Panic disorder (PD) patients usually react with more self-reported distress to voluntary hyperventilation (HV) than do comparison groups. Less consistently PD patients manifest physiological differences such as more irregular breathing and slower normalization of lowered end-tidal pCO(2) after HV. To test whether physiological differences before, during, or after HV would be more evident after more intense HV, we designed a study in which 16 PD patients and 16 non-anxious controls hyperventilated for 3 min to 25 mmHg, and another 19 PD patients and another 17 controls to 20 mmHg. Patients reacted to HV to 20 mmHg but not to 25 mmHg with more self-reported symptoms than controls. However, at neither HV intensity were previous findings of irregular breathing and slow normalization of pCO(2) replicated. In general, differences between patients and controls in response to HV were in the cognitive-language rather than in the physiological realm.
OBJECTIVES: Because hyperventilation, dyspnea, and a feeling of choking are often core features of a panic attack, respiration has been one of the most widely studied physiological parameters in panic disorder (PD) patients. A respiratory subgroup of PD, with distinct etiological pathways, has also been suggested. Investigation of the recovery phase following a respiratory challenge may be a reliable way to establish respiratory impairment in PD patients. The objective of the present study was to investigate the recovery phase from a 35% carbon dioxide challenge in PD patients and in healthy controls, and to test the hypothesis of a different respiratory pattern in patients, compared to control subjects.
METHODS: Eleven nonmedicated PD patients with or without agoraphobia, 11 medicated PD patients, and 11 control subjects took part in a 35% carbon dioxide and 65% oxygen inhalation challenge. Respiratory rate, partial pressure of carbon dioxide, heart rate, and blood pressure were recorded during the baseline phase (10 minutes) and the recovery phase (10 minutes). Visual Analogue Scale of Anxiety and Panic Symptom List scores were collected pre- and post-challenge.
RESULTS: Nonmedicated patients had increased variability in respiratory rate and partial pressure of carbon dioxide during recovery, compared with control subjects and medicated PD patients. Also, PD patients tended to have higher heart rates and to need more time to recover from the challenge than control subjects.
CONCLUSIONS: Results suggest that PD patients have less effective homeostatic control after their physiological equilibrium has been disrupted by a respiratory stressor.
OBJECTIVE: Posttraumatic stress disorder (PTSD) and panic disorder (PD) are two anxiety disorders with prominent psychophysiological symptoms. The PTSD criterion of persistent hyperarousal suggests autonomic dysregulation, and the disorder has been associated with elevated heart rate. In contrast, PD has been associated with respiratory abnormalities such as low end-tidal Pco(2). An integrated analysis of automatic and respiratory function in a direct comparison of these anxiety disorders is currently lacking.
METHODS: Electrodermal, cardiovascular, and respiratory psychophysiology was examined in 23 PTSD patients, 26 PD patients, and 32 healthy individuals at baseline and during threat of shock.
RESULTS: At baseline, the PTSD patients, in contrast to the other two groups, were characterized by attenuated parasympathetic and elevated sympathetic control, as evidenced by low respiratory sinus arrhythmia (a measure of cardiac vagal control) and high electrodermal activity. They also displayed elevated heart rate and cardiovascular sympathetic activation in comparison with healthy controls. PD patients exhibited lower Pco(2) (hypocapnia) and higher cardiovascular sympathetic activation compared with healthy controls. PTSD patients, but not PD patients, sighed more frequently than controls. During the threat of shock phase, the PTSD group demonstrated blunted electrodermal responses.
CONCLUSIONS: Persistent hyperarousal symptoms in PTSD seem to be due to high sympathetic activity coupled with low parasympathetic cardiac control. Respiratory abnormalities were also present in PTSD. Several psychophysiological measures exhibited group-comparison effect sizes in the order of 1.0, supporting their potential for enhancing differential diagnosis and possibly suggesting utility as endophenotypes in genetic studies of anxiety disorders.
OBJECTIVE: Findings showing that individuals with panic disorder (PD) are prone to experience panic attacks when inhaling CO2-enriched air have given rise to the hypothesis that physiological systems underlying the experience of suffocation may be important in the etiology of PD. In this study, we tested several predictions stemming from this view.
METHODS: Forty individuals with PD and 32 controls underwent both a breath-holding challenge and a CO2 rebreathing challenge. A wide array of physiological and psychological responses, including continuous measurements of subjective suffocation, was recorded.
RESULTS: Individuals with PD experienced elevated physiological reactivity to both challenges and greater levels of suffocation sensations during the rebreathing challenge. Furthermore, PD individuals who experienced a panic attack in response to the rebreathing challenge exhibited faster but shallower breathing during the challenge than did other PD individuals.
CONCLUSION: Findings are consistent with theories linking PD to hypersensitive brain systems underlying the experience of suffocation. The possibility that subjective suffocation was in part mediated by peripheral interoceptive disturbances (vs. brainstem dysregulation) is discussed.
OBJECTIVE: Considerable evidence suggests a connection between panic disorder and respiration, but the nature of the respiratory abnormalities in panic disorder remains unclear. The authors investigated the breath-by-breath complexity of respiration dynamics in panic disorder.
METHOD: Respiratory physiology was assessed in 40 patients with panic disorder and 31 healthy comparison subjects by using a breath-by-breath stationary system for testing cardiorespiratory function. Irregularity in the breathing pattern was determined by applying the approximate entropy index, which is an indicator of the irregularity and the "disorder" of the measure.
RESULTS: The patients with panic disorder showed significantly higher approximate entropy indexes than the healthy subjects for the measured respiratory parameters. Sighs contributed to the irregularity of breathing patterns but did not account for all the differences in approximate entropy between the patients with panic disorder and the comparison subjects. Anxiety state, severity of illness, and somatic and individual variables such as participation in sports and cigarette smoking did not seem to influence the results.
CONCLUSIONS: Patients with panic disorder showed greater entropy in baseline respiratory patterns, indicating higher levels of irregularity and complexity in their respiratory function. Greater respiratory entropy could be a factor in vulnerability to panic attacks.
BACKGROUND: Respiratory irregularity has been previously reported in patients with panic disorder using time domain measures. However, the respiratory signal is not entirely linear and a few previous studies used approximate entropy (APEN), a measure of regularity of time series. We have been studying APEN and other nonlinear measures including a measure of chaos, the largest Lyapunov exponent (LLE) of heart rate time series, in some detail. In this study, we used these measures of respiration to compare normal controls (n = 18) and patients with panic disorder (n = 22) in addition to the traditional time domain measures of respiratory rate and tidal volume.
METHODS: Respiratory signal was obtained by the Respitrace system using a thoracic and an abdominal belt, which was digitized at 500 Hz. Later, the time series were constructed at 4 Hz, as the highest frequency in this signal is limited to 0.5 Hz. We used 256 s of data (1024 points) during supine and standing postures under normal breathing and controlled breathing at 12 breaths/min.
RESULTS: APEN was significantly higher in patients in standing posture during normal as well as controlled breathing (p = 0.002 and 0.02, respectively). LLE was also significantly higher in standing posture during normal breathing (p = 0.009). Similarly, the time domain measures of standard deviations and the coefficient of variation (COV) of tidal volume (TV) were significantly higher in the patient group (p = 0.02 and 0.004, respectively). The frequency of sighs was also higher in the patient group in standing posture (p = 0.02). In standing posture, LLE (p < 0.05) as well as APEN (p < 0.01) contributed significantly toward the separation of the two groups over and beyond the linear measure, i.e. the COV of TV.
CONCLUSION: These findings support the previously described respiratory irregularity in patients with panic disorder and also illustrate the utility of nonlinear measures such as APEN and LLE as additional measures toward a better understanding of the abnormalities of respiratory physiology in similar patient populations as the correlation between LLE, APEN and some of the time domain measures only explained up to 50-60% of the variation.
Disordered breathing may play an important role in the pathophysiology of panic disorder. Several studies have now indicated that panic disorder patients have greater respiratory variability than normal controls. In this study, we examine baseline respiratory measures in four diagnostic groups to determine whether greater respiratory variability is specific to panic disorder and whether effective anti-panic treatment alters respiratory variability. Patients with panic disorder, major depression, or premenstrual dysphoric disorder, and normal control subjects underwent two respiratory exposures (5% and 7% CO(2) inhalation), while in a canopy system. Panic disorder patients returned after 12 weeks of either anti-panic medication or cognitive behavioral therapy, and were retested. Normal control subjects were also retested after a period of 12 weeks. Panic disorder patients had significantly greater respiratory variability at baseline than normal control subjects and patients with major depression. The premenstrual dysphoric patients also had greater variability than the normal control group. Panic disorder patients who panicked to 7% CO(2) inhalation had significantly greater baseline variability than panic disorder patients who did not panic. Anti-panic treatment did not significantly alter baseline respiratory variability. Our data suggest that increased respiratory variability may be an important trait feature for some panic disorder patients and may make them more vulnerable to CO(2)-induced panic.
