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Psychosomatic Medicine 68:331-339 (2006)
© 2006 American Psychosomatic Society

ORIGINAL ARTICLES

Blood-Injury Phobia With and Without a History of Fainting: Disgust Sensitivity Does Not Explain the Fainting Response

Alexander L. Gerlach, Dr Rer Nat, Gerd Spellmeyer, Claus Vögele, PhD, René Huster, Stephan Stevens, Günther Hetzel, MD and Jürgen Deckert, MD

From the Department of Psychology, Institute I-Psychological Assessment and Clinical Psychology, Westfalian Wilhelms University of Münster, Münster, Germany (A.L.G., S.S., R.H.); the Department of Psychiatry, University of Münster, Münster, Germany (G.S., G.H., J.D.); Clinical and Health Psychology Research Centre, School of Human and Life Sciences, Roehampton University, London, United Kingdom (C.V.).

Address correspondence and reprint requests to Dr Rer Nat, Alexander L. Gerlach, Westfalian Wilhelms University of Münster, Department of Psychology, Institute I-Psychological Assessment and Clinical Psychology, Fliednerstr. 21, 48149 Münster, Germany. E-mail: agerlach{at}uni-muenster.de


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: Individuals diagnosed with blood-injury phobia respond to venipuncture with strong psychophysiological responses. We investigated whether disgust sensitivity contributes to the fainting response and is associated with parasympathetic activation, as suggested by previous research.

Methods: Twenty individuals diagnosed with blood-injury phobia (9 with a history of fainting to the sight of blood, 11 without such a fainting history) and 20 healthy controls were compared. Psychophysiological responses and self-report measures of anxiety, disgust, and embarrassment were monitored during rest, a paced breathing task, and venipuncture. In addition, trait disgust sensitivity and blood-injury fears were assessed.

Results: Blood-injury phobics reported enhanced anxiety, disgust, and embarrassment during venipuncture. They also experienced heightened arousal, as indicated by heart rate, respiration rate, and minute ventilation. Blood-injury phobics without a fainting history tended toward higher anxiety and disgust scores. There was no evidence for increased parasympathetic activation in either blood-injury phobic subgroup or of an association of disgust and parasympathetic activation.

Conclusion: The tendency to faint when exposed to blood-injury stimuli may suffice as a conditioning event leading into phobia, without specific involvement of disgust sensitivity and parasympathetic activation.

Key Words: blood-injury phobia • specific phobia • fainting • vasovagal syncope • neurocardiogenic syncope • parasympathetic activation • sympathetic activation • respiratory sinus arrhythmia

Abbreviations: BIP+ = blood-injury phobia with a history of fainting; BIP– = blood injury phobia without a history of fainting; RSA = respiratory sinus arrhythmia; PSD HR = log-transformed power spectral density of heart rate oscillations (0.15–0.50 Hz); CMTR LV-HR = coherence-corrected magnitude of the transfer function-relating lung volume oscillations to heart rate oscillations at the peak respiratory frequency; BIFQ = blood-injury-fear questionnaire; FEE = Fragebogen zur Erfassung der Ekelempfindlichkeit.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Blood-injuryphobia is characterized by a persistent fear that is excessive or unreasonable and is triggered by the sight or anticipation of blood, wounds, syringes, and similar stimuli. The blood-injury-related stimuli are either avoided or endured only with intense anxiety, whereas the phobic person recognizes that the fear is excessive or unreasonable. Results from a recent epidemiologic survey employing DSM-IV criteria (American Psychiatric Association, 1994) yielded a lifetime prevalence of 3.5% and an early age of onset at around 5.5 years (1). Out of fear, patients may abstain from necessary medical treatment despite negative consequences for their health (2,3).

Fainting is a major reason why patients with blood-injury phobia are afraid of confrontation with the feared stimuli, and it is still not fully understood (4). The fainting response to blood-injury stimuli is considered an emotion-triggered form of the neurocardiogenic syncope (5–9). Historically, the role of the parasympathetic nervous system in the neurocardiogenic syncope has been highlighted. Graham et al. (6) have argued that vasovagal fainting is a diphasic response. The initial phase is characterized by an increase in sympathetic discharge and the second phase by parasympathetic excitation, accompanied by a substantial fall in heart rate and blood pressure. They argued that this parasympathetic excitation is activated by a reflex mechanism in the first phase (associated with anxiety) and is then left suddenly unopposed by the sympathetic activity when anxiety ceases. Indeed, Ruetz and coworkers (5) pointed out that fainting in blood donors often occurs after cessation of venipuncture.

Adding a trait aspect to this notion, some studies analyzed cardiac parasympathetic activity level in blood-injury phobics at rest not confronted with blood-injury stimuli. Results were mixed, with some of these studies finding increased respiratory sinus arrhythmia (RSA), an index of cardiac vagal activity, in blood-injury phobics compared with controls (e.g., 10–14). However, most of these studies neglected to control or measure tidal volume when estimating RSA or used student populations rather than diagnosed blood-injury phobics.

Parasympathetic excitation alone is not sufficient to explain syncope in most patients. For example, prevention of bradycardia in fainters through pharmacologic blocking or pacemakers has no effect on fainting rates (5,15). Loss of sympathetic tonus is also relevant since the final mechanism operative during syncope is withdrawal of sympathetic outflow to blood vessels in skeletal muscles (16). Additionally, in muscles there is an active cholinergic vasodilator mechanism (17). Finally, hyperventilation has also been implicated as a mechanism involved in fainting because cerebral vasoconstriction is part of the hypocapnic response (18,19). Hyperventilation, specifically increased ventilation, has been observed in fainting blood-injury phobics and in blood-injury-anxious students (5,7,20,21).

With respect to the emotional experience of the fainters, Page (22) argues that the vulnerability to faint in the presence of blood and injury is due to elevated disgust sensitivity. Confrontation with disgust stimuli may be accompanied by heart rate deceleration, a pattern reminiscent of the vasovagal response in blood-injury phobics (23). The parasympathetic nucleus of the solitary tract participates in cardiovascular control, the monitoring of tastes, and the rejection of inedible foods (24). Similarly, the medulla, via its vagal efferent, controls cardiac slowing, as well as nausea and vomiting (25). Parasympathetic activation associated with disgust may thus facilitate fainting in blood-injury phobics. However, although this notion is intriguing, some aspects are unclear. Most important, heart rate decelerations have only been found with disgust stimuli that were associated with blood-injury stimuli (26,27). Whenever disgust was elicited using non-blood-injury-related stimuli (e.g., smells, pictures of dirty toilets, etc.), a heart rate acceleration was observed (28–31).

In addition, in most studies investigating autonomic responses of blood-injury phobics, films or pictures were used (e.g., 32–34). Film stimuli, however, are quite different from the situations relevant for blood-injury phobics. Venipuncture is completed within a short time, whereas films often have a much longer duration. Furthermore, the pain stimulus present during venipuncture may be of particular importance when studying fainting (35). The few studies that employed venipuncture as a challenge (5,6) lacked sophisticated methodology in analyzing parasympathetic activation and did not perform parallel measurements of disgust and disgust sensitivity.

The present study serves to investigate the influence of disgust sensitivity on the autonomic responses to venipuncture in individuals diagnosed with blood-injury phobia. We tested the hypothesis that parasympathetic activation and disgust sensitivity are (1) higher in blood-injury phobics compared with controls and (2) higher in blood injury phobics with a history of fainting than in blood-injury phobics without a history of fainting. The second hypothesis is based on the consideration that in phobics with a history of fainting, the physiological mechanism promoting this reaction should be more pronounced. Furthermore, we tested (3) whether disgust sensitivity and parasympathetic activation are associated already at rest. As a methodologic improvement, we measured and controlled for both respiration rate and tidal volume when assessing RSA and included only blood-injury phobics with a confirmed diagnosis. Finally, we measured (4) parasympathetic activation before, during, and after cessation of venipuncture in order to estimate the influence of parasympathetic activation induced by venipuncture. Based on the Graham et al. (6) notion, we predicted that RSA should be increased in blood-injury phobics compared with controls during venipuncture and specifically during recovery.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
All phobic participants were recruited via newspaper articles describing blood-injury phobia. Healthy controls were recruited by advertisements asking for people without fear of venipuncture and without a history of fainting during venipuncture. After a telephone screening, participants who met the inclusion criteria (blood injury fear, no ongoing medication other than birth control, age between 18 and 65) were invited for a diagnostic assessment consisting of the German version of the SCID IV (36) and a short structured interview covering blood-injury phobia, both conducted by a licensed clinical psychologist. Three controls had to be excluded at this stage because of current mental disorders (one with panic disorder with agoraphobia, one with alcohol abuse, and one with a specific phobia of spiders); one participant in the phobic group had to be excluded because of multiple primary diagnoses other than blood-injury phobia (major depression, somatization disorder, social phobia). The resulting sample consisted of 20 controls and 20 individuals with a primary diagnosis of blood-injury phobia (DSM-IV). Diagnostic and demographic variables describing the two groups are presented in Table 1.


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  		TABLE 1. Description of the Study Sample

 

Ethical clearance had been obtained from the ethical committee of the University of Münster before data collection. Signed informed consent was acquired from all participants on arrival in the laboratory.

Participants' History of Fainting
Nine of the blood-injury phobics reported to have fainted in the past at the sight of blood-injury-related situations (BIP+), and 11 blood-injury phobics reported not to have fainted in these situations (BIP–). None of the controls had ever fainted at the sight of blood or injuries. Consequently, significantly more blood-injury phobics had fainted at the sight of blood or injury than controls ({chi}2 = 11.6129; p < .001).

The mean number of fainting episodes in the BIP+ group was 10.6 (SE: 2.2), with a minimum of 2 and a maximum of 20 fainting episodes (including fainting due to blood-injury stimuli, as well as other reasons). The respective numbers in the BIP– group (including only fainting due to other reasons) and the control group were 0.9 (SE: 0.5; min: 0; max: 5) and 0.8 (SE: 0.3; min: 0; max: 5). Mean age of first fainting episode (blood-injury stimuli) was 8.9 years (SE: 1.4; min: 3; max: 18 years) in the BIP+ group.

Six controls, 7 blood-injury phobics with a history of fainting, and 3 blood-injury phobics without a history of fainting reported to have fainted due to reasons other than the sight of blood or injections (e.g., orthostatic stress, diarrhea). The significant difference in fainting episode frequency between groups ({chi}2 = 6.9, p = .031) is due to the BIP+ group: more patients in this group had fainted due to other reasons than individuals in the BIP– ({chi}2 = 5.1, p = .024) or in the control group ({chi}2 = 5.7, p = .017). A comparison of the BIP– and the control group showed a similar proportion of individuals who had fainted due to non-blood-injury-related reasons ({chi}2 = 0.03, p = .8). Only three of the BIP+, none of the BIP–, and two controls reported relatives that had fainted due to confrontation with blood-injury.

Measures
Self-Report
In order to assess general and specific psychopathology, all participants completed a new questionnaire assessing fear and avoidance of blood-injury-related situations (blood-injury-fear questionnaire, BIFQ), a modified German version of the disgust scale (Fragebogen zur Erfassung der Ekelempfindlichkeit (FEE); 37), the German version of the Beck Depression Inventory (38), and the German version of the Symptom Check List (39). They additionally answered a number of questions concerning the fainting history of the person.

The BIFQ consists of two scales (fear and avoidance) with 28 items each and has been studied independently in a sample of 63 college students receiving course credit for participation. Each subscale has good reliability (Cronbach's {alpha} is 0.95 for the fear scale and 0.94 for the avoidance scale).

In order to assess the emotional state of the participants during the experiment, participants were asked to indicate their feelings of anxiety, embarrassment, and disgust at baseline and during venipuncture on a 10-cm visual analogue scale. Participants completed these scales immediately at the end of the baseline period and at the end of the recovery period.

Physiological Measures
Physiological recordings were made with the Kölner Vitaport II system (Temec Instruments, The Netherlands). We were mainly interested in three aspects of the peripheral physiological reaction: blood pressure to assess the magnitude of the fainting response and heart rate to assess the sympathetic activation resulting from anxiety; parasympathetic (vagal) control of the heart was assessed by means of two spectral measures, one of which required the measurement of respiration.

A continuous arterial blood pressure waveform was obtained from the index finger of the nondominant hand by means of the Finapres 2300 system (Ohmeda, Madison, WI) and sampled at 32 Hz. Beat-by-beat diastolic and systolic pressure values were identified as local maxima/minima in the arterial pressure waveform and edited manually. These measuring points were then interpolated using cubic splines and resampled at 4 Hz.

ECG was recorded at a 256 Hz sample rate from three electrodes attached to the chest. Heart rate was estimated with a program that calculated consecutive interbeat intervals. Outliers were identified based on an algorithm described by Berntson et al. (40) and edited manually. These data were resampled at a frequency of 4 Hz to generate an equally spaced time series.

Respiratory activity was monitored with elastic bands placed around the chest and abdomen and sampled at 32 Hz using inductive plethysmography (Respitrace, Ardsley, NY). Raw signals of the two bands were converted to lung volume change using calibration regression weights established by spirometry and the least-squares method (41). Respiratory rate and minute volume were calculated breath by breath using programs customized by the first author. Algorithms employed for these programs were based on work by a number of authors (41–45). The lung volume signal and the respiration rate were resampled at 4 Hz.

Vagal control of heart rate was estimated using two different methods, both published (46). Estimates of power spectral density of heart rate oscillations were summed across the frequency band associated with respiration (0.15–0.50 Hz). To normalize values, raw power was log-transformed (referred to in the following as PSD HR). In addition, coherence-corrected magnitude of the transfer function relating lung volume oscillations to heart rate oscillations at the peak respiratory frequency was calculated (referred to as CMTR LV-HR). This latter measure estimates vagal control of the heart while controlling for differences in tidal volume and respiration rate (e.g., 46–48).

Procedure
On arrival, participants were introduced to the equipment. Then the electrodes, the respitrace belts, and the Finapres finger cuff were attached. Participants were instructed to relax as best as they could before baseline measurements ensued for five minutes.

Participants were then instructed how to perform a paced breathing task. The experimenter explained that they would listen to a tone that changed its pitch and that they should breathe in while the pitch rose and breathe out while the pitch fell. They were also instructed not to breathe too deeply but rather to breathe normally. Then the paced breathing was started with the tone signaling a breathing rate of 10, 14, and 18 breaths per minute for two minutes for each breathing rate. This task results in uniform breathing frequencies in all participants and consequently allows assessing parasympathetic activity under standardized breathing conditions.

After completion of this task, participants were informed that the venipuncture was about to begin, that they had two minutes to mentally prepare and that this time period was signaled by a counter starting at 120 and counting backwards to 0 (anticipation). Then the experimenter and a medical doctor entered the room and the venipuncture was performed (venipuncture). Finally, physiologic monitoring continued for an additional two minutes (recovery).

Participants were asked not to speak during venipuncture and recovery, and they could choose to watch the procedure or not. Venipuncture followed a standard protocol: the accumulation conveyer and then a disinfectant were applied. After approximately 20 seconds, the remaining disinfectant was removed and a vein was penetrated with a syringe. Five milliliters of blood were taken, and after the accumulation conveyer was removed, the syringe was removed as well. The beginning and the end of this procedure were marked online. Finally, the experimenter noted whether the participants had watched the venipuncture.

During recovery, the medical doctor and the experimenter left the room while participants were monitored by means of the physiologic signals, a video screen, and an intercom system. Two participants fainted during recovery; in these cases, the reclining chair was lowered and the legs were raised while the physiologic measures continued.

Data Analysis
Each physiologic measure was first subjected to an ANOVA with GROUP (BIP+, BIP–, and controls) as between-subjects factor and TIME (baseline, anticipation, venipuncture, recovery) as within-subjects factor. If the GROUP and/or the interaction effect were significant, planned contrasts were calculated, first analyzing differences between blood-injury phobics and controls and then between the BIP+ and the BIP– groups. Self-report measures were additionally first subjected to a MANOVA, including all three self-report measures (anxiety, embarrassment, and disgust ratings). An {alpha} level of 0.05 was used for all statistical tests. Preliminary analyses with gender as an additional factor and age as a covariate revealed no effects relevant to the hypotheses tested in the current study. Consequently, gender and age were not included in the analyses presented here.

Since it cannot be ruled out that the fainting of two participants during recovery may have affected the results of the analysis of the physiologic measures, we tested additionally whether exclusion of these two participants would change the results. The patterns of the physiologic measures of these two fainters are depicted separately in the respective graphs and tables.

Finally, correlational analyses were conducted, looking at (a) intercorrelations of the self-report measures in order to estimate the degree to which these measures were actually measuring different emotions and (b) the correlations between measures of state and trait disgust and estimates of parasympathetic activation at baseline and during venipuncture and recovery. The latter correlational analyses were conducted to be able to estimate the association of self-report disgust (state and trait) with parasympathetic activation.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Paced-Breathing Paradigm
All three groups (controls, BIP+, and BIP–) were equally able to follow the paced-breathing instructions. There was no evidence for differences in breathing frequency or depth (minute volume in liters) between the three groups (F(4,72) = 0.17; p = .9; {eta}p2 < 0.01), nor was there a significant interaction between GROUP x RESPRATE (10, 14, 18 breaths per minute), F(8,68) = 1.6, p = .13, {eta}p2 = 0.16. Table 2 gives the respective means and standard errors. Showing the effect of the breathing instructions, the factor RESPRATE was highly significant (F(4,34) = 372,1; p < .001, {eta}p2 = 0.98). Exclusion of the two fainters did not change this pattern of results.


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  		TABLE 2. Means and Standard Error (in Brackets) of the Physiological Variables Relevant for the Paced Breathing Task

 

Surprisingly, neither the spectral heart-rate power (0.15–0.5 Hz) (GROUP: F(2,37) = 0.5; p = .6, {eta}p2 = 0.02; GROUP x RESPRATE: F(4,74) = 0.5, p = .7, {eta}p2 = 0.02) nor the CMTR LV-HR measure (GROUP: F(2,37) = 0.4; p = .6, {eta}p2 = 0.02; GROUP x RESPRATE: F(4,74) = 1.7, p = .14, {eta}p2 = 0.08) indicated differences in basic parasympathetic activation between the three groups. Again, RESPRATE was significant (PSD HR: F(2,74) = 115,6; p < .001, {eta}p2 = 0.73; CMTR LV-HR: F(2,74) = 3.4; p < .05, {eta}p2 = 0.08) demonstrating the effect of different breathing frequencies on RSA estimates. Note that the effect of RESPRATE is clearly reduced in the CMTR LV-HR measure as compared with the PSD HR measure ({eta}p2 = 0.73 versus {eta}p2 = 0.08), indicating the effects of controlling respiration rate and tidal volume. The results of these analyses were not changed by excluding the two fainters.

Venipuncture
Self-Report
A MANOVA with the between factor GROUP (BIP+, BIP–, controls) and the within-factor TIME (baseline and venipuncture) with all three self-report measures (anxiety, disgust, and embarrassment) as dependent variables produced highly significant effects for both factors and their interaction (GROUP: F(6,68) = 4.0, p < .001, {eta}p2 = 0.36; TIME: F(6,31) = 18.8, p < .001, {eta}p2 = 0.70; GROUP x TIME: F(12,62) = 7.3, p < .001, {eta}p2 = 0.45). Planned contrasts analyzing differences between controls and blood-injury phobics on all three self-report measures revealed higher anxiety ratings in blood-injury phobics (F(1,37) = 39.2, p < .001, {eta}p2 = 0.51), more disgust (F(1,37) = 4.8, p < .05, {eta}p2 = 0.11) and marginally more embarrassment (F(1,37) = 3.8, p < .08, {eta}p2 = 0.09) in response to venipuncture than in controls (compare Figure 1). This effect was complemented for all three self-report measures by a significant interaction TIME x GROUP (anxiety: F(1,37) = 59,8, p < .001, {eta}p2 = 0.61, disgust: F(1,37) = 10.1, p < .05, {eta}p2 = 0.14; embarrassment: F(1,37) = 24.8, p < .01, {eta}p2 = 0.22), indicating that only blood-injury phobics responded with an increase in anxiety, disgust, and embarrassment to venipuncture. In order to examine all differences in self-report measures between the BIP+ and BIP– groups, additional contrasts were calculated for the interaction of TIME x FAINT (BIP+ versus BIP–). Only the interaction for disgust was significant (F(1,36) = 4.8, p < .05). Contrary to our hypothesis, this last effect was due to a relatively greater increase in disgust ratings in the BIP– group. Importantly, the effect size for self-reported anxiety (BIP+: {eta}p2 = 0.76; BIP–: {eta}p2 = 0.94, controls: {eta}p2 < 0.01) was much larger than for either self-reported disgust (BIP+: {eta}p2 = 0.12; BIP–: {eta}p2 = 0.31, controls: {eta}p2 < 0.01) or self-reported embarrassment (BIP+: {eta}p2 = 0.31; BIP–: {eta}p2 = 0.37, controls: {eta}p2 < 0.01). Self-reported anxiety in the blood-injury-phobia group increased significantly more (4.7; 95% confidence intervals, 3.81–5.66) than either disgust (1.26; 95% confidence intervals, 0.05–2.47) or self-reported embarrassment (1.66; 95% confidence intervals, 0.51–2.81). The pattern of results of this analysis remained the same, if the two participants who had fainted during recovery were excluded from the respective analyses.


Figure 122
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  		Figure 1. Self-report anxiety: disgust and embarrassment during baseline and venipuncture. Error bars represent standard errors.

 

Behavior
None of the blood-injury-phobic participants and only 4 of the control participants watched the venipuncture. This difference between the two groups was significant ({chi}2 = 4.4; df = 01; p = .04).

Physiology
For an overview of F statistics regarding physiological variables, compare Table 3.


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  		TABLE 3. Result of the ANOVAs With the Factors GROUP (BIP+, BIP–; Controls), TIME (Baseline, Anticipation, Venipuncture, Recovery) and the Interaction of GROUP x TIME on the Seven Physiological Variables

 

Heart Rate
The analysis of heart rate revealed no effect of GROUP (F(2,37) = 1.1, p = .3, {eta}p2 = 0.06), a significant effect of TIME (F(3,111) = 23.9, p < .001, {eta}p2 = 0.4) and most important a significant interaction effect GROUP x TIME (F(6,111) = 4.4; p < .001, {eta}p2 = 0.2), reflecting the status of heart rate as the main physiologic indicator of anxiety-related arousal (49). During anticipation and venipuncture, heart rate increased more in blood-injury-phobic participants than in controls (quadratic contrast: F(1,38 = 13.4; p < .001, {eta}p2 = 0.26). However, there were no differences in heart rate increase between BIP+ and BIP– (quadratic contrast: F(1,18) = 0.1, p = .9, {eta}p2 < 0.01), indicating similar anticipation and venipuncture-related arousal in both these groups. Figure 2 illustrates this pattern. Exclusion of the data from the two fainters did not change this pattern of results.


Figure 222
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  		Figure 2. Heart rate and respiration rate at baseline, anticipation, venipuncture, and recovery. Error bars represent standard errors.

 

Blood Pressure
Surprisingly, no significant effects appeared in the analysis of systolic blood pressure (GROUP: F(2,37) = 1.1, p = .3, {eta}p2 = 0.06; TIME: F(3,111) = 2.2; p = .09, {eta}p2 = 0.06; GROUP x TIME: F(6,111) = 1.8; p = .10, {eta}p2 = 0.09). Exclusion of the two fainting participants had no effect on these results (Figure 3).


Figure 322
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  		Figure 3. Blood pressure at baseline: anticipation. venipuncture, and recovery. Error bars represent standard errors.

 

The analysis of diastolic blood pressure revealed a significant effect for TIME (F(3,111) = 6.3; p < .001, {eta}p2 = 0.15), a marginally significant interaction effect for GROUP x TIME (F(6,111) = 2.0; p < .07, {eta}p2 = 0.10), and no effect of GROUP (F(2,37) = 0.43, p = .6, {eta}p2 = 0.02). However, after exclusion of the two fainting participants, the interaction effect disappeared (F(6,105) = 1.6; p = .15, {eta}p2 = 0.08); only the TIME effect remained (F(3,105) = 3.8, p < .05, {eta}p2 = 0.10).

Summarizing the blood pressure analyses, with the exception of the two fainters, blood-injury phobics and controls did not differ meaningfully in their blood pressure patterns. Figure 4 illustrates these findings.


Figure 422
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  		Figure 4. Minute ventilation at baseline, anticipation, venipuncture, and recovery. Error bars represent standard errors.

 

Parasympathetic Activation
Again contrary to our expectations, when analyzing the two indices of parasympathetic activity, neither PSD HR (GROUP: F(2,36) = 0.2, p = .8, {eta}p2 = 0.01; TIME: F(3,108); F = 1.5; p = .2, {eta}p2 = 0.04; GROUP x TIME: F(6,108) = 0.6; p = .7, {eta}p2 = 0.03), nor CMTR LV-HR (GROUP: F(2,30) = 2.5, p = .1, {eta}p2 = 0.14; TIME: F(3,90) = 2.3, p = .08, {eta}p2 = 0.07; GROUP x TIME = F(6,90) = 1.5; p = .17, {eta}p2 = 0.09) indicated any significant differences between groups. Exclusion of the two fainters did not change this lack of findings.

Respiration
In the analysis of respiration rate, significant effects emerged for GROUP (F(2,37) = 3.4, p < .05, {eta}p2 = 0.16), TIME (F(3,111) = 17.9, p < .001, {eta}p2 = 0.34), and for GROUP x TIME (F(6,111) = 2.6; p < .05, {eta}p2 = 0.12). According to the contrasts, the combined group of blood-injury phobics had generally higher respiration rates than controls (F(1,38) = 6.4, p < .05, {eta}p2 = 0.14) but did not change differently, TIME (F(3,114) = 1.8, p = .15, {eta}p2 = 0.05). The BIP+ and BIP– groups had similar respiration rates (F(1,18) = 0.37, p = .55, {eta}p2 = 0.02), which changed marginally differently (F(1,18) = 2.4, p = .07, {eta}p2 = 0.12). This pattern of results remained the same when the two fainters were excluded from analysis.

Minute ventilation revealed again a significant effect for GROUP (F(2,37) = 3.7, p < .05, {eta}p2 = 0.17), TIME (F(3,111) = 4.8, p < .01, {eta}p2 = 0.11), and a significant interaction for GROUP x TIME (F(6,111) = 3.1, p < .01, {eta}p2 = 0.14). Blood-injury phobics had a higher minute ventilation than controls (F(1,37) = 6.7, p < .01, {eta}p2 = 0.14), but there was no difference between BIP+ and BIP– (F(1,37) = 0.9, p = .34, {eta}p2 = 0.03). Blood-injury phobics differed in their temporal pattern in minute ventilation from controls (F(3,36) = 3.6, p < .01, {eta}p2 = 0.23), but again, the temporal pattern of BIP+ and BIP– participants did not differ (F(3,16) = 0.5, p = .65, {eta}p2 = 0.09). Without the two fainters, the effect of GROUP on minute ventilation disappeared (F(2,35) = 2.2, p = .12, {eta}p2 = 0.11), but the effect of TIME (F(3,105) = 4.0, p < .01, {eta}p2 = 0.17) and the GROUP x TIME (F(6,105) = 3.4, p < .01, {eta}p2 = 0.16) interaction remained significant. Minute ventilation was still higher in blood-injury phobics than controls (F(1,36) = 4.6; p < .05, {eta}p2 = 0.11). BIP+ and BIP– phobics still did not differ in their overall minute ventilation (F(1,16) = 0.01, p = .91, {eta}p2 < 0.01). However, due to higher minute ventilation in blood-injury phobics during venipuncture, contrast analysis of the interaction of blood-injury phobics versus controls with TIME was significant even after exclusion of the two fainters (F(3,108) = 6.9, p < .01, {eta}p2 = 0.16). However, BIP+ and BIP– groups did not differ in minute volume levels (F(1,16) = 0.01; p = .9, {eta}p2 < 0.01) or in their minute ventilation pattern over time (F(3,48) = 0.04; p = .98, {eta}p2 < 0.01).

Correlation Analysis
All self-report measures (state and trait) were significantly correlated. Notably, self-report anxiety during venipuncture was significantly more highly correlated with the BIFQ (r = 0.81) than with either self-report disgust during venipuncture (r = 0.35; p < .01) or trait disgust (FEE I; r = 0.39, p < .01).

In order to test the notion that increased state and trait disgust were associated with increased parasympathetic activation, we calculated the correlation between (a) FEE I and self-report disgust with (b) CMTR LV-HR and PSD HR during venipuncture, recovery, and the paced breathing task (as an estimate of the parasympathetic activation at baseline). None of these correlations were significant (all p values >.2; 0.02 ≤ r ≤ 0.2).

Description of the Two Fainters
Two fainting episodes do not allow any statistical testing. It seems nevertheless indicated to describe the reactions of the two fainters. As can be seen in Figures 1 to 4, the most prominent change happens during recovery after cessation of venipuncture. Initially, from baseline to anticipation and venipuncture, an increase in heart rate can be observed. During recovery, heart rate then drops significantly. Similarly, respiration rate increases from baseline to anticipation and venipuncture but remains elevated during recovery. Minute ventilation follows the same pattern until it increases profoundly during recovery while the two fainters become unconscious. Interestingly, blood pressure measures (systole and diastole) initially increase from baseline to anticipation but start to drop already during venipuncture. Then, they drop pronouncedly during "recovery." In summary, fainting occurred in both patients after cessation of venipuncture. Unconsciousness was associated with increased minute ventilation and a drop in heart rate and blood pressure.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
We tested the hypothesis that parasympathetic activation and disgust sensitivity are higher in blood-injury phobics compared with controls and higher in blood-injury phobics with a history of fainting compared with blood-injury phobics without a history of fainting. Our results do not support these two notions. We found no evidence for chronically elevated levels of parasympathetic tone in blood-injury phobics, and there was no evidence of increased parasympathetic activation in blood-injury phobics during venipuncture or recovery from venipuncture. BIP+ and BIP– participants did not differ in parasympathetic activation at any time point during our experiment. Two out of 9 BIP+ participants fainted during recovery after the needle had been removed.

Again contrary to our hypothesis, disgust sensitivity was not elevated habitually in individuals diagnosed with blood-injury phobia. Whereas blood-injury-phobic participants reported more disgust on the "death" subscale of the German disgust sensitivity scale (37), they did not report more disgust sensitivity than controls on any of the other four scales. The increased scores of the blood-injury phobics on this subscale are likely artificially inflated because the item content of this scale refers to specific blood-injury-phobia situations. More important, however, the proponents of the disgust theory of blood-injection-injury phobia maintain that disgust should contribute to the fainting response by elevating vagal activation. Our results do not support this popular hypothesis. Firstly, blood-injury phobics with a fainting history do not report higher disgust sensitivity on any of the five subscales than the phobics without such history. Further disconfirming the hypothesis, BIP– participants reported more disgust compared with BIP+ during venipuncture. Notably, they also reported more anxiety and avoidance on the blood-injury fear questionnaire. Secondly, we did not find any indication that disgust was related to physiologic activation. According to our correlational analyses, parasympathetic measures were not related to any of the state or trait disgust measures employed in the present study. Generally, the effect sizes of these correlations were small, thus not encouraging confidence in our initial hypothesis.

Interestingly, BIP+ participants reported significantly more often to have fainted due to causes other than confrontation with blood- or injury-related stimuli than BIP– participants or controls. These reports support the notion that these patients have a generally increased risk to faint. However, other than Accurso et al. (12), we found no evidence for chronically increased parasympathetic activation in our group. Neither in the paced breathing paradigm, during venipuncture, nor during the recovery phase was parasympathetic activation in BIP+ participants alone, nor in blood-injury phobics combined (BIP+ and BIP–), higher than in controls. There are at least two other studies that report such a lack of increased parasympathetic activity in blood-injury phobics or even lowered activity (21,50). As pointed out in the introduction, we chose venipuncture as stimulus because of its immediate relevance for blood-injury phobics and because it entails a short pain stimulus. Previous studies have mostly used the confrontation with film stimuli depicting scenes of surgery. None of the phobic participants in the present study watched venipuncture. Consequently, there was no exposure to the sight of blood and no visual stimulation. Possibly, parasympathetic activation may only increase if a person is confronted with a visual blood-injury stimulus or if the person is able to vividly imagine such a stimulus. A further study comparing fainting during venipuncture while being visually stimulated is necessary to test and possibly confirm this post hoc hypothesis.

We found ample evidence for larger activation in blood-injury phobics compared with controls. This was evident in heart rate, respiration rate, and in minute ventilation. However, with the remarkable exception of the two fainters (both belonging to the BIP+ group) with their final increase in minute ventilation and decrease in blood pressure, BIP+ and BIP– did not differ physiologically. Anecdotally, we would like to add that two additional BIP+ participants fainted during treatment while watching a surgery film. This finding is surprising and highlights the sudden onset of fainting that is seemingly not predictable with the parasympathetic and sympathetic measures that we employed.

Three limitations of this study need to be discussed. It may have been better to assess an index of parasympathetic tone in a session separate from venipuncture. It cannot be ruled out that sympathetic activation due to anticipatory anxiety may have contaminated our measures of parasympathetic activation. Generally, with increased parasympathetic control, sympathetic control is reduced and vice versa (51). Also, we have neglected to measure a signal that could serve as a "pure" indicator of sympathetic activity, like electrodermal activity. Finally, whereas we do have enough statistical power to compare blood-injury phobics with controls, the analysis comparing BIP+ and BIP– participants may have suffered from small samples size.

In conclusion, our data do not support the notion that the physiologic disgust response promotes fainting in blood-injury phobics. In fact, although the only self-report state measure that differentiated between BIP+ and BIP– participants was disgust, the BIP– group had higher disgust ratings during venipuncture.

Quite often, authors associate blood-injury phobia with the fainting response. However, in the epidemiologic survey by Bienvenu and Eaton (1), only 25% of the patients with blood-injury phobia had a fainting history to the sight of blood. Physiologically, BIP+ patients were more likely to faint during venipuncture and also reported to have fainted more often in non-blood-injury-related situations than either controls or blood-injury phobics without a history of fainting. On self-report measures, we found that blood-injury phobics without a history of fainting reported more anxiety on a number of trait measures (BIP anxiety, BIP avoidance) and one state measure (disgust) compared with the BIP+ participants.

Page (22) suggested two pathways to acquire a blood-injury-related phobia. First, the vulnerability to blood-injury fears and avoidance may involve elevated trait anxiety. Second, the vulnerability to faint in the presence of blood and injury may involve elevated disgust sensitivity. Our result concerning higher anxiety and disgust levels in the BIP– group corroborates the first but not the second pathway. The tendency to faint in confrontation with blood-injury stimuli may in itself suffice as a conditioning event without specific involvement of disgust sensitivity and parasympathetic activation, in order to develop a blood-injury phobia.

Applied tension (52) is considered the standard treatment for blood-injury phobia. Yet in blood-injury-phobic patients who do not faint, applied tension may represent an avoidance or safety strategy and be thus counterproductive as its use may reduce the efficacy of exposure treatment (53,54). Our results suggest applying applied tension to patients with a history of fainting but confrontation therapy to achieve habituation in patients without such a fainting history.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 

This research was partially funded by the Association for the Advancement of Clinical Psychology and of Training in Psychotherapy, Münster. The authors would like to thank Prof. F. Rist for his invaluable help with this manuscript.

DOI:10.1097/01.psy.0000203284.53066.4b


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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