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Objective: Previous research has found differences in respiratory function between panic disorder and other anxiety disorder populations. These differences have been explained as reflecting either a) a specific feature of panic disorder, b) merely a sign of increased general arousal, or c) a result of population sampling error. The current study addressed the question of such differences by using improved methodology over previous research. A preliminary evaluation of respiratory symptoms during panic attacks was undertaken as a means of identifying a respiratory-sensitive subtype of the panic patient., Method: Seventeen panic disorder patients (PD), 18 patients with generalized anxiety disorder (GAD), and 20 normal control (NC) subjects were administered a psychophysiological evaluation composed of baseline, stressor, and recovery phases. Panic patients were measured for the severity of respiratory symptoms during panic attacks. End-tidal CO2 (EtCO2) and respiration rate were measured throughout the psychophysiological evaluation., Results: PDs demonstrated significantly lower baseline EtCO2 levels than the GADs and NCs, in spite of being equivalent to GADs on baseline anxiety levels. Moreover, panic patients reporting a high level of respiratory symptoms during panic attacks seemed to account for the bulk of observed differences., Conclusions: These findings lend support to a group of studies showing differences in respiratory function between panic disorder and other anxiety disorder populations. In addition, this study provides preliminary support for the presence of a distinct "hyperventilation subtype" of panic disorder. The implications of these findings for future research and treatment are discussed.

Functional disease is a common and difficult problem in clinical neurology. A thorough appraisal should be undertaken before concluding that a patient's problem is not physically based. This article describes symptoms and signs of potential value in the diagnosis of such disorder.

Whether multiple chemical sensitivity (MCS) is an organic disease initiated by environmental exposure or a psychologic disorder is a subject of controversy. The identification of pathophysiologic or psychophysiologic mechanisms occurring in patients with MCS after provocative challenges should be illuminating. Fifteen patients with MCS were challenged with their trigger substances and observed clinically. Prechallenge and postchallenge pulmonary function tests and PCO2, PO2, and oxygen saturation were measured. All of the patients whose symptoms were reproduced by the challenge (11 of 15) showed clinical evidence of acute hyperventilation with a rapid fall in PCO2 and no change or a rise in oxygen saturation. The symptoms and signs were consistent with an anxiety reaction with hyperventilation. Pulmonary function was unchanged; and recovery was rapid, aided in two cases by rebreathing into a paper bag. The most logical conclusion is that in these patients the MCS disorder is a manifestation of an anxiety syndrome triggered by their perception of an environmental insult, with at least some of their symptoms induced by hyperventilation.

Undergraduate women who scored in the top (n = 24) and bottom 15% (n = 24) on the Anxiety Sensitivity Index viewed randomly counterbalanced sets of three neutral and three dysphoric faces after having either hyperventilated or relaxed. Participants rated the amount of change they experienced in Happiness, Sadness, Fear, Anger, Surprise, Disgust, and Contempt after viewing each face. High Anxiety Sensitive (AS) women reported significantly greater changes on six of the seven emotions, even though pretreatment differences in somatically experienced anxiety were covaried out. Significant three-way interactions were found for participants self-rated changes in Fear and Surprise, with tendencies toward significance (p < .10) also emerging for Anger and Disgust. The pattern of interactions was identical for all four variables. Low AS women manifested greater reductions in these four emotions when viewing neutral as opposed to dysphoric faces, regardless of whether they hyperventilated or relaxed. High AS women who relaxed manifested similar discriminative abilities. High AS women who hyperventilated, however, reported no relative changes in emotional arousal to both dysphoric and neutral faces. The blunted discrimination shown by high AS women who hyperventilated suggests that, when these individuals are in a physiologically challenged state, they may be less responsive to "early warning" indicators of social distress displayed by others which may, in turn, cause them to experience subsequent interpersonal difficulties.

Study Objective: To determine the frequency of documented depression screening for adolescents presenting with somatic chief complaints to a pediatric emergency department., Methods: We conducted a retrospective chart review of 408 consecutive patients aged 11 to 17 years who presented to the ED with a chief complaint of chest pain, abdominal pain, headache, weakness/fatigue, dizziness/fainting, or hyperventilation., Results: Documentation of depression screening was noted in 4.2% of cases (17 of 408). For patients charts listing both a somatic chief complaint and a similar nonspecific discharge diagnosis, the documentation rate for depression screening rose to 7.5%. No change in screening documentation was noted for chronically ill patients. We did detect a significant difference in screening frequency between black adolescents and adolescents of all other races (P = .021)., Conclusion: Our findings demonstrate an extremely low frequency of documentation of depression screening in adolescents with somatic complaints presenting to the ED. Documentation of screening in black patients was still low but was performed at a significantly higher rate. These results indicate a need for education on the adolescent at risk for depression and suicide in the acute care setting.

The objective of this study was to validate the Asthma Symptom Checklist (ASC) so that it could be reliably used to assess the subjective symptomatology of asthma attacks in our context. Subjective symptomatology of asthma was examined in a group of 100 adult Spanish outpatients (57 women, 43 men; 17-69 years of age) with asthma. All of them completed the modified version of the ASC as well as questionnaires of depression, anxiety, and self-management of asthma (self-efficacy expectancies and health care utilization). Data about duration and severity of asthma, as well as dyspnea and %FEV1, were also recorded. The highest reliability Cronbach alpha indexes were for the panic-fear and fatigue scales. The oblique rotation of the ASC revealed five correlated factors (53% of the total variance explained): 1) panic-fear, 2) airways obstruction, 3) airways obstruction and panic-fear, 4) fatigue and irritability, 5) hyperventilation. The structure of factors was revalidated using orthogonal (varimax) rotation. Construct validity was examined by Person product-moment coefficient correlations, ANOVAs (asthma severity x ASC scores), and t-tests (sex by ASC scores). Panic-fear showed the best construct validity, as it was related to the severity of the asthma and the use of high-cost health care resources. There were no differences in ASC scores either on the basis of the asthma severity or on the sex of patients. The ASC factors represent stable components of subjective symptomatology of asthma attacks, especially with regard to the panic-fear and the hyperventilation subscales; however, the structure of the checklist as a whole was not identical to those reported in other studies. Correlations of the ASC with clinical variables related to asthma severity support the construct validity of the instrument and confirm its utility to evaluate the subjective symptomatology of asthma attacks in outpatients.

Objective: Assuming a subjective similarity between the experience of a hyperventilation episode and inhaling CO2-enriched air, we tested whether a respiratory challenge in association with a particular stimulus could result in altered respiratory behavior and associated somatic complaints upon presenting the stimulus only., Method: Psychosomatic patients (N = 28) reporting hyperventilation complaints participated in a differential conditioning paradigm using odors with a positive or negative valence as conditioned stimuli (CS+ or CS-) and 7.4% CO2-enriched air as the unconditioned stimulus (US). Three CS+ and three CS-acquisition trials were run. During the test phase, two CS(+)- and two CS(-)-only trials were run, followed by two new test odors (with a positive or negative valence). Respiratory frequency, tidal volume, end-tidal fractional concentration of CO2, and heart rate were measured throughout the experiment. Somatic complaints were registered after each trial., Results: We observed a) increased respiratory frequency and an elevated level of somatic complaints upon presenting the CS+ only; b) a selective association effect: conditioning was only apparent with the negatively valenced CS+ odor; (c) no generalization of respiratory responses and complaints to the new odors; (d) no conditioning effect on dummy complaints that are usually not reported when inhaling CO2; (e) in exploratory comparisons with normal subjects, stronger conditioning effects on typical hyperventilation complaints in patients, and, in female subjects, on respiratory frequency., Conclusion: Respiratory responses and psychosomatic complaints can be elicited by conditioned stimuli in a highly specific way. The findings are relevant for disorders in which respiratory abnormalities and/or psychosomatic complaints may play a role and for multiple chemical sensitivity.

The Hyperventilation Provocation Test (HVPT) has become a routine procedure in the diagnosis of hyperventilation syndrome (HVS). During an HVPT the patient voluntarily overbreathes for several minutes to produce hypocapnia. The test is considered positive if the induced symptoms are recognized by the patient as similar to those experienced in daily life. The present study tests the assumption that hypocapnia is the primary trigger for symptoms during an HVPT. In a randomized double-blind crossover design. 115 patients suspected of HVS and 40 healthy controls performed an HVPT and a placebo test (PT, isocapnic overbreathing). The HVPT induced more symptoms than the PT, especially more neuromuscular symptoms, cerebral symptoms, paresthesias, and temperature sensations. However, the absolute difference between the number of symptoms induced by the HVPT and PT was small. In patients, the PT induced 66% of symptoms induced by the HVPT. In the control group this percentage was 60%. The low specificity of the HVPT implies that symptom recognition during the HVPT is invalid as a diagnostic criterion for HVS.

We studied 23 consecutive patients with acute hyperventilation presenting to an inner-city emergency department, diagnosed on clinical grounds by the attending physician and confirmed by arterial blood gas values in 5 patients. An organic basis for the presenting complaints was excluded and chest radiograph, serum biochemistry, blood cell count, and thyroid function test results were normal. The male to female ratio was 12:11. Presenting complaints were dyspnea (61%), paresthesia (35%), chest pain or tightness (43%), muscle spasm (9%), dizziness (13%), palpitations (13%), and panic (30%). Similar previous episodes were reported in 74%. Misattribution of the presenting complaints to a cardiac or other life-threatening disorder was reported in 20 patients (87%) and was the main reason for their presentation to the hospital. Although no patients presented with clinical features of asthma, 7 (30%) were known asthmatics receiving treatment and another 10 (44%) had a history and investigation results suggestive of asthma. Only 2 had a history of anxiety or depression, but 17 (78%) patients exceeded the threshold for anxiety or panic on Clinical Interview Schedule (CIS-R) interview (score > or = 12). Marihuana or alcohol abuse were involved in 17% with a history of past abuse in 26%. When assessed 2 months after the attack, 13 (57%) had resting or stressor-induced hyperventilation with a significant (p < 0.05) association with asthma but not with a positive CIS-R score. These results illustrate the multifactorial basis of acute hyperventilation, the importance of misattribution, and the danger of using the term "hyperventilation syndrome" in the emergency department.

D.F. Klein (1993) proposed that patients with panic disorder (PD) have a hypersensitive suffocation monitor that predisposes them to experience panic attacks under certain conditions. The suffocation alarm theory predicts differential emotional responding to biological challenges that affect arterial partial pressure of carbon dioxide (PCO2). These PD patients should exhibit (a) lower fear and less likelihood of panic in response to biological challenges that lower PCO2 levels (e.g., hyperventilation), and (b) increased fear and greater likelihood of panic in response to biological challenges that raise PCO2 levels (e.g., inhalation of 35% CO2 gas). The following indicators of the suffocation monitor were assessed: (a) severity of dyspnea symptoms, (b) frequency of dyspnea symptoms, (c) heightened respiration rate, and (d) lowered PCO2 levels. Ratings of physiological and subjective responding, as well as panic, were obtained during both a hyperventilation and a 35% CO2 challenge. None of the classification methods predicted differential emotional responding to hyperventilation versus 35% CO2 challenge.

Background: Hyperventilation syndrome (HVS) describes a set of somatic and psychological symptoms thought to result from episodic or chronic hyperventilation. Recognition of symptoms during the hyperventilation provocation test (HVPT) is the most widely used criterion for diagnosis of HVS. We have investigated the validity of the HVPT and of the concept of HVS., Methods: In a randomised, double-blind, crossover design, the ability of 115 patients with suspected HVS to recognise symptoms during the HVPT was compared with the ability to recognise symptoms during a placebo test (isocapnic overbreathing, with carbon dioxide levels maintained by manual titration). 30 patients who had positive results on the HVPT underwent ambulatory transcutaneous monitoring of pCO2 to ascertain whether they hyperventilated during spontaneous symptom attacks., Findings: Of the 115 patients who underwent the HVPT and the placebo test, 85 (74%) reported symptom recognition during the HVPT (positive diagnosis HVS). Of that subset, 56 were also positive on the placebo test (false-positive), and 29 were negative on the placebo test (true-positive). False-positive and true-positive patients did not differ in symptom profile or in physiological variables. During ambulatory monitoring (15 true-positive, 15 false-positive) 22 attacks were registered. Transcutaneous end-tidal, pCO2 decreased during only seven. The decreases were slight and apparently followed the onset of the attack, which suggests that hyperventilation is a consequence rather than a cause of the attack. There were no apparent differences between false-positive and true-positive patients., Interpretation: The HVPT is invalid as a diagnostic test for HVS. Hyperventilation seems a negligible factor in the experience of spontaneous symptoms. The term HVS should be avoided.

Unlabelled: The goals of this study were to: a) confirm prior evidence that the respiratory stimulant doxapram induces panic attacks and produces excessive hyperventilation in patients with panic disorder and b) explore the impact of cognitive mediators on symptom and respiratory responses., Method: Thirty-two subjects (16 patients and 16 controls) received doxapram (0.5 mg/kg) and placebo infusions while symptom, respiratory, and heart rate responses were monitored. Subjects were randomly assigned to receive either a standard introduction or a cognitive intervention designed to reduce the panic responses of panic patients to laboratory challenges., Results: Doxapram was a potent and specific panicogenic agent, inducing panic in 75% of patients and 12.5% of controls. Compared with controls, patients also showed a greater decrease in end tidal carbon dioxide (CO2) and greater increases in minute ventilation, respiratory frequency, and heart rate. The cognitive intervention substantially attenuated the excessive hyperventilatory response of patients but did not fully normalize their breathing patterns. Tidal volume was the only respiratory measure not significantly altered by the cognitive intervention., Conclusions: In patients with panic disorder, doxapram (0.5 mg/kg) triggers panic attacks about as potently as 7% CO2 and more potently than 5% CO2 or lactate. Psychological factors can modulate the appearance of ventilatory abnormalities in panic patients, but persistent respiratory disturbances were still seen. Psychological factors and respiratory physiology both appear to be important phenomena in laboratory panic.

Ventilatory gas exchange during exercise was compared in patients with mild asthma (11 females and 11 males), hyperventilation syndrome (HVS, 11 females), and healthy subjects (11 females and 11 males) in order to assess hyperventilation during exercise and its association with exercise-induced bronchoconstriction. The asthmatics showed decreased working capacity and decreased maximal oxygen consumption, with no evidence of limitation due to impairment of ventilatory capacity. Ventilatory equivalents for CO2 and O2 (VE/VCO2 and VE/VO2) at rest did not differ between the controls and asthmatics, but they were significantly elevated in HVS. In female asthmatics, ventilatory equivalents during exercise were significantly (P < 0.05) elevated compared with those of healthy subjects; in female controls, VE/VCO2 was 30.1 +/- 3.3 at low exercise and 27.4 +/- 6.5 at maximal exercise. In female asthmatics, the corresponding figures were 34.9 +/- 6.1 and 36.7 +/- 5.3. Furthermore, VE/VCO2 individually related to percent of maximal oxygen consumption (VO2max) was significantly increased in female asthmatics both at low and high VO2. The highest ventilatory equivalents were obtained in HVS, 41.7 +/- 6.7 and 43.9 +/- 0.9, respectively. Significant exercise-induced bronchoconstriction (decrease of FEV1 > 15%) was found in 50% of the asthmatics. The ventilatory equivalents did not correlate with exercise-induced changes in FEV1 (r2 < 0.3). Mild exercise-induced hyperventilation which was observed in mild female asthmatics, did not appear to be related to exercise-induced bronchoconstriction.

The authors assessed airway impedance responses to psychological stressors among 113 individuals: 61 with asthma only (AS), 10 with asthma and panic disorder (ASPD), 24 with panic disorder only (PD), and 18 controls with neither condition (CON). Individuals with either AS or PD were affected by psychological stressors as measured by the forced oscillation technique. Individuals with PD (with or without AS) displayed lower airway impedance than those without PD. These data suggest that the airways of individuals with PD are in a chronic state of preparedness, which may promote hyperventilation.

An ambulatory monitor, body suit, and calibration procedure were developed to compare the respiration of seven patients with panic disorder and twelve normal volunteers. Subjects wore a body suit with Respitrace bands, connected to a portable respiratory monitor for a period of 24 hours. Breath by breath values for respiratory rate and tidal volume were computed every two minutes. There was a significant difference between patients and controls in their patterns of minute ventilation during sleep. Tidal volume, rather that respiratory rate increases characterized the periods of anxiety and limited symptom attacks.

The hyperventilation syndrome (HVS) can be regarded as a form of panic disorder associated with a relative increase in sympathomimetic tone, the effects of which can be counterbalanced by beta-adrenoceptor blockade. The efficacy of the beta-blocker bisoprolol was investigated in a double-blind placebo-controlled randomised crossover trial involving 60 patients from 17 general practices. Following a single-blind placebo prephase, patients who met the inclusion criteria were randomised to treatment with either 5 mg bisoprolol or an identical-looking placebo tablet once daily for three weeks. They were then crossed over to the other treatment arm. At the end of each treatment phase the number of hyperventilation attacks and the severity of symptoms were assessed and side effects recorded. The number of attacks decreased from 4.04 per week at baseline to 3.52 with placebo and to 1.26 with bisoprolol. The decrease of attacks with bisoprolol was significant (p < 0.05) compared to baseline and placebo. The severity of the complaints improved from 29 (scale 0 to 64) at baseline not significantly to 26 with placebo and significantly (p < 0.05) to 15 with bisoprolol. No serious side effects were reported. Five milligrams of bisoprolol once daily is effective and safe in the maintenance of symptom reduction in patients with the hyperventilation syndrome.

In a differential respiratory conditioning paradigm with normal Ss two odors (fresh smelling niaouli and bad smelling ammonia) were used as conditioned stimuli (CS+ or CS-) and 7.4% CO2-enriched air was used as the unconditioned stimulus (US). Three CS+ and three CS- trials were run during acquisition, followed on the next day by the same number of CS+ and CS- only trials. Respiratory frequency, minute ventilation, end-tidal fractional concentration of CO2 and subjective complaints were measured throughout the experiment. While during acquisition all measures were affected, the conditioning effects included only respiratory frequency and subjective complaints. A selective association effect appeared in that the conditioning effects were confined to ammonia as CS+: respiratory frequency increased and more somatic complaints were presented when compared to the CS- condition. The conditioning effect on complaints was not confined to complaints of general arousal, but included respiratory complaints as well. Correlational analyses showed that increases in complaints as caused by the conditioning procedure were predicted by changes in somatic variables, but not by individual differences in Negative Affectivity.

Hyperventilation is considered an important factor in the development of somatic symptoms or even panic attacks, though its role has recently been disputed. Arguments are often based on findings from the so-called Hyperventilation Provocation Test (HVPT), which is a procedure consisting of voluntarily overbreathing. The HVPT has been widely used for diagnosing Hyperventilation Syndrome and for experimentally eliciting panic attacks. Almost no attention, however, has been paid to standardizing the test and determining critical values with respect to depth and duration of hyperventilation. In the present study, symptom development was examined in 16 healthy subjects who underwent four HVPTs that differed in depth of hyperventilation (end-tidal PCO2 < 2.4 kPa or < 1.9 kPa), as well as duration of hyperventilation (2 or 5 min). Both depth and duration appeared to have an independent effect on the development of symptoms. In the 5-min condition, symptoms appeared mainly within the first 3 min. To be sure that the HVPT is long enough and deep enough to elicit symptoms in most people, a minimum duration of 3 min is advised, with end-tidal PCO2 decreasing to at least 1.9 kPa or dropping well over 50% of baseline.

This study investigated the physiological, subjective and behavioral responses to hyperventilation of four groups of Ss with: (1) clinical panic disorder (n = 13); (2) infrequent panic (n = 16); (3) no panic and high trait anxiety (n = 16); and (4) no panic and low trait anxiety. After completing a number of anxiety-related questionnaires, Ss participated in 2 min of hyperventilation during which heart rate and electrodermal activity were recorded continuously. Subjective sensations and cognitions during hyperventilation were assessed immediately following the task. After recovery, Ss could participate in a second, optional hyperventilation from which they could escape at any time. Analyses revealed no group differences in physiological responses to the hyperventilation, although group differences in subjective sensations and cognitions were found. Data are discussed with regards to the role of physiological processes vs subjective responses to anxiety-provoking stimuli in the psychopathology of clinical panic disorder.

Objective: The purpose of this comparative outcome study was to investigate whether the effects of exposure in vivo treatment for panic disorder with agoraphobia could be enhanced by adding interventions specifically for panic attacks before the start of exposure treatment. The additional effect of two types of treatment for panic attacks--pharmacological (fluvoxamine) and psychological (repeated hyperventilation provocations and respiratory training)--was examined. Thus, the combined treatment of panic interventions with exposure in vivo could be compared to exposure in vivo alone., Method: Ninety-six patients were randomly assigned to four treatment conditions: double-blind, placebo-controlled fluvoxamine followed by exposure in vivo, psychological panic management followed by exposure, and exposure in vivo alone. Outcome was assessed by self-report measures, a standardized multitask behavioral avoidance test, and continuous monitoring of panic attacks. Seventy-six patients completed the study., Results: All four treatments were effective and resulted in a significant decrease of agoraphobic avoidance. Moreover, the combination of fluvoxamine and exposure in vivo demonstrated efficacy superior to that of the other treatments and had twice as large an effect size (difference between pre- and posttreatment scores) on self-reported agoraphobic avoidance. The other treatments did not differ among each other in effectiveness., Conclusions: Results of the study indicate that the short-term outcome of exposure in vivo treatment can be enhanced by adding fluvoxamine treatment. Psychological panic management combined with exposure was not superior to exposure alone of equal duration.

Thirty-two patients suffering from panic disorder with agoraphobia were treated with repeated hyperventilation provocations and respiratory training, followed by exposure in vivo. The treatment was evaluated with a comprehensive set of outcome measures, including self-report questionnaires, a multitask behavioural avoidance test and continuous monitoring of panic. The treatment was found effective for the majority of patients in diminishing the frequency of panic attacks and agoraphobic avoidance. The clinical relevance of the treatment effect was evidenced by the considerable number of patients that recovered. The effect of the treatment was sustained over a three and six month follow-up period. The prognostic value of a number of variables for treatment outcome was also investigated. Three variables accounted for the majority of the variance in treatment outcome: a higher pretreatment level of agoraphobic complaints, use of psychotropic medication and a longer duration of the disorder were associated with poorer outcome. Other variables, such as the therapeutic relationship and the quality of the marital bond, had no prognostic value.

Respiratory abnormalities have been proposed as a central feature of panic disorder, but the literature is not unanimous. Symptoms of anxiety were quantitatively recorded with the Hamilton Rating Scale for Anxiety (HAM-A) in 72 psychiatric out-patients in two anxiety disorders clinics in Israel; 44 patients had panic disorder with or without agoraphobia and 28 patients had other anxiety disorders. Panic patients had more cardiovascular symptoms, but not more respiratory symptoms, than other patients. The relative importance of respiratory symptoms in panic disorder is not yet settled.

35 patients with vegetocirculatory dystonia and hyperventilation syndrome, but without the signs of organic lesion of nervous system were treated. The complex treatment included the breathing exercises with feedback mechanisms, the correction of psychovegetative and neurovascular disturbances, the massage of neck region and a head, psychotherapy, angioprotective, vegeto- and psychotropic drug therapy. The disappearance of acute vascular attacks and paroxysms of migrainous headache, the normalization of all breathing parameters and the improvement of vegetative status were observed in all patients.

Three studies were conducted to compare the ability of a measure of fear of physical sensations (Anxiety Sensitivity Index; ASI) and a measure of trait anxiety (State-Trait Anxiety Inventory; STAI) to predict response to hyperventilation. In the first study subjects (N = 43) were selected who differed in scores on the ASI but were equated on levels of trait anxiety. Two other studies were conducted in which subjects (ns = 63 and 54) varied randomly on ASI and STAI scores. The results indicate that scores on the ASI account for a significant proportion of variance in the response to hyperventilation that is not accounted for by scores on the STAI.

We examined the effects of hyperventilation and other manipulations of respiratory pace on parasympathetic nervous system function and subjective reactivity in 15 patients with panic disorder, 15 patients with social phobia, and 15 healthy control subjects. After a 30-minute rest period subjects completed a 2.5-minute trial of each of hypoventilation, normoventilation, and hyperventilation. Trials were separated by a 3 minute inter-trial interval. Incidence of panic attacks, symptom severity, vagal tone, heart rate, end-tidal carbon dioxide level, and respiratory frequency were measured throughout. Resting physiological measures did not differ between groups. Each respiratory manipulation resulted in the expected physiological changes (e.g., hyperventilation attenuated vagal tone), however, groups did not exhibit differential physiological reactivity to the manipulations. There were no panic attacks reported during either the hypoventilation or normoventilation phases; however, two social phobic subjects (13.3%) and two panic disorder patients (13.3%) reported panic attacks during hyperventilation. Although both groups of anxiety patients reported greater severity of hyperventilation-induced symptoms than did control subjects, symptom severity did not correlate significantly with vagal tone or heart rate. These results suggest that parasympathetic function is unlikely to be aberrant in PD patients and that diminished parasympathetic activity is not sufficient for the experience of panic attacks.

Forty-eight females were evaluated to detect differences in panic-related symptomatology and physiological responses to 2 min of hyperventilation. Ss were divided into 3 groups: infrequent panickers; no panic/high trait anxiety; and no panic/low trait anxiety. The low trait anxiety group scored significantly lower on various self-report measures of anxiety-related symptomatology compared to Ss with infrequent panic and high trait anxiety. Hyperventilation produced no significant group differences in physiological reactivity or recovery. However, Ss with low trait anxiety reported significantly less severe sensations and a significantly lower incidence of panic during hyperventilation than the infrequent panickers and the high trait anxiety group. Ss who panicked during hyperventilation reported more intense sensations and negative cognitions than those who did not panic. Thus, Ss were distinguished by their subjective, but not their physiological responses.

Cognitive models maintain that panic attacks may be initiated by fear resulting from the interpretation of somatic sensations as personally threatening or harmful. Similarly, several researchers have proposed that the enhanced response of panickers to biological challenge may result from the fear of induced anxiety sensations rather than from direct stimulation of aberrant biochemical systems. The present study examined the effects of both panic history and fear of anxiety sensations on subjective and cardiac responses to biological challenge. Eighty nonclinical subjects were chosen on the basis of level of anxiety sensitivity and history of previous panic attacks. High and low anxiety-sensitive panickers and nonpanickers (four groups of 20 subjects) were subjected to a 90 sec period of voluntary hyperventilation, during which heart rate was assessed. Regardless of panic history, total symptom scores did not differ between high and low anxiety-sensitive subjects at baseline or pre-hyperventilation, but did differ at post-hyperventilation. There were, however, no significant differences in post-hyperventilation measures of heart rate. The apparent mismatch of subjective and physiological responsivity to the challenge in high anxiety-sensitive individuals (i.e. more severe symptom self-reports in the absence of increased cardiac activation) provides support for the hypothesis that high anxiety sensitivity is associated with an enhanced tendency to panic in response to biological challenge.

In a critique of the study by Carr, Lehrer and Hochron (1992), Ley (Behaviour Research and Therapy, 32, 109-111, 1994) attributes the lack of confirmation for his dyspneic-fear theory among panic disorder patients to a basic flaw of that study: Ss were selected according to DSM-IIIR criteria. Ley argues that dyspneic-fear theory pertains exclusively to hyperventilatory (characterized by intense dyspnea) panic attacks not to all attacks that come under the classification of DSM-IIIR. We address the premise concerning the selection of Ss and argue that cognitive theory continues to offer a more convincing explanation of our study and of more recent findings by others.

Hyperventilation syndrome is not a rare disorder present primarily in children, but in adolescents too. It points to anxiety in children with or without family problems. The clinical picture is polymorphous and often without a clear connection with hyperventilation. That is why it is necessary for the physician to be aware of this problem in practice. The diagnosis is made on the basis of clinical picture and hyperventilation provocative test, when one expects this disorder might occur. We have reported five cases of children with this syndrome, with a special review concerning clinical picture and the way which led to the confirmation of diagnosis.

Thirty-six patients underwent assessment of behavioural breathlessness which included monitoring of breathing patterns and end tidal CO2 concentration and completion of questionnaires relating to hyperventilation (HV), anxiety and depression. Twenty-two patients had a positive assessment and underwent breathing retraining. Assessments were repeated immediately after re-training and 2 months later. Ten of the patients (Group A) had behavioural breathlessness either as the primary problem or secondary to an established clinical condition, and twelve (Group B) in association with chronic fatigue. Before re-training, resting end-tidal PCO2 was significantly lower in Group A than Group B (p < 0.05), but there was no significant difference in mean scores for HV-related symptoms, anxiety or depression. Following breathing retraining, both groups showed improvements in breathing patterns, end tidal CO2 levels and scores for HV-related symptoms which were sustained. In Group A the mean score for anxiety decreased (p < 0.01) and the score for depression was significantly lower than in Group B (p < 0.05). Although mean scores for anxiety and depression in Group B did not change significantly, some individuals in the group did show sustained improvement. There was no improvement in symptoms associated with chronic fatigue in Group B. In behavioural breathlessness, breathing retraining is of benefit, not only in restoring more normal patterns of breathing but also in reducing anxiety, particularly in patients without the complication of chronic fatigue.

Carr, Lehrer and Hochron (Behaviour Research and Therapy, 30, 251-261, 1992) attempted to test Ley's (Behaviour Research and Therapy, 30, 549-554, 1989) dyspneic-fear theory and concluded that while their results confirmed predictions for a sample of asthmatics, their results did not confirm predictions for a sample of panic-disorder patients. The present paper points to a basic flaw in the Carr et al. study which renders their conclusions regarding panic disorder indeterminate. The flaw in the Carr et al. study lies in their selection of panic-disorder patients. Whereas dyspneic-fear theory provides an explanation for panic fear experienced in hyperventilatory panic attacks, Carr et al. overlooked this fact and selected Ss based on the DSM-IIIR classification, a set of criteria which does not distinguish between hyperventilatory panic attacks and other types of panic attacks (see Ley, Behaviour Research and Therapy, 30, 347-357, 1992).

Sighing is a normal physiologic response, expanding the lungs to vital capacity, usually followed by a prolonged expiratory phase. Sighing dyspnea is a condition that may be mistaken for asthma, and should be considered in the atypical cases. Recognizing sighing dyspnea at the onset may save patients from having to undergo extensive diagnostic evaluations and treatments. This condition, once identified, can often be easily treated by explaining the benign nature and giving reassurance to the patient.

This study investigates the effects of partial exhalation to feelings of anxiety. Thirty five volunteer subjects (14 male, 21 female, mean age 40.6) were first trained in slow diaphragmatic breathing (SDB). Then subjects rated their anxiety levels on a scale from 1 (none) to 5 (extreme) in sequential conditions of SDB, 70% subjective exhalation, and SDB. During the 70% subjective exhalation phase, subjects were instructed to breathe and limit their exhalation to 70% of the inhaled volume during each consecutive breath. The 70% subjective condition significantly (P < .0005) increased subjects' anxiety levels as compared to the initial SDB baseline, while a return to SDB significantly reduced the anxiety levels. The 70% approach appears useful in demonstrating to the client that possible changes in breathing patterns can affect anxiety.

Background: Sighing breathing is observed in subjects suffering from anxiety with no apparent organic disease., Methods: Lung volumes and expiratory flow rates were measured in 12 patients with a sighing pattern of breathing and in 10 normal subjects matched for age, gender, and anthropometric data. In both groups the measurements were made by spirographic and plethysmographic techniques. In normal subjects functional residual capacity (FRC) and residual volume (RV) were measured during normal breathing and again during simulated sighing breathing to exclude technical artifacts resulting from hyperventilation during measurement by the helium closed circuit method., Results: Patients with a sighing pattern of breathing had a normal total lung capacity (TLC) but significantly different partitioning of lung compartments compared with normal subjects. The vital capacity (VC) was lower when measured by both spirographic and plethysmographic methods and RV was higher. The forced expiratory volume in one second (FEV1) was also lower in patients with sighing breathing. The FEV1/VC and the maximal expiratory flow rates at 50% and at 25% of the forced vital capacity (V50 and V25) were normal and similar in both groups. In normal subjects there were no differences in RV when measured during quiet or simulated sighing breathing., Conclusions: Subjects with sighing breathing have a normal TLC with a higher RV and lower VC than normal subjects. There was no obvious physiological or anatomical explanation for this pattern.

The 2-week prevalence of panic attacks according to DSM-III-R criteria was assessed in 102 general hospital patients with unexplained somatic symptoms suggestive of the hyperventilation syndrome (HVS). Thirty-six patients were classified as panickers. In comparison to nonpanickers, panickers reported more severe panic and hyperventilation symptoms and state anxiety during anxiety episodes in daily life and also obtained higher scores on measures for depression, generalized anxiety, agoraphobic anxiety, and agoraphobic avoidance. During the Hyperventilation Provocation Test, panickers reported more panic and hyperventilation symptoms and state anxiety and also rated their symptoms to be more similar to those occurring in daily life than nonpanickers. However, no differences were observed between panickers and nonpanickers in base excess values or in minute respiratory volume, respiratory rate, or fraction of end-tidal carbon dioxide during the resting, hyperventilation, and recovery phase. It is concluded that the prevalence of panic attacks in this group of patients is relatively high and that medical specialists must be more attentive to the occurrence of panic attacks or panic disorder in general hospital patients with unexplained somatic symptoms suggestive of HVS.

Hyperventilation is assumed to produce a set of somatic and psychological symptoms, the so-called Hyperventilation Syndrome (HVS). Recognition of symptoms during the hyperventilation provocation test (HVPT) is the most widely used criterion for diagnosing HVS, but additional physiological and symptom criteria have been proposed. The concordance of various diagnostic criteria for HVS is investigated in the present study. Forty-eight psychiatric patients with panic disorder and 90 somatic patients with symptoms suspective of HVS performed a HVPT. There was a strong interrelationship between the various symptom criteria as well as the physiological criteria. However, almost no association between symptom and physiological HVS criteria were found. Symptom recognition was significantly related to trait anxiety, agoraphobia and depression. These data do not only question the validity of the HVPT, but also of the concept of HVS. The results are more consistent with a cognitive approach to anxiety in which the HVPT is seen as an aspecific stressor during which more anxious patients anticipate an anxiety attack.

Arterial blood gases were measured and base excess calculated in 18 nonpanicking panic disorder (PD) patients, 12 subjects suffering from other anxiety disorders, and 18 normal control subjects. There was neither chronic nor clinically significant acute hyperventilation in either group.