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Samter’s Triad Syndrome - A Miracle Healing

Anna Coy completely healed herself of this genetic disease and has no symptoms whatsoever and eats a healthy diet full of hot chili peppers and everything under the sun. It was a miracle of mind and body and breathing that saved her life over and over during anaphylactic attacks that spanned for more than 12 years. Anna underwent for removal of polyps for the 5th time and aspirin desensitization with a course of 7 months on a regular dose of 350 mg of aspirin per day. She decided she was no longer willing to let this disease run her life and her food choices and went off the aspirin completely. She continued with her deep breathing exercises and focused on curing herself completely. To her doctors surprise she reversed her immune system to react normally to all food types and her lungs operate at maximum levels at all times. There is no trace of Samter’s Triad Syndrome left in Anna’s body.

Aspirin sensitivity, nasal polyposis, and asthma are examples of these conditions. Investigation has revealed that in the subset of patients with aspirin sensitivity, arachidonic acid metabolism is shunted into the highly inflammatory leukotriene pathway, which creates an uncontrollable inflammatory response. This highly upregulated situation (a veritable gasoline-on-the-fire) may, in the presence of genetic predisposition, lead to the formation of nasal polyps, anaphylactic episodes and mucosal flooding of the sinus cavities, restricted breathing and low immune function to ward off diseases. After surgery a further antinflammatory treatment is absolutely necessary otherwise polyps reoccur in 90% of the cases after weeks or months. Unfortunately there is so far no curative treatment. New drugs like cytokine or leukotriene receptor antagonists give hope for better results in treatment of aspirin intolerance in the future.

METHODS:

For this investigation 30 patients, who were undergoing adaptive desensitization for aspirin intolerance, were followed-up between 1 and 3 years. They received a maintenance dose of oral aspirin of only 100 mg a day after an initial application of higher doses. Their clinical course as well as their in vitro parameters of eicosanoid release were monitored throughout the individual observation period. RESULTS: Desensitization was successful in 25 of the 30 patients regarding the recurrence rate of nasal polyps, severity of bronchial asthma and sense of smell. There was a clear positive correlation between clinical and in vitro parameters. Discontinuing of aspirin therapy lead to worsening of clinical symptoms, regardless of the prior duration of treatment.

Breathing techniques for the nervous system

Florence Thomas
Asia Africa Intelligence Wire, July 29, 2004 pNA.
New Straits Times (Malaysia

“The human body should be under the control of the para-sympathetic nervous system but because of stress, control has been "pushed over" into the sympathetic section of the nervous system. (This system is intended to operate in emergencies only, and not on a day-to-day basis.)”

The parasympathetic nervous system takes over when one is breathing deeply and fully thus stimulating a relaxation response. Chemically there are endorphins, pain-killing peptides like enkephalin and serotonin released in the body and this combination along with other hormones and neuro-peptides make you feel calm. Tension in the muscles releases and the nervous system is in a relaxed state. 

If you walk around feeling like your nerves are frayed most of the time you may be a shallow breather.

Speaking and Breathing

American Salesman, April 1991 v36 n4 p10(6).
How to improve your speaking ability.
Frances Smith

Sales people can improve their speaking ability by doing deep breathing exercises, by increasing the blood circulation in their mouth by puffing out their cheeks slightly over their teeth, and by improving resonance, clarity, control, and range through simple spoken exercises.

Chronic Obstructive Pulmonary Disease

Respiratory rehabilitation programs, including endurance exercise training and breathing exercises have been shown to be effective in patients with chronic obstructive pulmonary disease (COPD).

Patient Care, May 15, 1984 v18 p128(18)
Ami S. Brodoff

COPD affects roughly 24 million Americans, and kills more than 119,000 each year

“Cigarette smoking is the principal cause of COPD.
Although a nonsmoker occasionally develops the disease, he or she is the exception.
Dusty jobs of any sort and occupations utilizing chemicals irritating to the lungs can cause a variety of pulmonary diseases and allergic diseases with pulmonary manifestations: These conditions are not obstructive lung diseases but can predispose to COPD and exacerbate existing disease, particularly when coupled with smoking. Cotton mill carders and spinners, for example, are exposed to raw, dirty cotton and can develop byssinosis. Chest tightness, wheezing, and cough usually develop in the beginning of the work week after a weekend of absence from the mill--hence, the term "Monday morning asthma."

There are many jobs where you can be exposed to chemicals and irritants that lead to possible COPD.

The classic symptom triad of COPD is:
 * Shortness of breath
 * Chronic productive cough
 * Episodic wheezing

 Frequent respiratory tract infections, fatigue, weight loss, and lack of libido should also increase your suspicion of COPD.

Asthma can be confused with COPD because both conditions cause dyspnea, cough, and wheezing. The differential diagnosis is complicated further because the airways obstruction of the patient with severe asthma may be largely irreversible while that of the patient with mild, early stage COPD may be substantially reversible.

Acute effects of deep diaphragmatic breathing in COPD patients with chronic respiratory insufficiency. M. Vitacca, E. Clini, L. Bianchi, N. Ambrosino. ERS Journals Ltd 1998.
 
Acute effects of deep diaphragmatic breathing in COPD patients with chronic respiratory insufficiency.

Vitacca M, Clini E, Bianchi L, Ambrosino N.
 Full article at erj.ersjournals.com

Fondazione Salvatore Maugeri IRCCS, Respiratory Department, Centro Medico di Gussago, Italy.

This study investigated the impact of deep diaphragmatic breathing (DB) on blood gases, breathing pattern, pulmonary mechanics and dyspnoea in severe hypercapnic chronic obstructive pulmonary disease (COPD) patients recovering from an acute exacerbation. Transcutaneous partial pressure of carbon dioxide (Ptc,CO2) and oxygen (Ptc,O2) and arterial oxygen saturation (Sa,O2), were continuously monitored in 25 COPD patients with chronic hypercapnia, during natural breathing and DB. In eight of these patients, breathing pattern and minute ventilation (V'E) were also assessed by means of a respiratory inductance plethysmography. In five tracheostomized patients, breathing pattern and mechanics were assessed by means of a neumotachograph/pressure transducer connected to an oesophageal balloon. Subjective rating of dyspnoea was performed by means of a visual analogue scale. In comparison to natural breathing deep DB was associated with a significant increase in Ptc,O2 and a significant decrease in Ptc,CO2, with a significant increase in tidal volume and a significant reduction in respiratory rate resulting in increased V'E. During DB, dyspnoea worsened significantly and inspiratory muscle effort increased, as demonstrated by an increase in oesophageal pressure swings, pressure-time product and work of breathing. We conclude that in severe chronic obstructive pulmonary disease patients with chronic hypercapnia, deep diaphragmatic breathing is associated with improvement of blood gases at the expense of a greater inspiratory muscle loading.

In conclusion, our study shows that in severe chronic obstructive pulmonary disease patients with chronic hypercapnia and reduced inspiratory muscle strength, recovering from an episode of acute respiratory failure, deep diaphragmatic breathing, a common component of respiratory rehabilitation programs, may induce an acute improvement in arterial blood gases while increasing inspiratory muscle effort and worsening dyspnoea. An increase in alveolar ventilation as suggested by the modifications of breathing pattern was likely to be the major mechanism through which diaphragmatic breathing improved the arterial blood gases.

PMID: 9551746 [PubMed - indexed for MEDLINE]
Biomed Pharmacother. 2003 Oct;57 Suppl 1:87s-91s.

Emphysema and Chronic Bronchitis

Emphysema and Chronic Bronchitis
They take your breath away.

Harvard Men's Health Watch, June 2003 v7 i11 pO.
Emphysema, Pulmonary Bronchitis, Lung diseases

“The lungs of patients with emphysema contain more air than normal, but the diseased lung tissues are not able to deliver normal amounts of critical oxygen to the bloodstream.”

In COPD, the bronchioles are narrowed by inflammation and mucus, making it harder for air to reach the air sacs, or alveoli. In patients with chronic bronchitis, the bronchioles bear the brunt of the problem, but in patients with emphysema, the alveoli themselves are over-inflated, inflamed, and damaged. Most patients with COPD have elements of both chronic bronchitis and emphysema.”

“In healthy people, rising blood levels of carbon dioxide tell the nervous system to speed up breathing, but in those with advanced lung disease low oxygen levels can do the same.”

“In emphysema the alveoli become hyper-inflated, filled with too much air. But pressure is not the main culprit in emphysema. Rather, it's inflammation triggered by inhaled irritants. White blood cells respond to the irritation, but instead of containing the damage, they release chemicals called cytokines, as well as elastase and other enzymes that damage and eventually destroy lung tissue.”

There are many protocols to follow when dealing with COPD, Emphysema and Lung Disease. It is best to consult your doctor if you suspect any problems with your lungs.

Monitored Exercise can help the muscles utilize oxygen better within the body but does not repair damaged lung tissue.

Deep breathing exercises can aid a person with COPD and emphysema in that you can learn to utilize the unaffected areas of the intercostals muscles and diaphragm to improve capacity. Increasing volume space within the torso to receive the most volume of oxygen possible into the lungs comfortably. Exercise makes patients with COPD huff and puff, but supervised, gradual exercise can actually help in the long run. It's called pulmonary rehabilitation, but it doesn't improve the lungs themselves. Instead, it helps the patient's muscles use oxygen more efficiently, so they get more mileage from their damaged lungs.

Lungs

Science of Breath 1904
Yogi Ramacharaka

“One of the functions of the lungs is to clean the blood. Nearly 35,000 pints of blood pass though the lower lobes of the lungs in one day.”

During your lifetime you will take about breathe 600 million breaths. A healthy young man will have an FEV1 of about 4 liters, or approximately 4 quarts.

Source:  Biological Sciences Review, Sept 2003 v16 i1 p36(8). Title:  Gas exchange in the lungs: this article explains how alveoli function and shows how some diseases disrupt normal physiology thus affecting the efficiency of gas exchange. Author:  Dianne Gull

“Humans have two lungs, each enclosed in a separate airtight region of the thoracic cavity. This means that if one lung is damaged, perhaps by a broken rib in an accident, the other lung can continue to function normally. The right lung is made up of three lobes and the left lung has two. There are two tree-like structures in each lung: the airway tree, which brings air to the respiratory surface, and the vascular tree, which brings blood to the respiratory surface. Blood flow is always matched to airflow. This ensures efficient exchange of carbon dioxide and oxygen--so when exercising, or recovering after exercise, heart rate and breathing rate increase or decrease together.
It takes only about a second for blood to pass through the capillaries of the lungs. In this time oxygen must be absorbed and carbon dioxide released. It is the structure of the alveolar wall that allows for this rapid and efficient exchange.

The diameter of the capillaries in the alveolus is about the same as that of the red blood cells themselves. This forces them to pass through the capillaries in single file. A thin layer of blood plasma between the plasma membrane of the red blood cell and the capillary wall acts as a lubricant.

Because the capillaries are an integral part of the alveolar wall, the actual distance across which gases must diffuse measures only about 0.5[micro]m--less than one-hundredth the thickness of a human hair. Alveolar macrophages move freely across the surface of the alveolus. They are highly phagocytic and remove inhaled dust particles. When you breathe out, you do not empty the lungs completely--a small volume of air, the residual volume, is always retained so that the alveoli deflate only partially.

Smoking And Lung Damage

“Smoking causes progressive damage to the respiratory system and sets in motion a series of changes. The initial stages are reversible, if the smoker gives up but the more serious damage is irreversible.

Cigarette smoke paralyses the cilia in the epithelium lining the trachea. Since the cilia move mucus, containing trapped dust particles and bacteria upwards out of the respiratory system (the so-called 'ciliary escalator') smokers have a characteristic cough and are prone to upper respiratory tract infections. Bronchitis, an infection of the bronchi, becomes increasingly common. Chronic bronchitis is caused by excessive production of mucus, which is a result of the irritation of the small bronchi by smoke.

The particles in tobacco smoke attract increased numbers of macrophages to the lungs. Macrophages possess a range of 'digestive' enzymes, which they use to destroy particles and pathogens that reach the lung surface. One of these enzymes is elastase. Elastase degrades the elastin fibres that give the lungs their elastic properties. Thus the higher than normal levels of elastase are responsible for the loss of elasticity of the lung tissue.

As the disease progresses, sufferers develop a characteristic barrel chest, caused by permanent inflation of the lungs. Exercise becomes impossible, and even walking on the flat may prove difficult

Suggestion. Stop smoking immediately in whatever way works for you. When you have a craving for a cigarette keep in mind that it will last for as little as thirty seconds. Find something to do for that time such as deep breathing exercises, munch on something crunchy like carrots or celery, shake or move your body with stretches or swinging your arms around in circles. Anything that gets your attention off the craving will do.

Begin a program of retraining your body to breathe better. Often times we go out to have a “Smoke Break”, consider that you are actually using the feeling of the smoke as it fills your lungs you are feeling yourself breathe. Most of the time you have to take a deep breath to bring the smoke into the lungs so you are already doing a deep breath only the smoke is the unhealthy part. So if you are already in the habit of taking a break why not make it a breathing break instead of a smoking break. Find a place away from smoker’s area and get some fresh air into the lungs. You will be getting the break and the fresh breath you need to step away from stress and into a more calm and peaceful state in a much healthier way.

Exercise and the Lungs

Exercise and the Lungs

Muscle & Fitness/Hers, March 2003 v4 i2 p56(4).
Title:  Air conditioning: how better breathing techniques can help improve your workouts. Author:  Karen Asp

“With a little work, however, you can learn to breathe better as you exercise, allowing you to access greater supplies of energy, and train harder and longer before feeling fatigued.

Feed the flame with oxygen. Your main source of energy comes from the foods you eat, including carbohydrates, protein and fat. This ingested food is broken down and stored as either glycogen or fat, which can be used later to produce energy. But for food to efficiently release this energy, it has to combine with oxygen. After oxygen enters your lungs, it's picked up by red blood cells and transported to working muscles. The more muscle you use, the more oxygen you need to produce energy. That's why it's important to develop good breathing techniques when you exercise. Poor breathing techniques force you to train at a lower intensity, and you may quit exercising sooner because it's more difficult to satisfy your muscles' oxygen and fuel requirements.

Obviously, everyone experiences some shortness of breath when exercising, but when your breath becomes too accelerated and uncontrolled, your body's saying you're pushing too hard. Excessive, pant-like breathing wastes energy and doesn't deliver enough oxygen to your lungs.

Breathing better might not take brains, but it does require practice. Focus on your breathing not only when you're exercising but also when you're sitting in traffic or picking up groceries, and you'll see the returns in your workouts.”

Obesity: How Excess Stress Factors on the Lung

Obesity: How Excess Stress Factors on the Lungs

Obesity - Health aspects
Full Text COPYRIGHT 1998 The Lancet Ltd.

“Symptoms of respiratory insufficiency were shortness of breath, wheezing, cough, and production of phlegm. Improving your breathing capacity can help you loose weight.
The continuing project monitoring cardiovascular health in the Netherlands (MORGEN) shows that waist circumference, body-mass index, and waist-to-hip ratio all relate closely and similarly to many indicators of chronic diseases.

Waist circumferences of, more than 102.0 cm in men and more than 88.0 cm in women (more than action level 2) have a strong likelihood of developing several disorders, including shortness of breath, hypercholesterolaemia, hypertension, and difficulty with basic activities of daily life. After adjustments for age and lifestyle factors, the likelihood of ill health was significantly raised, which suggests that weight management may be beneficial. Prevention of unwanted weight gain should be the primary goal, and slight waist reduction (5-10 cm) can result in improvements in several cardiovascular risk factors.

Mechanical ventilation in acute respiratory distress syndrome (ARDS): lung protecting strategies for improved alveolar recruitment

Ned Tijdschr Geneeskd. 2003 May 3;147(18):886-7; author reply 887

[Mechanical ventilation in acute respiratory distress syndrome (ARDS): lung protecting strategies for improved alveolar recruitment]

[Article in Dutch]

Schultz MJ, van Zanten AR, de Smet AM, Kesecioglu J.

Laboratorium Experimentele Geneeskunde, Academisch Medisch Centrum/Universiteit van Amsterdam, afd. Intensive Care Volwassenen, Meibergdreef 9, 1105 AZ Amsterdam. m.j.schultz@amc.uva.nl

For patients with acute respiratory distress syndrome (ARDS) the most important objective of mechanical ventilation is opening and keeping open the alveoli to achieve adequate oxygenation, without further damaging the lungs or negatively affecting the circulation. Alveolar recruitment is achieved by making use of positive end-expiratory pressure (PEEP). The best PEEP level is that with which the largest improvement in oxygen transport and lung compliance is achieved, without a decrease in the stroke volume of the left ventricle. In addition to the usual volume-controlled ventilation with PEEP, pressure-limited ventilation is also possible. In this a preselected pressure is never exceeded, whereas a maximum inspiratory airflow at the start of inspiration provides more opportunity for gaseous exchange. The oxygenation can possibly be further improved by increasing the inspiration-expiration ratio. As a result of the reduced expiratory period the alveoli which tend to collapse at the end of a normal expiration are kept open. Mechanical ventilation with a lower tidal volume decreases mortality. Ventilation in a prone position increases the end-expiratory lung volume and reduces the intrapulmonary shunt and the regional differences in the degree of ventilation. These factors possibly contribute to preventing ventilation-induced lung damage. Administration of natural surfactant during the ventilation of patients with ARDS seems to be a highly promising strategy; the clinical effectiveness still needs to be demonstrated.

Publication Types:
•    Review
•    Review, Tutorial

PMID: 12661116 [PubMed – LUNGS, ARDS
Ned Tijdschr Geneeskd. 2003 Feb 22;147(8):327-31.

Complementary and alternative medicine for bronchial asthma: is there new evidence?

Curr Opin Pulm Med. 2004 Jan;10(1):37-43.
Related Articles, Books, LinkOut
 
Complementary and alternative medicine for bronchial asthma: is there new evidence?

Gyorik SA, Brutsche MH.

Division of Respiratory Medicine, University Hospital Basel, Switzerland.

PURPOSE OF REVIEW:

Complementary and alternative medicine is widely used in bronchial asthma. Data on efficacy of these treatment modalities are lacking.

RECENT FINDINGS:

Studies published since June 2002 on complementary and alternative medicine in bronchial asthma were systematically reviewed.

SUMMARY:

Studies do not support the use of homeopathy, air ionizers, manual therapy, or acupuncture for asthma. These methods bear some risks to patients related to undertreatment and side effects. There might be a possible, but so far not clearly established, role for antioxidant dietary supplementation, and some natural antiinflammatory and immunomodulatory remedies. However, their effect size compared with the classical treatment and side-effect profile is not clearly established. Strategies influencing breathing technique or perception, such as breathing or retraining exercises, need to be studied over the next few years to establish their additive role in the treatment of asthma. Breathing exercises could improve lung function and quality of life in different studies. Psychotherapy-related methods such as relaxation, hypnosis, autogenic training, speleotherapy, and biofeedback might have a small effect in selected cases, but have not proven to be superior to placebo. Nevertheless, more randomized controlled trials of good methodological quality are required to allow firm conclusions.

Publication Types:
•    Review

PMID: 14749604 [PubMed

Exercise-induced bronchodilation in natural and induced asthma: effects on ventilatory response and performance.

J Appl Physiol. 2002 Jun;92(6):2353-60.
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Exercise-induced bronchodilation in natural and induced asthma: effects on ventilatory response and performance.

Crimi E, Pellegrino R, Smeraldi A, Brusasco V.

Dipartimenti di Medicina Interna e di Scienze Motorie e Riabilitative, Universita di Genova, 16132 Genova, Italy.

We studied whether bronchodilatation occurs with exercise during the late asthmatic reaction (LAR) to allergen (group 1, n = 13) or natural asthma (NA; group 2, n = 8) and whether this is sufficient to preserve maximum ventilation (VE(max)), oxygen consumption (VO(2 max)), and exercise performance (W(max)). In group 1, partial forced expiratory flow at 30% of resting forced vital capacity increased during exercise, both at control and LAR. W(max) was slightly reduced at LAR, whereas VE(max), tidal volume, breathing frequency, and VO(2 max) were preserved. Functional residual capacity and end-inspiratory lung volume were significantly larger at LAR than at control. In group 2, partial forced expiratory flow at 30% of resting forced vital capacity increased greatly with exercise during NA but did not attain control values after appropriate therapy. Compared with control, W(max) was slightly less during NA, whereas VO(2 max) and VE(max) were similar. Functional residual capacity, but not end-inspiratory lung volume at maximum load, was significantly greater than at control, whereas tidal volume decreased and breathing frequency increased. In conclusion, remarkable exercise bronchodilation occurs during either LAR or NA and allows VE(max) and VO(2 max) to be preserved with small changes in breathing pattern and a slight reduction in W(max).

PMID: 12015347 [PubMed - indexed for MEDLINE]

The interrelationship of nutrition and pulmonary function in patients with cystic fibrosis.

Curr Opin Pulm Med. 1996 Nov;2(6):457-61.
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The interrelationship of nutrition and pulmonary function in patients with cystic fibrosis.

Borowitz D.

Division of Pulmonary Medicine, Children's Hospital of Buffalo, NY 14222-2099, USA.

This paper reviews recent publications on the interrelationship of nutrition and pulmonary function in patients with cystic fibrosis. It is unclear whether low weight is a cause or an effect of declining pulmonary status in patients with cystic fibrosis. Epidemiologic studies suggest that low weight may be an independent predictor of mortality. Elevations in energy expenditure are not seen in presymptomatic infants. The elevations in energy expenditure seen in those with lung disease are not totally explained by increased oxygen cost of breathing and can be decreased by improving lung function. Although circulating levels of natural antioxidants and inflammation-modulating nutrients are low in patients with cystic fibrosis and can be increased with supplements, there are no recent data on their clinical effects. Nutritional intervention for patients with chronic illness needs to take into account psychosocial and adherence factors as well as nutritional prescriptions. Pancreatic enzyme supplementation should be limited to no greater than 2500 lipase units per kilogram per meal to decrease the risk of developing dose-related fibrosing colonopathy.

Publication Types:
•   Review

Breathing, voice, and movement therapy: applications to breathing disorders

1: Biofeedback Self Regul. 1994 Jun;19(2):141-53.
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Breathing, voice, and movement therapy: applications to breathing disorders.

Buchholz I.

KlangKoerperBewegung Institut, Munchen, Germany.

Elsa Gindler (1885-1961) developed a holistic approach to the human body and psyche via the movement of breath. Gindler experimented with movements to strengthen the deeper layers of the muscular system and improve the circulation of oxygen, movements that reduced tensions that had been preventing the breathing muscles from functioning properly. Subsequently, she founded a school for breathing and body awareness. The biggest breathing muscle in the human body is the diaphragm, the lowering of which can only take place when the jaw and the throat are relaxed, the belly is free, and the psoas (major and minor) and hip joints allow free leg-movement and flexibility in the lower back. When these conditions do not obtain, the body compensates by lifting the shoulders, pulling up the chest bone, and contracting the sphincter muscles in the throat, movements which weaken the muscles which assist the breathing process. Thus, the compensatory muscles are overburdened and the fine organization of the body is disturbed; the natural capacity to use the breath as a healing force is lost. The goal of breath therapy is to recognize and reestablish this capacity. Training sessions are devoted to relaxation; to exercises to rebuild muscle tone, strengthen weakened muscles, release contracted areas, and the use of the voice to stimulate the respiratory system. Sessions typically consist of (a) relaxation, (b) activation (experimenting with new, freer ways of moving), and (c) integration (application to everyday life). The therapist analyzes incidents of stress in the client's life where breathing is likely to be disturbed. This is especially important for asthmatics who can learn how to deal with an attack by relaxing rather than contracting. This work is especially beneficial for problems in (a) the skeletal structure, (b) respiration, (c) vital organs, and (d) general symptoms.

Publication Types:
•    Biography
•    Historical Article

Personal Name as Subject:
•    Gindler E

PMID: 7918752 [PubMed - indexed for MEDLINE]
•    Review, Tutorial

PMID: 9363185 [PubMed - indexed for MEDLINE]

Deep Breathing Exercises can improve respiratory muscle strength.

Am Rev Respir Dis. 1981 Aug;124(2):132-7.
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Deep Breathing Exercises can improve respiratory muscle strength.

The effects of intermittent positive pressure breathing on patients with respiratory muscle weakness.

De Troyer A, Deisser P.

Marked reductions in pulmonary compliance have been noted in patients with respiratory muscle weakness, which greatly contribute to the losses of lung volume. In an attempt to reverse this abnormality and to decrease the work of breathing, we evaluated the effects of a 15-min period of positive pressure, mechanical hyperinflation of the lungs in 10 patients with generalized neuromuscular disorders and long-standing involvement of the respiratory muscles. The vital capacity was 46, and the static expiratory lung compliance was 59% of control values. The recoil pressure of the lung at full inflation was 19 cm H2O. Using positive pressure breathing devices, we inflated the lungs either with inflation pressures ranging between 20 and 40 cm H2O or with volume that were at least twofold larger than the patients' natural inspiratory capacity. Lung volumes, including functional residual capacity, and static pulmonary compliance were not modified by these procedures. Maintaining 10 cm H2O of positive end-expiratory pressure did not alter the results. These findings suggest that (1) alveolar collapse, rather than a simple decrease in the compliance of the surface film of the lung, is the major cause of the low pulmonary compliance in patients with chronic respiratory muscle weakness; (2) these patients do not acutely benefit from intermittent positive breathing treatment.

PMID: 7020511 [PubMed - indexed for MEDLINE]

Natural and mechanical respiration therapy for chronic respiratory insufficiency

: MMW Munch Med Wochenschr. 1976 Jan 16;118(3):73-8.
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[Natural and mechanical respiration therapy for chronic respiratory insufficiency (author's transl)]

[Article in German]

Stresemann E.

Respiratory therapy of ventilation disorders involves a redistribution of the work of the respiratory musculature from above downwards, relieving the auxiliary musculature, increasing the excursion of the lower part of the thorax and relaxation of the diaphragm. It is pointless to provide respiratory techniques for use as exercises only when the body is in a state of rest; suitable respiratory techniques must rather be of the pattern of spontaneous respiratory movement which keeps control in stress situations also. The patient must learn to recognise the limit of his own pulmonary functional capacity, so that he can reduce the work load in good time before it is reached. Respiratory therapy is increased even more by passive positive pressure respiration which enables passive inspiration, sparing inspiratory respiratory work, with active exercise therapy in the expiratory phase, and which can be combined with inhalation treatment.

PMID: 814430 [PubMed - indexed for MEDLINE]

When should respiratory muscles be exercised?

Chest. 1983 Jul;84(1):76-84.
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When should respiratory muscles be exercised?

[No authors listed]

  1. Normal respiratory muscles have a large functional reserve.
  2. Muscles have a tremendous capacity for adaptation. Adaptation is task-specific (eg, muscles use similar motor units for the same tasks).
  3. Muscular fatigue results when motor units are required to perform an unaccustomed task. Continued effort in the face of fatigue, especially high-tension low-repetition effort, may produce a reversible "use atrophy" (eg, fiber damage, splitting, and regeneration).
  4. Exercising damaged or regenerating muscle may produce irreversible damage.
  5. Exercising the respiratory muscles of some patients may make them more susceptible to fatigue or, at least, produce no further improvement in function. Alternating rest and exercise improves pulmonary function tests in some patients.
  6. Retraining a weak or damaged muscle requires that it first be "shut down" and rested before attempting retraining.
  7. Training a rested muscle to different tasks--before these tasks are needed--may be the critical step in successful rehabilitation.
  8. Resistance breathing probably improves both respiratory muscle strength and respiratory muscle endurance.
  9. There are at least three immediate tasks for clinicians to define: Where in the present natural history of COPD should respiratory muscles be rested? How long should they be rested? How best can they be retrained?

Publication Types:
•    Case Reports

PMID: 6861548 [PubMed - indexed for MEDLINE]

Cognitive-behavioral pain management in children with juvenile rheumatoid arthritis.

MusculoSkeletal Research

1: Pediatrics. 1992 Jun;89(6 Pt 1):1075-9.
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Cognitive-behavioral pain management in children with juvenile rheumatoid arthritis.

Walco GA, Varni JW, Ilowite NT.

Schneider Children's Hospital of Long Island Jewish Medical Center, Albert Einstein College of Medicine, New Hyde Park, NY.

Decreasing chronic joint pain is a major goal in the management of juvenile rheumatoid arthritis. Cognitive-behavioral self-regulatory techniques were taught to children with juvenile rheumatoid arthritis to reduce musculoskeletal pain intensity and to facilitate better adaptive functioning. Subjects were 13 children between the ages of 4.5 and 16.9 years who had pauciarticular or systemic onset juvenile rheumatoid arthritis. Baseline data included an initial comprehensive assessment of pain, disease activity, and level of functional disability, as well as pain intensity ratings gathered over a 4-week period. Subjects were seen for eight individual sessions in which self-regulatory techniques (progressive muscle relaxation, guided imagery, meditative breathing) were taught, and parents were seen for two sessions in which key aspects of behavioral pain management techniques were reviewed. Results indicated that these techniques led to substantial reduction of pain intensity, which generalized to outside the clinic setting. Six- and 12-month follow-up data showed consistent decreases in pain as well as improved adaptive functioning. The data suggest that cognitive-behavioral interventions for pain are an effective adjunct to standard pharmacologic interventions for pain in patients with juvenile rheumatoid arthritis.

Diaphragmatic dysfunction in patients with idiopathic inflammatory myopathies.

1: Neuromuscul Disord. 2005 Jan;15(1):32-9.
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Diaphragmatic dysfunction in patients with idiopathic inflammatory myopathies.

Teixeira A, Cherin P, Demoule A, Levy-Soussan M, Straus C, Verin E, Zelter M, Derenne JP, Herson S, Similowski T.

UPRES EA 2397, Universite Pierre et Marie Curie Paris VI, Paris, France.

Polymyositis, dermatopolymyositis, and inclusion body myositis imply chronic inflammation of skeletal muscles. Pulmonary complications include aspiration pneumonia, interstitial pneumonitis, or respiratory muscle myositis. This study aims at better describing their impact on respiratory muscle. Twenty-three consecutive patients (12 PM, 5 DM, 6 IBM) were studied (static inspiratory and expiratory pressures; diaphragm function in terms of the mouth and transdiaphragmatic pressure responses to bilateral phrenic stimulation). Pulmonary parenchymatous abnormalities were mild (6 cases) or absent. The mouth pressure produced by phrenic stimulation was 6.83+/-3.01 cm H2O, with 18 patients (78%) diagnosed with diaphragm weakness (<10 cm H2O) and lower values in DM (4.35+/-1.48 cm H2O) than in IBM and in PM (P<0.05). Diaphragm weakness is frequent and probably overlooked in inflammatory myopathies. Further studies are needed to delineate the clinical relevance of these results.

PMID: 15639118 [PubMed - indexed for MEDLINE]

Psychological implications of respiratory health and disease

Psyche/Emotional Research
results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).

Sender's message:
 Sent on Sunday, 2005 May 15
 Select 1582453

1: Respiration. 2005 Mar-Apr;72(2):210-5.
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Psychological implications of respiratory health and disease.

Chetta A, Foresi A, Marangio E, Olivieri D.

Department of Clinical Sciences, Section of Respiratory Diseases, University of Parma, Parma, Italy. chetta@unipr.it

The possibility that a subject's psychological status may influence respiratory sensations and that chronic respiratory disease may have psychological consequences has sparked great interest among clinicians and researchers. This paper reviews the existing research on the association between respiratory symptom perception and the psychological status and between chronic respiratory diseases, such as asthma and chronic obstructive pulmonary disease, and psychological disturbances. Moreover, it focuses on the role of stressful events in determining asthma exacerbations. The recent literature suggests that in patients with chronic respiratory diseases, the evaluation of breathlessness perception, psychological disturbances and the recording of any stressful events should be considered as relevant as the physical and functional assessment of respiration. Copyright (c) 2005 S. Karger AG, Basel.

PMID: 15824535 [PubMed - in process]

Respiratory psychophysiology in hypertension research

1: Behav Modif. 2001 Sep;25(4):606-20.
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Respiratory psychophysiology in hypertension research.

Anderson DE.

The pathogenesis of hypertension results from an interaction of genetic and environmental factors. Behavioral factors might participate in sodium sensitive forms of hypertension via a cascade of physiological responses triggered by conditioned inhibition of breathing. When an individual decreases ventilation sufficient to increase pCO2 but not sufficient to activate chemoreceptor reflexes, plasma pH decreases transiently to stimulate a renal mechanism that can expand plasma volume via sodium retention. The combination of high resting pCO2 and high sodium intake elevates resting blood pressure in laboratory animals and healthy human participants. In the natural environment, this mechanism seems to be more important for the development of hypertension in women than in men, perhaps due to differential expression of anger and aggression. Studies are needed to clarify the role of breathing pattern in individual differences in resting pCO2 and the effects of breathing interventions on salt sensitivity and sodium sensitive forms of hypertension.

Publication Types:
•    Review
•    Review, Tutorial

PMID: 11530718 [PubMed –

Cardiorenal effects of behavioral inhibition of breathing

1: Biol Psychol. 1998 Sep;49(1-2):151-63.
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Cardiorenal effects of behavioral inhibition of breathing.

Anderson DE.

Laboratory of Behavioral Sciences, Gerontology Research Center, National Institute on Aging/NIH, Baltimore, MD 21224, USA.

This article reviews evidence that mild, but sustained, inhibition of breathing can affect blood pressure regulation via effects of increased PCO2 on sodium regulation. Experiments with micropigs are summarized which show that anticipation of the onset of a familiar avoidance task is accompanied by sustained increases in PCO2, increases in plasma hydrogen and bicarbonate ion concentrations, decreases in hematocrit, and increases in circulating levels of sodium pump inhibitors that are sensitive to plasma volume. Observational studies with humans using an ambulatory respiration monitor characterize episodes of inhibited breathing occurring in the natural environment. Experimental studies with human subjects show that voluntary maintenance of end-tidal CO2 near the upper end of the normal range results in decreases in renal sodium excretion, increases in plasma sodium pump inhibitors and inhibition of sodium pump activity. Together, these studies are consistent with the view that behavioral stress can influence blood pressure regulation via sustained inhibition of respiration which acidifies the plasma and increases sodium/hydrogen exchange in kidneys and blood vessels.

Publication Types:
•    Review
•    Review, Tutorial

PMID: 9792491 [PubMed - indexed for MEDLINE]

Inner speech and respiration: toward a possible mechanism of stress reduction

: Percept Mot Skills. 1994 Oct;79(2):803-11.
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Inner speech and respiration: toward a possible mechanism of stress reduction.

Chapell MS.

Department of Psychology, Temple University, Philadelphia, Pennsylvania 19122.

Stress reduction associated with slow, deep, regular, diaphragmatic-abdominal respiration has been attributed to arousal reduction and to diversionary effects on the cognitive mediation of stress. Evidence was presented to show that verbal inner speech, self-talk, is a primary cognitive mediator of stress and that inner speech is associated with speech musculature and irregular respiratory movements similar to those of external speech. It was proposed that, if with inner speech one uses and regulates speech musculature and irregular respiratory movements like external speech, then slow, deep, regular, diaphragmatic abdominal respiration may be incompatible with inner speech and may reduce stress by inhibiting stressful self-talk. In addition to describing a stress-reduction mechanism, a potential stress mechanism was suggested wherein fast, shallow, irregular, thoracic breathing and tension of speech musculature associated with stressful self-talk may promote the continuation of stressful self-talk.

Publication Types:
•    Review
•    Review, Tutorial

PMID: 7870507 [PubMed - indexed for MEDLINE]

Social and behavioral factors associated with episodes of inhibitory breathing.

1: J Behav Med. 1992 Dec;15(6):573-88.
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Social and behavioral factors associated with episodes of inhibitory breathing.

Haythornthwaite JA, Anderson DE, Moore LH.

Laboratory of Behavioral Sciences, National Institute on Aging, Baltimore, Maryland 21224.

Previous research has shown that episodes of inhibitory breathing, characterized by low-frequency breathing, occur both in laboratory animals during intervals preceding avoidance tasks and in humans in the natural environment. The present study investigated social and behavioral factors accompanying episodes of inhibitory breathing that occur in the natural environment. Breathing frequency and tidal volume of ambulatory subjects were monitored via inductive plethysmography. Information concerning location, social environment, behavior, and mood was self-recorded in a computerized diary. The percentage of episodes of inhibitory breathing was found to be significantly greater in social situations than when subjects were alone. Additional analyses eliminated talking as an explanation for these effects. Inhibitory breathing was more frequent when subjects were sedentary rather than active, and inhibitory breathing was not associated with changes in mood or appraisal. Additional research is needed to determine the nature of the social interactions that elicit inhibitory breathing, its physiological concomitants, and its long-term health implications.

PMID: 1484381 [PubMed - indexed for MEDLINE]

Self-regulation of response patterning: implications for psychophysiological research and therapy

Biofeedback Self Regul. 1976 Mar;1(1):7-30.
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Self-regulation of response patterning: implications for psychophysiological research and therapy.

Schwartz GE.

This paper develops the basic premise that learning to self-regulate a pattern of responses can have different consequences from those observed when controlling individual functions alone. It is suggested that the self-regulation of patterns of responses can be a particularly sensitive and effective procedure for (a) uncovering biological linkages and constraints between responses in the intact human, (b) investigating how multiphysiological systems combine to produce unique subjective experiences and effects on performance, and (c) enhancing the clinical effectiveness of biofeedback procedures by training patients to integrate and coordinate voluntarily specific patterns of cognitive, autonomic, and motor responses. These hypotheses are illustrated by basic research involving biofeedback training for patterns of blood pressure, heart rate and EEG activity, related experiments on the cognitive self-regulation of patterns of physiological responses using affective imagery and meditation procedures, and case studies of patients treated with biofeedback. The concept of electronic biofeedback as an "unnatural act" is presented with the goal of placing self-regulation within a more biobehavioral perspective emphasizing the natural patterning of physiological processes.

PMID: 990345 [PubMed - indexed for MEDLINE]

Sleep-disordered breathing and self-reported general health status

SLEEP Research
1: Sleep. 1998 Nov 1;21(7):701-6.
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Sleep-disordered breathing and self-reported general health status in the Wisconsin Sleep Cohort Study.

Finn L, Young T, Palta M, Fryback DG.

Department of Preventive Medicine, University of Wisconsin, Madison 53705, USA.

OBJECTIVE: To determine the relationship between sleep-disordered breathing and self-reported general health status. breathing status assessed by overnight in-laboratory polysomnography. SETTING: General Community. SUBJECTS: Employed men (n=421) and women (n=316), ages 30-60 years, enrolled in the Wisconsin Sleep Cohort Study. INTERVENTIONS: None. OUTCOME MEASURE: Self-reported general health profile and life satisfaction measured by the Medical Outcomes Survey Short Form-36 and obtained by interview. RESULTS: Sleep-disordered breathing was associated with lower general health status before and after adjustment for age, sex, body mass index, smoking status, alcohol usage, and a history of cardiovascular conditions. Even mild sleep-disordered breathing (apnea-hypopnea index = 5) was associated with decrements in the Medical Outcomes Short Form 36 Survey health constructs comparable to the magnitude of decrements linked to other chronic conditions such as arthritis, angina, hypertension, diabetes, and back problems. CONCLUSIONS: Sleep-disordered breathing is independently related to lower general health status, and this relationship is of clinical significance. Given the growing emphasis of the importance of patients' perceptions of health, these findings are relevant to estimating the overall impact of sleep-disordered breathing.

PMID: 11286346 [PubMed - indexed for MEDLINE]

Role of nose breathing in genioglossus muscle response to hypoxia

J Physiol Pharmacol. 2003 Sep;54 Suppl 1:48-54.
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Role of nose breathing in genioglossus muscle response to hypoxia in older and younger subjects.

Tafil-Klawe M, Klawe JJ.

Department of Physiology, Bydgoszcz Medical University, Bydgoszcz, Poland.

Several studies showed that nasal airway is an active component of the respiratory system. Clinical data suggest that nasal obstruction causes episodes of obstructive apnea or hypopnea. In the present study, a possible influence of breathing through the nose on genioglossus muscle (GG, dilator of upper airway) reactivity to hypoxic activation was studied. Two groups of 20-30 years and 41-55 years old, 35 healthy subjects each, were investigated. The GG-EMG-activity was recorded and analyzed during progressive normocapnic hypoxia. The subjects breathed through the nose (N) or mouth (M) alone and through the nose and mouth (N&M). Significantly smaller increases in the GG-EMG-activity in response to hypoxia were observed during M breathing, as compared with N and M&N breathings, in both groups. The older subjects also showed a reduced response of GG-muscle to hypoxia, which was most pronounced during M breathing. We suggest that breathing through the nose activates the dilator muscle of upper airways, preventing apnea events.

PMID: 15886411 [PubMed - in process]

Obstructive sleep apnea. Deep breathing techniques may help in retraining the body to breathe better while sleeping

Dis Mon. 1994 Apr;40(4):197-252.
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Obstructive sleep apnea. Deep breathing techniques may help in retraining the body to breathe better while sleeping

Wiegand L, Zwillich CW.

Division of Pulmonary and Critical Care Medicine, Milton S. Hershey Medical Center, Pennsylvania State University Hershey.

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society.

Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail.

During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse.

The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss.

Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.

Publication Types:
•    Review

PMID: 8143553 [PubMed - indexed for MEDLINE]

Pathophysiology and treatment of sleep apnea

1: Annu Rev Med. 1985;36:369-95.
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Pathophysiology and treatment of sleep apnea.

Ingbar DH, Gee JB.

The sleep apnea syndromes have attracted the interest of physicians and scientists in many different disciplines because the disorders involve the physiology of sleep, the control of respiration, the function of the upper airway, and the clinical sequelae upon cardiac, pulmonary, and psychological function. Over the eight years since this subject was last reviewed here (1), the pathophysiology of obstructive sleep apnea has become better understood. A variety of new treatments are now available. However, our clinical knowledge of the syndrome and its natural history have changed little. The high prevalence of these syndromes and related disorders such as snoring is only beginning to be apparent. This chapter reviews current understanding of these syndromes, with particular emphasis on recent advances, and highlights questions for future investigation. First, we consider normal upper airway function and the control of breathing during sleep. Then, we apply this information to a consideration of the pathophysiology, clinical features, and treatment of sleep apnea syndromes.

Publication Types:
•    Review

PMID: 3888057 [PubMed - indexed for MEDLINE]

Respiratory disorders of sleep

Am Rev Respir Dis. 1987 Sep;136(3):755-61.
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NHLBI workshop summary. Respiratory disorders of sleep. Pathophysiology, clinical implications, and therapeutic approaches.

Weil JV, Cherniack NS, Dempsey JA, Edelman NH, Phillipson EA, Remmers JE, Kiley JP.

The extensive investigation into complex interactions of breathing and sleep have produced answers to numerous important questions, but it is clear that many of the most important questions in this area remain unanswered. Our understanding of the mechanisms through which sleep alters breathing and how disordered breathing can, in turn, effect sleep is rudimentary. Although a large body of recent work has done much to elucidate the factors that act to maintain the patency of the upper airway during sleep, our understanding of such mechanisms and the relative importance of structure and function in this context remains primitive. A better understanding of these issues will be critical in elucidating the pathophysiology of respiratory disorders of sleep. Although some progress has been made in this area, new insights will be critically important to the design of novel, potentially more effective approaches to treatment. Therapeutic decisions are greatly hampered by major uncertainties regarding respiratory disorders of sleep and the clinical significance of symptoms, signs, and laboratory findings, and their relationship to morbidity and mortality. It seems clear that new information regarding the pathophysiology and natural history of these disorders will be important in the development of new, more effective strategies for therapeutic intervention, and this together with rigorous, systematic evaluation of new and future therapeutic approaches will be critical to clinical progress in this field.

PMID: 3115157 [PubMed - indexed for MEDLINE]