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Cardiovascular Psychophysiology
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Facts and Functions
The busy heartSix quarts of blood pumped per minute100,000 beats per dayTry it!
FunctionsTransport oxygen from lungs and nutrients from gutTransport waste productsTransport regulatory substances (e.g. endocrines)Thermal exchange between core and periphery
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Metabolic Demands
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Anatomy of the HeartCardiac Muscle (myocardium)
not striated, not smoothfour features distinguish from smooth or striate
Muscle has unstable resting potential – basis for intrinsic and rhythmic contractionAction potential freely conducted from one cell to another (lattice-like syncytial) network of cardiac fibersRepolarization lasts about 100 msecContraction phase = duration of cardiac action potentials (initial depolarization followed by sustained depolarization phase of 0.2-0.3 secs)
Four chambersRight AtriumRight VentricleLeft AtriumLeft Ventricle
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Anatomy of the Heart
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Human Circulatory System
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Circulation in a bit more
realistic detail
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Anatomy of the Heart
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More Valves
Aortic and Pulmonary ValvesRespond to relative pressure difference between ventricles and aorta or pulmonary arteryAs ventricles contract, pressure builds, and forces valves open when pressure exceeds arterial pressure
“Dub” in the Lub-Dub sound (sounds are valves closing or “slamming” shut)
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Neural Conduction of the HeartTwo Nodes
Sino-Atrial (SA) node – “Primary Pacemaker”Atrial-Ventricular (AV) node – “Yoked”
Nodes have intrinsic rythmicitySA node: 105 bpmAV node: 40-60 bpm
Denervated heart would still beat at over 100 bpmMust be extrinsic influences to slow or speed heart
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Neural Conduction of the Heart
Hierarchy ensures that normally the SA node “drives” the system
AV nodes provide a critical delay (allows atria to fully contract before ventricles do)AV nodes have important refractory period to prevent rapid successive ventricular contractions
A coordinated wave of depolarizationContraction of 4 chambers of heart must be precisely choreographed
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Nodes and Fibers
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The SA and AV Nodes in Action
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The Schematized EKG waveform
P = Atrial depolarizationQRS = Ventricular depolarizationT = Ventricular repolarizationNote that Atrial repolarization is not visible
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The EKG waveform
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http://mcdb.colorado.edu/courses/2115/units/Other/heartbeat%20animation.html
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The Cardiac Cycle
lub dub
Systole See also Fig 8.2 in Text
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http://www-medlib.med.utah.edu/kw/pharm/hyper_heart1.html
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Cardiac Output
HRxSVCO =
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Cardiac Chronoptropy
Heart rate regulated extrinsicallyVagal (PNS) influence
Slows HRSo too will dripping ACH on SA node ☺Likely that all changes below 100 bpm are predominately vagally induced
SNS influenceSpeeds HR, but impact not as strong as PNSMain effect is to increase contractility
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SNS and PNS influences
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HR change to simultaneous vagal and sympathetic stimulation
Levy & Zieske (1969). J Applied Phsyio, 27, 465-470
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Integrated Control Mechanisms
Baroreceptor ReflexPressure sensitive receptorslocated in the arch of the aorta and carotid sinus nervesJoin Vagal and Glossopharangeal nervesTerminate in regulatory centers in medullaWith increase in BP, causes compensatory decrease in HR, contractility, and SVQuickly adjusts to maintain BP
Valsalva Maneuver
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Valsalva Maneuver
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Integrated Control Mechanisms
Respiratory EffectsRespiratory Sinus Arrhythmia (RSA)
This arrhythmia is not a bad thing!
HR acceleration linked to inspirationHR deceleration linked to expiration
RSAIndexes strength of Vagal influenceMore later…
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Cardiac Inotropy
Contractility is predominately Sympathetically mediatedOften measured invasively, but can be
measured noninvasivelyEKG plus phonocardiogramImpedance cardiography
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SNS and PNS Integration: A CaveatRelatively easy to measure PNS: RSA or other metrics of HRVRelatively easy to measure SNS: Contractility via PEPBUT… one is measure of chronotropy, other is measure of inotropy
Changes in contractility can occur independently of changes in rateSNS inputs for inotropy primarily controlled by left-sided inputs to AV nodeSNS inputs of chronotropy primarily controlled by right-sided inputs to SA node
Thus, like “mixing apples and oranges”
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Cardiovascular Measures
Electrocardiogram (EKG)Phonocardiogram (PCG)Impedance cardiographyPhotoplethysmographyBallistocardiographyBlood Pressure
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EKGAC signalSample 200-500 Hz
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EKGAC signalSample 200-500 Hz
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Which Time?
Real timeHeart RateExpressed as beats per time (usually bpm)
Cardiac timeHeart Period; interbeat interval (IBI)Expressed in msec
Converting
bpmXHR
xHP
HR
60000,601000
1
000,601
==
=
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PhonocardiographyPosition microphone over heartLub-Dub is transduced to electrical signal
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Photoplethysmography
Three methods, all involve measuring light absorbed by peripheral vasulature
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The Photoplethysmographic Output
Increase in Pressure due to opening of Aortic Valve
Dichrotic Notch; closing of valve, end of ejection
~LVET
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Photoplethysmograph: Peripheral Vasoconstriction
T1 is onset of constrictionTop Panel: Pulse Volume (recorded with 1 sec time constant)Lower Panel: Blood Volume (no filter)
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PEP = Pre-ejection periodLVET = Left Ventricular Ejection
Time= Upswing of pressure
wave to S2Electromechanical Systole =
Q to S2PEP = EMS – LVET
PEP reflects sympathetic influence on cardiac contractility
Measuring contractility with EKG, PCG, and Photoplethysmography
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Measuring Blood PressureAuscultatory Technique•Not good for instantaneous readings
•Not good for repeated readings
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Ballistocardiography
ImagineOn a chair on a platform on an air hockey tableCardiac events cause movement of platform
New applications:Finding individuals hiding in vehiclesFinding individuals stuck in rubble
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ImpedanceCardiography
• Low energy high-frequency AC passed through thoracic region
• Changes in impedance to signal created by mechanical events of cardiac cycle, especially changes in thoracic blood volume
• ΔZ is change in impedance• Dz/dt is 1st derivative of
impedance signal Z• R-Z is time from r-wave to peak
ventricular contraction indicated in Z signal
• The “Heather” index – divide dz/dtby R-Z interval; putative measure of heart’s ability to respond to stress
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Measuring Vagal InfluenceDescending Vagal Influence slows HRRespiration interrupts this vagal influenceThe size of periodic oscillations due to respiration can therefore index the strength of the Vagal influence
Note, however, that under some circumstances, there can be dissociation between RSA and presumed central cardiac vagal efferent activity (cf., Grossman & Taylor, 2007)Concerns over changes in rate, and to lesser extent depthSee special issue of Biological Psychology, 2007 for more in depth treatment of these issues and more!
Demo with QRSTool
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Abbreviated History of HR Variability(with thanks to Porges, 2007)
Physiology treated HR as DV, similar to behaviorDominance of behaviorism emphasized control over the DV (behavior)Changes in HR unrelated to the manipulation considered noise
Lacey (1967) and Obrist (1981) had models related to attention, and metabolic demand, but HR variability did not fit in either modelVia appropriate experimental design, HR should be entirely under the control of experimental or environmental demands
Nonetheless, history of quantifying HR variability dates to the 1950’s with case report long before that:
1958: Lacey and Lacey, greater HRV associated with greater impulsivity1915: Eppinger and Hess, described a vagotonic syndrome with clinical features that included an exaggerated RSA Interest in HRV as an individual difference variable, however, really starts with the work of Steve Porges
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500
600
700
800
900
1000
1100
0 10 20 30 40 50 60 70 80Seconds
IBI (
mse
c)
-200-150-100
-500
50100150200
0 10 20 30 40 50 60 70 80
Seconds
IBI (
mse
c)
-200-150-100
-500
50100150200
0 10 20 30 40 50 60
Seconds
IBI (
mse
c)
500
600
700
800
900
1000
1100
0 10 20 30 40 50 60Seconds
IBI (
mse
c)
IBI Series (real time)
High Variability Subject Low Variability Subject
IBI Series (real time)
.12-.40 Hz filtered IBI Time Series .12-.40 Hz filtered IBI Time Series
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500
600
700
800
900
1000
1100
500 600 700 800 900 1000 1100
IBI(n) (msec)
IBI(n
+1) (
mse
c)
600
700
800
900
1000
1100
1200
600 700 800 900 1000 1100 1200
IBI(n) (msec)
IBI(n
+1) (
mse
c)High Variability Subject Low Variability Subject
Rate73.3 HR 85.7
832.3 IBI 707.7Total Variability
9.2 HRV 8.3112.4 SDNN 66.3132.8 RMSSD 27.7
"Sympathetic"1.4 CSI 4.7
"Parasympathetic"57.1 PNN50 10.897.6 MCD 22.05.3 CVI 4.58.8 RSA 5.3
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Cardiac Vagal Control and ModulationTwo Vagal Efferent Branches which terminate on SA Node (Porges 1995, 2003, 2007)
Reptilian “Dumb”: Dorsal Motor NucleusMassive reduction in HR & conservation of oxygen. Dive reflex -- cold water on the face during breath hold
Phylogentically newer “smart” VagusOrginates from Nucleus AmbiguousModualtes influence to:
Promote attentional engagement, emotional expression, and communication. Mobilizes organism to respond to environmental demands
Phasicly withdraws inhibitory influence, increasing HRUpon removal of the environmental stressor, resumes its efferent signal
Slowing heart rateAllows the organism to self-sooth
This polyvagal theory is not without its critics (e.g., Grossman & Taylor, 2007).
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Bradycardia observed in a diving seal. Data adapted from R.S. Elsner (1998), courtesy of http://www.deeperblue.net/article.php/225
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Porges, 2007
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Tonic Vs PhasicTonic Level indexes capacityPhasic change indexes actualization of that capacity
Attentionhigher vagal “tone” was associated with faster reaction time to a task requiring sustained attention Hyperactive kids treated with Ritalin (Porges, Walter, Korb, & Sprague, 1975).
attentional skills improved appropriate task-related suppression of heart rate variability was observed while performing the task requiring sustained attention
EmotionBeauchaine (2001):
low baseline vagal “tone” is related to negative emotional traits high vagal withdrawal is related to negative emotional states
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Task-related and Emotion-related modulation
6
6.2
6.4
6.6
6.8
7
7.2
7.4
Baseline Suppress Recovery
RSA
Low AnxHigh Anx
Movius & Allen, 2001
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Individual Differences in Cardiac VagalControl (aka “Trait Vagal Tone”)
InfantsVarious sick infants have lower vagal tone (Respiratory Distress Syndrome, Hydrocephalic)Infants with higher vagal tone (Porges, various years)
More emotionally reactive (both + & -)More responsive to environmental stimuli (behaviorally and physiologically)
Anxiety DisordersLower Vagal Tone in GAD (Thayer et al., 1996)Lower Vagal Tone in Panic Disorder (Friedman & Thayer, 1998)
DepressionDepression characterized by lower Vagal tone?Gender may moderate (Thayer et al., 1998)
Note small sample: 15 depressed, 11 controlsState dependent? (Chambers & Allen, 2002)
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0
20
40
60
80
100
120
MSD PPN50 HFP
Male NDMale DFemale NDFemale D
Data from Thayer et al., 1998, Bio Psychiatry
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Change in Vagal Tone
2.01.51.0.50.0-.5
Cha
nge
in H
RS
D S
core
10
0
-10
-20
-30
Chambers and Allen (2002) Psychophysiology
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Trait Vagal Tone (cont’)Defensive Coping (Movius & Allen, 2001)Integrative Developmental Model
Beauchaine (2001), Development and Psychopathology
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Beauchaine et al (2001) Journal of Abnormal Psychology
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6
6.2
6.4
6.6
6.8
7
7.2
7.4
Baseline Suppress Recovery
RSA
Low DefHigh Def
Movius & Allen, 2001
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Trait Vagal Tone as Moderator of Response following Bereavement
RSA
876543
BDI (
resi
dual
ized
on
base
line
BDI) 4
3
2
1
0
-1
-2-3
RSA
876543
BDI (
Res
idua
lized
on
Base
line
BDI) 4
3
2
1
0
-1
-2-3
Intervention Group Control Group
Bereavement as a period of cardiovascular riskDisclosure as an intervention for Bereavement (O’Connor, Allen, Kaszniak, 2005)Overall, all folks get better, but no differential impact of interventionBUT… Vagal Tone as moderator
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Orienting, Attention, and Defense
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SCR (by contrast)
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OR Vs DR