Diabetes might make COPD worse

A recent study performed by researchers at Liverpool Hospital in Australia has discovered that people suffering from diabetes, who are admitted to the hospital with exacerbation of COPD, have to stay in the hospital longer, and have a greater chance of dying.

According to this article from topnews.us, researchers say this might be because "that this may be because mutilation of their immune response owing to high blood sugar might lead to more austere contagions."

Of course not mentioned in this article is that systemic corticosteroids given in an attempt to reduce airway inflammation has the side effect of throwing glucose out of whack. This is one of the reasons why COPD patients admitted to the hospital will often have to have their sugar checked on a regular basis.

I recently wrote about another study that showed that COPD patients who were treated with oral corticosteroids instead of systemic corticosteroids were more likely to have a shorter length of stay in the hospital.

One would wonder if these two studies might correlate to a future where systemic corticosteroids are not used so much for COPD exacerbations to not only reduce lenth of stay, but reduce mortality, especially pertaining to COPD patients with diabetes.

Along with a reduction in systemic corticosteroids, improved control of diabetes might also work to reduce COPD related morbidity and mortality. Althought the key here might be improved patient compliance and education, and improved doctor involvement in patient care.

As I wrote before, however, changing the current protocols seems to be a problem among hospitals and physicians. Even if the the GOLD initiative for COPD guidelines change, it's still tough to get doctors educated prior to the release of new guidelines to change their own policy.

So, in leu of upcoming studies, I imagine we might see some major changes in the COPD protocols in the years to come.

COPDers should avoid wood smoke

A new study shows that patients who inhale both cigarette smoke and wood smoke have their risk for developing worsening COPD by a fourfold amount.

The study was first released in the online version of American Journal of Respiratory and Critical Care Medicine and reported on again at m medicalnewstoday.com, "Wood Smoke Exposure Multiplies Damage From Smoking increases Risk of COPD."

Inhaled smoke can be first or second hand, and wood smoke can be used for home heating or cooking or can be inhaled in the ambient air from other homes or businesses in the area. Either way, science already shows that the chemicals of cigarette smoke can damage the lungs and cause COPD.

Yet science now shows that inhaling wood smoke is "likely to (cause) epigenetic changes in the DNA that further increase their risk of COPD and related pulmonary problems," the medicalnewstoday.com article notes.

Dr. Yohannes Tesfaigzi and his colleagues studied sputum samples of over 1800 COPD patients and used their smoking and demographic information to come to their conclusion. They studied the eight genes known to be associate with lung cancer.

The medline article notes "They found that wood smoke exposure was significantly and independently associated with an increased risk of respiratory disease, especially among current smokers, non-Hispanic whites and men. Furthermore, wood smoke exposure was associated with specific COPD outcomes in people who had aberrantly methylated p16 or GATA4 genes, and both factors together increased the risk more than the additive of the two risk factors together. They also found that people with more than two of the eight genes analyzed showing methylation were also significantly more likely to have a lower than predicted FEV1 than those with fewer than two methylated genes."

This study is significant because not only does it prove there is a genetic link to developing COPD, it likewise provides evidence to COPD patients that if they smoke they should avoid heating their homes with wood. Likewise, it's evidence physicians and COPD experts can use to convince their patients to not heat their homes with wood, especially if the patient is a smoker.

Other studies also showed that inhaling cigarette smoke and wood smoke together increased the risk for worsening COPD as compared to inhaling just cigarette smoke or inhaling just wood smoke.

"We observed increased inflammatory response in mice that were exposed to both cigarette smoke and low concentrations of wood smoke compared to those exposed to cigarette smoke only. We would like to use this animal model to determine the mechanisms underlying this exacerbation," said Dr. Tesfaigzi.

Is using an expired inhaler bad?

Every day at MyAsthmaCentral.com we get lots of asthma related questions. Below are some questions I thought my readers at the RT Cave would enjoy.Your Question: can babies 9 weeks old have asthma

Your question: can you take advair and sprivia the same day

My humble answer: Absolutely. This medicine combination is used quite a bit for patients with lung disease, and they are proven safe and effective.

Your quesiton: I have mild asthma and my doctor thinks I should stop using Symbicort because he says I'm too dependent on it

My humble answer: Continue taking it. Symbicort is a very good medicine for controllilng asthma, and it's now recommended as a top line asthma therapy. It's very safe so long as you use it as prescribed. If you get worse when you stop taking it, that means it works for you and you should not quit taking it. If your doctor is a good asthma doctor he should have no problem with you taking a medicine that works so well for you. If he's worried about the safety of this medicine, check out this post.

Your question: Is using an expired inhaler bad?

My humble answer: Expired asthma medicines are still safe, although after a medicine has sat on the shelf a while it looses its efficacy. Ventolin is usually good for about a year, at which point the chemicals start to break down. I have used expired inhalers before, and most of the time they still work just fine for mild asthma. Yet if you're having an asthma exacerbation, an expired inhaler might not help you as well as a new inhaler would. Another problem with expired inhalers is the mist tents to taste like rotten mints (my opinion). I believe any pharmacist would recommend you throw your old inhalers out after a year and get new ones that are fully potent.

If you have any further questions email me, or Visit MyAsthmaCentral.com's Q&A section.

Asthma vaccine a posibility

To find a cure for asthma would be great, but could it be as easy as a simple vaccine. Thus was the topic of a recent Sharepost of mine at MyAsthmaCentral.com:

Is Vaccine to Cure Asthma/ Allergies Too Good to be True
By Rick Frea, Monday July 19, 2010, @MyAsthmaCentral.com

Studies show most asthmatics aren't compliant with their asthma controller meds. So wisdom has it life would be much easier for us asthmatics if only there was a simple shot that would prevent or even cure this dreaded disease.

A couple years ago I wrote a post entitled: "Asthma: A cure on the horizon." Little did I know that even as that post was being written scientists were working on a "jab" that is supposedly a vaccine to eradicate allergies to improve the lives of allergy, asthma and eczema sufferers.

The development of the vaccine was followed by a study where 63 asthmatics were either given a dummy drug, or what scientists like to refer to as CYT003-Qbg10, or the allergy/asthma/eczema vaccine.

According to the Telegraph, "'One size fits all' allergy jab for hay fever, asthma and eczema on the way," by Andrew Hough, the vaccine is thought to be a cure for many allergies, as the study results showed , of the asthmatics given the drug, asthma attacks or symptoms were cut by a third. Another study showed allergy symptoms were reduced by 39 percent, and quality of life was boosted by 42 percent.

Pending the results of a larger study, this vaccine "could" be available to the general public within the next few years. This is big news for asthmatics, since it is estimated that up to 75 percent of the 34.1 million asthmatics in the U.S. and 300 million worldwide also suffer from allergies that often trigger asthma.

Researchers also "concluded that a course of the vaccine was almost as good as steroids at keeping asthma under control," the article notes.

Does this sound too good to be true? Perhaps it is. Yet we'll have to wait and see how a larger study group responds to this vaccine before we get our hopes up.

The vaccine is composed of "synthetic DNA similar to those found in the bug that causes tuberculosis or TB. The DNA fools the body into thinking it is under attack from a dangerous bug, kick-starting a multi-pronged immune response," according to the Telegraph article.

I have written before that to me, allergies seem to be the cause of most of my asthma symptoms. Even while my asthma is controlled with newer medicines like Advair and Symbicort, exposure to large amounts of allergens still triggers asthma.

In fact, I wrote a post (click here) about all the things we asthmatics have to do to prevent the allergy response that causes runny nose, itchy and watery eyes, that downright miserable feeling, and the ultimate feeling of shortness of breath. I wrote that no method of avoiding allergens is anything remotely close to fun.

The experts say you should wear goggles when you garden. How geeky. They say you should keep your windows closed on spring and summer mornings when pollen counts are high. Well, we asthmatics like to enjoy that warm summer breeze too. They say you should put plastic coverings over your bedding. Of course then you have to hear the crinkle every time you roll -- how annoying.

As asthmatics, we have to learn to avoid visiting relatives and friends because they have pets, and we can't go hunting because we're allergic trees and animal hide, and we definitely can't go to the cabin because of molds and dust mites and cockroaches. Hepa filters work nice, but they're too expensive and need to be replaced too often.

It would be so much easier to just take a one size fits all vaccine and be done with it all. It would be nice to be normal. That's why I am joining the 300 million asthma sufferers around the world hoping this medicine turns out to be as efficient and safe as they say it will be.

So while this vaccine may not necessarily be a cure-all for asthma, it's definitely a gallant step in the direction. Even if it proves to be a junk vaccine, at least its proof scientists are making ground in the fight for an ultimate cure for asthma.

Here's why I hate government healthcare

The National Institute of Health and Clinical Excellence (NICE) has come to the decision that the asthma drug Xolair (Omalizumab) will no longer be available to children under the age of 12. This decision does not come without some controversy.

Xolair is a very expensive medicine, yet it is a great option for those asthmatics who do not respond well to other asthma therapies. It's an option for those asthmatics with hard luck asthma.

According to the examiner.com, "Asthma drug denied to young children" article notes that, "According to Wikipedia, Omalizumab (trade name Xolair) is a humanized antibody drug for patients with moderate-to-severe or severe allergic asthma, which is caused by hypersensitivity reactions to certain harmless environmental substances."

Likewise, "Like other protein and antibody drugs, Omalizumab causes anaphylaxis (a life-threatening systemic allergic reaction) in 1 to 2 patients per 1,000."

NICE responded to the "backlash" from physicians and concerned patients by noting that the cost of the medicine, and the risks, and studies that show Xolair is not effective for a large number of patients who try it, makes the medicine not worth the risk.

Yet why not let the patient and physician make that decision. If someone has asthma so bad it effects the quality of his life, and Xolair is an option, why not keep it as an option? Let the patient, and the patient's family choose. It's an individual right.

Yes, I am a believer in individual rights, as opposed to a government agency making a decision for the person. When a group of experts makes the decision, they are essentially implying they know what's best for everyone.

Respectfully disagree if you wish.

Advantages/ Disadvantages of day shift

Now that I've been working days for nearly six months I've had a chance to completely adjust. The following is what I find to be the advantages and disadvantages of working days.

1. Advantage: Doctors, they're always available to help the patients if you need them.

1. Disadvantage: Doctors, they're always available and sometimes irritatingly so.

2. Advantage: Doctor's orders. They keep patients ticking.

2. Disadvantage: Doctor's orders. Most are stupid.

3. Advantage: Bosses, they're always available

3. Disadvantage: Bosses, they're always available

4. Advantage: The Cafeteria is open.

4. Disadvantage: The cafeteria is open and the food is all fast food.

5. Advantage: Days off; you don't have to waste one to recuperate

5. Disadvantage: Waking up early.

6. Advantage: The RT bosses are always available.

6. Disadvantage: The RT bosses are always available.

7. Advantage: You're forced to use the stairs more often, which is good exercise.

7. Disadvantage: The elevators aren't where you left them, as what occurs on nights.

8. Advantage: With more RTs there's a greater likelihood you might get called off if it's slow.

8. Disadvantage: If its slow you get called off and have to use up vacation hours.

9. Advantage: More people available to help out.

9. Disadvantage: Too many people.

10. Advantage: You don't have to be up all night

10. Disadvantage: Fewer parking spots, and you have to park way out in BFE.

Puting the nurse on defense is fun -- sorta

I'm not the kind of RT to complain to nurses, at least most of the time. However, I am known to be honest, and let be known my opinion (the facts, in other words) in more subtle ways.

For example, I just did a breathing treatment in ER on a kid with a runny nose, harsh cough, clear lung sounds and good air movement. After the treatment the patient still had a runny nose, harsh cough, clear lung sounds and good air movement.

As I was leaving the ER, the nurse asked, "Is he doing any better."

"Nope. Lungsounds are still clear," I said.

Then she defends herself, "Well, he had a harsh cough, so I thought a treatment might help."

"That's fine," I say, and smile as I walk away.

I did this with a new doctor once. The patient had an audible wheeze. I could hear it really loud in the throat, and I could hear it radiating through the lung fields. While the patient had really good air movement, I knew that the untrained ear is often fooled into thinking this upper airway wheeze (often called stridor) is bronchospasm or asthma (I wrote about how to hear bronchospasm here)

When I walked out of the room, the doctor said, "So, did the treatment help?"

I said, "Nope. The patient still has stridor."

He said, with a suddenly vexed appearance, "He was wheezing."

"It sounded like stridor to me, and it was radiating throught the lungfields. But I could be wrong."

I was smiling as I left the ER.

Sometimes it's: "Nope, the crackles in the left base didn't go away."

Sometimes it's: "Nope, the patient's lungs still sound wet."

I like to do this, as it puts the person on the defense every time. It's interesting. It beats the, "What the hell does that patient need a treatment!" approach some of my coworkers use.

Yeah, it's tempting to be that way, but I like being on offense better.

Of course you have to leave the unit with a smile right away to stave off any further discussion and so they think you mean no hard feelings. And to leave with them still thinking. It's like the commercial that leads the customer to finish the ad.

Like, "It's the Heartbeat of America..."

Is nicotine addictive?

This is part 2 of a series by Tim Frymyer from over at Stopsmokinghelper.org. To view part 1 in this series, click here. To view part 3, "Stop smoking Aids" click here.

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Thanks again to Rick for letting me occupy the Respiratory Therapy Cave for another day to discuss the topic of smoking cessation. Today we’ll look at addiction. For over fifty years now, people have been telling us that smoking is addictive. The nicotine is said to increase the levels of dopamine in your brain which then gives the smoker that pleasure sensation or that feeling of satisfaction, every time they inhale. In fact, the brain produces more receptors to accommodate more and more nicotine, in an effort to get more of that feeling. Researchers state that over 85% of all smokers are addicted to nicotine. Given the low success associated with smoking cessation aids and the relatively high rate of recidivism or relapse, it is easy to see how one could come to the conclusion that nicotine is addictive. In fact, nicotine is said to be as or even more addictive than opium or cocaine.

The second part of habitual smoking is the behavioral side. We humans are creatures of habit and tend to associate certain activities together. For example, we all know people who smoke only when they drink. Those two behaviors are said to be associated or linked. Many smokers take cues from their environment which then trigger that smoking response. Often times these are simple cues like finishing a meal, driving to work, or some other basic, repeated cue that occurs throughout the day. Behaviorists say that the act of smoking takes on a Pavlovian response to environmental triggers. Adding this classic conditioning makes smoking a difficult one-two punch to beat.

However, new research from Tel Aviv is challenging the assumption that smoking causes a physiological addiction, like heroin. In the Journal of Abnormal Psychology, Dr. Reuven Dar examines the idea that smoking may be a simple case of mind over matter. His premise states that smoking's primary driver is behavioral. He feels these triggers are so strong, they cause the appearance of physiological addiction. His study looked at a simple measurement tool, craving intensity on regular smoking days, a voluntary day of abstinence and the required smoking cessation on the Sabbath.

His findings show that cravings on the Sabbath were less intense when the smoker knew they couldn't smoke. However, the cravings on the day of abstinence were just as strong as the regular smoking days. This lead Dr. Dar to conclude that when the individual knew they couldn't smoke, they were not showing the addictive calling card, intense cravings, that were present on every other day; in essence, mind over matter.

I think we all would agree that smoking addiction is a very complex physiological theme to dissect, though there just may be something to Dr. Dar's research. After treating thousands of patients in the hospital, it has been my experience that once the patient had made up their mind to stop smoking, it didn't really matter what method they used, they simply stopped. And they seemed to stop without any trouble. I’m sure you all have had similar experiences with your patients as well.

Skeptics, however, will argue this “mind over matter” concept. Research is still warranted to determine just which side of the addiction represents the most influencing motivation to smoke. In fact, there is also new research out of Duke University pointing to a smoking gene which, when present, can predict how successful a person will be when trying to quit. However, this genome testing is very expensive and still in it's infancy.

But I believe the idea founded in Dr. Dar’s research can give us a unique opportunity for education when we talk with our patients. Many patients feel quitting is just too difficult, especially in light of the very real stress they may be feeling about their current physical condition. However, we can give them hope and perhaps convince them that quitting may just be as simple as making a decision, followed by another decision and another. Simply resolving each day to quit, might be the “trick” our patients have been looking for

DVT, PE and pulmonary infarction

One of the biggest concerns among nurses and physicians is the prevention of deep vein thrombosis (DVT) and Pulmonary Embolism (PE). Collectively, these two diseases are referred to as venous thromboembolism (VTE).

This is important because DVTs may lead to PEs, and, according to Karen Ruffin, "The latest on preventing venous thromboembolism," Nursing Critical Care, March, 2009, research from autopsies has shown that 60% of patients who die in a hospital bed had an undiagnosed PE, and a diagnosis was missed in about 70% of those cases.

She writes that the CDC, federal Department of Health and Human services, FDA, and the surgeon general all note that the 100,000 people die each year from a PE, and this is among the most preventable -- which is why emphasis is on prevention, also known as prophylaxis.

Thus, with no prophylaxic care, and depending on the acuity of the diagnosis, Ruffin notes that any patient has a 10 to 48% chance of developing a DVT.'

The main reason that prevention is the main emphasis is because DVTs and PEs are so darn hard to diagnose because symptoms mimic so many other disease states.

What is a DVT?

Basically, a DVT is a blood clot that most commonly forms in the deep veins of the legs and thighs. When this clot breaks off, it can travel to the arteries of the lungs and cause a PE, which can be lethal.  According to MedicineNet.com a blood clot that forms in a blood vessel or the heart is called a thrombus. 

What is a PE?

According to Medscape Reference, pulmonary embolism was first described by Loschner in 1860.  Most PEs develop due to free floating thrombus.  How large the thrombus is will determine how far into the lungs it will travel before it becomes lodged, thus forming the PE. 

The PE will then occlude the blood vessel it is traveling in, and this will prevent blood flow from traveling to the portions of the lungs supplied by that blood vessel.  This results in ventilation/ perfusion (V/Q) mismatching, where that portion of the lung is ventilated but lacks circulation.

Medscapes describes taht mild PEs usually don't present with oxygenation problems. However, if oxygenation presents as a problem, clinical practitioners may be correct in assuming that the PE is massive and causing significant obstruction.  Your body will compensate for this type of V/Q mismatching with tachypnea (rapid breathing). 

If the PE is large this may result in increased pulmonary artery pressure which will result in right heart failure.  This is the result because the right heart will have to pump extra hard to push blood through that part of the lung. 

Generally speaking, as is noted in "Respiratory Disease: Principles of patient care," (Wilkins and Dexter, 1993, page 93), a small PE may be cause "little or no injury to the distal lung tissue, whereas large PEs may desrupt blood flow enough to destroy lung parenchyma" and thus cause an infarction (pulmonary infarction)of the lung. Although pulmonary infarction generally only occurs with COPD or those with left heart failure (CHF).

A PE will resolve itself in time as shortly after it's formed fibrinolysis occurs, and this is the "process of clot destruction in which blood-borne and vascular endothelial factors act to dissolve the clot," according to "Respiratory Disease." The authors further note that "clot resolution involves organization of the thrombus, attachment to the vascular wall, and return of blood flow."

Yet if the PE is too large, or compromise to risky or great, medical treatment will be necessary.

Normally conditions are ripe for smooth blood flow through vessels, although, according to experts, there are there main events that may causes DVTs:
1. Decreased flow of blood: Anything that may result in decreased mobility can cause blood to pool and clot off. Examples of this include:

• Prolonged bed rest
• Long flights or car rides
• Paralysis
• Atrial Fibrilation (blood pools in heart)
• Venous obstruction secondary to obesity
• Tumor
• Anesthesia that can cause venous dilation and decreased blood flow which can result in venous stasis and clotting.
• Age over 40
• Mycardial Infarction (heart attack) causes decreased cardiac output
• Stroke (less mobility)

2. Damage to blood vessel wall (inflammation): Damage to the endothelial lining of blood vessels can cause platelet activation.
Events that might cause cause inflammation or damage the vessel walls are:

• Past VTE
• Smoking
• Atherosclerosis
• Varicose veins
• Trauma
• Surgery
• Venipuncture
• Indwelling venous catheters
• Vasculitis
• Elevated blood glucose

3. Changes in blood composition: Any condition or state that decreases blood volume or increases blood viscocity (thickness).
Examples include:

• Dehydration
• Thrombocytosis
• Oral contraceptives
• Hormone replacement therapy
• Cancer
• Sepsis
• Inflammatory bowel disease
• Hematologic disorder
• Blood glucose over 200 mg/dl
• Blood transfusions
• Obesity (greater than 30 BMI)
• High estrogen states (pregnancy, post partum)
• Advanced age (over 40)
• Family history of VTE
• Smoking

Of course you can see, as Ruffin notes, "Risk factors for VTE are cumulative -- the more the patient has, the greater his risk for developing VTE.
How do blood clots form?

While blood normally flows freely through vessels, there are times when your bodies defense mechanism need to shut off flow by causing a clot. The two mechanisms are the clotting mechanism (platelets) and the thrombin system.

According to ehow.com, platelets are made in the bone marrow and float around in the blood waiting for a time when they are needed. When bleeding occurs, chemicals are released that change the composition of platelets, causing them to stick to the vessel wall. When enough platelets are present, a clot is formed to stop the bleeding. This is called a white clot.

Ehow.com also notes that as far as the thrombin system is concerned, several proteins become activated when bleeding occurs, and this results in chemical reactions that produce a substance called fibrin that sticks to the walls of the exposed vessels forming what is called a red clot.
Conditions that can cause a DVT are:

• Compression of veins (sitting or lying for a long time)
• Trauma
• Cancer
• Infections
• Stroke (increases inflammation)
• Heart Failure (increases inflammation)
• Nephrotic Syndrome (increases inflammation)

Things that increase risk for DVT include:

• Surgery
• Hospitalization
• Immobilization
• Smoking
• Obesity
• Over age 40
• Certain drugs (like estrogen)
• Certain contraceptives
• Thrombophilia
• Pregnancy
• High glucose (increases inflammation)

Tests used to diagnose DVTs are:

• D-Dimer
• Doppler Ultrasound of effected vein

A key for hospitals is to have an order set to make sure no patient is overlooked. This way all patients at risk can obtain the appropriate prophylactic therapy. An order set for one hospital looks something like this:

• PT, PTT on admission: These show the ability of the body to clot, and are usually rise as the blood becomes thinner and loses its ability to clot. This must be monitored because one of the preventative measures for clots is giving blood thinners. Both may be therapeutically high if patient is on a blood thiner. Critical would be a PT greater than 60, or a PTT greater than 40, and this would basically mean blood thinners should be scaled back.
• CBC and CMP on admission: Complete Blood Count (CBC) provides the doctor with a baseline level of white blood cells and red blood cells so this can be monitored during the course of the stay. Complete Metabolic Panel (CMP) are lab tests that provide the doctor with kidney function, liver function, electrolyte and acid base balance. For a list of lab values, click here.
• Leg elevated while in bed and pressure off heals: This keeps blood from pooling.
• No IM injections: Prevents trauma to the vessels
• Heparin IV protocol: This is a naturally occuring anti-coagulant to prevent the formation of clots. According to Wikepedia, it does not bust apart already formed clots, but "it allows the body's natural clot lysis mechanisms to work normally to break down clots that have formed."
• lovenox: According the Healthsquare.com, this is "used to prevent and treat harmful clots." This lowers the activity of clotting factors in your blood to keep your blood flowing smoothly. It's called a blood thinner, but it's more correctly termed an anti-coagulant like Heparin.
• Coumadin: An anticoagulant (blood thinner). It blocks the synthesis of certain clotting factors, and thus makes the blood thinner. It makes it so blood clots are unable to form.
• Surfak 1 capsule PO BID (hold if having loose stools): Used to prevent constipation. Hard stools can actually scrape the skin and cause bleeding and infection.
• HealthHype.com, Suddenly increased and decreased blood flow
• Compression stockings: They are stockings meant to prevent DVTs by preventing blood from pooling.
• Intermittent Pneumatic Compression (see picture): According to Encyclopedia.com, "a technique to prevent thrombosis in bedridden patients. It uses an inflatable device that squeezes the calf when it inflates, preventing pools of blood forming behind the valves in the veins, thus mimicking the effects of walking."

Regardless of prophylaxis, some patients will get DVTs which may progress at some point to PEs. Since it's hard to differenciate PEs from other disorders, it's important to think ahead.
Signs of PE are:

• Tachypnea: increased rate and depth (70% of cases)
• Rales (50% of cases)
• ABG may be normal, but may appear as thought patient is hyperventilating (low CO2) yet the patient is not hyperventilating
• Dyspnea (shortness of breath) at rest
• Diaphoretic
• Chest pain occurs suddenly and may worsen with deep breath, cough, movement
• Cough began suddenly
• May be bloody sputum
• Tachycardia (30% of cases)
• Anxiety
• Bluish or dusky skin
• D-Dimer is abnormal (70% false positive)
• V/Q scan (best indicator 87%)

Again, the best treatment is preventative, although you'll want to support ventilation and provide anticoagulants as noted above.
An interesting thing I'd like to add to this post is that, according to "Respiratory Disease," a PE is also associated with localized bronchoconstriction. The author's note, "the release of chemical mediators such as serotonin, histamine, and prostaglandins from platelets causing the bronchoconstriction, although the exact etiology is unknown. This causes ventilation perfusion mismatching and hypoxemia to go along with the shunting (blood shunted away from area PE is located) that is already occurring as a result of the PE.
So one would wonder if this might be the reason some doctors choose to treat PEs with regularly scheduled bronchodilator breathing treatments such as Albuterol.
Another pathological condition "Respiratory Disease" notes is associated with a PE is a reduction in surfactant 24 hours after the PE is formed, "which leads to decreased pulmonary compliance (lungs become stiffer), atelectasis, further ventilation/ perfussion mismatching, and hypoxemia.
A PE can also cause hemodynamic compromise, yet this is usually reserved for those patients who are already hemodynamically compromised, had a PE in the past, or have COPD. These patients may develop pulmonary hypertension.
So, several studies have shown that as VTE prophylaxis therapies and VTE protocols have increased the number of patients diagnosed with DVTs and PEs has steadily declined.

Researchers say mold may cause asthma

Harvard Medical School researchers believe mold and fungus in the home might be responsible for worsening asthma, and in some cases might even cause asthma.

According to this UPI.com article, "exposure to high levels of mold may increase the risk of severe asthma attacks

among people with certain chitinase gene -- CHIT1 -- variants."

Plus, "the presence of chitinases -- enzymes that break down chitin found in the cell walls of mold -- could be signaling inflammation."

Ann Wu of Harvard Medical School and Harvard Pilgrim Health Care Institute in Boston said "Our results support increasing evidence that CHIT1, which is primarily released in the lung, plays an important role in the pathophysiology of asthma in the proper environmental context of exposure to chitin, which was approximated by mold levels."

Thus, mold has been linked to worsening asthma, and asthma exacerbations requiring hospitalization. There was also a link found between mold and fungus and severe asthma attacks.

We knew mold was a major asthma trigger, yet this provide us with more evidence. This is why it is essential that asthmatics, and those with the asthma gene (asthma runs in your family) have their homes checked for mold.

You'll want to make sure there is no standing water in your home, and leaks should be fixed as soon as possible. Besides seeing your doctor regularly, and taking your asthma medicines exactly as prescribed, it is essential that you also do your part in avoiding your asthma triggers.

Pharmaceuticals may use this information to come up with a new medicine aimed at blocking chitinase enzyme activity to block the inflammatory response and prevent mold and fungus from causing or triggering asthma.

Here's how to know if you need asthma specialist

I've received many questions from asthmatics who were having difficulty managing their disease and were wondering what to do next. Often the answer is to seek an asthma specialist. Recently I wrote a post at MyAsthmaCentral.com regarding this topic.

Do You Need An Asthma Specialist?
By Rick Frea, Tuesday, May 25, 2010, @ MyAsthmaCentral.com

So, when is a good time to see an asthma specialist? That is a good question, and a common one.

Thanks to modern science and the National Heart, Blood and Lung Institute's asthma guidelines, most doctors are able to treat most asthmatics, and treat them well.

Yet, from time to time, there comes along an asthmatic whose asthma is difficult to control. When this occurs it's time for your doctor to call in the reinforcements: the asthma specialist or other specialist.

In my opinion, a wise person -- wise doctor in this case -- is one who knows the boundaries of his study, and knows when it's time to refer his patients to a specialist.

1. Asthma Specialists: According to the asthma guidelines, this constitutes:

• An Allergist: Specially trained in allergy and asthma
• A Pulmonologist: Specially trained in lung disease
• Ear, nose and throat doctor: They specialize in these areas
• Other: Any doctor who has extensive training and specializes in asthma

Thankfully, in today's medical world, doctors can refer to the asthma guidelines for a little help. The asthma guidelines (see page 71) recommend your physician refer you (or your asthmatic child) to an asthma specialist when:

• You had a life-threatening asthma attack
• You aren't meeting goals of asthma therapy after three to six months of treatment
• You have difficult-to-manage asthma (hardluck asthma)
• Your signs and symptoms of asthma are atypical
• Your doctor has trouble diagnosing your asthma
• Other conditions complicate your asthma, like allergies, sinusitis, nasal polyps, and severe rhinitis, GERD or COPD.
• Additional diagnostic testing is needed, such as allergy testing, scope of your nose (rhinoscopy), pulmonary function studies, or scope of your lungs (bronchoscopy)
• You need additional education or guidance. Let's face it, sometimes it's hard to adjust to this disease. You may need help learning what your asthma triggers are or how to avoid them. You also may need help remembering to take your medicines, or taking them correctly.
• Your doctor thinks you might benefit from allergy testing or allergy shots (immunotherapy)
• Your doctor suspects you need more than just typical asthma care, or need closer managing or specialized asthma medicines.
• You needed more than two bursts of corticosteroids within one year, or you needed to be hospitalized for your asthma
• Your asthma is being caused by something you inhaled at work or other environmental inhalant that is complicating your asthma or treatment.

2. Psychological and Social Specialists: Another thing that can complicate asthma are social or psychological circumstances. These, among other things, may trigger asthma or complicate your (or your childs) ability to care for yourself:

• Anxiety
• Depression
• Stress
• Substance abuse
• Marital problems
• Abusive spouse or parents
• Poverty

In this case, your doctor will want to refer you (or your child) to specialists such as a psychologist or social worker.

When I was 15 in 1985 my asthma was so bad that my doctor referred me to the specialists at National Jewish Health (NJH). While getting my asthma under control, my doctors realized anxiety was triggering my asthma and complicating my ability to care for myself.

I ended up staying at this asthma hospital for six months while they treated all these problems, and I have to admit, what I learned there still benefits me to this day.

While at NJH I also met kids who were addicted to cigarettes or -- believe it or not -- drugs. As you can imagine, these things complicated their asthma.

I also met a couple kids who had terrible home circumstances. One kid had alcoholic parents, the other abusive parents.

Thankfully there were, and are, specialists to help us get our lives and our asthma under control despite these exceptional circumstances.

3. Family Counseling: Sometimes family members, especially parents, need to see a specialist to learn how they can better take care of their family members, particularly their children.

The following are some examples of when family members might need help from a specialist:

• General guidance in how to manage asthma
• Parents of children with hardluck asthma
• Parents of children with anxiety or depression
• Parents in abusive homes
• Substance abuse in home
• Cigarette smoke in home

My parents received counseling before I left NJH to teach them what my asthma triggers were, and to show them how to make their home more asthma friendly. They also learned how to better help me manage my asthma.

While specialty hospitals like NJH are still around to help asthmatics and asthmatic parents, their programs are mostly outpatient orientated. Also, doctors are better educated today so most of us can get the care we need by specialists close to our homes.

And, while most doctors know when it's time to refer you to a specialist, sometimes you may need to nudge your doctor. After all, doctors are only human.

If you think you or your child needs to see a specialist, don't be afraid to talk to your doctor.

The perspective of getting an RT job

So you're trying to decide what career to choose, and you go to the school counselor, and he says, "Ninety-nine percent of our students get jobs when they leave school." Is he being honest?

Well, yes, he is being honest. Yet what he isn't telling you is that he's including in those statistics students who graduate to McDonalds or Burger King or Walmart because they don't get jobs in their respective fields.

Right now the economy is doing so poorly that the only place where real estate prices are going up is in Washington D.C., and that's because the only jobs that are available are government jobs.

By the way, government jobs also pay more than private jobs, and offer better benefits, and allow you to retire after 25 years. Yet that might change soon, because that's part of the reason government is failing us.

I was just talking with our nuclear technologist here at Shoreline Medical, and he said Ferris State University graduates 30 nuclear technologists every year. And in this past year's class all 30 are looking for jobs.

Of course you have to add into that that nuclear medicine is a new field, as Ferris's program only started in 1977. So the oldest person might be in his mid 50s, and few are ready to retire yet.

Likewise, most hospitals are tied in with respective schools, and by the time a hospital is ready to hire a new technologist one student has already been working, and it's from this base that new nuclear medicine technologists are hired.

It's a lot easier, and costs less, to hire those who already have experience at your hospital as opposed to training someone new.

Yet, when you talk to your counselor, he may honestly say 99% of our students get jobs upon graduation, and he can honestly say this, yet he may also not be telling you the complete truth.

In fact, the program at Ferris just expanded. This wouldn't happen if the counselor had said, "Well, this is a great field, yet the prospect of you getting a job in four years when you're done isn't very good. Only 5% get jobs upon graduation, the rest have to wait 5-10 years."

Here at the RT Cave we are honest with you. If you want to get a job as an RT, that's great. I wouldn't change careers for the world. I love being an RT. Still, when I have a student following me who is trying to decide between being an RT and an RN, I have to say: become an RN.

Why would I say this? Well, it's not easy getting an RT job. The turnover rate is very low. Likewise, if you get burned out at some point in your career and want to change jobs, the opportunities just aren't there.

If you're a medical/surgical nurse and you want a change, you can change to another department right within the hospital, or you can work at a nursing home, or do home care, or personal care, or etcetera. The opportunities are endless.

If you're an RT and you want to change jobs, chances are you'll have to relocate, unless you live in a city with many hospitals.

When I went to Ferris in 1988 I chose journalism and later advertising because I was told "99% of our students get jobs." What I wasn't told was that that job would be working as a desk clerk at a hotel.

So my advice to anyone seeking an education, make sure you scout out the career paths of your options. Know the hospitals in your region and what the turnover rate is. A good way of doing this is by shadowing an RT or an RN or whatever professional you're interested in becoming.

Most medical professions, especially Respiratory Therapy, are great professions and great careers. Yet just make sure you make the right decision for yourself, and choose a profession you can actually get a job in.

Suctioning: how deep do you go?

Your Question: I've actually looked in several places for this info before bugging you, but I can't seem to find it. How do you (or do you) measure how deep to place a suction catheter?

My preceptor asked me the other day just before I suctioned someone, and I wasn't really sure. I thought it should probably be to the depth of the carina, so I said I should measure from the sternal notch to the tip of the tube, but I was not terribly confident. It seemed to work fine. My preceptor just kinda eyeballed me.

My humble answer: First of all, any question any time is my policy. Your preceptor shouldn't give you a funny look because the purpose of clinicals is to learn. The same policy holds true at the RT Cave.

Actually, I think the sternal notch would be too deep. So that might explain the eyeball.

I actually think in RT school we were taught to go down to the corina. Actually, according to critical care nurse (aacnjournals.org), a study was performed and determined that up to 75% of those who suction patients regularly insert the suction catheter until they meet resistance.

And while studies like this show there is no conclusive evidence shallow tracheal suctioning is any better than deep tracheal suctioning, common sense might prevail here. However, other studies performed on animals has shown evidence of more necrosis and inflammation of tissues when deep suctioning was performed.

It is of my opinion, and the opinion of many of my colleagues, that banging into the corina with a narrow tip is not good practice. This is especially bad if the patient is on blood thinners such as coumadin, or if the patient has DIC. It can cause bleeding.

Other research shows it's not the actual suctioning process itself that causes most damage from suctioning, but the hitting of the corina with the suction catheter. To be blunt, this is common sense.

So what kind of trauma can deep suctioning do:

• Epithelial denudement (stripping of the surface of the tissues in that area)
  
• Hyperemia (more blood flow to damaged tissue due to increased tissue activity. In this case it's caused by tissue damage. It decreases oxygen and ph in that area. It also increases temperature and potassium ions in that area. Source: Wikepedia)
  
• Loss of cilia (due to banging the corina and the act of suctioning itself)
  
• edema (swelling of tissue)
  
• fibrosis (generally caused by the repair process of damaged tissue)
  
• granuloma formation (mass or nodule of caused by damaged tissue; infection)

According to critical care nurse, this damage can be made when tissue is sucked into catheter holes after the tissue is traumatized by the tip of the catheter banging into the corina. It can increase the risk of infection and bleeding.

As mentioned above, one study comparing deep and shallow suctioning of rabbits showed evidence of all the above types of damage in 100% of rabbits deep suctioned, and 0-10% in rabits shallow suctioned.

This is why it is important to suction gently:

• Use special tipped catheters when possible
• Use low levels of suction pressure when possible

Another thing to note is that intermittent suctioning has not been proven to reduce trauma. So again, it's not so much the suctioning process itself that causes damage to the patient, it's the tip of the catheter itself.

So there are generally four methods of inserting the suction catheter:

1. Insert the suction catheter until you meet resistance and suction
2. Insert catheter until you meet resistance, pull back 1cm, then suction
3. Insert catheter to corina the first time you suction, note the cm mark at lip, and during subsequent attempts suction suction 1cm above where you met resistance the 1st time.
4. Insert catheter 1cm beyond the end of the ETT. Insert suction catheter until the cm marker on ETT and suction catheter are aligned, and then insert 1cm further. Or, add the length of the ETT plus the adaper and add 1 cm. If ETT is shortened you'll have to adjust for this.
   
5. Eyeball it. Just try not to hit the corina. This may be needed if tape or other obstructs view of cm markers on the ETT

Obviously method #4 above is the best, and the most often recommended. That's the method I use. I find that by using this method the process is still very successful. The cm mark you determine should be marked at the bedside so everyone who suctions that patient knows how deep to insert the catheter.

Unfortunately some of the newer suction catheters don't have cm marks, and in this case you'll have no choice but to use method #5. Where I work this is the method we use, considering we so happen to have unmarked catheters.

Whether or not I use intermittent suctioning pretty much depends on the situation and the patient. If there's copious (lots) or thick tenacious secretions I find it's better to not use intermittent suction.

However, common sense applies. If you have a little lady or child who becomes hypoxic (low spo2) while suctioning you'll want to use intermittent suctioning.

Many RTs will pre-oxygenate a patient prior to suctioning. Most studies (like this one) show this is effective and should be performed. After suctioning make sure you properly reconnect the patient to the ventilator.

Ideally, however, you'll want to use inline suction catheters in order to prevent the loss of PEEP and to prevent ventilator acquired pneumonia. Actually, best practice evidence suggests the use of inline suction catheters, and these are now common at Shoreline medical.

Lavage and suctioning (as I wrote here) at least once per shift has also been proven to reduce the risk of infection. This can be done using the port on the inline suction catheter. However, from time to time, especially if you suspect a plug in the ETT, the patient may need to be removed from the ventilator to perform a good lavage and suction.

Sometimes you gotta wonder

It was a young lady I did a treatment on. She smoked, but that was beside the point.

When the treatment was finished I asked, "So, does your breathing feel better?"

She said, "Well, I still have a headache."

"No," I said, "Does your breathing feel any better?"

"Yes, I think my nose feels more clear."

"No, I mean your breathing, like, your lungs. Do your lungs feel any better?"

"Um, well, I guess they feel the same."

I reported this to the doctor, and he had laughed with me.

Vitamin E may prevent COPD

Researchers had suspected for some time now that supplementation of Vitamin E might help reduce the risk of COPD and heart disease, and results from a new study confirm this.

In fact the study, conducted by researchers at Harvard and Cornell, shows the risk was reduced by as much as 10% in both smokers and non-smokers.

According to the article, "The researchers believe vitamin E could be used as a component of a COPD prevention strategy. Vitamin E is a known anti-oxidant with numerous functions in our bodies. It helps to prevent age related diseases including heart disease, cancer, arthritis, signs of aging. Smokers are known to have higher levels of oxidation occurring in their bodies, due to their exposure to cigarette smoke."

One expert noted that, ""As lung disease develops, damage occurs to sensitive tissues through several proposed processes, including inflammation and damage from free radicals. Vitamin E May protect the lung against such damage."

Pending further studies, COPD experts may some day soon recommend taking vitamin E supplements to prevent COPD, especially those who might have the COPD gene (asthma gene).

It is my thought that some day newborn babies will have genetic testing done, and doctors will know what diseases they are prone to get. If the COPD gene is found, preventative measures can be taken.

How to keep your lab from failing inspections

ABG machines are a great device to have around, particularly in emergency situations. Yet recently the lab bosses have created new recommendations and policies for us to follow that are very inconvenient. However, as I have learned, a necessary evil.

An article in the May 10, 2010, issue of the AARC Times by John Campbell, "Preventing 'proficiency Referral' from happening to your health care organization," does a great job of detailing the importance of proper ABG and ABG machine handling in order to pass laboratory inspections to prevent mandatory lab closure.

We all have shortcuts, some of which we choose not to share for obvious reasons. One shortcut of many RTs in my department is we do so few ABGs that we rarely placed a sticker with the patient's name on them. We also rarely heeded the yellow warning lights on the ABG machine that warned that the equipment must be checked before further ABGs can be reported by the machine.

However, a recent crackdown has changed our behavior. The new policy is as follows:

• Identify patient
• proper sanitisers
• label syringe
• Check for yellow light on ABG machine
• If yellow, fix problem or run maintenance
• If question mark on ABG report throw it away.
• Run monthly control (every RT must do this once a year)

Some of those rules are common sense, although some are a pain in the arse, particularly the check the yellow light and do maintenance. You see, we used to have the ABG machine in the RT Cave, and the reason we gave it to lab was so we wouldn't have to do this anymore.

So here we are learning how to do it once again. In a way, it seems we might as well take care of it ourselves. Yet the RT Boss has decided it's best off in lab where they can do the appropriate check on it, after all, he noted, "They are the lab equipment experts."

Actually, I know of many RT departments that run their own ABG machine, and they do so just fine. So, technically speaking, there is no reason we can't do it ourselves. But, be it as it may, it's no longer our machine.

Inspections of labs are made at least once a year by MANY companies, including the Centers of Medicare and Medical Services (CMS), or some other CMS contracted agency commonly called CLIA inspection or by some other accredited agency that is deemed qualified to do these things such as the College of American Pathologies or the Joint Commission.

Once an inspection is done the hospital must not lapse, because new inspectors could arrive at anytime.

The reason for inspections are obvious: machines are expected to be accurate. Results are important for obvious reasons, and inspections -- however annoying or redundant -- are needed.

Here are some of the things inspectors look for:

• Only qualified and selected individuals handle and draw samples and run machine, etc.
• One person in charge of device responsible for making sure things are done in accordance to policies.
• ABGs are labeled properly. The inspectors are known to look in waste dispensers to make sure syringes are labeled.
• Proper documentation
• Critical values are noted and highlighted on ABG results
• A note on ABG stating that doctor or nurse was notified of critical values
• All staff rotate doing controls
• Problems immediately reported to lab director or medical director

Refusal or failure of procedure or evaluation will or MAY result in closing of the lab, which would mean we RTs would be unable to use the ABG machine. ABGs would have to be run to other hospitals and run through their ABG machine.

According to Campbell, "CMS gives 5 days notice to offending labs that its CLIA certificate is being revoked. This notice will hold that the proficiency referral was intentional even if, in fact, it was not. This notice can come by mail or even face, and the 5 day period also includes weekends."

Campbell notes there is an appeals process, yet CMS usually wins. Likewise, lab closings are reported to local newspapers, which can provide a bad image to the hospital. He notes monetary costs can be staggering, from $500,000 to a million in legal fees, decreased credibility and image, decrease confidence in your facility, and inability to run labs at your hospital.

So, however annoying, follow the ABG policy set at your hospital.

Why do my peak flows not decrease

The following question from medscapes.com was a great one, and one I though my readers would enjoy hearing the answer to.

Question: Why do my peak flow readings not decrease when I'm having an attack?

Yesterday morning I was out doing my rabbit chores and I was having shortness of breath upon exertion (lifting, etc). I went inside and checked my Peak Flow Reading and it was a little lower than usual, but not in my yellow zone; I used my rescue inhaler anyway. I went back outside and my shortness of breath was better. Later yesterday evening I started coughing and had chest tightness. My pfr was in my yellow zone. I woke up during the night once.

What I don't understand is how come I had shortness of breath that responded to albuterol, but had a pfr that was relatively ok? Was it a precursor to what happened later that evening and at night?

Thank you.

Answer #1 by Dr. Matthew M. Mintz: though peak flows do correlate with asthma symptoms, they are far from perfect. In children, for example, even some of the most severe asthmatics have normal lung functions. The purpose of doing peak flows was to identify an attack before it happened; however, this process is far from perfect. That said, current guidelines do recommend peak flow monitoring for patients with moderate to severe asthma.

Answer #2 by Stephen Gaudet, RRT and asthmatic: Also, Peak flow measurements represent the function of the larger airways. When your smaller airways are obstructed ( from inflammation, mucus or constriction), it's not always reflected in your peak flow numbers. You might also have some air-trapping, which could make you short of breath while still having near normal peak flows. In either case, albuterol usually helps.

Answer #3 by your humble RT: If it makes you feel any better, in February 1998 my asthma got so bad I required a breathing treatment every hour for about a week. However, my peak flow readings never wavered below my predicted normal. As a kid my peak flows were reliable predictors of oncoming asthma symptoms, yet as an adult this doesn't seem to be the case. Why?

My theory for this would coincide with what Steve said, that as a kid my airways were small, and the increased inflammation that occurs during an attack caused both my upper and lower airways to become obstructed. As an adult, my airways are bigger, and thus increased inflammation is more likely to effect my smaller airways. At least that's the theory we'll stick to for now.

So why do we have bronchiole muscles anyway?

In a recent post at MyAsthmaCentral.com I provide the answer about asthma you may never have thought of before, and neither until someone post it to me in an email.


Asthma: The appendix of the Lungs

by Rick Frea Monday, July 12, 2010 @MyAsthmaCentral.com

It's time for a change of pace and some fun trivia.

An asthma attack is caused when exposure to your asthma triggers causes the smooth muscles lining the air passages of your lungs to spasm and constrict. So why then do we have smooth muscles in our lungs anyway?

This was a question posed to me recently, and even though I've studied asthma extensively over the years, had never thought of this basic question. Thus, the answer eluded me until I did a little research.

For starters, here are some basic lung definitions. First, the air passages in your lungs are called bronchioles, and the smooth muscles lining them are bronchial muscles. I'm sure you knew that, I'm just saying.

When these muscles spasm it's called bronchospasm. This causes the bronchioles to constrict, which is duly called bronchoconstriction. (To view a good picture of this click here.)

Medicines like Albuterol and Xopenex are bronchodilators, and thus relax your bronchioles by stopping them from spasming.

Logic would have it that if we didn't have bronchial muscles, asthma wouldn't exist. So, then, to repeat our question: why did God line our lungs with muscles in the first place? It can't be just to have the ability to produce bronchospasm, can it?

The best article I found was in The American Journal of Respiratory Care Medicine published January 23, 2004 titled, "Airway Smooth Muscle: The Appendix of the Lungs," by Wayne Mitzner.

According to Mitzner, it has been "further suggested that perhaps airway smooth muscle was a vestigial remnant of its common embryologic origin with the gastrointestinal system, having no modern function."

In the gastrointestinal system smooth muscles lining your intestines are used to cause peristalsis, which is, according to Dictionary.com, "a progressive wave of relaxation of these muscles in order to create a wave that moves food through the intestines.

That in mind, Mitzner notes there have been some theories as to the use of bronchial smooth muscles:

1. To assist exhalation: This theory postulates contraction of these smooth muscles might assist with exhalation. Yet Mitzner concludes that, "However, the magnitude of such an effect, if it exists, must be quite small and of little physiologic significance. Gas exchange in the lung can be performed quite well with fully relaxed airway smooth muscle."

2. To aid expectoration (spitting up phlegm): Again, peristalsis might help move secretions from the lower airway to the upper airway to help you cough it up. Yet, evidence shows that cilia (small hair like structures in your lungs) work like an escalator to bring up mucus, and then you cough it up. There is no evidence that smooth muscles have any use in coughing up junk from your lungs.

3. Protecting the lungs: Believe it or not, your lungs are supposed to be sterile. Contracting of bronchial smooth muscle might prevent substances from entering the lungs. However, to maintain life, an organism must breath. And, to draw in air, lung muscles must be relaxed. If contracted for an extended time to "protect the lungs" one would not ventilate, and would therefore die. Thus, this theory holds little merit.

4. Other: Okay, so there have been many too difficult to explain reasons for bronchial smooth muscle. None, however, have been substantiated.

So, Mitzner writes that since most of these theories have pretty much been disproved, or at least remain as unpopular as asthma itself, there appears to be no modern reason at all for bronchial smooth muscle.

In a sense, bronchial smooth muscle is as useless as the appendix, hence his title: "Appendix of the Lungs." Bronchial muscles, like the appendix, may once upon a time have had a function, but all they do now is cause trouble for us humans.

Body hair serves no purpose, although at least body hair doesn't cause sickness.

Bronchial muscles are therefore like the appendix, or maybe even wisdom teeth, which also serve no modern purpose other than to cause us to bite our cheeks unless we have a dentist yank them out, which may also cause grief.

So, if you've ever wondered why there's smooth muscle in your lungs other than to cause asthma, now you know the rest of the story.

Asthma meds discontinued

Fair or not, the FDA is phasing out some once popular inhalers. This was the topic of a recent post of mine at MyAsthmaCentral.com

Seven Classic Asthma Meds to Be Discontinued

by Rick Frea Tuesday, July 06, 2010, @MyAsthmaCentral.com

Like it or not, the Food and Drug Administration (FDA) has made it official that seven classic asthma and COPD medicines will be phased out by December 2013. Yet there remain many medicinal options to help you maintain good control of your asthma, or maybe obtain even better control.

According to this press release from the FDA, the following are the affected products and there phase-out dates:

1. nedocromil (Tilade), June 14, 2010


2. metaproterenol (Alupent), June 14, 2010


3. triamcinolone (Azmacort), December 31, 2010


4. cromolyn (Intal), December 31, 2010


5. flunisolide (Aerobid), June 30, 2011


6. albuterol and ipratropium in combination (Combivent), December 31, 2013
   pirbuterol (Maxair), December 31, 2013

As you may have noticed, manufacturers have stopped making Tilade, Intal, Alupent and Azmacort.

The phase out is not because these meds no longer work for asthma and COPD patients, but due to "longstanding U.S. obligations under the Montreal Protocol" to get rid of substances that are believed to "deplete the ozone layer."

Basically, all of these inhalers "contain ozone-depleting chlorofluorocarbons (CFCs), which are propellants that move medication out of the inhaler and into the lungs of patients."

Azmacort and Aerobid are inhaled corticosteroids used to control the chronic inflammation in the air passages of the lungs, although better inhaled corticosteroids are now available, such as Flovent and Pulmicort Turbohaler.

Likewise, most asthmatics now get their inhaled corticosteroid fix in combination with long acting beta adrenergic (LABA) medicine like Serevent or Foradil via combination inhalers like Advair and Symbicort.

Intal and Tilade were mast cell stabilizers also used to treat chronic inflammation in the lungs. Newer medicines have proven to do the same job and better.

Alupent was the predecessor to Albuterol and Xopenex and pretty much outlived its usefulness anyway. It has more cardiac side effects than Albuterol. I remember my heart pounding after using it, something that rarely happens with Albuterol.

Maxair is another beta adrenergic medicine that I'm less familiar with, although it's been a nice alternative to Albuterol for many patients.

Combivent is the only medicine on this list that is still being used by a lot of patients, although not by many asthmatics. This is mainly a medicine to help COPD patients improve lung function. As you can see here, the makers of Combivent are working on a replacement medicine they hope to be available by the phase-out date.

Manufacturers could easily keep these products on the market by changing the CFC propellant to an HFA propellant, such as what occurred with Albuterol. However, the change would not be cost efficient with these seven medicines.

So you can see, most asthmatics shouldn't be affected so much by this phase out, as most of us are no longer prescribed them. However, as I can see by some of your comments to this q&a segment, some asthmatics are still taking one or more of these medicines, and are concerned.

Tilade or Intal seems to be the medicine some asthmatics are most concerned about. Some have noted they've been on this medicine for years, it has worked great to control their asthma, and they don't want to change.

Others have noted bad reactions to the more popular asthma meds, such as Flovent, Pulmicort, Singulair, Advair or Symbicort. It is for this reason they are on Intal or Tilade, and they don't want to change.

Another reason asthmatics have continued to take these medicines is because CFC inhalers are less expensive than the alternatives. Medicines like Advair, Symbicort and Singulair can be extremely expensive, especially for those without health insurance.

To be honest, and if I had my way, these asthmatics wouldn't have to make any changes. Yet I have no power, no magic potion, so if you're on one of these medicines you'll have no choice but to make a change.

So, if you are presently on one of these medicines, what can you do?

1. Work with your doctor on finding the best available medicine to control your asthma, or to keep your asthma under control. You might be surprised, though, because some of the newer medicines work better, and need to be taken less often.

2. You can become active and petition your local Congressman. Good luck if you choose this route.

Below I will list each medicine and some good alternatives you might discuss with your doctor:

1. Tilade or Intal: Singulair, Advair or Symbicort are good options to control your asthma. If you have a bad history with these meds don't give up, because there are still other options to discuss with your doctor.

2. Azmacort or Aerobid: No problem here. You can simply switch to better inhaled corticosteroids like Flovent. The newer corticosteroids are more powerful, last longer, and need to be taken less often.

4. Alupent or Maxair: Albuterol or Xopenex are your only options here.

5. Combivent: Atrovent and Albuterol are still available. You just won't have the option of taking them in one inhaler.

Some people still contend it's not fair the government has chosen to save the ozone based on a theory at the expense of asthmatics. As it is, you'll have no choice but to work with your doctor to find alternative medicine to control your asthma.

Don't fret, because you may just be surprised at all the better asthma options available to you. You may find, as I did a few years ago, that newer asthma meds result in even better asthma control for you.

Here's how to be the best at everything you do in life... and also how to get to Heaven

If you want to be a better person....

If you want to be the best person you can be.... If you want to be the best RT you can be... I you want to be seen by others in a positive light... If you want to give yourself the best chance of being observed by the bosses, and the best chance of moving up the latter... and if you want to get to Heaven, there are basically 2 things you need to do:

1. Love God with all your mind, heart and soul
2. Love your neighbor with all your mind heart and soul.

Basically, you can take every self help book ever made and you sum it down to these two things. You can even consider the 10 commandments, and they are all basically these two things. Don't kill, don't lie, don't covet thy neighbor's wife, don't covet thy neighbor's property, and the rest all tie into love thy neighbor.

So now we must define love. What is love?

Love is not an emotion or a feeling. Love is a choice. You have to choose to make sacrifices to put other people before yourself.

Examples of this include:

1. So you know breathing treatments are useless, yet you don't go wining to the doctor who wrote an order for pneumonia that he is an idiot. You treat him with love and respect.

2. So you and your wife go to a baseball game and it's 90 degrees. It's the best game you've ever watched, and you want to stay. Yet your wife wants to leave in the 5th inning. So you sacrifice the game to make your wife happy. You choose your wife over your game.

3. It's 90 degrees out and you want to sit inside in the air conditioning, yet in order to put food on the table you decide not to purchase air conditioning. You are frugal for love of your family. You choose your family over things.

4. It's 90 degrees out and you want to blog or gossip online, yet your son wants to play catch with you. Even though you're sweating your butt off, you play catch with a smile on your face.

Or, as I write here, it's important you keep your priorities in the right order.

If you love God and other people before all else, you should have to make no further effort at improving your image, the way people view you historically (note to politicians), and your ability to view your own life as a success.

Related links:

• Patients who believe in God are happier and more likely to get better quicker
• Ben Franklin's 13 subjects to becoming a better person
• 13 virtues of parenting
• 12 Virtues of respiratory therapy
  

No stereotypes where I work

There was this show my wife and I were watching where these people were having a person with a saw try to remove the chain off a locked up bike. They wanted to see if anyone would stop and try to stop it.

They had a white male person do this, and nobody stopped.

They had a white female do this, and some stopped to help her.

They had a black male do this, and many stopped to stop him.

So, as you can see, this proves our stereotype. Black people are treated differently than whites.

I thought of this because I saw a white lady looking lost in the halls of Shoreline, and I helped her find her way.

I saw a scraggly looking white guy, and I helped him find his way.

I saw black man and woman, and I helped them find their way.

I saw a Mexican woman, and I helped him find his way.

There, no stereotypes here. Every person I saw who looked lost, regardless of race or creed, was helped.

Now, you have to give me an exception for those times I'm burned out. Yet today I'm not burned out, and the help I give is equal.

This is work though. If I'm out in public, would I be willing to help a person out? Or would it be easier to not be inconvenienced? One can only know when the moment arises.

Assess-uterol

You know how I always say 80% of the breathing treatments ordered in hospitals are not indicated. Well, there is one other reason why so many useless breathing treatments are ordered, which might actually have something to do with the respect for us RTs.

The real reason for most breathing treatments that appear to be "unindicated" is so we RTs can assess the patient. The doctor knows we are the "experts" at assessing respiratory status, and want us in the room every 4 hours to make sure things are going well.

So what we have here is a simple case of Assess-uterol

Oxygen should be used as a drug with side effects

Oxygen is a drug, although often in the hospital setting we use it without thinking much about the consequences. Yet, like all drugs, there may be "side effects" to oxygen that often goes un-thought about.

Neonates are a great example. When a neonate is born and doesn't take a breath right away, it has always been standard practice to ventilate these newborns with positive pressure breaths with 100% oxygen. The theory is that 100% oxygen will help to increase oxygen tension in the lungs, and dilate vessels there. (click here for more reasons not to overoxygenate neonates)

However, newer studies show positive pressure alone will stimulate breathing, and that the 100% oxygen not only is not needed, but can be detrimental. Studies performed in the past 10 years have shown that, even in term infants that are otherwise healthy, a rapid increase in PO2 can increase their risk of developing cancer later in life.

Likewise, as this article notes, scientists have discovered that exposure to 100% oxygen even for as little as three hours can increase free radicals, and these free radicals attack lung cells exposed to 100% oxygen. When free radicals attack lung cells, isofurons are created.


By measuring isofurons, scientists have and will be able to study the effect of oxygen on lung damage, either now or in the future. So while 100% Fio2 exposure may be linked to future consequences, exposure for as little as 3 hours can increase chances of lung damage and risk for disorders such as ARDS

Physicians have known for years higher oxygen levels (FiO2 greater than 60) increased the risk of lung injury if used for extended periods of time. Yet they didn't know that an extended period of time may be considered anything over three hours.

Adult patients are often placed on 100% oxygen for various illnesses, although there have been a few times that we have had an ARDS patient in such a situation, and the patients were eventually cured of the ARDS, went home, only to come back a few years later with terminal cancer.

It just makes me wonder if, perhaps, we medical professionals are way too eager to use oxygen. That, perhaps, we ought to think twice about using it in such high doses. That, perhaps, we ought to try increasing CPAP and PEEP before going over, say, 40% FiO2.

It seems the only time we have doctors unwilling to go over 40% FiO2 at the present time is when the patient is a supposed CO2 retainer who uses the hypoxic drive to breath. Yet recent evidence shows that the hypoxic drive might be a myth that even RT schools are no longer teaching.

And even if a CO2 retainer does use the hypoxic drive to breath, it's a very rare occurrence that only occurs in 10% of COPD patients. Thus, if a patient is an end stage COPD patient (retainer or not) or a terminally ill patient, or otherwise critically ill patient who really needs it, I would say it's fine to use as much oxygen as you need.

Yet if you have a patient who is otherwise young and healthy, and has the prospects of living a normal life if he or she overcomes the present illness, I'd be thinking twice about using higher amounts of oxygen.

Allow me to note here that most patients who are truly CO2 retainers who are using the hypoxic drive only lose their drive to breath when they are in severe distress. If they need oxygen, it should be given. If they lose their drive to breath, that's when the patient should be intubated.

It's ironic that in the hospital setting oxygen is used often when it's not needed or shouldn't be used, and when it 's needed doctors are Leary of it. Yet, we should never lose sight of the fact oxygen is a drug, it has possible side effects, and it should be treated as a drug.