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Letter to the Editor   |    
Alveolar Ventilation During Hyperventilation by Panic Disorder Patients
IMRE JANSZKY, M.D.; MARIA KOPP, M.D., PH.D.
Am J Psychiatry 1999;156:667a-668.

To the Editor: We are concerned about the study on the hyperventilation test of panic disorder patients by Laszlo A. Papp, M.D., and colleagues (1). Their article is one of the most comprehensive studies on the psychophysiological parameters of panic patients; however, the study might have some additional value that escaped the authors’ attention during the discussion of their data.

We noticed that during cognitive behavioral psychotherapy for panic disorder, some patients, following our request to hyperventilate, started to breathe with sounds reminiscent of a dog panting in hot weather. According to physiological data, panting (high-frequency breathing with low tidal volume) by dogs increases minute ventilation, air change, and evaporation of the mucosa but avoids real hyperventilation. Because the effective part of a breath is the tidal volume minus the respiratory dead space, the result multiplied by the respiratory rate is the alveolar (minute) ventilation. In spite of the increase in minute ventilation, the alveolar ventilation during panting may be unchanged because of the decrease of tidal volume.

We hypothesize that our panic disorder patients tried to avoid real hyperventilation by using a similar, ineffective, formal hyperventilation with low tidal volume that can help them in natural panicogenic situations as well. This formal hyperventilation is the opposite of the (deep and not-so-fast) respiratory pattern of trained athletes.

According to the authors’ data, during the hyperventilation test, the "nonpanicker" panic disorder patients breathed with the lowest tidal volume. (The highest tidal volume belonged to the "panickers"; comparison subjects had medium values.) The difference between the data increases markedly if we consider the problem of respiratory dead space and alveolar ventilation. Estimating the alveolar ventilation of the subjects by using an average value of respiratory dead space (140 ml–150 ml), we found that while the alveolar ventilation of nonpanicker patients increased slightly (it almost remained stable), in the two other groups, the increase in alveolar ventilation was remarkable, especially among panickers. The patients can also be divided into two sets concerning alveolar ventilation: those who change their alveolar ventilation less, or more, than the comparison subjects. The group of nonpanicker patients contained not only those who did not really hyperventilate but also those whose panic attacks did not have any connection with the hyperventilation syndrome. We can assume that the difference between the "panters" and the patients who really hyperventilated would be more obvious if the subjects had not been encouraged to maintain a respiratory rate of 30 breaths per minute. Most likely, the "panters" would have increased their respiratory rate to over 30 breaths per minute so as to be more similar to the panting we observed in a large group of panic disorder patients.

Papp LA, Martinez JM, Klein DF, Coplan JD, Norman RG, Cole R, de Jesus MJ, Ross D, Goetz R, Gorman JM: Respiratory psychophysiology of panic disorder: three respiratory challenges in 98 subjects. Am J Psychiatry  1997; 154:1557–1565
[PubMed]
 
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References

Papp LA, Martinez JM, Klein DF, Coplan JD, Norman RG, Cole R, de Jesus MJ, Ross D, Goetz R, Gorman JM: Respiratory psychophysiology of panic disorder: three respiratory challenges in 98 subjects. Am J Psychiatry  1997; 154:1557–1565
[PubMed]
 
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