Biofeedback interventions like heart rate variability biofeedback (HRVB) target the cardiovascular system to
treat disorders as diverse as anxiety, depression, essential hypertension, migraine, post-traumatic stress disorder, Raynaud's
disorder, and stress.
Biofeedback monitors
blood pressure (BP), heart rate (HR), heart rate variability (HRV), pulse wave
velocity, temperature, and blood volume pulse modalities. There has been a paradigm shift in treating disorders like depression and heart failure. Clinicians increasingly teach clients to enhance HRV through exercises that strengthen parasympathetic nervous system (PNS) tone. PNS activity is also called vagal tone because the vagus is the primary component of this autonomic branch (Breit et al., 2018).
The brain receives more afferent projections from the heart than any other organ. Emerging evidence
suggests that the heart's intrinsic nervous system has extensive bidirectional connections with the brain (MacKinnon et al., 2013; Shaffer, McCraty, & Zerr, 2014).
Researchers increasingly recognize the importance of HRV as an index of vulnerability to
stressors and disease.
The PNS and baroreceptor system produce brief (≤ 5 minutes) resting HRV without a sympathetic contribution.
Patients can learn to increase the healthy variability of their hearts to treat disorders
like anxiety, asthma, depression, hypertension, and irritable bowel syndrome. HRV biofeedback training can help patients restore a healthy dynamic balance between the sympathetic and parasympathetic nervous systems.
Two patterns, coupling and fractionation, describe changes observed when
monitoring subjects. In response coupling, responses change together (HR
up, BP up). In response fractionation, responses change
independently
(HR down, BP up).
Coupling and fractionation reflect the multiple, independent processes
that jointly produce these physiological measures. Healthy systems
operate nonlinearly (unpredictably) to adapt to rapidly changing demands.
Whether
responses couple or fractionate during a specific observation period
depends on the complicated interplay of participant, task, and environmental
variables.
This unit addresses Descriptions of most commonly employed biofeedback modalities: Skin temperature, ECG and heart rate (III-A 1-2).
This unit covers Arteries, Three Measures of Peripheral Blood Flow, Veins, Capillaries, Arteriovenous Anastomoses (AVAs), Blood Pressure, the Heart, and Heart Rate Variability.
Please click on the podcast icon below to hear a full-length lecture.
Elastic arteries are large arteries like the aorta (shown below) that
distribute blood from the heart to muscular arteries.
Medium-sized
muscular arteries (like the brachial artery) circulate blood throughout
the body. They branch into small resistance arteries, which divide into arterioles.
About 400 million arterioles regulate capillary blood flow by controlling resistance.
The main source of resistance is the friction between blood and blood vessel walls. These microscopic vessels (15-300 μm in diameter)
deliver blood to capillaries and anastomoses. Arterioles divide into microscopic capillaries as they penetrate tissue. There are 3-5 levels of branching between arterioles and capillary beds, varying with the supplied organ or tissue (Jackson, 2021). Graphic adapted by minaanandag on fiverr.com.
Resistance arteries and arterioles help create peripheral vascular resistance, which is a major component of blood pressure (Segal, 2000). For example, arterioles contribute 50% of skeletal muscle vascular resistance (Fronek & Zweifach, 1975). Arterioles are responsible for most pulmonary vascular resistance due to their greater rigidity compared to larger arteries (Chaudhry et al., 2020).
The video below shows red blood cells
traveling through a pulsating arteriole.
The control of arteriole diameter, which is crucial to regulating
BP and hand temperature, is highly complex. Neural, hormonal,
and local controls regulate blood flow through arterioles.
These control mechanisms play varying roles across our body's organs. Modest degrees of vasoconstriction or vasodilation can greatly affect systemic vascular resistance (Tortora & Derrickson, 2021).
Generalized blood vessels have three layers or tunics surrounding a hollow lumen or
center.
The tunica interna (innermost layer) directly contacts circulating blood and responds to epinephrine (E) and
norepinephrine (NE) with vasodilation
(increase in lumen diameter and blood flow) in digits like the fingers.
The tunica media (middle layer) is composed of smooth muscle and elastic
fibers controlled by sympathetic constrictor fibers (C-fibers).
This is a site of neurally-controlled vasoconstriction (decrease in lumen
diameter and blood flow) in the digits. However, reduced sympathetic firing, exposure to nitric oxide, H+, lactic acid, or blood pressure changes relax the smooth muscle layer (Tortora & Derrickson, 2021).
Finally, the tunica externa or external layer is composed of a connective
tissue sheath. It supplies vessel walls with nerves and self-vessels and connects vessels to tissues.
Separate mechanisms produce hand-warming and hand-cooling. Hand-warming involves releasing a beta-adrenergic hormone and nitric oxide at the tunica interna. Hand-cooling is mediated by vasoconstrictor hormones and the firing of sympathetic C-fibers at the tunica media.
Human studies have demonstrated that hand warming involves the release of beta-adrenergic hormones and nitric oxide (NO). Beta-adrenergic receptors, particularly the ß3 subtype, are present in the cardiovascular system and are activated by catecholamines at high concentrations.
Activation of ß3-adrenergic receptors leads to the production of NO via endothelial NO synthase (eNOS), resulting in vasodilation and increased blood flow (Moens et al., 2010). Epinephrine is likely the more significant catecholamine for ß3 receptor activation, as it induces vasodilation through direct receptor activation and NO-mediated pathways (Arch, 2002; Gauthier, Langin, & Balligand, 1996).
Three Measures of Peripheral Blood Flow
Temperature, blood volume pulse, and pulse wave velocity depend on blood movement through arteries. Temperature and blood volume pulse provide relative measures of peripheral blood flow.
Temperature responds to stimuli in 20-30 seconds, while blood volume pulse reacts in a blazingly fast 0.5-2 seconds.
Temperature
Skin temperature indirectly indexes peripheral blood flow, which is primarily regulated by cutaneous arterioles (Peek, 2016).
Temperature is a gradual tonic index of blood flow. Following a stressor, it may take temperature 20-30 seconds to fall since arterioles must constrict, tissue perfusion with blood must drop, and a sensor called a thermistor must register this change.
"Temperature is the
modality most vulnerable to effort" (Khazan, 2019, p. 90). Since blood volume pulse and temperature monitor the same underlying physiology, "trying" can also produce large-scale disruptions in this modality.
Exposure to cold temperatures, overbreathing, trying too hard, stressors, and worrying can trigger hand-cooling. CO2 loss reduces nitric oxide release, which is needed to relax arteriole walls.
Note: Overbreathing graphic adapted from Inna Khazan.
Blood Volume Pulse
Blood
volume pulse (BVP) is the phasic (momentary) change in blood volume with each heartbeat.
It
is the vertical distance between the maximum value (peak) and the minimum value (trough) of a pulse
wave and is measured by the photoplethysmograph (PPG).
BVP responds to a stressor in 0.5-2 seconds. BVP is faster than temperature because it shines an infrared light on the skin surface instead of a sluggish temperature sensor.
The large-scale BVP changes in hands that are not
cold can help clients when
hand-warming stalls since BVP provides higher-resolution feedback.
The shape of the BVP waveform can indicate loss of arterial elasticity, and decreased pulse transit
time is associated with aging, arteriosclerosis, and hypertension (Izzo & Shykoff, 2001). Peper, Harvey, Lin, Tylova, and Moss
(2007) compared BVP waveforms and BP values for two parents and their teenage daughter in the
recordings below.
Caption: Comparison of finger BVP recording of parents (62-year-old father and 52- year-old mother) and child (17-year-old daughter). The mother has borderline hypertension. The absence of the dicrotic notch in the borderline-hypertensive (top) tracing suggests a stiffening of the arteries indicating increased BP.
BVP amplitude can provide valuable information about a client's cognitive and emotional responses, as shown in the
recording below from Peper, Harvey, Lin, Tylova, and Moss (2007).
Caption: This figure shows psychophysiological responses during a standardized stress protocol. The participant's responsiveness to internal and external physical and emotional stressors is vividly depicted in the variations of BVP amplitude. The pattern portrays decreases in amplitude in BVP signal in response to prompts such as sighs and claps that triggered SNS activation. In this participant, eye closure during the protocol evoked an unanticipated and large decrease in the BVP amplitude compared to any physical or imagined stress conditions. This unanticipated decrease in BVP may be interpreted as a kind of anticipatory anxiety.
Below is a BioGraph ® Infiniti blood volume pulse (BVP) display. Note the small dicrotic notch following
the peak of each waveform. The reduction or disappearance of a dicrotic notch may indicate the loss of arterial
flexibility seen in arteriosclerosis.
The ejection of blood from the left ventricle during systole produces a pulse
wave. Pulse wave velocity (PWV) is the rate of pulse wave movement through the
arteries. Practitioners measure PWV by placing pressure transducers (motion
sensors) at two points of the arterial system (like the brachial and
radial arteries of the same arm). The interval required for the pulse
wave to move between these points is called transit time (TT). Pulse wave
velocity is used as an indirect measure of BP change. During stress tests, researchers have reported correlations with average and systolic (but not diastolic) BP changes.
Veins
Veins are blood vessels that route blood from tissues back to the heart.
Veins contain the same three layers found in arteries.
Smooth muscle allows veins to
adjust diameter actively. The venous system is shown below in blue.
Systemic veins and venules serve as blood reservoirs that store 64% of blood volume at rest. The graphic of blood distribution at rest was created by the author.
A venule is a small vein (10-200 μm in diameter) that collects blood
from capillaries and delivers it to a vein. The low return pressure in
these vessels requires valves that prevent backward blood flow. Venules play an essential role in controlling return blood flow to the
heart due to narrow diameter, contractility, and extensive surface area. The smallest postcapillary venules (10-50 μm in diameter) exchange nutrients and wastes and allow the departure of white blood cells (Tortora & Derrickson, 2021).
Blood vessel graphic was redrawn by minaanandag on fiverr.com.
Capillaries
Capillaries may directly connect arterioles with venules or form extensive networks to rapidly exchange many substances (nutrients and waste products). "The mission of the entire cardiovascular system is to keep blood flowing through capillaries to allow capillary exchange, the movement of substances between blood and interstitial fluid" (Tortora & Derrickson, 2021, p. 781).
Capillaries are the smallest blood vessels (5-10 μm in diameter) and generally consist of a single layer of endothelium and
basement membrane. Change in capillary diameter is passive due to the
absence of a smooth muscle layer. True capillaries extend from
arterioles or metarterioles. A precapillary sphincter functions as a valve that controls blood flow to the tissues at the arterial end of a capillary.
Capillaries exchange nutrients and metabolic end-products
between blood vessels and cells. This exchange is aided by 1-micron-thick
walls, extensive branching, and massive surface area. Capillary
distribution is densest where tissue activity is highest.
Arteriovenous Anastomoses (AVAs)
Arteriovenous anastomoses (AVAs) are junctions of two or more vessels that supply the same
region.
These vessels contain the three
layers seen in both arterioles and venules. Smooth muscle allows
anastomoses to adjust diameter actively. AVAs between arteries reroute blood to tissues or organs when ordinary movements compress a vessel or circulation is obstructed by disease, injury, or a surgical procedure. AVAs also form between veins, arterioles, and venules (Tortora & Derrickson, 2021). Blood vessel graphic was redrawn by minaanandag on fiverr.com.
AVAs bypass capillaries, directly shunt blood from arterioles to venules, and help regulate temperature (Walløe, 2016).
AVAs are all closed when a naked human body is exposed to temperatures around 79 degrees F. They all open as the temperature approaches 97 degrees F. AVA dilation transfers blood from the
epidermis to the interior, cooling the skin. This mechanism is implicated in Raynaud's disease and
phenomenon.
Blood Pressure
Blood pressure is the force exerted by blood as it presses against blood
vessels. In clinical practice, BP refers to the pressure in
arteries.
Cardiac output is the amount of blood pumped by the heart in a minute
calculated by multiplying stroke volume by heart rate. A typical value for a resting adult is 5.25 liters/minute
(70 milliliters x 75 beats/minute). Stroke volume is the amount of blood ejected by the
left ventricle during one contraction.
Heart rate is the number of contractions per minute.
Blood leaving the left ventricle meets resistance or friction due to blood viscosity (thickness), length of blood vessels, and radius. Blood pressure equals cardiac output times resistance.
Self-regulation skills that lower BP reduce cardiac output,
resistance, or both.
Clinicians measure both systolic and diastolic BPs. Systolic
blood pressure (SBP) is the force exerted by blood on arterial walls during
contraction of the left ventricle (called systole). SBP is the upper
value when BP is reported and is about 120 mmHg in young
adult males at rest. Diastolic blood pressure (DBP) is the
force applied against arteries during ventricular relaxation (called
diastole). DBP is the lower value and is about 80 mmHg at rest.
The Heart
The heart is a hollow muscular organ about the size of a closed fist that pumps1,500 to 2,000 gallons of blood each day in the adult cardiovascular system.
You can label the heart's arteries, chambers, and valves on the back of your hand and then place it over your chest to display the relative positions of these structures.
These fibers continue to initiate heartbeats after
surgeons sever all cardiac nerves and remove a heart from the chest cavity for transplantation. Autorhythmic
fibers function as pacemakers and provide a conduction pathway for pacemaker potentials.
The SA node initiates each cardiac cycle in a healthy heart by spontaneously depolarizing its autorhythmic fibers. The SA node's firing of 60-100 action potentials per minute usually prevents slower parts
of the conduction system and myocardium (heart muscle) from generating competing potentials.
The AV node can replace an injured
or diseased SA node as a pacemaker and spontaneously depolarizes 40-60
times per minute. The signal rapidly spreads through the atrioventricular (AV)
bundle reaching the septum's top. Descending right and left bundle
branches conduct the action potential over the ventricles
about 0.2 seconds after the appearance of the P wave.
Conduction myofibers extend from the bundle
branches into the myocardium, depolarizing contractile fibers in the
ventricles (lower chambers). Ventricular depolarization generates the
QRS complex. The ventricles contract (ventricular systole)
soon after the emergence of the QRS complex. Their contraction continues through
the S-T segment. Ventricular contractile fiber depolarization generates the
T wave about 0.4 seconds following the P wave. The ventricles
relax (ventricular diastole) 0.6 seconds after the P wave begins (Tortora & Derrickson, 2021).
Clinicians should examine ECG morphology for evidence of arrhythmias, ischemia, and prolonged Q-T
intervals that could endanger client safety as part of client assessment for HRV biofeedback
training (Drew et al., 2004).
Regulation by the Cardiovascular Center
The cardiovascular (CV) center located in the medulla regulates blood pressure and tissue perfusion by changing HR, stroke volume, systemic vascular resistance, and blood volume. Interconnected neuronal, hormonal, and local negative feedback systems are responsible for immediate (e.g., rushing to class) and long-term BP regulation and redistribution of blood flow (e.g., increased perfusion of skeletal muscles during exercise).
Interconnected CV center neurons
regulate blood vessel diameter, HR, HRV, stroke volume. The CV center contains cardiostimulatory, cardioinhibitory, vasoconstrictor, and vasodilator centers consisting of clusters of neurons. The cardiostimulatory center speeds HR, and the cardioinhibitory center slows it. The vasoconstrictor center narrows blood vessels and the vasodilator center dilates them.
While the SA node generates the normal heartbeat cardiac rhythm, autonomic motor neurons and circulating hormones and ions influence the
interbeat interval (time between adjacent heartbeats; HR) and myocardial contraction force (stroke volume; Tortora & Derrickson, 2021).
Autonomic Control
The CV center regulates the heart and vasomotor tone. Sympathetic cardiac accelerator nerves target the SA node, AV node, and the bulk of the myocardium (heart
muscle). Action potentials conducted by these motor neurons release NE and E. These neurotransmitters bind to beta-adrenergic (β1) receptors located on cardiac muscle fibers. This speeds spontaneous SA and AV node depolarization, increasing HR and strengthening atria and ventricle contractility. In failing hearts, the number of beta-adrenergic receptors is reduced, and their cardiac muscle contraction
in response to NE and E binding is weakened (Ogletree-Hughes et al., 2001).
Parasympathetic
vagus (X) nerves also innervate the SA node, AV node, and atrial cardiac muscle. Graphic adapted by minaanandag on fiverr.com.
Firing by
these motor neurons triggers acetylcholine release and binding to muscarinic (mainly M2) receptors. Cholinergic binding decreases
the rate of spontaneous depolarization in the SA and AV nodes (slowing heart rate). Since there is sparse vagal
innervation of the ventricles, vagal tone minimally affects the ventricular contractility (Tortora & Derrickson, 2021).
Autonomic Balance
There is a dynamic balance between
sympathetic nervous system (SNS) and
parasympathetic nervous system (PNS) influences in a healthy heart. The synergistic relationship between these autonomic branches is complex: sometimes reciprocal, additive, or subtractive (Gevirtz, Schwartz, & Lehrer, 2016).
PNS control predominates at rest, resulting in an
average HR of 75 beats per minute (bpm) that is significantly slower than the SA node's intrinsic rate,
which decreases with age, from an average 107 bpm at 20 years to 90 bpm at 50 years (Opthof, 2000).
The
PNS can slow the heart by 20 or 30 beats per minute or briefly stop it (Tortora & Derrickson, 2021). This control illustrates the response called accentuated antagonism (Olshansky et al., 2011). Parasympathetic nerves exert their effects more
rapidly (< 1 second) than sympathetic nerves (> 5 seconds) (Nunan et al., 2010; Shaffer, McCraty, & Zerr, 2014; Tortora & Derrickson, 2021).
While the SNS can suppress PNS activity, it can also increase PNS reactivity (Gellhorn, 1957). Parasympathetic rebound may occur following high stress levels, resulting in increased nighttime gastric activity (Nada et al., 2001) and asthma symptoms (Ballard, 1999).
Cardiac Regulation by Hormones and Ions
Circulating hormones and ions also influence the heart. Epinephrine, norepinephrine, and thyroid hormones increase
HR and contractibility. The
cations (positive ions) K+, Ca2+, and Na+ significantly affect
cardiac function. While elevated plasma levels of K+ and Na+ decrease HR and
contraction force, high intracellular Ca2+ levels have the opposite effect (Tortora & Derrickson, 2021).
Vasomotor Tone
CV center vasomotor nerves continuously adjust the diameter of the smooth muscle in blood vessel walls. SNS neurons leave the spinal cord via thoracic and first and second lumbar spinal nerves to arterioles, particularly those in the skin and abdominal viscera. These impulses establish
vasomotor tone, moderate tonic vasoconstriction, and resting systemic vascular resistance. SNS signals to most veins result in venoconstriction that empties blood from venous blood reservoirs and raises BP (Tortora & Derrickson, 2021).
Heart Rate
Heart rate (HR; also called stroke rate) is the number of heartbeats per
minute. This value is 75 beats/minute for a resting young adult male.
Resting rates slower than 60 beats/minute (bradycardia) and faster than
100 beats/minute (tachycardia) may indicate a cardiovascular disorder. Typical non-athlete HRs are 60-80 bpm. Athletes may have HRs between 40-60 bpm (Khazan, 2019).
Abnormal or irregular rhythms are called arrhythmias or dysrhythmias (Tortora & Derrickson, 2021).
Elevated HR Is Associated with Dementia and Cognitive Decline
Imahori et al. (2021) conducted a cohort study of 2147 adults ≥ 60 who were free of dementia when they entered the study. Resting heart rates (RHR) ≥80 (compared with 60-69 bpm) were associated with a greater risk of dementia and more rapid cognitive decline, independent of cardiovascular disease (CV).
Elevated HR Limits HRV
Heart rate is significant because a high rate can reduce heart rate variability. Faster HRs allow less time between successive heartbeats for HR to vary. This lowers HRV.
Analysis of HRs in healthy individuals reveals a chaotic pattern.
Heart rate values are not constant but are unpredictable due to multiple hormonal and neural control systems. Successive values might be 65, 78,
72, 86, illustrating the variability of a healthy heart that can
rapidly adapt to changing workloads. Variability is severely reduced in
hearts damaged by cardiovascular disease.
Below is a three-dimensional BioGraph ® Infiniti
heart rate variability (HRV) display of the ECG power spectrum. HRV biofeedback training aims at increasing the power at 0.1 Hz (6
breaths per minute) to maximize healthy variability.
Heart Rate Variability (HRV)
Heart rate variability (HRV) consists of changes in the time intervals between
consecutive heartbeats (Task Force of the European Society of Cardiology and the North American Society of Pacing
and Electrophysiology, 1996). BCIA's Biofeedback Blueprint covers HRV briefly since it offers a separate HRV Biofeedback Certification and Certificate of Completion.
Respiratory sinus arrhythmia (RSA), heart rate speeding and slowing across each breathing cycle, is the primary and entirely parasympathetic source of HRV (Gevirtz, 2020).
Graphic adapted from Elite Academy.
Inhalation partially disengages the vagal brake, speeding heart rate. This is purely parasympathetic. Graphics inspired by Dr. Richard Gevirtz.
Exhalation reapplies the vagal brake, slowing heart rate.
The baroreceptor reflex, which exerts homeostatic control over acute BP changes, is the second-most-important and entirely parasympathetic source of HRV (Gevirtz, 2020).
Slow-paced breathing increases RSA by stimulating the baroreceptor system at its unique resonance frequency (~ 0.1 Hz). The resonance frequency is caused by the delay in the baroreflex (Lehrer et al., 2004). Before HRVB, respiration and the baroreflex are usually out of phase resulting in weak resonance effects.
Resonance is simple physics (Lehrer, 2020). The baroreflex system exhibits resonance since it is a feedback system with a fixed delay. Inertia due to blood volume in the vascular tree accounts for most of this delay.
Resonance frequency breathing also modulates BP changes since HR and BP oscillations are 180° out of phase (DeBoer, Karemaker, & Strackee, 1987; Vaschillo et al., 2002).
Graphic adapted from Evgeny Vaschillo.
Caption: The bottom line represents respiration. A rising black bar is inhalation. and a falling black bar means exhalation. The next lines represent HR and BP. This diagram allows us to see the changes in HR and BP produced by breathing. Starting at the bottom left, inhalation speeds the heart, and about 5 seconds later, BP falls. During exhalation, the heart slows and about 5 seconds later, BP increases.
Before HRVB, respiration and the baroreflex are usually out of phase resulting in weak resonance effects. Graphic adapted from Elite Academy.
HRV biofeedback training slows breathing to the baroreflex's rhythm, which aligns these processes and significantly increases resonance effects. Graphic adapted from Elite Academy.
Slowing breathing to rates between 4.5-6.5 bpm for adults and 6.5-9.5 bpm for children increases RSA (Lehrer & Gevirtz, 2014). Increased RSA immediately "exercises" the baroreflex without changing vagal tone or tightening BP regulation. Those changes require weeks of practice. HRV biofeedback can increase RSA 4-10 times compared to rest (Lehrer et al., 2020b; Vaschillo et al., 2002).
Caption: The red waveform shows HR oscillations while resting without breathing instructions or feedback. The blue waveform shows HR oscillations with HRV biofeedback and breathing from 4.5-6.5 bpm.
You can observe the effect of a breathing rate on RSA during paced breathing and select the rate that produces the largest HR oscillations.
Adult breathing from 4.5-6.5 bpm shifts the ECG peak frequency from the high-frequency band (~0.20 Hz) to the cardiovascular system’s resonance frequency (~0.10 Hz). This more than doubles the energy in the low-frequency band of the ECG (0.04-0.15 Hz).
We train clients to increase low-frequency power and RSA so that high-frequency power and time-domain measures like the RMSSD will increase during baselines when breathing at typical rates (Lehrer, 2020).
Why Is Heart Rate Variability Important?
A healthy heart is not a metronome. When the time intervals between heartbeats significantly change
across successive breathing cycles, this shows that the cardiovascular center can effectively modulate vagal tone.
Dan S@unclebelang on fiverr.com created this Real Genius episode.
The record below shows healthy variability. The time intervals between successive heartbeats differ. Graphic created by Dani S@unclebelang on fiverr.com.
"The complexity of a healthy heart rhythm is critical to the maintenance of homeostasis because it provides the flexibility to cope with an uncertain and changing environment...HRV metrics are important because they are associated with regulatory capacity, health, and performance and can predict morbidity and mortality" (Shaffer, Meehan, & Zerr, 2020).
"... HRV is associated with executive function, regulatory capacity, and health... Cardiac vagal control indexes how efficiently we mobilize and utilize limited self-regulatory resources during resting, reactivity, and recovery conditions" (Shaffer, Meehan, & Zerr, 2020).
Vagal tone modulation helps maintain the dynamic autonomic balance critical to
cardiovascular health. Autonomic imbalance due to deficient vagal inhibition is implicated in increased morbidity
and all-cause mortality (Thayer, Yamamoto, & Brosschot, 2010).
Heart Rate Variability Is a Marker for Disease and Adaptability
Since a healthy cardiovascular system integrates multiple control systems, its overlapping oscillatory patterns
are chaotic.
The double compound pendulum animation from Wikipedia shown below illustrates chaotic behavior.
Slightly changing the pendulum's starting condition results in a radically different trajectory.
A healthy heart exhibits complexity in its oscillations and rapidly adjusts to sudden physical and psychological
challenges due to its effective interlocking cardiac control systems. A healthy heart illustrates the concept of
allostasis or the achievement of stability through change. In contrast, an
aging or diseased heart shows noncomplex oscillations and ineffectively responds to sudden demands due to the
breakdown of its control mechanisms (Lehrer & Eddie, 2013). Check out the YouTube video Heart Rate Variability (HRV) Biofeedback by Mark Stern.
HRV appears to index autonomic functioning, BP, neurocardiac functioning, digestion, oxygen and carbon dioxide exchange, vascular tone (diameter of resistance vessels), and possibly facial muscle regulation (Gevirtz et al., 2016). HRV reflects the vagal contribution to executive functions, affective control, and social self-regulation (Byrd et al., 2015; Laborde et al., 2017; Mather & Thayer, 2018).
Vagal tank theory (Laborde et al., 2018) argues that vagal traffic to the heart indicates how efficiently we mobilize and use scarce self-regulatory resources.
Heart rate variability biofeedback is extensively used to treat various disorders (e.g., asthma and depression) and enhance performance in various contexts (e.g., sports; Gevirtz, 2013; Lehrer et al., 2020a; Tan et al., 2016).
Lehrer et al. (2020) observed that "HRVB has the largest effect sizes on anxiety, depression, anger, and athletic/artistic performance and the smallest effect sizes on PTSD, sleep, and quality of life" (p. 109).
Although the final targets of these applications may differ, HRVB increases vagal tone (Vaschillo et al., 2006) and stimulates the negative feedback loops responsible for homeostasis (Lehrer & Eddy, 2013).
Whereas HRV is desirable, BP variability can endanger health. We require BP stability under constant workloads (Gevirtz, 2020). Graphic adapted from Dr. Gevirtz by Minaanandag on fiverr.com.
Dan S@unclebelang on fiverr.com created this Real Genius episode.
Reduced HRV Is Associated with Disease and Loss of Adaptability
In the early 1960s, researchers found that changes in HRV preceded fetal distress (Hon & Lee, 1963).
Reduced HRV is associated with vulnerability to physical and psychological stressors and disease (Lehrer, 2007).
Prospective studies have shown that decreased HRV is the strongest independent predictor for the progression of coronary atherosclerosis (McCraty & Shaffer, 2015).
Low HRV is a marker for cardiovascular disorders, including hypertension, especially with left ventricular
hypertrophy; ventricular arrhythmia; chronic heart failure; and ischemic heart disease (Bigger et al., 1995;
Casolo et al., 1989; Maver, Strucl, & Accetto, 2004; Nolan et al., 1992; Roach et al., 2004). Low HRV predicts
sudden cardiac death, especially due to arrhythmia following myocardial infarction and post-heart attack survival
(Bigger et al., 1993; Bigger et al., 1992; Kleiger et al., 1987).
Depression in myocardial infarction (MI) patients increases mortality. Depressed patients are twice as likely as non-depressed individuals to have lower HRV (16% vs. 7%). Lower HRV is a strong independent predictor of post-MI death (Craney et al., 2001). HRVB might reduce anxiety and depression associated with low vagal activity because it increases vagal tone. From Friedman’s (2007) perspective, the problem is not “a sticky accelerator.” HRVB may fix “bad brakes” (p. 186).
Reduced HRV is also seen in disorders with autonomic dysregulation, including anxiety and depressive disorders,
and asthma, and vulnerability to sudden infant death (Agelink et al., 2002; Carney et al., 2001; Cohen &
Benjamin, 2006; Giardino, Chan, & Borson, 2004; Kazuma, Otsuka, Matsuoka, & Murata, 1997). Lehrer (2007) believes that HRV indexes adaptability and marshals evidence that increased RSA represents more
efficient regulation of BP, HR, and gas exchange by synergistic control systems.
Heart-Brain Interactions
Thayer and Lane (2000) outline a neurovisceral integration model that
describes how a central autonomic network (CAN) that links the brainstem NST with forebrain structures
(including the anterior cingulate, insula, and ventromedial prefrontal cortex, and the amygdala and
hypothalamus) through feedback and feed-forward loops. They speculate that a breakdown in negative feedback may
produce the increased SNS arousal that characterizes anxiety disorders. Thayer et al. (2012, p. 754) contend
that regions that include the amygdala and medial prefrontal cortex, which evaluate "threat and safety,"
help regulate HRV through their connections with the NST.
Shaffer, McCraty, and Zerr (2014) propose that interconnected cardiac ganglia create an intrinsic nervous system within the heart
that influences the S-A and A-V node pacemakers and forms reciprocal connections with the extrinsic cardiac
ganglia found in the chest cavity and the medulla. The sensory, interconnecting, afferent, and motor neurons within the heart can function independently and constitute a "little brain" on the mammalian heart.
The ascending afferent nerves help to regulate the heart and its rhythms physiologically and influence efferent SNS and PNS activity. From 85-90% of vagus nerve fibers are afferents and more afferents from the heart target the brain than any other major organ.
Afferent signals from the intrinsic cardiac nervous system may affect attention, motivation, perceptual sensitivity, and emotional processing (Shaffer, McCraty, & Zerr, 2014).
MacKinnon, Gevirtz, McCraty, and Brown (2013) reported that HRV influences the amplitude of heartbeat event-related potentials (HERPs). The amplitude of these negative EEG potentials that appear about 200-300 ms after each R-spike indexes cardiac afferent communication with the brain. Both negative and positive emotion conditions reduced HRV and HERP amplitude. In contrast, resonance frequency breathing increased HRV and HERP amplitude above baseline.
The authors speculated that resonance frequency breathing reduces interference with vagal afferent signal transmission from the heart to the cerebral cortex.
0.1 Hz biofeedback: training to concentrate ECG power around 0.1 Hz in the low
frequency (LF) band by teaching patients to breathe diaphragmatically at their resonance frequency around 6
breaths per minute and experience positive emotional tone to maximize HR variability.
accentuated antagonism: the ability of PNS neurons to slow or stop the heart.
allostasis: the maintenance of stability through change by mechanisms that anticipate challenge and adapt through behavior and physiological change.
alpha-adrenergic receptors: G protein-coupled receptors for the catecholamines
epinephrine and norepinephrine. The binding of these catecholamines to arteriole alpha-adrenergic receptors can produce hand-cooling.
arrhythmias: abnormal or irregular rhythms, also called dysrhythmias.
artery: blood vessels that carry blood away from the heart and are
divided into elastic and muscular arteries and arterioles.
arteriole vasoconstriction: the decreased diameter of an arteriole's lumen
due to activation of vasoconstricting sympathetic nerves that act on alpha-adrenergic receptors, circulating
hormones, and local chemical factors.
arteriole vasodilation: the increased diameter of an arteriole's lumen due
to the circulation of a beta-adrenergic agent in the blood. There are no vasodilating nerves in the fingers.
arteriole: an almost-microscopic blood vessel that
delivers blood to capillaries and anastomoses.
arteriovenous anastomoses (AVAs): an end-to-end joining of blood vessels.
atrioventricular (AV) bundle: cardiac cells that conduct electrical impulses
from the AV node to the top of the septum.
atrioventricular (AV) node: one of two internal pacemakers primarily
responsible for the heart rhythm, located between the atria and the ventricles.
baroreflex: the baroreceptor reflex that provides negative feedback control of
BP. Elevated BP activates the baroreflex to lower BP, and low BP
suppresses the baroreflex to raise BP.
β-adrenergic agent: a molecule that binds to a beta-adrenergic receptor to
start the cascade that causes hand-warming.
β3-adrenergic receptors: G protein-coupled receptors activated mainly by epinephrine and norepinephrine, leading to vasodilation directly and through nitric oxide (NO) release.
β-adrenergic receptors: G protein-coupled receptors for the catecholamines
epinephrine and norepinephrine. Catecholamine binding to the lumen of an arteriole is
responsible for hand-warming.
blood pressure: the force exerted by blood as it presses against arteries.
blood reservoir: systemic veins and venules contain 64% of blood in a resting body.
blood volume pulse (BVP): the phasic change in blood volume with each
heartbeat. It is the vertical distance between the minimum value (trough) of one pulse wave and the maximum value
(peak) of the next measured using a photoplethysmograph (PPG).
bundle branches: fibers that descend along both sides of the septum (right and
left bundle branches) and conduct the action potential over the ventricles about 0.2 seconds after the appearance of the
P wave.
capillary: blood vessels found near almost all cells that may directly connect arterioles with venules or form extensive networks for rapid exchange of a large volume of substances (nutrients and waste products).
cardiac accelerator nerves: SNS neurons that increase HR and the force of the heart's contraction.
cardiac cycle: one cycle consists of systole (ventricular contraction) and
diastole (ventricular relaxation).
cardiac output: the amount of blood pumped by the heart in a minute
calculated by multiplying stroke volume times HR. In a normal, resting adult, this is 5.25 liters/minute (70 milliliters x 75 beats/minute).
cardioinhibitory center: CV center neurons that inhibit the heart.
cardiostimulatory center: CV center neurons that stimulate the heart.
cardiotachometer: device that measures the frequency of ventricular
contraction beat-to-beat.
cations: positive ions like K+, Ca2+, and Na+.
chaos: unpredictability due to non-linear dynamics.
conduction myofibers: the fibers that extend from the bundle branches into the
myocardium, depolarizing contractile fibers in the ventricles.
diastole: the period when the ventricles or atria relax.
diastolic blood pressure (DBP): the force applied against arteries during
ventricular relaxation.
dilation: an increase in blood vessel lumen diameter.
dysrhythmias: arrhythmia.
elastic artery: large arteries like the aorta that distribute blood from the
heart to muscular arteries.
electrocardiogram (ECG): a recording of the heart's electrical activity using an electrocardiograph.
frequency-domain measures of HRV: the calculation of the absolute or relative power of the HRV signal within four frequency bands.
hand-cooling: reduced peripheral blood flow mainly controlled by
vasoconstricting sympathetic nerves that act on alpha-adrenergic receptors. Circulating hormones and local factors
also reduce the arteriolar diameter.
hand-warming: increased peripheral blood flow primarily due to
circulating hormones and local vasodilators. There are no vasodilating nerves in the fingers, although they exist
in the forearm.
heart: the hollow, muscular organ, about the size of a closed fist that contains
four chambers (two ventricles and two atria) that function as two pumps.
heart rate: the number of heartbeats per minute, also called stroke rate.
heart rate variability (HRV): beat-to-beat changes in HR, including changes in the RR intervals between consecutive heartbeats.
high coherence: a single high amplitude peak in the 0.09-0.14 Hz range.
high-frequency (HF) band: ECG frequency range from 0.15-0.40 Hz representing the inhibition and activation of the vagus nerve by breathing (RSA).
interbeat interval (IBI): the time interval between the peaks of successive
R-spikes (initial upward deflections in the QRS complex). This period is also called the NN (normal-to-normal)
interval.
left atrium: the heart's upper chamber that receives oxygenated blood from
the pulmonary veins and pumps it to the left ventricle.
left ventricle: the heart's lower chamber that receives oxygenated blood
from the left atrium and pumps it through the aorta.
low-frequency (LF) band: ECG frequency range of 0.04-0.15 Hz that may
represent the influence of PNS and baroreflex activity when breathing at the resonance frequency.
medium-sized muscular arteries: arteries like the brachial artery that receive
blood from elastic arteries and distribute blood throughout the body.
neurovisceral integration model: a hypothesis that a central autonomic network (CAN) links the brainstem NST with forebrain structures
(including the anterior cingulate, insula, and ventromedial prefrontal cortex, and the amygdala and
hypothalamus) through feedback and feed-forward loops.
nitric oxide: an endothelium-derived signaling molecule that induces peripheral vasodilation by activating guanylate cyclase in vascular smooth muscle cells, increasing cyclic guanosine monophosphate (cGMP) levels, and promoting muscle relaxation and increased blood flow.
nucleus ambiguus system: the nucleus dorsal to the inferior olivary nucleus of the
upper medulla that gives rise to vagus nerve motor fibers.
P wave: an ECG structure produced as contractile fibers in the atria depolarizes and culminates in the atria's contraction (atrial systole).
parasympathetic vagus (X) nerves: cranial nerves that arise from the medulla's
cardiovascular center, decrease the rate of spontaneous depolarization in SA and AV nodes, and slow the HR
from the SA node's intrinsic rate of 100 beats per minute.
person effect: Taub and School's (1978) observation that biofeedback training
is a social situation and that a client's relationship with the therapist may be the most critical aspect of
training.
photoplethysmograph (PPG): a device that measures the relative amount of blood
flow through tissue using a photoelectric transducer.
postcapillary venule: the smallest venules that exchange nutrients and wastes and allow the departure of white blood cells.
precapillary sphincter: in capillaries, a valve at the arterial end of a
capillary that controls blood flow to the tissues.
pulse wave velocity (PWV): the rate of pulse wave movement through the arteries that is
measured by placing pressure transducers (motion sensors) at two points of the arterial system (like the
brachial and radial arteries of the same arm).
QRS complex: the ECG structure that corresponds to the depolarization of the
ventricles.
Raynaud's patients: individuals diagnosed with Raynaud's disease or
phenomenon exhibit abnormal anastomoses dilation in response to mild cold-related
stimuli.
regulatory capacity: the ability to adaptively respond to challenges like exercise and stressors.
respiratory sinus arrhythmia (RSA): respiration-driven heart rhythm that
contributes to the high frequency (HF) component of HRV. Inhalation inhibits vagal nerve
slowing of the heart (increasing HR), while exhalation restores vagal slowing (decreasing HR).
response coupling: responses that change together (HR up, BP
up).
response fractionation: responses that change independently (HR down,
BP up).
resonance frequency: the frequency at which a system, like the cardiovascular
system, can be activated or stimulated.
right atrium: the heart's upper chamber that receives deoxygenated blood
and pumps it into the right ventricle.
right ventricle: the heart's lower chamber that receives deoxygenated blood
from the right atrium and pumps it into the pulmonary artery.
R-spike: the initial upward deflection in the QRS complex of the ECG.
sinoatrial (SA) node: the heart node that initiates each cardiac
cycle through spontaneous depolarization of its autorhythmic fibers.
skin temperature: an indirect index of peripheral blood flow, primarily regulated by cutaneous arterioles.
spectral analysis: the division of HRV into its component
rhythms that operate within different frequency bands.
S-T segment: the ECG structure that connects the QRS complex and the T wave.
Ventricular contraction continues through the S-T segment.
stroke volume: the amount of blood ejected by the left ventricle during one contraction.
sympathetic cardiac accelerator nerves: nerves that arise from the medulla's
cardiovascular center that increase the rate of spontaneous depolarization in the SA and AV nodes and increase
stroke volume by strengthening the contractility of the atria and ventricles.
systole: the contraction of the left ventricle.
systolic blood pressure (SBP): the force exerted by blood on arterial walls during
contraction of the left ventricle.
T wave: the ECG structure that represents ventricular repolarization.
transit time (TT): in pulse wave velocity, the interval required for the pulse
wave to move between two points of the arterial system.
tunica externa: the external layer of an artery composed of a connective
tissue sheath.
tunica media: the middle layer of an artery composed of smooth muscle and elastic fibers and controlled by sympathetic constrictor fibers (C-fibers). This layer is a site of neurally-controlled
vasoconstriction (decrease in lumen diameter and blood flow) in the digits.
ultra-low-frequency (ULF) band: ECG frequency range below 0.003 Hz. Very slow biological processes that may contribute to this band include circadian rhythms, core body temperature, metabolism, and the renin-angiotensin system. There may also be PNS and SNS contributions.
vagal tank theory: the hypothesis that vagal traffic to the heart indicates how efficiently we mobilize and use scarce self-regulatory resources.
vagal withdrawal: the sympathetic suppression of parasympathetic activity association with anxiety, effort, and fear.
vagus nerves: the parasympathetic vagus (X) nerves decrease the rate of
spontaneous depolarization in the SA and AV nodes and slow HR. HR increases may reflect
reduced vagal inhibition.
vasomotor nerves: SNS neurons that innervate arterioles and veins.
vasomotor tone: the moderate arteriole constriction that creates resting systemic vascular resistance.
vein: blood vessels that return blood from tissues back to the heart.
venule: a microscopic vessel formed by
capillaries that delivers blood to a vein.
very-low-frequency (VLF): ECG frequency range of 0.003-0.04 Hz may represent temperature regulation, gastric, plasma renin fluctuations, endothelial, physical activity influences, possible intrinsic cardiac nervous system, PNS, and SNS contributions.
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Assignment
Now that you have completed this module, describe how this module has
changed your understanding of hand-warming. Also, explain when blood
volume pulse feedback could be more useful than temperature biofeedback.
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