Panic Attacks During Placebo Procedures in the Laboratory

Goetz, Raymond R.; Klein, Donald F.; Gully, Robert; Kahn, Jeffrey P.; Liebowitz, Michael R.; Fyer, Abby J.; Gorman, Jack M.

doi:10.1001/archpsyc.1993.01820160050006

Cited by 46 publications

(28 citation statements)

References 25 publications

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“…Our findings of an increase in RR during CCK-5-induced PA are also supported by results of other studies that used different panic challenges and that showed an increase in V T and RR during induced PAs (Gorman et al, 1988(Gorman et al, , 2001). Interestingly, Goetz et al (1993) have described a marginally significant increase in RR during PA induced by placebo infusion in PD patients, with a peak of the RR around the same time (30 s) as the peak in RR that we observed (40 s) (Figure 4). Another human study testing the effects of CCK-4 on airway resistance found no differences in spirometric variables after CCK-4-induced panic symptoms (Shlik et al, 1997).…”

Section: Discussionsupporting

confidence: 75%

Pulmonary and Systemic Nitric Oxide Measurements During CCK-5-Induced Panic Attacks

Lara

Chrapko

Archer

et al. 2003

Neuropsychopharmacol

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Nitric oxide (NO) plays a major role in cardiopulmonary regulation as illustrated by the alterations of the NO system described in cardiopulmonary illnesses. Recent studies have found an association between panic disorder and cardiovascular death and illness, as well as pulmonary diseases. Our objective was to investigate whether pulmonary or systemic NO production was altered during induced panic attacks (PAs). We used a double-blind placebo-controlled crossover design with randomization of the order of an injection of placebo and pentagastrin, a cholecystokinin-B receptor agonist that induces PAs in healthy volunteers (HVs). A total of 17 HVs experienced a PA after pentagastrin challenge. Exhaled NO and NO metabolites were measured by chemiluminescence. During pentagastrin-induced PAs, HVs displayed significant decreases in plateau concentrations of NO exhaled, which were associated with proportional increases in minute ventilation. There were no significant changes in pulmonary or systemic NO production. These results suggest that the decrease in exhaled NO concentration observed during pentagastrin-induced PAs is related to the associated hyperventilation, rather than to any change in lung NO production. This study is the first to evaluate changes in NO measurements during acute anxiety.

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Section: Discussionsupporting

confidence: 75%

Pulmonary and Systemic Nitric Oxide Measurements During CCK-5-Induced Panic Attacks

Lara

Chrapko

Archer

et al. 2003

Neuropsychopharmacol

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“…Goetz et al [1994] reported a high degree of symptom consistency and self-rated similarity between symptom arrays during a typical panic attack and lactate-induced panic. Addressing panic attacks somewhat closer to the experience of a natural panic attack, our group [Goetz et al, 1993] reported the physiological data from 17 PD patients who experienced "situationally provoked panic" during the saline infusion period of a lactate infusion protocol; however, individual symptom data were not reported at that time. These API-17 data (unpublished data available on request) are now available and indicates that the following symptoms differed from baseline to the point of panic (among patients experiencing these lactate-induced attacks) at the alpha level of 0.002: fear in general (effect size = 1.6); dyspnea (2.2); fear of dying (1.8); confusion (1.8); difficulty concentrating (2.5), doing one's job (2.1), and speaking (2.6); sweating (1.5); and twitching/trembling (3.3).…”

Section: Discussionmentioning

confidence: 99%

“…In previous publications, we have shown that prominent cardiorespiratory responses occur during situationally provoked (laboratory setting) panic attacks [Goetz et al, 1993], and that levels of baseline fear and dyspnea, as well as lactate-induced increments in fear and dyspnea, are the most salient features of the panic response to lactate infusion [Goetz et al, 1996]. Ley, in a series of reports [1987,1989,1992], noted the salience of fear and dyspnea in panic disorder, which he attributed to hyperventilation.…”

Section: Introductionmentioning

confidence: 89%

Acute panic inventory symptoms during CO2 inhalation and room-air hyperventilation among panic disorder patients and normal controls

et al. 2001

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There is scant literature on anxiety symptoms induced during respiratory challenges developed to induce panic symptoms and attacks. Here we report on the prevalence of Acute Panic Inventory (API) symptoms during three consecutive respiratory challenges to patients with panic disorder (PD) and normal controls (NC). The challenges performed using a closed canopy system included voluntary room air hyperventilation (RAH), inhalation of 5% CO(2), and 7% CO(2)-enriched air. The PD patients were 41 men and 53 women whose mean age was 33.4 (SD = 8.55). The normal comparison group consisted of 35 men and 27 women with a mean age of 31.3 (SD = 9.21). The diagnosis of panic disorder was made using the Structured Clinical Interview for DSM-III-R. All potential normal controls underwent structured clinical interview using the Schedule for Affective Disorders and Schizophrenia-Lifetime Version Modified for the Study of Anxiety Disorders (SADS-LA), and must have been free of a lifetime history of anxiety disorders, affective disorders, substance use disorders, and schizophrenia. All participants also had a complete medical evaluation and were in good health. The experiment consisted of seven experimental epochs: three baseline/recovery periods each followed by a respiratory challenge, and then a final recovery epoch. The API was administered at the end of each epoch. Clinical staff trained and experienced in rating panic attacks rated participants' response during each challenge as panic or no panic. Three groups were defined for analysis: PD patients who panicked, PD patients who did not panic, and NC who did not panic. Staff ratings indicated that the 7% CO(2) challenge was the most panicogenic, followed by the 5% CO(2), and the RAH challenges. Conventional statistics (analysis of variance and partial correlations) indicated that many baseline symptoms as well as symptom increments differed across groups, and were associated with the outcome of panic/no panic during each challenge. However, logistic regression analysis indicated that only a few symptoms independently predicted the panic/no panic outcome because many symptoms were redundant. The symptom cluster of fear in general, dizziness, difficulties with concentrating, and doing one's job predicted panic to RAH. The cluster of fear in general, confusion, dyspnea, and twitching/trembling predicted the response to 5% CO(2). Finally, fear in general, confusion, twitching/ trembling and dizziness predicted the response to 7% CO(2). While univariate analyses indicated that many symptoms distinguished between panic and no panic outcome, logistic regression revealed that group differences were subsumed under a few prominent symptoms, namely, fear in general, confusion, dizziness, twitching/trembling, and dyspnea. The results are discussed in the context of patient (having a diagnosis of PD) and panic effects (rated as panicking to a challenge).

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“…Even though the SNS is instrumental in the etiology of anxiety disorders, experimental evidence suggests that the PNS may be responsible for the maintenance of elevated physiology in psychopathology (15). For instance, the administration of catecholamine (SNS) antagonists prior to induced panic attacks does little to reduce heart rate, suggesting that the SNS plays a minor role in such attacks (19). However, lactate, which is a known suppressor of vagal (PNS) activity, accumulates during panic attacks (20), and is even administered in laboratory studies to induce panic attacks (21) and stimulate PTSD symptoms (22).…”

Section: Psychophysiology Of Ptsdmentioning

confidence: 99%

Posttraumatic Stress, Heart Rate Variability, and the Mediating Role of Behavioral Health Risks

Dennis

Watkins

Calhoun

et al. 2014

Psychosomatic Medicine

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Objective Posttraumatic stress disorder (PTSD) has been linked to reduced heart-rate variability (HRV), which is in turn a risk factor for cardiovascular disease and death. Although hyperarousal and anxiety are thought to underlie this association, behavioral health risks, including smoking, alcohol dependence, obesity, and sleep disturbance, represent potential mechanisms linking PTSD and HRV. Methods To test this hypothesis, a combination of short-term laboratory-based and 24-hour ambulatory measures of HRV were collected from 227 young adults (18-39 years old), 107 of whom were diagnosed with PTSD. Latent variable modeling was used to assess the relationship of PTSD symptoms with HRV along with potential behavioral health mediators. Results PTSD symptoms were associated with reduced HRV, β = -.21, p = .002. However, this association was reduced in models that adjusted for cigarette consumption and history of alcohol dependence, and was rendered non-significant in a model adjusting for sleep disturbance. Independent mediation effects were deemed significant via bootstrapping analysis. Together the three behavioral health factors (cigarette consumption, history of alcohol dependence, and sleep disturbance) accounted for 94% of the shared variance between PTSD symptoms and HRV. Abdominal obesity was not a significant mediator. Conclusions These results indicate that behavioral factors—specifically smoking, alcohol overuse, and sleep disturbance—mediate the association between PTSD and HRV-based indices of autonomic nervous system dysregulation. Benefits from psychiatric and psychological interventions in PTSD may therefore be enhanced by including modification of health behaviors.

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Panic Attacks During Placebo Procedures in the Laboratory

Cited by 46 publications

References 25 publications

Pulmonary and Systemic Nitric Oxide Measurements During CCK-5-Induced Panic Attacks

Pulmonary and Systemic Nitric Oxide Measurements During CCK-5-Induced Panic Attacks

Acute panic inventory symptoms during CO2 inhalation and room-air hyperventilation among panic disorder patients and normal controls

Posttraumatic Stress, Heart Rate Variability, and the Mediating Role of Behavioral Health Risks

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