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).
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 subject, task, and environmental
variables.
I. HRV Anatomy and Physiology: A. Cardiac Anatomy and Physiology.
Professionals completing this unit will be able to discuss:
A. How the ECG is generated
B. Sympathetic and parasympathetic influences
C. Heart-brain interactions
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. Arterioles are almost microscopic (8-50 microns in diameter)
that deliver blood to capillaries and anastomoses. Graphics by minaanandag on fiverr.
Arterioles are responsible for roughly 50% of peripheral resistance through their narrow diameter,
contractility, and massive surface area. The video below shows red blood cells
traveling through a pulsating arteriole.
The control of arteriole diameter, which is crucial for regulating
BP and hand temperature, is highly complex. Neural, hormonal,
and local controls cooperate to regulate blood flow through arterioles.
These control mechanisms play varying roles across our body's organs.
All arteries have three layers or tunics surrounding a hollow lumen or
center. The tunica interna (innermost layer) 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.
Finally, the tunica externa or external layer is comprises a connective
tissue sheath.
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.
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, 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.
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 using 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 BVP signal amplitude 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 the physical or imagined stress conditions. This unanticipated decrease in BVP may be interpreted as 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.
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 along 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.
Researchers have reported correlations with average and systolic (but not
diastolic) BP changes during stress tests.
Veins
Veins are blood vessels that route blood from tissues back to the heart.
Veins contain the same three layers found in arteries.
A venule is a small vein (less than 2 millimeters 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 are essential in controlling return blood flow to the
heart due to their narrow diameter, contractility, and extensive surface area.
Graphic redrawn by minaanandag on fiverr.com.
Capillaries
Capillaries may directly connect arterioles with venules or form extensive networks to rapidly exchange a large volume of substances (nutrients and waste products).
A capillary generally consists 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.
AVAs bypass capillaries, directly shunt blood from arterioles to venules, and help regulate temperature (Walløe, 2016).
These vessels contain the three
layers seen in both arterioles and venules. Smooth muscle allows
anastomoses to adjust diameter actively. Graphic redrawn by minaanandag on fiverr.com.
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 both Raynaud’s disease and
Raynaud’s 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), blood vessel length, and blood vessel
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 (under resting conditions). 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 (under resting
conditions).
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 top of the septum. 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 an assessment for HRV biofeedback
training (Drew et al., 2004).
Regulation by the Cardiovascular Center
While the SA node generates the normal heartbeat cardiac rhythm, autonomic motor neurons, circulating hormones, and ions influence the
interbeat interval (time between adjacent heartbeats) and myocardial contraction force. The
cardiovascular center, located in the medulla of the brainstem, integrates sensory information from
proprioceptors (limb position), chemoreceptors (blood chemistry), and baroreceptors (BP) as well as
information from the cerebral cortex and limbic system. The cardiovascular center responds to sensory and higher
brain center input by adjusting autonomic balance via sympathetic and parasympathetic motor neurons (Tortora & Derrickson, 2021).
Sympathetic Control
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 on cardiac muscle fibers. This speeds spontaneous SA and AV node depolarization (increasing HR) and strengthens the atria and ventricles' 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 Control
Like cardiac accelerator nerves, the left and right parasympathetic
vagus (X) nerves also innervate the SA node, AV node, and atrial cardiac muscle.
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 of 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, 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).
Heart Rate
Heart rate (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).
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, and 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).
Clinicians can monitor HRV using ECG and respiration sensors, as shown below.
Heart-Brain Interactions
Thayer and Lane (2000) outline a neurovisceral integration model that
describes how a central autonomic network (CAN) links the brainstem NST with forebrain structures
(including the anterior cingulate, insula, ventromedial prefrontal cortex, 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.
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 above baseline and increased HERP amplitude.
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.
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.
arteries: blood vessels that carry blood away from the heart and that 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.
arterioles: the almost-microscopic (8-50 microns in diameter) blood vessels that
deliver blood to capillaries and anastomoses. Arterioles may control up to 50% of peripheral resistance through
their narrow diameter, contractility, and massive surface area that follows a fractal pattern.
arteriovenous anastomoses (AVAs): junctions of two or more vessels that
supply the same region, directly shunt blood from arterioles to venules, and help to regulate temperature.
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: 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.
beta-adrenergic agent: a molecule that binds to a beta-adrenergic receptor to
start the cascade that causes hand-warming.
beta-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 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.
capillaries: blood vessels that are 7-9 microns in diameter, found near almost
all cells, and may directly connect arterioles with venules or form extensive networks for rapid exchange of
a large volume of substances (nutrients and waste products).
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. This is 5.25 liters/minute (70 milliliters x 75 beats/minute) in a
normal, resting adult.
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: 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: increased lumen diameter.
dysrhythmias: an arrhythmia.
elastic arteries: 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: a 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 upper chamber of the heart that receives oxygenated blood from
the pulmonary veins and pumps it to the left ventricle.
left ventricle: the bottom chamber of the heart that receives oxygenated blood
from the left atrium and pumps it through the aorta.
low-frequency (LF) band: the ECG frequency range of 0.04-0.15 Hz that may
represent the influence of PNS, SNS, and baroreflex activity (when breathing at resonance frequency).
medium-sized muscular arteries: arteries like the brachial artery that receive
blood from elastic arteries and distribute blood throughout the body.
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.
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 along the arterial system (like the
brachial and radial arteries of the same arm).
QRS complex: an ECG structure that corresponds to the depolarization of the
ventricles.
Raynaud's patients: medical patients diagnosed with Raynaud’s disease or
Raynaud’s 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 change together (HR up, BP
up).
response fractionation: responses 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 upper chamber of the heart that receives deoxygenated blood
and pumps it into the right ventricle.
right ventricle: the lower chamber of the heart 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 node of the heart that initiates each cardiac
cycle through spontaneous depolarization of its autorhythmic fibers.
skin temperature: an indirect index of peripheral blood flow, which is primarily regulated by cutaneous arterioles.
spectral analysis: the division of HRV into its component
rhythms that operate within different frequency bands.
S-T segment: an 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: 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 along 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: the 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 withdrawal: sympathetic suppression of parasympathetic activity associated with anxiety, effort, and fear.
vagus nerve: the parasympathetic vagus (X) nerve decreases the rate of
spontaneous depolarization in the SA and AV nodes and slows the HR. Heart rate increases often reflect
reduced vagal inhibition.
veins: blood vessels that route blood from tissues back to the heart and
contain the same three layers found in arteries. These layers are thinner in veins due to lower pressure.
venule: a small vein (less than 2 millimeters 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.
very-low-frequency (VLF): the ECG frequency range of 0.003-.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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Berntson, G. G., Quigley, K. S., & Lozano, D. (2007). Cardiovascular psychophysiology. In
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