The Hyperventilation Syndrome – Dr. Frances Ames Part I

Dr. Frances Ames was a remarkable woman from South Africa. She was a neurologist, psychiatrist, and human rights activist. During her infancy in the early 1920s, her mother was abandoned by her husband and left penniless with three daughters. Despite this hardship, she achieved academic success and qualified as a doctor in 1942. In 1964, she was the first woman to be awarded an MD degree, medical doctor, at Cape Town University.

Ames was a proponent of the therapeutic benefits of cannabis, as she observed first-hand how cannabis relieved spasm in MS patients and helped paraplegics in the spinal injuries ward of her hospital. Her work is cited extensively throughout the cannabis literature.

When Nelson Mandela honored Dr. Ames with South Africa’s highest civilian award, the Star of Africa, in 1999, he did so not for her achievements in the medical field but for the role she played in bringing to book the doctors who had acquiesced in the torture and death of the black activist Steve Biko.

In December 1952 she submitted the comprehensive thesis The Hyperventilation Syndrome, for the degree of Doctor of Medicine to the University of Cape Town.

INDEX – THE HYPERVENTILATION SYNDROME

  1. Introduction
  2. Historical Review
  3. Clinical Symptoms and Signs
  4. Diagnosis and Differential Diagnosis
  5. Treatment
  6. Experimental Section
  7. Discussion
  8. Summary and Conclusions
  9. Appendix of Case Histories
  10. References
  11. Acknowledgments

CHAPTER 1 – INTRODUCTION

The hyperventilation syndrome is the name given to a distinctive group of symptoms and signs which are caused by an increase in the depth and rate of breathing. This abnormal breathing is nearly always the result of emotional stress.

The association between emotional stress and disorders of breathing is well-known: sighing with grief, gasping with rage, panting with fear, heaving with resentment. Of its origin, Darwin said, “Men, during numberless generations, have endeavored to escape from their enemies by headlong flight, or by violently struggling with them; and such great exertions will have caused the heart to beat rapidly, the breathing to be hurried, the chest to heave and the nostrils to be dilated…..And, now, whenever the emotion of fear is strongly felt, though it may not lead to any exertion, the same results tend to reappear through the force of inheritance and association.”

Cannon (1920) described hyperventilation as a preparation for flight or fight:

The forced respirations in deeply emotional experiences can be interpreted, therefore, as an anticipatory reduction of the carbon- dioxide in the blood, a preparation for the augmented discharge of carbon- dioxide into the blood as soon as great muscular exertion begins.”

Primitive man could and did take to his heels or use his fists if afraid. Modern man, inhibited by cultural and social traditions of behavior, is unable to do so. So the age-old physiological preparation for flight or fight is not carried over into any functional motor activity. This is when trouble arises. A strong emotional reaction with no motor outlet turns on itself to cause a physical upset. 

In this paper, a study is made of the symptoms and signs by which to recognize this syndrome, and of some of the physiological mechanisms which are brought into operation.

CHAPTER 2 – HISTORICAL REVIEW

The first description of the effects of overbreathing in man appeared as a footnote to an article by Haldane and Poulton (1908), the physiologists. They used forced breathing on themselves during experiments on the effect of want of oxygen on respiration, and the footnote comments: “Poulton, after about a minute of forced breathing, began to feel tingling in the hands and to a less extent in the feet. This became very painful, the pain reaching a maximtµn usually about half a minute after the apnoea had begun. The tingling was accompanied by numbness and sweating of the hands and a peculiar sense of giddiness and abnormality almost resembling the effects of anoxemia. Except for the feeling of abnormality these symptoms were absent in Haldane even after 5 minutes of forced breathing.”

They mentioned that forced breathing had been used to produce partial anesthesia for slight operations and attributed the disturbance of consciousness to loss of carbon dioxide. “Deficiency of CO2 appears to produce a condition of diminished excitability, but the explanation of the tingling sensations is by no means clear.” They were impressed by the apnoea following overbreathing and mentioned that Cingalese pearl divers hyperventilate before diving as a form of religious ceremony. Poulton demonstrated to the Physiological Society the effect on himself of forced breathing. During the period of apnoea “some of those present thought that something was wrong with Poulton and could hardly be restrained from performing artificial respiration. One or two of them were so affected that they became faint or sick and had to retire hastily. The face gradually assumes the leaden corpse-like hue of great anoxemia and it may be about a minute after this change begins before any desire to breathe is experienced.”

Henderson (1909) made a study of the effects of overbreathing. He hyperventilated sixty subjects for 45-90 seconds and concluded that the effects were similar to those of shock. He, too, was impressed by the apnoea and warned that it might be a danger in prolonged overbreathing. He cited experiments on anesthetized dogs, where, he said, 25-30 minutes of artificial respiration led to apnoea so prolonged that the heart failed after 7-8 minutes from lack of oxygen. He considered that apnoea almost invariably followed overbreathing and found it absent in only two or “possibly three” of his sixty subjects. Symptoms following overbreathing were more severe in these people. There appears to have been a tacit assumption by all subsequent workers that the majority of subjects after overbreathing experience this cessation of breathing during which time the CO2 of the alveolar air is built up again.

It was not until 1946 that Mills, describing the respiratory pattern after 1-1 1/2 minutes of overbreathing in thirty-five subjects selected at random, found that only ten of these showed apnoea fairly consistently after hyperventilation. Eight of his subjects continued to overbreathe, often with great vigor. The remaining 17 showed an intermediate picture. Mills could not find any obvious physiological reason for the hyperpnoea of eight of his subjects and concluded that “it results directly from that same cortical activity which is initially responsible for the forced breathing.” 

The circulatory derangements after overbreathing were again emphasized by Hill and Flack (1910). They found that “polygraph tracings show acceleration and enfeeblement of the pulse during forced breathing; the pulse can be felt to become weak or even disappear with each inspiratory effort, to return with expiration. Systolic blood pressure falls considerably with each inspiration.” In 1928 Vincent and Thompson investigated blood pressure changes during overbreathing. They found that 90% of people showed an average fall of 25 mmHg in systolic pressure. The remainder showed an average rise of 37 mmHg. The only difference between the two groups was that the subjects whose blood pressure rose had very slow initial pulse rates.

In 1938 Soley and Shock made an interesting observation: “We have been impressed by the peripheral vasoconstriction which is so marked during forced breathing that the fingers must be stabbed deeply to obtain blood for chemical studies“. Kety and Schmidt (1946) did continuous blood pressure readings and measured cardiac output in five volunteers. They found that the blood pressure did not fall, in fact, it tended to rise in some cases, though not significantly. Cardiac output was reduced 11% during passive hyperventilation, but during active hyperventilation, it was maintained by a constant tachycardia. 

The neuromuscular effects of overbreathing were first noted by Vernon (1909). He had suggested that divers might remain underwater for 9-10 minutes by combining oxygen inhalation with hyperventilation and utilizing the subsequent apnoea. On trying it on himself he was struck by the fact that after 6 minutes of overbreathing his hands passed into a condition of tonic rigidity and for the first 1 ½ minutes of the subsequent apnoea were “completely paralyzed“. 

More than 10 years passed before the clinical importance of this observation was realized. Then Grant and Goldman (1920) recognized that many of the symptoms and signs following overbreathing corresponded with those or tetany. The fact was driven home to them in a dramatic fashion during an experiment with Goldman as the subject. Grant describes it thus: “After breathing very deeply for 30 minutes A.G. suddenly went into a complete tetanic convulsion. At the onset, he involuntarily gave a loud high-pitched scream, probably due to the contraction of the muscles of respiration and the forcing of air out through contracted vocal cords. The entire body was rigid, all the muscles being contracted in tetanic spasm. The back was arched somewhat and all extremities extended completely. Relaxation occurred within 30 seconds, and there was no further spasm“. They also noted, unlike Vernon, that the tetanic spasm could be overcome by an act of will and mentioned that this is also possible in the spasm of idiopathic tetany. 

The next step was to explain the pathogenesis of this tetany of hyperventilation. Grant and Goldman thought that it was primarily due to an alkalosis in the body. The reduction of CO2 in the alveoli by overbreathing caused a reduction of CO2 in the blood. This disturbed the B2CO3 : NaHC03 ratio and produced an alkalosis because CO2 is washed out of the blood more rapidly by overventilation than NaHco3 is decreased by excretion or other means.

Although they considered the alkalosis to be of primary importance they also attempted to find a link with the familiar tetany of hypocalcemia. Serum calcium levels in their cases were normal so they suggested that when the “CO2 of the blood is reduced by overventilation, a portion of the calcium is in some way rendered inactive though still present in the circulating blood“. 

Estimation of serum calcium appeared as almost a routine investigation during experiments on hyperpnoea after this. The only workers who claimed a significant calcium change were Barnes end Greaves (1936), who found a diminished calcium level in the cerebrospinal fluid after overbreathing. Their work was promptly refuted the following year by Mccance and Watchorn (1937), and independently by Cumings and Carmichael (1937). All subsequent workers agreed that the serum calcium level either remains unchanged during hyperventilation, (Schultzer and Lebel (1939), O’Donovan (1943), or shows a slight rise (Fowweather, Davidson, and Ellis (1940). Fowweather et al. reported a marked drop in phosphate levels in the blood immediately after overbreathing but this work has not been confirmed. 

During the year that Grant and Goldman’s article appeared, Collip and Backus (1920) were also occupied with the cause of the symptoms of overbreathing. They found that during hyperventilation the CO2 tension of the alveolar air fell 44% and the CO2 combining the power of the venous blood fell 14.3%. They also noted that the acidity of the urine was markedly decreased, a diuresis occurred and the rate of elimination of phosphates was increased. They concluded that the development of definite tetany and “muscle cramps” in many subjects during hyperpnoea was due to an alkalosis of the tissue. Alkalosis is today a well-recognized cause of tetany and the tetany following hyperventilation is generally accepted as being due to an alkalosis produced by the “washing out of carbon dioxide” from the blood. 

In 1922 Goldman made a further significant contribution by showing that some people hyperventilate involuntarily thus producing symptoms. He gave the credit for the first description of such a case to Barker and Sprunt (1922) who described involuntary overbreathing with tetany production in a patient convalescing from epidemic encephalitis.

The first of Goldman’s eleven cases was a medical student who, during an attack of gall bladder colic, involuntarily hyperventilated and found that this lessened his pain. In subsequent attacks, he deliberately overbreathed to achieve this analgesic effect. He diagnosed the cause of his ultimate tetany himself, as he had often seen Goldman demonstrate the effect of hyperventilation during lectures. Five cases were students who had become tetanic during a class fight and in them, Goldman attributed this to excessive hyperpnoea following the acidosis of violent exercise. Two cases had acute infections with upper respiratory tract symptoms and one case had abdominal distension and vomiting. The remaining two cases were hysterical and Goldman commented that “some cases of hysterical pseudo tetany are undoubtedly real cases of tetany due to over respiration”.

It was only several years later that it became clear that involuntary hyperventilation in otherwise healthy individuals was usually the result of emotional stress. In 1929 White and Hahn drew attention to the symptom of “sighing dyspnoea” and described it as a valuable indicator of nervous tension. In 1934 Baker describing several cases stressed the importance of “sighing dyspnoea” as a manifestation of emotional stress. The same year Maytum and Willius (1934) recognized sighing dyspnoea as a form of hyperventilation. The following year Christie (1935), describing neurotic respiratory patterns, claimed that patients with conversion hysteria characteristically complained of “an inability to return air into the lungs so that in mild cases deep sighing respirations were characteristic while in severe cases a paroxysm of hyperventilation leading to hyperventilation tetany might occur“.

In 1942 Silverberg emphasized the importance of careful history taking in patients complaining of dyspnoea because in this way the breathing difficulty resulting from emotional stress could be readily differentiated. from that of organic disease. Although healthy, individuals occasionally hyperventilate because of heat – Bazett and Haldane (1921), Wingfield (1941) and Dibden (1949), or because of excessive overbreathing after exertion – Goldman (1922) and Dibden (1949), most people do so as a result of emotional stress.

The effects of hyperventilation on the neuromuscular system led Rosett (1924) to advocate overbreathing as a simple, harmless technique for unmasking central nervous system disease. He took the view that the main effect of hyperventilation was on the cerebral cortex. “In disease of the cerebrum, the manifestations referable to the particular system involved become vastly exaggerated under hyperpnoea. In injury of the pyramidal system, so slight as to escape detection by ordinary means, definite signs and symptoms are observable. Every form of abnormal involuntary movement referable to a disorder of the striatal system becomes exaggerated to the greatest possible extent. Mental abnormalities assert themselves in pronounced abnormal behavior“. Hyperventilation is still used nowadays in an attempt to render doubtful neurological signs, for example, an equivocal plantar response, more definite. 

The individual susceptibility of people to the effects of hyperventilation was emphasized by McCance (1932). He reported the cases of two women who “with scarcely noticeable overbreathing” went into tetanic spasm. He could not find any cause for this phenomenon. In 1939 Schultzer and Lebel again drew attention to the “hypersensitive type” and in 1943 O’Donovan described these people as individuals who, breathing at the rate of 55 – 60 breaths a minute, develop tetany in less than 2 minutes or who experience such severe symptoms within 2 minutes as to prevent them from continuing overbreathing. O’Donovan was inclined to think that predisposition to alkalosis could be induced “so that with each hyperventilation the nervous system becomes more easily excited and responds in an increasing degree until tetany appears with a relatively small stimulus“. He claimed that in some cases this hypersensitivity could be abolished by vitamin or other hypercalcemia therapy.

The clinical concept of hyperventilation was extended by Kerr, Dalton, and Gliebe (1937) who introduced the term “hyperventilation syndrome” to cover the many symptoms which had been observed in patients who overbreathed involuntarily. They recognized that emotional stress lay at the root of the syndrome in most cases and made the important point that patients seldom presented with tetanic spasms but commonly did so with rather vague ill-defined symptoms. There is a risk here, however, of widening the concept too much and obscuring the fact that hyperventilation involves definite mechanisms which set a limit to symptoms and signs. Kerr et al. seem to have identified the hyperventilation syndrome with the anxiety state. Significantly, the following year Soley and Shock (1938) attributed all the symptoms and signs of “effort syndrome” to hyperventilation. 

In 1938 a useful contribution came from Fraser and Sargant who described twenty cases of “hyperventilation fits” and differentiated them from hysterical and epileptic seizures. 

In 1940 Fowweather, Davidson and Ellis thought that there was much justification for the term hyperventilation syndrome. They sought to explain the wide variation in clinical symptoms and signs by a tissue alkalosis which manifested itself in tetany in those individuals whose voluntary musculature was particularly susceptible, or in “effort syndrome” in those whose circulatory systems were susceptible and so on. 

Later many workers thought that the term hyperventilation syndrome was being used to include too much. Guttman and Jones (1940), Wood (1941), and Friedman (1945) agreed that effort syndrome could not be wholly explained by hyperventilation. The fact remains, ho ever, that the Kerr school has made a valuable contribution in (to quote Gliebe and Auerback (1944) emphasizing hyperventilation “as an important mechanism of psychosomatic disease – it demonstrates one means whereby emotional disturbances can produce physiological and biochemical changes and physical symptoms”. 

World War II focused attention on the occurrence of the hyperventilation syndrome among aircrew. Boothby, while learning to fly, experienced distressing symptoms which he afterward recognized were due to overbreathing and in collaboration with Hinshaw (1941), investigated the effects of hyperventilation on coordination and cerebration. They suggested that the phenomena in pilots of “blacking out” and “freezing to the controls’‘ might in some cases be due to overbreathing. Hyperventilation at low altitudes was due to emotional stress; at high altitudes, lack of oxygen was an additional factor. Carryer (1943, 1947) was another investigator who emphasized the importance of hyperventilation in aviation medicine. 

With the increasing recognition of the syndrome, the various specialties began to contribute knowledge of its manifestations in their own particular fields. 

That hyperventilation could produce inversion of T waves in the electrocardiogram was shown as early as 1932 by McGance. This became of increasing importance later because the combination of precordial pain (not uncommon in the hyperventilation syndrome) and electrocardiographic changes led to the erroneous diagnosis of myocardial infarction in anxious patients. In 1943 Thompson demonstrated marked electrocardiographic abnormalities, consisting either of late inversion of T or S-T depression with marked lowering of T in any or all leads of the electrocardiogram during overbreathing in patients with normal hearts. They thought that alkalosis was the main factor in causing these abnormalities.

In 1946 Christensen reported sinus tachycardia, depression of S-T segments, and iso-electric, diphasic, or inverted T waves during overbreathing. He explained them as resulting from interference with coronary blood flow “by increased intramyocardial tension due to hypocapnia”. In 1947 Scherf and Schlacluran described lowering of R and T waves in lead 1. They stated that “as long as a marked increase in heart rate was avoided and the respirations were not sufficiently rapid and shallow to cause anoxia, no depression of the RS-T segment was observed.” They thought that the changes which did occur resulted from positional changes of the heart. 

The co-existence of organic heart disease and hyperventilation was stressed by Stead and Warren (1943) who described patients with compensated heart disease whose “dyspnoea” was wrongly attributed to congestive heart failure. 

In 1946 Herxheinier reported that asthma could be precipitated in susceptible subjects by overbreathing. He suggested that it might play a part in the pathogenesis of psychologically triggered asthmatic attacks. 

In 1947 McKell and Sullivan found that 5.8% of consecutive ambulatory patients with gastrointestinal complaints were, in reality, suffering from the effects of the hyperventilation syndrome. They suggested that anxious patients often got a feeling of fullness which initiated air-swallowing. “‘This interferes to some extent with the respiratory rhythm and seems to initiate the hyperventilation in some cases.” 

Engel, Ferris, and Logan (1947) reviewing the subject stated that “hyperventilation may occur as a more or less nonspecific reaction to the experience of terror, extreme anger, severe pain or other intense emotions in essentially healthy individuals or it may be a symptom of neurosis.” 

They divided the symptoms resulting from overbreathing into two more or less separate groups – one related to the reduction in consciousness and one related to the tetany. They found that there was a close correlation between the “degree of slowing of frequency of the encephalogram and the degree of reduction of awareness“. They thought that the symptom of tetany had received an undue amount of attention and that the “reduction in consciousness develops much earlier and is much more disturbing to the patient”. 

In 1949 Dibden reviewed the subject very fully and stressed the importance of recognizing the syndrome because “the dramatic demonstration of the nature of the syndrome symptoms by a hyperventilation test so impresses the patient as to create an excellent rapport with the psychiatrist“. 

In 1950 Rice claimed that during 1,000 routine interviews 10% of patients complained of symptoms and signs of the hyperventilation syndrome. He described the symptoms in detail and discussed their pathogenesis.

The present position is, that overbreathing is recognized as a cause of disturbing symptoms; that involuntary overbreathing is a definite clinical entity; that a wide variety of symptoms and signs have been grouped under the term hyperventilation syndrome; and that the most common cause of this syndrome is stress.

Next Chapter
Chapter 3 – Clinical Symptoms and Signs

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Anders Olsson is a lecturer, teacher and founder of the Conscious Breathing concept and the author of Conscious Breathing. After living most of his life with a ”hurricane of thoughts” bouncing back and forth in is head, Anders was fortunate enough to come across tools that have helped him relax and find his inner calm. The most powerful of these tools has undoubtedly been to improve his breathing habits, which made Anders decide to become the worlds most prominent expert in breathing. This is now more than 10 years ago and since then he has helped tens of thousands of people to a better health and improved quality of life.

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