Hyperventilation in panic disorder and asthma: Empirical evidence and clinical strategies

https://doi.org/10.1016/j.ijpsycho.2010.05.006Get rights and content

Abstract

Sustained or spontaneous hyperventilation has been associated with a variety of physical symptoms and has been linked to a number of organic illnesses and mental disorders. Theories of panic disorder hold that hyperventilation either produces feared symptoms of hypocapnia or protects against feared suffocation symptoms of hypercapnia. Although the evidence for both theories is inconclusive, findings from observational, experimental, and therapeutic studies suggest an important role of low carbon dioxide (CO2) levels in this disorder. Similarly, hypocapnia and associated hyperpnia are linked to bronchoconstriction, symptom exacerbation, and lower quality of life in patients with asthma. Raising CO2 levels by means of therapeutic capnometry has proven beneficial effects in both disorders, and the reversing of hyperventilation has emerged as a potent mediator for reductions in panic symptom severity and treatment success.

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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