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Organic Disease Presenting As Hyperventilation Syndrome
Organic Disease Presenting As Hyperventilation Syndrome JOSEPH M. KIELY, M.D.
• The hyperventilation syndrome is a mani- having primarily symptoms of hyperventilafestation of anxiety neurosis characterized tion, and the true nature of the underlying by feelings of apprehension, breathlessness, organic disorder was revealed only after subpalpitation, chest discomfort, dizziness, and sequent study. Adequate therapy of the basic paresthesia.'·4 This disorder may mimic vari- disease completely eliminated the hypervenous organic diseases". The symptoms induced tilation symptoms in these patients. by acute or chronic overbreathing in subjects REPORT OF CASES with anxiety neurosis are usually interpreted Case 1 (Pheochromocytoma). A 1:>7-yearby the patient as manifestations of serious, old housewife was seen at the Mayo Clinic in 1968 and often life-threatening, disease. Usually, with a complaint of "spells" of 10 years' duration. the alert clinician quickly recognizes the She had undergone three abdominal operations, "functional" nature of the problem, demon- in addition to nasal surgery, between 1933 and strates to the patient the mechanism of the 1957. Hysterectomy for menorrhagia was persymptoms, and reassures him about the ab- formed in 1958, and shortly thereafter the "spells" began. These episodes occurred as often as four sence of significant "organic" pathology. Espe- times daily, and each usually lasted 10 to 20 cially since World War II, the frequency and minutes. During the episode, she noted air hunger importance of emotional factors in the pro- .and breathed very rapidly and deeply. In addition, duction of physical symptoms have been she experienced numbness of the arms, facial palrepeatedly emphasized. General practitioners lor, light-headedness, tremulousness. and a "very nervous feeling." and internists, particularly, have been taught The patient was normotensive, and results of to recognize functional symptoms in their pa- the physical examination were normal. Hyperventients and have been admonished not to over- tilation for 45 seconds reproduced a "spell," and look the emotional components of "organic" a preliminary diagnosis of hyperventilation syndisease. Some of us have taken this advice drome was made. A provocative glucagon test did n-ot elevate too literally, and are now overlooking organic her blood pressure, but the patient reported a diseases in patients whose illnesses initially typical "spell" during the test; and levels of urinary metanephrines and catecholamines were appear to have an emotional basis. elevated. Nephrotomography revealed a right This report emphasizes that symptoms of adrenal tumor, and at laparotomy a well-encapthe well-known hyperventilation syndrome sulated pheochromocytoma was removed. may mask the presence of serious underlyAt a follow-up examination 3 months after ing organic disease. Four brief case summaries surgery, she reported that the "spells" had ceased of patients with pheochromocytoma, por- and she felt considerably improved. Case 2 (Porphyria). - A 47-year-old housephyria, brain tumor, and hypoparathyroidism, wife was seen at the Mayo Clinic in 1957 because respectively, are presented. These patients of "dizzy spells." She had had four of these were all initially regarded by the clinician as "spells" during the 4 months prior to examinaDr. Kiely is from Department of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota. Read at the Annual Meeting of the Academy of Psychosomatic Medicine, Scottsdale, Arizona, November 21, 1969. 326
tion. Characteristically, the attacks began with a "feeling of fright," followed by rapid and deep breathing, and then paresthesia of the extremities, giddiness. and palpitation. These symptoms had occurred intermittently over a period of 4 days during one of the "spells." Results of physical examination were unremarkable, except for slight facial hirsutism. A Volume XI
HYPERVENTILATION SYNDROME-KIELY preliminary diagnosis was hyperventilation syndrome. Further questioning elicited a history of intermittent severe colicky abdominal pain since childhood. Between 1934 and 1943, appendectomy and separate surgical procedures on both ovaries were performed without symptomatic benefit. She complained of hot flushes "every 45 minutes both day and night" for 13 years after removal of her remaining ovary in 1943. A duodenal ulcer deformity was noted on roentgenologic study in 1944. The urine contained both uroporphyrin and coproporphyrin but was negative for porphobilinogen. The stool contained significantly increased amounts of protoporphyrin, coproporphyrin, and uroporphyrin. After the diagnosis of porphyria had been established, chlorpromazine therapy relieved both the episodic abdominal pain and the symptoms of the hyperventilation syndrome over a 10-year follow-up period. Case 3 (Brain-Stem Tumor). - A 27-year-old housewife was seen at the Mayo Clinic in 1968 with complaints of headaches and "spells." Her father had frequent headaches, and during childhood the patient also had had frequent "sick headaches." During the year prior to examination at our clinic, the headaches had increased in frequency and severity. The pain was bilateral and throbbing and was associated with nausea, vomiting, and photophobia. Previous studies, including brain scan, spinal-fluid examination, and bilateral carotid angiograms, had revealed no abnormalities. For 2 months prior to the evaluation, she had had frequent "spells" that were characterized by breathlessness, dizziness, tightness of the throat, and paresthesia of the upper extremities. The initial physical examination revealed no abnormal findings. but during later interviews she sighed frequently, swallowed air, and belched loudly. Routine laboratory studies and skull roentgenogram showed no abnormalities. The Minnesota Multiphasic Personality Inventory test showed significant elevations of the hypochondriasis and hysteria scales and a normal depression scale. A typical episode of hyperventilation was observed, and the symptoms were promptly relieved by having her rebreathe into a paper bag. The internist's diagnosis was anxiety state with aerophagia, hyperventilation syndrome, and vasodilating headaches. Further evaluation by the ophthalmologist and neurologist revealed slight horizontal nystagmus. The pneumoencephalogram showed no air filling of the ventricles. and the ventriculogram revealed a very large fourth ventricle compatible with obstruction to its outlet. A suboccipital craniotomy was performed, and a low-grade ependymoma was found. After a Torkildsen shunt procedure and
radiotherapy, the headaches and episodes of hyperventilation were completely relieved during a 6-month follow-up. Case 4 (Primary Hypoparathyraidism). - A 56-year-old man was seen at the Mayo Clinic in 1952 because of "choking spells." He had suffered 12 such episodes in the 3 months prior to examination here. The "spells" began abruptly and lasted only a few seconds. They were characterized by an inability to inhale or exhale and were associated with a fear of death. Previous diagnoses of "cardiac neurosis" and "chronic nervous exhaustion" had been made, and in 1938 he underwent gastroenterostomy for duodenal ulcer. Physical examination revealed no abnormalities. The laryngologist found the hypopharynx and larynx to be normal, and the internist made a diagnosis of anxiety state. A routine electrocardiogram showed prolongation of ventricular repolarization (Q-T interval 0.44 second). The serum calcium concentration was significantly reduced (4.8 and 5.0 mg/100 ml), and the serum protein content was normal. No intracranial calcification was noted on the skull roentgenograms. The endocrinologist noted the presence of Chvostek and Trousseau signs and made a diagnosis of primary hypoparathyroid'sm with intermittent laryngeal stridor. Adequate replacement therapy returned the serum calcium concentration toward normal, with complete relief of the "choking spells." DISCUSSION
The confusing clinical pictures presented by these patients led us to review the mechanism of symptom production in anxiety neurosis and hyperventilation syndrome. In 1894, Freud6 distinguished anxiety neurosis from what was then called "neurasthenia." He carefully delineated the symptoms that occur with episodic anxiety attacks - palpitation, disturbance of respiration with dyspnea, sweating, tremor and shuddering, hunger and giddiness, vertigo, and paresthesia. It is remarkable to note that these symptoms which he tabulated as existing in the acute anxiety attack are precisely those now recognized as characteristic of the hyperventilation syndrome 7 • 8 • Regardless of the precipitating process, the initial link in the pathogenetic chain is sustained overbreathingD• This lowers the arterial carbon dioxide tension and results in respiratory alkalosis, which in turn reduces 327
July-August 1970
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PSYCHOSOMATICS
the concentration of ionized calcium in the plasma and interstitial fluids. The neurovascular and neuromuscular changes which then occur underlie the multiple clinical manifestations. The onset of these symptoms usually is a frightening experience and tends to enhance and prolong the overbreathing thus establishing a cyclic, self-perpetuating process. In addition, autonomic and hormonal changes accompany this secondary fear response'o. Pitts and McClure" have reported a controlled study of the effects of sodium lactate infusions in a group of patients with anxiety neurosis compared to controls. They concluded that a high concentration of lactate ion can produce some anxiety symptoms in almost anyone, that it regularly produces acute anxiety attacks mimicking the hyperventilation syndrome in patients with anxiety neurosis but not in controls, and that calcium ion largely prevents the symptoms in both patients and controls. They commented on the great similarity of the symptoms of acute anxiety attacks to those of pretetanic hypocalcemia. Their study suggests that anxiety symptoms may have a common determining biochemical end mechanism involving possibly the chelating of ionized calcium at the surface of cell membranes by lactate. The biochemical mechanism of lactate chelating of ionized calcium may help explain why acute anxiety attacks develop during hyperventilation in patients with chronic anxiety neurosis, in contrast to most normal persons in whom overbreathing produces only mild paresthesia. Other studies had shown an abnormality in lactate metabolism in patients with anxiety neurosis'~. Such patients show a significantly greater increase in levels of blood lactate in response to mild exercise than do normal controls. The appearance of anxiety symptoms evoked in patients by exercise appeared to be concomitant with the extremely rapid increase in blood lactate levels. Normal persons did not develop anxiety symptoms with exercise and showed only the expected normal increase in lactate levels. Catecholamines, such as epinephrine, increase lactate production by acting on adrenergic receptor 328
sites on the cell surface to activate the glycolytic enzyme system of the cell. Patients with anxiety neurosis may overproduce epinephrine and other catecholamines, and thus have a lower level of ionized calcium at the surface of the cell membrane as a result of the increased production of lactate. Hyperventilation by producing respiratory alkalosis further lowers the concentration of ionized calcium and thus may produce the symptoms of an acute anxiety attack. It is of particular interest that the most disturbing symptoms reported by many patients with the hyperventilation syndrome are related to the cardiovascular system. These symptoms are similar to those described in the effort syndrome," in the essential circulatory hyperkinesis syndrome," in the hyperkinetic heart syndrome,"-' and in the hyperdynamic ~-adrenergic circulatory state syndrome.'r. These syndromes appear to be related to increased responsiveness of the ~ adrenergic receptor site in such patients. Some patients with these disorders appear to have anxiety neurosis with predominantly cardiovascular symptoms. The ~-adrenergic blocking drug propranolol has been reported to relieve the disturbing cardiovascular symptoms in such patients."'!" By reducing the production of lactate induced by epinephrine and other catecholamines, this agent should also prove useful in the management of hyperventilation syndrome. SUMMARY
The hyperventilation syndrome may be the presenting manifestation of a basic underlying organic disease. Symptoms of acute anxiety attacks and hyperventilation syndrome are identical, and both may have a common biochemical mechanism. Increased affinity of the ~-adrenergic receptor sites on cell surfaces in patients with anxiety neurosis and certain organic disorders is one possible explanation for increased production of lactate, with resulting reduction in the concentration of ionized calcium at the surface of cell membranes in response to circulating catecholamines. Volume XI
HYPERVENTILATION SYNDROME-KIELY REFERENOE8
1. Carryer, H.M.: The Hyperventilation Syndrome. Med. Olin. N. Amer. July, 1947. (pages 845-849. 2. Engel, G.L., Ferris, E.B., and Logan, M.: Hyperventilation: Analysis of Clinical Symptomatology. Ann. Intern. Med. 27: 683, November, 1947. 3. Rice, R.L.: Symptom Patterns of the Hyperventilation Syndrome. Amer. J. Med. 8: 691, June, 1950. 4. Singer, E.P.: The Hyperventilation Syndrome in Clinical Medicine. New York J. Med. 58: 1494, May I, 1958. 5. Gliebe, P. A., and Auerback, A.: Sighing and Other Forms of Hyperventilation Simulating Organic Disease. J. Nero. Ment. Dis. 99: 600, January, 1944. 6. Freud, S.: Oollected Papers. New York: The International Psycho-analytical Press, 1924. Vol. 1. (pages 76-106). 7. Kerr, W.J., Dalton, J.W., and Gliebe, P.A.: Some Physical Phenomena Associated with the Anxiety States and Their Relation to Hyperventilation. Ann. Intern. Med. 11: 961, December, 1937. 8. Kolb, L.C.: Anxiety and the Anxiety States. J. Ohronic Dis. 9: 199, March, 1959. 9. Okel, B.B., and Hurst, J.W.: Prolonged Hy·
10.
11.
12. 13.
14.
15. 16.
17.
18.
perventilation in Man. Arch. It/tern. Med. (Ohicago) , 108: 757, November, 1961. Lewis, B. I.: Hyperventilation Syndromes: Clinical and Physiologic Observations. Postgrad Med, 21: 259, March, ]!l57. Pitts, F. N., Jr., and McClure. J. N.: Lactate Metabolism in Anxiety Neurosis. New E.ng J Med, 277: 1329, December 21, 1967. Pitts, F. N., Jr.: The Biochemistry of Anxiety. 8ci Amer, 220: 69, February, 1969. Wood, P.: Da Costa's Syndrome (or Effort Syndrome). Brit Med J, 1: 767, May 24,1941 Gottsegen, G., Okos, G., and Romoda, T.: Essential Circulatory Hyperkinesis. Amer J Oardiol, 10: 785, December, 1962. Gorlin, R.: The Hyperkinetic Heart Syndrome. JAMA, 182: 823, November 24, 1962. Frohlich, E. D., Tarazi, R. C., and Dustan, H. P.: Hyperdynamic B-Adrenergic Circulatory State. Arch. Intern. Med. (Ohicago),123: I, January, 1969. Bollinger, A., Gander, M., Pylkkti.nen, P.O., Forster, G.: Treatment of the Hyperkinetic Heart Syndrome with Propranolol. Oardiologia (Basel), 49 (Suppl 2): 68, 1966. Granville-Grossman, K. L., and Turner, P.: The Effect of Propranolol on Anxiety. Lancet, 1: 788, April 9, 1966.
First International Collegium in Psychosomatic Medicine The Fifth World Congress of Psychiatry will take place in Mexico City, November 28 to December 4, 1971. It will be followed by the First International Collegium in Psychosomatic Medicine in Guadalajara, Mexico, December 5 to 8. Further details will be published as they become available. Those interested may contact either Edwin Dunlop, M.D., 150 Emory Street, Attleboro, Mass. (U.S.A.) or Dr. Roberto Kertesz, San Jose de Calasanz 431, Buenos Aires, Argentina (abroad). Both are serving as executive secretaries for the International Collegium.
July-August 1970
329
• The hyperventilation syndrome is a mani- having primarily symptoms of hyperventilafestation of anxiety neurosis characterized tion, and the true nature of the underlying by feelings of apprehension, breathlessness, organic disorder was revealed only after subpalpitation, chest discomfort, dizziness, and sequent study. Adequate therapy of the basic paresthesia.'·4 This disorder may mimic vari- disease completely eliminated the hypervenous organic diseases". The symptoms induced tilation symptoms in these patients. by acute or chronic overbreathing in subjects REPORT OF CASES with anxiety neurosis are usually interpreted Case 1 (Pheochromocytoma). A 1:>7-yearby the patient as manifestations of serious, old housewife was seen at the Mayo Clinic in 1968 and often life-threatening, disease. Usually, with a complaint of "spells" of 10 years' duration. the alert clinician quickly recognizes the She had undergone three abdominal operations, "functional" nature of the problem, demon- in addition to nasal surgery, between 1933 and strates to the patient the mechanism of the 1957. Hysterectomy for menorrhagia was persymptoms, and reassures him about the ab- formed in 1958, and shortly thereafter the "spells" began. These episodes occurred as often as four sence of significant "organic" pathology. Espe- times daily, and each usually lasted 10 to 20 cially since World War II, the frequency and minutes. During the episode, she noted air hunger importance of emotional factors in the pro- .and breathed very rapidly and deeply. In addition, duction of physical symptoms have been she experienced numbness of the arms, facial palrepeatedly emphasized. General practitioners lor, light-headedness, tremulousness. and a "very nervous feeling." and internists, particularly, have been taught The patient was normotensive, and results of to recognize functional symptoms in their pa- the physical examination were normal. Hyperventients and have been admonished not to over- tilation for 45 seconds reproduced a "spell," and look the emotional components of "organic" a preliminary diagnosis of hyperventilation syndisease. Some of us have taken this advice drome was made. A provocative glucagon test did n-ot elevate too literally, and are now overlooking organic her blood pressure, but the patient reported a diseases in patients whose illnesses initially typical "spell" during the test; and levels of urinary metanephrines and catecholamines were appear to have an emotional basis. elevated. Nephrotomography revealed a right This report emphasizes that symptoms of adrenal tumor, and at laparotomy a well-encapthe well-known hyperventilation syndrome sulated pheochromocytoma was removed. may mask the presence of serious underlyAt a follow-up examination 3 months after ing organic disease. Four brief case summaries surgery, she reported that the "spells" had ceased of patients with pheochromocytoma, por- and she felt considerably improved. Case 2 (Porphyria). - A 47-year-old housephyria, brain tumor, and hypoparathyroidism, wife was seen at the Mayo Clinic in 1957 because respectively, are presented. These patients of "dizzy spells." She had had four of these were all initially regarded by the clinician as "spells" during the 4 months prior to examinaDr. Kiely is from Department of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota. Read at the Annual Meeting of the Academy of Psychosomatic Medicine, Scottsdale, Arizona, November 21, 1969. 326
tion. Characteristically, the attacks began with a "feeling of fright," followed by rapid and deep breathing, and then paresthesia of the extremities, giddiness. and palpitation. These symptoms had occurred intermittently over a period of 4 days during one of the "spells." Results of physical examination were unremarkable, except for slight facial hirsutism. A Volume XI
HYPERVENTILATION SYNDROME-KIELY preliminary diagnosis was hyperventilation syndrome. Further questioning elicited a history of intermittent severe colicky abdominal pain since childhood. Between 1934 and 1943, appendectomy and separate surgical procedures on both ovaries were performed without symptomatic benefit. She complained of hot flushes "every 45 minutes both day and night" for 13 years after removal of her remaining ovary in 1943. A duodenal ulcer deformity was noted on roentgenologic study in 1944. The urine contained both uroporphyrin and coproporphyrin but was negative for porphobilinogen. The stool contained significantly increased amounts of protoporphyrin, coproporphyrin, and uroporphyrin. After the diagnosis of porphyria had been established, chlorpromazine therapy relieved both the episodic abdominal pain and the symptoms of the hyperventilation syndrome over a 10-year follow-up period. Case 3 (Brain-Stem Tumor). - A 27-year-old housewife was seen at the Mayo Clinic in 1968 with complaints of headaches and "spells." Her father had frequent headaches, and during childhood the patient also had had frequent "sick headaches." During the year prior to examination at our clinic, the headaches had increased in frequency and severity. The pain was bilateral and throbbing and was associated with nausea, vomiting, and photophobia. Previous studies, including brain scan, spinal-fluid examination, and bilateral carotid angiograms, had revealed no abnormalities. For 2 months prior to the evaluation, she had had frequent "spells" that were characterized by breathlessness, dizziness, tightness of the throat, and paresthesia of the upper extremities. The initial physical examination revealed no abnormal findings. but during later interviews she sighed frequently, swallowed air, and belched loudly. Routine laboratory studies and skull roentgenogram showed no abnormalities. The Minnesota Multiphasic Personality Inventory test showed significant elevations of the hypochondriasis and hysteria scales and a normal depression scale. A typical episode of hyperventilation was observed, and the symptoms were promptly relieved by having her rebreathe into a paper bag. The internist's diagnosis was anxiety state with aerophagia, hyperventilation syndrome, and vasodilating headaches. Further evaluation by the ophthalmologist and neurologist revealed slight horizontal nystagmus. The pneumoencephalogram showed no air filling of the ventricles. and the ventriculogram revealed a very large fourth ventricle compatible with obstruction to its outlet. A suboccipital craniotomy was performed, and a low-grade ependymoma was found. After a Torkildsen shunt procedure and
radiotherapy, the headaches and episodes of hyperventilation were completely relieved during a 6-month follow-up. Case 4 (Primary Hypoparathyraidism). - A 56-year-old man was seen at the Mayo Clinic in 1952 because of "choking spells." He had suffered 12 such episodes in the 3 months prior to examination here. The "spells" began abruptly and lasted only a few seconds. They were characterized by an inability to inhale or exhale and were associated with a fear of death. Previous diagnoses of "cardiac neurosis" and "chronic nervous exhaustion" had been made, and in 1938 he underwent gastroenterostomy for duodenal ulcer. Physical examination revealed no abnormalities. The laryngologist found the hypopharynx and larynx to be normal, and the internist made a diagnosis of anxiety state. A routine electrocardiogram showed prolongation of ventricular repolarization (Q-T interval 0.44 second). The serum calcium concentration was significantly reduced (4.8 and 5.0 mg/100 ml), and the serum protein content was normal. No intracranial calcification was noted on the skull roentgenograms. The endocrinologist noted the presence of Chvostek and Trousseau signs and made a diagnosis of primary hypoparathyroid'sm with intermittent laryngeal stridor. Adequate replacement therapy returned the serum calcium concentration toward normal, with complete relief of the "choking spells." DISCUSSION
The confusing clinical pictures presented by these patients led us to review the mechanism of symptom production in anxiety neurosis and hyperventilation syndrome. In 1894, Freud6 distinguished anxiety neurosis from what was then called "neurasthenia." He carefully delineated the symptoms that occur with episodic anxiety attacks - palpitation, disturbance of respiration with dyspnea, sweating, tremor and shuddering, hunger and giddiness, vertigo, and paresthesia. It is remarkable to note that these symptoms which he tabulated as existing in the acute anxiety attack are precisely those now recognized as characteristic of the hyperventilation syndrome 7 • 8 • Regardless of the precipitating process, the initial link in the pathogenetic chain is sustained overbreathingD• This lowers the arterial carbon dioxide tension and results in respiratory alkalosis, which in turn reduces 327
July-August 1970
-
PSYCHOSOMATICS
the concentration of ionized calcium in the plasma and interstitial fluids. The neurovascular and neuromuscular changes which then occur underlie the multiple clinical manifestations. The onset of these symptoms usually is a frightening experience and tends to enhance and prolong the overbreathing thus establishing a cyclic, self-perpetuating process. In addition, autonomic and hormonal changes accompany this secondary fear response'o. Pitts and McClure" have reported a controlled study of the effects of sodium lactate infusions in a group of patients with anxiety neurosis compared to controls. They concluded that a high concentration of lactate ion can produce some anxiety symptoms in almost anyone, that it regularly produces acute anxiety attacks mimicking the hyperventilation syndrome in patients with anxiety neurosis but not in controls, and that calcium ion largely prevents the symptoms in both patients and controls. They commented on the great similarity of the symptoms of acute anxiety attacks to those of pretetanic hypocalcemia. Their study suggests that anxiety symptoms may have a common determining biochemical end mechanism involving possibly the chelating of ionized calcium at the surface of cell membranes by lactate. The biochemical mechanism of lactate chelating of ionized calcium may help explain why acute anxiety attacks develop during hyperventilation in patients with chronic anxiety neurosis, in contrast to most normal persons in whom overbreathing produces only mild paresthesia. Other studies had shown an abnormality in lactate metabolism in patients with anxiety neurosis'~. Such patients show a significantly greater increase in levels of blood lactate in response to mild exercise than do normal controls. The appearance of anxiety symptoms evoked in patients by exercise appeared to be concomitant with the extremely rapid increase in blood lactate levels. Normal persons did not develop anxiety symptoms with exercise and showed only the expected normal increase in lactate levels. Catecholamines, such as epinephrine, increase lactate production by acting on adrenergic receptor 328
sites on the cell surface to activate the glycolytic enzyme system of the cell. Patients with anxiety neurosis may overproduce epinephrine and other catecholamines, and thus have a lower level of ionized calcium at the surface of the cell membrane as a result of the increased production of lactate. Hyperventilation by producing respiratory alkalosis further lowers the concentration of ionized calcium and thus may produce the symptoms of an acute anxiety attack. It is of particular interest that the most disturbing symptoms reported by many patients with the hyperventilation syndrome are related to the cardiovascular system. These symptoms are similar to those described in the effort syndrome," in the essential circulatory hyperkinesis syndrome," in the hyperkinetic heart syndrome,"-' and in the hyperdynamic ~-adrenergic circulatory state syndrome.'r. These syndromes appear to be related to increased responsiveness of the ~ adrenergic receptor site in such patients. Some patients with these disorders appear to have anxiety neurosis with predominantly cardiovascular symptoms. The ~-adrenergic blocking drug propranolol has been reported to relieve the disturbing cardiovascular symptoms in such patients."'!" By reducing the production of lactate induced by epinephrine and other catecholamines, this agent should also prove useful in the management of hyperventilation syndrome. SUMMARY
The hyperventilation syndrome may be the presenting manifestation of a basic underlying organic disease. Symptoms of acute anxiety attacks and hyperventilation syndrome are identical, and both may have a common biochemical mechanism. Increased affinity of the ~-adrenergic receptor sites on cell surfaces in patients with anxiety neurosis and certain organic disorders is one possible explanation for increased production of lactate, with resulting reduction in the concentration of ionized calcium at the surface of cell membranes in response to circulating catecholamines. Volume XI
HYPERVENTILATION SYNDROME-KIELY REFERENOE8
1. Carryer, H.M.: The Hyperventilation Syndrome. Med. Olin. N. Amer. July, 1947. (pages 845-849. 2. Engel, G.L., Ferris, E.B., and Logan, M.: Hyperventilation: Analysis of Clinical Symptomatology. Ann. Intern. Med. 27: 683, November, 1947. 3. Rice, R.L.: Symptom Patterns of the Hyperventilation Syndrome. Amer. J. Med. 8: 691, June, 1950. 4. Singer, E.P.: The Hyperventilation Syndrome in Clinical Medicine. New York J. Med. 58: 1494, May I, 1958. 5. Gliebe, P. A., and Auerback, A.: Sighing and Other Forms of Hyperventilation Simulating Organic Disease. J. Nero. Ment. Dis. 99: 600, January, 1944. 6. Freud, S.: Oollected Papers. New York: The International Psycho-analytical Press, 1924. Vol. 1. (pages 76-106). 7. Kerr, W.J., Dalton, J.W., and Gliebe, P.A.: Some Physical Phenomena Associated with the Anxiety States and Their Relation to Hyperventilation. Ann. Intern. Med. 11: 961, December, 1937. 8. Kolb, L.C.: Anxiety and the Anxiety States. J. Ohronic Dis. 9: 199, March, 1959. 9. Okel, B.B., and Hurst, J.W.: Prolonged Hy·
10.
11.
12. 13.
14.
15. 16.
17.
18.
perventilation in Man. Arch. It/tern. Med. (Ohicago) , 108: 757, November, 1961. Lewis, B. I.: Hyperventilation Syndromes: Clinical and Physiologic Observations. Postgrad Med, 21: 259, March, ]!l57. Pitts, F. N., Jr., and McClure. J. N.: Lactate Metabolism in Anxiety Neurosis. New E.ng J Med, 277: 1329, December 21, 1967. Pitts, F. N., Jr.: The Biochemistry of Anxiety. 8ci Amer, 220: 69, February, 1969. Wood, P.: Da Costa's Syndrome (or Effort Syndrome). Brit Med J, 1: 767, May 24,1941 Gottsegen, G., Okos, G., and Romoda, T.: Essential Circulatory Hyperkinesis. Amer J Oardiol, 10: 785, December, 1962. Gorlin, R.: The Hyperkinetic Heart Syndrome. JAMA, 182: 823, November 24, 1962. Frohlich, E. D., Tarazi, R. C., and Dustan, H. P.: Hyperdynamic B-Adrenergic Circulatory State. Arch. Intern. Med. (Ohicago),123: I, January, 1969. Bollinger, A., Gander, M., Pylkkti.nen, P.O., Forster, G.: Treatment of the Hyperkinetic Heart Syndrome with Propranolol. Oardiologia (Basel), 49 (Suppl 2): 68, 1966. Granville-Grossman, K. L., and Turner, P.: The Effect of Propranolol on Anxiety. Lancet, 1: 788, April 9, 1966.
First International Collegium in Psychosomatic Medicine The Fifth World Congress of Psychiatry will take place in Mexico City, November 28 to December 4, 1971. It will be followed by the First International Collegium in Psychosomatic Medicine in Guadalajara, Mexico, December 5 to 8. Further details will be published as they become available. Those interested may contact either Edwin Dunlop, M.D., 150 Emory Street, Attleboro, Mass. (U.S.A.) or Dr. Roberto Kertesz, San Jose de Calasanz 431, Buenos Aires, Argentina (abroad). Both are serving as executive secretaries for the International Collegium.
July-August 1970
329