AFP 50 Years Ago
Am Fam Physician. 2000 Dec 1;62(11):2409-2412.
This feature is part of a year-long series of excerpts and special commentaries celebrating AFP's 50th year of publication. Excerpts from the two 1950 volumes of GP, AFP's predecessor, appear along with highlights of 50 years of family medicine.
This feature, titled “Hyperventilation Syndrome,” and written by O. Brandon Hull, M.D., Lubbock, Texas, is reproduced from the September 1950 issue of GP. The commentary is provided by Sumi Makkar, M.D., editorial fellow for AFP.
Hyperventilation syndrome is produced when a patient has some stimulus leading to overbreathing with a resultant loss of carbon dioxide from the lungs. Although the physician sees such a case practically every day and the symptoms follow a fairly definite pattern, too often it is incorrectly diagnosed.
Hyperventilation syndrome is a symptom complex seen practically every day of a physician's practice. It has been estimated by Kerr (1937) to account for 25 to 33⅓ percent of the general practitioner's cases. Too often this type of case goes unrecognized and undiagnosed, the patient being considered by the attending physician as a “neurotic” in order to account for the multiplicity of complaints. Or, all too frequently, the patient is diagnosed as having a serious illness, generally heart disease. It is the purpose of this paper to stress the common occurrence of this syndrome in the everyday practice of the general practitioner, the internist, and every other specialist. Because of its bizarre manifestations and its basic etiology, it is seen by everyone regardless of the limitation of one's practice.
Too many of us have been lulled into a sense of false security by medical school teachings. We were taught to diagnose all organic diseases and have been exposed to those stressing psychosomatic complaints. Most of us find, however, that we fall short when it comes to dealing with cases having many vague complaints, for all too often a supposed complete history, physical, and laboratory work-up fail to reveal actual pathology. Hyperventilation syndrome is in this category. We have heard of it in medical school, maybe read an occasional article. There is no question in our own mind but what we could easily diagnose a case of tetany without assistance. But do we recognize the mild symptoms seen in most of these cases? The usual teachings fail to associate these common experiences in daily practice, and since one has to draw upon his own experience and ingenuity to explain them, he frequently remains confused or makes an erroneous diagnosis. Unless a case shows definite signs of tetany, we may miss the chronic or mild forms with early signs and symptoms.
Let's discuss briefly the physiologic mechanism producing hyperventilation syndrome, the common complaints, and then present case histories of the type encountered in every practice.
Although much work has been done on the physiology and biochemistry of this subject, it is not completely understood. The scope of this paper does not include the experimental side of the problem but rather calls to your attention the practical significance of the studies of Haldane (1908) and others through Goldman (1922) to Kerr, Kerr having introduced the term hyperventilation syndrome in 1937. Suffice to say, hyperventilation syndrome is produced when a patient has some stimulus which produces overbreathing and overventilation with the resultant loss of carbon dioxide from the lungs. This produces a change in the blood pH, and alkalosis results. There is some argument that this is the complete story, but one gets lost in the observations of the biochemist and physiologist. The basic change is essentially as described, and for further study as to whether alkalosis is the sole cause for the actions the adrenals play and many other factors, one is referred to the literature on the subject.
Hyperventilation syndrome produces a multiplicity of sensations to the patient and a multitude of symptoms and complaints for the physician to understand. They follow a fairly definite pattern: more commonly, headache, lightheadedness, dizziness, constriction around the chest, dyspnea, palpitation, numbness and tingling of the extremities, drawing of the hands, even sharp chest pain, and a sensation of suffocation. And to quote some of the patients, “I hurt all over,” “My hands tingle,” “I can't breathe,” “I can't get any air,” and the list may go on, depending on the description of various people. These have been produced experimentally by Fraser (1938) and Sargant (1940), Hinshaw and Boothby (1941). Soley (1948) and Shock (1938) have explained the “effort syndrome” on a hyperventilation basis.
The important thing to recognize is that the hyperventilation syndrome varies in degrees from patient to patient. The stimulus may be so different as to completely baffle the physician. A student nurse ordinarily in excellent health starts having menstrual cramps and hyperventilates producing all the symptoms listed above, even to the point of tetany. A politician gets excited listening to the election returns and develops a supposed heart attack, or it may be a young man with a chill at the onset of pneumonia, a patient with ulcer pain, or a truck driver after a minor traffic entanglement.
One must rely solely on a very careful history and elicit time of onset and place to get a possible lead if it is a patient complaining of having had “fainting spells,” “heart attack,” “dizzy spells,” or any symptoms as listed above. A patient who sighs frequently or “Can't breathe below here,” pointing toward the sternum, and stating “I can breathe but the air doesn't do me any good,” is one to be observed closely and to be given a hyperventilation test in an effort to reproduce the symptoms. If one sees the patient in an attack, usually as an emergency, one has an advantage because then he understands the situation and can obtain a more reliable history, especially if one observes the environment and surroundings….
Treatment of hyperventilation cases reduces to a few basic facts.
A complete, careful, detailed history including the time, place, and circumstances preceding the attack or attacks.
Complete physical examination and any laboratory work deemed necessary.
Hyperventilation test by having the patient breathe rapidly 15 to 30 times a minute through the mouth with a full expansion of the chest will reproduce many of the symptoms that occurred with the attack. Maybe not all because of the different type of stimulus. Breathing into a paper bag restores it normally within one to three minutes. One takes a small paper bag, holding it over the nose and mouth so that the patient may rebreathe for one to three minutes, and, in rebreathing the carbon dioxide, the symptoms subside gradually, usually within three minutes. When this is done, it gives the physician the opening he needs to convince the patient that hyperventilation is the cause of his complaints.
Many physicians have shown little interest, have spent too little time to thoroughly recognize the significance of such a variety of complaints in the so-called “neurotic.” The patient who is reassured without adequate explanation or told “it's all in your head” or “you are just imagining your symptoms” remains unsatisfied and all too frequently seeks a cultist who will spend time on the patient. Any organic lesion must be described and treated, but to prevent hyperventilation syndrome the patient must have an explanation in terms he can understand and must be taught to control it. The general practitioner and internist must then decide how much can be accomplished by treating the organic lesion and preventing the initial stimuli from producing hyperventilation. If it is purely on an anxiety state and too fixed for the physician, then a psychiatric consultation should be advised. Medication such as phenobarbital or ammonium chloride may help temporarily in mild anxiety states and get temporary results, but the cause must be found and eliminated in all cases if satisfactory results are to be obtained.—O. BRANDON HULL, M.D.
Dr. Hull describes an important phenomenon that is likely underappreciated and underdiagnosed. In a review of the literature from the past four years, few articles were found that were entirely devoted to hyperventilation syndrome. One review article in Chest acknowledges the complexity of the syndrome and the scarcity of information written on the subject.1 The term has been applied in multiple contexts, including psychiatry and physiology, and its usefulness as a single entity for any discipline has been questioned. A study of 23 patients who presented to the emergency department with hyperventilation further emphasizes the uncertainty surrounding the nature of the syndrome.2 The authors of this study suggest that the etiology of the syndrome is multi-factorial, including anxiety and, possibly, asthma.3 Despite the lack of information about the cause of hyperventilation syndrome, the physiologic changes induced by hypocapnia are very real to the patient.
Curiously, I have for the most part used the term “hyperventilation” to describe patients in the setting of intensive care or patients with acidosis and secondary respiratory alkalosis. Neither in teaching rounds nor in formal lectures has it been emphasized that the constellation of symptoms including dyspnea, lightheadedness, and numbness and tingling of extremities can be attributed to hyperventilation syndrome.4 Instead, I suspect we have all been taught to first and foremost consider diagnoses like myocardial infarction, pulmonary embolus, arrhythmias and stroke. In this medicolegal era, fear of the consequences of missing serious conditions leads us to disregard diagnoses that are not lifethreatening.
Retrospectively, I can recall several patients who anxiously presented in an outpatient setting with atypical chest pain, shortness of breath or dizziness. After a review of their cardiovascular risk factors, a preliminary examination and often electrocardiography, I generally reassured the patients and sent them home. Although I attributed their symptoms to anxiety, some patients were not relieved with that explanation. Perhaps if I had asked them to hyperventilate in the office and triggered their symptoms (hyperventilation provocation test), I could have revealed a more believable cause for their symptoms. Even though the diagnostic value of the hyperventilation provocation test has been questioned, it is certainly a handy tool that can ease a patient's distress.5,6
While “25 to 33⅓ percent of the general practitioner's cases” seems a gross overestimation of hyperventilation syndrome, it is likely more prevalent than we think. Maybe today's generation of doctors is more excited about diagnosing conditions like chronic fatigue syndrome, irritable bowel syndrome or fibromyalgia. Nonetheless, hyperventilation syndrome is a common source of distress among patients now, just as it was 50 years ago. In the face of rising health care costs, it is prudent to consider this syndrome in our differential diagnoses.—sumi makkar, m.d.
1. Gardner WN. The pathophysiology of hyperventilation disorders. Chest. 1996;109:516–34.
2. Saisch SG, Wessely S, Gardner WN. Patients with acute hyperventilation presenting to an inner-city emergency department. Chest. 1996;110:952–7.
3. Singer EF. Acute hyperventilation in the emergency department. Chest. 1997;112:294–5.
4. Rosen P, ed. Emergency medicine: concepts and clinical practice. 4th ed. St. Louis: Mosby Year Book, 1998:1466.
5. Hornsveld H, Garssen B. The low specificity of the Hyperventilation Provocation Test. J Psychosom Res. 1996;41:435–49.
6. Vansteenkiste J, Rochette F, Demedts M. Diagnostic tests of hyperventilation syndrome. Eur Respir J. 1991;4:393–9.
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