ارزشیابی واکنش پذیری همودینامیک در یک عامل استرس زای طبیعی را پیش بینی می کند
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|39067||2010||8 صفحه PDF||سفارش دهید||6677 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : International Journal of Psychophysiology, Volume 77, Issue 1, July 2010, Pages 35–42
Abstract Prior research has shown that appraisals are predictive of hemodynamic reaction patterns. The current study examined the relationship between appraisal and hemodynamic responding in a real-life stressful situation. Twenty-four men aged 19–28 wore a blood pressure monitor while presenting a paper in a class. Participant's appraisal self-reports were obtained prior to the stressor. Multilevel regression models were used to analyze the relationships between appraisal and myocardial responding (as measured by cardiac output) and vascular resistance (as measured by TPR). Pre-stressor appraisals were significantly associated with CO, both during the stressor (Z = 2.03 p < .05) as well as during the 30-minute anticipation period preceding the stressor (Z = 2.43 p < .01). In line with the predictions, relatively challenged participants showed higher CO. Pre-stressor appraisals significantly predicted TPR during anticipation (Z = 2.70 p < .01) but these associations failed to reach significance during the stressor (Z = 1.82, n.s.). As was predicted, during anticipation, increased threat was associated with increased TPR. Thus, during the anticipation period prior to the stressor, increased challenge was associated with decreased vascular resistance and increased myocardial reactivity. Further, increased threat was associated with increased vascular resistance and decreased myocardial reactivity. During the stressor increases in challenge were associated with further increases in myocardial responding but relationships between appraisal and vascular resistance were not significant. The current study shows that the relationship between appraisal and hemodynamic reactivity seen in laboratory studies are also present during naturally occurring stress. Our findings suggest that threat appraisals to naturalistic stressors contribute to an, arguably unhealthy, vascular reaction pattern.
. Introduction It is widely held that the cardiovascular response to psychological stress is a risk factor for cardiovascular disease, the reactivity hypothesis (Krantz & Manuck, 1984). Cardiovascular reactivity is usually assessed by measuring the CV response to laboratory stressors. The assumption underlying the use of laboratory stressors is that the responses seen in the laboratory are typical of those that occur in everyday life such that individuals who show a large response to laboratory stressors also show larger or more frequent responses in everyday life. While rarely made explicit it is also assumed that the processes underpinning cardiovascular reactivity are similar in laboratory and field settings. There has been extensive research on the generalisation of the CV reactivity from laboratory to field and while results are mixed (Kamarck & Lovallo, 2003, Linden et al., 2003 and Schwartz et al., 2003) there is some evidence of generalisation to both specific naturalistic stressors and self reported stress in everyday life (Johnston et al., 2008). However there have been few attempts to determine if the psychophysiological processes determining CV reactivity to naturalistic stressors are the same as those established by laboratory studies. Blood pressure reactivity is determined by two hemodynamic parameters; the output of the heart (Cardiac Output [CO]) and vascular resistance (Total Peripheral Resistance [TPR]) (Berne & Levy, 1997 and Guyton & Hall, 2000). Hemodynamic response patterns differ among individuals and these characteristics appear to be relatively stable. Thus, individuals may be labelled as myocardial, vascular or mixed responders (Kasprowicz et al., 1990 and Sherwood & Turner, 1995). A vascular reaction pattern may contribute to structural adaptations of the heart and the vasculature. Short-term vascular responsiveness may promote vascular hypertrophy due to recurring stimulation of vascular muscle (Sherwood & Turner, 1995). Furthermore, stress-induced vascular responsiveness has been shown to predict left ventricular hypertrophy (Sherwood & Turner, 1995). Steptoe and Marmot (Steptoe & Marmot, 2005) found that vascular responsiveness was predictive of increased BP 3 years later. Ottaviani et al. (Ottaviani et al., 2007) recently found evidence suggesting a link between a vascular recovery pattern and inflammatory cardiovascular risk factors. Hemodynamic reactivity patterns are affected by a person's reaction to a stressor, which is in turn related to the perception or appraisal of the stressor. Differential hemodynamic response patterns are elicited in reaction to active and passive coping. Active coping with a stressful situation is associated with a myocardial response (Obrist, 1981). In contrast, passive coping is associated with a vascular response pattern (Sherwood et al., 1986 and Brownley et al., 2000). More recently, Tomaka and colleagues (Tomaka et al., 1993 and Tomaka et al., 1997) showed that appraisals are predictive of hemodynamic reaction patterns. Challenge and threat appraisal were predictive of myocardial and vascular reactivity, respectively. The concepts of challenge and threat appraisal stem from the work of Lazarus and Folkman (Lazarus, 1966 and Lazarus & Folkman, 1984). Blascovich and Tomaka (1996) operationalise appraisal as the outcome of a comparison of perceived situational demands and perceived resources. Challenge appraisals result when resources are perceived to be sufficient or nearly sufficient in comparison to perceived demands. A threat appraisal is made when perceived resources are considered insufficient to meet the demands (Blascovich and Mendes, 2000). Correlational studies provided evidence suggesting that during active coping tasks, challenged individuals showed a myocardial response whereas threatened individuals showed a vascular response (Tomaka et al., 1993, Heffner et al., 2002 and Quigley et al., 2002). In addition, experimental manipulations of stressor appraisal provided further evidence for the hypothesised links between appraisal and hemodynamic responding. In these studies, challenge and threat appraisals were manipulated by using challenging or threatening task instructions or situational characteristics (Tomaka et al., 1997, Blascovich et al., 1999, Blascovich et al., 2001, Mendes et al., 2002 and Weisbuch-Remington et al., 2005). Research on hemodynamic reaction patterns in relation to appraisal has been carried out in the laboratory, using a limited range of mental stress tests. Relatively recently, non-invasive ambulatory equipment has been developed that allows the study of hemodynamic reaction patterns in everyday life situations. Nevertheless, to date, we are not aware of any research that has been carried out on the hemodynamic response to everyday life stress and relating this to appraisal. The current aim is to test whether the relationships between appraisal and hemodynamic responding observed in the laboratory are found in everyday life stressful situations. It is examined whether the appraisal-related hemodynamic differences can be found, even in the face of uncontrollable nuisance variables that are characteristic of naturalistic settings. In the current study, participants' hemodynamic reactivity was measured before, during and after performance of a speech, a task used successfully to study the generalisation of the magnitude of CV responses from laboratory to field (Johnston et al., 2008). Giving a speech is an active coping task that can be characterised as a motivated performance situation that is goal-relevant (i.e. having real or imagined consequences). Public speaking is a task that has a social-evaluative component, and self-presentation concerns make such a task highly goal-relevant. Accordingly, it may be argued that task involvement will be uniformly high for all participants. These characteristics make the current stressor suitable to test the hypothesized relationships between appraisal and hemodynamic reactivity. It is hypothesised that, during the stressor, challenged participants will show a myocardial response, whereas threatened participants are hypothesised to show a vascular response. Anticipation of the stressor is more difficult to characterise, as it may involve both active and passive components. It may be argued that that the anticipation phase is a (relatively) passive stressor since active coping with the stressor (public speaking) is impossible before the start of this stressor. At the same time, stressor anticipation may involve active coping such as rehearsal of the talk. Finally, it is hypothesised that, during recovery, cardiovascular arousal levels will return to baseline levels. In the current conceptual framework no predictions are specified for the relationship between appraisal and changes in hemodynamic parameters.
نتیجه گیری انگلیسی
. Results 3.1. Self-reported stressfulness As was described above, prior to stressor exposure, participants were asked ‘How stressful do you expect the presentation to be’ on a scale ranging from 1 (not at all) to 7 (extremely). Post stressor ratings were obtained by the question ‘How stressful was the presentation? The mean of the stressfulness ratings was 4.08 (95% C.I.: 3.50–4.67). Post-stressor ratings of perceived stressfulness had a mean of 3.2 (95% C.I.: 2.87–3.53). These ratings suggest that the stressor was perceived as moderately stressful. The stressfulness ratings were significantly (positively) correlated with the appraisal ratio (r = .65, p<.001). 3.2. Cardiovascular arousal levels before, during and after the stressor Fig. 1 and Fig. 2 show the changes in HR and MBP over time for the anticipation, stressor and recovery phases. For each phase the means for the tertiles of total phase duration are displayed in order to accommodate the differences in stressor duration between participants. HR during the first, second and third tertile of the duration of the ... Fig. 1. HR during the first, second and third tertile of the duration of the anticipation, stressor and recovery phases, error bars represent the standard error of the mean. Figure options Full-size image (18 K) Fig. 2. MBP during the first, second and third tertile of the duration of the anticipation, stressor and recovery phases, error bars represent the standard error of the mean. Figure options In order to evaluate cardiovascular arousal levels during the stressor, these were contrasted with CV arousal levels during anticipation and recovery. Furthermore, anticipation CV levels were compared to those obtained during recovery. Analyses showed that the BP variables (SBP, MBP and DBP), as well as TPR significantly increased from anticipation to stress. On the other hand, SV decreased from anticipation to stressor. The BP variables, as well as CO and HR all decreased from stressor to recovery. Changes in CVR as a function of recovery compared to stressor were nonsignificant in SV and TPR (see Table 1.1). In comparison to recovery, anticipation levels of SBP, HR and CO were significantly elevated while TPR was significantly higher during recovery (see Table 1.2). Table 1.1. Regression estimates in the prediction of cardiovascular responding during anticipation, stressor and recovery from phase. The β1 and β2 estimates represent the contrasts between stressor and recovery levels and recovery and stressor levels, respectively. Variable β0 constant SE β0 β1 anticipation v. stressor SE β1 β2 recovery v. stressor SE β2 Variance Components Person level Intercept (σ2u0) SE Phase level Intercept (σ2e) SE Systolic Blood Pressure 165.23* 4.57 − 13.04* 4.19 − 21.48* 3.81 235.84 69.16 291.71 9.56 Diastolic Blood Pressure 102.91* 2.79 − 8.75* 2.37 − 11.62* 2.48 90.56 26.52 101.51 3.33 Mean Blood Pressure 126.70* 3.36 − 10.57* 3.04 − 15.23* 2.93 123.16 36.14 157.49 5.16 Heart Rate 96.52* 4.22 − 3.64 2.31 − 12.47* 2.35 320.08 92.74 107.82 3.49 Cardiac Output 7.19* 0.39 0.31 0.21 − 0.62* 0.20 2.61 0.76 1.44 0.05 Stroke Volume 76.66* 3.65 6.27* 1.92 2.83 2.37 244.51 71.05 128.95 4.2 Total Peripheral Resistance 1135.76* 63.98 − 137.72* 41.38 − 50.81 49.61 50146.32 14652.65 49662.13 1613.3 Note. All beta estimates are unstandardized. Robust SE's are reported. Phase (anticipation, stressor, and recovery) is dummy-coded. For the anticipation dummy variable: anticipation is coded as 1 and both stress and recovery are coded as 0. Similarly, for the recovery dummy variable: recovery is coded as 1 and both anticipation and stress are coded as 0. *p < .0. Table options Table 1.2. Regression estimates in the prediction of cardiovascular responding during anticipation, stressor and recovery from phase. The β1 estimate represents the contrasts between anticipation and recovery levels. The β2 estimate that was used to contrast stressor and recovery periods is not reported in this table, as it is already displayed in Table 2.1 a. Variable β0 constant SE β0 β1 anticipation v. recovery SE β1 Variance Components Person level Intercept (σ2u0) SE level Intercept (σ2e) SE Systolic Blood Pressure 143.75* 3.18 8.44* 3.39 235.84 69.16 291.71 9.56 Diastolic Blood Pressure 91.29* 2.02 2.87 2.00 90.56 26.52 101.51 3.33 Mean Blood Pressure 111.47* 2.38 4.66 2.51 123.16 36.14 157.49 5.16 Heart Rate 84.05* 3.46 8.83* 1.90 320.08 92.74 107.82 3.49 Cardiac Output 6.58* 0.30 0.93* 0.14 2.61 0.76 1.44 0.05 Stroke Volume 79.49* 2.99 3.44 1.93 244.515 71.05 128.96 4.2 Total Peripheral Resistance 1084.94* 45.38 − 86.91* 42.72 50,146.18 14,652.73 49,662.12 1613.28 Note. All beta estimates are unstandardized. Robust SE's are reported. Phase (anticipation, stressor, and recovery) is dummy-coded. For the anticipation dummy variable: anticipation is coded as 1 and both stress and recovery are coded as 0. Similarly, for the stress dummy variable: stress is coded as 1 and both anticipation and recovery are coded as 0. *p < .0. Table options 3.3. Appraisal and hemodynamic responding The mean of the pre-stressor appraisal ratios self reports was 0.79, with a range of 0.14–1.25. Since the average appraisal ratio is smaller than 1, on average, ratings for perceived resources were higher than those for perceived demands. 3.3.1. Anticipation During anticipation, appraisal significantly predicted changes in TPR and CO. The relationship between appraisal and TPR was positive; an increase in the appraisal ratio predicted increases in TPR. Thus, relatively threatened participants showed increased TPR during anticipation. The relationship between appraisal and CO was negative; participants who were relatively challenged showed an increase in CO (see Table 2.1). Table 2.1. Regression estimates in the prediction of cardiovascular responding from appraisal ratio during anticipation. Variable β0 constant SE β0 β1 appraisal ratio SE β1 Variance Components Person level Intercept (σ2u0) SE Minute level Intercept (σ2e) SE Cardiac Output − 3.22 2.96 − 1.39* 0.57 1.02 0.32 1.38 0.08 Total Peripheral Resistance 2776.61* 492.86 243.24* 90.0 28,210.04 8588.37 29,473.94 1628.78 Note. All beta estimates are unstandardized. Robust SE's are reported. Not reported here but included in the analyses are the control variables; BMI, age, audience size, whether the presentation is marked or not and number of alcohol units ingested in the past 24 h. * p < .05. Table options 3.3.2. Stressor During the stressor, appraisal significantly predicted changes in CO, such that relatively challenged individuals showed increased CO (see Table 2.2). Table 2.2. Regression estimates in the prediction of cardiovascular responding from the appraisal ratio during the stressor. Variable β0 constant SE β0 β1 appraisal ratio SE β1 Variance Components Person level Intercept (σ2u0) SE Minute level Intercept (σ2e) SE Cardiac Output − 1.97 3.21 − 2.06* 1.01 1.97 0.6 0.74 0.05 Total Peripheral Resistance 3184.77* 556.94 345.73 189.72 61,844.8 18,831.85 31,344.52 2062.34 Note. All beta estimates are unstandardized. Robust SE's are reported. Not reported here but included in the analyses are the control variables; BMI, age, audience size, posture (whether participants sat or stood), whether the presentation is marked or not and number of alcohol units ingested in the past 24 h. *p < .05. Table options 3.3.3. Recovery During recovery, no significant associations were found between pre-stressor appraisal and CO or TPR (see Table 2.3). Table 2.3. Regression estimates in the prediction of cardiovascular responding from the appraisal ratio during recovery. Variable β0 constant SE β0 β1 appraisal ratio SE β1 Variance Components Person level Intercept (σ2u0) SE Minute level Intercept (σ2e) SE Cardiac Output − 0.22 3.06 − 1.47 0.81 1.15 0.35 1.01 0.06 Total Peripheral Resistance 2223.23* 624.83 241.54 168.86 41,163.65 12,431.69 29,838.92 1633.94 Note. All beta estimates are unstandardized. Robust SE's are reported. Not reported here but included in the analyses are the control variables; BMI, age, audience size, whether the presentation is marked or not and number of alcohol units ingested in the past 24 h. * p < .05.