Unveiling the True Essence of the Statue of Liberty

In recent times, misconceptions have clouded the genuine meaning behind the Statue of Liberty. Many believe it symbolizes the U.S. extending a welcome to the impoverished, poorly educated, and unfortunate of other nations, citing the famous inscription: "Give me your tired, give me your poor, give me your huddled masses."

However, a closer examination reveals a different narrative, one rooted in the celebration of freedom and liberty rather than immigration. The statue, dedicated on October 28, 1886, was France's expression of gratitude to the United States for being the first nation to demonstrate that freedom and liberty were attainable.

The commonly quoted phrase, "Give me your tired, give me your poor, give me your huddled masses," engraved on the statue's base, was part of a poem titled "The New Colossus" written by Emma Lazarus in 1883. Surprisingly, it wasn't included on the pedestal until 1903.

Lazarus wrote the poem as part of a campaign to raise funds for the statue's pedestal, and its original intent was not focused on immigration but rather on freedom and liberty. The statue was meant to be a torchbearer, with Lady Liberty stepping forward to carry the torch of liberty from the United States to the rest of the world.

Contrary to the prevailing misconception, the Statue of Liberty is not a beacon for immigrants tired, poor, huddled, hungry, or thirsty seeking refuge in the United States. Its purpose is to illuminate the path to liberty for the global community. Over the years, Lady Liberty symbolically offered freedom to France and Europe, inspiring these regions to formulate their own interpretations of freedom.

While various countries developed their versions of freedom, none paralleled the unique form established by the United States. The U.S. was the pioneer in embracing freedom, signing the Declaration of Independence and crafting a Constitution designed to protect the natural rights of individuals by limiting the government's authority.

Despite the passage of time, the true meaning of the original documents—such as the Declaration of Independence, U.S. Constitution—and the Statue of Liberty appears to elude many. Those who misunderstand or intentionally misinterpret these symbols risk altering the United States into something contrary to the founders' intentions.

In essence, the Statue of Liberty is a testament to the enduring spirit of freedom. Its light does not guide immigrants to the United States but illuminates the path to liberty for the entire world. Understanding this fundamental truth allows us to appreciate the rich historical significance of Lady Liberty and the principles she represents.\

Busting Health Fads Is a Mission Of This Blog

There are people trying to control the way you live. They want you to wear sunscreen because they make money off sunscreen. Even studies showing sunscreen doesn't protect against melanoma are brushed off. It's because they know if they tell you to do something you will abide and do it. It will become a fad of sorts. It will become a myth that can't be unbusted.

But then you have people like me. I'm a skeptic. When everyone is thinking something, I become skeptical. And then I look into what they're saying and find that there's not one iota of evidence to support it. But, despite that, every doctor says you need to wear sunscreen. Even when studies show it's not true, they say, "Nope! You still need to wear sunscreen! Doesn't matter what the evidence shows!"

Poppycock

You have these scientists who have a political agenda. They can't get politics out of their science. And so even when the studies they perform disprove their agenda, they find some way of spinning it, even within their own studies. You have industries controlling the research. A good example is pharmaceuticals. Who do you think funds much of the inhaler research? It's not non-profits. Most of it is funded by big pharma.

Keep reading my blog and I will give you plenty of examples of this. I mean, how may global warming believers have chimed at some point that we only have ten years to live if we don't do something to stop it. And then that ten years comes up and we are still here and nothing has changed and no one ever calls them on their poppycock fear mongering. No one! Except people like me. And I bet there's those reading this that think I'm the idiot Because I don't go with the fad. I"m not the sheep, so I'm the idiot.

So, when I hear these things I think to myself, "Where's the evidence?" And even if they offer evidence, is it real. A good example of this is global warming. They offer lots of evidence that there is global warming. But, 100% of this evidence is computer modulated data. Did you know that computer modulated data is only as good as the data put into it. If you put crap into it you will get crap out. So, in reality, it's not evidence.

So, that's why I question even this global warming/ Global cooling/ Climate change stuff. It's just industries, political activists, trying to push forth their agenda. And good people buy into it hook, line, and sinker. I won't let that happen to me. And I hope you don't either.

Don't get me wrong. I love the environment. As God fearing person, I will do everything in my being to keep the Earth safe and clean. But I'm not buying into a fad. No way. Not this guy. I'm not going to support a theory, where the solution to it is destroying the economy.

And when you do what they say, and you make the changes they want, and nothing changes, no one calls them on it. Ha Ha. So many times this happens. Then they blame people like me who didn't support it. But they fail to look at their own beliefs to really see if they are truly valid.

Do they work? Is their science unbiased? Do their policies truly work? I'm the skeptic who says it probably doesn't work and it's probably not true. Evidence is that we are still here on God's Green Earth.

So, they say it's conventional wisdom. But, conventional wisdom is not always right. Sometimes, it's even proven false and they won't admit it. They just continuing to push forth their myth on behalf of a political agenda on behalf of industries.

10 Weight Loss Myths Busted

Healthcare has a history of myths. In fact, medical history is about 99.9% mythical. And this runs even into our modern medicine. Sad to say, much of what is known today about medicine is a mythical. I have given many examples of this on this blog. And there's no better place to start than with weight loss.

You have to drink 8-10 glasses of water every day to lose weight.

Not true.

You have to quit drinking to lose weight.

Not true.

You can't eat McDonald's and birthday cake when you're trying to lose weight.

Not true.

You have to exercise to lose weight.

Not true.

Running is bad for your knees.

Not true.

You can't eat saturated fat and lose weight.

Not true.

You can't eat eggs on a diet.

Not true.

You should limit salt on any diet.

Not true.

You have to eat breakfast to lose weight.

Not true.

Diet pop causes you to gain weight.

Not true.

So, now you know about weight loss myths. This should help you find a better weight loss program that works for YOU. Personally, I'm working on a program that allows me to continue doing and continue eating the things I enjoy.

Myth Buster: You Can Lose Weight And Gain Muscle At Same Time

Two friends were discussing dieting. Friend A said he wanted to lose weight and gain muscle. Friend B said, "You can't do both at the same time." 

I intervened: "That's a myth because you can.

Friend B said, "No you can't. It's impossible." 

I said, "It is possible, and I have. That's the entire premise of work out programs like the Body-For-Life." 

"Do you have proof?" he said.  

"Yes. As a matter of fact, I have loads of proof. I have articles. I have myself."

"What do you mean, you have yourself." 

"I am proof. I have lost weight and gained muscle lots of times. I have lost up to 40 pounds while gaining muscle. I mean, I'm no Arnold, but I do have some muscle tone that didn't exist."

See, that was the end of the discussion. But this highlights the difference between common sense and what they teach in colleges and universities. They teach conventional wisdom. They teach the same stuff that has been said over and over and over without citation. 

You have to eat breakfast. You can't eat eggs. You can't lose weight and gain muscle at the same time. Cholesterol causes heart disease. Salt causes high blood pressure. All of these are myths that do nothing but cause people to eat boring foods that are not satisfying. Foods that make it harder to lose weight.

So, just ignore them all. I mean, do your research. Sometimes the conventional wisdom people are right. When they right give it to them. Let them know they are right. But, when they are wrong, ignore them. You don't have to argue with them. But when it's your children, I think you ought to share what you know. 

Go to Hussmanfitness.com. John Hussman is a doctor. He's also a weight loss expert. He proves how you can lose weight and gain muscle at the same time. So, don't just take my word for it. I mean, I've done it. But, take the experts advice before mine. 

In fact, there are lots of people I know who have lost weight. They all look good. But those who participated in a muscle training program developed muscle tone while they lost weight. Anyone who loses weight looks nice. But those who also gained muscle look all the sharper. 

Further reading:

• Hussman Fitness: You really do change from the inside out

Myth Buster: Eggs Do Help You Lose Weight After All

So, I started a weight loss program in 1998. Eggs were not on the recommended food list. I ate fake eggs, but they were expensive and no fun. Today it appears eggs are now recommended. They are now the staple of my diet. So, what has changed?

When did I start eating eggs? Why? Well, it started when I was listening to a radio program on the radio. This would have been sometime in 2015. A pediatrician was being interviewed. He said researchers were studying why children pooped out during the course of the day.

He said a theory was that they were eating foods high in carbohydrates for breakfast. They were eating lots of foods like cereal. By the third hour and before lunch, their carbohydrate levels tanked. This made it hard to pay attention. This affected grades for the third hour.

I'm simplifying this, but this is the gist of it.

I'm sure they developed various theories attempting to explain this. Should lunch be earlier? Or did it have to do with what kids were eating for breakfast?

As part of one study, they had two groups. The study group ate eggs and bacon for breakfast. The control group ate what they normally ate, which was cereal. It turned out that those who ate eggs and bacon did better in school. They did not tank at the third hour. Their grades were better.

Now, this was just one study. But other studies showed the same thing. Kids who ate hearty breakfasts performed better in school.

Then there were other studies done regarding eggs and bacon for breakfast. You had the study and control groups. It turned out that those who ate eggs and bacon for breakfast lost more weight than those in the control group.

Actually, it was simpler than that. Initial studies showed that those who ate eggs and bacon for breakfast were less likely to binge during the course of the day. They were less likely to have those weak moments where they craved cookies and cake. They were less likely to give into these low points in the day.

They conclusion theorized this was due to the increase in protein.

Another similar theory is that a good hearty meal increases the release of dopamine. Dopamine is a happy hormone. It makes you feel good. Dopamine makes you feel satisfied. So, you are less likely to binge the rest of the day.

But eggs will cause cholesterol levels to rise? Studies proved this was also a myth. Eggs did not cause a rise in choleserol levels. In fact, it was learned that eggs contain low density lipoproteins, which is good cholesterol.

Other studies showed that they did not cause a rise in cholesterol. Other studies showed that cholesterol does not cause heart disease. In fact, even the government now recognizes this.

So, weight loss gurus now recommend eggs for breakfast.

It was initially thought this had to be for breakfast. But, this is not true either. It just has to be the first meal of the day, no matter when that meal is. I discussed this in my post, "Myth Buster: You Must Eat Eggs For Breakfast."

Further reading:

• Thrillist: Scientists Insist You Eat Eggs And Bacon For Breakfast
• Daily Mail: Breakkfast like a king: Why a high fat bacon and eggs meal is healthiest start to the day (but only first thing)

Myth Buster: Saturated Fat Causes Heart Disease

When it comes to medicine we have to be careful what we read. This is particularly true when it comes to conventional wisdom, especially when something is said without citation. Something like, "High-fat foods may cause weight gain and heart disease."

We are fed a barrage of information about fatty foods causing weight gain and heart disease. Seldom is there a reference supporting this. It's just said as though it were a fact, similar to the one that says, "Humans are causing global warming."

Evidence, please?

At least with global warming, it's computer moderated information. What they don't tell you is that the information that comes out is only as good as what comes it. So, if what goes in is junk, what comes out is junk. But, when it comes to fatty foods causing weight gain and heart disease, there's no evidence to be heard from.

In this case, it seems that someone just made this up because it sounds good. Then everyone else just kind of went with it. Then it becomes conventional wisdom. And it's thought to be a fact. When in fact it's just a myth.

A few years ago I wrote a good article on this blog. It was called "Myth Busted: Junk Food Doesn't Cause Heart Disease." So true I turned out to be. Nina Teicholz discussed this in the Wall Street Journal in her article: "The Questionable Link Between Saturated Fat and Heart Disease."

She said the myth was started by one person by the name of Ancel Keys. This lead to a 50-year campaign to convince people not to eat meat, eggs, and whole fat dairy.  Despite this campaign, there has never been one scientific piece of evidence to show this to be true. 

She said:

"Saturated fat does not cause heart disease"—or so concluded a big study published in March in the journal Annals of Internal Medicine. How could this be? The very cornerstone of dietary advice for generations has been that the saturated fats in butter, cheese and red meat should be avoided because they clog our arteries. For many diet-conscious Americans, it is simply second nature to opt for chicken over sirloin, canola oil over butter.

The new study's conclusion shouldn't surprise anyone familiar with modern nutritional science, however. The fact is, there has never been solid evidence for the idea that these fats cause disease. We only believe this to be the case because nutrition policy has been derailed over the past half-century by a mixture of personal ambition, bad science, politics and bias.

She provides us with the history of the myth.

Our distrust of saturated fat can be traced back to the 1950s, to a man named Ancel Benjamin Keys, a scientist at the University of Minnesota. Dr. Keys was formidably persuasive and, through sheer force of will, rose to the top of the nutrition world—even gracing the cover of Time magazine—for relentlessly championing the idea that saturated fats raise cholesterol and, as a result, cause heart attacks.

This idea fell on receptive ears because, at the time, Americans faced a fast-growing epidemic. Heart disease, a rarity only three decades earlier, had quickly become the nation's No. 1 killer. Even President Dwight D. Eisenhower suffered a heart attack in 1955. Researchers were desperate for answers.

As the director of the largest nutrition study to date, Dr. Keys was in an excellent position to promote his idea. The "Seven Countries" study that he conducted on nearly 13,000 men in the U.S., Japan and Europe ostensibly demonstrated that heart disease wasn't the inevitable result of aging but could be linked to poor nutrition.

Critics have pointed out that Dr. Keys violated several basic scientific norms in his study. For one, he didn't choose countries randomly but instead selected only those likely to prove his beliefs, including Yugoslavia, Finland and Italy. Excluded were France, land of the famously healthy omelet eater, as well as other countries where people consumed a lot of fat yet didn't suffer from high rates of heart disease, such as Switzerland, Sweden and West Germany. The study's star subjects—upon whom much of our current understanding of the Mediterranean diet is based—were peasants from Crete, islanders who tilled their fields well into old age and who appeared to eat very little meat or cheese.

 As we know, once something becomes established in the medical community, it becomes conventional wisdom. Once something becomes conventional wisdom, it becomes almost impossible to disprove. Global warming is a perfect example of this. Now, it appears, that saturated fat is another.

But, don't worry. The American Heart Association still lists Saturated fat as a big no-no. No citation. I'm not criticising the AHA here because they do lots of good things. I'm just saying, it's so easy to become a victim of a myth.

And, besides. Modern evidence does show that only some people have heart disease genes. So, it would seem to me that a better thing to teach is, "If you have a family history of heart disease, you might want to be careful with high-fat foods and cholesterol."

But that's not how we are in this world. We continue to repeat myths long after they have been disproven. Hypoxic Drive Hoax anyone?

Further reading:

• Wall Street Journal: "The Questionable Link Between High Fat And Heart Disease."  
• MRT Cave: Myth Busted: Junk Food Doesn't Cause Heart Disease

Myth: Epinephrine is stronger than albuterol, and better at ending asthma attacks

Sus-Prhine was once a top-line
treatment for asthma
in emergency rooms.

I am a victim of a myth. I am guilty. I believed, and have for a long time, that epinephrine is better at opening airways and ending asthma attacks than albuterol. I am guilty of thinking, at times, "Why don't we just give epinephrine?" However, truth be told, according to studies, epinephrine is not any better than albuterol.

This is one of the few times where the medical profession dispelled a myth and realized the truth before me. Various studies in the late 1980's and early 1990's showed that albuterol was equally effective as epinephrine at opening airways. It was also shown to be far safer.

The most convincing study was published in 1991, and I wrote about it in my post, "1991: Study finds albuterol works just as well as albuterol."

The study gave albuterol and epinephrine to various children of an average age around 8-years-old, and the various testing done showed that both medicines were equally effective at ending asthma attacks.

So, it is basically for this reason why doctors give albuterol to asthmatics rather than epinephrine. Epinephrine is sometimes offered as a last resort prior to intubating asthmatics, but it's either never given because albuterol eventually works (or, more likely, the systemic corticosteroids start working), or it is given and fails to work. It fails to work because albuterol was already probably given ad nauseum, and epinephrine is not better than albuterol.

Even recently I have wondered why we don't just give epinephrine to some asthmatic patients who come in with asthma exacerbations. Here we have access to this shot that could just open them up in a matter of minutes, as opposed to giving albuterl ad nauseum.

The reason I am such a victim of this myth is because epinephrine benefited me so many times when I was a kid. I'd go to the doctor's office or emergency room and the shot would start opening my airways within five minutes. It created a feeling of euphoria. I mean, if you can't breathe and all of a sudden you can, you'd feel euphoria too. Although, some of this effect was probably the product of the medicine.

The last time I was given it was in 1991. When I asked for Sus-phrine, which was basically a long-acting form of epinephrine, the doctor had no idea what I was talking about. At this point, it had been six years since I had needed it or asked for it.

However, the pharmacist found a vial, and I was given it. And it opened my airways up. A few months later I went to the emergency room again. This time the doctor convinced me to try this new medicine called albuterol. I had actually had an albuterol inhaler, but never tried the solution before.

To my surprise, it worked just as well as the epinephrine at opening my airways up. I remember being excited about this new medicine. When I asked about it the therapist said it was a safer version of Alupent (the solution I had at home at the time).

A week later I had my own prescription for albuterol. I have been using it ever since.  Still, it never dawned on me that this new albuterol thing was equally as effective as epinephrine for another 16 years. I mean, it's kind of a "Duh!"  But, you know, it was hard for me to give up on the idea that a medicine that saved my life so many times could be replaced.

If you want to learn more about epinephrine, Sus-phrine, or gain access to the study referenced here, check out the following links.

Further reading:

• 1900: The discovery of epinephrine
• 1981: Sus-Phrine: The greatest asthma medicine ever
• 1991: Study finds albuterol works just as well as epinephrine
• 1900-current: The evolution of asthma rescue medicine

It's time to stop the war on salt

So, New York City has now received permission to fine chain restaurants for serving up too much salt, or for not using icons to warn customers of salty food. This ruling allows me to segue into a topic I've been meaning to get into for quite some time: What if they are wrong? What if too much salt is not harmful? If salt is proven to be safe, will New York change this ruling?

This subject kind of touches home with me because my mom suffered for many years with hypertension, and still does. She used to have to drink these horrid tasting drinks to keep her blood pressure in check. I think they were potassium drinks, but I'd have to ask her. My mom was also encouraged not to eat foods that contained salt, so she never added salt to anything she cooked. She never ate foods like potato chips, and used a salt substitute.

The science makes sense. The theory has it that eating salt raises the level of sodium chloride in your bloodstream, and this salt is absorbed into cells lining the bloodstream. This, in turn, causes these vessels to constrict, thereby raising blood pressure.

Even before I became a respiratory therapist, which was prior to 1995, I remember reading studies showing that, while this theory seems to make sense, it might not be true. Since then various studies show that cells only take in so much sodium chloride, and what is not used is simply excreted by kidneys. So, the evidence seems to show that too much salt does not cause hypertension.

In fact, even more recent studies show that, to the contrary, too little salt is more likely to cause hypertension than too much salt. Too little salt increases your risk of stroke and heart disease, not too much salt.

So, this brings me back to my original question: will this new evidence cause New York to change this ruling? Will evidence showing that too much salt will not cause high blood pressure, and that too little salt might, cause progressives to stop their push to limit salt intake? Or is there so much at stake here that they will not stop their quest no matter what the evidence shows?

Recently I was diagnosed with hypertension. My doctor prescribed a blood pressure medicine for me, told me to take one pill every day and then he said, "Well, you should probably limit your salt intake. In fact, the evidence seems to show it doesn't matter. So, if you want to continue to add salt to food to make it taste better, and your blood pressure is under control, go for it!"

So, my doctor seems to have caught on to modern wisdom. He understands that while the science shows one thing, analytical data shows another. This is one more old medical myth that appears to be out the window, and yet progressives continue to push for laws to make food taste worse. So, my argument is for progressives to stop the war on salt, and find something else to do with their time.

Myth Buster: Exercise causes weight loss

I think I wrote about this before on this blog, that you can't lose weight just by exercising alone. I tried it last winter, and I actually ended up gaining weight.

You see ads galore trying to get you to buy one gadget or another to lose weight. They show you a picture of the gadget, and a picture of some guy with six pack abs and say, "This could be you if you buy this product."

The truth is, that person never lost weight using that product. If fact, he probably had that six pack long before the product was ever even invented.

Truth is, it doesn't matter what product you buy, you will not lose weight by exercising alone. You have to diet. Losing weight is a matter of ins and outs. If you take in less than what goes out of your body, you will naturally lose weight.

Yes, there are advantages to exercising. I've written about them too on this blog and my asthma blog. The benefits of exercise is overwhelming, and I highly recommend you do it.  Exercising strengthens your heart and lungs, improves your immune system and makes you feel better overall.

Yet exercise alone will not result in weight loss.  It may help you burn fat faster, but it will not cause you to lose weight if you do not also eat a healthy diet.

I've always believed this, yet trying to find proof in a world dominated by marketers, and a media, that is content to have you believe that exercise is the key to weight loss so they can brainwash you to buy their products is never easy.

However, I found an article at time.com called, " Why Exercise Won't Make You Thin," by John Cloud (Thursday, Aug. 06, 2009) that explains quite simply why exercise alone won't make you thin.

Cloud said that if exercise alone made people thin, the fact that the percentage of people exercising increased from 47% to 57% from 1980 to 2000 would result in a thinner society. Yet, the opposite is true, as America is fatter than ever before.

He said:

"The basic problem is that while it's true that exercise burns calories and that you must burn calories to lose weight, exercise has another effect: it can stimulate hunger. That causes us to eat more, which in turn can negate the weight-loss benefits we just accrued. Exercise, in other words, isn't necessarily helping us lose weight. It may even be making it harder."

He also mentions a study where 464 women were asked to maintain their normal diet. Most were told to exercise, while one group was told not to exercise.

The results:

"The findings were surprising. On average, the women in all the groups, even the control group, lost weight, but the women who exercised — sweating it out with a trainer several days a week for six months — did not lose significantly more weight than the control subjects did....Some of the women in each of the four groups actually gained weight, some more than 10 lb. each."

He said that a paper written by a group of psychologists explains why this happens:

"Many people assume that weight is mostly a matter of willpower — that we can learn both to exercise and to avoid muffins and Gatorade. A few of us can, but evolution did not build us to do this for very long. In 2000 the journal Psychological Bulletin published a paper by psychologists Mark Muraven and Roy Baumeister in which they observed that self-control is like a muscle: it weakens each day after you use it. If you force yourself to jog for an hour, your self-regulatory capacity is proportionately enfeebled. Rather than lunching on a salad, you'll be more likely to opt for pizza."

It is possible, Cloud concludes, that the recent trend to get people to exercise more has caused America to get fatter?

Originally published on 8/17/2009; edited

Further reading:

• Why exercise won't make you thin -- by John Cloud in Time
• Jogging may not be bad for joints
• Myth Buster: You must eat a breakfast to feel good 
• Exercise: The News You Don't Want to Hear -- Huffington Post

Myth Buster: Measles not caused by ignorant parents

I'm personally not against vaccinations.  I've had all mine, particularly my mandatory flu vaccination that reduces my chance of getting the flu by a whopping 23 percent.  Yet I certainly don't think the government should have the kind of power that mandates that people get them.

This is a subject that has risen once again as a bunch of people in California have contacted the Measles, a disease that was conquered in this country a long time ago.  Up until recently the disease did not even exist.

So making it mandatory to get the measles vaccination is not the issue here.  There is some other agenda at hand here.  I mean, everybody is blaming the un-vaccinated and no one wants to talk about why we need them in the first place.

Yet, considering this is a politically incorrect blog, I am going to tell you what the real cause of the Measles outbreak is: it is lapsed border control.

I know people don't want to hear it, but it's true.  If we secured our borders so that people could only get into our country by legal means, those with diseases would be screened at the border and not let in.  Diseases like the Measles would stay out.

Yet both republicans and democrats alike don't want to talk about this issue for fear that they might lose votes.  They have, in effect, put their own political ambitions ahead of their nation.  They would prefer to make laws forcing us to give up some (more) of our liberties so they look like they are solving problems and can get re-elected.

Simply put, if our borders were secure, there would be no measles in this country right now.  That's what this is all about.  That is the root cause of the Measles outbreak, not the American men and women who choose not to get their children vaccinated for whatever educated or ignorant reasons they have (CBS News Reports on the current debate).

But instead of looking at the root cause of the problem (lapsed borders), you have people in this country, those who want more government control over our lives, claiming that anyone who is anti-vaccine is a moron and a dunce.  So what if they are: people have a constitutional right to be stupid.

But I don't think the choice not to vaccinate makes anyone stupid.  It actually take courage and intelligence to challenge the consensus view.  It shows the ability in this country to think for yourself and the freedom to act in the way you choose as opposed to just being sheep and acting like everyone else.

It generally shows the fear that there may still remain risks to anything you put into the human body, particularly the body of a newborn baby.

Look, this is a free country.  And people have been given the choice to vaccinate or not to vaccinate themselves and their children for forever, and the Measles and many other diseases were exterminated in this country.

So now people with diseases are coming into this country with diseases, and the people getting blamed are not the people whose main job is to keep us safe from this type of thing, but innocent Americans.

Our ancestors fought so hard for us to "finally" obtain the right to choose, and now some of us are so eager to just give that up.  To me this is a sad day in American history to even be discussing this.

Again, I am not against vaccinations.  I am actually for them.  There are a few vaccinations I won't let my kids get, such as the HPV vaccination, but that's a discussion for another day.

Vaccinations are a wonderful invention, but they should not be mandatory. People have a God given right to choose what they put into (and what they don't put into) their bodies and the bodies of their children.

Further Reading:

• To the Parent of the Immunocompromised Child Who Thinks My Kid is a Threat

Myth Buster: A high FiO2 is protective

So you have a patient come into the emergency room in severe respiratory distress, possibly heart failure, but the SpO2 is normal. In the past it was acceptable to place these patients on a nonrebreather to prevent the patients condition from deteriorating, thus allowing you time to react. This, however, may no longer be acceptable.

I think doctors have gotten much better at not panicking in this regard, as even patients with heart failure, while the used to always get a nonrebreather, that seems to no longer be the case. As with chest pain and any other condition, no oxygen is given unless the SpO2 drops below 94%.

The reasoning for the change was described in an October, 2013, article in Respiratory Care, by Thomas Blakeman.  He said:

According to Downs, the only true indication for prophylactic hyperoxyxgenation is prior to tracheal intubation. Downs furher states that, hypothetically, a patient on FiO2 of 100% and having a PaO2 of 650 m Hg, could drop to 90 mm Hg due to lung function deterioration over a period of 15-20 minutes, but the SpO2 would not drop below 98%. This drop would not be enough to indicate a problem. But over the next 5 minutes the SpO2 wold drop to 92%, alerting the caregiver to investigate. In this scenario the elapsed time until a problem is detected would be 20-25 minutes. If that same patient was on an FiO2 of 30% with a PaO2 of 90 mm Hg and an SpO2 of 99% and experienced the same problem, the SpO2 would decrease to 94% within 10 minutes, alerting caregivers to a problem much earlier. Additionally, if a patient is already receiving FiO2 of 100%, there is no room to increase once a problem is detected."

So, over-oxygenating, a common occurrence in hospitals, may mask an underlying problem, delaying treatment.

References:

1. Blakeman, Thomas C., "Evidence for Oxygen in the Hospitalized Patient: Is more Really the Enemy of Good," Respiratory Care, October, 2013, volume 58, number 10, pages 1679-1693

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Myth Buster: FiO2 less than 60% is safe

One of the myths of respiratory therapy is if we get the FiO2 down to 60% we are safe.  In fact, most of us were taught in school that an FiO2 greater than 60% produced more side effects than an FiO2 less than 60%.

This apparently is a myth, and the following is the evidence:

1. Register et al conducted a study with subjects under going open heart surgery, all of whom were breathing room air preoperatively  It was found that in subjects administered FiO2s of 0.50 postoperatively had a greater degree of hypoxemia on room air on postoperative day 2 than those given sufficient oygen to maintain SpO2 (greater than) 90%.  After repeating the study using only room air intra- and post-operatively, and finding that most subjects did not have a decrease in blood oxygen levels, as compared to preoperative values, it was postulated that the hypoxemia experienced in the first study was due to the use of oxygen during and after surgery.

1. Garner et al exposed rats with peritonitis to FiO2 of 0.80, 0.4, or 0.21. Mortality was lowest in the FiO2 O.21 group, and highest in the Fio2 0.80 group.  Upon postmortem examination it was found that lung pathology did not differ between the groups but there was substantial liver damage with FiO2 (greater than) 0.21.  It was postulated that free radical formation caused the liver damage. 

This is yet another example that oxygen should not be administered unless necessary, and that every effort should be made to reduce oxygen as soon as possible.  Thankfully, most hospital oxygen protocols call for maintaining an SpO2 of somewhere in the range of 88-94%.  

References:

1. Blakeman, Thomas C., "Evidence for Oxygen in the Hospitalized Patient: Is more Really the Enemy of Good," Respiratory Care, October, 2013, volume 58, number 10, pages 1679-1693

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Myth Buster: Routine use of oxygen is safe

There is now ample evidence that oxygen is a drug with side effects.  No longer should health care providers administer oxygen under the philosophy "it may not help, but it won't hurt."

Oxygen used to be considered useful, or at least harmless, for any of the following situations, despite lack of evidence it does any good:

• Emergency departments
• Post-anasthesia care units
• Conscious sedation
• Chest pain
• Shortness of breath
• Critical Care Units

ACLS used to recommend 2-4lpm by nasal cannula for chest pain. The idea here is that if a low flow of oxygen to the heart is causing the chest pain, the oxygen "might" help.  

However, there was never any science to show this.  Plus, it makes no sense, because if you are getting an SpO2 reading of 98%, then you know the heart has an ample amount of oxygen.  If it's not getting enough oxygen it's because of a blockage in the coronary arteries, not the supply of oxygen to the heart. 

ACLS currently recommends oxygen only if the SpO2 is less than 94%.  This makes much more sense to me.  

Plus, most hospital-wide oxygenation protocols call for an SpO2 of 90-94%, and even 88% is often acceptable.  This makes sense particularly if you look at the deoxyhemoglobin curve.  

One of the main reasons why it's important not to oxygenate until the SpO2 decreases is that the use of supplemental may mask that an underlying problem may be occurring.  

A patient may have decreased ventilations, but this will not be recognized because the SpO2 is already artificially maintained with supplemental oxygen.  When such a patient is not on oxygen, a dip in SpO2 would be noticed at a routine check, and oxygen could be administered at this time, with appropriate measures being taken to recognize and resolve the underlying cause. 

The new policies make sense, especially when you consider that oxygen is a drug with side effects and an expense. To oxygenate based on a myth that it will help but won't hurt is not good medicine. 

References:

1. Blakeman, Thomas C., "Evidence for Oxygen in the Hospitalized Patient: Is more Really the Enemy of Good," Respiratory Care, October, 2013, volume 58, number 10, pages 1679-1693

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Myth Buster: You must eat a breakfast to feel good

I remember back in the 1970s watching these videos in class called Mulligan Stew, where the gang would inculcate into our little heads the importance of breakfast. Mulligan would meet kids who were "grouchy and don't eat right."  The gang would say things like "if you don't eat breakfast you get headaches and get grumpy during the day."

Mulligan Stew was a show that was boring and no one wanted to watch.  It was so unpopular, in fact, that it was cancelled after only six episodes were aired in 1977. But educators liked it so much that they forced us kids to watch it ad nauseum, forcing the theme "4-4-3-2" on us: four servings of bread and cereal, four servings of fruits and vegetables, three servings of milk, and 2 servings of meat."  You could get started on this early by eating a good breakfast.

New evidence, however, suggests that this is not true.  In fact, modern researchers suggest there was never any evidence to show that breakfast was essential to begin with, that it just sounded like it must be true.

New evidence suggests that you do not need breakfast to start your metabolism after all, and therefore breakfast is not needed to lose weight. They also proved that breakfast is not needed to keep you from getting headaches and grumpy, as Mulligan proclaimed.

The August issue of The American Journal of Clinical Nutrition reported on various studies that proved that breakfast is not essential.  The studies showed that people who were not morning people could skip breakfast and burn just as many calories as those who ate breakfast.

The studies showed that those who did not eat breakfast had just as much energy as those who did not, lost an equal amount of weight, and did not necessarily become so hungry that they ate too much at lunchtime.  Those are all things we were told would happen if we did not eat breakfast.

New evidence suggests that if you want to skip breakfast you can do so without harm to your health or well-being.  Besides, skipping breakfast will allow you to put fewer calories into your body, thus allowing you another opportunity to keep your weekly calorie intake less than your calorie output.

New evidence suggests that if you like breakfast, great!  But, if you are one of those folks who prefers to skip breakfast, that's fine too.  Still, as with most myths, the idea that breakfast is essential to good health and well-being will probably continue to be inculcated into our heads because it sounds good.

To read about more myths busted at the RT Cave click here.

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How does NIV help with CHF?

There have been a few physicians who have explained to me that noninvasive ventilation helps patients with congestive heart failure (CHF), or pulmonary edema, because it forces fluid out of the lungs.  But this is a myth.

The true value of NIV for CHF is best described by Jeffrey Sankoff, MD, from Emergency Physicians: 

Contrary to popular belief, NIMV does NOT push edema fluid out of the lungs. Patients with acute CHF have an imbalance in the CO (cardiac output) of the right and left sides of the heart. With the inciting event (detailed above) the left ventricle becomes compromised but the right ventricle usually does not. So the right ventricle continues to pump forward a normal volume of blood but the left ventricle becomes unable to keep pace. Fluid backs up into the lungs resulting in capillary leak and pulmonary edema. With NIMV, the resultant positive intra-thoracic pressure decreases venous return (blood flowing back to the heart). This reduces right-sided CO to a level that the left heart can equal or even exceed. Fluid ceases to back up and will even begin to be reabsorbed as left ventricular CO improves. Pulmonary edema ceases to worsen and may even diminish, often rapidly.

I think it's essential to understand this, because I have also had physicians place patients on NIV with the hope that it would help with their breathing, but also that it might improve their blood pressure.  The truth is, however, the low blood pressure is a contraindication for NIV, and now you know why.

Alternatives to the hypoxic drive theory

Since 1960, several studies have demonstrated what really happens when CO2 retainers are exposed to supplemental oxygen.  The best explanation comes from John Haldane himself in what is now referred to as the Haldane Effect, and another process we refer to as ventilation/ perfusion (V/Q) mismatching.

1.  The Haldane effect:   This law was created by John Haldane, a pioneer of oxygen therapy.  He proved that as Deoxygenation of the blood increases its ability to carry carbon dioxide.  Thus, the less oxygen on hemoglobin, the more CO2 on hemoglobin.  CO2 attaches to unsaturated hemoglobin molecules. Oxygen is more soluble in water and therefore has a higher affinity for hemoglobin, so if you increase oxygen in the blood by supplemental oxygen, CO2 molecules are forced off hemoglobin and oxygen takes its place.  This causes an increase in CO2 in the blood, or an increased PaCO2.

Most people would simply increase their respiratory rate and blow off this CO2. Yet COPD retainers who are in respiratory distress may not have the capacity to increase their respiratory rate, so their respiratory rate remains the same.  This causes their PaCO2 to rise.

Now consider that this patient may have an elevated hemoglobin level after years of oxygen deprivation, and you're going to have lots of extra CO2 molecules roaming around the blood stream.  This may be on top the patients already elevated CO2 retention.

All these CO2 molecules are transported back to the lungs for ventilation to take place.  Yet because many alveoli are poorly ventilated (V/Q mismatching), and because the patients ability to increase ventilation is tapped out, PaCO2 levels will rise.

The Haldane effect was proven by a study described in 1996 in Critical Care Medicine, "Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease." (1)

2.  V/Q mismatching:  Consider that V = Ventilation and P = Perfusion.  So, generally this is Ventilation/ Perfusion mismatching.  It is caused by increased airway narrowing due to airway remodeling, bronchospasm, and increased sputum production.  Where this occurs, the lungs are perfused but poorly ventilated.  It means that in areas of the lungs where V/Q mismatching occurs do not allow CO2 to enter the lungs, and oxygen to enter.

When an alveoli is poorly ventilated the vasculature around it will constrict so oxygen goes to alveoli that are ventilated well.  This is how that patient's body has made efficient use of his diseased lungs.

Now add 100% oxygen and you screw up this naturally occurring phenomenon.  Now the vasculature around that non-ventilating alveoli dilates, and this causes blood to be sent to the non functioning alveoli.  Now you have even greater V/Q mismatching and more CO2 that doesn't get out of the blood.  The end result, therefore, is an increase in PaCO2.

This theory was proven via a study completed in 1980 and reported in American Review of Respiratory Disorders, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure," (2)

These two theories are far more viable than the hypoxic drive theory, and both have been proven by science.  Regardless, the hypoxic drive theory continues to be the gold standard theory.

References:

1. Hanson, et all, "Causes of hypercapnia with Oxygen Therapy in patients with Chronic Obstructive Pulmonary Disease," Critical Care medicine, 1996, volume 24, pages 23-28 (abstract available by link)  Source #3 above also indicates support for this theory (Caruano-Montaldo, ibid, page 218), and reference # 12 (Robinson, ibid, page 1527), and #13 (Dick, C.R., ibid)
2. Aubier, M, et al, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure", American Review of Respiratory Diseases,  1980, Volume 122, pages 747-754 (abstract available by link) Source #3 above also indicates support for this theory (Caruano-Montaldo, ibid, page 218)

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What evidence proves the hypoxic drive theory wrong?

Ironically, and surprisingly, there has never been a real scientific study done to prove the hypoxic drive theory.  On the contrary, many studies have shown the theory to be nothing more than a myth.

For instance, in 1989 Greggory A. Schmidt M.D. and Jesse B. Hall M.D. wrote an article, "Oxygen Therapy and Hypoxic Drive to Breath:  Is There Danger in the patient with COPD?" that was published in Critical Care Digest questioning the popular hypoxic drive theory.  (1)

Schmidt and Hall reported that little science was used in coming up with this theory.  No COPD patients were given oxygen and had their ventilations simultaneously measured.  (1)

In fact, they report that in one study COPD patients were given oxygen and they found that "the rise in CO2 could not be accounted for by hypoventilation."

Likewise, a follow up study determined that supplemental oxygen to COPD patients caused decreased ventilation in some, unchanged ventilation in some, and normal ventilation in some. They wrote that "The commonest pattern was of early hypoventilation followed by a return to baseline.

Schmidt and Hall "attributed the rise in CO2 to an increase in the dead space to tidal volume ratio (also referred to as ventilation/ perfusion mismatching) consequent to oxygen therapy, though the mechanism for this change is unclear."

Abier et al in 1980 showed that 20 COPD patients in acute respiratory failure receiving 5lpm oxygen for 30 minutes showed a 14% reduction in minute ventilation with only a small rise in PaCO2, despite a large rise in PaO2.  They concluded that there was no correlation with the rise in PaCO2 and the fall in ventilation. (2)

Abier et al in 1980 also studied the effects of 100% oxygen on minute ventilation in COPD patients presenting with acute respiratory failure.  The concluded, once again, that despite the slight rise in CO2 and drop in minute ventilation, there was no correlation with the rise in PaCO2 and the fall in ventilation. (3)

In a 2000 study by Robinson et al, 22 COPD patients were given 100% oxygen and ventilations fell by an average of 20% for those who were CO2 retainers, yet the cause was determined to be due to ventilation/ perfusion mismatching, "not just a failure of ventilatory response to the increase in PaCO2."  (4)

A 2007 by Dick et al showed that oxygen induced hypercarbia was not caused by knocking out the drive to breathe.  In stable patients with COPD given 100% oxygen over a period of 15 minutes, oxygen saturations increased by about 7.6% and PaCO2 rose by about 6.6 mmgH, while minute ventilation was unchanged in all those studied. (5)

A 2014 study by Savi et all concluded the following:

Our results support the hypothesis that increasing the FiO2 in CO2-retaining COPD subjects on NIV does not cause any clinically important change in CO2 retention.  (6)

The also note:

The PaCO2 commonly rises somewhat when a patient with COPD receives supplemental oxygen, but carbon dioxide narcosis due to oxygen therapy is uncommon, and patients should not be kept hypoxemic for fear that oxygen therpay could aggravate carbon dioxide retention. The increase in CO2 is probably due to a change in dead space or shift of the hemoglobin-oxygen binding curve, rather than decreased respiratory drive.  The expected rise should not be specifically treated unless it is excessive, resulting in a trend toward acute respiratory acidosis on serial arterial blood gas analysis, with cenetral nervous system or cardiovascular side effects.  Carbon dioxide narcosis may occur with excessive FiO2, but is much less likely with low flow, controlled oxygen therapy.(6)

Despite all these studies, the hypoxic drive theory continues to be the gold standard theory regarding treatment of patients with COPD.  However, enough evidence now exists to support that supplemental oxygen is not as detrimental to COPD-CO2 retainers as once suspected.

References:

1. Schmidt, Greggory A., Jesse B. Hall M.D "Oxygen Therapy and Hypoxic Drive to Breath:  Is There Danger in the patient with COPD?" Critical Care Digest, 1989, 8, pages 52-53
2. Aubier M., Murciano D, Fournier M, Milic-Emili J, Pariente R, Derenne JP, "Central respiratory drive in acute respiratory failure of patients with chronic obstructive pulmonary disease, American Review of Respiratory Disease, 1980 volume 122, number 2, pages 191-199
3. Aubier M, Murciano D, Milic-Emil J, Touaty E, Daghfous J, Pariente R, Derenne JP, "Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure," American Review of Respiratory Disorders, 1980, volume 122, number 5, pages 747-754
4. Robinson, Tracey D., et al, "The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnia during Acute Exacerbations of Chronic Obstructive Pulmonary Disease," American Journal of Respiratory adn Critical Care Medicine, 2000, volume 161, pages 1524-1529
5. Dick, C.R., et al, "O2-induced change in ventilation and ventilatory drive in COPD," American Journal of Respiratory and Critical Care Medicine," volume 155, no. 2, Feb., 1997, pages 609-614
6. Savi, Augusto, et al, "Influence of FiO2 During Noninvasive Ventilation in Patients with COPD," Respiratory Care, March, 2014, Volume 59, Number 3, pages 383-387

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How the hypoxic drive theory was born

While oxygen was discovered as early as the 18th century, it was not routinely used therapeutically until the early 21st century.  Still, it wasn't until the 1940s that physicains started realizing their were risks associated with its use, and 1960 when the hypoxic drive theory was born.

Oxygen was discovered in 1777 by Joseph Priestley. Despite its availability, it was not routinely used to treat medical conditions mainly because there was no convenient means of producing, storing, and delivering oxygen to patients.  Yet by the turn of the 21st century the first two of these obstacles were resolved, and it was up to John Haldane to resolve the third.

In 1922, Haldane wrote about his own research on oxygen in "The Therapeutic Administration of Oxygen."  During WWI he had developed a mask to conveniently deliver oxygen to soldiers suffering from pulmonary edema due to poison gas.  After the war he continued his experiments in hospitals.

Soon thereafter oxygen tanks became more and more common at the patient bedside, and oxygen was tried on patients with pulmonary edema and pneumonia, although sometimes for patients with cystic fibrosis, asthma, emphysema and chronic bronchitis.  (7)

Once oxygen was administered to COPD patients, it was soon realized that some of these patients became lethargic and lost their drive to breathe.  It was soon learned that it was the oxygen causing this because it caused their carbon dioxide (CO2) to rise.

In 1949 a case was documented where a man with emphysema "lapsed into a coma after receiving oxygen therapy but rapidly recovered after the oxygen was removed," according to Nicola Cooper, Kirsty Forrest, Paul Cramp in their 2006 textbook, "Essential guide to acute care."

The text also explains that "in 1954 a decrease in ventilation in 26 out of 35 patients with COPD given oxygen therapy, with a rise in PaCO2 and a fall in pH.  No patient with a normal baseline PO2 showed these changes.  In a further study it was showed that stopping and starting oxygen therapy led to a fall and rise of PaCO2, respectively."  (8)

The concern became so great that in the 1950s a study was performed that ultimately lead Dr. EJM Campbell to give a lecture to pulmonologists in 1960 about the dangers of giving too much oxygen to COPD patients.  It was this lecture that forever linked hypoxic drive with COPD, and gave birth to the hypoxic drive theory.  (9)

Yet instead of a scientific theory being treated as a scientific theory it was treated as scientific fact, and this began the accepted practice of keeping patients in much need of supplemental oxygen hypoxic.

The medical profession decided the hypoxic drive theory sounded good so it must be good. The Hypoxic Drive Theory thus became the law of COPD land. Any evidence to the contrary would be rejected.

Of interest here is that the study Campbell referred to in his lecture consisted of only four COPD patients. Regardless, the theory quickly gained acceptance by the medical community, and became the gold standard when taking care of patients with COPD

Since then a few studies have confirmed the theory, although many have shed doubt on the theory.  Regardless, due to Campbell's presentation, the theory had already stuck in the minds of physicians and medical professors.  They had now become dogmatic to the theory, and closed minded to any evidence to the contrary.   (10)

References:

1. Schmidt, Greggory A., Jesse B. Hall M.D "Oxygen Therapy and Hypoxic Drive to Breath:  Is There Danger in the patient with COPD?" Critical Care Digest, 1989, 8, pages 52-53
2. Wilkins, Robert L, James K. Stoller, ed. "Egan's Fundamentals of Respiratory Care," 2009, pages 309-310
3. Caruana-Montaldo, Brendan, et al, "The Control of Breathing in Clinical Practice," Chest, 2000, 117, pages 205-225 (This article also provides a good review of the central and peripheral chemoreceptors and the drive to breathe)
4. Wojciechowski, William V., "Entry Level Exam Review for Respiratory Care:  Guidelines for success," 3rd edition, 2011, U.S., page 487?
5. Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusettes, page 24
6. Tines, John Hudson, "Exploring the History of Medicine," 1999, great read for obtaining a pithy history of medicine
7. Glover, Dennis W. , "History of Respiratory therapy," 2010, page 94, great read for obtaining a pithy history of respiratory therapy
8. Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusettes, page 24
9. Campbell, E.J.MRespiratory Failure,"  The British Medical Journal,  June 1965, 1451-1460 (article provided by link)

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What is the hypoxic drive theory?

The hypoxic drive theory was born in the 1950s, was given credulity in 1960, and was first disproved in 1987.  (1)  Since then the theory, known to some as the myth or the hoax, has become one of the most hotly debated theories in all of medicine.

The crux of the theory is that the main drive to breath comes from neurons in the medulla oblongata at the base of the brain.  These neurons receive signals from central chemoreceptors on the medulla and peripheral chemoreceptors located in the bifurcations of the aortic arteries and the aortic arch.

Respiratory rate is adjusted to maintain a normal acid base balance (pH) throughout the body.  The majority of the times, the central chemo receptors send signals to the brain that control breathing. They monitor carbon dioxide (CO2) levels.  When CO2 levels are high a signal is sent to speed up the drive to breathe to blow off the excess CO2.  In this way, CO2 is our main drive to breathe.

The peripheral chemo receptors send a signal to breathe when the partial pressure of oxygen in the arteries (PaO2) is less than 60. This is referred to as the hypoxic drive.  This hypoxic response is far slower than signals sent by central chemoreceptors, and therefore the hypoxic drive has only a minor role in breathing.

In COPD patients, chronic airway obstruction due to bronchospasm and increased mucus secretion blocks air passages, and as a result many alveoli become ineffective at ventilating (CO2 cannot get out and oxygen cannot get in).  For these patients, this results in a chronically elevated CO2 (greater than 50), and lowered oxygen levels (SpO2 less than 90 and Po2 less than 60). (2)

As CO2 rises, bicarbonate (HCO3) falls in order to compensate and prevent acidosis (a drop in pH, or a pH less than 7.35).  The result here is that many of these patients normally live with something like a PaCO2 of 50, a PaO2 of 50, and a Bicarb of 30.  These patients are aptly referred to as CO2 retainers, or simply retainers.

In many instances students are incorrectly taught that all COPD patients are retainers who breathe under influence of the hypoxic drive.  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.

In fact, of patients who present to hospitals in respiratory distress, half will have reversible CO2 retention, and half will be chronic CO2 retainers.  (5)

The hypoxic drive theory has it that the high CO2 may make the chemoreceptors tolerant of the high CO2, and thus CO2 ceases to be that person's drive to breath.  These patients are your prototypical CO2 retainers. The hypoxic drive theory, thus, states that many of them are hypoxic drive breathers.

Those who believe in the theory believe if you give these patients too much oxygen, enough to drive their PO2 above 70, then you will blunt their hypoxic drive and knock out their drive to breathe.  Their respiratory rare will slow, their CO2 will therefore rise even more, acidosis will occur, the patient will become lethargic (very sleepy or somnolent), and ultimately they will stop breathing.

It is for this reason that most medical experts champion for never over-oxygenating patients who are CO2 retainers. The experts recommend using a nasal cannula set at 2-4lpm, and never higher.  Or, if their respiratory rate is sporadic, to use a venturi mask set no higher than 40% FiO2.

These experts say that if the CO2 rises, that the FiO2 should be lowered.  This has resulted in many physicians accepting PO2s in the lower 80s and even the upper 70s in certain patients.

Yet this often results in the ire of caregivers taking care of these patients, because they are the ones who have to watch them suffer from dyspnea, or air hunger, or the feeling they can't catch their breath.

It has also resulted in ire because many of these patients are placed on 100% oxygen with no ill effect.  Many of these patents have been given breathing treatments using oxygen, estimated to be about 60%, and have never seen any patient drop dead during a breathing treatment.

It was evidence like this that made clinicians second guess the hypoxic drive theory.  It was from here that various studies were done to show, once and for all, whether the hypoxic drive theory is a fact, or whether it's nothing more than a medical myth.

What in turn happened was that, even though most studies proved the theory was in fact a myth, the subject became even more controversial.

References:

1. Schmidt, Greggory A., Jesse B. Hall M.D "Oxygen Therapy and Hypoxic Drive to Breath:  Is There Danger in the patient with COPD?" Critical Care Digest, 1989, 8, pages 52-53
2. Wilkins, Robert L, James K. Stoller, ed. "Egan's Fundamentals of Respiratory Care," 2009, pages 309-310
3. Caruana-Montaldo, Brendan, et al, "The Control of Breathing in Clinical Practice," Chest, 2000, 117, pages 205-225 (This article also provides a good review of the central and peripheral chemoreceptors and the drive to breathe)
4. Wojciechowski, William V., "Entry Level Exam Review for Respiratory Care:  Guidelines for success," 3rd edition, 2011, U.S., page 487?
5. Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusettes, page 24

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Running linked to a shorter lifespan

Some people think the more they run, the longer they run, the healthier they will be and the longer they will live.  Yet the evidence doesn't support this theory.

I don't know if most people know this, but despite what we have been taught in schools and by the media, running on a treadmill does not make your heart stronger and prevent diseases like heart disease.  Studies show that this simply is not true, even though it's what we have been taught.

In fact, the only reason that you would get on a treadmill -- and they're doing this out in California -- is to run the power to the gym itself. Otherwise it's wasted energy. The only adaptation occurs in your muscles not your heart.

Now, I know this is going to be hard to swallow for some people, but this is what the evidence shows.  According to CBS News: 

"Going for runs on a regular basis has been linked to a multitude of health benefits in countless research studies, but recent research suggests that too much running is tied to a shorter life span."

So, according to modern evidence, too much running is the antithesis of a healthy heart and a long life.

But, look, this is not a new idea. The subject was discussed on this blog before, and when I find it I will put a link here.  But this is not a new idea.

Anyway, I saw a chart back in a book I read in about losing weight that showed that those who were sedentary had the shortest lifespan, those who ran a lot had the second shortest lifespan, and those who ran moderately had the longest lifespan.  Actually, this updated study discusses those same results.

The experts say they don't know why this is, but I do.  It comes down to something my mom said my grandpa always said, "Anything in moderation is good for you." The people who exercise moderately are those who live the longest.

Studies show the advantages of exercising, of running, are abounding.  It makes you healthier all the way around.  If you are too sedentary, you are an an increased risk of unhappiness.  On the other hand, of those studies, those who ran over 20 miles a day, plus those who ran 20 miles a day and took various painkillers and prescription medicine for pain associated with "too much wear and tear", increased their risk factors for diabetes, high blood pressure, and family history of chronic illness.

The experts suggest a 'sweet spot' for running is a slow to moderate pace for a total of about 2.5 hours each week.

So, this idea is not new. While some athletes think that lifting a ton of weights and running fast, long distances every day might help them become better athletes, it actually results in a greater risk for injuries and a shorter lifespan.