Carbon dioxide hypersensitivity, hyperventilation, and panic disorder

OBJECTIVE: The purpose of this article is to offer a comprehensive, data-based explanation of the relationship between hyperventilation and panic disorder linking CO2 hypersensitivity, cognitive/behavioral factors, and the respiratory effects of antipanic pharmacologic and psychological treatments....

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Veröffentlicht in:The American journal of psychiatry 1993-08, Vol.150 (8), p.1149-1157
Hauptverfasser: PAPP, L. A, KLEIN, D. F, GORMAN, J. M
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container_title The American journal of psychiatry
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creator PAPP, L. A
KLEIN, D. F
GORMAN, J. M
description OBJECTIVE: The purpose of this article is to offer a comprehensive, data-based explanation of the relationship between hyperventilation and panic disorder linking CO2 hypersensitivity, cognitive/behavioral factors, and the respiratory effects of antipanic pharmacologic and psychological treatments. METHOD: The authors conducted a computerized search of MEDLINE for relevant articles. RESULTS: Some panic patients have a chronic, subtle respiratory disturbance. Acute hyperventilation is neither necessary nor sufficient for panic to occur. Respiratory abnormalities in panic patients may adaptively aim at coping with a hypersensitive CO2 chemoreceptor system. Pharmacologic panicogens also stimulate the respiratory system, causing hyperventilation. Triggering this hypersensitive respiratory control mechanism may incite panic. Antipanic medications may reset the receptor threshold. Misattribution and catastrophic interpretation of somatic symptoms or the sense of loss of control may contribute to panic symptoms. Behavioral interventions such as desensitization or breathing retraining may block the full-blown attack. Cognitive strategies through cognitive control of respiration may supplement and accentuate these interventions. CONCLUSIONS: Panic disorder may be due to an inherently unstable autonomic nervous system, coupled with cognitive distress.
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Acute hyperventilation is neither necessary nor sufficient for panic to occur. Respiratory abnormalities in panic patients may adaptively aim at coping with a hypersensitive CO2 chemoreceptor system. Pharmacologic panicogens also stimulate the respiratory system, causing hyperventilation. Triggering this hypersensitive respiratory control mechanism may incite panic. Antipanic medications may reset the receptor threshold. Misattribution and catastrophic interpretation of somatic symptoms or the sense of loss of control may contribute to panic symptoms. Behavioral interventions such as desensitization or breathing retraining may block the full-blown attack. Cognitive strategies through cognitive control of respiration may supplement and accentuate these interventions. CONCLUSIONS: Panic disorder may be due to an inherently unstable autonomic nervous system, coupled with cognitive distress.</abstract><cop>Washington, DC</cop><pub>American Psychiatric Publishing</pub><pmid>8392296</pmid><doi>10.1176/ajp.150.8.1149</doi><tpages>9</tpages></addata></record>
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subjects Adult and adolescent clinical studies
Alkalosis, Respiratory - chemically induced
Alkalosis, Respiratory - complications
Anxiety disorders. Neuroses
Biological and medical sciences
Carbon dioxide
Carbon Dioxide - adverse effects
Cognitive Therapy
Humans
Hyperventilation
Hyperventilation - chemically induced
Hyperventilation - complications
Lactates - pharmacology
Lactic Acid
Medical disorders
Medical sciences
Neuroses
Panic Disorder - etiology
Panic Disorder - physiopathology
Panic Disorder - therapy
Panic disorders
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Receptors, Cell Surface - drug effects
Receptors, Cell Surface - physiology
Relationship
Respiratory Center - drug effects
Respiratory Center - physiopathology
Respiratory system
Social research
title Carbon dioxide hypersensitivity, hyperventilation, and panic disorder
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