Should it be illegal to smoke in front of kids?

I have no problem with people smoking, so long as they do so in the privacy of their own homes or vehicles where no one else is being forced to inhale their stale, polluted air.  However, when little kids are involved, I draw the line.

This past spring and summer I attended many t-ball games where my 5-year-old daughter and her friends participated in a friendly we-don't-keep-score-and-just-play-for-fun game of t-ball.  Yet at every single one of those games some individual kept lighting up cigarette after cigarette after cigarette, forcing me and everyone else -- including the kids -- to inhale their smoke.

I have asthma too, and the smoke bothers me.  But I'm thinking of the kids first.  I have trouble fathoming the idea that an adult, addicted or not, can't go one hour without lighting up.

Liberty means to exercise  human rights in any manner a person chooses so long as it does not interfere  with the exercise of the right of others.  Going by this, all people have a right to smoke cigarettes, but that right should stop as soon as nonsmokers are in the room.

As an adult, I can easily avoid your stale, polluted air.  However, your children cannot.  For this reason, it should, by default, be illegal to smoke in front of children.

Seriously folks, I'm not a champion for more laws, as I believe every law takes away some liberty.  However, if that law would protect innocent children, then I'm all for it.  I think it is absolutely cruel to force children to inhale polluted air because you choose to smoke cigarettes.

There are already enough studies to show that second hand smoke is harmful, and especially to asthmatic children. When I was a kid I remember suffering heartily when adults smoked around me, and I make every effort to make sure that never happens to my kids.

Now, evidence suggests that even third hand smoke, the remnants of smoke that stick to carpet and furniture, can be inhaled with consequences.  Evidence suggests it may trigger asthma, and a new study shows that it may even cause cancer.

I don't like to judge people.  I don't want to make laws forcing people to take certain actions, or not to take certain actions.  But if people are going to continue to light up around people -- people who have a natural right to inhale pure air -- then it might be time to take action against it.

Further reading:

• 20 reasons to quit
• 10 tips to help you quit smoking

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Alarms and alarm fatigue.

You should expect to hear a lot about alarm fatigue, and methods of resolving it, in the coming years.  This was made into one of the top priorities of the Joint Commission for 2014.

A good article can be found in an editor's note in the June, 2013, edition of RT: For Decision Makers in Respiratory Care called "Joint Commission Goal: Cause for Alarm."

Another good article is by Erich Faust at Advance for Respiratory and Sleep Disorders, "Preventing Alarm Fatigue."

Faust defined fatigue this way:

Alarm fatigue occurs when clinicians become overwhelmed by the high number of patient alarms and fail to respond to potentially critical patient alarms. The issue is recognized by many clinical organizations as a significant hazard to patient safety and care. In fact, the ECRI Institute has published the "Top 10 Health Technology Hazards" list annually since 2011 and "alarm hazards" has been on the list since its inception, topping the list in 2012 and 2013.

Faust also described how the movement was born. He said:

In 2013, The Joint Commission released a Sentinel Event Alert on "Medical device alarm safety in hospitals." The Joint Commission recognizes this issue as a "frequent and persistent problem" with 98 alarm-related events reported between January 2009 and June 2012 - 80 resulting in death and 13 in permanent loss of function. They also cite alarm fatigue as "the most common contributing factor" to alarm-related events.

As a result, The Joint Commission has made a number of recommendations to address the issue, including the implementation of The Joint Commission National Patient Safety Goal, in two phases. Phase I requires hospitals to establish alarms as an organization priority and identify the most important alarms to manage based on their own internal situations. In Phase II, hospitals will be expected to develop and implement specific components of policies and procedures.

With these recommendations in mind, there is a clinical need to develop more intelligent alarm management strategies to reduce clinically-insignificant alarms while identifying alarm conditions that require intervention. Device manufacturers are taking significant steps to develop smarter alarm management systems and remote patient monitoring systems that have the potential to reduce clinically insignificant alarms while alerting caregivers to clinically-significant events.

Furthermore, he said "nuisance" alarms are a constant cause of alarm apathy, especially considering "85-99 percent of alarms do not require an intervention." The negative effect of this is the medical clinician becoming deconditioned to to alarms.

Potential remedies noted are:

• Proper education as to where to set the alarm limits
• The addition of "smart alarms" to existing medical technology
• Educating staff as to importance of responding to all alarms.
• Creating alarms with a soft, or pleasant cadence 
• Remote patient monitoring

I actually attended a conference a few years back where the keynote speaker gave a presentation about alarm fatigue and efforts made to combat it.  He displayed a pulse oximeter that had an alarm that was smart, or a smart alarm.  It was designed so it would not go off every time the patient's pulse ox reading was, say, 88%.  It would only go off if the SpO2 was consistently low.  This way the patient doesn't get awakened every time he gets into a deep sleep and his sat dips ever so slightly, and the staff doesn't get annoyed or deconditioned to the alarm.

While at the present time such devices are expensive, I would imagine they will be the wave of the future.  There might even be an effort to add this technology into ventilators and other medical equipment that is already in use.  Smart ventilator alarms would only alarm when a patient consistently has a minute ventilation out of range, or a consistent leak is sensed. This would allow for the patient to get better rest, and would come a long way toward reducing therapist apathy toward alarms.   

Another neat thing about these smart alarms is that, instead of being an annoying screech, they would provide a soft, pleasant sound. This would make sure that the appropriate people are notified that something needs attention, but the cadence would be soothing to the patient.  

Remote patient monitoring is already being done to some extent at hospitals. "Remote monitoring systems help busy clinicians manage the constant stream of alarms from bedside devices by allowing them to observe patient data from a central location or on the care floor using a pager/smart phone," said Faust.

While this technology is currently used with telemetry systems that monitor heart rhythm strips, it might eventually include similar alarms for IVs, ventilators, and other important equipment.

The advantage of remote monitoring is, said Faust, that "By providing remote visibility to alarms and information from bedside devices, clinical caregivers are better able to prioritize their responses to better manage the needs of patients."

So expect to hear more about this in the not so distant future.

Further reading: 

1. The Joint Commission Issues National Patient Safety Goal and Requirements for Medical Device Alarm Management
2. Answering the Call to Alarm Safety: Getting Ready for Joint Commission's Patient Safety Goal 
3. The Joint Commission Announces 2014 Patient Safety Goals

Will your kids outgrow their asthma?

The following was published August 2, 2013, at healthcentral.com/asthma.

Can kids outgrow asthma? 

There used to be a myth that asthma goes away with age. I was told my asthma would go away many times when I was a kid, and now at 43 I still have it. Today, doctors know asthma never goes away, although it does sometimes go into remission.

The million dollar question of the day is: How do you know which kids will eventually "outgrow" their asthma?

Personally, even as my doctors told me I'd outgrow it, I knew it was too good to be true. I guess it was a good thing I reasoned this way, because it prevented a let down when, ahem, my asthma never did go away. It's controlled, but it's still there.

However, a new study by Swedish researchers, and reported by Reuters, concluded that kids with severe asthma who are allergic to animals have an 82 percent chance of still having asthma when they grow up.

Well, I had severe asthma as a kid, and I was allergic to dogs, cats, horses, and probably any other animal that walked the earth. I also still have asthma. So, it would appear the study might be right.

But it might not. As with all studies, you have to take it with a grain of salt. Still, it's pretty neat.

The researchers followed 248 Swedish children aged 7-8 in 1996, and the parents of these kids were interviewed every year until the kids were 19.

Other study results:

• Being male, not having severe asthma, and not having an animal allergy as a child nearly doubled the chance of asthma going into remission
• Having a parent with asthma had no affect on whether childhood asthma would go into remission (other studies do find a link here, however)
• Living in a damp or rural home had no affect on whether childhood asthma would go into remission
• Parental smoking had no affect on whether childhood asthma would go into remission. Again, this is only one study, but if it turns out to be true, it's pretty neat. 

What we do know for sure is that allergies sure complicate asthma. I can tell you that from personal experience. Allergies plus asthma evidently appear to be an indicator that childhood asthma will probably not go away.

Or, as noted by one of the experts quoted in the Reuters article, "It seems clear that the mixture of asthma and allergy in childhood is not such a good thing in terms of asthma going away."

I don't know about you, but if I'm a kid with asthma (or a parent of one, as I am), I'd like to know if my asthma (or my child's) has a good chance of some day going away. Or whether I need to prepare myself (or my child) for a lifetime of this disease. What do you think?

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Does hospital reimbursement laws impact disease trends?

Your question:  My friends were arguing about government involvement in medicine.  One said it's good, but the other said government involvement make it difficult, if not impossible, to track trends in various diseases.  What do you think of this? Do you think it's true? Why?

My answer:  Without delving too deep into politics, I'll try to explain what your friend was probably trying to say.  Asthma rates have skyrocketed since 1980.  So does that mean more people are getting asthma?  Maybe.  But it was just prior to 1980 that DRGs were created, and this made it so physicians and hospitals were reimbursed based on diagnosis rather than procedure.  For instance, insurance companies only pay for pulmonary function testing if there is a diagnosis of asthma.  So, some speculate this has caused many physicians to write "asthma" on the diagnosis line even when there is not asthma. So are there actually more asthmatics today than in 1980? Some say it's hard to know because of government intervention.

Similarly, pneumonia and COPD are highly reimbursable.  However recent laws have made it so CMS will not reimburse the hospital when pneumonia and COPD patients are readmitted within so many days.  Now, since patients with COPD have nearly a 50-50 chance of getting readmitted, physicians, you might expect, might be less likely to write "COPD" on the diagnosis line.  However, since pneumonia patients are less likely to be readmitted, that will likely be the diagnosis.  Thirty years down the line it might look like there are fewer COPD patients and more pneumonia patients.  Experts will be looking at these diseases like we look at asthma today: are these trends accurate?

The bottom line is money.  While CMS will say they are doing this to help patients and improve patient care, the true reason is to save money. The result is that it has become difficult, if not impossible, for experts to know the true cause of whether disease rates are rising and falling.   In my opinion, it would be best to allow doctors to treat and diagnose as they feel is appropriate, and not on whether they will be reimbursed.

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What are the advantages of NIV?

Sometimes there is confusion regarding the advantages of NIV, otherwise referred to as BiPAP. I have had doctors order it because it "forces fluid out of the lungs" in heart failure, and because it "increases blood pressure." Yet neither of these are actual benefits of NIV. That said, what are the benefits of NIV? The are:

1. IPAP increases ventilation and helps to blow off CO2 
2. CPAP increases FRC and therefore keeps the lungs open so the next breath comes in easier
3. Both IPAP and CPAP help to reduce work of breathing
4. Both the IPAP and CPAP help reduce work of heart

So, how does BiPAP reduce work of heart because the increased intrathoracic pressure decreases preload to the heart, thereby decreasing cardiac output, and thereby decreasing blood pressure.  In this way, it helps to decrease the patients work of heart.  That is how it helps with heart failure.  It does not force fluid out of the lungs. It does not increase blood pressure.

Is asthma psychological?

The following was originally published on May 13, 2013 at healthcentral.com/asthma.

Is asthma all in your head?

In a series of articles written throughout the 1850s, Dr. Henry Hyde Salter, himself an asthmatic, wrote a series of articles about asthma that were published in the book "On Asthma: It's Pathology and Treatment." In this book he wrote that "Asthma essentially a nervous disease." 

He offered the following proof:

• Many patients feel fine as soon as they enter the doctor's office
• Mental emotion can bring on a paroxysm of asthma
• Mental emotion can resolve a paroxysm of asthma
• Remedies that relax the nervous system resolve asthma, such as tobacco,antispasmodics, sedatives, and nervous depressants. Examples include tobacco, alcohol, morphine, and especially chloroform.

So there you have it: asthma is a nervous disease. This was the belief about asthma that prevailed even up to the 1980s, and even beyond that. This myth continued to live on despite it being disproved in the 1950s.

Dr. Salter did such a good job inculcating the idea that asthma was nervous, that many asthma websites and books have to go to make light of it even to this day. In noting the common triggers of an asthma attack, the experts atNational Jewish Health note:

Emotions do not cause asthma, but can make asthma worse because strong feelings can lead to changes in breathing patterns. Times of "good" stress and "bad" stress can cause problems for people with asthma. However, it is important to express your emotions, and good asthma management can minimize the effect of stress.

Dr. Salter was a very good doctor for his time, yet his idea asthma was "all in your head" was incorrect. Yet he wasn't the only asthma expert of old who was fooled, as so too were Hippocrates (the father of medicine) around 400 B.C.,Galen of the 1st century, Thomas Willis and Jean Baptise van Helmont in the 17th century, and William Osler (the father of modern medicine) in the late 19th and early 20th century. They were all fooled.

They were fooled mainly because asthma, in its uncomplicated or pure form anyway, left no visible scars on the body. Even upon autopsy, doctors found the lungs of asthmatics to be normal. So they simply speculated it must be nervous in nature.

We don't fault them, however, because they didn't know about the immune system. Dr. Osler probably knew about it, but knowledge of it during his time was primitive. Yet the link between the immune system and asthma was eventually discovered, and now we know asthma is not nervous at all.

Today we know asthma is a disorder of the immune system; it's an autoimmune disease. It occurs because your immune is tricked into thinking things that are innocuous (harmless) -- like dust mites, mold, fungus, cockroach urine -- to most people are harmful to your body.

So instead of ignoring these things when inhaled, yoor body develops a defense against them, and attacks them, and this is why you have an asthma attack. So I personally don't fault doctors like Dr. Salter for thinking asthma was nervous.

Reference: 

1. Salter, Henry Hyde, "On Asthma: It's Pathology and Treatment," 1868, London, page 24-30. Other references are provided in the posts linked to above.

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Emotional State Lexicon

The following are the emotional states.

• Anxiety/ nervousness: An emotional state; indicative of a patient watching every movement; asthma, respiratory failure, hypoxia
• Depressed: An emotional state indicative of quiet, denial, in hospital too long
• Anger/ combative/ irritable: An emotional state which often presents with electrolyte imbalance
• Euphoria: An emotional state which usually presents with drugs or overdose.
• Panic: An emotional state which resents often with hypoxia, tension pneumothorax, status asthmaticus

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Level of consciousness lexicon

The following are the levels of consciousness.

• Lethargic: somnolence: sleepy
• Stuporious: confused: responds inappropriately, OD, intoxication
• Semi-comatose: responds only to painful stimuli
• Comatose: does not respond to painful stimuli
• Obtunded: drowsy, maybe decreased cough/gag reflex

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Types of breathing lexicon

The following are terms associated with types of breathing.

• Unconscious breathing: Most of the time you don't think about breathing, yet you continue to do it. This is an important safety net for life, because if we had to think about breathing 24-7 we'd accomplish little and most life would cease to exist. Air goes into your lungs because a negative pressure is created that sucks air in, kind of like a vacuum. Normal exhalation is passive. Normal unconscious breathing is generally called quiet breathing.
• Diaphragm: The main muscle of respiration is this large muscle that contracts during inspiration. When it contracts it moves downward making more room in the lungs and creates a negative pressure, causing air to be drawn in.
• External Intercostal Muscles: These are positioned between the ribs and contract during normal breathing, pulling the ribcage outward. These assists the diaphragm in lifting the rib cage and creating negative pressure in the lungs. They also assist with expiration.
• Scalene: This might assist the diaphram.
• Exhalation: Normally passive. It occurs when the muscles of respiration relax. When this occurs the rib cage is drawn in, and the lungs are compressed. This increases the pressure in the lungs, and air is pushed out. This is also referred to as normal elastic recoil of the lungs.
• Conscious breathing: When you take in a breath by thinking about it. When you do so you will be using your accessory muscles of respiration. 
• Normal Muscles of Respiration: These are the muscles you use during most breaths. Generally, these include the diaphragm, external intercostals and scalene muscles.
• Negative recoil of lungs: Natural relaxation of muscles of respiration causing air to be released from the lungs.
• Forced exhalation: If the lungs lose their elasticity (if they become stiff and unable to recoil), your body will have to use all the above mentioned muscles to force air out of your lungs. This is generally called active forced breathing or forced exhalation. It is generally active or conscious, and is often referred to as labored breathing. Other examples of this are emphysema and pulmonary fibrosis .Muscles that assist with forced exhalation include: Abdominal Muscles, Internal Intercostals, and Innermost Intercostals
• Diaphragmatic breathing: When you are breathing normally you are using your diaphragm. This allows you to get the most out of each breath. When this occurs, your stomach moves out, and your chest does not move.
• Accessory Muscles of Respiration: Muscles you normally don't use to inhale, and when you do use them they will be sore the next day. Examples include: 

The main accessory muscles are:

• Sternocleidomastoid (neck)
• Scalene (neck)

The minor accessory muscles are:

1. Serratus Anterior (minor role, side of chest)
2. Pectoralis Major (minor role, chest)
3. Pectoralis Minor (minor role, chest)
4. Upper Trapezius (back, shoulder and neck)
5. Latissimus Dorsi (side of chest and abdomen)
6. Erector Spinae (deep back)
7. Iliocostalis Lumborum (deep back)
8. Serratus Posterior (mid back)
9. Serratus Inferior (mid back)
10. Serratus Superior (mid back)
11. Levatores Costarum (chest)
12. Tranversus Thoracis (chest)
13. Subclavius (chest)

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Lung Anatomy Lexicon

The following is basic lung anatomy terms.

• Nares (nostrils): You waft through the nasal openings, barely inching between hairs meant to keep particles out. This begins the upper airway.
• Nose: It's not just an organ of smell, it also aids in phonation and easily lets air in. It's also the first line of defense against inhaled particles. 
• Epithelial cells: You'll see these cells lining the air passages from the oropharynx to the respiratory bronchioles. Their main function is protection of underlying tissue and secretion. Note the wavelike movement of hair-like structures on the surfaces.
• Goblet cells: These are specialized epithelial cells that are randomly scattered along the way. Their job is to secrete mucin, which dissolves in water to form mucus.
• Mucus: This is formed by goblet cells and traps particles in inspired air to prevent them from getting to the lungs. It then rides up on those fine hair-like structures to the mouth. Once in the mouth it's called sputum.
• Cilia: These are those fine hair-like structures referred to above. They wave in rhythmic fashion and act as an escalator to move mucus to the mouth. Each ciliated cell has 200 cilia, and there are 1 to 2 billion cilia per square centimeter.
• Nasal septum: This is what divides the two nasal passages from the nare to the nasopharynx. 
• Vestibule: This is the main cavity of the nose. Air is warmed to 98.6° Fahrenheit and humidified.
• Turbinates: These are three bone-like shelves that project into the nasal cavity from the lateral wall. They help with the sense of smell and warm and humidify inspired air. 
• Pharynx: This is a funnel shaped passage where are travels from the nasal cavity to the larynx. It too aids in phonation. Both food and air travel this way.
• Nasal pharynx: This is the upper portion of the pharynx.
• Oropharynx: This is the middle portion of the pharynx, and from here you travel to the larynx. Look down! That dark opening is called the glottis, and those white objects on either side are the vocal cords.
• Vocal cords: These are only open when you inhale. This is another means to keep particles out of the lungs. As air brushes past them when you breathe out they vibrate, creating sound.
• Epiglottis: This is the object projecting upward and guarding the opening to the glottis. When you swallow it lies down to keep food out of the lungs. 
• Glottis: Only air is allowed to pass (yet a few particles sneak by). This is the opening to the Larynx.
• Larynx: This is a very short passage that protects the lungs during swallowing, helps produce a voice, and is often referred to as the voice box.
• Laryngeal skeleton: The larynx is kept open by nine cartilages, the largest of which is the thyroid cartilage, better known as the pomas adamus, or Adams Apple. Just inferior to the Thyroid cartilage you'll see the cricoid cartilage in the neck.
• Trachea: This is the main tube-like passage to the lungs, and is often referred to as the windpipe. It's kept open by 16-20 c-shaped cartilages.
• Carina: This is a fork in the road. Go right to the right lung, and left to the left lung. The respiratory tract from this point is called the lower airway.
• Lungs: The lungs are normally kept sterile by many of the mechanisms we described on our journey. Occasionally particles make it this far and cause havoc. Yet healthy lungs move particles out within 24 hours. Most particles are filtered by the upper airway. A porous and spongy organ, the lungs provide a space whereby large amounts of air and blood can come in contact for rapid exchange of gases to occur.
• Right lung: It's actually larger than the left and has three lobes.
• Left lung: This side has only two lobes. Can you guess why? I'll give you a clue. Listen! Lub dub... lub dub... lub dub... lub dub... lub dub...
• Bronchus (large airways): This is the passage air takes as it begins its travel through the lungs. Air passes through the lobar region, segmental, then subsegmental. These airways divide into smaller and smaller but more numerous airways.
• Bronchioles (small airways): These airways continue to get smaller and divide exponentially. Air travels through the terminal then respiratory airways. There's no cartilage to keep the airways open here, which isn't good during an asthma attack (see picture). 
• Bronchial tree: The bronchus, bronchioles and alveoli make up the bronchial tree.
• Bronchial Smooth Muscle: Crisscrossing and spiralling the outside the bronchial airways are smooth muscle fibers. During asthma these spasm and contract, narrowingthese hallways, making it hard to breathe.
• Beta 2 Adrenergic Receptors: On the bronchial walls are tiny receptors. When you inhale beta-adrenergic medicine like Ventolin or Xopenex, the medicine binds to these receptors, and the reaction causes bronchial muscles to relax, opening the airway, and making breathing easier.
• Alveolar Duct: The respiratory bronchioles leads air to these fine ducts that terminate in clusters of 10-16 fine balloon-like structures called alveoli.
• Alveoli: Most adults have over 300 million of these in their lungs, and this is where most gas exchange occurs. Oxygen molecules inhaled wait here for an available hemoglobin molecule.
• Red Blood Cells (RBC): These look like little red boats or donuts. In the middle is a protein called hemoglobin. RBCs ride single file down the capillary beds in the lungs where they come into contact with the alveoli.
• Capillary: These tiny vessels transports RBCs that have carbon dioxide (a cellular waste product) attached to the hemoglobin instead of oxygen. These RBCs are purplish-blue in color.

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Basic respiratory therapy lexicon

Here are some basic terms used by respiratory therapists.

• Ventilation: Moving air in and out of the lungs. Measured by respiratory rate, tidal volume, chest movement, breath sounds, Measurement of Carbon Dioxide (PaCO2), etc. This is your first priority in an emergency (establish and open the airway)
• Oxygenation: Getting oxygen from the air, to the lungs, and then to the bloodstream. Measured by Heart rate, color, sensorium, Oxygen (PaO2 and SpO2), color (cyanosis, gray or normal), sensorium, etc. This is your second priority in an emergency (increase FiO2). This is also the most common problem.
• Circulation: Moving the blood through the body. Measured by pulse and heart rate and strength, cardiac output (blood pressure). This is your third priority in an emergency (chest compressions, defibrillate, heart drugs, etc.)
• Perfusion: Getting blood and oxygen to the tissues. Measured by blood pressure (cardiac output), sensorium, temperature, urine output, hemodynamics. This is your fourth priority in an emergency, raise the blood pressure.
• Signs: Objective information, those things that you can see or measure. Examples include color, pulse, edema, blood pressure, pulse ox, etc.
• Symptoms: Subjective information, those things that the patient must tell you. Examples include dy spnea, pain, nausea, muscle weakness, etc.
• Objective:  Judgement not based on personal feeling; opinions based on fact; what you find upon assessment; examples include blood pressure, pulse oximetry, lung sounds, temperature, level of consciousness, etc. 
• Subjective:  Judgement or opinion based on personal feelings.  Examples include pain level, level of dyspnea, anxiety, etc. 
• Smoking history: How many years and how many packs per day. Measured by # of packs per day times years smoked.
• Advanced directives: Set of instructions documenting what treatment a patient would want if he was unable to make medical decisions on his own. Does the patient want to be a full code, or does he want all measures to be taken to restart his heart if it stops beating. Does he want to be placed on a ventilator. These are questions that should be answered.
• Do not Resuscitate (DNR): This is an order from a patient requesting that no efforts be made to restart the heart if it should so happen to stop, and no efforts should be made to intubate the patient (No Mechanical Ventilation) should he stop breathing. Otherwise, the patient should be treated, but no invasive procedures should take place.
• Arterial Blood Gas: A sampling of arterial blood drawn from the radial, brachial or femerol arteries to determine PAO2, PCO2, HCO3 and accurate SaO2, and pH. Used to monitor respiratory status and metabolic status.
• Venous Blood Gas: In a patient who is not showing signs of respiratory distress, recent research shows this should be just as useful as an ABG (unless your goal is to monitor oxygenation status). Venous pH and HCO3 are basically similar, and PO2 is expected to be a normal of 75, so if it is low, you can be assured PO2 is low. Actually, VBG is just as useful as ABG so long as you can momitor oxygen status with a pulse oximeter (SpO2).
• Capilary Blood Gas: Used to determine pH, HCO3 and pH values in a newborn, especially when no cord blood access is available, or if it's difficult to get an ABG. With the exception of oxygen status, the values are similar as an ABG and just as useful. CBGs are now coming back into play, as for a while they were not being ordered much.
• Pulmonary Function Test: A test that measures lung function. It measure how much air you exhale, and how fast this air flows.  It's a very useful tool to help physicians diagnose various lung diseases.
• Urine output: This is the measure of the normal output of a person per day. Normal is 40 ml/hour or 1 liter per day. When input is greater than output, this results in weight gain, electrolyte imbalance, increased hemodynamic pressures, decreased lung compliance, etc. (see central venous pressure below)
• Sensible water loss: Water lost by urine, vomiting.
• Insensible water loss: Water lost by lungs and skin
• Hypervolemia: Too much fluid in the body.
• Hypovolemia: Too little fluid in the body, dehydration, also indicated by a high hematocrit.
• Level of Consciousness: Normal is awake, alert and orientated (AAOx). Abnormal is lethargic, somnolent, stuporiouis, confused, obtunded, coma.
• Lethargic: Very sleepy, somnolent. May be too many sedatives or possible CO2 toxicity (although rare).
• Confused: Stuporious; change in mental status; responds inappropriately from patients normal; also consider drug overdose, too many sedatives (valium, morphine, psychotropic drugs, etc.)
• Obtunded: This is a drowsy state where the patient is so tired he can barely plop his eyes open. At this point you should consider high CO2, decreased gag reflux and decreased cough. May consider drug toxicity, respiratory failure, sepsis, etc. You'll have to problem shoot.
• Coma: Patient does not respond even to painful stimuli. This may be an end stage disease condition, or it may be drug induced, or it may be a sign of drug toxicity, etc. You'll have to problem shoot. May also be normal in a ventilated patient to allow their lungs and system to relax while the body heals.
• Orthopnea: Shortness of breath when lying down, have to be sitting up to breath. Common with congested heart failure
• Malaise: Geneeral feeling of nausea or pain; flu-like symptoms, headache, tired, weakness, fatigue.
• Dyspnea: A feeling that you can't catch your breath. It's a subjective measure.   It's the medical description of shortness of breath (see #73). Shortness of breath, or breathing discomfort, or uneasy breathing feelings. You may feel dyspnea after a long sprint, and this is normal and it resolves itself. More severe is dyspnea at rest. Dyspnea while slowly walking is less severe than dyspnea while walking fast. Chronic end stage lung patients may feel dyspnea doing normal tasks like shaving, preparing food, etc.
• Clubbing of fingers: This is caused by any disease that caused chronic hypoxia, such as lung cancer of cystic fibrosis. The anlge of the nails is increased, almost smooth looking.
• Venous distention: A popping out of the veins, especially in the neck. Common in patients with end stage lung disease due to high pressure needed to pump blood through lungs and body
• Edema: This is excess fluid somewhere in the body, causing swelling, such as in the ankles. It's common with heart failure, or kidney failure.
• Ascites: Accumulation of fluid in the abdomen; liver failure
• Diaphoresis: Sweating. May be sign of heart failure (CHF), fever, infection, anxiety, nervousness, etc.
• Jaundice: Yellow skin; liver failure; increased biliruben (new born infants). If newborn, patient may be placed under radiant light and the problem will resolve itself.
• Barrel Chest: Increased a/p diameter of chest, and a result of air trapping. This may be a short term condition (asthma) or chronic (end stage emphysema, COPD)
• Nasal flaring: A flaring out of the nostrils during inspiration. This is usually a signs of respiratory distress in newborn babies and infants
• Retractions: This is a sucking in of the chest during inspiration, and is a sign of respiratory distress in neonates. The higher up in the chest the retractions are the more severe the respiratory distress.
• Grunting: A grunting on expiration, and is usually a common sign of respiratory distress in neonates. It's the patients natural attempt to keep the alveoli open and get more oxygen.
• Tracheal deviation: This is when the trachea is moved either to the left or right. The trachea is usually pushed away from pathologies such as pleural effusions, tension pneumothorax, neck or thyroid tumors, large mediastinal masses. ( or things that take up space in the lungs). It moves toward pulmonary atelectasis, pulmonary fibrosis, pneumonectomy and diagphragmatic paralysis (or things that make more room in the lungs).
• Crepitis: A crunchy feeling felt by the hand over the chest wall, neck, and around a chest tube. It's usually air that creeps and bubbles under the skin. Subcutaneous emphysema.
• Vesicular: Normal lung sounds
• Bronchial: Normal lung sounds heard over the upper airway (trachea and bronchi).
• Adventitious: Abnormal lung sounds (wheezing, rhonchi, rhales, crackles, etc.)
• Coarse lung sounds: Rhonchi (see rhonchi below)
• Wheezes: High pitched sound heard on inspiration and or expiration, and is usually indicitive of bronchospasm. Don't get upper airway wheezes confused for bronchospasm, because all that wheezes is not necessarily bronchospasm. Usually, if it's audible, it's not a wheeze technically speaking.
• Crackles:  The sound of fluid in the lungs or the alveoli popping open with inspiration.  There are two types:  1) Coarse crackles (a.k.a. rhales) are heard on inspiration and expiration and represent fluid in the lungs, 2) Fine crackles are heard on inspiration only and represent alveoli popping open with inspiration; often a sign of atelectasis; may be sign of early pneumonia.
• Fluid challenge: If you have a patient who has a low blood pressure, shock, hypovolemia, etc. you'll challenge him with a rapid bolus of fluid to try to get blood pressure up.
• Blood pressure: Normal is 120/80. Greater than 140/90 should be treated as hypertension, and less than 90/60 should be treated as hypotension. Consider normal values for patinet however.
• Pulmonary Hypertension: High blood pressure in the lungs, which is usually indicative of end stage pulmonary disease, such as COPD, lung cancer, pulmonary fibrosis, cystic fibrosis, etc. It means the heart is working extra hard to push blood through the lungs, and often results in a large right heart (Cor pulmonale) that eventually results in a large left heart and heart failure.
• Cor pulmonale: An enlarged right heart secondary to long term high pulmonary blood pressure (pulmonary vascular resistance) secondary to end stage chronic lung disease.
• Auscultation: Listening to lung sounds
• Bronchial Hygene therapy: positioning a patinet to drain secretions (done in cystic fibrosis patients)
• Chest percussion: Clapping with cupped hands over chest wall to create vibrations in an attempt to move thick and stubborn secretions so they may be expectorated.
• Expectoration: Spitting up phlegm
• Chest physiotherapy (CPT): Using bronchial hygene and chest percussion to stimulate expectoration of secretions; pulmonary toilet.
• Pulmonary toilet: Doing whatever is necessary to help a patient expectorate thick and stubborn secretions; COPD; breathing treatment with bronchodilator and sometimes with Mucomyst; chest physiotherapy; PEP therapy, Flutter valves, etc.
• Suctioning: Removing secretions from the patients airway by artificial means. It is invasive and should never be done on any patient who is awake and alert. It can traumatize the patient and the airway. It is a necessary procedure in an intubated patient.
• Intubation: The process of inserting an endotracheal tube into a patients airway to the lungs to facilitate breathing for that patient. It is necessary for patients who cannot breath on their own. A patient is usually hooked up to mechanical ventilation.
• Mechanical Ventilation: The process of breathing for a patient with a machine called a ventilator.
• Prone position: Lying on belly
• Supine position: Lying on back
• Fowlers position: Sitting up straight
• Semi fowlers position: Sitting up withe the head of bed at a 30-40 degree angle.
• Death Rattle: Increased saliva and secretions in throat due to loss of ability to swallow and clear oral secretions. It's harmless to the patient, but can often be stressful for the family member not familiar with it, or not ecucated about it.
• Cardiac Wheezes: These are usually coarse wheezes, sometimes audible, and often of the upper airway that are caused because of increased pressure around the bronchial tree of the lungs due to heart failure and increased pulmonary edema. The increased pressure and fluid actually squeeze the bronchial tubes, thus causing them to wheeze. This presents similar to asthma, and is often confused as asthma, thus the name.
• Cardiac Asthma: See Cardiac Wheeze. This is asthma-like symptoms caused by heart failure. It presents as dyspnea at rest or on exertion and wheezes. It is often confused for asthma
• Ventilator Delirium: (synonym is psychosis) According to RT Magazine: "Delirium, as defined by the DSM-IV, requires an acute disturbance of consciousness with reduced clarity or awareness of the environment (eg, an inability to focus or to sustain or shift attention) and either (1) a new cognitive change (eg, deficits in memory or orientation, or a language disturbance) or (2) a new perceptual disturbance (eg, hallucinations or misinterpretations).2 Delirium frequently develops over hours or days, and fluctuates over time.
• Ventilator Acquired Pneumonia: This is pneumonia acquired once a patient is on a Vent. For the most part, a vent cannot cause pneumonia, however the term sticks.
• Circadian Rhythm Sleep Disorder: This is what happens to people who work nights. It's the totally whacking out of your circadian rhythm, thus making it difficult to sleep. The only cure is to stop working nights.
• Concurrent therapy:  See treatment stacking
• Treatment stacking:  When you do more than one breathing treatment at a time. 
• Nauseated: You feel sick
• Nauseous:  You make others feel sick
• Shortness of breath (SOB): It's a subjective measure. It's how your breathing feels to you. Do you feel winded? Do you feel you can't get air in? Do you feel dypneic. (see above)

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Indications and contraindications for NIV

Noninvasive ventilation (NIV) is commonly ordered, and in many cases allows an opportunity for a patient to recover in lieu of intubation and mechanical ventilation. 

According to the National Institute of Health, the following are the indications:

• Acute respiratory failure 
• Acute or chronic respiratory insufficiency 
• Documented sleep apnea

However nice NIV is, there are times when it is contraindicated.  It is up to the respiratory therapists to remind the attending physicians of these contraindications when they arise.  

Contraindications for NIV are

• Absence of a drive to breathe
• Inability to maintain a patent airway
• Inability to adequately clear secretions 
• Acute sinusitis or otitis media 
• Risk for aspiration of gastric contents 
• Hypotension (NIV may decrease cardiac output, decrease venous return)
• Pre-existing pneumothroax or pneumomediastinum 
• Epistaxis 
• Recent facial, oral or skull surgery or trauma 
• History of allergy or sensitivity to mask materials where the risk from allergic reaction outweighs the benefit of ventilatory assistance 

All asthmatics have a little bit of Joe Goofus

The following originally published at healthcentral.com/asthma on 3/4/13

We all have a little Joe Goofus in us -- even me

I thought it was funny (well, not really) when I visited my mother's house a few weeks ago and realized I forgot my rescue inhaler (So that makes me a goofus asthmatic right?)

My mother said, "You can use mine."

I said, "Awesome."

Then I squirted it and it tasted like rotten eggs.  Plus the puffer worked poorly.  I checked the date on the inhaler and saw it expired in 2010.  The medicine worked -- sort of, but not very well.  I suppose, by my rules, that makes my mom a goofus asthmatic too.

The funny thing about this (okay, so it's not funny) is my inhalers never expire because they never last long enough to expire, unless I happen to find a lost one under a couch cushion or under the bed or something like that (that ever happen to you?)

If you get to a point where your asthma is acting up and you need your rescue inhaler, it sure would be nice if you had one.  And if you had one, it sure would be nice if there was some medicine in it.  And if there's medicine in it, it would be nice if the medicine wasn't expired so you get the most bang for your puffs.

So my advice to all you asthmatics out there, (especially all you potential Joe Goofus asthmatics -- you know who you are) is to make sure you do all of the following:

1. Get a prescription for a rescue inhaler from your doctor
2. Carry your rescue inhaler (Albuterol or Xopenex) with you, or have it nearby, at all times
3. When the counter shows you have only 20 puffs left, call in for a new prescription
4. If your inhaler is a year old, toss it out and get a new one

Follow these simple rules and you'll be well on your way to removing yourself form Goofus status.

As far as my mom, well, I encouraged her to get a new prescription, and I encouraged her to put a date on it.  I also encouraged her to toss it out after the expiration date.

My mother was raised by parents who lived through the Great Depression, so she tends to be quite frugal.  Yet I explained that when it comes to your asthma medicine, you need to toss the old one even if there's some left in there,and get a new inhaler.  Will she do this?  I have no control over my mother.  

I do, however, have control over my own actions.  I usually am a good asthmatic and carry my rescue medicine with me like a good boy.  However, we all have our off days, which is probably why we'll all have a little of Joe Goofus in us.

What do you think?

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Does a double dose of claritin benefit allergic asthma?

Your Question:  I have allergic asthma and take claritin because it does help. However, on some nights I wake up and the allergies as so bad that nothing seems to do anything. I was wondering if a double dose of claritin would benefit me on those days?

My answer; For the record, the standard dose of Claritin (loratadine) is 10 mg, and you're talking about doubling that dose to 20 mg.  Since I am not an expert on allergic medicine, I am going to allow the physicians over at healthtap.com answer your question.

1.  Dr. Luis A. Matos:  It may make you drowsy.  The full adult dose of Loratadine in other parts of the world is 20 mg. This amount caused a 12-14% drowsiness rate. The 10 mg dose was tested in the us in order to find a non-drowsy dose and it worked. If your allergy symptoms are controlled with Diphenhydramine (benadryl-50% drowsiness) and not 10 mg loratadine, you can try a second 10 mg dose and it may help with a lot less drowsiness.

2.  Dr. James W. Ferguson:  Studies of loritadine show the medication is well tolerated at twice the recommended 10 mg dose. However, the same studies show no added benefit of the double dose in symptom relief over the regular dose schedule.

Concusion:  So it appears that it is safe to try a second of Claritin if you want, although it's important to understand there is no evidence it will do any good, and that there will be a slight increase in your risk for side effects, of which the main one is somnolence.

Types of Asthmatics Lexicon

Types of Asthmatics:

Bronchodilatoraholic: A person who takes more than two puffs twice a week of a rescue inhaler. Some are bronchodilator abusers, and some are simply Hardluck Asthmatics. You can read my experience here and and take the test to see if you are one by clicking here.

Bronchodilator Abuser: A person who abuses his rescue inhaler when what he should be doing is checking in with his asthma physician. Overuse of an inhaler is the #1 sign of uncontrolled asthma.

Hardluck Asthma: Despite all the best asthma medicines and wisdom, these asthmatics continue to have trouble with their asthma. I wrote about one such asthmatic here and here, and I wrote about my experience here. Plus you can click on "my story" under the banner to read more of my story growing up with Hardluck Asthma.

Gallant Asthmatic: She is the asthmatic who does everything right, and has great control of his asthma. He avoids his asthma triggers, has worked with his doctor on an Asthma Action Plan, and follows it to a tee. He is also very compliant with his asthma medicines and sees his asthma physician at least twice a year, but ideally twice a year. I write about Gallant Asthmatics often, such as this post and this post.

Goofus Asthmatic: He's the asthmatic who does everything wrong. He fails to go out of his way to avoid his asthma triggers, only goes to see his doctor when he has to, and does not have an asthma action plan. If he does have one he doesn't follow it. He is not compliant with his medicines, as he takes them only when he is feeling symptoms. He is the asthma type who is most likely to be seen in the ER. On a similar note, since his asthma is so out of control and since he is not on his controller meds, he is most likely to be admitted to the hospital. I write about Goofus Asthmatics on occasion, such as this post.

Phlegmatic Asthmatic: She's the calm, cool and collected asthmatic who takes everything in stride. He could be having an asthma attack right in front of you and you'd never know it (unless you had a keen eye for asthma.) How do you know you're dealing with a phlegmatic asthmatic? You won't unless they tell you they have asthma. These are the zen asthmatics who appear to be accepting of their condition, don't lose their cool and quietly deal with breathing trouble. I am a phlegmatic asthmatic

Actor Asthmatic: He is the asthmatic who always seems to have trouble breathing when you need him most. If it's time to haul in wood for the fire, his asthma flares. If he's dreading going to work he might run laps around the living room to ignite his asthma. When it's time to haul in the groceries he'll be seen puffing on his inhaler. He'll do anything to get out of work and avoid stress. Synynom: Exaggeration of Asthma. The actors are fun to write about.

Martyr Asthmatic:They could by dying and they still don't go to the ER. They are usually tough, macho adult men who only go to the ER at the insistence of their spouses. Their biggest fear, although they won't admit it, is that they will be told their asthma is all in their head, and then they'll feel stupid. So, they think it's easier just to pretend they are fine.

Recovered Asthmatic: Child asthmatics who grow up and no longer have asthma symptoms so they do some unwise things -- like smoke. When their asthma comes back, they are in a world of hurt.

Doubting Thomas: These are mostly adult-onset asthmatics who, all of a sudden, develop mild asthma symptoms, but don't want to admit they have asthma. They would rather suffer at home than seek treatment. But when the RT gives them a treatment they will say, "Wow, I didn't even realize I was short-of-breath." Famous Olympic swimmer Dara Torres may have been this kind of asthmatic. But now, I'm sure, she is a Gallant asthmatic.

Sometimer Asthmatic: Synonym: Asthmatics in Denial: They live normal lives, feel good 95% of the time, and so are in denial about their asthma and don't take their preventative medicines. These are your adult asthmatics who sometimes have mild symptoms, and when they do they take a puff or two or three or four of their inhaler until they feel better.

Poor Patient Asthmatic: These asthmatics would be okay is they had different doctors. We RTs hate to bad mouth doctors, but we know that since this patient has been in the ER 10 times in the last year, he should be on some type of preventative, anti-inflammatory medicine and not just a bronchodilator. Poor patients may also be children whose parents don't have a clue how to manage the asthma.

Bronchodilatoraholic: These are people who use a bronchodilator frequently. Some may be abusing their medicine, but many are gallants who simply have hard luck asthma.Abusers don't work with their doctor on an asthma action plan and they may not bother with controller, anti-inflammatory medications. For them, puffing away is like a bad habit - like biting your fingernails. In contrast, some hard-luck asthmatics may just need their bronchodilator frequently - many times a day, every day.We'll learn more about bronchodilatoraholics on another post.

Unfortunate Asthmatic: These asthmatics don't have access to a healthcare provider, and cannot affort to get their prescriptions refilled. They give the appearance of Goofus Asthmatics, although they are not. Many live in downtrodden city homes filled with allergens they cannot escape. Their homes are often exposed to the elements due to things like a leaky roof, flooded and musty basement, broken windows covered with plastic and duct tape, broken plaster and peeling paint. They have poor ability to remove asthma triggers from clothing due to lack of washer and drier, or inibility to afford to pay the water bill. They are often exposed to second hand smoke due to inibility to choose their surrounding environment. Good asthma control may be hard to come by no matter hard they try.

Best asthma you can be: This is the more realistic asthma type. They strive to be the best they can be, although they are not perfect because, if you think about it, perfection is not achievable. Normal asthmatics will miss an occasional dose of medicine, and will take an occasional extra puff on their inhaler, and may even use their rescue inhaler without a spacer.

Vulnerability: (1)A feeling you get when you realize you're not going to live forever. It most often occurs when you require prolonged or frequent stays in a hospital. (2) The realization if you want to live a long, healthy life you have to take care of your self, which may include making some changes (like quitting smoking, avoiding allergens, etc.
Vulnerability: (1)A feeling you get when you realize you're not going to live forever. It most often occurs when you require prolonged or frequent stays in a hospital. (2) The realization if you want to live a long, healthy life you have to take care of your self, which may include making some changes (like quitting smoking, avoiding allergens, etc.

Bronchodilator anxiety: The feeling of anxiety because you don't have your rescue inhaler on your posession. This may bring about an asthma attack just because you don't have it.

Asthma forgetfulness: The tendency of some asthmatics to forget they have asthma because they are feeling well, and do things that they shouldn't. Examples: quit taking meds, rake leaves, clean musty basement, etc.

Hypoxic Drive Theory: Here are the evidence that disproves it

The hypoxic drive theory was established in 1960.  Since then many studies have shed doubt on this theory, in favor of the Haldane Effect and ventilation-perfusion mismatching.  Listed here is all the evidence that either proves or disproves these theories.

1. Hoyt, John. W., "Debunking the Myths of Chronic Obstructive Pulmonary Disease", Critical Care Medicine, 1997, Volume 25, Number 9, pages 1450-1451 (you'll have to obtain a prescription to view article)
2. Campbell, E.J.M, "Respiratory Failure,"  The British Medical Journal,  June 1965, 1451-1460 (article provided by link)
3. Arnottt, W.M, "Respiratory Failure,"  Lancet,  January 1960, Volume 25, Issue 7114, pages 1-7 (you'll have to subscribe to view article)
4. Campbell, E.J.M, "The J. Burns Amberson Lecture - Management of Acute Respiratory Failure in Chronic Bronchitis and Emphysema," The Journal of Occupational and Environmental Medicine, June 1968,  Volume 10, issue 6, pages 329-332  (You'll have to become a member to veiw article)
5. Campbell, E.J.M, "The J. Burns Amberson Lecture - Management of Acute Respiratory Failure in Chronic Bronchitis and Emphysema," American Review of Respiratory Diseases, October 1967, Volume 96, Issue 4 (no link available)
6. Scano,G, A. Spinelli,  R. Duranti, M. Gorini, F. Gigliott i, P. Goti, J. Milic-Emili, "Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia," Europe Respiratory Journal, 1995, Volume 8, pages 78-85 (full pdf provided by link)
7. Robinson, Tracy D  David B. Freiberg, Jeff A. Regnis and Iven H. Young, "The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnea during Acute Exacerbation of Chronic Obstructive Pulmonary Disease," American Journal of Respiratory and Critical Care Medicine, 2000, volume 161, pages 1524-1529 (full pdf provided by link)
8. 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)
9. 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)
10. Lazic, D, et al, "The influence of oxygen therapy on the hypercapnia in patients with chronic obstructive pulmonary disease,"  July 2008, Volume 65, Issue 7, pages 521-524 (abstract available by link)
11. Sassoon, C.S., et al, "Hyperoxic-induced Hypercapnea in Stable Chronic Obstructive Pulmonary Disease," American Review of Respiratory Disease, 1987, 144, pages526-530 (abstract available by link)
12. Chien, et al, "Uncontrolled Oxygen Administration and Respiratory Failure in Acute Asthma," Chest, March 2000, Volume 117, Issue 3, pages728-733 (abstract available by link, or pdf here)
13. Caruana-Montaldo, et al, "The Control of Breathing in Clinical Practice," January 2000, 117/1, pages 205-225 (Article available by link)
14. Dunn, et al, "Oxygen-Induced Hypercarbia in Obstructive Pulmonary Disease," American Review of Respiratory Disease, 1991, 144, pages 526-530
15. Gosselink, R, H, Stam editors, Lung Function Testing, 2000 chapter 3, "Control of Breathing," , page 51 (chapter 5 provided for viewing only, supports Campbell)
16. Rudolf, et al, "(Hypothesis) Hypercapnea During Oxygen Therapy in Acute Exacerbation of Chronic Respiratory Failure," Lancet, September 3, 1977, pages 4483-486 (Abstract available by link, prescription needed to view article)
17. Stradling, J.R, "(Editorial) Hypercapnia during oxygen therapy in airways obstruction: a reappraisal," Thorax, December 1986, 41(12) pages 897-90202 (have to subscribe to veiw article)
18. Siafakas, N. M, editor, Mitrouska, I, N. Tzanakis, N.M. Siafakas, Management of Chronic Obstructive Pulmonary Disease, Chapter 18,  "Oxygen Therapy in Chronic Obstructive Pulmonary Disease," 2006, pages 302-308
19. Crossley, et al, "Influence of inspired oxygen concentration on deadspace, respiratory drive, and paCO2 in intubated patients with chronic obstructive pulmonary disease," Critical Care Medicine, 1997, volume 25, Number 9, pages 1522-1526 (abstract available by link)
20. Plantt, et al, "One year prevalence study of respiratory acidosis in acute exacerbations of COPD:  implications for the provision of non-invasive ventilation and O2 administration," Thorax, 2000, 55, pages 550-554 (full pdf available by link, for abstract click here).
21. Molfino, et al, "respiratory arrest in Near-Fatal Asthma," New England Journal of Medicine, 1991, 324: pages 285-288 (abstract available by link,  another abstract available here or full pdf available here)  Correspondence to this article from pages 205-206 here.
22. McFadden, "(Editorial) Fatal and Near Fatal Asthma," New England Journal of Medicine, 1991, 324: pages 409-411
23. Burnell, et al, "(Case Report) Extreme Obesity Associated with Alveolar Hypoventilation- A Pickwickian Syndrome," , American Journal of Medicine, 1956, 21:811-818 (abstract available by link)
24. Wagner, et al, "Ventilation-perfusion inequality in chronic obstructive pulmonary disease," The Journal of Clinical investigations, February 1977, Volume 59, pages 203-216 (full article available by link)
25. Dick, et al, "O2-Induced changes in Ventilation and Ventilatory Drive in COPD," American Journal of Critical Care Medicine, 1997, Volume 115, pages 609-614 (abstract available by link)
26. Gasparini, et al, "Inter-Individual Variability of the Response to Oxygen Administration in Hypercapneic Patients," European Journal of Respiratory Disease,  1986, 69 (suppl 146) 427-443 (no abstract or pdf availaable)
27. Schiavi, "Acute Respiratory Failure in Chronic Obstructive Pulmonary Disease," Clinical Pulmonary Medicine, May 1998
28. Gomersall, Charles D, et al, "Oxygen therapy for hypercapnic patients with chronic obstructive pulmonary disease and acute respiratory failure: A randomized, controlled pilot study," Critical Care Medicine, January 2002, 1: 113-116 (abstract available by link)
29. Simpson, Stephen Q, "(Editorial) Oxygen-induced acute hypercapnia in chronic obstructive pulmonary disease: What's the problem?" Critical Care Medicine, January 2002, 1, page 258
30. Day, Rene A, Beverly Williams, Brunner and Suddarth's Textbook of Canadian Medical-Surgical Nursing, 2009, page 654
31. French, William A, "The Hypoxic Drive Theory Revisited," RT:  For Decision Makers in Respiratory Care, " February/ March, 2000
32. "Hypoxic Drive Theory: A Myth -- the why and how," Myparamedicblog.wordpress.com, 2009, http://paramedicblog.wordpress.com/2009/11/19/hypoxic-drive-theory-myth-the-why-and-how/
33. Siobal, Mark, "Hypoxic Drive in Chronic Obstructive Lung Disease: Is the fear of oxygen therapy based on fact or myth," UCSF San Fransisco General Hospital," power point presentation: PPT
34.  Beachey, Will, "Breathing Control in Chronic Hypercapnia," RT:  For Decision Makers in Respiratory Care, " June/ July, 2000
35. "Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients prehospital setting: randomized controlled trial," British Medical Journal, 2010, page 341, C5462
36. Correspondence (Aubier and Stradling regarding study cited in #8 above), American Review of Respiratory Disease, Oct. 16, 1986
37. Aubier, et al, "Central Respiratory Drive in Acute Respiratory Failure of Patients with Chronic Obstructive Pulmonary Disease," American Review of Respiratory Disease, 1980, Volume 122, pages 191-99
38. Grief, Robert, et al, "Supplemental perioperative oxygen to reduce the incidence of surgical wound infection," The New England Journal of Medicine, Jan. 20, 2000, volume 342, no. 3
39. Jonnson K, et al, "Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients," Ann Surg, Nov. 1991, 214 (5), pages 605-13
40. La Van, FB, TK Hunt, "Oxygen and wound healing," Clin Plast Surg, July, 1990, 17 (3), pages 463-72
41. Bartells, Matthew N., John M. Gonzales, Woojin Kim, Ronald E. De Meersman, "Oxygen Supplementation and Cardiac-Autonomic Modulation in COPD, Chest, 2000, 118, pages 691-6
42. Noriaki, et al, "the relationship between chronic hypoxemia and activation of the tumor necrosis factor-x- system in Patients with Chronic Obstructive Pulmonary Disease, American Journal of Respiratory and Critical Care Medicine, April, 2000, Vol. 161, Number 4, pages 1179-1184
43. Mannix, ET, F. Manifredi, MO Farb er, "Elevated O2 cost of ventilation contributes to tissue wasting in COPD," Chest, March, 1999, volume 115, no. 3, pages 708-13
44. Macnee, Skwarski, "The pathogenisis of peripheral edema in Chronic Obstructive Pulmonary Disease," Clinical Pulmonary Medicine, Nov., 1997
45. "Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema.  Report of the Medical Research Council Working Party, Lancet, 1981, 1(8222), pages 681-6
46. Plywaczewski, et al, "Incidence of nocturnal desaturation while breathing oxygen in COPD patients undergoing long-term oxygen therapy," Chest, 2000, 117, pages 679-83
47. Burnell, et al, "(Case Report) Extreme obesity associated with aleolar hypoventilation -- a pickwickian syndrome," American Journal of Medicine, 1956, 21, pages 811-18
48. Steven M., Scharf, Michael R. Pinsky, Sheldon Magder, ed., "Respiratory-circulatory interactions in health and disease," 2005, New York, pages 656-658.  This provides a great review of all the evidence that disproves the hypoxic drive theory up to this date.  Great read for those interested. 
49. Cooper, Nicola, Kirsty Forrest, Paul Cramp, "Essential guide to acute care," 2nd edition, 2006, Massachusettes, page 24
50. Moulton, Chris, David W. Yates, "Lecture notes:  Emergency Medicine," 3rd ed., 2006, pages 215-16
51. 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
52. Young

Note:  Various individuals contributed to this list, most notably Jeffrey Whitnack and Dana Oachs. 

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