Biofeedback Training to Increase P co2 in Asthma With Elevated Anxiety: A One-Stop Treatment of Both Conditions?

OBJECTIVE: Anxiety is highly prevalent in individuals with asthma. Asthma symptoms and medication can exacerbate anxiety, and vice versa. Unfortunately, treatments of comorbid anxiety and asthma are largely lacking. A problematic feature common to both conditions is hyperventilation. It adversely affects lung function and symptoms in asthma and anxiety. We examined whether a treatment to reduce hyperventilation, shown to improve asthma symptoms, also improves anxiety in asthma patients with high anxiety. METHOD: One hundred twenty English- or Spanish-speaking adult patients with asthma were randomly assigned to either Capnometry-Assisted Respiratory Training (CART) to raise P co2 or feedback to slow respiratory rate (SLOW). Although anxiety was not an inclusion criterion, 21.7% met clinically relevant anxiety levels on the Hospital Anxiety and Depression Scale (HADS). Anxiety (HADS-A) and depression (HADS-D) scales, anxiety sensitivity (Anxiety Sensitivity Index [ASI]), and negative affect (Negative Affect Scale of the Positive Affect Negative Affect Schedule) were assessed at baseline, posttreatment, 1-month follow-up, and 6-month follow-up. RESULTS: In this secondary analysis, asthma patients with high baseline anxiety showed greater reductions in ASI and PANAS-N in CART than in SLOW ( p values ≤ .005, Cohen d values ≥ 0.58). Furthermore, at 6-month follow-up, these patients also had lower ASI, PANAS-N, and HADS-D in CART than in SLOW ( p values ≤ .012, Cohen d values ≥ 0.54). Patients with low baseline anxiety did not have differential outcomes in CART than in SLOW. CONCLUSIONS: For asthma patients with high anxiety, our brief training designed to raise P co2 resulted in significant and sustained reductions in anxiety sensitivity and negative affect compared with slow-breathing training. The findings lend support for P co2 as a potential physiological target for anxiety reduction in asthma. TRIAL REGISTRATION: Clinicaltrials.gov Identifier: NCT00975273 .

Respiratory muscle tension as symptom generator in individuals with high anxiety sensitivity.

OBJECTIVE: Anxiety and panic are associated with the experience of a range of bodily symptoms, in particular unpleasant breathing sensations (dyspnea). Respiratory theories of panic disorder have focused on disturbances in blood gas regulation, but respiratory muscle tension as a source of dyspnea has not been considered. We therefore examined the potential of intercostal muscle tension to elicit dyspnea in individuals with high anxiety sensitivity, a risk factor for developing panic disorder. METHODS: Individuals high and low in anxiety sensitivity (total N=62) completed four tasks: electromyogram biofeedback for tensing intercostal muscle, electromyogram biofeedback for tensing leg muscles, paced breathing at three different speeds, and a fine motor task. Global dyspnea, individual respiratory sensations, nonrespiratory sensations, and discomfort were assessed after each task, whereas respiratory pattern (respiratory inductance plethysmography) and end-tidal carbon dioxide (capnography) were measured continuously. RESULTS: In individuals with high compared to low anxiety sensitivity, intercostal muscle tension elicited a particularly strong report of obstruction (M=5.1, SD=3.6 versus M=2.5, SD=3.0), air hunger (M=1.9, SD=2.1 versus M=0.4, SD=0.8), hyperventilation symptoms (M=0.6, SD=0.6 versus M=0.1, SD=0.1), and discomfort (M=5.1, SD=3.2 versus M=2.2, SD=2.1) (all p values<.05). This effect was not explained by site-unspecific muscle tension, voluntary manipulation of respiration, or sustained task-related attention. Nonrespiratory control sensations were not significantly affected by tasks (F<1), and respiratory variables did not reflect any specific responding of high-Anxiety Sensitivity Index participants to intercostal muscle tension. CONCLUSIONS: Respiratory muscle tension may contribute to the respiratory sensations experienced by panic-prone individuals. Theories and treatments for panic disorder should consider this potential source of symptoms.

Hypoventilation training for asthma: a case illustration.

Hyperventilation-induced hypocapnia is common among asthma patients. This case study illustrates both methodology and results from a patient undergoing training in capnometry-assisted respiratory training (CART). CART is a 4-week training aimed at normalizing basal and acute levels of end-tidal carbon dioxide (PCO(2)) using a portable capnometer. In the presented case, basal levels of PCO(2) increased from hypocapnic to normocapnic range over the course of treatment. Improvements were accompanied by improvements in lung function and reductions in diurnal lung function variability. Improvements remained stable throughout follow-up.

Respiratory and cognitive mediators of treatment change in panic disorder: evidence for intervention specificity.

OBJECTIVE: There are numerous theories of panic disorder, each proposing a unique pathway of change leading to treatment success. However, little is known about whether improvements in proposed mediators are indeed associated with treatment outcomes and whether these mediators are specific to particular treatment modalities. Our purpose in this study was to analyze pathways of change in theoretically distinct interventions using longitudinal, moderated mediation analyses. METHOD: Forty-one patients with panic disorder and agoraphobia were randomly assigned to receive 4 weeks of training aimed at altering either respiration (capnometry-assisted respiratory training) or panic-related cognitions (cognitive training). Changes in respiration (PCO2, respiration rate), symptom appraisal, and a modality-nonspecific mediator (perceived control) were considered as possible mediators. RESULTS: The reductions in panic symptom severity and panic-related cognitions and the improvements in perceived control were significant and comparable in both treatment groups. Capnometry-assisted respiratory training, but not cognitive training, led to corrections from initially hypocapnic to normocapnic levels. Moderated mediation and temporal analyses suggested that in capnometry-assisted respiratory training, PCO2 unidirectionally mediated and preceded changes in symptom appraisal and perceived control and was unidirectionally associated with changes in panic symptom severity. In cognitive training, reductions in symptom appraisal were bidirectionally associated with perceived control and panic symptom severity. In addition, perceived control was bidirectionally related to panic symptom severity in both treatment conditions. CONCLUSION: The findings suggest that reductions in panic symptom severity can be achieved through different pathways, consistent with the underlying models.

Changes in respiration mediate changes in fear of bodily sensations in panic disorder.

The purpose of the study was to examine whether changes in pCO(2) mediate changes in fear of bodily sensation (as indexed by anxiety sensitivity) in a bio-behavioral treatment for panic disorder that targets changes in end-tidal pCO(2). Thirty-five panic patients underwent 4 weeks of capnometry-assisted breathing training targeting respiratory dysregulation. Longitudinal mediation analyses of the changes in fear of bodily symptoms over time demonstrated that pCO(2), but not respiration rate, was a partial mediator of the changes in anxiety sensitivity. Results were supported by cross lag panel analyses, which indicated that earlier pCO(2) levels predicted later levels of anxiety sensitivity, but not vice versa. PCO(2) changes also led to changes in respiration rate, questioning the importance of respiration rate in breathing training. The results provide little support for changes in fear of bodily sensations leading to changes in respiration, but rather suggest that breathing training targeting pCO(2) reduced fear of bodily sensations in panic disorder.

Changes in pCO2, symptoms, and lung function of asthma patients during capnometry-assisted breathing training.

In a recent pilot study with asthma patients we demonstrated beneficial outcomes of a breathing training using capnometry biofeedback and paced breathing assistance to increase pCO(2) levels and reduce hyperventilation. Here we explored the time course changes in pCO(2), respiration rate, symptoms and lung function across treatment weeks, in order to determine how long training needs to continue. We analyzed in eight asthma patients whether gains in pCO(2) and reductions in respiration rate achieved in home exercises with paced breathing tapes followed a linear trend across the 4-week treatment period. We also explored the extent to which gains at home were manifest in weekly training sessions in the clinic, in terms of improvement in symptoms and spirometric lung function. The increases in pCO(2) and respiration rate were linear across treatment weeks for home exercises. Similar increases were seen for in-session measurements, together with gradual decreases in symptoms from week to week. Basal lung function remained stable throughout treatment. With our current protocol of paced breathing and capnometry-assisted biofeedback at least 4 weeks are needed to achieve a normalization of pCO(2) levels and reduction in symptoms in asthma patients.

Feedback of end-tidal pCO2 as a therapeutic approach for panic disorder.

BACKGROUND: Given growing evidence that respiratory dysregulation is a central feature of panic disorder (PD) interventions for panic that specifically target respiratory functions could prove clinically useful and scientifically informative. We tested the effectiveness of a new, brief, capnometry-assisted breathing therapy (BRT) on clinical and respiratory measures in PD. METHODS: Thirty-seven participants with PD with or without agoraphobia were randomly assigned to BRT or to a delayed-treatment control group. Clinical status, respiration rate, and end-tidal pCO(2) were assessed at baseline, post-treatment, 2-month and 12-month follow-up. Respiratory measures were also assessed during homework exercises using a portable capnometer as a feedback device. RESULTS: Significant improvements (in PD severity, agoraphobic avoidance, anxiety sensitivity, disability, and respiratory measures) were seen in treated, but not untreated patients, with moderate to large effect sizes. Improvements were maintained at follow-up. Treatment compliance was high for session attendance and homework exercises; dropouts were few. CONCLUSIONS: The data provide preliminary evidence that raising end-tidal pCO(2) by means of capnometry feedback is therapeutically beneficial for panic patients. Replication and extension will be needed to verify this new treatment's efficacy and determine its mechanisms.

Targeting pCO(2) in asthma: pilot evaluation of a capnometry-assisted breathing training.

OBJECTIVES: This pilot study aimed to evaluate the feasibility and potential benefits of a novel biofeedback breathing training for achieving sustained increases in pCO(2) levels. METHODS: Twelve asthma patients were randomly assigned to an immediate 4-week treatment group or waiting list control. Patients were instructed to modify their respiration in order to change levels of end-tidal pCO(2) using a hand-held capnometer. Treatment outcome was assessed in frequency and distress of symptoms, asthma control, lung function, and variability of peak expiratory flow (PEF). RESULTS: We found stable increases in pCO(2) and reductions in respiration rate during treatment and 2-month follow-up. Mean pCO(2) levels rose from a hypocapnic to a normocapnic range at follow-up. Frequency and distress of symptoms was reduced and reported asthma control increased. In addition, mean PEF variability decreased significantly in the treatment group. CONCLUSIONS: Our pilot intervention provided evidence for the feasibility of pCO(2)-biofeedback training in asthma patients.

Psychophysiological effects of breathing instructions for stress management.

Stressed and tense individuals often are recommended to change the way they breathe. However, psychophysiological effects of breathing instructions on respiration are rarely measured. We tested the immediate effects of short and simple breathing instructions in 13 people seeking treatment for panic disorder, 15 people complaining of daily tension, and 15 controls. Participants underwent a 3-hour laboratory session during which instructions to direct attention to breathing and anti-hyperventilation instructions to breathe more slowly, shallowly, or both were given. Respiratory, cardiac, and electrodermal measures were recorded. The anti-hyperventilation instructions failed to raise end-tidal pCO(2) above initial baseline levels for any of the groups because changes in respiratory rate were compensated for by changes in tidal volume and vice versa. Paying attention to breathing significantly reduced respiratory rate and decreased tidal volume instability compared to the other instructions. Shallow breathing made all groups more anxious than did other instructions. Heart rate and skin conductance were not differentially affected by instructions. We conclude that simple and short instructions to alter breathing do not change respiratory or autonomic measures in the direction of relaxation, except for attention to breathing, which increases respiratory stability. To understand the results of breathing instructions for stress and anxiety management, respiration needs to be monitored physiologically.

Voluntary hyperventilation in the treatment of panic disorder--functions of hyperventilation, their implications for breathing training, and recommendations for standardization.

Hyperventilation has numerous theoretical and empirical links to anxiety and panic. Voluntary hyperventilation (VH) tests have been applied experimentally to understand psychological and physiological mechanisms that produce and maintain anxiety, and therapeutically in the treatment of anxiety disorders. From the theoretical perspective of hyperventilation theories of anxiety, VH is useful diagnostically to the clinician and educationally to the patient. From the theoretical perspective of cognitive-behavior therapy, VH is a way to expose patients with panic disorder to sensations associated with panic and to activate catastrophic cognitions that need restructuring. Here we review panic disorder treatment studies using breathing training that have included VH. We differentiate the roles of VH in diagnosis, education about symptoms, training of breathing strategies, interoceptive exposure, and outcome measurement--discussing methodological issues specific to these roles and VH test reliability and validity. We propose how VH procedures might be standardized in future studies.

Respiratory feedback for treating panic disorder.

Panic disorder patients often complain of shortness of breath or other respiratory complaints, which has been used as evidence for both hyperventilation and false suffocation alarm theories of panic. Training patients to change their breathing patterns is a common intervention, but breathing rarely has been measured objectively in assessing the patient or monitoring therapy results. We report a new breathing training method that makes use of respiratory biofeedback to teach individuals to modify four respiratory characteristics: increased ventilation (Respiratory Rate x Tidal Volume), breath-to-breath irregularity in rate and depth, and chest breathing. As illustrated by a composite case, feedback of respiratory rate and end-tidal pCO2 can facilitate voluntary control of respiration and reduce symptoms. Respiratory monitoring may provide relevant diagnostic, prognostic, and outcome information.

Breathing training for treating panic disorder. Useful intervention or impediment?

Breathing training (BT) is commonly used for treatment of panic disorder. We identified nine studies that reported the outcome of BT. Overall, the published studies of BT are not sufficiently compelling to allow an unequivocal judgment of whether such techniques are beneficial. This article discusses problems with the underlying rationale, study design, and techniques used in BT, and it identifies factors that may have determined therapy outcomes. The idea that hypocapnia and respiratory irregularities are underlying factors in the development of panic implies that these factors should be monitored physiologically throughout therapy. Techniques taught in BT must take account of respiration rate and tidal volume in the regulation of blood gases (pCO2). More studies are needed that are designed to measure the efficacy of BT using an adequate rationale and methodology. Claims that BT should be rejected in favor of cognitive or other forms of intervention are premature.