppress these peripheral chemo receptors, thereby depressing ventilatory drive."

Since a person's breathing is how they blow off excess CO2, you can see how this could be detrimental to a person who already has a high CO2 level.

Thus, since the high FiO2 (say 100%) is signalling the peripheral chemo receptors to slow down breathing, a person with a chronically high CO2 may end up with a critically high CO2. In cases like this, I've seen CO2s in COPD patients as high as 110. This is not good. And usually these patients become lethargic. Yet many times they surprise us and they do not lose consciousness.

Usually, according to William A. French, "Hypoxic Drive Theory Revisited," rtmagazine.com (Issue: February/March 2000), CO2 must generally reach a level above 90 mm Hg for" a patient to become lethargic.

However, sometimes these patients are so used to high CO2 levels, that they remain conscious even with a high CO2 level. If you have ever seen a COPD patient in this situation, you will observe that they are usually blue, and this is where we get the term blue bloaters from. The patient is blue due to low oxygen.

And they also are jittery or shaky. That is the high CO2 at work. If they are lethargic, that is usually due to the high CO2 level, but as the hypoxic drive theory states, it may also be due to the high level of oxygen the medical staff provided to the patient.

That is the theory. Keep in mind it is a theory that doctors believe in to the point of ad nauseam. I personally think it is inhumane to allow a person's oxygen to stay low, when this could kill them. However, that's just my opinion.

This brings me to my next point. According to Egan himself, right in his book. And I think it is these next two paragraphs that will help me disprove the hypoxic drive theory, of which I will attempt to do in my next couple posts.

Egan writes that "the rise in PaCO2 that is observed in some patients is due mainly to impaired gas exchange, not depression of ventilation."

And, he writes:

"Regardless of mechanism then, hyperventilation is a potential hazard of O2 therapy in patients with chronic lung disease, however, this harmful effect should never stop us from giving oxygen to a patient in need. Preventing hypoxia should always be the first priority."

Thus, according to Egan, "in order to prevent hypoxia but avoid hypoventilation (breathing to slow down) in these patients, we should aim for an arterial PO2 between 50 and 60 torr. Generally, this approach provides adequate oxygenation, while minimizing the likelihood of hypoventilaiton."

In layman's terms, a normal blood PO2 is over 100. A PO2 of 100 would usually generate a sat (SPO2) of about 98% (this is the % of oxygen in inspired air that gets to the arteries). A PO2 of 50 to 60 would therefore generate a sat of 80 to 90%. So, if you werent' familiar with these medical terms, now you are. And now you know what to look for on the monitor besides heartrate, respiratory rate and blood pressure.

To maintain a sat of 80 to 90%, usually we RTs use 2-3 LPM via nasal cannula. Or, if a patient needs more oxygen, or is breathing laboriously, we will use a venti-mask at no more than 30 to 40% FiO2 (oxygen). (For the record, there is 21% oxygen in the air you breath).

However, what happens if a chronic COPD patient is on a 40% venti-mask and the sat on the monitor still reads 70%? Now what do you do. You give them more oxygen. You give them 100% oxygen if they need it.

Or, as I've seen many times, you walk up to the doctor to get an order for more oxygen, and he says, "keep it right where it is. We don't want to knock out his drive to breath." And he looks at you like you are an idiot.

Or, another scenario is you do a blood gas that shows a PO2 of 45 and a CO2 100. The patient is awake and alert and talking to you just fine. The doctor says, "decrease the oxygen. We need to see if we can get that CO2 down."

This is where you roll your eyes in frustration.

(To view part four click here. To return to part one click here.)

This topic came up in the comments section of my blog and Amy's blog, and my most recent response became so long I decided just to turn it into a post.

Here's the deal. There is this "really cute cat" down the street from us, and it is "free."

My wife is trying to convince me that Singulair should prevent an asthma flair. Plus, she read somewhere that most people aren't allergic to cats per se, but to their saliva. Cats lick themselves to clean themselves, and that causes the allergic response. So, as per her source, if you wash the cat daily, you shouldn't have a problem with allergies.

Now, the gamble is, once you have a pet in your house, it walks the whole house, and if you do find out you are allergic to it, there's no way you will ever get all of the allergen out of your house. It will be there forever.

That's the argument I hang to when the subject "CAT" comes up. Now she has my 5 YO winking her cute little eyes at me saying, "Please, dadda, please..." It's not easy saying no to that.

(Ironically, I wrote about cats on my other blog just yesterday. Go figure.)

On a side note, we haven't done so well with pets in the past. When we first got married we simply "had to" get a dog. Mind you, I love dogs, but when you live in town, a barking dog can cause a lot of stress for an owner, especially when the neighbors keep calling the police.

But that wasn't the half of it. We had a fenced in yard, and we thought that would suffice. But the dog learned that it could dig a whole under the fence, and roam the town, causing havoc with other dogs. After the police gave me a ticket for this, I had no choice but to find a new loving home for this dog, even though I really liked it other than these two things. I even taught it to walk on two legs.

We "had to" get a hamster once too. But it somehow kept getting out of its cage. About the fourth time this happened I realized that my boy, then four, was opening up the cage every time he went to the bathroom alone.

Well, one day the hamster didn't look so good. We figured it got into the rat poison in the basement. No more hamsters.

We had fish too, but for the life of me (no pun intended), I could not keep fish alive either.

Thank God we are better at raising humans than raising pets.

So, now "we just have to" have a cat.

I'm not allergic to dogs or hamsters, and even though cats don't bother me, the test did show a positive result for cats. So, I'm sticking to that argument.

However, my wife and both my kids ask me at least 20 times a day. All it takes is one weak moment, so their strategy might pay off.

Besides, how can a dad say no to the little girl in the pic.

"Daddy, please..."

The hypoxic drive theory: Why do we breathe?

(This is part two of a six post series. To return to part one, click here.)

When you are thinking about it, you can control your breathing on your own. Most of the time you are alive, however, you will have other things to think about, yet your breathing continues.

So, how does this work?

(For further reading you can click here.)

There are basically two reasons for breathing. One is to maintain homeostasis (balance) within the body, and the other is for the exchange of gas. By homeostasis I mean maintaining a normal level of oxygen (PO2), carbon dioxide (CO2) and acid base balance (pH or hydrogen ions). By exchanging gas, I mean breathing in oxygen, and blowing out CO2.

According to Donald F. Egan's "Fundamentals of Respiratory Care", breathing is controlled by the Central Nervous System, and originates "in the brain stem, mainly from neurons located in the Medulla Oblongata. For the most part, and skipping a bunch of crummy detail, this gland controls breathing by messages it receives from Chemo receptors.

There are two sets of chemo receptors: the central and the peripheral. The central sit right on the Medulla, and the peripheral are located in the "bifurcations" of both carotid arteries and the arch of the aorta, or somewhere between your shoulders and above your heart.

These chemo receptors send messages to the brain (the Medulla) based on changes in CO2 and PO2. However, for the most part, the main driver of non-spontaneous breathing is carbon dioxide (CO2) way more so than oxygen (PO2).

Allow me to put it simple, when CO2 goes up above a certain point, your breathing speeds up. This is evident quite often in COPD and asthma patients who are suffering an exacerbation. They are having great trouble breathing, and ultimately they start to poop out, and their CO2 starts to build up. Thus, their breathing speeds up.

A normal CO2 is 40. Say it goes up to 100. By this point, when CO2 is 20% or greater above the normal value, CO2 starts to act like a sedative, and slows breathing down. Thus, as CO2 continues to rise, this is a sign doctors watch out for that a person is pooping out, and may need aggressive therapy.

The majority of the time, the central chemo receptors send signals to the brain that control breathing. The peripheral chemo receptors only have a minor roll during normal respirations, and only send a signal to breathe when the PO2 is less than 60. Either way, this response is far slower than the signal sent by the central chemoreceptors. Thus, the peripheral chemoreceptors only play a minor role in breathing, unless a patient is a chronic CO2 retainer (so the theory goes), of which we will discuss in a moment.

Thus, we will focus on the central chemo receptors for purposes of simplicity.

Let me confuse you a minute. The real drive of breathing is actually hydrogen ions . As hydrogen ions increase, your breathing speeds up. But, since hydrogen ions are not allowed to cross the blood brain barrier so that the pH of the brain can be different from the pH of the body, it cannot directly be used to stimulate breathing.

Thus, CO2 is used. CO2 is allowed to cross the blood brain barrier. Excess levels of CO2 arrive in the brain and are received by the Central Chemo receptors. Thus, "elevations in CO2... cause rapid diffusion of the gas into the CSF (Cerebral Spinal Fluid), where it dissociates into hydrogen ions and lowers the CSF, thereby stimulating the central chemo receptors. The central chemo receptors, in turn, signal the medulary centers to increase ventilation."

So you can see, CO2 "indirectly" causes changes in respiration's.

If the CO2 becomes chronic, or is still hanging at a high level after a day or two, according to Egan, the stimulatory effect of the high CO2 diminishes because the kidneys will try to compensate for the high CO2 by creating more buffers (bicarbonate or HCO3), thus causing the pH of the CSF to go back to normal. The medulla thus receives a signal that CO2 is normal, even though it is actually elevated.

It therefore is easy to tell which patients are chronic retainers because their HCO3 level will usually be high, and usually something greater than 30.

And, in Chronic COPD patients, this CO2 level may stay high while at the same time maintaining homeostasis (a normal pH), and, thus, CO2 has less of an effect on breathing as it would on a normal person (in theory anyway).

In effect, it may be normal for a COPD patient to have a CO2 of 50, and a PO2 of 50. We call these guys members of the 50/50 club, or chronic CO2 retainers or simply chronic retainers.

Changes in PO2 have no direct effect on Central Chemo receptors.

As anything in life, this process is far more complicated than I just explained, but you can see from what I have described here why in many COPD patients CO2 may lose its ability to stimulate a person's drive to breath, especially when CO2 is chronically elevated (or so the theory will have it).

And this is where the gold standard of RT comes into play. As, when a patient has a chronically elevated CO2, it is believed that it stops being the drive to breath. In these patients, it is believed that oxygen becomes their main drive to breath.

Thus, we must take a look at peripheral chemo receptors. According to Egan, "Peripheral chemo receptors are not very sensitive to CO2 changes... their primary role appears to be in response to hypoxia."

Normal PO2 is 104. It does not effect the peripheral chemo receptors until it is less than 60. To put this in perspective, a PO2 of 60 will usually generate a sat (SPO2) of about 90%. As the PO2 falls from 60 to 30 torr (SPo2 of 90% to 60%), the rate of breathing should be expected to be increased due to signals sent from the peripheral chemo receptors.

Now, as we've explained, CO2 is normally the drive to breath. But, if a patient with COPD is having so much trouble breathing that there is no way possible that he can speed up his breathing further to blow off that excess CO2 "regardless of patient effort," CO2 no longer is the drive to breathe, and PO2 becomes the drive to breathe.

This is called the hypoxic drive theory.

And this, my fellow readers, is why doctors soooooo do not want to put a COPD patient on more than 2LPM even though their oxygen levels continue to be low.

This is why many COPD patients are allowed by many doctors to have sats in the mid to low 80s even though low levels of oxygen may be deadly to the heart. This is why many doctors refuse to put many COPD patients on 100% oxygen, because they are afraid they will knock out their drive to breath. They are afraid the patient will become lethargic and die.

The hypoxic drive theory is the gold standard of respiratory therapy, but is it a fallacy or a reality? This is a debate that may be ending.

(To view part three click here. To return to part one click here.)

Here is a case study for you guys

After Dr. Krook assessed the mild-SOB out-of-town smoker who so happened to be camping at one of Shorelines parks, he ordered 3 Q-20 minute treatments. How does he know that a second or even a third treatment will be indicated when I haven't even given the first and reported the results?

Later, before she or I even went into the patient's room, Dr. Krane ordered me to do Q1 hour breathing treatments. Upon assessment the patient was was a smoker, but her chief complaint was mild dyspnea and a cough and nasal drainage. What's wrong with this picture?

Two very interesting patients

Here is something interesting that I doubt happens very often.

It started out as just your typical breathing treatment. She was a 66-year-old end-stage COPD patient who was a regular. I knocked and entered the room.

In bed #1 was her room mate, a lady who looked younger and healthier than my patient. Since she was new to me, and since I was going to be in and out of the room all night, I introduced myself. "Hey, I'm Rick from RT. I'm here to annoy your room mate."

"She's a pretty nice person," the lady in bed #1 said, smiling.

I approached the more sickly looking patient in bed #2. "Hey, Mrs. Lunger, it's time for your before bed peace pipe."

"I'm ready," she said.

Banter ensued between the two very pleasant patients and myself. But that's not what made this encounter so interesting. My patient kept referring to the lady in bed one as "Mommy."

At first I never thought anything of it, just thought these two ladies just got along very well as room mates.

Later, however, as I was wrapping up the treatment and stuffing it into the bag, my patient said, "So, what do you think of my mommy. She looks pretty good, hey."

They both giggled.

I never would have guessed.