gevirtz on hrv

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Mediational Models in Psychophysiological Disorders

Richard Gevirtz, Ph.D.CSPP at Alliant International U.-San Diego

[email protected]: 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

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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

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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


.08 5 .06 4 .05 3 .03 2 .02 1


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


.08 5 .06 4 .05 3 .03 2 .02 1


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


.08 5 .06 4 .05 3 .03 2 .02 1


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


.08 5 .06 4 .05 3 .03 2 .02 1


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


.08 5 .06 4 .05 3 .03 2 .02 1


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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05/03/23 Gevirtz 130

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

05/03/23 Gevirtz 132

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

05/03/23 Gevirtz 135

05/03/23 Gevirtz 136

05/03/23 Gevirtz 137

05/03/23 Gevirtz 138

05/03/23 Gevirtz 139

05/03/23 Gevirtz 140

05/03/23 Gevirtz 141

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


363840424446485052

SGRQ on 60 pt scale

St. George's Resp Quest.


0200

400

600

800

1000

1200

1400

1600

RSA spontanious


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


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


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


05/03/23 Gevirtz 224

mm

Hg

8

10

12

14

16

18

DBP RSA biofeedbackDBP Waiting list


Mean Diastolic BP

05/03/23 Gevirtz 225

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

05/03/23 Gevirtz 226

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

05/03/23 Gevirtz 227

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.

05/03/23 Gevirtz 228

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)

http://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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