The Psychophysiology of Appreciation: Implications for Organizational Contexts based on research by Carlo A. Pruneti, Ph.D. Dept. of Clinical and Esperimental Medicine, University of Parma, Italy Rollin McCraty, Ph.D. Institute of HeartMath, Boulder Creek, CA, USA
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The Psychophysiology of Appreciation: Implications for Organizational Contexts based on research by Carlo A. Pruneti, Ph.D. Dept. of Clinical and Esperimental.
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The Psychophysiology of Appreciation:
Implications for Organizational Contexts
based on research by
Carlo A. Pruneti, Ph.D.
Dept. of Clinical and Esperimental Medicine, University of Parma, Italy
Rollin McCraty, Ph.D.
Institute of HeartMath, Boulder Creek, CA, USA
Dual Systems and Bi-directional Flow
Pictures from The Autonomic Nervous System, Hudler (1998)
Parasympathetic"Rest & Digest"
Sympathetic"Fight or Flight"
Decrease Heart Rate Increase Heart RateDecrease Force of
Synchronized electrical activity (i.e., knowledge sharing) between the brain and other body systems underlies our ability to perceive, feel, focus, learn, reason and perform at our best.
Stress is the disruption in the harmonious synchronization of nervous system activity.
In Summary:
Emotions such as anger, frustration, or anxiety, lead to erratic and disordered heart rhythms, indicating less synchronization in the reciprocal action between the parasympathetic and sympathetic branches of the autonomic nervous system (ANS). Positive emotions, such as appreciation, or care, are associated with a highly ordered or coherent patterns in the heart rhythm, reflecting greater synchronization between the two branches of the ANS, and a shift in autonomic balance toward increased parasympathetic activity (McCraty, Atkinson, & Tiller, 1995; McCraty, Atkinson, Tiller, Rein, & Watkins, 1995; Tiller,
McCraty, & Atkinson, 1996).
A measure of neurocardiac function that reflects heart-brain interactions and autonomic nervous system dynamics.
* Identify patients with autonomic abnormalities who are at increased risk of arrhythmic events.
Renin angiotensinsystem
Heart Rate Cardiac outputBlood pressure
Parasympathetic Nervous system
SympatheticNervous system
*Regolazione del Sistema Renina - Angiotensina * Il complesso sistema rennina-angiotensina presiede alla regolazione
della pressione arteriosa, cioè della forza esercitata dal sangue sulle pareti delle arterie, da cui dipende l'adeguata perfusione di sangue a tutti i distretti corporei; tale pressione è influenzata, tra l'altro, dalla quantità di sangue che il cuore spinge quando pompa, dalla sua forza di contrazione e dalle resistenze che si oppongono al libero scorrere del torrente ematico. Ebbene, il sistema renina-angiotensina agisce da un lato incrementando il volume del sangue (attraverso lo stimolo su sintesi e rilascio di aldosterone dalla corteccia surrenale), e dall'altro inducendo vasocostrizione.
*La vasocostrizione - vale a dire la diminuzione del lume dei vasi sanguigni - indotta dal sistema renina-angiotensina, aumenta significativamente la pressione arteriosa. Ci accorgiamo di questo fenomeno quando innaffiando l'orto con un tubo di gomma ne riduciamo il calibro con le dita per aumentare la distanza raggiunta dal getto d'acqua. Altrettanto intuitivo è il fatto che questo, e con esso la pressione idrica, aumenta e diminuisce mano a mano che apriamo o chiudiamo, rispettivamente, il rubinetto. Lo stesso effetto è indotto dall'aldosterone, ormone sintetizzato dalla corteccia del surrene sotto lo stimolo del sistema renina-angiotensina. L'aldosterone agisce infatti sulla parte distale dei nefroni (unità funzionali del rene), dove determina una diminuzione dell'escrezione di sodio e di acqua, ed un aumento dell'escrezione di potassio e ioni idrogeno. La ritenzione di sodio e acqua da parte del rene aumenta il volume plasmatico e la pressione arteriosa, proprio come nell'esempio dell'acqua e del rubinetto.
*Fluctuations in HR (HRV) are mediated by sympathetic (SNS) and parasympathetic (PNS) inputs to the SA node.
*Rapid fluctuations in HR usually reflect PNS control only (respiratory sinus arrhythmia).
*Slower fluctuations in HR reflect combined SNS and PNS + other psychological and emotional influences.
•“Rapid” fluctuations in HR are at >10 cycles/min (respiratory frequencies)
•Vagal effect on HR mediated by acetylcholine binding which has an immediate effect on SA node.
•If HR patterns are normal, rapid fluctuations in HR are vagally modulated
The Acetylcholine Neurotransmitter binds to a receptor on a muscle once released from a neuron.
*“Slower” fluctuations in HR are <10 cycles per min.
*SNS effect on HR is mediated by norepinephrine release which has a delayed effect on SA node
*Both SNS and vagal nerve traffic fluctuate at >10 cycles/min, but the time constant for changes in SNS tone to affect HR is too long to affect HR at normal breathing frequencies.
NE blinds to the beta-receptor (Alpha subunit of G-protein).
After binding, G protein links to second messenger (adenyl cyclase) which converts ATP to cAMP. cAMP activates protein kinase A which breaks ATP to ADP+phosphate which phosphorylates the pacemaker channels and increases HR
Sympathetic activation takes too long to affect RSA
Approach 1
*Physiologist’s Paradigm
HR data collected over short period of time (~5-20 min), with or without interventions, under carefully controlled laboratory conditions.
Longer-term HRV-quantifies changes in HR over periods of >5min.
Intermediate-term HRV-quantifies changes in HR over periods of <5 min.
Short-term HRV-quantifies changes in HR from one beat to the next
Ratio HRV-quantifies relationship between two HRV indices.
Approach 1: How much variability is there?Time Domain and Geometric Analyses
Approach 2: What are the underlying rhythms? What physiologic process do they represent? How much power does each underlying rhythm have?
Frequency Domain Analysis
Approach 3: How much complexity or self-similarity is there?Non-Linear Analyses
Time Domain HRV
• SDNN-Standard deviation of N-N intervals in msec (Total HRV)
• SDANN-Standard deviation of mean values of N-Ns for each 5 minute interval in msec (Reflects circadian, neuroendocrine and other rhythms + sustained activity)
Longer-term HRV
• SDNNIDX-Average of standard deviations of N-Ns for each 5 min interval in ms (Combined SNS and PNS HRV)
• Coefficient of variance (CV)- SDNNIDX/AVNN. Heart rate normalized SDNNIDX.
Time Domain HRV
Intermediate-term HRV
Time Domain HRV
• rMSSD-Root mean square of successive differences of N-N intervals in ms
• pNN50-Percent of successive N-N differences >50 ms
Calculated from differences between successive N-N intervals
Reflect PNS influence on HR
Short-term HRV
Geometric HRV
HRV Index-Measure of longer-term HRV
From Farrell et al, J am Coll Cardiol 1991;18:687-97
Examples of Normal and AbnormalGeometric HRV
*Based on autoregressive techniques or fast Fourier transform (FFT).
*Partitions the total variance in heart rate into underlying rhythms that occur at different frequencies.
*These frequencies can be associated with different intrinsic, autonomically-modulated periodic rhythms.
What are the Underlying Rhythms?
One rhythm5 seconds/cycle or12 times/min
5 seconds/cycle= 1/5 cycle/second
1/5 cycle/second= 0.2 Hz
What are the Underlying Rhythms?
Three Different Rhythms
High Frequency = 0.25 Hz (15 cycles/minLow Frequency = 0.1 Hz (6 cycles/min)Very Low Frequency = 0.016 Hz (1 cycle/min)
*Only normal-to-normal (NN) intervals included
*At least one normal beat before and one normal beat after each ectopic beat is excluded
*Cannot reliably compute HRV with >20% ectopic beats
*With the exception of ULF, HRV in a 24-hour recording is calculated on shorter segments (5 min) and averaged.
Longer-Term HRV
• Total Power (TP)
Sum of all frequency domain components.
• Ultra low frequency power (ULF)
At >every 5 min to once in 24 hours. Reflects circadian, neuroendocrine, sustained activity of subject, and other unknown rhythms.
Frequency Domain HRV
Intermediate-term HRV
• Very low frequency power (VLF)
At ~20 sec-5 min frequencyReflects activity of renin-angiotensin system, vagal activity, activity of subject.Exaggerated by sleep apnea. Abolishedby atropine
• Low frequency power (LF)
At 3-9 cycles/min Baroreceptor influences on HR, mediated by SNS and vagal influences. Abolished by atropine.
Frequency Domain HRV
Short-term HRV
• High frequency power (HF)
At respiratory frequencies
(9-24 cycles/minute, respiratory sinus arrhythmia but may also include non-respiratory sinus arrhythmia). Normally abolished by atropine.