Here's how NIV benefits CO2-retaining COPD patients

I often tell my patients that nothing I do cures any ailment.  To the contrary, I tell them that the procedures I perform treat acute symptoms, while the doctor and nurse do other things that will provide the cure.

A perfect example of this is with noninvasive ventilation (NIV) for treatment of acute respiratory distress due to chronic obstructive pulmonary disease (COPD). Savi et al, 2014, notes the following:

Noninvasive ventilation benefits patients with COPD, and it seems reasonable to expect that NIV would increase tidal volume and improve CO2 elimination, and thus reduce respiratory drive.

The note the studies have proven that NIV results in the following when used on COPD patient's presenting to the emergency room with flare-ups:

• Reduction of treatment failure
• Lower mortality
• Fewer complications
• Lower Intubation rates

However, the studies also conclude that:  "In these patients CO2 elimination is increased but overall ventilation-perfusion mismatch is not changed during NIV. 

What does improve ventilation, the authors note, are the following:

• Treating precipitating factors (eg, infection with antibiotics)
• Increase expiratory flow (eg, with beta agonists)
• Reduce pulmonary inflammation (eg, with corticosteroids)
• Manage gas exchange (eg, improve oxygenation)

Without NIV, studies have shown, patient's who have COPD with CO2 retainers should receive an FiO2 just enough to maintain an SpO2 of 88-92%, as higher FiO2s (either due to the loss of hypoxic drive, or V/Q mismatching) have been shown to cause a rise in PaCO2.  

However, this effect is negated with NIV.  Savi et al concludes:

During NIV with an FiO2 sufficient to maintain a normal PaO2, a further increase in FiO2 does not result in an increase in PaCO2 in CO2-rataining COPD patients, since no changes occur in (minute ventilation).

Crossley et al had similar results, concluding, that "CO2-retaining COPD patients following a period of mechanical ventilation with PaO2 in the normal range can safely receive supplemental oxygen without retaining CO2 or a depression of respiratory drive.  A new ventilation-perfusion relationship is established during ventilation to normoxia, and it is not altered by further increasing FiO2," Savi et all reports.

Since NIV helps COPD patients take deeper breaths, thus improving their ventilation (allowing them to blow off CO2), high levels of oxygen do not cause rising PaCO2 levels while a patient is receiving NIV therapy.  However, we often find that, while using NIV, many patients require less oxygen compared to prior to the NIV start.

Bottom line:  NIV is beneficial to CO2-retaining COPD patients because it increases their tidal volume, increases CO2 elimination, and reduces their drive to breathe.  By treating these symptoms, caregivers are provided an opportunity to do whatever is necessary to treat the cause of the exacerbation (even if that means utilizing higher oxygen levels).

References:

1. Savi, Augusto, Jucara Gasparetto Maccari, Tulio Frederico Tonietto, Ana Carolina Pecanha Antonio, Roselaine Pinheiro de Oliveira, Marcelo de Mello Rieder, Evelyn Cristina Zignani, Emerson Boschi da Silva, and Cassiano Teixeira, "Influence of FiO2 on PaCO2 During Noninvasive Ventilation in Patients With COPD," Respiratory Care, March, 2014, volume 59, number 3, pages 383-387

Will COPD be divided into sub-groups?

It's possible that chronic obstructive pulmonary disease (COPD) may soon be classified into subgroups.  This may be necessary because certain features of the disease may require unique treatments.

For instance, studies seem to show that COPD patients who respond well to bronchodilators, or who show partial reversibility with bronchodilators, may also respond well to inhaled corticosteroids, according Ortega et al.

These patients tend to present with hyperactive airways, similar to asthma.  They may also present with elevated eosinophils in induced sputum samples, and have higher concentrations of exhaled nitric oxide, similar to patients with asthma.

Furthermore, COPD patients with positive reversibility tend to have a slower annual reduction in FEV1, and may be a predictor of longevity.

However, COPD patients with a positive response to bronchodilators have a higher risk of developing respiratory symptoms, and, as Ortega et al concludes, a shorter time to exhaustion in endurance exercise testing, and a shorter shuttle-walk distance.

The study notes that about 70-90% of asthmatics have exercise induced bronchospasm, and that these patients often respond better to exercise after inhalation of bronchodilator.  COPD patients with positive reversibility respond in a similar way with exercise post bronchodilator.

Ortega et al suggests a possible treatment for dyspnea caused by exertion may be bronchodilators after exertion, as this seems to improve lung function.

So, COPD patients with positive reversibility may be classified as one subgroup, while COPD patients with negative reversibility may be classified as another subgroup.  Treatment for both groups may be different, requiring different sets of guidelines.

References:

1. Ortega, Francisco, Eduardo Marquez-Martin, Borja Valencia, Pilar Cejudo, Ana Rodriquez, Jose Luis Lopez-Campos, and Emilia Barrot, “Impat of Bronchodilator Responsiveness on Quality of Life and Exercise Capacity in Patients With COPD,” Respiratory Care, January, 2014, volume 59, number 1, pages 81-89

Depression and anxiety in COPD increases morbidity and mortality, study shows

Many patients with chronic obstructive pulmonary disease (COPD) feel depressed or anxious due to their disease.  It is important for physicians to recognize and treat this, because studies sow COPD patients who are anxious or depressed have a 1.25% greater risk of dying compared to COPD patients who are not depressed.

It makes sense that so many patients with COPD become depressed, considering the disease affects so many different areas of their lives.  For instance, according to Peian et al:

• They feel useless
• Experience reduced sexual activity
• Depend on others for their personal care
• Lose interest in future projects

Peain also reports:

Tobacco may provide psychological relief for some individuals.  Continuing smokers with COPD are more at risk of depression than those who quit.  A longitudinal cohort study showed that continuous smokers had a much steeper decline in lung function than those who stopped smoking.  We also found that with an increasing duration of smoking and the amount of smoking, the number of deaths was increased.  These results may be attributed to the interaction between depression and smoking.  Furthermore, there was an interaction between former smoking and depression, which may be due to short duration of quitting.  Most of te former smokers quit only when they suffered from a serious condition.  In addition, smoking cessation was reported to be associated with an increased rate of depression.  These results suggest that COPD patients should stop smoking as soon as possible.

Likewise, the study reported on anxiety.

Elevated anxiety in cOPD patietns is more common in current smokers than in nonsmokers.  Smoking is a common reason to explain the high association of anxiety with COPD.  Tobacco use is widely acknowledged as the single most important environmental risk factor for the development of COPD, and a high level of anxiety is a risk factor for starting to smoke.  A roportion of patients who develop COPD as a consequence of smoking show higher levels of anxiety than in the general population.  Taken together, it is likely that there is an interaction between current smoking and anxiety.   In fact, our study shows that this interaction is increased with a long duration of smoking and a large number of pack-years. 

The study further concluded that 48-60% of th deaths in COPD subjects were explained by an interaction between smoking and depression symptoms, and 49-55% of the deaths of COPD subjects were explained by an interaction between smoking and anxiety symptoms."

Bottom line, the researchers suggest that "quitting smoking may help depressed or anxious patients with COPD forestall death.  Given the difficulty in the treatment of depression or anxiety in certain COPD patients, a recommendation to quit smoking may be an inexpensive and practical means of delaying death from COPD."

References:

1. Lou, Peian, Peipei Chen, Pan Zhang, Jiaxi Yu, Yong Wang, Na Chen, Lei Zhang, Hongmin Wu, and Jing Zhao, “Effects of Smoking, Depression and Anxiety on Mortality of COPD Patients: A Prospective Study,” Respiratory Care, January, 2014, Volume 59, Number 1, pages 54-61

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Adult Onset Croup

Croup is a common disease in children.  While rare, can still occur in adults, yet when it does it is more severe, often requiring care in intensive care units. 

Croup is caused by inflammation and swelling around the vocal cords, and can cause a harsh barky cough, and may also lead to breathing difficulty if the air passages becomes partially blocked.  If severe, it may lead to death.  

The simplest treatment for croup may be to place the child in a hot, steamy bathroom. This tends to ease some of the swelling.  Another treatment may be to go outside in the cool, fresh air.  However, when these simple treatments don't work, a visit to a physician, or an emergency room, may be required. In some instances, a stay in a hospital may be required.  Death, however, from croup is rare.

The cause of croup is most often a virus, but occasionally it can be caused by a bacteria.  Croup is contagious, as the germs that cause it may be exhaled and transferred through the air in droplets.  The best way to prevent the spread of it is to wash your hands frequently, clean up surfaces touched by those who are infected, and to cover your mouth when you sneeze or cough.  

While croup is a lot less common in adults than it is in children, it is possible for a rare form of croup to affect adults, so it is best to take precautions to avoid contracting croup, even if you are an adult. Here are some everyday tips on how to keep your lungs clean: http://www.healthcentral.com/copd/cf/slideshows/9-ways-to-keep-your-airways-clear-and-lungs-clean

I found a really nice case study on adult croup by Karger: Medical and Scientific Publishers, "Adult Croup: A Rare but More Severe Condition."  Basically, 11 cases of adult croup were reviewed. All required a stay in the hospital ranging anywhere from 3-35 days. While ten of the patients required care in an intensive care unit, none of them died. So, adult onset croup tends to be more severe than child onset croup, although it is not deadly if treated properly.

It's also interesting to note that the presumed reason croup is more common in children is because they have narrower airways than adults. Because their airways are narrow, even slight inflammation may partially block their air passages, causing the symptoms of croup (harsh voice, barky cough, shortness of breath, fever, etc.)

Usually when adults get the same virus, they simply get a common cold. However, in some instances, the inflammation may become so severe that it causes adult croup.
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People with end stage COPD now living longer

The natural progression of Chronic Obstructive Pulmonary Disease will eventually lead to heart failure.  When this happens the disease is considered to be in its end stages.  Good news here is that, while the prognosis is still quite poor, it has now been extended from two years to four hears, according to a study reported on in 2013 by the American Heart Association.  

Sometimes heart failure is caused by the aging process, simply by the it getting weak with age.  However, often it is secondary  to to the heart working too hard to pump blood through diseased lungs.  Patients with cystic fibrosis, bronchiectasis, and chronic obstructive pulmonary disease (COPD) are some of the lung diseases that may lead to heart failure. 

When heart failure is secondary to pulmonary disease, this usually begins by the right heart becoming enlarged (hypertrophic) from years of working too hard.  It then becomes an inefficient pump.  This is called cor pulmonale. 

Cor pulmonale may eventually lead to left heart failure, whereby the heart fails to meat the demands of the body.  Venous return to the heart increases, leading to blood becoming backed up in the legs, ankles, and lungs.  When blood backs up in the lungs this is called pulmonary edema.  It's also referred to as acute heart failure, or congested heart failure. 

There is no cure for heart failure, although the symptoms can be treated.  There are medicines to strengthen the force and contractility of the heart, and medicines to help remove the fluid from the lungs and ankles.  Acute heart failure may also be treated with noninvasive ventilation to reduce venous return and reduce cardiac output and blood pressure.  

Generally speaking, when patients with COPD develop heart failure it is considered end stage COPD.  This is where the patient will need to be monitored closely by a physician, and may require frequent physician and hospital visits in order to treat flare ups.  

At this point, flare ups may be caused by exposure to COPD triggers such as strong smells and cigarette smoke, but they may also be caused by heart failure. This is when treating the disease becomes difficult

Usually, patients with lung diseases develop atrial fibrilation prior to heart failure, so this may be a sign that it's time to consider heart failure.  

What is PEP?

Studies have shown that Positive Expiratory Pressure (PEP) by using an acapella, along with medicated aerosols, may help patients with asthma, COPD and cystic fibrosis clear secretions from their airway.
Inhaled medicines have the following effect:

1. Promote hydration
2. Reduce secretion viscosity
3. Optimize mucociliary clearance 

PEP therapy has the following effect:

Improve collateral ventilation to allow better distribution of gas beyond occluded airways

PEP works by creating a positive pressure to splint open and stabilize airways, preventing bronchial collapse. So when a treatment is given in conjunction with a nebulizer, it may result in better distribution of the medicine while enhancing secretion clearance.

Reference:

1. Mesquita, Fabricio, et al., "Scintigraphic Assessment of radio-Aerosol Pulmonary Deposition With the Acapella Positive Expiratory Pressure Device and Varoius Nebulizer Configurations," Respiratory Care, March, 2014, volume 59, number 3, pages 328-333

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What is the best method of giving acapella with nebulizer?

Shown here is nebulizer distal to acapella.
Studies show this is not best method.

Your question:  When giving a breathing treatment with Acapella, where is the best place to put the nebulizer?

My answer:  A recent study by Mesquita et tested airway distribution by placing the nebulizer distal to the acapella as the manufacturer suggests, and airway distribution by placing the nebulizer between the acapella and the and the patient airway.  The researchers concluded that placing the nebulizer distal to the acapella resulted in less lung distribution compared to placing the nebulizer between the acapella and the patient's airway.  \

Reference:

1. Mesquita, Fabricio, et al., "Scintigraphic Assessment of radio-Aerosol Pulmonary Deposition With the Acapella Positive Expiratory Pressure Device and Varoius Nebulizer Configurations," Respiratory Care, March, 2014, volume 59, number 3, pages 328-333

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Does albuterol treat pneumonia?

Many times in the hospital setting physicians order scheduled albuterol breathing treatments for patients admitted with pneumonia.  The question of the day is: does ventolin have any effect on pneumonia?

First of all, what is pneumonia?  Pneumonia is an inflammatory disease of the peripheral airways, particularly the alveolar (air) sacs.  The air sacs may become filled with fluid or pus, causing symptoms such as cough with colorful phlegm, fever, chills, and dyspnea.

So, what is the evidence that albuterol benefits pneumonia?  So far I have not been able to find any studies in this regard.  I am told there was a study done in the late 1980s, and the results were inconclusive.

Lacking studies, let's investigate the available wisdom.

1.  Pneumonia is an inflammatory disease.  To this date there is no evidence that albuterol has anti-inflammatory properties.

2.  Albuterol is attracted to beta 2 (B2) adrenergic receptors lining the smooth muscles that line the air passages in the lungs.  There is no evidence of smooth muscles in the alveoli, and no evidence of B2 receptors in the alveoli.

3.  Nebulizers are ideal for the inhalation of B2 adrenergic medicine because it creates aerosolized particles the size of 0.5 microns, an ideal size for medicine to get to the air passages.  For the medicine to get to the alveoli the nebulizer would have to produce aerosolized particles 0.1 to 02 microns.

4.  Pneumonia may cause a cough with increased secretions.  There is evidence that albuterol may increase mucociliary clearance and enhance cough.  However, in order to produce this effect a dose greater than the standard dose of 2.5 mg (0.5cc) would be necessary.  Studies regarding albuterol and mucociliary clearance were reviewed by Dr. Ruben D. in the September, 2007, issue of Respiratory Care, "Inhaled Adrenergics and Anticholinergics in Obstructive Lung Disease: Do They Enhance Mucociliary Clearance?"

5.  Some patients diagnosed with pneumonia who will claim to breathe easier after a treatment with albuterol.  However, the reason for this is because some patients with pneumonia present with bronchospasm secondary to pneumonia. The albuterol will treat the bronchospasm.  This is most likely to occur in patients with underlying or undiagnosed asthma.  While clinical evidence may suggests albuterol opens up air passages and breaks up secretions to enhance cough, no studies have been done to show this.

6. Cavallazzi R, et al shows that inhaled corticosteroids (mainly Budesonide) are the most widely used agents to treat pneumonia, as they are shown to have anti-inflammatory properties. They are generally recommended, with albuterol, to prevent COPD exacerbations in patients with severe COPD.  However, inhaled steroids may be systemically absorbed and have immonosuppresant effects.  The evidence that inhaled steroids may actually lead to pneumonia is modest.

7.  Systemic steroids are shown to reduce inflammation associated with pneumonia, and are a common treatment option. 

8.  Antibiotics are also frequently prescribed for pneumonia, considering most are caused by bacterial agents.

Conclusion:  There is no evidence that albuterol particles even make it to the alveoli, and even if they did make it there, there is no evidence they would produce any effect on the pneumonia. The best treatment for pneumonia should be inhaled or systemic steroids and antibiotics.

However, an initial treatment of albuterol may prove beneficial in opening up air passages when bronchospasm is present, and help break up secretions to enhance cough and expectoration.  This author recommends a trial and then PRN if the trial proves beneficial.  

Do inhaled corticosteroids reduce COPD exacerbations?

There has been an increase in the number of physicians ordering inhaled corticosteroids for patients suffering with pneumonia and chronic obstructive pulmonary disease.  So, is there any evidence to support this treatment regime.

Let's review the evidence:

1.  Norton JL et al notes that the use of inhaled steroids is among the most common treatment for pneumonia.  However, they also reduce the immune response and, therefore, slightly increase the risk of being diagnosed with pneumonia.

2.  An article in the April 15, 2011, issue of American Thoracic Society's Journal of Respiratory and Clinical Critical Care Medicine, reported on a review of clinical studies, which concluded that inhaled corticosteroids help to reduce mortality compared to those who were not taking inhaled corticosteroids. They concluded inhaled steroids reduce exacerbations by reducing the underlying inflammation in the air passages. However, while it decreases exacerbations, it also increases the risk for catching pneumonia.  Those using inhaled steroids had a 30 day mortality rate of 10%, and those not using it had a 13.6% mortality rate. The 90 day mortality rate was 17.3% for those who used ICS, and 22.8 for those not using ICS.

3.  Ritesh Agarwal et al studied the effects of ICS on COPD patients and concluded: "There is only a modest benefit of ICS in preventing COPD exacerbations, which is not related to the level of baseline lung function on metaregression analysis. The benefits of ICS in preventing COPD exacerbations thus seem to be overstated."

Conclusion:  There does seem to be evidence that inhaled corticosteroids reduce exacerbations of COPD.

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Do B2 agonists increase mucociliary clearance?

Along with improving lung function, there is some evidence that beta adrenergic agonists (B2) might enhance secretion clearance.  This might provide another reason for physicians to order scheduled B2 agonist therapy.

There have been a variety of studies on the subject, and they were all summed up well by Dr. Ruben Restrepo in the September, 2007, issue of RCJournal, "Inhaled Adrenergics and Anticholinergics in Obstructive Lung Disease: Do They Enhance Mucociliary Clearance?"

How beta agonists stimulate mucus secretion is a complex process.  Restrepo explains it this way:  

The effects of the B2 adrenergics on the airway are mediated by stimulation of the B2 receptors, which increases cyclic adenosine monophosphate, which is a regulator of ciliary beat frequency in human airway epithelia.  Because of their effect on ciliary beat frequency, B2 adrenergics have been considered mucokinetic medications and cough clearance promoters.  B2 adrenergic agonists increase passive movement of watter across the airway surface, via active transport of ions across the airway epithelium.  They also stimulate secretion production, primarily from their action on mucus-secreting cells and submucosal glands.  These actions combined increase the amount of mucus in the airways.  

The following are the studies:

1. Sabeter et al showed that when studied with ipatropium bromide and placebo, only albuterol (Ventolin) and Salmeterol (Serevent) enhanced mucociliary clearance in sheep up to 12 hours after the breathing treatment. Salmeterol had the longest acting effect.
2. Jones and Reid albuterol increased the number of secretory cells in rats, particularly in the most peripheral airways. However, they concluded that larger than normal doses were required for "maximal short-term effects on mucociliary clearance, which increases the risk of increased viscious mucus secretion."
3. Guleria et all found no difference in mucociliary clearance with either albuterol, ipatropium bromide, beclomethasone and placebo.
4. Both albuterol and salmeterol produced only a "slight (less than 20%) increase increase in ciliary beat frequency above baseline."
5. Laube et al showed that a single administration of albuterol significantly improved mucoliliary clearanc, compared with baseline values.
6. Cleary et al found that inhaled levalbuterol does not increase mucociliary clearance or cough clearance, compared to albuterol or placebo.
7. Wong et al found a 4-fold increase in ciliary beat frequency 30 minutes after administration with fenoterol.  It also showed increased  mucus clearance, more coughs, lower sputum viscosity, and more sputum production 24 hours after treatment.
8. Studies show that salmeterol stimulates faster and stronger ciliary beat frequency than does albuterol.  
9. Piatti et all studies salmeterol on COPD and pneumonia patients, and "confirmed the ability of salmeterol to enhance 'only to a modest degree' ciliary beat frequency in both normal and COPD nasal epithelium.  
10. Mossberg et all confirmed the "minimal stimulation effect of B2 adrenergics in chronic bronchitis."
11. Bennet et al "suggested that the observed enhanced clearance with salmeterol may be primarily from its effect on the mucociliary apparatus, as opposed to the cough mechanism. There were many studies done on salmeterol.
12. Hasani et al found no significant enhancement of mucociliary clearance in patients with asthma following 2 weeks of salmeterol versus placebo, and concluded that salmeterol's mucociliary clearance benefit was a result of increased airway patency.
13. Melloni and Germouty studied the effects of formoterol, and discovered an increase in mucociliary clearance.  There are only minimal studies done on fenoterol.
14. Studies are inconclusive as to the mucoliliary clearance of B2 agonists in patients with cystic fibrosis.  Some showed that it had an effect, while others show no effect. 
15. Studies showed that there was no increase in mucociliary clearance after inhalations of ipatropium bromide.
16. Tiotropium may marginally enhance mucociliary clearance. 
17. Norton J. et al (2013 study) suggests that clenbuterol modestly enhanced mucociliary clearance in horses.

Conclusions:  

1.  It appears that both albuterol (Ventolin) does have mucociliary clearance abilities, although for maximal effect more than 0.5cc must be given with each treatment.  

2.  Albuterol seems to have better mucociliary clearance abilities than levalbuterl (Xopenex).  Albuterol seems to be the prescription of choice for patients admitted to hospitals, and this may explain why physicians insist on ordering albuterol Q4 or QID for patients, even those who present with no dyspnea, presenting with chronic bronchitis, emphysema, asthma, cystic fibrosis, and pneumonia

3.  Formoterol (Symbicort) probably has mucociliary clearance properties, although there have only been a few studies as to this date. It can probably be prescribed for this purpose.

3.  Salmeterol (Serevent, Advair) has greater mucociliary clearance abilities than albuterol, and therefore should be the prescription of choice for mucociliary cearance.

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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Placebo Effect: Misinterpreted Study Proves It

Once again, folks, we have a medical study misenterpreted by the so called experts.  They are now said to have proven "inhaling Albuterol helps asthmatic lungs work better, yet patients who get it don't feel much better than those treated with a placebo inhaler."  That's the results of a study, and they have totally blown it.

Thankfully you have me to give you guys an accurate analysis of these study results, because they show something the researchers have completely missed.

Let me put it this way.  Since I started this blog I've been telling you that doctors think that all pulmonary diseases should be treated as asthma.  They think all dyspnea, regardless of the cause, should be treated as asthma.  They think all dyspnea, regardless of the cause, can be treated with albuterol.  

So you have a patient come into the emergency room with dyspnea and wheezing, and the doctor automatically orders up an Albuterol breathing treatment.  Upon your pre and post treatment assessment the patient neither looks better nor worse, yet then you pose the question:  "Do you feel better?"  The answer is almost always a resounding, "Yes!  I do feel better."  Yet you often wonder:  Is the patient accurate?"

My theory has always been that many patients say they feel better when they actually don't.  In fact, many times a patient will say something like, "Yeah, my breathing is better.  My nose isn't as stuffed as it was before the treatment."  Of course then you know the treatment only had a perceived effect.  

A study was done recently and reported in the New England Journal of Medicine that studied the perceived benefits of Albuterol on subjects, half that were given actual Albuterol and half that were given a placebo.  A good review of this study was written by Reuters "Treatment, not medicine, helps asthma patients feel better: study."  

The test was only done on a small sample of 39 mild to moderate asthmatics.  Of those who received Albuterol, 50 percent reported improvement.  Of those who received a placebo, 50 percent reported improvement.

Thus, the researchers conclusion, as the headline to the Reuters post suggests, is that of the placebo effect, whereby just the mere presence of a medical care worker is all that's needed to help asthmatics feel better. They conclude that the presence of a doctor -- or in this case the RT -- is just as beneficial as acupuncture. In this case, the medicine is Palbuterol. 

Yet I think the researchers have totally blown these results.  I think these results tell a completely different story than the researchers are telling us, and this is not surprising.  I think the conclusion we should be drawing from this study is that patients have no clue whether or not they feel better.  I think these asthmatics only had a perceived benefit from Albuterol.  I think what these results tell us is the patient is unreliable.

This goes back to common asthma wisdom that says that the only true way to determine if an Albuterol nebulizer has improved lung function is to either do a pre and post pulmonary function test or to have the patient use a peak flow meter.  To go by what the patient says isn't enough.

Obviously if you have an asthmatic who is short of breath and the Albuterol provides instant relief in breathing then the patient is going to be accurate when he says, "I feel better."  Yet if the patient's dyspnea and wheezing is caused by a cold, or heart failure, or pneumonia, or kidney failure, or lung cancer, or rickets, the Albuterol will have no effect, and yet the patient will feel the placebo effect. 

As to be expected, the researchers got it all wrong. Yet your humble RT here is once again proven right. I've written before that Albuterol should be renamed Palbuterol because the medicine may not have any effect, but the presence of an RT will.

This is interesting to say the least.  We know that albuterol really does make breathing easier in patients who are having actual bronchospasm.  However, evidence also suggests that giving albuterol to anyone who is short of breath may produce the placebo response.  So now you know why doctors treat all pulmonary diseases as asthma.

Once again the results of a study are misinterpreted.  Thankfully your humble RT is on the job because these study results prove that Albuterol doesn't cure all dyspnea and wheezing.

Allergy meds linked to obesity, heart disease

This new study shows that allergies might be linked with heart disease, the leading cause of death in the United States, and this new study shows that antihistamines used to treat allergy symptoms might be linked with putting on extra pounds.

How's that for a double whammy to start your week. Of course I also have another post,"Does Advair cause weight gain," where I explain the concern that inhaled corticosteroids (such as what is in Advair) may also be linked to putting on extra poundage. Plus we all know by now that a nice big black box warning is on Advair linking it with asthma related deaths.

The thing is, though, that allergies cause such miserable symptoms, we asthmatics often have no choice but to take antihistamines like Claratin. Ironically, just prior to writing this post I woke up with the sniffles and popped a Walatin, a generic form of Clariton. What else was I to do, suffer?

If you've ever suffered from allergy symptoms, you'll know it's nothing you want to just take lying down, and sniffling, and wiping, and perhaps even wheezing. Just that downright miserable feeling -- kind of like a bad cold -- pretty much forces your hand at taking some medicine, if available, to ease the suffering.

Likewise, as with any medicine, you have to weight the advantages with the disadvantages, and in the case of antihistamines it's worth it.

However, it must also be noted that allergies/asthma has also been linked with obesity, as you can read here. And obesity itself increases your risk for heart disease, as we all should know by now.

Likewise, obesity is also linked to worsening asthma, as you can read here. Scientists believe that certain chemicals released from fat tissue may trigger bronchospasm.

Plus those with asthma/ allergies may have a lowered self esteem and not adhere to their medicine regime and not take care of their bodies by eating right and exercising as they should.

Yet this also provides us asthmatics/ allergy sufferers another added incentive to eat right and to exercise. Not only will this help us shed the pounds, it will also make our lungs and even our heart stronger.

New asthma cause found; may lead to new meds

Health.usnews.com, "Potential Cause of Asthma-Like Symptoms Spotted in Mice," reports that scientists have discovered the cause of asthma in mice, and this might some day prove to be a useful way of treating asthma in adults.

The post notes that researchers now believe "that an inflammation-causing protein called interleukin-17 (IL-17A) is the major cause of severe asthma-like symptoms in mice. The animals used in the study had been bred to have a genetic resemblance to humans with severe susceptibility to asthma."

This is key, because if researchers can somehow develop a medicine to block IL-17A pathways, they might be able to better treat severe forms of asthma.

Of course we must not get too excited here, because animal studies do not always translate to humans. Yet it's progress nonetheless.

Even doctors are prone to mis-diagnose

Here's an interesting post from Men's Health at MSNBC.com, "5 most common misdiagnoses for men." Several of us who are diagnosed with allergies, bronchitis and sinus headaches may actually have something else wrong with us.

The post notes that some men go to their doctors complaining of allergy-like symptoms of runny nose, watery eyes, and that downright miserable feeling and be diagnosed with allergies. When in actuality what they have is vasomotor rhinitis.

The article states it's rare to develop allergies in your 20s and 30s unless you change jobs or move to a new location. "Instead, your symptoms may be the result of vasomotor rhinitis, a condition triggered by non-allergen irritants, such as perfume, smog, and cigarette smoke, that inflame your nasal mucous membranes, says Patricia Wheeler, M.D., an associate professor of family medicine at the University of Louisville. The allergy medicines you're prescribed won't provide relief."

While sinus headaches are often diagnosed when men come in complaining of facial pressure, they are diagnosed with sinus headache, yet sinus headache medicine doesn't work. What they really have is a migraine headache, which is treated a completely different way.

Bronchitis is often the diagnosis when men come in because they are "hacking up" a bad cold. Yet the culprit may be something "hidden," such as asthma.

There's actually quite a few times as I'm digging through charts that I suspect a diagnosis of "bronchitis" is actually asthma. Of course we know asthma is treated quite different than bronchitis, and asthma can be prevented if treated daily with asthma controller medicines.

Then again, quite often I see patient's diagnosed with pneumonia when there is no indication for this diagnosis: no pneumonia on x-ray, no elevated white blood count, etc. Yet this misdiagnosis is probably due to reimbursement criteria more so than ignorance.

So as you're perusing through charts, or dealing with your own health, just be aware that your doctor is, after all, only human. And Lord knows all humans are prone to error.

New study to determine how long we live

According to this post from Healthscout.com, scientists have "grouped together a series of genetic variants" that can help determine who will live long and who has the genetic disposition to die young. Ultimately, the goal of this research is to determine who is likely to die young, and to make sure these people get the medical intervention they need to live longer.

Experts who performed the study said it can be determined how long people will live simply by learning how long their parent's lived, yet events such as this study will be better capable of helping scientists pave the way for "advances in science."

Right now about 6,000 people have obtained the age of 100, and, so long as one has his mental capacity, I personally think this would be an awesome age to obtain. Could you imagine if this blog were still going, say, in 2070. If that were the case, this blogger would have been retired, hopefully, for 40 years.

But can you just imagine the changes in respiratory care in that time? Can you imagine the stories we'd be able to tell? I think it would be awesome.

Now there are many who don't want to know their genetic trends, yet I think it would be a great idea. Obviously I have a genetic disposition to asthma, yet science has proven that mild to moderate asthma (most cases of asthma) do not alter the length of someone's life. Thus, the average lifespan right now is 80. Yet perhaps in another 20 years or so that number will be increased to, say, 100.

Of course that wouldn't be so good if there were a bunch of 80 to 100 year old blobs of skin with no brains in their heads; people dependent on the government; on the hands who feed and clothe and place them in wheelchairs each morning so they can roll around mindlessly in some building redolent of pee and bleach.

The people paying the medical bills, and socialists, wouldn't like this system would they?

Yet, being the optimist I am, I believe we could be around longer, and we could enjoy life longer, so long as we continue to move forth science as this study purports to do. I think longevity is a good thing.

If, say, it is determined I have a genetic predisposition to heart disease, then my doctor would know this and be able to help me with preventative measures. I could make sure I get plenty of exercise, and never start smoking, and eat right for starters. And, if necessary, he may look into medicinal options.

So anyway, I think studies like this, however trivial they seem to you and me, are a great step forward. While we are right now in the communication era, I bet the next era may be the genetics era, where there are mega advancements in genetics and, perhaps, length of life.