Monday, April 27, 2015

Understanding Asthma Action Plans

The following was originally published on May 27, 2014, at

Most asthma experts recommend every asthmatic have an asthma action plan, sometimes called an asthma management plan.  It’s a plan you work on with your doctor to determine what action you should take to manage your asthma both long and short term.  

Asthmatic air passages have some degree of chronic (it’s always there) inflammation. This makes your lungs hypersensitive, or over sensitive, to certain asthma triggers in the world around you. To learn more about asthma triggers check out my post: “Learn how to avoid your asthma triggers.”

When exposed to your asthma triggers, this inflammation may become worse, causing an acute (it’s happening now) asthma attack (flare-up, exacerbation).

This causes:
  • Muscles lining your air passages to spasm or constrict, and this obstructs the air passages, causing shortness of breath.
  • Goblet cells lining your air passages produce secretions that also obstruct air passages, causing shortness of breath. 
So there are two stages of asthma: chronic and acute. These correlate with the two parts of an asthma action plan:
A. Long-term management:  This part of the plan includes your actions to treat the underlying chronic inflammation and, therefore, prevent asthma from flaring up. It includes all the medicine you take every day, such as Flovent, Qvar, Advair, Symbacort, Dulura and Breo.

B.  Short-term asthma management:  This part of the plan includes your actions to treat acute asthma symptoms. There are two methods of monitoring your asthma to help you determine the action you need to take.
  1. Peak flow monitoring:  This is where you use a peak flow meter to help you determine how well your lungs are working.  This type of monitoring works great because it provides an objective number to help you decide what action to take.
  2. Symptom monitoring:  This is where you monitor your asthma signs and symptoms to help you determine how well your lungs are working.  This type of monitoring is subjective and does not require the use of a device.
  3. Both:  This is where you use both peak flow monitoring and symptom monitoring to help you determine how well your lungs are working.  An ideal plan will include both.
Asthma journal:  An important part of any plan is an asthma journal, which may be something as simple as a spiral notebook.  In this journal you will record your daily peak flows and your daily symptoms.  

Once you have a journal, and when you are feeling well, you should blow into your peak flow meter every day for two weeks and record the results in the  journal.  The peak flow value that is highest during this time will become your personal best.  You then use this value to determine the following:
  • Green range: 80% or better means you are in your safe zone and no action is needed (see below).
  • Yellow range: 60-80% means you are in your caution zone, and action is needed.  Follow your plan for the correct action to take. 
  • Red range:  Less than 60% means you are in your danger zone and action is needed. Follow your plan for the correct action to take.
You will then continue to use your peak flow meter every day, and continue monitoring your asthma symptoms, to help you decide what action to take.

A typical plan will go something like this:

Early warning symptoms:  These may include feeling tired, irritable, anxiety, itchy chin, funny feeling in chest, coughing, trouble sleeping, cold symptoms, sneezing, headache, increased sputum, inability to exercise, breathing changes, and your peak flows are 80% or better of your personal best.  (For signs and symptoms of asthma in infants check out my post “What Are the Signs and Symptoms of Asthma in Infants.

Action:   Continue taking all the medications recommended as part of your long-term asthma action plan.  If your doctor recommends it, pretreat yourself before you exercise.  If necessary, remove yourself from known asthma triggers.   

Acute asthma symptoms: These may include wheezing, coughing, shortness of breath, chest tightness, and peak flow numbers 50-80% of your personal best.  

Action: Get away from what is triggering your asthma.  May also include taking your rescue medicine, such as 4-8 puffs on your albuterol rescue inhaler 2-5 minutes apart or taking an albuterol breathing treatment.  If your symptoms do not improve, or your peak flow values do not return to your green range,  your plan may include a second dose of the above medicines.  If, within 20-30 minutes of taking action, your symptoms or peak flows do not improve, you should call your physician, who may recommend increasing the frequency you use your rescue medicine (such as taking it every four hours for a while). Systemic steroids may also be recommended.

Late asthma symptoms: These may include uncontrollable coughing, chest tightness, leaning on things to breathe, shoulders raised, unable to move or walk, bluish skin around lips and fingers, and sucking in stomach and lifting shoulders to breathe (paradoxical breathing). It also includes peak flow values of less than 60% of your personal best.

Action:  Take your rescue medicine by inhaler or nebulizer immediately.  Your plan may include repeated doses.  Call your doctor or 911 right away.  If you are this bad you will need to be seen by an expert.  

Make sure you continue to monitor your peak flows and symptoms every day, and record them in your asthma journal.  When you visit your doctor, it is important to take this journal with you. This will help you and your physician recognize trends, such as that your asthma gets worse when you are around horses, or worse in the spring or summer.  This way you and your physician can make changes to your plan as necessary.  

Bottom line:  An asthma action plan is essential for good asthma control.  It should include the medicines you take every day to control and prevent asthma symptoms, and the actions necessary to treat your asthma when it does flare up.    

The plan should also be simple, written on one side of a piece of paper, and kept in a place that is easy to access, such as on the refrigerator or bedside table, wallet, or purse.  This way it is easy to find when you need it.  Check out for example asthma action plans for adults, children and infants.

Friday, April 24, 2015

100 B.C.: The beginning of the decline of wisdom

In order to understand the medicine of a given point in time, it's essential to understand the people of that time.  So here is a glimpse into the era of ancient Rome at the time when Christianity was just forming.

The ancient Greeks significantly advanced wisdom for the ancient world, and this knowledge was a gift handed to the Romans. The problem was that the gift was only available to the chosen few, while the majority continued to live in abject poverty.

This is key here, because the way the Roman majority was treated by the ruling class would help set up the entire structure of the Jewish way of life. This lead to the planting of the seeds of Christianity, which slowly grew into a full and flourishing tree that provided hope to the majority, although at the expense of wisdom.

So, life for the majority was not very good. This was explained best by medical historian Thomas Lindsley Bradford in his 1898 book "Quiz questions on the history of medicine:"
Draper tells us that just before the coming of Christ Rome was very wicked. Rome then contained two millions and a quarter of inhabitants, but of these only about ten thousand were of the gentry, the upper ten; there were about one hundred and twenty-five thousand populace or plebs. The plebs were often paupers in feeling, many of them were given public alms; they had cheap board, free admission to the theatres and gladiatorial shows, where the combats of the gladiators was not calculated to impress with fine feeling. There was about a million slaves, held as chattels, in the most abject misery. They might be killed at the will of their masters, and sometimes they were horribly mutilated, the physicians often having to perform these acts. There was no middle class at Rome. All these were kept in order by the numerous guards, generally mercenaries and foreigners. In Caesar's time, Rome the city which ruled the world was terribly depraved. Politicians had become demagogues; the concentration of power and increase of immorality proceeded equally. The Roman power included one hundred and twenty millions of people. Wealth was the only standard of social distinction. Law was of no value; the suitor was compelled to deposit a bribe before a trial could be had. Draper in his intellectual development of Europe says of this period of Roman history: The social fabric was a festering mass of rottenness. The people had become a populace; the aristocracy was demoniac; the city was a hell. No crime that the annals of human wickedness can show was left unperpetrated—remorseless murders; the betrayal of parents, husbands, wives and friends. Poisoning was reduced to a system; adultery degenerated into incest, and crimes that cannot be written. Women of the higher class were so depraved, lascivious and dangerous, that men could not be compelled to contract matrimony with them; marriage was displaced by concubinage; even virgins were guilty of inconceivable immodesties; great officers of state and ladies of the court of promiscuous bathings and naked exhibitions. In the time of Caesar it had become necessary for the government to put a premium on marriage. He gave rewards to women who had many children; prohibited those women under forty-five years of age and having no children, from wearing jewels and riding in litters, hoping by such social distinctions to correct the evil. It went from bad to worse, so that Augustus in view of the general avoidance of legal marriage, and resort to concubinage with slaves, was compelled to impose penalties on the unmarried—to exact that they should not inherit by will except from relations.The Roman women reckoned the years not from the consuls but from the men they had lived with. Gluttony was carried to loathsomeness. It was said of them—they eat that they may vomit, and vomit that they may eat. At the taking of Perusium, three hundred of the most distinguished citizens were solemnly sacrificed at the altar of Divius Julius by Octavius. Moral principle was extinct, it was a nation of atheists. Religious sentiment was entirely effaced. It was skeptical thought that governed the minds of the scholars; Varro, one hundred and ten years B. C, said that the gods were to be received as mere emblems of the forces of matter. Lucretius recommends that the mind be emancipated from the fear of the gods; Cicero was a skeptic. Some thought a virtuous life should be lived; some were cynics, some stoics. Epictetus (55-135 A.D), the slave and philosopher, taught that suicide was man's privilege. Seneca (4 B.C.-65 A.D.) said that time is our only possession, and that nothing else belonged to man. And we may well understand the influence all this must have had on the medical doctrines of the physicians of that time.
Bradford then posed the question: "What effect had Christianity on medicine?" His answer:
Rutherford Russell says that it is likely that Christianity must at first have acted injuriously on medicine. Jesus Christ was celebrated as a healer; he went about healing the sick and restoring to life. To the people of his time his principal occupation was the healing of the sick. This power possessed by the Saviour was given by him to his disciples. Luke had been a physician; but how could he prescribe after the manner of men, when he was able to heal by the grace of God? Thus medicine based as an art on the natural order of things, was for a time superseded by the preternatural power of certain men. But between religion and science there was a barrier great and unsurmountable.
So while Christianity did help to improve the plight of the poor, it did so (at least initially) by taking away from the aristocracy the gift of wisdom from the Greeks. It would be another thousand years before wisdom would come back to the civilized world, and another 1700 years before a system was created to encourage common folks to use their wisdom to improve medicine for all the masses.

  1. Bradford, Thomas Lindsley, writer, Robert Ray Roth, editor, “Quiz questions on the history of medicine from the lectures of Thomas Lindley Bradford M.D.,” 1898, Philadelphia, Hohn Joseph McVey
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Thursday, April 23, 2015

Diffusion of oxygen from air to tissues

Today we're going to take a molecule of oxygen, and show how it travels from the air inhaled, through the lungs, the blood and then to the tissues.  Then we'll do the same for carbon dioxide, showing how it travels from the tissues to the lungs to be exhaled.

Basically, it must be understood that a gas travels from areas of high pressure gradient to areas of lower pressure gradient.  There are a couple laws of physics to help explain how this is possible.

Please note that all the numbers and percentages in this post are either estimates or averages.

Fick's First Law of Diffusion.  The rate of oxygen diffusion is proportionate to the concentration difference of oxygen and the surface area.  In other words, it travels from areas of high pressure to areas of lower pressure.  This explains how oxygen travels through tissues.

Henry's Law.  Gases dissolve in liquids in proportion to their partial pressures, depending also on how soluble they are in specific fluids and on the temperature.  This is important because most oxygen inside the body is stored in fluid, such as blood.  Inside the nose it is hunidified, and the alveoli are saturated with water vapor which has its own partial pressure.  

Total Pressure.  This is the tension given off by a molecule of a gas if it were to be confined inside a container.  The pressure is caused by movement of the molecules, and the pressure or tension they cause by constantly impacting the surface of the container.  The total pressure of a gas is summed up by the total pressure of all the molecules contained in it.

Partial Pressure.  This is the pressure exerted by a single gas component in a mixture.  It is the pressure of an individual gas of a mixture.

Dalton's Law.  The total pressure of a mixture of gases equals the sum of the partial pressures of the individual gases in that mixture. 

Room Air.  Contains about 79% nitrogen and 21% oxygen (There are other gases in the air, although they will be omitted here for to make this easier to understand).  Usually, 21% is generally designated as the Fraction of Inspired Oxygen in Room Air.  

Total Pressure of Atmospheric Air as sea level:  760 mmHg
  • Partial Pressure of Nitrogen (PN2) in room air:   600 mmHg
  • Partial Pressure of Oxygen (PO2) in room air:  160 mmHg
These pressures may vary depending on the temperature, humidity, and atmospheric pressure. 

Diffusion:  Pressure moves, diffuses, from areas of higher pressure to lower pressure.  So, by the natural process of respiration, air is inhaled.  It is humidified and warmed to body temperature by the nasal passages.  
  • PNO2 after humidified and heated to normal body temperature (37°C): 564 mmHg
  • PO2 after humidified and heated to normal body temperature (37°C):  149 mmHg
It then makes it's way though air passages to the alveoli.  

Partial Pressure of Alveolar Oxygen.  Designated as PAO2 = 104 mm Hg.  

This may be estimated by FiO2 * 5 (21% * 5 = 105).  There are other more accurate formulas, although this one is the simplest to perform in the clinical setting.  Remember that it is just an estimate using numbers that are rounded off for simplicity purposes. 

PAO2 may also be lowered due to disease processes.  As the formula suggests, the PAO2 may be higher when higher concentrations of oxygen are inhaled (FiO2 22-100%).  Likewise, less oxygen may be inhaled when breathing is relaxed while sleeping.  Less oxygen may also be inhaled due to lung disease, causing the PAO2 to become lowered.  This may be reflected by a measure of PaO2 as obtained from an arterial blood gas (ABG).

Again, oxygen, unlike CO2, requires a high pressure gradient to diffuse.  

Partial pressure of capillary venous blood (PvO2):  PO2 is 40

So oxygen moves from the alveoli, across the respiratory membrane, to the capillary blood because of the pressure difference:
  • 104-40 = 64 mmHg pressure difference. 
This pressure difference, or pressure gradien is perfect for oxygen diffusion to occur from the alveoli to the capillary system.  

So our oxygen molecule is now inside the bloodstream.  Due to its high affinity for oxygen, the oxygen molecule attaches to a hemoglobin molecule.  The hemoglobin molecule has no impact on the partial pressure of oxygen.

However, the accumulation of oxygen in the arterial system causes a build-up of tension that results in the partial pressure rising to 104, the same as it was in the alveoli. So, by the time arterial blood reaches the left atrium, the PO2 is now 104.

Capillary bloodstream (CvO2) = 104 mmHg. 

So now...

After the diffusion of oxygen from the alveoli to the capillary occurs, this oxygenated blood moves to the pulmonary vein to the left atrium.  This blood contains a PaO2 of 104, on average.  This blood constitutes 98% of cardiac output.  Another 2% of the cardiac output comes from the bronchial veins, and this blood has a PaO2 of 40.  This unoxygenated blood is shunted into the pulmonary vein, and mixes with arterial blood.  It is because of this natural shunt that a normal saturation is 98% and not 100%.  This in turn brings the PO2 of left ventricle down to 97 mmHg

The PO2 of the left atrium:  97 mmHg

The heart contracts, and sends oxygenated blood through the arterial system.

Partial Pressure of Arterial Oxygen.  Designated as PaO2.

Because of normal variations in PAO2 (as explained above), the PaO2 may likewise vary.  So, that said, the following is generally considered as true of PaO2. 
  • Normal: 80-100
  • Hypoxemia:  60-80
  • Severe Hyupoxemia:  40-60
So now, the oxygen molecule is attached to a hemoglobin molecule, and rides the bloodstream until it finds a cell that has a low enough PO2 for it to diffuse into that cell.

Partial Pressure of Tissue Oxygen.  
  • Varies from tissue to tissue
  • Some tissues have a PO2  of 22-35
  • The PO2 varies in different areas of a cell
Once oxygen leaves the arterial system, this leaves the hemoglobin in venous blood without oxygen. This blood then returns to the lungs via the venous system to get some more oxygen. 

Partial Pressure of Venous Oxygen.  Designated as PvO2, is 40.

Now the system starts all over again.  However, if we determine that the patient has a disease process that causes hypoxemia (defined as PaO2 less than 60), and the patient is given a higher FiO2 than what is in room air (22-100%), the rate of diffusion of oxygen from the lungs to the tissues will increase.

Once in the cell, the oxygen is quickly absorbed into the mitochondria and is used as part of cellular respiration.  Energy is the byproduct, and this allows the cell do perform its work.  A wasteproduct is Carbon Dioxide (CO2)

About 200 ml of CO2 is produced by each cell per minute. This CO2 has to be quickly eliminated from to prevent acidosis.  CO2 is 20 times more soluble than oxygen, and therefore diffuses quickly.
Likewise, while oxygen requires a high pressure gradient to diffuse, CO2 requires only a small pressure gradient.

Partial Pressure of  Venous Carbon Dioxide (PvCO2):  46 mm Hg

Partial Pressure of Alveolar Carbon Dioxide (PACO2): 40 mmHg

Partial Pressure of Arterial Carbon Dioxide (PaCO2):  40 mmHg

Partial Pressure of Room Air Carbon Dioxide:  0.2

So even while the pressure gradient between the venous system and alveoli is only 6, this is enough for CO2 to diffuse through the system.

Therefore, under normal conditions, CO2 is easily diffused through the body, and exhaled.  Oxygen is inhaled and easily diffuses through the body to the cells.  Of course, effecting these are atmospheric variations like humidity and temperature, disease processes like COPD, and aging.

References and further reading.

Wednesday, April 22, 2015

Interview: Debunking the Hypoxic Drive Theory

The following post was originally published at Advance for Respiratory Care and Sleep Medicine, and written by Rebecca Mayer Knutsen on January 12, 2015.

Oxygen and COPD: Debunking the hypoxic drive theory

In patients with chronic obstructive pulmonary disorder (COPD), inflammatory changes impact their ability to breathe properly. Patients will eventually retain carbon dioxide (CO2) as their efforts to maintain normal CO2 levels proves difficult. Experts have long debated whether chronically elevated carbon dioxide levels affect how a patient handles oxygen. As a result, a theory developed that administering oxygen obliterated the drive to breathe.

The problem with the Hypoxic Drive Theory is that it's a myth concocted on incomplete evidence and often elicits a controversial response, according to John Bottrell, RT, Spectrum Health Ludington Hospital, and COPD/asthma expert for

For hypoxemic patients with COPD, most medical experts now recommend administering the lowest amount of oxygen needed to maintain SpO2 of 88% to 92%, according to Bottrell.

The Controversy of Hypoxic Drive Theory

In hypoxic drive, Bottrell told ADVANCE, the peripheral chemoreceptors located at the bifurcations of the aortic arteries and the aortic arch monitor partial pressure of arterial oxygen (PaO2). This drive only becomes active when the PaO2 is less than 60 mmHg. "This hypoxic response is far slower than signals sent by central chemoreceptors, and therefore the hypoxic drive has only a minor role in breathing," he explained.

When patients with COPD need oxygen, healthcare practitioners should give it to them because doing otherwise will further compromise their health, Bottrell observed. "If the patient goes into respiratory failure, then he should be treated with either noninvasive ventilation or mechanical ventilation," he shared.

Spectrum Health Ludington Hospital tests include arterial blood gas (ABG) collection, pulse oximeter and end tidal CO2 monitor. End tidal CO2 monitor is a noninvasive device that can be connected to special nasal cannulas or endotracheal tubes. The test determines the ETCO2, which is an estimation of the amount of CO2 exhaled. This percentage can be used to estimate PaCO2. In a person with healthy lungs, the EtCO2 is about 2 to 5 mmHg less than PaCO2.

Historical Perspective on Hypoxic Drive Theory

Oxygen was first used for patients with COPD in the late 1940s and 1950s. Around that time, experts observed that some patients became lethargic or lapsed into a coma after receiving high levels of oxygen, Bottrell told ADVANCE. Initial studies showed a decrease in ventilation in 26 of 35 patients with COPD given oxygen therapy, with a rise in CO2and a fall in pH. A further study showed that stopping and starting oxygen therapy led to a fall and rise in CO2 respectively.

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

"The hypoxic drive theory states that some patients with COPD develop chronically elevated arterial CO2 levels, and as a result, their hypercapnic drive becomes blunted, causing them to use their hypoxic drive to breathe instead," Bottrell said. "Therefore, giving high amounts of oxygen to these patients may blunt the hypoxic drive as well, thus completely blunting their drive to breathe."

This occurrence may cause PaCO2 levels to rise to critical levels, resulting in narcosis and possible death. For this reason, COPD patients with suspected CO2 retention are limited to 2 to 3 lpm by nasal cannula, or 40% by venturi mask.

According to Bottrell, the study cited by Campbell included only four patients with COPD, and later studies failed to validate this theory. "Yet it has continued to be a gold standard theory when dealing with COPD patients," he observed.

"Under the guise of this theory, many patients who desperately need higher levels of supplemental oxygen to survive are deprived of it," Bottrell relayed. "Plus, as many respiratory therapists, nurses, and physicians have observed, when these patients are given the oxygen they need, rarely does this lead to complications."

Bottrell believes patients might go into respiratory failure regardless of how much oxygen they receive. "And while higher levels of oxygen may cause CO2 to rise, it's not due to oxygen blunting their hypoxic drive, which the hypoxic drive theory postulates, it's due to either the Haldane effect or V/Q mismatching," he said.

The Haldane effect was postulated by John Haldane, a pioneer in oxygen therapy. He proved that the deoxygenation of arterial blood increases its ability to carry carbon dioxide. "In other words, as fewer oxygen molecules are attaching to hemoglobin, more CO2 are attaching to hemoglobin," Bottrell said.

Oxygen is more soluble in water, and therefore, has a higher affinity for hemoglobin. "So if you increase oxygen in the blood, CO2 molecules are forced off hemoglobin and oxygen takes its place," Bottrell shared. "This causes an increase in PaCO2."

Out of respect for this theory, according to Bottrell, COPD patients should be maintained on the lowest level of oxygen required to maintain an oxygen saturation between 88% to 92%.

According to Bottrell, modern evidence suggests that the hypercapnic drive is never completely blunted, and therefore even COPD patients with chronically elevated PaCO2 will not stop breathing in the presence of higher oxygen levels. "There is such a thing as the hypoxic drive, but the hypoxic drive theory is a myth," he said.

Rebecca Mayer Knutsen is on staff at ADVANCE.

To view the complete interview, read my post "How does too much oxygen effect COPD?"

Tuesday, April 21, 2015

What is rescue medicine?

The following was originally published on November 18, 2014 on

What is rescue medicine? defines “rescue” in part as “to free from violence or danger.” Since an asthma flare-up (attack) is a violent reaction within your air passages that places you in impending danger, it’s only fitting that the medicine discovered to end asthma flare-ups be referred to as “rescue medicine.”

Asthma is a medical condition where the cells lining the air passages (bronchioles) are chronically inflamed. When exposed to asthma triggers, the inflammation worsens, causing muscles lining these air passages (bronchial muscles) to spasm and contract. These muscles, in essence, squeeze the air passages, making it difficult for air to get out of your lungs, creating a feeling that you can’t catch your breath (air hunger, dyspnea, fish out of water).

Since asthma is a reversible disease, it can be reversed either by waiting it out, or by using medicine. For most of history, since most medicine caused only mild relief, most asthmatics were forced to suffer until the symptoms ceased on their own.

So, what exactly does this mean? What is rescue medicine? This means that the medicine, once injected or inhaled, is attracted to and attaches to beta 2 (B2) adrenergic receptors that line the respiratory tract. A chemical reaction then occurs that causes bronchial muscles to relax, causing air passages to open up (dilate), thus ending the asthma flare up.

While this type of medicine is generally referred to as rescue medicine, it is also commonly referred to as bronchodilators, beta 2 adrenergic medicine, or simply B2 agonists.

While epinephrine worked great to make breathing easier, it also worked like a charm as a vasopressor. In other words, while it was a great asthma rescue medicine, this came with many systemic and undesirable side effects, such as increased blood pressure, fast and pounding heart rate, tremors, increasd anxiety and nervousness.

The good news is that, over the years, scientists learned to make synthetic medicine (made in a factory) that mimics the B2 response of epinephrine but avoids the B1 and A1 response. This means that the medicine works better than epinephrine with negligible side effects.

Epinephrine is still available, although it's mainly reserved for emergency situations in hospitals. The most commonly prescribed asthma rescue medicines today include albuterol (Ventolin), which was introduced to the market in 1969, and levalbuterol (Xopenex), which was introduced to the market in 1999.

Albuterol and levalbuterol are available in hospitals and for home use by asthmatics, and are inhaled into the lungs by either using a rescue inhaler or a nebulizer.
  • Rescue Inhaler: This is an small, easy to use portable device that can easily fit into a pocket and can be taken with you wherever you go. It usually takes just one or two puffs to end an asthma attack. While generally referred to as rescue inhalers, they may also be called “asthma inhalers” or "puffers.” Because they are easily portable, inexpensive, and easy to use, they work fine for most asthmatics in most instances. Check out my post "How to use an inhaler."
  • Nebulizer: This a small cup with a mouthpiece. The medicine for this comes in tiny plastic amps. The amps are opened and the medicine is poured into the nebulizer cup. The nebulizer is then connected to a small air compressor that turns the medicine into a mist to be inhaled using the mouthpiece over 10-20 minutes. These are not as portable as inhalers, although most asthmatics say that they work better during severe asthma attacks. Check out my post "How to properly take a breathing treatment" and "What is a nebulizer?"
Most asthma guidelines recommend that all asthmatics have some form of rescue medicine on hand at all times, whether it be in the form of an inhaler, nebulizer, or both. Providing asthmatics with a prescription for rescue medicine is usually the first thing an asthma physician will do once the diagnosis of asthma is made.

While every asthmatic should have access to rescue medicine, it is no longer considered a top line asthma medicine. This is because emphasis has been changed from treating acute asthma symptoms (flare-ups, asthma attacks) when they occur, to preventing and controlling asthma.

Today, asthma is generally controlled using asthma controller medicines, such as Flovent, Advair, Symbicort, Dulera and Singulair. Studies show that when these medicines are used every day, they help to both control and preventasthma, thus eliminating (or greatly reducing) the need for rescue medicine.

Yet even people with controlled asthma may still have asthma flare-ups from time to time, and it's for this reason every asthmatics should have both anAsthma Action Plan, and a rescue inhaler or nebulizer available at all times.

Monday, April 20, 2015

Asthma may cause bone loss

The following was originally published at on April 28, 2014

Asthma May Contribute to Bone Loss, Study Says

Modern science has shown asthma is “more than just a lung disease.” It has now been linked with the immune system, mind, stomach, nose, eyes, and skin. The latest evidence suggests it may even be linked with bone loss.

Both and reported on a study where researchers studied the medical records of over 7,000 adults in Seoul, Korea. They concluded that those with “hyperactive airways” were at an increased risk for bone loss and bone fractures.

The term “hyperactive airways” is a technical term for asthma. It means that a person has chronically inflamed air passages that are hypersensitive, or overreactive, to certain triggers around them. Asthma triggers include things such as dust mites, mold, pollen, pollution, cockroach urine, strong smells, and smoke.

At the present time, the experts do not know why asthmatics are at an increased risk for bone loss. They also do not know why asthma might cause bone loss, although there are theories.

1. Inhaled corticosteroids: Medicines such as Flovent, Qvar, Pulmicort, Advair and Symbicort are used to treat the underlying inflammation in order to control and prevent asthma. While systemic steroids were linked to bone loss as far back as 1983, the link between inhaled steroids and bone loss remains unknown.

2. Bone loss: The researchers could not rule out that the bone loss did not come before the asthma. It may be possible the factors that contribute to bone loss may also contribute to the development of asthma.

3. Low vitamin D: Studies have already shown a possible link between asthma and vitamin D deficiency. This vitamin is supplied by the sun and diet, and is needed to absorb calcium. Theories here suggest that poor asthma control may result in less time outdoors, or a diet that does not include enough vitamin D.

4. Low activity levels: When an asthmatic isn’t breathing well, or fears that exertion will trigger an attack, this results in less physical activity. Less weight bearing activity can result in bone loss and weaker bones.

5. Increased anxiety: Studies have linked asthma with anxiety. People suffering with anxiety are at an increased risk of abusing alcohol. Likewise, some people believe that smoking might reduce anxiety. Both smoking and alcohol abuse have been linked with bone loss.

More research is needed on this topic. In the meantime, enough studies have linked asthma with bone loss to take this seriously. The Mayo Clinic lists the following things you can do to ensure proper bone health.

1. Include plenty of calcium in your diet: You should receive at least 1,000 mg of calcium every day. Foods to consider are broccoli, kale, sardines and soy products, such as tofu. You may also try calcium supplements.

2. Pay attention to vitamin D: You should ideally receive at least 600 iU every day, and 800 iU for those over 71. Sources include sunshine, and foods such as milk, cheese, fish, fish oils, egg yolks, and fortified foods like cereal. You may also try vitamin D supplements.

3. Include physical activity in your daily routine: Weight bearing exercises are essential to build healthy bones and slow down bone loss. For tips on how to exercise with asthma you can check out “14 Tips for Exercising with Asthma.”

4. Avoid inhaling cigarette smoke: While many believe smoking decreases anxiety, studies suggest quitting smoking reduces anxiety. Besides, smoking is a severe asthma trigger, and should be avoided by asthmatics at all costs anyway.

5. Avoid consuming more than 2 alcoholic beverages a day: Studies suggest “Long-term alcohol consumption can interfere with bone growth.” Besides, alcohol has also been linked with worsening asthma, so it should be avoided anyway.

The overriding theme here seems to suggest that asthmatics must pay special attention to their bodies in order to maintain good health, including their bones.

Saturday, April 18, 2015

400-1743: The first use of the term influenza

In the ancient world all diseases were attributed to the wrath of the "diety." If a Pandemic ravaged a village, town or nation, it was attributed to an angry god or spirit.  Both the ancient Greek poet Homer (800-701) and Hippocrates (460-370) described pandemics during their lifetimes.  It's probable some of these were attributed to the influenza virus.

Homer describes how Zeus used his thunderbolt to "punish impiety," and "for vengeance for an insult offered to his priest, the shafts of the Sun-god carried sickness into the Argive camp, destroying first the dogs and mules, and then thousands of warriors," writes Arthur Hopkirk, in his 1914 book "Influenza."  (1, page vii and viii)

In reality these warriors may have died of a pandemic caused by a virus or bacteria, such as influenza.  Although the ancients had no clue about the internal workings of the human body, nor about invisible invaders of the human body.  It was easier for them to believe in fake gods and attribute them when bad things like plagues happened.
"On mules and dogs th' infection first began;
And last, the vengeful arrows fix'd in man."
Those described as having sweats and chills (signs of a fever) were the most likely to succumb to the disease.  In man's desire to help his fellow man, the following were the remedies tried (1, page 15-16):
  • Purging
  • Venesection
  • Bleeding by the ranal vein
  • Emetics
And sometimes the remedy wreaked more havoc than the plague.  If ruthless venesection was performed, this in and of itself could have been the killer.  Yet the plague was blamed nonetheless.

The plague struck again and again.  In 412 B.C. the following was written regarding a plague in Rome (1, page 16):
“A plague, however, which broke out at that time and gave more alarm than it proved destructive, diverted the people’s attention from the forum and political disputes to look after their families and take care of their health. The city was all over oppressed with sickness, though no great mortality ensued.”
It struck again (or so historians think) in (1, page 20-26)...
  • 827 A.D. in France and Germany
  • 876 in Italy
  • 889 in Germany
  • 927 in France and Germany
  • 996-97 in England
  • 1173 in Germany and Italy (it was called "a dense fog" in Italy, first authentic outbreak)
  • 1239
  • 1311
  • 1323 in Italy and France
  • 1327-28
  • 1357
  • 1287 in France and Germany
  • 1403 in Paris, France
  • 1404
  • 1410-11 in France
  • 1413-14 in France
  • 1427 in France caused a "Poisonous air."
  • 1438
  • 1482
  • 1505
  • 1510
The following quote comes from 1323 (3):  
In the year, 1323, and in the month of August, there was a pestilential wind, which caused nearly all the inhabitants of Florence to fall sick of cold and fever, and the same thing took place throughout almost of whole of Italy.
And the following from 1327 (3):
In the said year and month, there was throughout the whole of Italy an infection fever caused by cold; but few people died of it.
Regarding the 1387 outbreak, the following was written (4):
There came a general pestilence in the whole country, with cough and influenza, so that hardly one among ten remained healthy. 
Regarding the 1427 outbreak, an anonymous chronicler from St. Albans wrote (1, page 25-6):
In the beginning of October, a certain rheumy infirmity which is called 'mure' invaded the whole people, and so infected the aged along with the younger, that it conducted a great number to the grave. 
The remedy for the 1387 pandemic, which took few lives, was "decoctions of chamomile and coriander berries, sweetened with syrup and poppies; clymasta; diaphoretics; and low diet." (1, page 23)  This would have been a more pleasant remedy compared to what the ancient Greeks treated the symptoms.  

Many of the deaths that resulted occurred on the fifth or sixth day, and Hippocrates notes that death usually occurred on the seventh day.  Later, in the first century A.D., Galen agreed with Hippocrates that death usually occurred on the seventh day.  (1, page 17)

At some point in our history, sometime in the ancient world, the concept that little creatures in the air may be responsible for spreading some diseases was postulated, although who postulated this theory, and when, remains a mystery.
Hopkirk says the first to write of this concept may have been the Greek "polyhistorian" Varro (117-36 B.C.), who wrote the following:
It is to be observed that wherever there are marshy districts certain most minute animals will grow, which cannot be discerned by the eye; but, carried by the air, reach the body through the mouth and nostrils, causing serious disease." (1, page x)
Varro was referring to the malaria plague in "Corfu when Pompey was there with an army and fleet."  Although the same concept may be applied to other contagious diseases, such as influenza.  Varro recommended the following to prevent the spread of the disease malaria: (1, page x)
  • Isolation
  • Ventilation
  • Destruction of insanitary dwellings
  • Etc.
Influenza is known to cause much grief for those afflicted with it, although it causes only a few deaths.  Usually those who die from it are over the age of 65 or have some chronic underlying medical condition that is complicated by influenza.

Prior to the 16th century influenza was referred to by various names, depending on the geographic region of the person describing it.  Sometimes it was simply referred to as a pest, pestilence, or plague.  Historians determine if the "plague" was influenza by descriptions of the symptoms, a high morbidity, yet low mortality rate.  If many deaths resulted, chances are that particular plague was not influenza. (1, page 4-5)

The term influenza may actually have come from a misinterpretation of the Italian word influence.  The idea here is that around 1357 people believed the position of the stars "influenced" outbreaks of the disease.  Although how this term superseded all the other terms and made it's way into medical nomenclature remains a mystery.  (1, page 6)(2, page 31)

The following are just a few other names used to describe various pandemics or endemics most historians figure were influenza (1, pages 8-9):
  1. Burzelen:  1307 in Germany (meaning to stumble?)
  2. Le tac or le horion:  1411 in France
  3. Tonawasches Fieber:  1414 in Germany (Because occurred in Danube district)
  4. Coqueluche: 1414 in France (Caused oppressive pain in the head)(Victims wore cap on head)
  5. Ladendo:  1427 in France
  6. Schafkrankheit or Schafhusten:  1580 in Germany (Sheep's disease, cough)
  7. Galanteriekrankheit or Modefieber: 1709 in Germany (Galant malady, fashionable fever)
  8. Le Grippe:  1743 in France (from "agripper," meaning to sieze quickly and cause sore throat
  9. Petite poste or petite courrier:  1762 in France
  10. Zamporina:  Brazil in 1780
  11. La Coquette:  France 1780-81
  12. Russische Krankheit (lightning catarrh):  1782 in Germany (due to its sudden onset)
  13. Corcunda (hunchback disease):  Brazil in 1816.  Violent cough made you hunch your back
  14. Polka Fever:  1846-7 in Brazil
In Great Britain during the 14th and 15th centuries, common names were faucht and slaodan.  Creatan was a word derived from creat (chest), and was another common name.  In 1562 it was called "the newe acquayntance.  In 1580 "the gentle correction."  It was also referred to as "the jolly rant," "the new delight," "the Dunkirk rant," and "the knock-me-down fever." (1, page 9)

An outbreak in Britain in 1485 was described as "English Sweat." It was so back that "King Henry VII had to postpone his coronation," according to Evelyn Kelly and Claire Wilson in their 2011 book "Investigating Influenza and Bird Flu."  "The disease was treated with tobacco juice, lime juice, and bloodletting." (2, page 32)

Finally, in 1743, the term influenza was used to describe influenza.  No one knows why, but this is the term that stuck, and has since made it's way to medical nomenclature.  The only exception was in Germany, where the Grippe was the term commonly used as of 1743.  

While the names varied through early history, the "grip" the disease held on it's victims were similar:
  • Catarrh:  Inflammation of the respiratory tract (nasal congestion)
  • Fever:  Usually over 100 degrees
  • Chills:  Associated with the fever
  • Headache:
  • Body or muscle aches: Especially of the back, arms and legs
  • Dry cough: Helps spread the disease from one victim to the next
  • Fatigue and weakness:  General feeling of tiredness
  • Suspended Business: Many stopped working to take care of their families
It's generally the commonality of symptoms described, the high rate of morbidity, and low mortality, that has allowed historians to feel confidence these epidemics and pandemics were probably influenza.  

  1. Hopkirk, Arthur F., "Influenza: It's History, Nature, Cause and Treatment," 1914, New York, Charles Scribner and Sons
  2. Kelly, Evelyn B., PhD and Claire Wilson, "Investigating influenza and Bird Flu: Real facts and real lives," 2011, Enslow Publishers, U.S., Chapter 2, "The History of Influenza," pages 29-47
  3. Hopkirk, op cit,Gluge, "in the course of his argument, quotes the following passages from Buoninsegni’s Istoria Fiorentina, Florence, 1580." The passages are recorded on page 21 of Hopkirk's book.  
  4. Hopkirk, op cit, from Jakob von Konigshoven Stassburg Chronicles, of 1387, as recorded by Hopkirk on page 22 of his book
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