Below is some additional material on Carbon Dioxide, Hyperventilation, and The Buteyko Breathing Method.

Provides information regarding the exact condition that is hyperventilation

Debates the complexity of Carbon Dioxide and its involvement in asthma

Debates the issue of reduced PETCO2 leading to possible hyperventilation

Provides medical definitions of hyperventilation relating to asthma

Discusses the biological effects of respiratory alkalosis

Hyperventilation and Asthma- The link 

By Patrick McKeown

Taken from Appendix Two of the book Asthma Free Naturally

At this point, it's reasonable to ask if there is any evidence available from Western medical experts that helps to clarify the link between hyperventilation and asthma.

A number of scientific and medical papers have been written that prove hyperventilation plays a predominant role in the onset of asthma symptoms. Some experts have argued that asthma symptoms arise because of a loss of carbon dioxide while others cite additional effects of hyperventilation such as water and/or heat loss from the airways. More significant is the existence of a number of studies and papers in the Western world that support the premise of Buteyko's theory.

In an article entitled Hyperventilation Syndrome and Asthma, Demeter notes: Hyperventilation whether spontaneous or exercise induced, is known to cause asthma.1

His study shows that a large number of patients with hyperventilation syndrome also had asthma, and that treatment by bronchodilating drugs and explanation proved to be highly effective in reducing symptoms. The paper lists a number of symptoms of hyperventilation, including chest tightness, dyspnea (difficult breathing), palpitations, dizziness and others with which most asthmatics will be familiar.

Furthermore, Demeter states that these symptoms are the result of hyperventilation rather than its cause. Demeter possibly offers an explanation as to why hyperventilation syndrome receives very little attention in the treatment of asthma. Firstly, he explains that it is very difficult to make a diagnosis of hyperventilation in laboratory tests and secondly no mention is made of any link between hyperventilation syndrome and asthma.1

For a paper by Elshout et al which was published in the highly respected medical journal Thorax, a study was done to determine what happens to airway resistance when there is an increase of carbon dioxide (hypercapnia) or a decrease (hypocapnia).2 Altogether, 15 healthy people and 30 with asthma were involved. It was found that an increase of carbon dioxide determined by measuring end tidal CO2 resulted in a significant fall in airway resistance in both normal and asthmatic subjects. This simply means that an increase of carbon dioxide caused the airways to become less restricted, resulting in a reduction of asthma symptoms.

On the other hand, a carbon dioxide decline did have a negative effect on the airways of asthmatic subjects, but led to no change in the healthy persons. The conclusion drawn was that hypocapnia may contribute to airway obstruction in asthmatic patients, even when water and heat loss is prevented.2

So while a loss of carbon dioxide has no affect on individuals without asthma, it does cause airway obstruction leading to asthma symptoms among those with asthma.

In another paper, entitled The mechanism of bronchoconstriction due to hypocapnia in man, Sterling writes that hypocapnia (loss of carbon dioxide) due to voluntary hyperventilation in man causes increased resistance to airflow.

Furthermore, when subjects inhaled an air mixture containing five per cent carbon dioxide bronchoconstriction was prevented, indicating that it had been due to hypocapnia, not to mechanical factors associated with hyperventilation3

The following is a quotation from a paper entitled Demonstration and treatment of hyperventilation causing asthma: Hyperventilation, leading to airways cooling, will cause bronchoconstriction in vulnerable individuals but, because attacks of asthma are accompanied by hyperventilation of physiological origin, the role of hyperventilation in causing asthma attacks may be overlooked.

In the study, a twenty-year-old man with a lifelong history of asthma was taught breathing exercises over a period of five sessions of thirty minutes each over five months. The patient resumed physical activities and became capable of performing levels of exercise never previously achieved.

The article concludes that this case demonstrates that training in controlled breathing can help patients who hyperventilate to avoid some attacks of asthma.4

We already know that when hyperventilation occurs over a small period of time, it's not a problem. In this situation, the respiratory centre senses the decrease of carbon dioxide and so automatically reduces or stops the breathing process to enable it to restore to preset levels. In this situation therefore, hyperventilation is only a short-term phenomenon.

However, if overbreathing is prolonged over a long period of time, physiological changes occur in the body resulting in hyperventilation becoming a more permanent state

Let's amalgamate this with Buteyko's theory. The lifestyle of modern man increases breathing volume which in turn causes a loss of carbon dioxide, resulting in asthma for persons genetically predisposed.

As increased respiratory volume is a common symptom of an attack, asthma plays a role in increasing hyperventilation and therefore symptoms. Simply because an asthma attack can occur over a relatively long period of time, the respiratory centre can become used to accepting a lower level of carbon dioxide. In turn, this leads to increased breathing volume over the long term.One feeds the other; hyperventilation leads to an increased breathing volume, and this in turn leads to further hyperventilation.

Another area not altogether separate from prolonged hyperventilation is that of exercise-induced asthma [EIA]. Exercise-induced asthma affects up to ninety per cent of asthmatics. While the main theories explaining EIA are water loss or cooling of the airways, 7, 8, 9 Buteyko and others 2, 12 cite loss of carbon dioxide.

On commencement of physical exercise, the volume of breathing increases. The airways are therefore required to condition a greater volume of air and this causes the dehydration and cooling effect which plays a primary role in producing asthma symptoms. According to Anderson, the greater the volume of ventilation, the greater the loss of water and cooling of the airways and so the greater the severity of bronchoconstriction.

It is interesting to note that similar effects to EIA can be reproduced by voluntary hyperventilation. In other words, asthmatic symptoms similar to those caused by exercise can be produced by taking in large volumes of air through the mouth over the course of a few minutes. 11, 12, 13

Therefore, it can be accepted without question that the volume of air inhaled and the condition of this air plays a noteworthy role in producing symptoms. It is also logical to state that the airways become dryer and cooler with a greater volume of air passing through. This is not just solely applicable to people undergoing exercise; it also relates to the volume of air inhaled during rest.

So how does this relate to Professor Buteyko's work?

In summary, prolonged hyperventilation causes a resetting of the body's acceptable level of carbon dioxide, allowing the respiratory system to maintain chronic overbreathing. This larger volume of breathing is the primary element in producing asthma symptoms. Therefore, breathing exercises aimed at reversing hyperventilation should have a vital role in reducing asthma symptoms.

Quite simply, the more you reverse your overbreathing, the greater the improvement to your asthma. Your control pause will indicate the extent of the correction of your breathing. At forty seconds, your breathing will be corrected and asthma will not be presenting any symptoms. It is as simple as that.

The role of carbon dioxide in causing asthma has often been a contentious issue among medical professionals, and it is very difficult to prove. Carbon dioxide can be a difficult gas to measure and some methods involve considerable medical risk, such as puncturing an artery. More commonly, carbon dioxide is measured by an instrument called a capnograph.

A capnograph measures the amount of carbon dioxide in exhaled air, which is equal to the content within the lungs. However, for the following reasons, the measurement of end tidal carbon dioxide is not as straightforward as it would seem:

Apart from the evidence documented above, along with positive verbal feedback from many thousands of people worldwide, there is anecdotal evidence which may prove helpful in demonstrating the link between asthma and over-breathing.

For example, why would asthma get worse following a long period of time talking; fits of laughter; a stressful period; a large meal; a night sleeping with the mouth open; being in a stuffy warm environment, or blowing into a peak flow meter or Spirometry a number of times? Quite simply, all of these cause over-breathing and over-breathing causes asthma symptoms.

 

It's accepted that swimming is a very beneficial exercise for people with asthma. It's known that the maximal breathing volume per minute is lower during swimming than during other sports such as running or cycling.19, 20, 21 While the effect of reduced asthma symptoms is primarily believed to be due to the inhalation of warm air,19, 20 the role of carbon dioxide can offer a realistic explanation. For example, if inhaling warm air is beneficial, then remaining in the shower under hot water for an hour each day may help to reduce attacks. A more plausible explanation is that during swimming, reduced breathing results in an increase of carbon dioxide causing bronchodilation.Unfortunately swimmers are not aware of this link and may spend the rest of their day overbreathing or worse ...mouth breathing.

Late onset asthma is becoming more common among women and it usually occurs following a stressful period. While a person may be overbreathing for their entire life, the additional increase of breathing due to a stressful event can push their carbon dioxide levels to fall and asthma is activated as a defence mechanism. The respiratory centre becomes set at this lower level of carbon dioxide and so breathing is maintained at a high and unhealthy volume. 

The incidence of asthma increases relative to modern affluence. This is due to the changes in our lifestyle; it isn't anything to do with our genetic make-up, because this takes thousands and millions of years to evolve. What we call modern civilization culminates in a greater consumption of processed foods, overeating, over-clothing, stress and lack of physical activity. All of these factors contribute to over-breathing and are common in countries with the highest incidence of asthma.

Why do some children grow out of asthma and others don't? Again, Buteyko Breathing can offer a possible explanation for this. Some children automatically and unconsciously reduce their breathing. Those who don't continue to have asthma into adulthood.

Doctors used to recommend breathing into and out of a brown paper bag to stop an asthma attack. While this is not an altogether safe practice, it's based on the concept of restoring the carbon dioxide level to dilate the airways. This is based on the same Buteyko Breathing concept...the restoration of CO2 levels. Buteyko breathing, however, relies on natural accumulation of carbon dioxide by reduced breathing and so is therefore safer.

GREGORY J. MAGARIAN MD; DEBORAH A. MIDDAUGH MD, and DOUGLAS H. LINZ MD, Portland

Topics in Primary Care Medicine Diagram Omitted. Please refer to source for complete article.

"Topics in Primary Care Medicine" presents articles on common diagnostic or therapeutic problems encountered in primary care practice. Physicians interested in contributing to the series are encouraged to contact the series' editors. --BERNARD LO, MD, STEPHEN J. McPHEE, MD Series' Editors

Refer to: Magarian G J, Middaugh DA, Linz DH: Hyperventilation syndrome: A diagnosis begging for recognition (Topics in Primary Care Medicine). West J Med 1983 May; 138:733-736. From Ambulatory Care and Medical Services, Veterans Administration Medical Center, and the Division of General Medicine, Department of Medicine, Oregon Health Sciences University, Portland. Supported in part by HEW grant No. 1-028-PE10051-02. Reprint requests to Gregory J. Magarian, MD, Ambulatory Care Service (llC), Veterans Administration Medical Center, Portland, OR 97207.

Beginning with the American Civil War, military physicians seeing soldiers under the stress of combat have described a syndrome characterized by breathlessness, lightheadedness or dizziness, pronounced fatigue and exercise intolerance, numbness and paresthesias and chest pain. Rarely have organic diseases been found to account for the symptoms in such cases, yet despite reassurance, symptoms commonly persist for prolonged periods despite removal from the apparent stress setting. This syndrome has been given many names including irritable heart, soldier's heart, Da Costa's syndrome, effort syndrome, neurocirculatory asthenia and, more recently, hyperventilation syndrome.

Since the original descriptions in soldiers, it is now recognized that hyperventilation occurs in many persons under stresses of daily living. It is manifest not only in those overtly stressed, anxious and depressed but also in those who appear outwardly calm as they "bottle up" their feelings, often because of undeveloped or lack of acceptable emotional outlets. Physicians and lay persons alike readily recognize acute hyperventilatory attacks occurring under acute stress. However, chronic or recurrent hyperventilation problems often are unrecognized probably for a variety of reasons, including the frequent lack of obvious overbreathing, a tendency to focus on one or two complaints that alone are not particularly suggestive of hyperventilation, minimal discussion of the topic in medical school and cursory coverage in medical textbooks.

Although precise delineation of the relationship between physiologic responses and symptoms of hyperventilation is lacking, an understanding of known physiologic mechanisms does provide insight (Table 1). Hypocapnea and respiratory alkalosis develop rapidly upon onset of hyperventilation and can easily be maintained indefinitely, by nearly imperceptible hyperventilation, such as by taking an occasional deep breath while maintaining a normal respiratory rate. Without knowing this, physicians may directly observe the subtle, chronic form of hyperventilation without recognizing it or, upon considering the diagnosis, inappropriately reject it because the anticipated hyperventilatory respiratory pattern is not present.

Hypocapnic, respiratory alkalosis Hyperadrenergic state Increased oxygen binding to hemoglobin (Bohr effect) Hypophosphatemia Initial vasodilatory, later vasoconstrictive cardiovascular responses Reduced cerebral perfusion Possible coronary vasospasm

Stress is often associated with a hyperadrenergic state that is known to provoke hyperventilatory responses in humans. Beta-blocking drugs may reduce not only stress levels but also ventilatory responses to catecholamine stimulation and have recently been shown to improve performance levels in stressful situations.

Respiratory alkalosis increases the avidity of oxygen binding to hemoglobin such that oxygen becomes less readily released to tissues (the Bohr effect). Hypophosphatemia develops rapidly and persists for the duration of respiratory alkalosis, probably related to intracellular shifts of phosphorus. With persistent hyperventitation, hypophosphatemia would impair generation of 2,3-diphosphoglycerate (2,3- DPG), further reducing oxygen availability for tissue utilization.

It is estimated that a 2 percent reduction in cerebral blood flow occurs for every decline of 1 mm of mercury in arterial carbon dioxide tension. This, along with the Bohr effect, leads to reduced cerebral oxygenation. Cerebral hypoxia, however, produces a vasodilatory response that may compensate for the initial reduction in cerebral perfusion.

Cardiovascular responses are variable and seem to be in large part related to the duration of hyperventilation. The initial response is a reduction in systemic vascular resistance and blood pressure with an increase in heart rate and cardiac output. Within four to seven minutes of sustained hyperventilation, however, this response diminishes or disappears.

Finally, several investigators have shown coronary vasoconstriction induced by hyperventilation in some patients with Prinzmetal's angina and others with fixed coronary occlusive disease.

How does the hyperventilation syndrome develop? Although hyperventilation may have organic or physiologic causes, the syndrome of hyperventilation is usually associated with emotional triggers and thoracic breathing tendency. Indeed, many persons who are anxiety-laden, stressed or depressed have hyperventilatory breathing patterns and complain of their inability to obtain satisfying deep breaths. Anxiety, anger and other emotions produce increases in both rate and depth of respirations probably mediated by a hyperadrenergic state. Once hyperventilation is initiated, persisting stresses of everyday living or the stresses of new bothersome symptoms from hyperventilation create the potential for a self- perpetuating cycle of chronic hyperventilation

Persons who hyperventilate more commonly exhibit obsessional behavior, excessive body consciousness, phobias, feelings of inadequacy and maladjustments in many stages of life. Lum believes that an exaggerated tendency to breathe using thoracic musculature is an important factor allowing for the development and, once developed, the persistence of the hyperventilatien syndrome.

Among the most difficult and frustrating. patients for physicians are those with multiple complaints involving many organ systems who, despite seeing numerous physicians, fail to obtain a satisfactory explanation or relief from their symptoms. They often have a "positive review of systems." After numerous physicians have been seen and multiple diagnostic tests have been done, which have excluded organic disorders, such patients are often dismissed as having nothing wrong with them or having a severe neurosis, anxiety, depression, hypochondriasis or hysteria, despite the persistence of symptoms that may be disabling in their work and other aspects of everyday living. Unfortunately, this scenario continues to be a common occurrence and is the frequent setting in which the hyperventilation syndrome is recognized, months or years after its onset. Previous studies have shown that 5 percent to 10 percent of patients seeking care from primary care physicians have at least some complaints related to hyperventilation.

Weakness, fatigue, sleep disturbances, blurred vision

PSYCHIATRIC Anxiety, depression, phobias, feeling far away, sensations of unreality

NEUROLOGIC Paresthesias in extremities or periorally, lightheadedness, dizziness, disorientation, impaired thinking, seizures, syncope, headaches

CARDIOLOGIC Palpitations, chest pain

RESPIRATORY Dyspnea often without provocation characterized as being unable to take a satisfying deep inspiration, exaggerated thoracic breathing, sighing, yawning

GASTROINTESTINAL Dry mouth, bloating, belching, flatulence

MUSCULAR Cramping, spasm, musculoskeletal chest wall pain (chest wall syndrome)

The hyperventilation syndrome may be associated with a myriad of symptoms (Table 2), affecting both men and women equally. The most frequent complaints for which medical attention is sought are lightheadedness or dizziness, dyspnea and chest pain. Substantial weakness, exercise intolerance, fatigue and peripheral or perioral numbness and tingling, occurring in isolation or in concert with other hyperventilatory symptoms, are almost always present. Many patients have multiple other complaints. When symptoms are taken in isolation, the syndrome is often not considered. However, when taken together, the entire symptom complex often makes the diagnosis rather obvious.

The dizziness of hyperventilation may be described as lightheadedness or an unsteady, giddy feeling, similar to drunkenness or vertigo. In one review of 104 patients who presented to a specialty clinic for the evaluation of dizziness, 23 percent had hyperventilation as the sole or prominent contributing factor. There may also be some degree of disorientation and mental impairment.

Breathlessness is a common complaint and is usually described as the inability to inhale a satisfyingly deep breath. It may be manifested by periodic, predominantly thoracic deep breaths, sighing and yawning. Sighing dyspnea is not a manifestation of cardiac failure. Although the hyperventilation syndrome rarely is associated with an obvious increase in respiratory rate, astute observers usually will note an increase in thoracic respiratory efforts. Paradoxically, whereas many people take deep breaths in an effort to relax, they may be provoking the very state they wish to avoid. The dyspnea of the syndrome may arise from fatigued respiratory muscles, overworked from chronic, excessive respiratory efforts. Since this type of dyspnea rarely occurs in the absence of other related symptoms, it is important that other manifestations of the hyperventilation syndrome be sought in all cases of otherwise unexplained dyspnea.

Gastrointestinal manifestations include dry mouth, bloating, belching and flatulence, related to aerophagia associated with overbreathing. Depression with attendant anorexia and weight loss may mimic systemic disease.

Cardiovascular symptoms of the syndrome are primarily palpitations and chest pain, which may mimic angma. Continuous ambulatory electrocardiographic monitoring of hyperventilators has shown frequent sinus tachycardia and supraventricular arrhythmias, even during sleep. Hyperventilatory symptoms without apparent provocation may occur during these times.

The chest pain of hyperventilation is variably described. It may be sharp and stabbing, thought to be related to pressure on the diaphragm from gastric distention or diaphragmatic hypertonicity related to a generalized hypertonic muscular contractile state. Other types of chest pain have features that may strongly suggest angina including location and radiation patterns. The pain may be described as dull, gnawing, burning or constricting and localized to the precordial or retrosternal area but is often rather diffuse and of greater duration than is typical of angina pectoris. It is not predictably associated with events that usually provoke angina, frequently occurring at rest or after exertion, and is not reliably relieved by nitroglycerin. Occasionally, "pseudoischemic" electrocardiographic patterns may be seen in patients with chest pain from hyperventilation. It currently remains uncertain whether hyperventilation- induced coronary vasospasm and myocardial ischemia contribute to the chest pain associated with the hyperventilation syndrome. Unfortunately, a diagnosis of noncardiac chest pain, while initially gratifying, usually does not result in a significant reduction in outpatient clinic or emergency room visits as symptoms often persist. Therefore, in evaluating chest pain, the historical data base should include questions directed toward the possibility of hyperventilation lest the etiologic basis of the chest pain be dismissed as noncardiac, yet unrecognized as hyperventilatory.

Other symptoms of hyperventilation are usually present but rarely offered voluntarily. Apart from other disorders the patient may have, the physical examination is often normal. Patients often do not appear overtly anxious though they are frequently depressed. Obvious hyperventilation is usually lacking although occasional deep breaths, sighing or yawning and palpable chest wall tenderness may be noted. The diagnosis of chest wall syndrome requires exclusion of the hyperventilation syndrome which may be its basis. It is critical to recognize that the presence of the syndrome does not exclude the presence of an organic disease. In fact, reaction to the symptoms of an organic disease may be a prime factor provoking hyperventilation.

Management of Hyperventilation Syndrome As many patients with the syndrome have had symptoms for months or years and have seen other physicians without appreciating the cause of their symptoms, it is important that the patient be confronted with the cause-and-effect relationship between hyperventilation and their symptoms. A hyperventilatory trial is crucial for therapeutic success. This can be accomplished by having the patient breathe deeply at a rate of 30 to 40 times per minute. Most patients with the hyperventilation syndrome will recognize at least some of their symptoms within several minutes and often in seconds. This recognition and subsequent explanation of hyperventilation greatly enhances the potential for improvement. An explanation and reassurance without the patient actually experiencing the cause-and- effect relationship of overbreathing at the time is often without therapeutic benefit.

After provocation of symptoms .during a hyperventilatory trial, breathing into a lunch bag-sized brown paper bag will result in resolution of those symptoms that are directly related to hypocapnea. Dyspnea and chest pain, however, may persist in that they are not caused by hypocapnea, but more likely by the excessive use of thoracic musculature.

Because many patients have experienced substantial adverse effects on their employment and social interactions it is beneficial for a spouse or a friend to be present during a hyperventilation trial. Family and friends may be highly skeptical that something as simple as overbreathing can be having such devastating effects on the patient and indirectly upon them as well. Convincing both the patient and others provides support for the patient as he or she attempts to regain control.

Although some believe bag rebreathing is of little value, we have found it to be useful, allowing patients an escape from symptoms. Initially, we encourage patients to attempt bag rebreathing, relax and get away from the situation that may have triggered the response. As a result, patients appreciate a newfound control. This greatly reduces the anxiety and stress that fuel the hyperventilation cycle.

Long-term control may be achieved by relaxation therapy and retraining patients to become diaphragmatic rather than thoracic breathers. Referral to behavior modification experts may be of value in particularly difficult patients with long-standing symptoms. In anxious and depressed persons with chronic hyperventilation we have rarely seen substantial benefit from the use of anxiolytic or antidepressant medications when the hyperventilatory component was unrecognized or being inadequately addressed. in conjunction with therapeutic measures directed toward the hyperventilatory tendency these drugs may be of additional benefit though we often find them unnecessary.

GENERAL REFERENCES Evans DW, Lure LC: Hyperventilation: An important cause of pseudoangina. Lancet 1977; 1: 155-157 Heistad DD, Wheeler RC, Mark AL, et al: Effects of adrenergic stimulation on ventilation in man. J Clin Invest 1972; 51:1469-1475 Lary D, Goldschlager N: Electrocardiographic changes during hyperventilation resembling myocardial ischemia in patients with normal coronary arteriograms. Am Heart J 1974; 87:383-390 Lurm LC: Hyperventilation: The tip of the iceberg. J Psychosom Res 1975; 19:375-383 Magarian GJ: Hyperventilation. syndromes: Infrequently recognized common expressions of anxiety and stress. Medicine 1982; 61:219-236 Pfeiffer JM: The aetiology of the hyperventilation syndrome. Psychother Psychosom 1978; 30:47-55

On May 9, 1794, during the Reign of Terror, Antoine-Laurent Lavoisier died by the guillotine. This event closed the first and greatest chapter in the physiology of carbon dioxide: for the principle of the production of carbon dioxide and its relation to oxygen in fire and the in life which Lavoisier had discovered shortly before his death was, and still is, the most fundamental of all contributions to knowledge in this field. Truly, as his colleague Lagrange said:"It took but a moment to cut off a head, the like of which a hundred years may not reproduce."

Likeness of Life to Fire.-Lavoisier's supreme contribution to science, and particularly to physiology was the demonstration that, in their broad outlines, combustion in a fire and respiratory metabolism in an animal are identical. Both consist in the union of oxygen from the air with carbonaceous material: and both result in the liberation of heat and the production of carbon dioxide.

Carbon dioxide had, indeed been discovered previously by Black in 1757, and oxygen had been described by Mayow, Scheele and Priestly. But it was Lavoisier who first showed the part played by oxygen and the process by which carbon dioxide is produced.

A century later the standard textbook of physiology in the English language was that of Sir Michael Foster of Cambridge University. This book supplied the early training of many of the physiologists who during the past 35 years have contributed to the development of respiration and to the increasing recognition of the part played in the economy of the body by carbon dioxide. The facts and conceptions presented by Foster show, therefore both the advance of 100 years from Lavoiser and the starting point of modern investigation. If the first chapter of the physiology of carbon dioxide was contributed by Lavoisier and closed with his death, the second chapter is presented by Foster, and is nearly coextensive with the 19th century; which the third chapter, with which this paper will chiefly deal, is the product of the generation that has done its experimental work in the first 3 decades of the 20th century, and from its theoretical results is now making valuable contributions to clinical medicine and surgery, and particularly to therapeutics.

Contrast Between Life and Fire.--- The most important advance in the physiology of respiration as presented by Foster, beyond the conception left by Lavoiseir, was that the oxidation in living matter, although like a fire in materials and products, is profoundly different in its process and control. If a fire is supplied with pure oxygen instead of air, it burns with enormously augmented intensity. But when a man or animal breathes oxygen, or enriched with oxygen, no more of that gas is consumed, no more heat is produced and no more carbon dioxide is exhaled than when air alone is breathed. Although clinicians still find it hard to believe, oxygen is in no sense a stimulant to living creatures. It is merely en essential food; it is a food of which the body cannot be induce to take more , or to get along on appreciably less, than its own interior regulation determines according to its needs. Even in rarefied air, or in cases of heart disease—conditions in which a man may suffer severely from the deficient supply of oxygen—the body actually consumes practically a normal amount. The asphyxial symptoms are the expression of the strain on the body to obtain this amount. It gets it, or it dies.

Lavoiser had supposed that the vital combustion must occur in the lungs where the inspired air comes in contact with the blood. Spalanzani, the Italian physiologist, soon recognized, however, that in fact the oxidation does not occur in the lungs: it is in the tissues, to which oxygen is transported by the blood. That such is the fact was proved by Magnus, a German physiologist, who first extracted the gases from blood by means of the vacuum pump and showed that arterial blood contains more oxygen and less carbon dioxide than does venous blood. Then Hoppe-Seyler, one of the first of the biochemists, separated hemoglobin, the coloring matter of the red blood corpuscles, in the form of pure crystals, and showed that this substance forms a loose chemical compound with oxygen. Hemoglobin is the means by which the blood transports oxygen.

Blood Alkali as Carrier of Carbon Dioxide . ---- Later, in the 19th century, Zuntz, in Berlin, recognized that carbon dioxide, unlike oxygen, is not carried by hemoglobin, but that hemoglobin is nevertheless an essential factor in the transportation of this gas but the blood. He showed that in the blood carbon dioxide is combined with bases, chiefly as sodium bicarbonate. He thus demonstrated, for the first time, what is now generally, but rather unwisely, called the "alkaline resevere." It were better to call the bicarbonates of the plasma the "alkali in use"; the true reserve alkali is combined with hemoglobin and is given off to unite with carbonic acid, or to neutralize stronger acids. As carbon dioxide is given off in the lungs, the amount of alkali thus set free recombines with hemoglobin.

This mode of transportation of carbon dioxide is one of the most extraordinary features of the blood and respiration. The evidence for it rests upon 2 facts demonstrated by Pfluger and others during the great epoch of German physiology in the second half of the 19th century. One of these facts is that the blood plasma, if separated from its corpuscles, will part with little of its carbon dioxide even in the presence of a vacuum. The other fact is that all the carbon dioxide in the plasma, both that in simple solution and that combined with alkali into the bicarbonates, comes off readily if the red corpuscles of the blood are present. Thus, the hemoglobin of the red corpuscles, by supplying or recombining with alkali, dominates the capacity of the plasma to transport carbon dioxide; it thus enables the blood to take up this gas in the tissues and to give it off in the lungs under very slight differences of pressure. Meanwhile, another problem of primary importance was attracting the attention of investigators: the problems not only of how we breathe, and why, in the sense of the need, by also why, in the sense of the cause and stimuli. It is one of the commonest observations of life that physical exertion, owing to its increased consumption of oxygen and production of carbon dioxide, is accompanied by the breathing of an increased volume of air. The need is evident. But what is the nature of the stimulus and what is the controlling mechanism which together induce this adjustment of the ventilation of the lungs to the respiratory needs of the body? This matter was long debated. Nearly every champion of every shade of opinion for more than 50 years contributed some particle of truth on one phase or another. But every contributor was in error who claimed for any one factor an exclusive control; for breathing is the resultant of many factors.

Nervous and Chemical Regulation of Breathing. ---- The factors thus revealed were 2 main classes: nervous and chemical..Throw a bucket of cold water over a man and he draws one or more deep breaths. Irritate an afferent nerve, causing pain, and he cries out. Tickle his nose or throat and he sneezes or coughs. These are all respiratory reflexes excited by nervous impulses coming to the respiratory center. But more important than any other nervous element in breathing are the vagus nerves whose
may fibers there are some which have endings in the lungs and convey impulses from them to the respiratory center in the medulla oblongata. Through these pathways, as Hering and Breuer showed, each expiratory deflation of the lungs stimulates the center to discharge a reflex to the diaphragm and other respiratory muscles inducing inspiration; and contrariwise, each inspiration induces reflexly an expiration. To this mechanism breathing owes its rhythmic character; or, as an engineer would express it, breathing is a reciprocating mechanism.

Over against this explanation, based upon nervous factors, evidence gradually accumulated indicating a chemical control of respiration. The blood flowing to and through the respiratory center was found to exert a dominating influence upon the activity of breathing. Whenever the blood was rendered venous, the center was stimulated to produce a counteracting increase of the volume of breathing. If, on the contrary, the blood were overventilated in the lungs, the activity of the center ceased for a time and apnea resulted. In this state, the subject neither breathes nor feels any desire to do so.

As this conception of the chemical control of breathing developed, its advocates separated into 2 groups. One held that it is primarily the degree to which the blood is oxygenated which influences the respiratory center and controls its activity. The other presented evidence indicating that is rather the amount of carbon dioxide in the blood which is the determining factor. In this matter also both sides of the controversy contributed experimental facts of value and each was in part correct. Respiration is,
indeed, influenced fundamentally by the oxygen pressure to which the individual is acclimatized: a pressure which depends upon the elevation of his home above sea level. But acclimatization to altitude is very slow, requiring days or weeks. It is only under conditions of sudden extreme oxygen deficiency, verging on asphyxia, or after intense muscular exertion, that respiration is stimulated—in fact, as we shall see later, over stimulated—by an urgent demand for oxygen.

On the other hand, nature provides that in a healthy man or animal, except under intense exertion, the oxygen supply is always ample and its influence upon breathing is therefore, under normal conditions relatively slight. It is the variations in the amount of carbon dioxide produced n bodily rest and exercise that afford the stimulus inducing the adjustments of breathing to the varying energy needs of the body. Foster, in his book above referred to held that the evidence then available indicated that oxygen is a

more important control than carbon dioxide. But even as early as 1885, Miescher, a Swiss physiologist, in a paper that is one of the masterpieces of physiology, had summarized all the evidence then available and reached the conclusion that it is the variations in the amount of carbon dioxide which principally induce the immediate adjustments of respiration. In a classic phrase inspired by the insight of genius he wrote: "Over the oxygen supply of the body carbon dioxide spreads its protecting wings."

He died before he could complete his work and his death may be said to have closed the second chapter in the history of respiration and the functions of carbon dioxide in the body.

The Breath of Life.---- The first 3 decades of the present century have witnessed an extraordinary reversal of standpoint and increase of interest in regard to the functional importance of carbon dioxide in the animal body. Moreover, discoveries in this field, which were initially purely scientific and theoretical, are now finding a wide range of clinical applications for the alleviation of suffering and the saving of life.

Before considering these matters, it will be best that the mind be cleared of certain deep rooted misconceptions that have long opposed the truth and impeded its applications. It will be seen that carbon dioxide is truly the breath of life.

The human mind is inherently inclined to take moralistic view of nature. Prior to the modern scientific era, which only goes back a generation or two, if indeed it can be said as yet even to have begun in popular thought, nearly every problem was viewed as an alternative between good and evil, righteousness and sin, God and the Devil. This superstitious slant still distorts the conceptions of health and disease; indeed, it is mainly derived from the experience of physical suffering. Lavoisier contributed unintentionally to this conception when he defined the life supporting character of oxygen and the suffocating power of carbon dioxide. Accordingly, for more than a century after his death, and even now in the field of respiration and related functions, oxygen typifies the Good and carbon dioxide is still regarded as a spirit of Evil. There could scarcely be a greater misconception of the true biological relations of these gases.

PHYSIOLOGY.-----Relations of Carbon Dioxide and Oxygen in the Body.---- Carbon dioxide is, in fact, a more fundamental component of living matter than is oxygen. Life probably existed on earth for millions of years prior to the carboniferous era, in an atmosphere containing a much larger amount of carbon dioxide than at present. There may even have been a time when there was no free oxygen available in the air. Even now, such animals as ascaris will live and be active in an atmosphere of hydrogen and entirely without oxygen. In vertebrates, the process of muscular contraction is fundamentally anaerobic.

A frog's muscle will contract effectively and repeatedly under suitable stimulation in an atmosphere of pure nitrogen. In contraction, a muscle produces lactic acid, partly by reconversion into sugar. In other words, oxygen is not one of the primary factors in muscular work. The reserve store of oxygen in the body is small. Vigorous breathing does not take place before an exertion; the exertion is first made and then the oxygen needed to clear the system in preparation for another exertion is absorbed. The demand for oxygen for this scavenging of waste and restoration of power is termed by A.V. Hill the "oxygen deficit" of exercise.

On the other hand, present knowledge indicates that carbon dioxide is an absolutely essential component of protoplasm. It is one of the factors in the balance of alkali and acid for the maintenance of the normal pH of the tissues. Acapnia, that is diminution of the normal content of carbon dioxide, involves therefore, a disturbance of one of the fundamental conditions of life.

Another natural, but very obstructive misconception is that oxygen and carbon dioxide are so far antagonistic that in blood a gain of one necessarily involves a corresponding loss of the other. On the contrary, although each tends to raise the pressure and thus promote the diffusion of the other, the 2 gases are held and transported in the blood by different means; oxygen is carried by the hemoglobin in the corpuscles, while carbon dioxide is combined with alkali in the plasma. A sample of blood may be high both gases, or low in both gases. Moreover, under clinical conditions low oxygen and low carbon dioxide—anoxemia and acapnia—generally occur together. Each of these abnormal states tends to induce and intensify the other. Therapeutic increase of carbon dioxide, by inhalation of this gas diluted in air, if often the effective means of improving the oxygenation of the blood and tissues. Under such conditions of acute deprivation of oxygen as those in carbon monoxide asphyxia, the body suffers from an excessive elimination of carbon dioxide: and the restoration of carbon dioxide is in itself helpful. In a drowned man or a non-breathing newborn child, the deprivation of oxygen does not cause and excess of carbon dioxide. On the contrary, in the absence of oxygen, lactic acid and other primary decomposition products of the tissues acannot be converted into carbon dioxide; for that conversion oxygen is necessary. The saying of Miescher, quoted at the end of a previous section, has therefore, a depth of truth and breadth of application greater than he could possibly have realized.

As a factor in the Acid-base Balance of the Blood.---- Modern physiology has shown that, in addition to the control and regulation exerted by the nervous system, there are many chemical substances produced in the body that influence function and form. To these active principles Starling gave the name of "hormones." Among the hormones are epinephrine ( often called adrenaline), pituitrin, thyroxin, insulin and many other products of the glands of internal secretion and other organs. Carbon dioxide is the chief hormone of the entire body; it is the only one that is produced by every tissue and that probably acts on every organ. In the regulation of the functions of the body, carbon dioxide exerts at least 3 well defined influences: (1) It is one of the prime factors in the acid-base balance of the blood. (2) It is the principal control of respiration. (3) It exerts an essential tonic influence upon the heart and peripheral circulation.

In recent years, an extensive literature has grown up on the subject of the so-called "alkaline reserve," the acid-base balance, and the pH or hydrogen ion concentration of the plasma. There have also appeared many investigations and discussions of the real or assumed relations of these features of the blood to clinical acidosis and alkalosis. In the complicated adjustments of the physico-chemical equilibrium in the blood, carbon dioxide is, more than any other factor, subject to disturbance by every variation in bodily activity or heat production; but it is also that factor which is most immediately readjusted. The automatic reactions which effect this readjustment are the increase or decrease of the volume of breathing. This volume depends upon the depth more that the rate of respiration; or rather, it is the product of depth and rate. It determines the degree of the ventilation of the blood as its passes through the lungs. Normally, it is so adjusted that the carbon dioxide in the alveolar air of the lungs is maintained at a partial pressure of a little more that 5% of an atmosphere. This amount of carbon dioxide gas in the alveolar air produces exactly that amount of carbonic acid in solution in the blood needed to balance the normal amount of alkali and thus to induce and maintain normal pH. This is the principle expressed by the equation of L.J. Henderson:

If, however, because of some disturbance of the function of the kidneys or other organs, the blood alkali in use is not of normal amount, the pH of the blood would also be rendered abnormal, except for the counteracting control of respiration over the carbon dioxide in the alveolar air and thus over the carbonic acid in solution in the blood. Whenever the blood alkali is lower than normal, respiration increases and maintains a more vigorous pulmonary ventilation. The object and effect of its augmentation are that alveolar carbon dioxide is mixed with more fresh air and diluted. Consequently, the carbonic acid of arterial blood-pressure is decreased proportionally. This is the explanation of the increased respiration occurring in the acidosis of acute nephritis and in diabetic coma, and developing into air hunger as death approaches: an increase of respiration is the natural compensation for a decrease of blood alkali. On the other hand, if the amount of carbon dioxide is deficient simultaneously with a normal or excessive blood alkali, respiration is decreased or fails entirely. These respiratory reactions depend upon the relating influence of carbon dioxide in its chemical balance with the blood alkali; for, if the carbon dioxide and alkali are even slightly out of balance, the respiratory center is powerfully stimulated or depressed.

Whether the physiological reactions to carbon dioxide are due directly to a specific effect of this substance, or rather to the pH of the blood and of other humors in which carbon dioxide is an important factor, is still under active investigation. It is, however, noteworthy that the existence of these reactions renders invalid much of the now prevalent conception of the chemistry of clinical acidosis and alkalosis. It is not correct chemistry or physiology to infer that, because the amount of the alkali in use is
high or low, the pH of the blood must be correspondingly affected. A high or low blood alkali needs merely a corresponding affected. A high or low blood alkali needs merely a corresponding decrease or increase of the volume of breathing for its compensation to afford an normal pH. If, therefore, in nephritis or diabetes or other disorders, the pH is really abnormal and the blood actually becomes even slightly more acid or more alkaline than normal. There must be some disturbance of the respiratory regulation of the alveolar carbon dioxide as yet not understood. A normal regulation of the carbon dioxide pressure is adequate to compensate either a high or a low blood alkali in practically all conditions compatible with the continuance of life.

The part normally played by the kidneys and the influences of abnormal conditions and processes in them in other organs in determining the amount of alkali in use in the blood, both in health and in such disorders as diabetes and clinical acidosis and alkalosis, are beyond the scope of this article. The problems which these matters present are, indeed, as yet only incompletely analyzed.

In the Control of Respiration and the Circulation.--- The modern development of the knowledge of the part played by carbon dioxide in the control of respiration began with a classic paper by Haldane and Priestly, entitled "The Regulation of the Lung Ventilation," and was followed by other important papers by Haldane and Douglas. In these papers it was shown by observations on normal men that breathing quite unaffected either by inhalation of oxygen-rich air by such a moderate decrease of oxygen as occurs on first going to an altitude. On the other hand the breathing changes its volume automatically in such close adjustment to the amount of carbon dioxide produced in the body that the alveolar air is kept nearly constant in this respect. Carbon dioxide is the chief immediate respiratory hormone.

A few months after the first paper by Haldane and his collaborators showed the influence of carbon dioxide upon respiration, Henderson had his collaborators began the publication of a long series of papers dealing with the influence of carbon dioxide upon the circulation. They showed that acapnia may induce acute disturbance of the heart and failure of the peripheral circulation. These conditions resemble the functional depression of shock in patients after prolonged anesthesia and major operations. On the other hand it was found that if the carbon dioxide content of the body is conserved by partial rebreathing, the vitality of an animal, even under prolonged and extensive operation and trauma, is but little depressed.

These observations upon the circulation showed also that in animals reduced to a state of shock the carbon dioxide of the blood, or as it now be generally termed, the "alkaline reserve," is greatly reduced. This experimental result was later confirmed by the observations of Cannon upon wounded soldiers during the war.

The observations upon the respiration of animals under a mode of anesthesia that was intentionally made to imitate inexpert administration showed that the failure of breathing which was formerly one of the principal hazards of the operating room is largely due to excessive breathing during the stage of excitement. If, during the initial stage of anesthesia, an excessive elimination of carbon dioxide is induced and then the sensitivity of the respiratory center is depressed by a sight excess of anesthetic, respiration ceases. It does not return until the chemical stimulus of the blood gases and the sensitivity of the respiratory center are sufficiently restored to induce again the natural activity of breathing.

THERAPEUTICS. ----In Anesthesia.--- In 1920, Henderson, Haggard and Coburn carried their observations to the clinic and found that when inhalations of carbon dioxide ( 8% ) in air were administered to patients after major surgical operations under open ether anesthesia, the effects were strikingly beneficial. With the return of deep breathing, the cyanosis then common after anesthesia disappeared. The cutaneous circulation improved. The skin changed in color and temperature, from blue- gray and cold to pink and warm. The volume of the pulse, previously thready, rapidly became full; and arterial pressure was restored to normal. Owing to the increased volume of breathing, the anesthetic (ether) was rapidly ventilated out of the blood and consciousness returned within a few minutes, even after profound anesthesia. Nausea and vomiting were either greatly reduced or entirely absent and after the inhalation the patient dropped off to sleep.

In continuation of these observations, White found that when slow hemorrhage occurs after operations upon the brain, the rate of breathing gradually decreases until death is imminent. In several of such cases life was saved by stimulation of respiration with inhalation of carbon dioxide.

The use of this inhalation has now become general in connection with anesthesia. Nearly every American anesthetic apparatus now has an attachment for a cylinder of carbon dioxide, or of a mixture of carbon dioxide and oxygen. By this means any tendency to failure of breathing on the operating table is counteracted. At the close of the operation, an inhalation of carbon dioxide is given to stimulate respiration and induce rapid elimination of a large part of the anesthetic. By this inhalation a vigorous heart action and the tonus of the peripheral circulation are also restored.

Postoperative Atelectasis and Pneumonia.---Prophylaxis.--- From the use of carbon dioxide for the purposes just described, another even more important application has developed, i.e., the prevention of postoperative atelectasis and pneumonia. Many observers have noted that after major surgical operations, the vital capacity of the lungs is often reduced to as little as one-third of the preoperative volume. The diaphragm may be elevated toward the thorax by several centimeters. In x-ray pictures, this condition of partial collapse of the chest is found to continue to some extent for several days. The position of the thorax is essentially like that which occurs in a normal man for a few minutes after vigorous forced breathing. It is, therefore, a phenomenon of acapnia.

This acapnial position of the thorax may leave considerable parts of the lungs unventilated. The airways to these parts may become obstructed and the occluded air is then absorbed into the blood.

As a result, atelectasis of a lobe, or even a massive collapse of an entire lung, may develop. From this condition, as Coryllos and Birnbaum have demonstrated experimentally, pneumonia may develop, for if pathogenic organisms happen to be present, they find in an atelectatic lung conditions favorable to their growth.

The essential correctness of this conception of the origin of postoperative atelectasis and pneumonia is attest by the prophylactic and therapeutic means that have been found effective to counteract or prevent them. In many surgical clinics in America and Germany, results have been obtained which show that when the inhalation of carbon dioxide is administered to all cases after anesthesia and operation, the lungs are reexpanded, the tonus of the respiratory muscles is restored, atelectasis is prevented, and the risk of postoperative pneumonia is virtually eliminated.

Pneumonia.---The possible benefits of a similar inhalational treatment of medical pneumonia, for example after influenza, arejust now under active investigation. Henderson, Haggard, Coryllos and Birnbaum have shown that in dogs, in which pneumonia has been experimentally induced, the lungs may be cleared and the pneumonia cured by placing the animals in an atmosphere of about 8% carbon dioxide for 12 to 24 hours. In support of the claim that these are real cures is the fact that pneumococci are inhibited in growth or even killed by a lowering of pH no greater than carbon dioxide may induce. A lowering of the pH by carbon dioxide contributes also to the autolysis and liquefaction of the exudate responsible for the consolidation of the lungs in pneumonia. Many cases of pneumonia have now been treated with inhalation of carbon dioxide in oxygen; and a special tent for this treatment is being introduced by Henderson and Haggard. It is believed by those who have used it that this treatment is
decidedly superior to that with oxygen alone.

Asphyxia.---Very similar to the use of carbon dioxide inhalation after anesthesia is the modern treatment of carbon monoxide asphyxia. This form of asphyxia is the cause of many thousands of deaths annually. Its commonest causes are city manufactured gas, which usually contains 20 to 30 % of carbon monoxide, and the exhaust from automobiles. Carbon monoxide forms a combination with hemoglobin which displaces oxygen. The compound is not so firm, however, as was once believed, for the
carbon monoxide may be, in turn, displaced. The oxygen-carrying power of the blood is thus restored. The critical feature of carbon monoxide poisoning is the asphyxia, especially of the nervous system, because of the diminished capacity of the blood to transport oxygen. It seemed, therefore, at first that inhalation of oxygen would be the logical treatment. In practice, however, oxygen alone was found to be much less beneficial than was expected.

Investigating this problem, Henderson and Haggard found that in the development of carbon monoxide asphyxia the victim overbreathes and blows off an excessive amount of carbon dioxide. He thus develops acapnia, as well as anoxemia. On removal from the noxious atmosphere, the victim may exhibit a marked depression of breathing. The administration of oxygen is therefore, only slightly effective; for it is not adequately inhaled.

In experiments on asphyxiated animals these investigators showed that by administering a mixture of oxygen and carbon dioxide the respiration could be so stimulated, and the elimination of carbon monoxide so accelerated, that rapid recovery was induced.In the beneficial results, the relief of acapnia is almost as important as the elimination of carbon monoxide and the restoration of an ample supply of oxygen.

A special form of apparatus, the H-H Inhalator, for the administration of a mixture of oxygen and carbon dioxide to asphyxiated patients was, therefore, devised and has been widely introduced. This treatment has been so successful that many thousands of these inhalators are now in use: several hundred, for instance, in metropolitan New York, and a number corresponding to the population in Chicago and other cities. The rescue crews of the fire and police departments, the gas and electric companies, and now also the hospital ambulances generally have them. At first a mixture of 5% carbon dioxide in oxygen was used, but 7% has proved even more beneficial.

The value of this treatment is not merely for the saving of life, but also for the prevention of such postasphyxial sequelae as pneumonia, injury to the heart, and permanent nervous impairment. In many cases of brief but intense asphyxiation the patient is completely restored within an hour; he may then voluntarily and safely go back to work.

The same treatment is effectively used for resuscitation from a wide range of other noxious gases occurring in industry.

Asphyxia of the Newborn.---Out of this treatment of carbon monoxide poisoning has developed the use of inhalation for the relief of a far more common form of asphyxia: that of the newborn. The story of this development is interesting. In it the men of the rescue crews of the Chicago Fire Department have played somewhat the same part that the milkmaids immune to smallpox did in the discovery of vaccination.

Many times it happened that a physician in Chicago who had seen a resuscitation of a case of carbon monoxide asphyxia had occasion soon after to deliver a baby that would not breathe. After swinging, spanking, and dipping the child in cold and hot water, the accoucheur, unable to induce active, natural breathing, thought to telephone for one of the rescue crews and their inhalator. The ministrations of these men were in many cases so successful that within a couple of years the fire department had developed a considerable practice in this field. With justifiable pride, it claimed the saving of several hundred babies.

When this information came to the attention of the writer it occurred to him that on theoretical grounds inhalation of oxygen and carbon dioxide is exactly the method that should be most effective in combating asphyxia of the newborn. As a result of this discovery, chemical stimulation and support for the depressed respiratory center of the newborn child by inhalation of carbon dioxide is now rapidly replacing the older, and often ineffective, methods of resuscitation depending upon cutaneous stimulation.

Neonatal Pneumonia.---Prophylaxis.--- The lungs at birth are atelectatic. The first cry effects a partial dilation. Later breaths should dilate them further; but the dilation is often incomplete for several days, or even for some weeks. If during this time, pathogenic organisms happen to be present, they find conditions favorable for their growth in any part of the lungs that are still atelectatic. The number of deaths from this cause during the neonatal period is often as high as 4 for each of 100 live births. To forestall this hazard, it has long been the custom to stimulate the child to cry at least once daily. For this purpose some painful stimulus, such as stinging of the soles of its feet with an elastic rubber band, is applied. Experience demonstrates, however, that a premature or weak child may not be adequately stimulated and pneumonia may develop. A more humane, scientific and effective method of inducing dilation of the lungs is the routine administration to all babies during the first week or two of life of 5 or 10 minute inhalations of oxygen and 7 or 8 % carbon dioxide. The mixture is entirely safe for general use by nurses and midwives. Higher concentrations can be used effectively on difficult cases, but preferably only by those who have experience in the use of such concentrations in connection with anesthesia.

Angina Pectoris and Intermittent Claudication.----In most of the applications of inhalational treatment discussed in the foregoing pages the influence of carbon dioxide upon respiration is chiefly involved. The equally important influences of carbon dioxide upon the hear and the peripheral blood- vessels have not as yet been exploited to an equal degree. Henderson and his collaborators showed many years ago that under certain experimental conditions the heart tends to develop a partial tetanus or cramp, and that this condition may be overcome by means of carbon dioxide. They showed also that, owing to the loss of muscular tonus in animals under prolonged anesthesia and operation, the blood stagnates in the peripheral vessels, the venous return to the right heart decreases progressively, and the circulation finally comes to a standstill.

With these considerations as a physiological background, the influence of carbon dioxide inhalation has recently been tried on several cases of angina pectoris. This is not an emergency treatment, but a therapy for prolonged application. It is administered for 10 to 15 minutes at a time 2 or 3 times a day. The method of inhalation is essentially like that applied by Henderson,, Haggard and Coburn, and by White, after anesthesia and operation. As the inhalation consists of carbon dioxide in air, instead of in oxygen, its cost, aside from the control apparatus, is small.

The effects of this treatment are a distinct improvement in the color and temperature of the lips and skin, indicating an effect upon the peripheral circulation somewhat like that of amyl nitrate. Arterial pressure and the pulse rate are not increased, although a markedly fuller circulation is evident. The sense of oppression in the chest and the pain referred to the shoulder and arm is considerably decreased; it may cease altogether for some hours after the inhalation. After some weeks of daily inhalations, the capacity to take moderate exercise is markedly increased.

This inhalation has also been used upon a few cases of intermittent claudication. A marked improvement in the local circulation resulted both under the inhalational and as a cumulative effect of the treatment for some weeks. When it was discontinued , the patients soon relapsed into their previous condition.

Drowning and Electric Shock.--- The accepted treatment of the victims of drowning and electric shock is the Shafer prone pressure method of artificial respiration. Experience has demonstrated that the return of natural breathing is considerably aided and accelerated by the administration oxygen and carbon dioxide from an inhalator, while artificial respiration is being applied. Not only are the lungs thus supplied with a high concentration of oxygen, but the depressed respiratory center is also stimulated by the carbon dioxide to an earlier renewal of neural activity than would otherwise occur.

Catatonia.---Finally, mention may be made of the extraordinary observations reported by the late A.S. Lovenhart, in which he found that inhalation of carbon dioxide to cases of catatonia induced a temporary restoration of intelligence and mental responsiveness. The simplest explanation of the results in these cases is attained by postulating an habitual contraction of blood-vessels in the brain of the catatonic patient, similar to that in the heart and limbs of the cases discussed in the previous section. If this view is correct, the beneficial effects of the inhalation are due to improvement in the circulation in the brain under the influence of carbon dioxide upon the finer blood vessels.

Yandell Henderson,
New Haven, Connecticut

The extensive literature of this subject may be found through the references accompanying the following works: Haldane, J.S.: Respiration, Yale University Press, 1922 Henderson, Y.: Physiological Regulation of the Acid-Base Balance of the blood and Some Related Functions, Physical. Rev. 5:131 ( April) 1925; The Dangers of Carbon Monoxide Poisoning and Measures to Lessen These Dangers, J.A .M.A> 94: 179 ( Jan.18) 1930; Acapnia as a Factor in Post-operative Shock, Atelecasis and
Pneumonia, Ibid. 95: 572 ( Aug.23) 1930; Incomplete Dilation of the Lungs as a factor in Neonatal Mortality, Ibid. 96: 495 (Feb.14) 1931.

Articles and references which support Buteyko's Method and the hypothesis that stands behind it:

James T, Doctors Gasp at Buteyko Success, Australian Doctor, April 1995., Buteyko KP.,Genina VA.,The Results of the Approbation of the BBL Method in the Department of Childrens Disease in the First Moscow Medical Institute of E.M. Sechenov 27.2.81 Ameisen P.J Every Breath you take. Lansdowne. Graham,T, ASTCC Self Management of Asthma through Normalisation of Breathing. Drake,C, The Diverse and Beneficial Effects of Respiratory Reconditioning. Harley Respiratory Clinic 1997 Y. Henderson, Carbon Dioxide,The Cylcopedia of Medicine 1940. Askaanazi, J, Silverberg, PA, Foster RJ, Hyman, AI, Milic-Emil, J and Kinney, J, 1980. Effects of respiratory apparatus on breathing pattern. American Physiological Society. 0161-7567/80/.Blauw. GJ, Westendrop, R G I, 1995. Asthma deaths in New Zealand: whodunit? Commentary in the Lancet, 345, January 7th. Bowler, S, Green, A., Mitchell, C & Graham, T., 1995. Buteyko breathing in asthma: controlled trial. Mater Hospital, South Brisbane, Queensland. Buteyko K.P, 1990 Method: the experience of implementation in medical practice-Kiev, Moscow,, Novosibirsk., Patriot Press, Moscow. Buteyko K.P. The Theoretical Understanding of the Buteyko Method. Kasimov, The Biochemical Analysis of the I.S.D.R. Method. Demeter, SL & Cordasco, EM, 1986. Hyperventilation Syndrome and asthma, The American Journal of Medicine, 81,889-994 Donnelly, P M,1991. Exercise-induced asthma: the protective role of CO

during swimming. The Lancet, 337.179-108 Fried, R.,1990. The breath connection. Plenum Press, New York, p 177 Gardner, W, Orehek J. Grimaud C, Charpin J, 1975. Bronchoconstrictor effects of a deep aspiration in patients with asthma. American Review Respiratory Disease,111:433-439 Graham, T, Stalmatsky, A & Drake C, 1995 The Buteyko asthma breathing technique. The Medical Journal of Australia, 162, Jan 1995. Hibbert C, Pilsbury D, 1988. Demonstration and Treatment of hypevenilation causing asthma. British Journal of Psychiatry, 53;687-689. Hombrey, J, Jacobi, M S, Patil, CP, Saunders, KB, 1988. CO

response and pattern of breathing in patients with symptomatic hyperventilation compared to asthmatic and normal subjects, European Respiratory Journal, 1, 846-852. Selroos O. et al, 1988. Effects of Early vs Late Intervention with Inhaled Corticosteroids in asthma. Chest, 108,1228-1234 Stalmatsky, A.,1993 (pers comm.) Buteyko Breathing Practitioner Training. Rama, Ballentine R, Hymes A The Science of Breath, The Himalayan Institute Press. Stiller K et al, (1994) The effects of efficacy of breathing and coughing exercises in the prevention of pulmonary complications after coronary artery surgery. Chest 105,741-747 Sunday Telegraph 17/3/96, referring to a report in the Royal Australian College of General Practitioners Journal, Australian Family Physician by Dr R Pierce. Taylor DR, Sears MP, Herbison GP et al, 1993. Regular inhaled beta agonists in asthma: effects on exacerbations and lung function. Thorax,48;134-8. Tobin,MJChadha,TS,Jenouri.,G,Birch., SJ,Gazeroglu,HV ,& Sakner,MA ,1983.

Breathing Patterns, 2. Diseased subjects. Chest84,287-294

 

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