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Temporal changes in hemodynamic reactivity before, during and after a real-life stressor. Ydwine J. Zanstra Professor Derek W. Johnston. Health Psychology Group University of Aberdeen. Cardiovascular reactivity. Psychological stress may play a role in the etiology of cardiovascular disease
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Temporal changes in hemodynamic reactivitybefore, during and after a real-life stressor Ydwine J. Zanstra Professor Derek W. Johnston Health Psychology GroupUniversity of Aberdeen
Cardiovascularreactivity • Psychological stress may play a role in the etiology of cardiovascular disease • Link between stressor appraisals and exaggerated or maladaptive cardiovascular reaction patterns
Cardiovascularreactivity:hemodynamic reaction patterns Research into the pathogenic role of stress in the etiology of cardiovascular disease and hypertension will benefit from examining hemodynamic reaction patterns (Ottaviani et al., 2006; Sherwood & Turner, 1995)
Cardiovascularreactivity:hemodynamic reaction patterns hemodynamic reaction patterns : changes in the parameters underlying blood pressure: Blood Pressure = Cardiac Output *Total Peripheral Resistance
Cardiovascularreactivity:hemodynamic reaction patterns Hemodynamic changes in response to a stressor are typically examined in the laboratory • threat appraisals have been shown to be associated with increased Total Peripheral Resistance • challenge appraisals were associated with increases in Cardiac Output. (e.g. Tomaka et al., 1993, 1997; Blascovich & Tomaka, 1996)
Objective to obtain ambulatory measures of changes in hemodynamic variables : • Cardiac Output (CO), • Total Peripheral Resistance (TPR), • Mean Blood Pressure (MBP) and • Heart Rate (HR) in response to a real-lifestressor
Methods Participants: 12 men aged 20-27. Within-subjects design: • Ambulatory blood pressure • measured during before and after performance of a presentation: • anticipation, stressor, recovery
Methods: ambulatory blood pressure Portapres Ambulatory non-invasive blood pressure measurements: Consists of: • Two finger cuffs • Belt (pump, battery and memory card) • Height correction system Records: • Continuous measurement • Sampling rate = 100 Hz Hemodynamic variables (e.g. Cardiac Output, Total Peripheral Resistance) can be derived from blood pressure waveform
Analysis • Heart Rate values were derived from the blood pressure waveform. • Modelflowanalysis was used to derive beat-to-beat values for Total Peripheral Resistance and Cardiac Output. • After artefact correction, one-minute means were calculated for all variables. • T-tests were used to compare stressor levels to those during the anticipation and recovery periods. • Repeated measures analysis was performed on all variables for the 52 minutes preceding the stressor, (anticipation) and the 45 minutes after the stressor (recovery).
Results T-tests: 1. anticipation vs. stressor the mean of the of the first two minutes of the stressor compared to the last two minutes of the anticipatory period 2. stressor vs. recovery the mean of the of the first two minutes of the stressor compared to the first two minutes of the recovery period Significant effects in Mean Blood Pressure only: • anticipation vs. stressor was significant (t(11) = 2.57, P = .026) • stressor vs. recovery approached significance (t(11) = -1.93, P = .080)
Results anticipation (last two minutes), stressor (first two minutes), and recovery (first two minutes)
Results anticipation (last two minutes), stressor (first two minutes), and recovery (first two minutes)
Results: anticipation and recovery Repeated measures analysis of; analysis of changes during anticipation and changes during recovery: Heart Rate and Mean Blood Pressure Anticipation: significant, upward linear trends in Mean Blood Pressure (F(1,11)=6.21, P=.03) and Heart Rate (F(1,11)= 8.56, P=.014) Recovery: Mean Blood Pressure values decrease over time (n.s.) Heart Rate decreased during recovery, linear trend approached significance (F(1,11)= 3.43, P=.087).
Results: anticipation and recovery Anticipation: significant, upward linear trends in Mean Blood Pressure and Heart Rate Recovery: • Mean Blood Pressure values decrease over time (n.s.) • Heart Rate decreased during recovery; linear trend approached significance Mean Blood Pressure and Heart Rate as a function of time during anticipationand recovery
Results: anticipation and recovery Repeated Measures analysis of changes during anticipation and changes during recovery: Cardiac Output and Total Peripheral Resistance: Anticipation: Cardiac Output showed a quadratic trend approaching significance (F(1,11)=3.36, P=.094). Values increased initially and decreased just prior to the start of the stressor. Total Peripheral Resistance showed a quadratic trend that approached significance (F(1,11)=3.49, P=0.088). Initial decrease was followed by an increase Recovery: no significant results
Results: anticipation and recovery Anticipation: Cardiac Output • quadratic trend approaching significance. Values increased initially and decreased just prior to the start of the stressor. Total Peripheral Resistance • quadratic trend that approached significance: Initial decrease was followed by an increase Recovery: no significant results Cardiac Output and Total Peripheral Resistance as a function of time during anticipationand recovery
Summary of main findings • Both heart rate and mean blood pressure increased initially. • The anticipatory increase in mean blood pressure appears to be at first mediated by early rises in Cardiac Output. • However, just before the start of the stressor, Cardiac Output decreases. • Total Peripheral Resistance continues to rise throughout the anticipatory period and appears to be increasingly responsible for the continuing rise in mean blood pressure. • Changes during recovery were nonsignificant
Discussion • Changes in hemodynamic parameters over time can be measured in real-life • Linear increases in blood pressure may be mediated by more complicated patterns of change in hemodynamic parameters • Future analysis will focus on the relationship of hemodynamic reaction patterns with stressor appraisal
References • Blascovich, J., & Tomaka, J. (1996). The biopsychosocial model of arousal regulation. Advances in experimental social psychology, 28, 1-51 • Ottaviani, C., Shapiro, D., Goldstein, I. B., James, J. E., & Weiss, R. (2006). Hemodynamic profile, compensation deficit, and ambulatory blood pressure. Psychophysiology, 43(1), 46-56. • Sherwood, A., & Turner, J. R. (1995). Hemodynamic responses during psychological stress: Implications for studying disease processes. International Journal of Behavioral Medicine, 2(3), 193-218. • Tomaka, J., Blascovich, J., Kelsey, R. M., & Leitten, C. L. (1993). Subjective, physiological and behavioural effects of threat and challenge appraisal. Journal of Personality and Social Psychology, 65(2), 248-260 • Tomaka, J., Blascovich, J., Kibler, J., & Ernst, J. M. (1997). Cognitive and Physiological Antecedents of Threat and Challenge Appraisal. Journal of Personality and Social Psychology, 73(1), 63-72.
Temporal changes in hemodynamic reactivitybefore, during and after a real-life stressor Ydwine J. Zanstra Professor Derek W. Johnston Health Psychology GroupUniversity of Aberdeen
Artefact correction The artefact detection and correction procedure was carried out using CARSPAN software (Mulder, 1988): • moving averages were calculated for time windows of 60 seconds • a value was identified as an artefact if it exceeds a confidence interval of +/- 4 S.D.’s around that moving average. • Artefact correction involved linear interpolation between two preceding and two successive values
Modelflow AlgorithmsFor computing hemodynamic parameters MAP=CO*TPR Given: • MAP (Mean Arterial Pressure) • HR (Heart Rate) Unknown: • SV (Stroke Volume) • CO (Cardiac Output) • TPR (Total Peripheral Resistance) • SV = Asys*/Zao** • CO (l/min) = SV (l) * HR (beats/min) • TPR (dyne-s · cm-5) = (MAP (mmHg) / CO (l/min)) x 80 • *=area under the systolic portion of the pressure wave • **=characteristic impedance of the aorta