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Lectures 2, and 3 Are Risk factors Causal? Biological Plausibility: cardiovascular Reactivity.

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Presentation on theme: "Lectures 2, and 3 Are Risk factors Causal? Biological Plausibility: cardiovascular Reactivity."— Presentation transcript:

1 Lectures 2, and 3 Are Risk factors Causal? Biological Plausibility: cardiovascular Reactivity

2 General reading in Health Psychology To make the most of this course you should read the relevant sections in one of the recommended introductory texts, either Taylor or Sarafino. In Taylor you should read Chapter 2 “Systems of the body” Pages (nervous, endocrine and Cardiovascular systems). Chapter 6 “Stress” Complete Chapter (pages ). Chapter 7 “Moderators of the stress experience” (pages ) (Combined as “Stress & Coping” in earlier editions. In Sarafino the equivalent chapters are essentially Chapter 2 pages 31-40, 49-51, and Chapters 3, 4 & 5 (pages ).

3 More Reading Another good general book is Baum, Gatchel and Krantz An introduction to Health Psychology, Chapters 2, 3 and 5. For those who wish to find out more about of Obrist and Brod (mentioned in Lecture 2) the references are below. Not required reading. Obrist,PA,Gaebelein,CJ,Teller,ES,Langer,AW,Grignolo,A,Light,KC, McCubbin,JA,(1978) The relationship among heart rate, carotid dp/dt and blood pressure in humans as a function of the type of stress Psychophysiology,15, Brod J Fencl, V, Hejl, Z, Jirka, J (1959). Circulatory changes underlying blood pressure elevation during acute emotion stress (Mental arithmetic) in normotensive and hypertensive subjects. Clin Sci, 18,

4 Cardiovascular Reactivity: Some reading The most cited reference on the topic of CV reactivity is Krantz DS & Manuck SB (1984). Acute psychophysiologic reactivity and risk of cardiovascular disease: a review and methodological critique. Psychol. Bull., 96, While old it is an important paper. It is demanding reading. The sections on CV disease will be relevant to later lectures. It can be found on PsycArticles in library Metalab There was special section of Psychosomatic Medicine devoted to Cardiovascular Reactivity in Read Linden WL, Gerin & Davidson K (2003) Cardiovascular reactivity: Status Quo and a research agenda for the New Millennium. Psychosomatic Medicine, 65, 5-8

5 CV Reactivity Kamarck TW & Lovallo WR (2003) Cardiovascular reactivity to psychological challenge: conceptual and measurement issues. Psychosomatic Medicine, 65, When discussing appraisal I shall lean heavily on the studies reported in: Tomaka, Blascovich, Kelsey & Leitten (1993) Subjective, physiological and behavioral effects of threat and challenge appraisal. J. Per. Soc. Psychol., 65, Tomaka, Blaskovich, Kibler & Ernst (1997). Cognitive and physiological antecedents of threat and challenge appraisal J. Per. Soc. Psychol, 73, Blascovich & Tomaka present a fuller account of their views in Blascovich & Tomaka (1996) The biopsychosocial model of arousal regulation. Adv. Exp. Soc. Psychol., 28, 1-51.

6 References on social support and cardiovascular reactivity Kamarck T (1992) Recent developments in the the study of cardiovascular reactivity: contributions from psychometric theory and social psychology. Psychophysiology, 29, Lapore SJ et al, (1993) Social support lowers cardiovascular reactivity to an acute stressor. Psychosomatic Medicine, 55, Lapore SJ (1995). Cynicism, social support and cardiovascular reactivity. Health Psychology, 14,

7 When is a risk factor casual TemporalityStrength of relationship ConsistencyBiological gradient Biological PlausibilityCoherence Outcome SpecificityIntervention evidence

8 Causality (cont) Temporality: are there prospective studies demonstrating that x precedes development of disease? Strength of relationship: How much of the variance in disease incidence explained by x? Consistency: Are studies consistent in their findings? Biological gradient: is severity and/or frequency of x associated with increasing risk of disease? Biological plausibility: what pathogenic mechanisms link x to disease?

9 Causality 3 Coherence: Does evidence for the relation between x and disease come from different samples (population, patient, animal models)? Outcome specificity: Is the risk associated with x exclusive to one disease? Intervention Effects: Is the disease prevented if x is treated early enough?

10 Basic Model The Reactivity Hypothesis: excessive cardiovascular response to stress is a risk factor for cardiovascular disease.

11 Simplified model of the cardiovascular (i.e., heart and blood vessels) system

12 CV system

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15 Cardiovascular measures Heart Rate (HR): Number of cardiac cycles per minute Systolic Blood Pressure (SBP): Maximum blood pressure in a cardiac cycle Diasystolic Blood Pressure (DBP): Minimum blood pressure in a cardiac cycle Mean Arterial Pressure (MAP): Average blood pressure over a cardiac cycle

16 Cardiovascular measures (cont.) Stroke Volume (SV): Amount of blood pumped in a cardiac cycle Cardiac Output (CO): Amount of blood pumped in unit of time CO = SV x HR Total Peripheral Resistance (TPR): The total resistance in circulatory system to the flow of blood. MAP= CO x TPR

17 One participant from Brod 1959

18 Participants from Brod 1958 split into cardiac and vascular responders

19 Obrist et al, Hard but not impossible produces Active Copying

20 Obsrist et al Active Coping (RT, Reaction time task) has larger cardiac effect than Passive Coping (CP – cold pressor) or watching pornographic film. NB. Effect of Active Coping much reduced by Beta Blocking drug which largely removes effect of sympathetic nervous system on the heart.

21 Obrist et al Carotid dp/dt measure of force of heart contracting. Large effect of Active Coping.

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23 Manuck. Comparison of Cardiac & Vascular Reactors on Mental arithmetic (active coping task, cf Brod)

24 Manuck. All subgroups similar on mirror tracing task

25 Autonomic Nervous System- seriously simplified Sympathetic Nervous System - quite diffuse Neurotransmitter Noradrenaline ReceptorsAdrenoreceptors Beta - Heart - Increase HR & Contractility Alpha - Smooth Muscle (e.g, vasculature) - contract small blood vessels Parasympathetic Nervous System- quite specific Neurotransmitter acetylcholine Receptorscholinergic Heart- slows heart rate, minor effect on Contractility

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27 Lazarus: Transactional Model of Stress & Coping. Most influential model of stress that underpins Tomaka & Blascovich studies

28 Tomaka & Blascovich, following Lazarus & Folkman: 2 common stress related appraisals Threat : perception of danger greater than perception of coping abilities Challenge: perception of danger less than perception of coping Threat associated with negative emotions - However challenge associated with more CV activation (Obrist Active passive distinction) Tomaka & Blascovich attempt to clarify this. Task: Mental arithmetic (Active Coping) Threat: rating of threat greater than rating of ability to cope (Primary/Secondary). Challenge: rating of coping greater than rating of threat. After task ratings of experienced stress obtained.

29 3 studies, Study 1 preliminary. Study 2. Mental arithmetic. Subjects classified into threatened or challenged. Results Subjective & Behavioural Threat group More Stress 3.85 v 2.85 on 7 point scales Threat group performed less well 2.19 v 2.85 (self ratings) and produced less correct answers, 10.5 v NB results most clear cut first time tasks carried out. Physiological ….

30 Challenge has cardiac effects, threat vascular. NB Pre-ejection period relates to force that heart contracts. It shortens with challenge and more usual to show changes as negative

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32 Tomaka et al (1997) Cont. They attempted to test causality of appraisal by 1.Manipulating appraisal. Threat: emphasis on speed, accuracy. Challenge: See task as challenge and yourself as someone who can do it. (see next slide) 2. Manipulating physiological response (reverse causality) 1.Exp 2. Alter CO with exercise- no effect on appraisal 2.Exp 3. Alter TPR with cold pressor- no effect on appraisal

33 Experimental manipulation of threat and challenge has predicted effects

34 Social Support reduces risk of heart disease. Does it affect reactivity? Is effect of social support a main effect or does it buffer effect of stress?

35 Presence of friend reduces CV response.

36 Effect of social support only clear under high threat. Buffering?

37 Lepore (1993) study of Social Support. Presence of non-supportive person increases BP

38 Effects of Social support may depend on personality of recipient

39 Study by Kamarck of social support (or a related process?) in real life.

40 Cardiovascular Reactivity (CR). Things that should be true if CR is a risk factor Is it an individual difference variable? Is it reliable? Is it one factor? Does it generalise?

41 Steptoe & Vogele 1991 Reliability of CV response to mental stress testing Test-retest correlations HR.62 SBP.52 DBP.30

42 Cardiovascular Reactivity. Issues. Is it an individual difference variable? Is it reliable? Is it one factor? Does it generalise?

43 Kamarck 1992 again. Most corr. large and positive

44 Cardiovascular Reactivity. Issues. Is it an individual difference variable? Is it reliable? Is it one factor? Does it generalise?

45 Anastasiades & Johnston (1991)

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47 Median split on laboratory reactivity HR Control HR Tutorial Low Reactors High Reactors Johnston D.W., Tuomisto M.T., & Patching, G.R. (2008) The Relationship between Cardiac Reactivity in the Laboratory and in Real Life. Health Psychology. 27, 34-42

48 High Reactors Low Reactors Johnston, 2004, Relationship between subjective arousal & HR in HI and LO cardiac reactors

49 Does CR to stress generalise. Appears to generalise to a range of stressful situations Suggests that people who are vulnerable and produce large CV response may be at risk if exposed to stress, i.e., Stress and diathesis (or vulnerability) model Mechanisms? Zanstra


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