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Title of Thesis: “Anxiety Sensitivity, Body Vigilance, Interoceptive Acuity, and
Cardiovascular Reactivity in the Genesis of Panic”
Name of Candidate: Julie M. Storey,
Department of Medical and Clinical Psychology
Master of Science
2000
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Julie-J^. Storey, CaptHlSA^C^^^
Department of Medical and CliniCaHP^ychology
Uniformed Services University of the Health
Sciences
11
ABSTRACT
Title of Thesis: Anxiety Sensitivity, Body Vigilance, Interoceptive Acuity, and
Cardiovascular Reactivity in the Genesis of Panic
Julie M. Storey, Master of Science, 2000
Thesis directed by: Michael Feuerstein, Ph.D., Professor, Department of Medical and
Clinical Psychology
Cognitive conceptualizations of panic require both the experience of arousal symptoms
and their catastrophic interpretation. The tendency to interpret arousal symptoms as
threatening is known as anxiety sensitivity (AS), but it is unclear if increased vigilance,
greater physiological reactivity, or enhanced perception are responsible for reported
physiological symptoms. Each of these mechanisms has been empirically supported in
clinical, but not nonclinical, populations. The current investigation examined the ability
of AS, body vigilance, cardiovascular reactivity, and interoceptive acuity to predict
fearful responding to a 35% CO 2 inhalation in a nonclinical population. A main effect
was found for AS (R^ = .13; p < .01). Two interaction effects were found (AS x Heart
Rate, AR^ = .05, p < .05; AS x Diastolic Blood Pressure, AR^ = .05, p < .05). Results
support cognitive theories of panic and suggest physiological reactivity combined with
AS elicit more fearful responses than either alone.
ANXIETY SENSITIVITY, BODY VIGILANCE,
INTEROCEPTIVE ACUITY, AND CARDIOVASCULAR
REACTIVITY IN THE GENESIS OF PANIC
by
Julie M. Storey, Capt, USAF
Thesis submitted to the Faculty of the
Department of Medical and Clinical Psychology Graduate Program of the
Uniformed Services University of the Health Sciences
in partial fulfillment of the requirements for the degree of
Master of Science 2000
IV
TABLE OF CONTENTS
Approval Sheet. i
Copyright Statement. ii
Abstract. Hi
Title. iv
Table of Contents. v
List of Tables. vi
List of Figures. vii
Introduction. 1
Physical Symptoms in Panic. 1
Body Vigilance . 2
Interoceptive Acuity . 4
Cardiovascular Reactivity . 6
Catastrophic Interpretation of Symptoms in Panic. 9
Study Hypotheses. 11
Methods. 12
Sample and Procedures. 12
Physiological Measures. 14
Psychological Measures. 15
Biological Challenge Procedure. 16
Protocol Overview. 17
Data Analytic Strategy. 18
Results. 19
V
Descriptive Statistics. 19
Missing Data. 20
Main Effects. 21
Interaction Effects. 22
Discussion. 23
Limitations of the Study. 26
Conclusions.27
References. 29
vi
LIST OF TABLES
Table 1: Contact Results for 1516 Phone Numbers
Table 2; Descriptive Statistics for the Sample
Table 3: Descriptive Statistics for the Predictor Measures
Table 4; Correlations Among Predictor Variables
Table 5: Summary of Hierarchical Regression Analysis for Variables Predicting Post
CO 2 Fear
Table 6: Summary of Hierarchical Regression Analysis for Cross Products Predicting
Post CO 2 Fear
vu
LIST OF FIGURES
Figure 1: Interaction Between Anxiety Sensitivity and Heart Rate Reactivity for
Predicting Post CO 2 Fear
Figure 2: Interaction Between Anxiety Sensitivity and Diastolic Blood Pressure
Reactivity for Predicting Post CO 2 Fear
Introduction
The central features of a panic attack, as defined by the Diagnostic and Statistical
Manual of Mental Disorders, Fourth Edition (DSM-FV; American Psychiatric
Association, 1994), are intense fear accompanied by somatic and/or cognitive symptoms.
This theoretically singular entity is estimated to affect 28-34% of individuals across their
lifetimes (Norton, Harrison, Hauch, and Rhodes, 1985) and is linked to a broad range of
psychological and physical outcomes. While some individuals report an isolated,
uncomfortable event, others report a debilitating disorder (e.g., panic disorder).
Since the inclusion of panic attacks and panic disorder in the DSM-III (Diagnostic
and Statistical Manual of Mental Disorders, Third Edition; Ajnerican Psychiatric
Association, 1980), this amalgam of physical and emotional complaints has been a topic
of much research and debate. Significant advances have been made in our understanding
of the maintenance and clinical course of these entities (McNally, 1994). Cognitive
theory, applied to panic attacks and panic disorder in the mid-1980’s, proved to be an
important impetus for panic research. Cognitive conceptualizations of panic suggest that
a panic attack results when benign physical symptoms are catastrophically interpreted
(Clark, 1986; Reiss and McNally, 1985). Two key components identified by this
conceptualization are: the experience of physical symptoms, and the interpretation of
them in a catastrophic framework.
Physical Symptoms in Panic
Much debate abounds regarding the actual and perceived physical symptoms
“experienced” by individuals plagued by panic attacks. Ehlers (1993) identified three
hypotheses regarding increased symptom perception in panic disorder. Patients with
1
2
panic disorder may be more apt to perceive autonomic sensations because of: increased
attention to levels of physiological arousal; enhanced ability to perceive normal
physiological aberrations; and/or greater physiological reactivity to situations
experienced as anxiogenic.
Body vigilance. In cognitive theory, a systematic preference for certain types of
information is known as an attentional bias (Clark and Fairbum, 1997). An attentional
bias for somatic changes has been suggested and observed to play a role in the perception
of physical sensations (Ehlers, 1993). Pennebaker, Gonder-Frederick, Cox, and Hoover
(1985) observed that increased attentional focus on the body increases the likelihood of
perceiving potentially threatening interoceptive cues. Although this assertion has
historically been reserved for patients with hypochondriacal concerns (i.e., concerned
with the onset or presence of serious physical illness), recent evidence suggests it may be
true for panic disorder patients as well as individuals with subclinical somatic concerns.
Investigations into panic disorder have labeled this tendency to selectively attend to
somatic changes as body vi^lance (Schmidt, Lerew, and Trakowski, 1997). In a multi¬
study investigation of the relationship between body vigilance and anxiety pathology,
Schmidt and colleagues (1997) found body vigilance to be normally distributed in a
nonclinical sample and to be related to a history of spontaneous panic attacks, anxiety
sensitivity, and anxiety symptomatology. Additionally, individuals with panic disorder
reported higher levels of body vigilance relative to social phobics and nonclinical
controls and showed reductions in body vigilance associated with reported reductions in
panic symptoms following a cognitive-behavioral intervention.
3
It has additionally been suggested that this heightened vigilance exists only for
somatic disturbances related to autonomic nervous system arousal (e.g., heart palpitations
and shortness of breath) but not for non-autonomic sensations (e.g., muscle aches or
stomach pains) in panic disorder patients (Pilkington, Antony, and Swinson, 1998). In a
study involving anxiety disordered patients and nonclinical volunteers, Pilkington and
colleagues found vigilance for autonomic sensations to be significantly elevated in panic
disorder patients relative to nonclinical controls, specific phobic patients, social phobic
patients, and obsessive-compulsive patients. Panic disorder patients were no more
vigilant for non-autonomic bodily sensations than nonclincal controls.
These data suggest an attentional bias for symptoms of autonomic arousal in panic
disordered patients. Evidence for such a bias, and indirect evidence for the relevance of
body vigilance in the maintenance of panic disorder, can be gleaned from Horenstein and
Segui (1997) and Asmundson, Sandler, Wilson, and Walker (1992). Both of these
studies were reaction time studies using panic disorder patients, clinical controls, and
nonclinical controls. Two words were presented simultaneously to the subject, one word
was a neutral word, and the other a threatening word. A probe dot then replaced one of
the words, and the latency to detection of the probe was measured. Panic disorder
patients were quicker to detect the probe when it replaced the threatening word rather
than the neutral word. Asmundson et al. (1992) found a similar pattern, but only for
physically threatening words (e.g., collapse and death). Socially threatening words (e.g.,
failure and stupid) did not enhance reaction time.
Although a relatively young construct, these preliminary investigations suggest that
body vigilance to be a behavioral sequela of catastrophic cognitions and a mechanism by
4
which individuals with panic disorder detect changes in their somatic states leading to
self-perpetuating anxiety responses.
Interoceptive acuity. Whereas body vigilance involves attention to somatic
perturbations, interoceptive acuity involves accuracy in detecting such changes.
Although results have been somewhat mixed, some research suggests that panic disorder
patients, in addition to heightened vigilance, may also have an enhanced accuracy in the
perception of internal somatic cues (Ehlers and Breuer, 1992). Although empirical
support is relatively recent, the notion that certain people are more attuned to changes in
their soma is not a new one. Tyrer (1976) reports that patients with somatic anxiety are
better at perceiving bodily states than other subjects, and Shands and Schor (1982)
described panic disorder patients as “interoceptive experts, being able to describe changes
in almost every organ system and region of the body” (p. 108). Because cardiovascular
symptoms are common during panic, evaluation of interoceptive acuity in panic disorder
patients has typically focused on the accuracy of detecting one’s heart rate (Ehlers and
Breuer, 1992; McLeod and Hoehn-Saric, 1993).
Early studies of interoception began as studies of vigilance - focusing more on
patient’s self-reported awareness and not on their objective accuracy. These early
investigations suggest that panic disorder patients believe they are more aware of somatic
(usually cardiovascular) aberrations and act accordingly (fearfully) when they “perceive”
such changes. For example, subjects with high state or trait anxiety have shown greater
reported cardiac awareness than non-anxious subjects (Schandry, 1981; Montgomery and
Jones, 1984), and nonclinical subjects who report good heartbeat perception are
emotionally more responsive to stressors than subjects who do not (Katkin, 1985;
5
Schandry, 1983). Ehlers and Breuer (1992) foimd panic patients, as well as infrequent
panickers, reported greater baseline cardiac sensitivity than either patients with other
anxiety disorders or nonclinical controls. Additionally, self-reported cardiac awareness
has been found to be related to the degree of agoraphobic avoidance behavior among
frequent and infrequent panickers. Anxiety patients, but not healthy volimteers, report
increases in anxiety and exhibit increases in physiological arousal when they hear false
auditory feedback indicating a surge in heart rate (Ehlers, Margraf, Roth, Taylor, and
Birbaumer, 1988). Although such self-reported awareness indirectly suggests heightened
accuracy, self-reports of interoceptive sensitivity and objective measures of accuracy tend
to have low correlations (Shands and Schor, 1982; Tyrer, 1973, 1976; Whitehead,
Drescher, Heiman, and Blackwell, 1977).
Some studies investigating objective accuracy suggest panic disorder patients are
more accurate at perceiving their heart beats than patients with simple phobias, infrequent
panickers, and nonclinical controls, although panic disorder patients are not typically
completely accurate (Ehlers and Breuer, 1992). Ehlers (1995), in a prospective
evaluation of panic disorder patients, infrequent panickers, simple phobics, remitted
panickers, and controls found maintenance of the disorder as well as relapse to be
associated with good heartbeat perception, in addition to anxiety sensitivity, and degree
of avoidance.
Although evidence suggests panic disorder patients have heightened awareness of
their cardiac sensations, it is unclear whether increased cardiac awareness is present
before the onset of panic attacks or whether it is acquired later in the course of the
disorder (Ehlers and Breuer, 1992). It has been hypothesized that interoceptive acuity
6
may evolve from frequent pulse taking or changes in attentional focus that increase the
probability that panic patients will be aware of normal cardiac changes (e.g.,
tachycardias, arrhythmias) that occur frequently in many people but go unnoticed (Ehlers
and Breuer, 1992). As interoceptive acuity improves, such changes are more likely to be
detected by vulnerable subjects (i.e., subjects with high anxiety sensitivity), and a panic
attack is apt to be triggered. At least one study (Ehlers and Breuer, 1992) found
infrequent panickers to be no better than nonclinical controls in detecting their heart rate,
suggesting accuracy of heart rate detection, if it in fact exists in panickers, may be a result
of long-term experience with panic attacks more than a cause.
Cardiovascular reactivity. Changes from baseline functioning of the heart or
vasculature induced by experimental or in vivo demands are known as cardiovascular
reactivity . Largely due to the fact that symptoms frequently reported by anxiety disorder
patients suggest an increase in cardiovascular functioning (e.g., palpitations, chest pain,
chest tighmess), the literature is replete with investigations into the relationship between
cardiovascular measures and anxiety symptomatology. Although results are not entirely
consistent, a large portion of the evidence suggests baseline cardiovascular profiles,
which include heart rate and blood pressure measures, of individuals with anxiety
pathology do not differ significantly from those of nonclinical controls (Braune, Albus,
Froehler, and Hoen et al., 1994; Hoehn-Saric and McLeod, 1988; Sandler, Wilson,
Asmundson, Larsen, et al., 1992). However, it appears as individuals with anxiety
pathology begin to experience anxiety, they may experience larger changes in their
cardiovascular functions, including greater elevations in heart rate, systolic blood
7
pressure and diastolic blood pressure (Hoehn-Saric and McLeod; 1988; Pauli, Marquardt,
Hartl, Nutzinger, Holzl, and Strian, 1991).
Heart rate reactivity. Several laboratory studies have demonstrated the presence of
elevated heart rate responses to physiological challenges in panic disorder patients when
compared to nonclinical controls. Patients with panic disorder have been shown to
demonstrate greater heart rate reactivity to treadmill exercise (Taylor, King, Ehlers et al.,
1987), to an orthostatic challenge (Stein, Papp, Klein, et al., 1992), to a biological
challenge (vanZijderveld, TenVoorde, Veltman, and van Doomen, 1997), and to certain
psychomotor tasks (Hoehn-Saric, McLeod, and Zimmerli, 1991) when compared with
nonclinical controls, social phobics (Veltman, van Zijderveld, Tilder, and van Dyck,
1996), and blood phobics (Friedman, Thayer, Borkoved, Tyrrell, Johnson, Columbo,
1993; Friedman and Thayer, 1998). As with many constructs implicated in anxiety
pathology, however, it remains unclear if this increased reactivity is a risk factor for panic
or a consequence of cognitive (fear) and behavioral (avoidance of exercise) sequelae of
panic.
Blood pressure reactivity. Studies of blood pressure reactivity, especially in relation
to diastolic blood pressure reactivity, have yielded equivocal results. Although most
investigations report elevated systolic blood pressure reactivity in panic disorder patients
during ambulatory monitoring and in response to a variety of stressors (e.g., a mental
stress task, epinephrine challenge; Bystritsky, Craske, Maidenberg, Vapnik, and Shapiro,
1995; Hoehn-Saric et al., 1991; Shear et al, 1992; White and Baker, 1987; vanZijderveld,
TenVoorde, Veltman, and van Doomen, 1997), diastolic reactivity differs depending
upon the type of stressor and the time of measurement (Bystritsky and Shapiro, 1992;
8
Yeregani, Meiri, Pohl, Baton, Desai, and Golec, 1990; vanZijderveld, TenVoorde,
Veltman, and van Dooraen, 1997). However, Bystritsky and Shapiro (1992) reported
elevated diastolic blood pressure reactivity in panic disorder patients during a carbon
dioxide challenge, and three different investigations of ambulatory blood pressure
indicate significantly elevated diastolic blood pressure reactivity prior to and during panic
in a naturalistic setting (Bystritsky et al, 1995; Shear et al, 1992; White and Baker, 1987).
Although evidence to date suggests cardiovascular reactivity’s role in the
maintenance of anxiety pathology, few studies have investigated its role in development
of these disorders. Sandler, Wilson, Asmundson, Gordon, Larsen et al. (1992) compared
infrequent panickers to nonpanicking controls and discovered that infrequent panickers
did not evidence the heightened autonomic activation that is often found in individuals
with panic disorder. This study, while not conclusive, suggests that cardiovascular
reactivity may be a systemic response to repeated, intense autonomic arousal and not a
causal mechanism in the development of panic. To date, no studies have prospectively
investigated cardiovascular reactivity, and few have reported its relationship to fear in a
nonclinical sample. Shostak and Peterson (1990) investigated the relationship between
anxiety sensitivity and physiological changes in nonclinical subjects following a mental
arithmetic task and found comparable muscle activity and systolic blood pressure across
three levels of anxiety sensitivity. However, one might logically question the relevance
of a mental stress task for individuals high in anxiety sensitivity. Similarly, Asmtmdson,
Norton, Wilson, and Sandler (1994) failed to find heart-rate reactivity differences
between high and low anxiety sensitive nonclinical subjects following a hyperventilation
challenge. In this investigation, Asmundson and colleagues failed to provide evidence of
9
arousal in either group, bringing into question the efficacy of the stressor and thus the
acciu'acy of their conclusions.
Catastrophic Interpretation of Symptoms in Panic
The second component of the cognitive conceptualization of panic is the
misinterpretation of innocuous, internal bodily sensations as threatening (Barlow, 1988,
Clark, 1986). Identified as threatening, these sensations may trigger anxiety, increased
arousal, and self-perpetuating fear. According to this model of panic, the mere
experience of physical arousal is insufficient to elicit panic. The individual must believe
that the physical arousal may have negative consequences.
The extent to which an individual believes that autonomic arousal can result in
catastrophic consequences in known as anxiety sensitivity (Reiss and McNally, 1985).
Individuals high in anxiety sensitivity may believe that shortness of breath signals
suffocation or that heart palpitations indicate a heart attack, whereas those low in anxiety
sensitivity experience these sensations as uncomfortable but innocuous (McNally, 1994).
Evidence suggests that anxiety sensitivity is a stable, trait-like characteristic that emerges
from experiences (both personal and observational) that yoke aversive consequences with
arousal (McNally, 1994).
Empirical support for anxiety sensitivity’s role in panic is fairly strong. Elevated
anxiety sensitivity has been shown to be typical of anxiety disorders in general (Taylor,
Koch, and McNally, 1992), with panic disorder patients scoring two standard deviations
greater than controls, and significantly higher than patients with generalized anxiety
disorder (McNally, Amir, Louro, Lukach, Riemann, and Calamari, 1994). Additionally,
anxiety sensitivity has been shown to predict diagnostic severity of panic disorder (Jones
10
and Barlow, 1991, c.f., Telch, Silverman, and Schmidt, 1996) and has been shown to
diminish with the reduction of anxiety symptomatology (McNally and Lorenz, 1987;
Telch, Lucas, Schmidt, Hanna, Jaimez and Lucas, 1993).
Empirical evidence garnered via multiple methods and across multiple populations
suggests anxiety sensitivity may play a prominent role in the pathogenesis and the
maintenance of panic disorder (McNally et al., 1998). Most notably, prospective
investigations have identified anxiety sensitivity as a risk factor for the development of
panic attacks and panic disorder (Donnell and McNally, 1990; Ehlers, 1995; Mailer and
Reiss, 1992; Schmidt et al., 1997). For example, Ehlers (1995) found high baseline
anxiety sensitivity to be associated with the occurrence of a first panic attack during a
one-year follow-up period. In the laboratory, anxiety sensitivity has been found to
predict emotional and physical responding to various biological challenges regardless of
panic history and diagnostic status (Donnell and McNally, 1989; Schmidt and Telch,
1994; Rapee and Medoro, 1994; Telch and Harrington, 1993; Telch et al., 1996;
Holloway and McNally, 1987). Telch and Harrington (1992) found subjects with high
anxiety sensitivity without a history of panic attacks exhibit rates of CO 2 -induced panic
comparable to panic disorder patients. Eke and McNally (1996) found that psychological
variables reflecting fears of bodily sensations are better predictors of response to carbon
dioxide challenge than either behavioral sensitivity to carbon dioxide or general trait
anxiety.
While research concerning anxiety sensitivity, body vigilance, interoceptive acuity,
and cardiovascular reactivity has shed considerable light upon the maintenance of panic,
the focus has only recently turned to the enlightenment of its pathogenesis (Mailer and
11
Reiss, 1992; Schmidt, Lerew, and Jackson, 1997; Ehlers and Breuer, 1992; Schmidt et al.,
1997). Additionally, prior investigations into risk factors for anxiety pathology have to
date involved the sole consideration of the singular effects of each of the suspected risk
factors. Very few studies have investigated the relationship between anxiety sensitivity,
cardiac reactivity, and heartbeat perception in nonclinical subjects.
In one of the few existing investigations into these constructs in a nonclinical
sample, Sturges and Goetsch (1996) exposed nonclinically anxious (i.e., high anxiety
sensitivity) women and nonanxious (i.e., low anxiety sensitivity) women to caffeine-
induced arousal and compared heart rate and skin conductance reactivity and
interoceptive accuracy and failed to find an effect. However, methodological difficulties,
such as the failure to measure blood pressure and the allowance of practice trials on the
heart beat tracking task, may have masked or ignored important differences between the
groups. The authors also did not investigate interactive effects between the variables of
interest, and they failed to include a measure of symptoms and subjective distress in
relation to the caffeine challenge.
Thus, the principle aim of the present study was to investigate the hypotheses
proposed by Ehlers (1993) by evaluating the singular and interactive effects of anxiety
sensitivity, body vigilance, heartbeat perception, and cardiovascular reactivity in
predicting fearful responding to a biological challenge in individuals with no history of
spontaneous panic or any anxiety disorder diagnosis.
Study Hypotheses
Ehlers’s (1993) hypothesized that individuals with panic disorder are more likely to
perceive physical symptoms for one of three reasons: they pay more attention to them;
12
are more accurate at perceiving them; or they are more reactivity physiologically to
anxiogenic physical stimuli. Additionally, recent research into the role of cognitions in
panic suggests the catastrophic interpretation of physical symptoms is important in the
genesis of anxiety and fear. Therefore, it was hypothesized that:
- Catastrophic interpretation of symptoms will predict fearful responding to a carbon
dioxide challenge in a nonclinical sample.
- Catastrophic interpretation will mediate the roles of somatic vigilance, interoceptive
acuity, and cardiovascular reactivity in self-reported fear. That is, neither body
vigilance, heartbeat perception, nor cardiovascular reactivity (i.e., changes in heart
rate, systolic and diastolic blood pressure) will predict fearful responding unless they
are catastrophically interpreted.
Methods
Sample and Procedures
72 (27 males and 45 females) non-clinical subjects from Washington, D.C. and
Montgomery County, Maryland participated in the study. Potential subjects were
contacted by phone from a list of 1,516 phone numbers selected randomly by city block
and purchased from a national survey sampling company (See Table 1). Of the 1,516
phone numbers, 107 eligible residences expressing interest in the study were identified.
These 107 households contained a total of 135 eligible people.
Respondents were administered a brief, preliminary telephone interview to
determine their eligibility. The data presented in this paper were collected as part of a
13
Table 1
Contact Results for 1516 Random Phone Numbers
Status
Count
Business (nonresidential) Numbers
131
Couldn’t Contact
639
Disconnected Numbers
288
Fax Numbers
87
Hang-ups
20
Ineligible Households
203
Age: 156
Medical: S
Psych Hx: 5
Other: 37
Not Interested
41
Interested/Eligible households
107
Total
1516
larger, prospective study of risk factors for anxiety pathology. Based upon
epidemiological data that suggest young adults to be at highest risk for the development
of anxiety pathology (Weissman and Merikangas, 1986; Bums and Thorpe, 1977),
eligible respondents were between the ages of 18 and 35 and without a history of
spontaneous panic or a DSM-FV Axis I disorder. Additionally, eligible respondents were
without significant, current medical illness (e.g., renal, cardiovascular, neurological, or
pulmonary disease), which could accoimt for differences in physiological indices at
baseline and in response to the biological challenge task. Due to the format of the current
protocol, all respondents were able to comprehend spoken and written English. All
eligible individuals living in the selected household were accepted into the study and
were asked to come in for one lab session.
14
Physiological Measures
Vital capacity. A Respirodyne II Plus respirometer and disposable flow sensors
were used to measure each subject’s yital capacity (VC). VC is the maximum yolume of
air that can be moyed in and out of the lungs and is measured in liters. VC was assessed
three times and ayeraged to yield a VC index.
Heart rate and blood pressure. Heart rate, systolic and diastolic blood pressure were
recorded using a Critikon Dynamap Vital Signs Monitor, Model 1846 SX. The monitor
was set to read blood pressure and heart rate at one-minute interyals during the 10-minute
baseline. Measures were suspended during the interoception protocol (see below).
Following each inhalation, 2 immediate blood pressure and heart rate measures were
taken.
Vagal tone. A single channel, three lead signal from an electrocardiographic pre-
amplifler (VTMII, Scope Services, Bethesda, Maryland), proyided yisual, computerized
numeric output of heart rate which allowed for precise assessment of the subject’s
interoceptiye accuracy.
Interoceptiye accuracy. Interoceptiye accuracy was assessed yia the mental tracking
paradigm designed by Schandry (1981) and modified by Ehlers and Breuer (1992).
Subjects were instructed to count their heartbeats silently during interyals of 35 seconds,
25 seconds, and 45 seconds without taking their pulses or using other perception
strategies. In order to minimize random guessing, subjects were specifically instructed to
count only the heartbeats they actually perceiye and not to count just because they know
their heart should be beating (Zoellner and Craske, 1999). Each interval began with the
experimenter asking if the subject was ready, and upon a positive response stating, “Go.”
15
Simultaneously, another experimenter counted actual R-waves from electrocardiogram
(ECG) recordings of the VTM-II. Interoceptive accuracy was defined as the absolute
value of the actual number of heartbeats minus the number of perceived heartbeats
divided by the actual number of heartbeats multiplied by 100. The resulting quotient is
identified as heart beat accuracy (HBA).
Psychological Measures
Structured clinical interview . In order to assess Axis I psychiatric disorders, the
Structured Clinical Interview for Axis IDSM-IV Disorders, Patient Edition (SCID-I/P-
Version 2.0; First, Spitzer, Gibbon, and Williams, 1996) was administered to all subjects
by a graduate student trained in its administration. The SCID-I/P has shown high validity
and good test-retest reliability in diagnosing Axis I disorders in a variety of populations
(Williams, Spitzer, and Gibbon, 1992).
Acute Panic Inventory. The Acute Panic Inventory (API) is a 24-item inventory for
assessing symptoms of arousal associated with panic attacks (Liebowitz et al., 1984).
Subjects rate the severity of each symptom from 0 (absent) to 3 (severe). Examples
include, “Did you feel faint?”, and “Were you afraid of dying?”. The API includes two
self-report visual analog scales of the subject’s current level of fear and highest level of
fear (0 - no fear at all, 100 - extreme fear).
Anxiety Sensitivity Index. The Anxiety Sensitivity Index (ASI) is a 16-item
questionnaire that measures fear of somatic symptoms related to arousal (Peterson and
Reiss, 1992). Each item assesses a concern about the possible negative consequences of
anxiety symptoms on a 0 to 4 point likert scale. This test is scored by summing each
response to provide a total score. The ASI has demonstrated adequate internal
16
consistency (Telch, Shennis, and Lucas, 1989) and test-retest reliability (Mailer and
Reiss, 1992). The ASI appears to tap into fear of anxiety symptoms as opposed to state
or trait anxiety (see McNally, 1994). The mean for nonclinical samples has been
observed to be 19 (Peterson and Reiss, 1992).
Body Vigilance Scale. The Body Vigilance Scale (BVS; Schmidt et al., 1997) is a
4-item self-report inventory that was designed to assess attentional focus to internal body
sensations. The first three items assess degree of attentional focus, perceived sensitivity
to changes in bodily sensations, and the average amount of time spent attending to bodily
sensations. The fourth item involves separate ratings for attention to 15 sensations (e.g.,
heart palpitations) that include all of the physical symptoms described for panic attacks in
the DSM-IV (American Psychiatric Association, 1994). Scores on item 3 are divided by
10. Ratings for the 15 sensations are averaged to yield a single score for item 4. The
BVS total score is the sum of items 1-4. The BVS has been shown to have adequate test-
retest reliability and high internal consistency, and the mean score for nonclinical
subjects has been reported to be 18.0 (Schmidt et. al., 1997).
Biological Challenge Procedure
Prior to exposing the subject to the CO 2 challenge, the subject’s vital capacity (VC)
was measured. The experimenter provided instructions and a demonstration of the VC
procedure. The subject inhaled as much air as possible, placed his/her mouth around the
flow sensor making a tight seal, and exhaled through the flow sensor. Following three
VC measurements, the subjects were given the following instructions: “Next you will
take two deep breaths. One breath will be of normal room air, and the other will be a
mixture of oxygen and carbon dioxide. The oxygen and carbon dioxide mixture will
17
produce some short-lived sensations. You will not be told which one you will receive
first in order to ensure your response will not be biased. As I said before, you will take
one single breath of each gas. I will ask you to hold the inhalation while I count to five,
and then you can exhale.” Next, the experimenter demonstrated taking a vital capacity
breath from the venti-comp bag. The order of presentation of the two gases was
determined by coin flip prior to the initiation of the protocol. The experimenter then
assisted the subject in taking a vital capacity breath of each of the gases (35% carbon
dioxide and 65% oxygen, and room air). The mixture was delivered to subjects via 4.8
liter venti-comp bags filled to capacity. The patient, with nostrils closed, exhaled all of
the air in his/her lungs and then inhaled from the venti-comp bag via a one-way flow
valve with the goal of inhaling as much of the mixture as possible. The challenge phase
consisted of the inhalation period plus 30 seconds following COi inhalation. The CO 2
intake volume was assessed by measuring the amount of CO 2 remaining in the venti-
comp bag. The API was obtained after each phase. The patient was then disconnected
from the apparatus.
Protocol Overview
After reviewing the consent forms and administering the SCID-I/P, subjects were
given a battery of self-report inventories including the ASI, BVS, and the STAI. After
completing these questionnaires, subjects were then connected to the VTM-II and
dynamap and asked to sit still and quietly for a 10-minute baseline. At the end of the
baseline period, subjects completed the Interoceptive Accuracy paradigm and then the
CO 2 challenge.
18
Data Analytic Strategy
Total scores were calculated for the ASI and the BVS according to their
standardized scoring algorithms. Measures of reactivity for each of the cardiovascular
indices (heart rate, diastolic blood pressure, and systolic blood pressure) were calculated
by partialling out the variance in scores accounted for by baseline measures (i.e., for each
cardiovascular measure, a linear regression analysis was performed using the measure’s
baseline level and room air reactivity level as independent variables and the CO 2
reactivity level as the dependent level. The unstandardized residuals of these regressions
were used as the reactivity variable for each of cardiovascular indices).
Two hierarchical multiple regression analyses were performed to examine the
predictors of self-reported fear in response to the CO 2 challenge. The dependent variable
was the subject’s level of fear reported immediately after the biological challenge on the
visual analog scale of the API. The six independent variables for this analysis
represented fear of arousal symptoms (ASI) and Ehlers’s (1993) hypothesized
mechanisms for perception of physical symptoms (BVS, HBA, AHR, ADBP, ASBP).
The independent variables were entered stepwise, and the order of entry was based on
cognitive theory and prior research findings discussed in the Introduction.
The second regression analysis was designed to identify interaction effects
between the ASI and each of the other five independent variables on the dependent
variable, post-C02 self-reported level of fear. The independent variables were entered in
six steps. The first step contained the main effects for ASI, BVS, HBA, AHR, ADBP,
ASBP. Steps two through six contained the cross-products of the ASI and each of the
19
other five variables. The cross products were entered stepwise, and the order of entry
was based on cognitive theory and prior research findings discussed in the Introduction.
Results
Descriptive Statistics
Table 2 gives descriptive statistics for the initial sample of 72 subjects. The sample
primarily included young, healthy Caucasian women with at least a high school diploma.
The sample means on the anxiety sensitivity index (ASI), the body vigilance scale (BVS),
and baseline cardiovascular measures were within the normal range but were lower than
previously reported means for nonclinical subjects (Table 2).
Table 2
Sample Descriptive Statistics
n
%
Gender
Female
45
62.5%
Male
27
37.5%
Ethnicity
Caucasian
40
54.9%
African American
20
28.1%
Hispanic
5
7.2%
Asian
3
4.2%
Other
4
5.6%
Range
MfSDl
Age(yrs)
18-35
26.9(4.6)
Education (yrs)
11-18
14.7(2.1)
20
Missing Data
As Table 3 indicates, each predictor variable had missing data points. Most of these
missing data points were due to time constraints and equipment difficulties. None of the
missing data points were due to subject refusal to complete the protocol, and no single
subject was missing more than 2 data points. Pairwise deletion of subjects with missing
data yielded a reduced sample of 48. As a result, statistical analyses included
replacement of missing data with the sample mean for that measure.
Table 3
Descriptive Statistics for the Predictor Measures
Missing
data
Variable
Range
MfSDl
n
%
Anxiety Sensitivity Index
1-37
14.58(8.2)
7
9.7
Body Vigilance Scale
0 - 35.3
10.81(8.2)
5
6.9
Heartbeat Accuracy (% inaccurate)
3.4 - 100
87.12(21.0)
4
5.5
Baseline Systolic Blood Pressure
84-150
111.53(13.1)
7
9.7
Post CO 2 Systolic Blood Pressure
91 - 164
120.48(16.4)
8
11.1
Baseline Diastolic Blood Pressme
48-92
66.91(9.1)
7
9.7
Post CO 2 Diastolic Blood Pressure
52-99
73.46(10.0)
8
11.1
Baseline Heart Rate
41-96
64.76(11.0)
7
9.7
Post CO 2 Heart Rate
45-104
67.77(11.4)
6
8.3
Correlation Matrix
Table 4 contains the correlations among the six independent variables. Significant
correlations (p<.05) existed between the ASI and SBP reactivity, and SBP reactivity and
HR reactivity.
21
Table 4
Correlation Matrix for Predictor Variables
Variable
1
2
3
4
5
6
1. ASI
“
.101
.077
-.099
-.270
.327*
2. BVS
“
.230
.035
-.035
o
1
3. HBA
--
-.163
-.172
.082
4. AHR
—
.152
-.365*
5. ADBP
—
.056
6. ASBP
—
•g < .05
Table 5
Summary of Hierarchical Regression Analysis for Variables Predicting Post COo Fear
QLzl2}
Variable
B
SEB
P
Anxiety Sensitiyity Index (ASI)
.07
.02
.36**
Body Vigilance Scale (BVS)
-.03
.02
-.15
Heart Beat Accuracy (HBA)
.00
.01
-.06
Heart Rate Reactiyity (AHR)
.03
.02
.18
Diastolic Blood Pressure Reactivity (ADBP)
.02
.02
.14
Systolic Blood Pressure Reactiyity (ASBP)
.01
.02
.06
Note. R~= .13 for Step 1 fp < .01)
♦*E<.01
Main Effects
The anxiety sensitiyity index (ASI), body vigilance scale (BVS), heartbeat accuracy
index (HBA), diastolic blood pressure reactivity (ADBP), systolic blood pressure
reactivity (ASBP), heart rate reactivity (AHR) were entered hierarchically in the order
22
indicated in Table 5. The ASI was the only significant predictor, accounting for 13.2% of
the variance in self-reported fear after the CO 2 challenge. Adding each of the other
predictors did not significantly increase the variance explained.
Table 6
Summary of Hierarchical Regression Analysis for Cross Products Predicting Post CO;
Fear (N = 72 )
Variable
B
^B
3
Step 1
Anxiety Sensitivity Index (ASI)
.079
.774
.44**
Body Vigilance Scale (BVS)
-.031
.022
-.17 ■
Heart Beat Accuracy (HBA)
.000
.021
.00
Heart Rate Reactivity (AHR)
.033
.008
.19
Diastolic Blood Pressure Reactivity (ADBP)
.021
.021
.13
Systolic Blood Pressure Reactivity (ASBP)
.009
.020
.06
Step 2
ASIxBVS
.000
.002
.02
Step 3
ASIxHBA
.000
.001
-.23
Step 4
ASIxAHR
.007
.003
.58*
Step 5
ASIxADBP
.005
.003
.54*
Step 6
ASIxASBP
.004
.002
.42
Note. = .21 for Step 1; AR^ = .05 for Step 4; AR^ = .05 for Step 5 (gs < .05)
''‘p< .05. •*£< .01.
Interaction Effects
Table 6 represents the second multiple regression analysis examining the effects of
23
the cross products of the ASI and the other five independent variables. ASIxAHR cross
product (Step 4) increased the value to .266, a significant improvement over Step 3,
indicating anxiety sensitivity’s effect on fear is not the same for different levels of heart
rate reactivity. A graphical representation of the ASI/AHR interaction is depicted in
Figure 1.
Similarly, the ASIxADBP cross product significantly increased the R^ value to .312.
A graphical representation of the ASIxADBP interaction is depicted in Figure 2. The
addition of the other cross products did not contribute significantly to the model. The
overall model explained 34.5% of the variance in post-COi self-reported fear.
Discussion
Cognitive notions of panic assert the preeminence of catastrophic thought processes
in the development and maintenance of panic, and the findings from the present study
lend support to this notion. When considering anxiety sensitivity, cardiovascular
reactivity, body vigilance, and interoceptive accuracy, anxiety sensitivity emerged as the
only significant factor associated with self-reported fear of carbon dioxide-induced
arousal. These results suggest anxiety sensitivity to be a dispositional factor that
contributes to fearful responding to symptoms of arousal independent of panic history.
Additionally, the findings are consistent with the formulation that when one perceives
arousal as threatening, one is more apt to respond fearfully to arousal-inducing agents and
activities regardless of one’s prior history of panic attacks. These findings have been
reported in previous studies investigating the role of anxiety sensitivity in nonclinical
24
subjects exposed to biological challenges (Holloway and McNally, 1987; Schmidt and
Telch, 1994; Telch et al., 1996).
The remaining results will be discussed in light of Ehlers’s (1993) hypotheses
regarding the role of heightened somatic perception in panic, namely increased vigilance,
enhanced interoceptive acuity, and greater physiological reactivity. In the current,
nonclinical sample, increased vigilance did not emerge as a significant factor associated
with self-reported fear, neither singularly nor in interaction with anxiety sensitivity. The
failure of vigilance to be associated with fearful responding to autonomic arousal
suggests that vigilance, although potentially important in the maintenance of panic, is
unlikely to be a substantial contributor to the development of panic.
The results suggest a similar conclusion with regard to interoceptive acuity.
Although accuracy in detecting somatic changes may foster and sustain panicogenic
cognitions and behaviors, the current findings do not implicate it as a significant
contributor to fearful responding in subjects without histories of panic.
As for Ehlers’s third hypothesis, that individuals who experience panic are more
physiologically reactive, the current findings are more encouraging. Although none of
the cardiovascular reactivity measures (i.e., heart rate, diastolic blood pressure, systolic
blood pressure) singularly contributed to self-reported fear, heart rate reactivity and
diastolic blood pressure reactivity, when considered with anxiety sensitivity status,
appears to be a significant factor. As hypothesized, an anxiety sensitivity and diastolic
blood pressure reactivity interaction emerged as a significant contributor to fearful
responding to the carbon dioxide challenge, indicating high heart rate and diastolic blood
pressure reactivity may increase fearful responding in individuals who also have high
anxiety sensitivity. Because these findings emerged in this nonclinical sample, the results
suggest these factors to be potential risks for the development of panic. This finding is
26
consistent with previous reports from ambulatory monitoring of individuals with panic
disorder showing increased diastolic blood pressure reactivity during and near panic
(Shear et al., 1992; White and Baker, 1987; Bystritsky et al., 1995) and with reports of
elevated diastolic blood pressure in individuals with panic disorder in response to CO 2
challenge.
Additionally, a trend towards an anxiety sensitivity and systolic blood pressure
interaction emerged in the analyses (AR^ = .033, p < .09), indicating the potential role of
systolic blood pressure reactivity or the potential role of a general measure of reactivity
(e.g., mean arterial pressure) that should be investigated in future studies with greater
statistical power.
Limitations of the Study
The primary limitations of this study were the small sample size, missing data, and
the cross-sectional design. The small sample size was a direct result of the methodology
used for recruitment of subjects. Although random digit dialing techniques theoretically
render a more representative sample, people today are inundated with tele-marketers and
phone solicitors, so much so that many households were unwilling to speak to us and
unwilling to return our phone calls. This method of subject recruitment could have
resulted in an additional bias in that, intuitively, it seems that more anxious people would
be less willing to commit to driving across a large metropolitan area to participate in a
research study.
To some extent, this bias is supported by the sample’s low scores relative to other
nonclinical samples on the anxiety sensitivity index (McNally, 1996), and the body
vigilance scale (Schmidt et al., 1997). Additionally, the sample’s high degree of
27
inaccuracy in detecting heart rates, and lower than average baseline blood pressures and
heart rates (Guyton and Hall, 1996) are indicative of such a selection bias. Subjects’ low
level of fearful responding to the CO 2 challenge could have also been influenced by the
selection bias and other methodological limitations. For example, Telch and colleagues
(1996) found that the emotional responding of nonclinical subjects with high anxiety
sensitivity is influenced by perceived control (i.e., their ability to regulate their CO 2
intake).
In our study, subjects were told they could leave the study at any time, and they
would be paid for the portion of the protocol they completed. This could have resulted in
diminished emotional responding in an already nonanxious sample. The low scores on
the SUDS scale indicating fear of the CO 2 challenge are suggestive of this fact (M = I -2,
SD = 1.9, possible range, 0-10). The recruitment methodology also resulted in a small
sample size, which significantly diminished the statistical power of the analyses.
Missing data points were another source of concern in the current study. Due to the
small sample size and the wide distribution of missing values, it was not possible to
discard subjects with missing data. No single subject was missing more than 2
independent variable measures, but 24 subjects were missing at least one independent
variable. Substitution with the mean was implemented for these subjects.
Conclusions
Although many questions remain regarding the genesis of panic and other anxiety
disorders, the results of this study, interpreted in light of results from other nonclinical
examples, have potential theoretical ramifications for current theory. The present
findings suggest improved accuracy for detecting one’s heart rate and vigilance for
28
symptoms of arousal may be common sequelae, but appear to be neither necessary nor
sufficient links in the anxiety pathology chain. Prospective studies of nonclinical
subjects will best be able to pursue these findings further. This study additionally
provides added support to the notion that aberrant, catastrophic cognitions regarding the
meaning of somatic symptoms may be necessary, and at times sufficient, to induce
fearful responding to such sensations. As well, an individual’s physiology, specifically
one’s cardiovascular reactivity, may be an important mediator in the genesis of fear.
29
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