Behar. Res. Ther. Vol. 28, NO.4. pp. 389-295.1990 ooO5-7967 90 53.00 + 0.00 Pnnred in Great Bnrain. All rights reserved Copyright C 1990 Pergamon Press plc TYPES AND CORRELATES OF BLOOD/INJURY-RELATED VASOVAGAL SYNCOPE RONALD A. KLEINKNECHT, JOSEPH LENZ, GREG FORD and Scorr DEBERARD Department of Psychology, Western Washington University, Bellingham, WA 98225, U.S.A. Summary-This study investigated by interview, the initial syncopal episode of 103 blood/injury-related vasovagal fainters in order to examine two competing hypotheses concerning their origins. Graham zyxwvutsrqponmlk (Circulation, 23.901-906, 1961) postulated that the faint resulted when sympathetic nervous system (SNS) activity ceased on termination of a threat, leaving parasympathetic nervous system (PNS) activation unopposed. Engel [Fainring (2nd edn), 1962; Annals of Infernal Medicine, 89.901-906, 19781 proposed that when in the face of threat with SNS activation, escape is blocked, the PNS becomes activated as the conservation-withdrawal reponse, leading to syncope. We found cases clearly conforming to each of these formulations as well as some with characteristics of both, and some who fainted in response to blood or injury but with no perception of threat. The Graham and Engel types did not differ in terms of fear or avoidance of blood, injury, or medically-related situations nor did they differ in the frequency with which their parents reported blood/injury-related syncopal episodes. It is proposed that both may be activated by a common psychological mechanism involving cessation of a defensive posture. In contrast. the non-threat fainters showed significantly less medically-related avoidance and had a greater percentage (94%) of parents with positive faint histories. Fainting associated with blood, injuries, or mutilation is a relatively common response of adults, being found in as many as 15% of blood donors (Graham, 1961) and reported in as many as 19% of college students (Kleinknecht, 1987, 1988; Kleinknecht & Lenz, 1989). This fainting has generally been considered a vasovagal response (Graham, 1961; Engel, 1962, 1978; Sledge & Boydstun, 1979; Vingerhoets, 1984, 1985) and is also seen in approx. 80% of blood/injury phobics seeking treatment for their fear (Ost, Sterner & Lindahl, 1984; Thyer, Himle & Curtis, 1985). Blood /injury appears to be the only phobia in which fainting is a common response component (Ost et al., 1984; Ost & Hugdahl, 1985). Although highly related, fear and fainting are at least partially independent: some B/I phobics do not faint and some people who faint in the presence of B/I stimuli are neither phobic nor fearful (Kleinknecht & Lenz, 1989; Rachman, 1990). Most investigators in this area agree that a blood/injury-related vasovagal faint is the result of a diphasic cardiovascular response (e.g. Graham, Kabler & Lundsford, 1961; Engel, 1962, 1978; Vingerhoets, 1984, 1985). The first phase is the sympathetically-mediated ‘fight or flight’ response. This SNS activation is followed by the onset of increased parasympathetic activity which then leads to the faint. Two explanations, each with some support, have been presented to explain onset of fainting in response to blood/injury-related stimuli. The two positions agree that the first phase involves anxiety and associated SNS arousal over a perceived threat and that the faint results from the second phase. They disagree, however, on the mechanism that triggers the second, or syncopal phase. The explanation proposed by Graham (1961) begins by characterizing the first phase as the result of anxiety arousal in the face of perceived threat. When the threat is removed, either by passing or by actually having been carried out, ‘relief’ activates the second, or syncopal phase. Physiologically Graham postulated that threat stimulates hyperdynamic circulation. The faint results when reflexes antagonistic to the first phase (i.e. holding cardiovascular activity in check and keeping it from rising out of control) are suddenly left unopposed when relief from threat reduces anxiety. Blood pressure and pulse rate plummet producing bradycardia and even asystole. This formulation will be referred to here as the ‘Relief’ hypothesis. Its behavioral presentation would include pre-faint anxiety and the occurrence of the the faint after threat had passed. Engel (1962, 1978) proposed that fainting was the result of two conflicting escape mechanisms being simultaneously activated: the SNS-mediated ‘fight or flight’ response and PNS-mediated ‘conservation-withdrawal response’. The conditions necessary for a vasovagal faint to occur include the perception of impending physical injury or threat thereof and the perception that this threat 289