~ Carbon dioxide (CO2) studies reveal insights into panic disorder (PD). ~ Breathing in 5% or inhaling 35% CO2 can trigger panic attacks more often in PD individuals. ~ PD patients describe these CO2-induced panic attacks as similar to their regular ones. This suggests a link between PD and aberrant respiratory responses. ~ Cognitive factors influence respiratory responses in PD, with perceived control playing a crucial role.
The intricate relationship between carbon dioxide (CO2) and panic attacks has long intrigued researchers, shedding light on the peculiarities of panic disorder (PD). Specifically, studies have consistently shown that the continuous re-breathing of 5% CO2 or even a single or double inhalation of 35% CO2 can trigger panic attacks more frequently in individuals with PD than in those with other anxiety disorders. Remarkably, PD patients undergoing these CO2-induced simulations often describe the resulting panic attacks as indistinguishable from their regular ones. This intriguing phenomenon lends credence to the hypothesis that PD might be intricately linked to an aberrant respiratory system.
The control of respiratory processes hinges on three crucial parameters: arterial blood levels of CO2, oxygen (O2), and hydrogen ions (H+). Among these, CO2 levels wield the most potent influence. Chemoreceptors, located both in the medulla (central control of respiration) and in the carotid bodies (peripheral control of respiration), play a pivotal role in regulating these parameters. While both types of chemoreceptors respond to changes in arterial blood, it is primarily the central chemoreceptors that mediate the respiratory response.
For instance, when PD individuals succumb to a panic attack after re-breathing 35% CO2, their breathing patterns have become notably shallower and more rapid compared to PD individuals who do not exhibit a similar reaction under the same experiment. This observation underscores the intricate link between PD and aberrations in respiratory response.
However, not all PD participants exhibit this exaggerated response, hinting at potential subgroups within PD with distinct etiological pathways. Particularly illuminating are the findings from a study involving the administration of a respiratory stimulant to two PD groups. The first group was informed to expect “harmless” physical sensations and given control over reducing the intensity of the challenge, while the second group was given no instructions. Intriguingly, this subtle cognitive manipulation led to reduced subjective respiratory responses within the first group compared to those who received no such instructions. This underscores the profound impact of subjective perception on PD’s respiratory response. The more individuals with PD feel in control of their respiration, the less distressing their breathing becomes.
In essence, the interplay between CO2 and panic disorder offers a multifaceted perspective on the condition’ s underlying mechanisms. These insights not only deepen our understanding of PD but also underscore the role of perception and cognition in shaping the experience of panic attacks. As research continues, it holds the promise of unveiling new avenues for therapeutic interventions and improved management of panic disorder.
Reference:
Rassovsky, Y., Abrams, K., & Kushner, M. G. (2006). Suffocation and respiratory responses to carbon dioxide and breath holding challenges in individuals with panic disorder. J Psychosom Res, 60(3), 291-298. doi:10.1016/j.jpsychores.2005.08.005