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05/03/23 Gevirtz 1
Mediational Models in Psychophysiological Disorders
Richard Gevirtz, Ph.D.CSPP at Alliant International U.-San Diego
rgevirtz@alliant.eduWebsite: WWW.Alliant.edu/faculty/gevirtz
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Outline I I. Epidemiology II. Mediational model :
Psychophysiological disordersDisorders with central mediation
III. Mediators A. Respiration B. Limbic or RAS B. Sympathetic n.s. C. Parasympathetic n.s.
• 1. Vagal mechanisms• 2. Porges Polyvagal Theory• 3. Neurovisceral Integration
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Outline II IV. HRV-I: Underlying Physiology
A. Sources of variance• 1. respiration• 2.blood pressure/baroreceptors• 3. sympatheic vascular tone?
B. Spectral analysis VI. HRV-II: Measurement VII. HRV-III: Feedback
A. Effect on spectral B. Resonance
VIII. Treatment Protocol
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Outline III IX. Applications
A. Autonomic mediators• Hypertension/hypotension• Chronic muscle pain• Dysreflexia• IBS/RAP• Asthma
B. Respiration• COPD• Asthma• Panic
C. Inflammation• Asthma
D. CNS• FM• CRPS
Evidence of efficacy, HRV Biofeedback Asthma-Lehrer et al., Chest, 2004 COPD- Giardino et al., APB, 2004 CAD- Del Pozo et al. (AHJ, 2004), van Dixhoorn et al. Performance- Strack et al., Gruzelier’s group (APB, 2005) Stress, performance, etc., McCraty et al (Har. Bus Rev, 2003; Physio Beh Sci,
1999; numerous HeartMath reports) IBS/RAP- Humphreys & Gevirtz (JPGN, 2000) Sowder, Gevirtz,et al. (2007) FM- Hasset et al. APB,(2007) Altitude sickness-Bernardi (2001& in press) MDD, Karavadis et al., APB, (2007), Zucker et al.(2007), Rene et al.(2007) Congestive Heart Failure-(Bernardi, 2002, Circulation) Swanson, Gevirtz, et
al. (2007) Hypertension- (Schein et al, 2001, J. Human Hypertension; Herbs & Gevirtz,
1994, Abstract, APB; Lehrer et al.,( 2004) Reinke, Gevirtz, et al. (2007) PTSD Zucker et al., White et al.,(2008) GAD Murphy, Hoffmann et al. (2008)
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Estimates of Primary Care Visits
IBS8% Panic+
15%
HA/Back20%
Other7%
Cold/Flu40%
F Cardio10%
IBSPanic+HA/BackOtherCold/FluF Cardio
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Alternative Medicine in the U.S.
0
200
400
600
800
1990 1997
Alternative vs. Dr. Visits (in millions)
AlternativePrimary Dr.
0
10
20
30
Spending in Billions of $
Dr. ServicesAlternative
JAMA, 1998The $21.2 billion is up 45% since 1990
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Alternative Medicine: Out-of-Pocket Expenditures
$12.2 billion out-of-pocketThis exceeds 1997 out-of-pocket
expenditures for all hospitalizations in the U.S.
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Most Common Reasons for Seeking Alternative Medicine Therapies
Headaches 32%Arthritis 27%Fatigue 27%Allergies 17%Back Pain 49%
0 50
Therapy UsedRelax,ChiroRelax, ChiroRelax, MessageHerbal, RelaxChiro, Massage
About 40% of patients inform their physician of alternative therapies.
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Percentage of Americans Using Alternative Therapy
05
1015202530354045
Percent
1990 1997
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Stigma of PainMental health disorders are so stigmatized in our
culture that disorders that may only partially involve psychological/emotional factors are considered just as shameful as mental disorders.
“Physicians in particular need to be sensitized to the fact that people with pain generally expect to experience stigmatizing attitudes among health care practitioners, especially regarding the use of pain medication.” Zelman, 2004
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Physical Symptoms
Physiological Systems
Cognitive/Emotional Factors
Early Developmental Factors Genetics
Social &CulturalFactors
“hysteria”
Mediational Model of Psychophysiological Disorders
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Respiratory System
Downloaded from: StudentConsult (on 14 August 2006 08:36 PM)© 2005 Elsevier
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Normal lung Emphysema
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Respiratory Tasks in Normal BreathingAdequate saturation of blood with oxygenAdequate saturation of blood with CO2-dissolved
as carbonic acidAlkaline buffer-bicarbonateMaintain pH of blood at 7.4removal and retention of alkaline and acidic
products by the kidneysmaintain breathing drive at optimal levels
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Blood pH: A critical tight band 7.4 (+or-.5) blood pH - since scale is log, a .2 difference
means a doubling of the hydrogen ions present pH controlled primarily by CO2
CO2 is end product of cell metabolism is analogous to ash or smoke in pure form, deadly converted to carbonic acid to protect tissue builds quickly with exercise, but so does oxygen
demand
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Breathing volume than controls these parameters: “Therefore changes in breathing volume relative
to CO2 production regulate the moment to moment concentration of pH in the bloodstream…There is a tight interaction between the breathing volume, the amount of CO2 , production, the partial pressure of CO2 in the arterial blood ( indicated as Pa CO2 ), and the blood pH. Note that concentration of CO2 in the blood, not the amount of oxygen, is the major regulator of breathing drive”
Gilbert (in press) in Multidisciplinary Approaches to Breathing
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The Bohr Effect
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From, Chaitow, Bradley, & Gilbert (2002), Multidisciplinary Approaches to Breathing Pattern Disorders
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“As a consequence of hyperventilation, the decrease in PCO2 will reduce the caliber of the arteries and thereby impede the flow of blood to body tissue (ischemia), and the increase in blood pH will reduce the amount of oxygen that hemoglobin can release to the body tissue (hypoxia). Therefore, the heart must pump more frequently and with greater vigor in order to compensate for the decrease in pCO2 and increase in pH.” { Ley, 1987, p.309}
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40 torr
30 torr
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This is your brain on normal breathing.
This is your brain on hyperventilation.
Low blood flow High blood flow
Mechanics of Breathing
DiaphragmChest wall muscles – intercostal musclesAccessory muscles – scalene musclesRetraction of abdominal muscles is sign of
distress
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Diaphragmatic and Pursed Lip Breathing
Many sources available to incorporate these techniques Freid (1987,1993) Chaitow, Bradley, & Gilbert(2002) Gevirtz in Schwartz and Andrasik (2003) Bradley( 1998) Clifton-Smith (1999)
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Autonomic Nervous System (ANS)
The ANS is divided into three divisions: the parasympathetic, with cranial and sacral connections, the Sympathetic, with central nervous connections in the thoracic and lumbar segments of the spinal cord, and the enteric nervous system which occupies the digestive tract(MacArthur Research Network)
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Sympathetic Nervous System
Muscle spindle increased intrafusal firing
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“…compared with our ancestors, modern lifestyles have all but eliminated the danger of predatory aggression, and we rarely engage the central autonomic networks developed by evolutionary pressure to cope with the most stressful challenges to homeostasis.” (p.683)
Parasympathetic Nervous System
Overall Models
Balance Model vs. Regulatory Model
PNS Activation
SNS Activation
Co-Activation model
Reciprocal or Balance
Cardiac Vagal Tone
Context dependentReflects input from vagal afferent nerve
fibers as well as brain structures (cardiorespiratory center, amygdala, and hypothalamus)
Neuroanatomy Complex
Pre and post ganglionic fibers Efferent and afferent components
Efferents CNS to target organs Two components
• Brachial motor-voluntary muscles of the pharynx, larynx, and part of tongue• Visceral motor- glands and smooth muscle of the pharynx, larynx, and thoracic
abdominal organs ( heart, lungs, liver, pancreas, and gut Afferents
Target organs to CNS Three components
• Visceral sensory-info from larynx, esophagus, trachea, visceral organs. Also chemoreceptors and stretch receptors in aorta
• General sensory- pharynx, tympanic membrane, and external auditory meatus Special Sensory- taste sensation in epiglottis
CNS Cell BodiesMedullary Structures
Brachial motor neurons• Nucleus Ambiguus (NA)
Visceral motor neurons• Dorsal motor nucleus (DMNX)
Afferents just outside of CNS- Superior and inferior ganglia
Transmit from receptors in target organs to the nucleus of the Solitary Tract (also in the medulla) from there info (gut distention, blood pressure, etc) is sent to hypothalamus and NA, regulating vagal and sympathetic efferents (baroreflex).
Age
Both sympathetic and parasympathetic influence on the SA node of the heart decline with age (Craft and Schwartz, 1995)
RSA and Glucose Metabolism IMany studies have found that diminished glucose
regulation is associated with decreased RSA. Cause or effect?
Pancreas and liver have vagal input, but poorly understood.
Falling plasma glucose activates the sympathetic system leading to release of epinephrine from the adrenal medulla. This stimulates hepatic and renal glucose production and gluconeogenisis. It also stimulates skelatal muscle to uptake glucose.
RSA and Glucose Metabolism IIStimulation of the vagal efferent nerve fibers
results in insulin release by pancreatic β-cells, while liver efferents increases glucogen formation.
Hypoglycemia->sympathetic activation-increased glucose production.
Hyperglycemia parasympathetic activation decreased glucose production and increased storage.
Parasympathetic Insufficiency
“Impaired parasympathetic regulation of glucose is therefore a risk factor for hyperglycemia and hyperinsulinemia-precursors of Type II diabetes.” (Masi et al., 2007)
Vagal function early sign of insulin dysregulation or could long term vagal dysfunction be a risk for the development of insulin reistence and diabetes.
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Parasympathetic (PSNS) Activity
Parasympathetic activity: Decreases heart rate, polarizes cells. Acts through acetylcholine, high turnover in
cells means beat-to-beat regulation. Acts to stabilize the cardiac membrane and re-
establish homeostasis. Usually exceeds SNS activity.
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Polyvagal Theory of Stephen Porges
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Stage ANS Component Behavioral Component
III Myelinated vagus(ventral vagal complex)
Social communication, self-soothing and calming, inhibit symp-adrenal-influences
II Sympathetic-adrenal-system(sympathetic nervous system)
Mobilization, fight/flight, active avoidance
I Unmyelinated vagus(dorsal vagal complex)
Immobilization, death feigning, passive avoidance, shutdown.
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Porges’ Evolutionary Theory of Emotion
Porges, S. (1997) Emotion: An Evoutionary By-Product of the Neural Regulation of the Autonomic Nervous System in C.S. Carter, I. Lederhendler, B. Kirkpatrick (eds.) The integrative neurobiology of affiliation. Annals of the New York Academy of Sciences, 807.
Porges, S. (1995) Orienting in a defensive world: Mammalian modifications of our evolutionary heritage. A Polyvagal theory. Psychophysiology:32,301-318.
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Porges, S. (2001) The polyvagal theory: phylogenetic substrates of a social nervous system. Intl J. Psychophysiology, 42, 29-52.
Love: an emergent property of the Mammalian autonomic nervous system. Psychoneuroendocrinology, 23,:837-61
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Autonomic Nervous System Components
Name Characterization
Visceral Afferents-“feelings” Feedback from gut, heart,lungs
Sympathetic Nervous System& Hypothalamic PituitaryAxis
Mobilization of metabolicresources cardiovascularoutput, digestive functions
Parasympathetic NervousSystem- emotional “states”
Foster growth & restoration-complex cardiac brakingsystem
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Phylogenetic Hierarchy in Cardiovascular Response to Stress
Chromaffin DMNX SNS Adrenal Med NA
Cyclostomes
Cartilaginous fish
Advanced fish
Amphibians
Reptiles
Mammals *
*Allows rapid regulation of
metabolic output:useful in social regulation
DMNX=dorsal motor nucleus
SNS=sympathetic nervous system
NA= nucleus ambiguous
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Polyvagal Theory Proposes: Three global evolutionary phases:
“…primitive unmyelinated visceral vagus that fosters digestion and responds to threat by depressing metabolic activity.”-immobilization
“…sympathetic nervous system that is capable of increasing metabolic output and inhibiting the visceral vagus to foster mobilization for ‘fight or flight’.”
The third stage, unique to mammals, is characterized by a myelinated vagus that can rapidly regulate cardiac output to foster engagement and disengagement with the environment”-linked to cranial nerves and facial muscles
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Social Engagement and the PNSPorges (In Press) Annals of the NY Acad of Sciences
There are well defined neural circuits to support social engagement behaviors and the defensive strategies of fight, flight, and freeze.
These neural circuits form a phylogenetically organized hierarchy. Without being dependent on conscious awareness the nervous system
evaluates risk in dangerous, or life threatening environments. Social engagement behaviors and the benefits of the physiological
states associated with social support require a neuroception of safety. Social behaviors associated with nursing, reproduction, and the
formation of strong pair bonds require immobilization without fear Immobilization without fear is mediated by the co-opting of the neural
circuit regulating defensive freezing behaviors through the involvement of oxytocin, a neuropeptide in mammals involved in the formation of social bonds.
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Cortex
Brainstem
Cranial NervesV, VII, IX, X, XI
Bronchi
Heart
HeadturningPharyanxLarynxFacial
muscles
MiddleEar
muscles
Muscles ofmastication
Environment
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ResultsPNS Activity and Marital Satisfaction
• Correlation of vagaltone (HF) and maritalsatisfaction resulted insignificant correlationfor recovery periodfollowing a neutraldiscussion period
00.050.1
0.150.2
0.250.3
0.350.4
0.450.5
Base
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Even
tsDi
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sion
Reco
very
1*
Reco
very
2
Confl
ictDi
scus
sion
Reco
very
3
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Example of RSA
Notice how heart rate increases with inhale. Heart rate decreases with exhale. This pattern shows high vagal tone (high PSNS activity) and a high amount of heart rate variability.
Respiration Heart Rate
Inhale Exhale
Peak/valley differences= vagal tone when resp is
in normal range
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Vagal Withdrawal: An alternative to Sympathetic Activation .: Neurosci Biobehav Rev. 1995 Summer;19(2):225-33.
Cardiac vagal tone: a physiological index of stress.
Porges SW.
Institute for Child Study, University of Maryland, College Park 20742, USA.
Cardiac vagal tone is proposed as a novel index of stress and stress vulnerability in mammals. A model is described that emphasizes the role of the parasympathetic nervous system and particularly the vagus nerve in defining stress. The model details the importance of a branch of the vagus originating in the nucleus ambiguus. In mammals the nucleus ambiguus not only coordinates sucking, swallowing, and breathing, but it also regulates heart rate and vocalizations in response to stressors. In mammals it is possible, by quantifying the amplitude of respiratory sinus arrhythmia, to assess the tonic and phasic regulation of the vagal pathways originating in the nucleus ambiguus. Measurement of this component of vagal tone is proposed as a method to assess, on an individual basis, both stress and the vulnerability to stress.
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Worrying about being late for an appointment. See FFT B
Driving. See FFT A
13 Br/Min
33 Br/min
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Anxiety attack while driving home
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Vagal modulation of responses to stress in PTSDSahar, Shalev, and Porges (2001)Biol. Psychiatry, 49,637-43
29 trauma survivors 14 with PTSD (PTSD active) 15 w/o (Non PTSD)
Stress profile focus on PNS measuresPTSD showed blunted RSA during MACoupling of RSA/IBI only in the Non-PTSD
group (r=.75)Responses to challenge may be dominated by the
SNS in PTSD
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Levine’s Approach to Trauma Treatment
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“Rather, Levine looks to the process of what happens when we experience trauma. He sees recovery as getting past a series of mental vortexes that can block our ability to continue traveling down life's stream. As we travel down the stream, our relationship with the traumas changes, just as our relationship with a loved one who has died changes as we continue to live, and they do not. When we get caught in the vortexes created by our traumatic histories we become struck, and whirling within the vortexes, we can relive the traumas - through flashbacks, anxiety, or actual repetitions of particular aspects of the trauma. Levine doesn't minimize the importance of our memories, but emphasizes the primacy of our feelings, of our body states, and of our body's need to physically remove the traumas in order to heal. In this sense, he reminds me of Stan Grof's work on healing the body through breathwork. But the methods proposed here are considerably gentler.”
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Bessel van der Kolk Abnormal psychophysiological responses in PTSD have been demonstrated on two different levels: 1) in response to specific reminders of the trauma and 2) in response to intense, but neutral stimuli, such as acoustic startle. The first paradigm implies heightened physiological arousal to sounds, images, and thoughts related to specific traumatic incidents. A large number of studies have confirmed that traumatized individuals respond to such stimuli with significant conditioned autonomic reactions, such as heart rate, skin conductance and blood pressure (20,21,22,23, 24,25). The highly elevated physiological responses that accompany the recall of traumatic experiences that happened years, and sometimes decades before, illustrate the intensity and timelessness with which traumatic memories continue to affect current experience (3,16). This phenomenon has generally been understood in the light of Peter Lang's work (26) which shows that emotionally laden imagery correlates with measurable autonomic responses. Lang has proposed that emotional memories are stored as "associative networks", that are activated when a person is confronted with situations that stimulate a sufficient number of elements that make up these networks. One significant measure of treatment outcome that has become widely accepted in recent years is a decrease in physiological arousal in response to imagery related to the trauma (27). However, Shalev et al (28) have shown that desensitization to specific trauma-related mental images does not necessarily generalize to recollections of other traumatic events, as well.
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Stephen Porges started off the day with a lecture on his research: "Application of Polyvagal Theory to Clinical Treatment". Most of it was in understandable English, because Porges is a U of Illinois professor and knows how to teach. According to the conference bio, "his polyvagal Theory of Emotion led to the discovery of an integrated neural system that regulates social engagement behaviors." His lecture today focused on the need for face-to-face interactions for bonding to occur. When there’s a violation of the interaction—someone doesn’t make eye contact, when a supposed intimate is speaking, the speaker experiences distress: anger/shame/alienation. Safety creates proximity creates contact creates bonding. There might be more bonding in sleeping together than in sex. Porges commented on the dysfunction in the Seinfeld rule, "No sleepovers!“ (We know that those people were all attachment disordered!) I can’t recount the whole lecture, but I can give you tidbits:Facial muscles go down to the heart. Talking, listening, and smiling calm us down. Two vagal nerve systems. The old one, from lizard days, shuts us down completely. It’s the one from which we can swoon, be literally scared shitless, or become selectively mute, when distressed. The new vagus is linked to face and is protective of mobilization systems.
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It works socially. Our nervous system can relax us through the meyelinated vagus, if we are experiencing safety; mobilize us, through the sympatheticand adrenal system, if we sense dangere, or completely immobilize us, through the old, lizard unmeyelinated vagus, if we think our life is in danger, feigning death like a mouse fooling a cat. (Doug, out birding during the day, caught and pet a horned lizard, who didn’t move at all. It was in the immobilization vagal phase.) Social behavior enables us to function better. Social engagement systems: prosody (tone and music of our voices), gaze, facial expressivity, posture during social engagement, mood, affect, and behavioral state regulation.
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Environment can be interpreted, based on our state. Borderline cutters, in a study, lost vagal control of their hearts while watching emotional videos. Controls, did fine. Very autistic kids attend to low (more frightening) tones. They stay scared and "mobilized" most of the time and try to soothe by doing weird stuff, not be connecting with others. If you play them music with all the low tones filtered out, over time, they will become socially engaged, like normal kids. I saw the video, it wasway cool.
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HRV
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What Is Heart Rate Variability?
HRV is the spontaneous change in HR. HRV is related to interaction between
sympathetic and parasympathetic influences at sinoatrial node in the heart.
HRV interacts with respiratory and blood pressure regulation.
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Measurement of R-WaveThe time between R-wave peaks is interbeat interval or heart
period. It is also called “NN” (normal to normal) interval.
R-Wave Interbeat Interval
Measured in msi.e.1000ms=60 BPM
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HRV Defined (MacArthur Network)
Heart rate variability (HRV) refers to the beat-to-beat alterations in heart rate. Under resting conditions, the ECG of healthy individuals exhibits periodic variation in R-R intervals. This rhythmic phenomenon, known as respiratory sinus arrhythmia (RSA), fluctuates with the phase of respiration -- cardio-acceleration during inspiration, and cardio-deceleration during expiration. RSA is predominantly mediated by respiratory gating of parasymphathetic efferent activity to the heart: vagal efferent traffic to the sinus node occurs primarily in phase with expiration and is absent or attenuated during inspiration. Atropine abolishes RSA.
Reduced HRV has thus been used as a marker of reduced vagal activity. However, because HRV is a cardiac measure derived from the ECG, it is not possible to distinguish reduced central vagal activity (in the vagal centers of the brain) from reduced peripheral activity (the contribution of the target organ -- the sinus node -- or the afferent/efferent pathways conducting the neural impulses to/from the brain).
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Respiratory Influences
HR changes related to respiration are called respiratory sinus arrhythmia (RSA).
HR increases with inhalation. HR decreases with exhalation.
Amount of HR change with breathing is used as an index of vagal “tone”.
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Respiratory Activity Continually Perturbs Cardiovascular hemodynamics
“In the brain stem, respiration modulates the activity of most sympathetic and vagal efferents both through direct coupling between the respiratory and autonomic centers and through modulation of central sensitivity to baroreceptor and other afferent inputs. The autonomic efferents in turn modulate heart rate (HR) and peripheral vascular resistance with respiratory periodicities.”
Saul JP at. Al.Transfer function analysis of the circulation: unique insights into cardiovascular regulation. Am J Physiol. 1991 Oct;261(4 Pt 2):H1231-45
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Allostatic Load and HRV What aspect of allostasis does HRV potentially measure? Although our understanding of the meaning of HRV is far from complete, it seems
to be a marker of both dynamic and cumulative load. As a dynamic marker of load, HRV appears to be sensitive and responsive to acute stress. Under laboratory conditions, mental load -- including making complex decisions, and public speech tasks -- have been shown to lower HRV. As a marker of cumulative wear and tear, HRV has also been shown to decline with the aging process. Although resting heart rate does not change significantly with advancing age, there is a decline in HRV, which has been attributed to a decrease in efferent vagal tone and reduced beta-adrenergic responsiveness. By contrast, regular physical activity (which slows down the aging process) has been shown to raise HRV, presumably by increasing vagal tone.
In short, HRV appears to be a marker of two processes, relevant to the conceptualization of allostatic load: (1) frequent activation (short term dips in HRV in response to acute stress); and (b) inadequate response (long-term vagal withdrawal, resulting in the over-activity of the counter-regulatory system -- in this case, the sympathetic control of cardiac rhythm).
More from McEwen Allostatic load
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How is HRV measured? Originally, HRV was assessed manually from calculation of the
mean R-R interval and its standard deviation measured on short-term (e.g., 5 minute) electrocardiograms. The smaller the standard deviation in R-R intervals, the lower is the HRV. To date, over 26 different types of arithmetic manipulations of R-R intervals have been used in the literature to represent HRV. Examples include: the standard deviations of the normal mean R-R interval obtained from successive 5-minute periods over 24-hour Holter recordings (called the SDANN index); the number of instances per hour in which two consecutive R-R intervals differ by more than 50 msec over 24-hours (called the pNN50 index); the root-mean square of the difference of successive R-R intervals (the rMSSD index); the difference between the shortest R-R interval during inspiration and the longest during expiration (called the MAX-MIN, or peak-valley quantification of HRV); and the base of the triangular area under the main peak of the R-R interval frequency distribution diagram obtained from 24-hour recording; and so on. So far, experimental and simulation data appear to indicate that the various methods of expressing HRV are largely equivalent, and there is no evidence that any one method is superior to another, provided measurement windows are 5 minutes or longer.
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What contributes to the variability in sequential R-waves
Underlying physiology of HRV Sympathetic Parasympathetic Baroreceptors Peripheral vascular influences
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Baroreflex Sensitivity (BRS)Sensitive prognostic indicator of
cardiovascular health (Osterzeil et al., 1995, Br. Heart J, 73, 517-522)
Can be reliably estimated with .1 Hz paced breathing (Davies et al., 2002, Am. Heart J, 143,441-7)
Measure IBI (in msec) from valley to peak during .1 Hz paced breathing
Correlates r=.81 with finipres methodsSuperior to: Bolus phenylephrine, alpha
index, and sequence method (Davies et al., 1999, Clinical Science, 97, 515-522)
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The baroreceptor vagal reflex is an important part of the cardiovascular control system. It may be defined as the biological neural control system responsible for short-term blood pressure regulation.
The schematic of the baroreceptor vagal reflex is shown in Fig. 1. Baroreceptors (first-order cells) located in the great arteries provide sensory information to second-order barosensitive neurons located in the nucleus tractus solitaire (NTS) in the lower brainstem. Via a number of intermediate medullary neural networks, the second-order NTS neurons effect motor neurons which in turn control heart rate and total peripheral resistance and thus blood pressure.
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Baroreceptor Sensitivity
A rise in BP stimulates the baroreceptor to signal to the SA node through the PNS to brake the HR
A drop in BP stimulates the baroreceptor to increase HR through the SNS
The ability of BP to regulate HR is called “Baroreceptor Sensitivity” (BRS)
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Chemoreceptors: Control of Respiratory Drive Peripheral Chemoreceptors
Located primarily in the carotid and aortic bodies(in humans mostly carotid)
Increase firing rapidly primarily in response to hypoxia, but also to hypercapnia
Control ventilation Central Chemoreceptors
Sensitive to pH of cerebral spinal fluid Also have important effects on cardiovascular system
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Chemoreceptors (Cont) Respiratory and Cardiovascular systems highly intertwined “Chemoreceptor stimulation causes a marked increase in ventilation
and sympathetic nerve activity, while baroreceptor activation causes a mild decrease in ventilation and a sharp reduction in sympathetic nerve activity.”
“Baroreceptor activation…has a particularly potent inhibitory effect on the sensitivity to peripheral chemorecptor stimulation, with little (if any) inhibitory effect on the sensitivity to central chemoreceptor firing.”
“Increases in ventilation cause a complex cascade of pulminary and cardiovascular effects, including activation of the stretch receptors and an elevation in arterial blood pressure: these make it difficult to isolate the direct cardiovascular effects of chemostimuli in a spontaneously breathing subject.”
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Chemorecptors (cont)
“Nevertheless, despite their complexity, these relationships appear to form a stable network, which in normals allows each subsystem to be adequately regulated , while allowing appropiate cross-talk between systems. In the disease states, such as chronic heart failure, there is breakdown of the normal magnitude (and in some cases direction) of the cardiorespiratory reflexes, which can lead to potentially maladaptive feedback loops.” (Francis, Coats, & Ponikowski, 2002)
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Synthesis of interactions among some of the important reflexes of the cardiovascular and respiratory systems (Francis et al. 2002)
Baroreceptors
IncreasedBP Increased Sympathetic
nerve activity
Cardiovascularintegration center
Ventilatoryintegration center
LungStretchLower pCO2
Higher PO2
PeripheralChemoreceptors
CentralChemoreceptors
Increased Ventilation
+
++
+
-
-
-
- -
Cardiovascularsystem
Respiratorysystem
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Frequency Domain Measures
The power spectrum
05/03/23 Gevirtz 1031 4 1512106 20 25Breaths per minute
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Hertz to Breaths per minute Hz B/min .5 30 .25 15 .2 12 .18 11 .16 10 .15 9 .13 8 .12 7 .10 6
.08 5 .06 4 .05 3 .03 2 .02 1
B/min/60=Hz Hz x 60 = B/min
05/03/23 Gevirtz 105
Temperature Rhythms
Temperature
Time [s]
Tem
pera
ture
[D
egre
e C
]
400 450 500 550 600 650
33.9
34.0
34.1
34.2
34.3
05/03/23 Gevirtz 106
Hertz to Breaths per minute Hz B/min .5 30 .25 15 .2 12 .18 11 .16 10 .15 9 .13 8 .12 7 .10 6
.08 5 .06 4 .05 3 .03 2 .02 1
B/min/60=Hz Hz x 60 = B/min
05/03/23 Gevirtz 107
Temperature Spectrum
Temperature Spectrum
Frequency [Hz]
PS
D [
Deg
ree
C^2
/Hz]
0.0 0.1 0.2 0.3 0.4 0.5
0.0
0.1
0.2
0.3
05/03/23 Gevirtz 108
Hertz to Breaths per minute Hz B/min .5 30 .25 15 .2 12 .18 11 .16 10 .15 9 .13 8 .12 7 .10 6
.08 5 .06 4 .05 3 .03 2 .02 1
B/min/60=Hz Hz x 60 = B/min
05/03/23 Gevirtz 109
Heart Rate Rhythms
Heart Rate
Time [s]
HR
[bp
m]
50 100 150 200 250
70
80
90
05/03/23 Gevirtz 110
Hertz to Breaths per minute Hz B/min .5 30 .25 15 .2 12 .18 11 .16 10 .15 9 .13 8 .12 7 .10 6
.08 5 .06 4 .05 3 .03 2 .02 1
B/min/60=Hz Hz x 60 = B/min
05/03/23 Gevirtz 111
Heart Rate Spectrum
Heart Rate Spectrum (general)
Frequency [Hz]
PS
D [
bpm
^2/H
z]
0.0 0.1 0.2 0.3 0.4 0.5
0
1000
2000
3000
05/03/23 Gevirtz 112
Hertz to Breaths per minute Hz B/min .5 30 .25 15 .2 12 .18 11 .16 10 .15 9 .13 8 .12 7 .10 6
.08 5 .06 4 .05 3 .03 2 .02 1
B/min/60=Hz Hz x 60 = B/min
05/03/23 Gevirtz 113
RRI Spectrum
Frequency [Hz]
PS
D [
ms^
2/H
z]
0.0 0.1 0.2 0.3 0.4 0.5
0
10000
20000
30000
40000
05/03/23 Gevirtz 114
Hertz to Breaths per minute Hz B/min .5 30 .25 15 .2 12 .18 11 .16 10 .15 9 .13 8 .12 7 .10 6
.08 5 .06 4 .05 3 .03 2 .02 1
B/min/60=Hz Hz x 60 = B/min
05/03/23 Gevirtz 115
Respiration Spectrum at Normal Breathing Pace
Respiration Volume Spectrum
Frequency [Hz]
PS
D [
ml^
2/H
z]
0.0 0.1 0.2 0.3 0.4 0.5
0
250
500
750
1000
05/03/23 Gevirtz 116
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LF/HF Ratio
Often cited as a measure of “sympathovagal balance” with high scores indicating sympathetic dominance
Still controversial (see Eckberg et al.)Does correlate (r=.97) with a fractal
measure of entropy
05/03/23 Gevirtz 131
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Relationship between In(LF/HF) ratio and alpha 1 , a detrended fluctuation measure,( a fractal measure).
05/03/23 Gevirtz 133
24 Hour LF:HF Ratio
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
16 17 18 19 20 21 22 23 24 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Time
LF:HF Ratio
Morning Evening
** *
Severise, Gevirtz et al., 2008
05/03/23 Gevirtz 134
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Determinants of Heart Rate (IBI)
Intrinsic Pacemaker1-2 Hz (110-120 b/m)
Sympathetic Influences on the Sino-Atrial NodeA paced accelerator
Parasympathetic Influences on the Sino-Atrial NodeA paced brake
Baroreceptor Feedback System
CardioPro.lnkIBI
MedullaryInfluences
VascularInfluences
05/03/23 Gevirtz 142
Based on an interview with Laceys in 1977
05/03/23 Gevirtz 143
05/03/23 Gevirtz 144
Cardiac Parasympathetic Afferent System
Vagal afferent pathways from the heart to the brain exceed brain to heart
These can affect: cortical function EEG Emotional memory system
05/03/23 Gevirtz 145
Heart as a Separate Nervous System
Neural CardiologyElaborate neural plexus Sensory neuritesAfferents can effect cortical functioning and
performance
05/03/23 Gevirtz 146
Heart as Endocrine “Gland”
Heart produces: Atrial peptides Oxytocin Dopamine Epinephrine Norepineprine
Pulsing of impulses greatly affect communications in the Endocrine System
05/03/23 Gevirtz 147
Fascinating Rhythms
05/03/23 Gevirtz 148
Role of OscillationsIn healthy individuals, a degree of interaction
between activity of SNS and PSNS allows more effective responses to demands. This interaction occurs as oscillations of SNS and PSNS activity.
This interaction produces variability in HR. Oscillations in HR interact with other systems (hormones, blood pressure, respiration, emotion, etc).
05/03/23 Gevirtz 149
More on Oscillations
Oscillations help bring the physiology back to equilibrium after stressors and contribute to stability of the system.
Oscillations allow for a timed sequence of events to occur (e.g., firing of all sets of cells necessary to contract the ventricles) and for the repetition of those events.
05/03/23 Gevirtz 150
More on Oscillations
Oscillations help predict daily events, e.g., circadian changes in HRV.
Pathology arises when these oscillations are disturbed, leading to a LOSS of variability and a decrease in ability to adapt.
05/03/23 Gevirtz 151
Heart Rate Variability (HRV) and Health>150,000 Medline ciataions (2000)“Importantly, decreased HRV is almost
uniformly associated with adverse outcome.” (Kleiger et al., 1992 Cardiology Clinician)
Predictor of mortality(all causes)Especially sudden deathHundreds of citations on methodology,( see
the Task Force Report, 1996)
05/03/23 Gevirtz 152
HRV in Health
Changes in the amount of HRV are related to change in autonomic activity in: Aging: decreases vagal tone. Exercise: improves HRV. Stress: HRV decreases with SNS arousal. Circadian rhythms: HRV changes with time of
day.
05/03/23 Gevirtz 153
HRV as a Risk Factor
HRV has been widely reported to be a risk factor for CHD, for all cause mortality, and even cancer mortality.
< 50 ms vs > 50 ms Ors often 3-4 This means that a shift SDNN (standard
deviation of R-R on ECG) from low to moderate decreases risk of mortality by 4 to 1
Kleiger et al. 1987, Am J. Cardio.
05/03/23 Gevirtz 154
HRV as an Outcome Measure
Since HRV: is not changed by placebo (Kleiger et al., 1991,
Vybrial et al, 1993, De Ferrari et al., 1993, Casadei et al., 1996, Venkatesh et al., 1996)
is stable ( Kleiger et al., 1991, Bigger et al., 1992, Stein et al., 1995)
It is an excellent candidate for an outcome measure for txs of anxiety, depression,etc. (Pignotti & Steinberg, 2000)
05/03/23 Gevirtz 155
HRV may be a sensitive marker of changes in depression
Nahshoni et al (2001) Am J Geriatric Psychiatry, 255-60 Cardiac vagal activity increased after ECT in
11 elderly depressed patients compared to controls.
Similar to many medication studies
05/03/23 Gevirtz 156
Power-law Relationship of Heart Rate Variability as a predictor of Mortality in the Elderly
“Power-law relationship of 24-hour HR variability is a more powerful predictor of death than the traditional risk markers in elderly subjects”(Huikuri et al., 1998, American Heart Journal)
Cerebro-vascular adjusted relative risk= 2.84Cardiac mortality adjusted relative risk= 2.05
05/03/23 Gevirtz 157
Criteria for Sampling
R-wave (and ECG) needs to be sampled at at least 256 samples/second
Need a sharp peak for r-wave detectionPPG reading may not always be satisfactory
due to lack of sharp peak
05/03/23 Gevirtz 158
HF(.15-.4Hz)LF(.08-.14Hz)
VLF(.001-.07Hz)
05/03/23 Gevirtz 159
Fig.1. Here is an example of the various frequencies displayed in a spectral format. Note the bottom graphic shows activity in the bands (the x axis) of VLF (0-.04Hz), LF (.05-.11Hz), & HF (.12-.4 Hz). The Y axis is power or amplitude, and the z axis represents 32 sec time epochs
HF LF
VLF
05/03/23 Gevirtz 160
Fig. 2. Note the high level of VLF activity accompanying rumination, worry or performance anxiety.
05/03/23 Gevirtz 161
Fig.3. The “meditators peak” in the .08-.11 range. Note that the patient has learned to both “quiet her mind” while breathing slowly and diapragmatically.
05/03/23 Gevirtz 162
Early stages of Resonant Frequency Acquisition
05/03/23 Gevirtz 163
RFT Continued
05/03/23 Gevirtz 164
Achievement of “meditators peak” through Resonant Frequency Training
05/03/23 Gevirtz 165
The “meditators peak”
05/03/23 Gevirtz 166
Patient after 10 minutes of RFT
Evidence of efficacy, HRV Biofeedback Asthma-Lehrer et al., Chest, 2004 COPD- Giardino et al., APB, 2004 CAD- Del Pozo et al. (AHJ, 2004), van Dixhoorn et al. Performance- Strack et al., Gruzelier’s group (APB, 2005) Stress, performance, etc., McCraty et al (Har. Bus Rev, 2003; Physio Beh Sci,
1999; numerous HeartMath reports) IBS/RAP- Humphreys & Gevirtz (JPGN, 2000) Sowder, Gevirtz,et al. (2007) FM- Hasset et al. APB,(2007) Altitude sickness-Bernardi (2001& in press) MDD, Karavadis et al., APB, (2007), Zucker et al.(2007), Rene et al.(2007) Congestive Heart Failure-(Bernardi, 2002, Circulation) Swanson, Gevirtz, et
al. (2007) Hypertension- (Schein et al, 2001, J. Human Hypertension; Herbs & Gevirtz,
1994, Abstract, APB; Lehrer et al.,( 2004) Reinke, Gevirtz, et al. (2007) PTSD Zucker et al., White et al.,(2008) GAD Murphy, Hoffmann et al. (2008)
05/03/23 Gevirtz 168
Heart Rate Variabilty Biofeedback
“Increasing RSA”
05/03/23 Gevirtz 169
Ordinary Breathing produces three HR frequencies,
HF,LF,&VLF
Progression to approx. 6 BPM, (Diaphragmatically) in experienced breathers produces single summatedpeak at about .1hz:
RESONANT FREQUENCY
Daily practice in this state increases
homeostatic reflexes
Vaschillo’s Resonant Vaschillo’s Resonant Frequency Frequency
TheoryTheory
05/03/23 Gevirtz 170
HFLFVLF
05/03/23 Gevirtz 171
RFT : Notice trend from three waves to a dominant .1 Hz Wave
05/03/23 Gevirtz 172
05/03/23 Gevirtz 173
ResonanceDictionary Definition:
The increase of amplitude of oscillations of an electric or mechanical system due to a periodic force whose frequency is equal or very close to the natural undamped frequency of the system
Transfer functions, phase angles, and suchResonance Frequency Biofeedback Training
05/03/23 Gevirtz 174
40
45
50
55
60
65
70
75
80
85
1 12 23 34 45 56 67 78 89 100
111
122
133
144
155
166
177
188
Time (sec)
Hea
rt R
ate
(bea
t/min
)
Biofeedback Rest
EFFECTS OF HRV BIOFEEDBACK ON HEART RATE
05/03/23 Gevirtz 175
Spectrums of Biofeedback-inducedRRI and SBP
0.0 0.1 0.2 0.3 0.4 0.5 0.6
ms2
/Hz
0.0
5.0e+4
1.0e+5
1.5e+5
2.0e+5
2.5e+5
Hz0.0 0.1 0.2 0.3 0.4 0.5 0.6
mm
Hg2 /
Hz
0
200
400
600
800
1000
Biofeedback-induced RRI and SBP
0 20 40 60 80 100 120 140
ms
750800850900950
1000105011001150
Seconds0 20 40 60 80 100 120 140
mm
Hg
105
110
115
120
125
130
135
05/03/23 Gevirtz 176
Resonance and Effects of HRV Biofeedback
Paul Lehrer, Ph.D.UMDNJ Dept of PsychiatryPiscataway, N.J.
05/03/23 Gevirtz 177
Resonance in Physiological Systems
Resonance is a property of an oscillating system in which perturbations at specific frequencies produce large increases in oscillation amplitudes.
A system has resonance properties if two processes (functions) of the system interplay against each other in a feedback relationship. R
esonce system
05/03/23 Gevirtz 178
Reaction of Aperiodic and Resonance Systems to Perturbation Stimuli
Aperiodic system Resonance system
Perturbation Stimuli
Output Function(Response to stimuli)
Time
Time
Time
Time
T[s]
Resonance frequency:
F[Hz] = I/T[s]
05/03/23 Gevirtz 179
Pendulum as a Resonance System The pendulum may
oscillate because kinetic and potential energies of mass are linked with each other by feedback. The process of kinetic energy change elicits a process of potential energy change and vice versa.
Stimuli
05/03/23 Gevirtz 180
To understand why human beings are more sensitive to some frequencies than to others, it is useful to consider the human body as having sub-systems, where each sub-system has its own resonant frequency.
The Human Body Consists of Many Resonant Systems
05/03/23 Gevirtz 181
EACH BODY SUB-SYSTEM HAS A RESONANCE FREQUENCY BAND
Mechanical Resonance
05/03/23 Gevirtz 182
ResonanceWe found that the human cardiovascular
system has resonant features. Each person has a specific resonant
frequency in the range of .055 - .12 Hz. Breathing at resonant frequency causes high
amplitudes in both heart rate (HR) and blood pressure (BP) oscillations.
We have found that breathing at resonant frequency trains the reflexes of the cardiovascular system, in particular, the baroreflex.
05/03/23 Gevirtz 183
The Cardiovascular System Has The Cardiovascular System Has the Property of Resonancethe Property of ResonanceHR, BP, vascular tone, and other functions of the
cardiovascular system continually change in healthy people.
These changes are as important for the autonomic nervous system as movements for the nervous-muscular system.
HR and BP variability reveal resonant properties of the cardiovascular system.
05/03/23 Gevirtz 184
Biofeedback Is Based Biofeedback Is Based on Resonant on Resonant Properties of the Properties of the Cardiovascular SystemCardiovascular System
Resonant frequency HR variability biofeedback gives people the ability to increase HR variability at a specific resonant frequency.
The biofeedback procedure produces high- amplitude oscillations in cardiovascular functions.
05/03/23 Gevirtz 185
The Baroreflex Provides The Cardiovascular System with Resonant Properties
If BP changes, the baroreflex produces contingent changes in HR and vascular tone (VT).
The increases in BP produce decreases in HR and VT, and decreases in BP produce increases in HR and VT.
By mechanical action increases in HR and in VT produce increases in BP, while BR-induced decreases in HR and in VT produce decreases in BP.
05/03/23 Gevirtz 186
HR and BP Reactions to Stimuli if the Baroreflex Does Not Work
Blood Pressure
Heart Rate
Delay~5 sec
Stimuli
Time
Time
Time
05/03/23 Gevirtz 187Stimuli
Heart Rate
Blood Pressure
Delay~ 5 sec
HR and BP Reactions to Stimuli if the Baroreflex Works
Time
Time
Time
Functional Resonance
Stimuli elicit HR changes which, after a delay, change BP.BP changes, in turn elicit, HR changes due to baroreflex activity.
05/03/23 Gevirtz 188Respiration
Heart Rate
Blood Pressure
Delay~ 5 sec
Time
Time
Time
HR and BP Oscillations Elicited by the Stimulus of Respiration
05/03/23 Gevirtz 189
Two Closed-Loop Baroreflex Model
W(HR-target)
Blood pressure(BP) control system
Heart rate (HR)control system
Baroreceptors
Vascular tone (VT)control system
Brain
HR VTW(BP-HR) BP
Closed loop of HR baroreflex
VTHR
BP
05/03/23 Gevirtz 190
POSITIVE RESONANCE at 0.1 Hz (6/minute, or period of 10 sec)
Heart rate oscillations are at their maximum Heart rate and blood pressure oscillations are 180o out
of phase Baroreflex causes HR to decrease/increase just as
biofeedback also is causing it to decrease/increase Note-- Blood pressure effects are at their minimum
(perhaps because vascular tone baroreflex effects resonate negatively with biofeedback effects at this frequency)
05/03/23 Gevirtz 191
The highest HR oscillations are at a target frequency of ~ 0.1 HzThe phase of HR and the stimulus (breathing?) at that frequency is ~ 0o
05/03/23 Gevirtz 192
Transfer function: Respiration to HRV (n = 6)
Vaschillo et al, Chest, in press
05/03/23 Gevirtz 193
Transfer Functions of Blood Pressure with Regard to Heart Rate (Baroreflex Effect of BP) and HR with Regard to StimulusMax HR Oscil is at ~0.1 Hz (180o HR:BP Phase)Min HR Oscil is at ~0.03 Hz (0o HR:BP Phase)
05/03/23 Gevirtz 194
Therefore, HRV biofeedback stimulates the baroreflexVoluntary maximization of HRV requires
people to breathe at their resonant frequency (~6/min)
180o HR:BP phase relationship implies baroreflex (BR) stimulation
BR and HRV are maximizedBR is “exercised” and trainedNeuroplasticity of the BR is demonstrated
05/03/23 Gevirtz 195
Effects of Biofeedback Instruction to Increase HRV
Slows breathing to resonant HRV frequencyHRV and respiration are in phaseHRV and blood pressure are 180o out of
phaseLarge increase in HRV at a single
frequency
05/03/23 Gevirtz 196
We have found that:The cardiovascular system has at least two
resonant mechanisms. It is seems the baroreflex underlies these mechanisms.
HR resonance occurs in the frequency range (.075-.11 Hz) (4.5-6.6 times/min).
BP resonance occurs in frequency range (.02-.05 Hz) (1-3 times/min).
Every person has individual HR and BP resonant frequencies.
05/03/23 Gevirtz 197
Resonant Frequency Varies Across Individuals(cycles / min)
Spectral LF Power(Subject 7281)
Respiration Rate (breath/min)4 5 6 7
Spe
ctra
l LF
Pow
er (m
s^2)
0
2000
4000
6000
8000
10000
12000
14000
16000
R-R Intervals(Subject 7281)
Respiration Rate (breath/min)
4 5 6 7
800
RR
I (m
s)
R-R Intervals(Subject 7311)
Respiration Rate (breath/min)
4 5 6 7
RR
I (m
s)
800
Spectral LF Power(Subject 7311)
Respiration Rate (breath/min)4 5 6 7
Spe
ctra
l LF
Pow
er (m
s^2)
0
1000
2000
3000
4000
5000
6000
7000
05/03/23 Gevirtz 198
Examples of Individual Resonant Frequencies
05/03/23 Gevirtz 199
ID numberSess 1 Sess2 Sess3 Sess4 Sess5 Sess6 Sess7 Sess8 Sess9 Sess10
717 6 6 6 6 5.5 5.5 6 5.5 6 6718 5.5 5.5 5.5 6 6 5.5 6 6 6 6
721 6 5.5 5.5 5.5 5.5 5.5 5.5 5.5 6 6
724 5.5 5.5 5.5 5 5 5 5.5 5.5 5.5 5.5725 6 6 6 6 6 6 6 6 5.5 5.5
726 5.5 5.5 5.5 5.5 5.5 6 5.5 5.5 6.5 6728 5 5 5 5 5 5 5.5 5.5 5.5 5.5731 6 6 6.5 6.5 6.5 6.5 6 6 6.5 6.5745 5.5 5.5 5.5 5.5 5.5 5.5 5.5 5.5 5.5 5.5755 4.5 5 5 5 5 5 5 5 4.5 4.5
Individual Resonant Frequency (breath/min)
05/03/23 Gevirtz 200
Mean of the Resonant Frequency (Vertical lines present 1.98 standard error)
4.64.8
55.25.45.65.8
6
Allsubjects
Asthma Healthy Women Men
Tim
es p
er M
inut
e
P<0.0001
n=56 n=32 n=24 n=37 n=19
05/03/23 Gevirtz 201
Height
55 60 65 70 75 80
Res
onan
t Fre
quen
cy
4.5
5.0
5.5
6.0
6.5
7.0
r = -.55p < .0001
Regression of Height on Resonant Frequency
05/03/23 Gevirtz 202
Resonant Frequency
HeightWeightAge
The correlation coefficients (r) between resonant frequency
and age, height, and weight
r=-0.6 P<.0001
r=0.01 P<0.9 r=0.02 P<0.82
05/03/23 Gevirtz 203
Regression of Height by Resnant Frequency
Height
55 60 65 70 75 80
Res
onan
t Fre
quen
cy
4.5
5.0
5.5
6.0
6.5
7.0
r = -.55
05/03/23 Gevirtz 204
Heart Rate Variability Amplitude at Reasonant Frequency
Asthma Healthy0 1 2 3
Bea
t/min
0
2
4
6
8
10
12
14
16
Heart Rate Variability Amplitude at Reasonant Frequency
Asthma Healthy0 1 2 3
Bea
t/min
0
2
4
6
8
10
12
14
16
05/03/23 Gevirtz 205
ConclusionConclusion1) Each person has a specific resonant frequency.
2) The resonance frequency range is between 4.5 to 6.5 (times/min).
3) Asthma does not affect the resonant frequency.
4) Asthma decreases the amplitude of HR oscillation at the resonant frequency.
05/03/23 Gevirtz 206
HRV biofeedback stimulates the baroreflexVoluntary maximization of HRV requires
people to breathe at their resonant frequency (~6/min)
180o HR:BP phase relationship implies baroreflex (BR) stimulation
BR and HRV are maximizedBR is “exercised” and trainedNeuroplasticity of the BR is demonstrated
05/03/23 Gevirtz 207
ImplicationsBaroreflexes are systematically stimulated with
each breath, producing very high amplitude outputDoes exercise improve baroreflex function?Voluntary increase in HRV (or BP variability?)
requires breathing in phase with HR (BP) changesDoes phase with respiration improve breathing?
05/03/23 Gevirtz 208
HRV Biofeedback Also Can Improve Respiratory Function
05/03/23 Gevirtz 209
Function of Respiratory Sinus Arrhythmia
Yasuma & Hayano (2004): promotes respiratory efficiency HR increases during inhalation More blood to alveoli when O2 concentration is
highest
05/03/23 Gevirtz 210
HRV and Pulse Oxyimetry Biofeedback for COPDGiardino, et al, 2004, App Psychophysiology and Biofeedback, 29,121-133
05/03/23 Gevirtz 211
HRV and Pulse Oxyimetry Biofeedback for COPDGiardino, et al, 2004, App Psychophysiology and Biofeedback, 29,121-133
050
100150200250300350400450
distance in meters
6minwalk
PretreatmentPosttreatment
434445464748495051
% of predicted FEV1
5Pred Fev1
PretreatmentPosttreatment
363840424446485052
SGRQ on 60 pt scale
St. George's Resp Quest.
PretreatmentPosttreatment
0200
400
600
800
1000
1200
1400
1600
RSA spontanious
PretreatmentPosttreatment
RSA ms2/Hz
Lower scores indicate higher function
05/03/23 Gevirtz 212
BUT 0o phase relationship in intact humans occurs only during resonant-frequency breathing
05/03/23 Gevirtz 213
Learning to Judge Resonant Frequency
The correlation between resonant frequency and height was nonsignificant when examined only for the first session
Thus:Subjects gradually learned to find their RFSubjects gradually learned to breathe at a single sustained rate
05/03/23 Gevirtz 214
Learning to Judge Resonant Frequency
The correlation between resonant frequency and height was non-significant when examined only for the first session
Thus:Subjects gradually learned to find their RFSubjects gradually learned to breathe at a single sustained rate
05/03/23 Gevirtz 215
L. Bernardi’s research: 6/min breathing Increases tolerance to lower SaO2
Increases respiratory gas exchange efficiencyDecreases dyspneaGreater resistance to hyperventilationLowers hypoxic ventilatory response Increases baroreflex response in chronic heart
failure Bernardi, L., et al Lancet, 351,1308-1311., 1998 Bernardi L. et al, J Hypertens, 19:2221-2229,2001 Bernardi, L. et al, Circulation 105 143-145, 2002.
05/03/23 Gevirtz 216
Yogis and Sherpas breathe at this Rate and Tolerate Altitude
Low hypoxic ventilatory response in laboratory Resist hyperventilation Higher SaO2
Low hemoglobin Low minute volume ventilation No mountain sickness High exercise tolerance
•Spicuzza et al, Lancet 356:1495-1496, 2000
•Keyl, C. et al. J Appl Physiol. ;94:213-219, 2003
05/03/23 Gevirtz 217
Possible Reason??
In phase respiration and respiratory sinus arrhythmia at resonant frequency
More efficient ventilationHigher baroreflex gain, stronger autonomic
modulation
05/03/23 Gevirtz 218
Controlled Study of 56 Healthy Subjects
Increase RSA amplitude vs. Waiting List10 20-min weekly sessions with home
practicePhysiological assessment at sessions 1, 4, 7,
10
05/03/23 Gevirtz 219
05/03/23 Gevirtz 220
ms2
/ hz
0
1000
2000
3000
4000
5000
6000
7000
LF RRI RSALF RRI Waiting List
SESSION 1 SESSION 4 SESSION 7 SESSION 10
Low Frequency RRI power
05/03/23 Gevirtz 221
High Frequency RRI powerm
s2 /
Hz
0
500
1000
1500
2000
2500
RSAWaiting List
R1
B1
B2
R2
SESSION 1 SESSION 4 SESSION 7 SESSION 10
R1
B1 B2
R2R1
B1 B2
R2
R1
B1
B2
R2
05/03/23 Gevirtz 222
Mean R-R Intervalm
sec
780
800
820
840
860
880
900
920
940
RSA biofeedbackWaiting listRegression lines
SESSION 1 SESSION 4 SESSION 7 SESSION 10
REST
REST
REST
REST
REST
RESTREST
REST
BFK
BFK
BFK
BFK
BFK
BFK
BFK
BFK
Tx x Task p < .02Tx x Session p < .08Tx x Task x Session p < .04
05/03/23 Gevirtz 223
Total RRI powerm
sec2
2000
3000
4000
5000
6000
7000
8000
TOTAL RRI POWER RSATOTAL RRI POWER WL
SESSION 1 SESSION 4 SESSION 7 SESSION 10
05/03/23 Gevirtz 224
mm
Hg
8
10
12
14
16
18
DBP RSA biofeedbackDBP Waiting list
SESSION 1 SESSION 4 SESSION 7 SESSION 10
Mean Diastolic BP
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Mean Systolic BPm
illim
eter
s H
g
100
102
104
106
108
110
112
114
116
118
120
Systolic BP RSA biofeedbackSystolic BP Waiting List
Session 1 Session 4 Session 7 Session 10
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Respiratory Activity Continually Perturbs Cardiovascular hemodynamics
“In the brain stem, respiration modulates the activity of most sympathetic and vagal efferents both through direct coupling between the respiratory and autonomic centers and through modulation of central sensitivity to baroreceptor and other afferent inputs. The autonomic efferents in turn modulate heart rate (HR) and peripheral vascular resistance with respiratory periodicities.”
Saul JP at. Al.Transfer function analysis of the circulation: unique insights into cardiovascular regulation. Am J Physiol. 1991 Oct;261(4 Pt 2):H1231-45
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There Are Many Types of Breathing Procedures to Control
Body Condition Eastern medicine includes respiratory
training. Special respiratory training procedures are
developed (e.g., by Eric Peper, Buteiko, Strelnikova).
Heart rate variability biofeedback includes respiratory training at resonance frequency of the cardiovascular system. In order to reach the highest therapeutic effect, individual needs to breath at his/her own resonant frequency.
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Heart Rate Variability Biofeedback Improves Autonomic
Functions Regulation:
- Increases baroreflex gain and peak expiratory flow; Lehrer, P., at al. Heart rate variability biofeedback increases
baroreflex gain and peak expiratory flow. Psychosom Med. 2003 65(5):796-805.
- Improves efficiency of pulmonary gas exchange. Giardino, N., at al. Respiratory sinus arrhythmia is associated with
efficiency of pulmonary gas exchange in healthy humans. Am J Physiol Heart Circ Physiol. 2003 May;284(5):H1585-91.
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Forced Oscillation Pneumography
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RFT & Baroreflex FunctionBaroreflex Gain
11
11.5
12
12.5
13
13.5
14
ms/mmHg
Pre Post
TrainingControl
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FullProtocol
HRValone
Placebo
WaitingList
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PRESCRIBED MEDICATION
Session
Med
icat
ion
Leve
l
4
5
6
7
8
9
FULL
HRVAlone
Placebo
WaitingList
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Heart Rate RSA Biofeedback Training: A Treatment Manual
Resonant Frequency (RFT) TrainingBased on Lehrer, Vashillo, & Vashillo (2000)
Applied Psychophysiology and Biofeedback, 25, 177-191
Richard Gevirtz, Ph.D.CSPP at AIU, San Diego, CA
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Assessment Using an EKG for the office procedure (Currently two are readily
available: Thought Technology Infiniti or CardioPro and J& J Use 2, C-2 System), turn screen away from patient and allow at least 5 minutes of “free breathing”. It is useful to distract the patient by having them listen to an audio tape of neutral material (National Geographic, travelogs, etc)
RFT determination: Instructions: (Show screen such as Fig. 1 or 2) “On this screen you will see
your breath wave, your heart rate updated every beat, and a breath pacer. Try and breath at the pace of the pacer, but keep it as effortless as possible.”
Set pacer at 7, 6.5, 6, 5.5, 5, 4.5 breaths per minute. Use 2-3 minutes for each interval. Observe 1) peak valley differences in B/M, and LF power or relative power. Write down maximum values. For example, 24 B/M and .4 ms.
If you have a capnometer, watch for signs of HV
CardioPro.lnk
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Peak78
Valley65
LF Power
Fig. 1. J&J Screen showing HR, Resp,temp, Skin Cond,and a spectral analysis. Peak valley differences are about 14 B/M (79-65), LF is .1.
BreathPacer
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Fig. 2.1. CardioPro screen for HR and Resp
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Fig. 2.2. CardioPro Training Screen Breath Pacer
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Treatment IOnce RF is determined, Use instructions such as
the following: (from Lehrer, Vaschillo, and Vaschillo, p.184, italics mine)
Your heart goes up and down with your breathing. When you breathe in, your heart tends to go up. When you breathe out, your heart tends to go down. These changes in heart rate are called “Respiratory Sinus Arrhythmia” or RSA. RSA triggers very powerful reflexes in the body that help to control the whole autonomic nervous system (including your heart rate, blood pressure, and breathing). We will train you to increase the size of these heart rate changes. Increasing the size of these heart rate changes will exercise these important reflexes, and help them to control your body more efficiently. As`a part of this treatment we will give you information about the swings in your heart rate that accompany breathing. That will be the RSA biofeedback. You will use this information to teach yourself to increase your RSA. If you practice the technique regularly at home, you will strengthen the reflexes that regulate the autonomic nervous system. This should help you manage your health (or IBS, or Pain, etc) and ability to manage every day stress.”
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HFLFVLF
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Treatment IITraining procedes:EZ Air (BFE.org)(click on support)
Use pacer or Breathsounds (www.BreathSounds.com) at first, but let the patient take over the pace when ready.
Encourage home practice• Biosvyaz, St. Peterberg, Russia (www.biosvyaz.com)• Heart Math Freeze Framer(www.heartmath.com)• Heart Tracker (BioCom Technologies, www.biocomtech.com)• Temp monitor (about $20) available from BMI ( or Future
Health (www.futurehealth.org)
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Bio-Medical Instruments (www.bio-medical.com)
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Treatment IIICheck for RF peak and pattern at the beginning of
each session with the screen hidden from the patient.
Once evidence for a good RF is found, challenge the patient with stressors and then instruct them to resume training.
Watch for VLF elevations. They represent either chronic sympathetic activation or vagal withdrawal (as in chronic worry).
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