Hyperventilation in panic disorder and asthma: Empirical evidence and clinical strategies
Section snippets
The study of hyperventilation in health and disease
Hyperventilation, or hypocapnia, has been a pervasive topic in the general psychophysiology of emotion and performance (Wientjes, 1992, Ley and Yelich, 1998) as well as the clinical psychophysiology of anxiety disorders (e.g., Ley, 1992, Roth et al., 2005) and asthma (Herxheimer, 1946, Clarke and Gibson, 1980, Bruton and Holgate, 2005). Hyperventilation is caused by increased alveolar ventilation relative to metabolic carbon dioxide production. Consequently, alveolar carbon dioxide pressure
Symptom experience of panic patients and respiratory theories of panic disorder
Abnormalities in respiration have been postulated to play a central role in the development and maintenance of panic disorder. The clinical literature abounds with observations of panic patients presenting with a variety of physical complaints for which no organic origin is apparent. Among the most frequent and distressing symptoms reported by panic patients are sensations of shortness of breath, together with palpitations and dizziness (McNally et al., 1995, Meuret et al., 2006). Other
Hypocapnia in asthma
In the following, we will review the evidence for hypocapnia in asthma. As with studies examining the prevalence of hypocapnia in panic disorder, studies have reported a heightened prevalence of hypocapnia symptoms, reduced PCO2 levels, and an exaggerated increase in ventilation in response to a variety of stimuli in asthma. Experimental evidence that demonstrates adverse effects of hyperventilation in asthma will be reviewed. Furthermore, we will discuss circumstantial evidence linking
Therapeutic capnography
Reversing hypocapnia with the goal of achieving normocapnic levels has long been hypothesized to be beneficial (e.g., Laffey and Kavanagh, 2002). Although it seems plausible that interventions aimed at reversing hypocapnic states would validate their efficacy by means of objective measurements of CO2, this has rarely been done (Meuret et al., 2003). Thus, evaluating the effectiveness of most breathing trainings is greatly complicated by the lack of the most central measure, PCO2. One of the
General conclusion
Since its first introduction to panic and asthma treatment, breathing training has continued to evolve. However, lay conceptions about the benefits of individual breathing techniques (“deep breathing”) and a lack of mechanistic studies have impeded progress in this area for some time. The recently developed therapeutic capnometry for panic and asthma offers the advantage of a plausible and testable psychophysiological rationale for the expected treatment effects. For panic treatment, this is a
Acknowledgements
Preparation of this manuscript was partly funded by a National Institutes of Health/National Heart, Lung and Blood Institute grant, R01 HL-089761 (to both authors), and the generous support of the Beth and Russell Siegelman Foundation (Meuret).
We gratefully acknowledge the role of Dr. Walton T. Roth in inspiring and mentoring the authors' pursuit of respiratory psychophysiology in clinical psychology research.
We thank Dr. Karleyton Evans for valuable suggestions on an earlier version of this
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