Characteristics of sighing in panic disorder - Wilhelm et al. (2001)
Patients with panic disorder (PD) have larger, more frequent sighs than non-PD patients
CO2 levels take longer to return to normal after a sigh in PD patients
Sighing might be a key cause of resting hypocapnia (low CO2) in PD patients
The Breathing Diabetic Summary
This paper examines sighing in patients with panic disorder (PD). The authors had performed a previous study where they found that PD patients sighed more frequently than non-PD patients. To understand this better, they aimed to analyze sighs in PD patients, identify potential triggering mechanisms, and see if excessive sighing can help explain the low resting CO2 (hypocapnia) observed in PD patients.
The study had 16 patients with PD, 15 with general anxiety disorder (GAD), and 19 healthy controls. The subjects were instructed to sit in a quiet room for 30 minutes and breathe through their noses while keeping their eyes open. The authors statistically examined the 3 breaths leading up to a sigh and the 3 breaths after one. They did the same for non-sigh breaths, so that they had 7-breath-sequences for each sigh or non-sigh breath.
The results showed that the PD patients actually breathed slower than the controls. However, their tidal volumes were larger. Using the data presented in their table, the controls had an average minute volume of ~5 L whereas the PD patients had an average minute volume of ~6 L. As we discussed before, breathing slowly does not necessarily mean breathing less. The tidal volume distributions of the PD patients also was skewed toward larger values, indicating more sigh-like breaths.
The authors believe that the 5 L vs. 6 L difference is not significant and that it is actually the ensemble of sigh-like breaths that is causing low CO2 values in PD patients. They suggest that not all breaths are created equal: Bigger breaths contribute disproportionately more to lowering CO2. Thus, they conclude that excessive sighing in PD patients might explain chronic hypocapnia observed in these patients.
The results also indicate that the triggering mechanism for sighing is associated with the suffocation theory of PD. The authors believe that this trigger could lower the set point for CO2 regulation, making sighs and large breaths more frequent. This process would lead to a positive feedback loop, where excessive sighing lowers the CO2 set point, which causes more large breaths, and so on. This also helps explain the chronically low CO2 observed in PD patients.
Overall, this paper showed that sighing is extremely important in PD. Their results suggest that sighing might help explain chronically lowered CO2 values in PD patients. For us, observing how often we sigh might help us understand our anxiety/panic levels.I have definitely become more conscious of sighing and can easily associate increased sighing with increased anxiety or stress. This is a great thing. When we notice increased sighing, we can then practice slow, light, wu-wei breathing to calm ourselves, restore CO2 levels to normal, and restore respiratory balance.
Abstract from Paper
BACKGROUND: Sighs, breaths with larger tidal volumes than surrounding breaths, have been reported as being more frequent in patients with anxiety disorders.
METHODS: Sixteen patients with panic disorder, 15 with generalized anxiety disorder, and 19 normal control subjects were asked to sit quietly for 30 min. Respiratory volumes and timing were recorded with inductive plethysmography and expired pCO(2), from nasal prongs.
RESULTS: Panic disorder patients sighed more and had tonically lower end-tidal pCO(2)s than control subjects, whereas generalized anxiety disorder patients were intermediate. Sighs defined as >2.0 times the subject mean discriminated groups best. Sigh frequency was more predictive of individual pCO(2) levels than was minute volume. Ensemble averaging of respiratory variables for sequences of breaths surrounding sighs showed no evidence that sighs were triggered by increased pCO(2) or reduced tidal volume in any group. Sigh breaths were larger in panic disorder patients than in control subjects. After sighs, pCO(2) and tidal volume did not return to baseline levels as quickly in panic disorder patients as in control subjects.
CONCLUSIONS: Hypocapnia in panic disorder patients is related to sigh frequency. In none of the groups was sighing a homeostatic response. Panic disorder patients show less peripheral chemoreflex gain than control subjects, which would maintain low pCO(2) levels after sighing.
Wilhelm FH, Trabert W, and Roth WT (2001), Characteristics of sighing in panic disorder, Biological Psychiatry, 49(7), 606 – 614.