Normal blood pressure (BP) is now defined as below 120/80 mmHg. This diagnostic change in 2017 increased the number of patients who are candidates for behavioral and medical intervention.
Biofeedback has demonstrated efficacy and
cost-effectiveness in
cardiovascular disorders like essential
hypertension. In essential hypertension, research has shown that effective
interventions share critical components and that models predict treatment success and the size of BP reductions.
For many clients, weight loss, stress management training, and SEMG and temperature biofeedback are among the best-documented
cardiovascular interventions.
The treatment paradigm for cardiovascular disorders is
shifting from only fixing a "stuck accelerator" to also fixing "bad brakes." Instead of exclusively addressing SNS overactivity, clinicians increasingly explore interventions that increase vagal tone and heart rate variability.
This unit addresses the Pathophysiology, biofeedback modalities, and treatment protocols for specific ANS biofeedback applications (V-D).
This unit covers Essential Hypertension, Vasovagal Syncope, Heart Failure and Coronary Artery Disease, and Cardiac Arrhythmias.
Please click on the podcast icon below to hear a full-length lecture.
EVIDENCE-BASED PRACTICE (4TH ED.)
We have updated the efficacy ratings for clinical applications covered in AAPB's Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).
Essential Hypertension
Blood Pressure Mechanics
Blood pressure (BP) is the product of
cardiac output (amount of blood
pumped by the heart) and systemic vascular
resistance. Systemic vascular resistance represents all systemic blood vessels' total resistance and is influenced by blood viscosity (thickness) and blood vessel length and radius.
Cardiac output is the product of
stroke volume (amount of blood ejected with each beat) and
stroke rate (number of beats per minute).
Arterioles (small arteries) play a
significant role in controlling systemic vascular resistance. A minor
adjustment in arteriole diameter can significantly change systemic
vascular resistance and, consequently, BP and tissue
perfusion (Tortora & Derrickson, 2019).
Stage 1 hypertension (elevated BP) is defined when systolic BP (SBP) is 130 mmHg or higher and/or diastolic BP (DBP) is > 80 mmHg or higher.
The 2017 American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines (Whelton et al., 2017) are shown below.
The 2017 guidelines classify 103 million Americans as hypertensive instead of 72 million under the 2003 National Heart, Lung, and Blood Institute (NHLBI) guidelines. Under the 2017 guidelines, 50% of men and 38% of women are considered hypertensive.
The NIH Systolic Blood Pressure Intervention Trial (SPRINT) treatment of high-risk hypertensive patients 50 years or older to a SBP of 120 mmHg reduced cardiovascular events by 30% and all-cause mortality by almost 25%, compared to a target of 140 mmHg (Medscape, 2015).
McEvoy and colleagues (2016)
warned that medical treatment to reduce SBP below 140 mmHg should not allow DBP to fall below 70 mmHg, particularly below 60 mmHg, because this could threaten the delivery of blood to the heart. Low DBP values were independently associated with progressive heart damage, coronary heart disease, and death.
Demographics
One-third of Americans and two-thirds over 60 are hypertensive (Benjamin et al., 2018). African Americans and patients diagnosed with diabetes have a higher prevalence of hypertension. Patients with elevated BP may progress to hypertension without lifestyle and drug intervention (Huether et al., 2020).
Hypertension Symptoms
While elevated BP can be "silent," diverse symptoms like blurred vision and swelling ankles (edema) may accompany this chronic health condition.
Hypertension Complications
Researchers have reported that slight blood pressure elevations in middle age are associated with a 30% greater risk of dementia or cognitive impairment in two decades. Medication that lowers BP can reduce this risk (Hughes et al., 2020).
Goedde, Kabins, and Koenig (2007) explored the effects of
patient speech on BP in a study that involved 55 undergraduates (28 men and 27 women). SBP was 11.4 mmHg lower, and DBP was 11.6 mmHg lower during silence than speech. These findings suggested that patient conversation while taking BP could elevate their readings.
The infographic below, adapted from Elizaveta Galkina in the December 16, 2024 the Wall Street Journal article, "Your Blood Pressure Reading Is Probably Wrong," summarizes mistakes that can elevate blood pressure measurements.
Do not ingest caffeine within 30 minutes of measurement.
Essential hypertension is a heterogeneous disorder produced by diverse
genetic and environmental factors that impact circulating blood volume and peripheral vascular resistance.
Autonomic imbalance, involving sympathetic overactivity and parasympathetic
underactivity, plays an vital role in developing essential hypertension. Demographic factors (age,
gender, and ethnicity) and psychological factors (depression, anger, and anxiety) influence BP
(McGrady & Moss, 2013).
Based on twin studies and the Framingham Heart Study, the heritable component of BP ranges from 33-57% (Madhur, 2014).
Recommended Lifestyle Changes
Potential SBP reductions for hypertensive patients will vary by individual. Weight loss is the most effective lifestyle change due to the multiple pathways by which obesity can increase BP. About 60% of hypertensive patients and 25% of normotensive individuals are salt-sensitive. From 4-5% of individuals experience lower BP when they ingest salt (Harvard Heart Letter, August 2019). Stress management can make valuable contributions to BP control.
The main drugs used to treat hypertension include diuretics, ACE
inhibitors, beta-blockers, and calcium channel blockers.
Diuretics reduce blood volume by
removing water and salt in urine.
ACE inhibitors block angiotensin II
formation, resulting in vasodilation (reducing systemic vascular
resistance) and reduced aldosterone secretion.
Beta-blockers inhibit renin secretion and decrease heart rate
and cardiac contractibility. Finally, calcium
channel blockers slow Ca2+ entry into myocardial fibers,
reducing the heart's workload and contraction force.
Biofeedback
interventions can interact with anti-hypertensive medication resulting
in significant BP reductions. Patients should monitor their
BP daily and discuss medication adjustments with
their physician before making changes on their own.
A Pathways Model Intervention
Click on the Read More button to learn about hypertension treatment using McGrady and Moss' Pathways Model.
Richard was a 45-year-old mildly overweight Caucasian male with a 10-year history of stage 1 hypertension. While his BP was well controlled using a combination of an ACE inhibitor and beta-blocker, he wanted to reduce his reliance on medication. His Level One interventions were to (1) track his daily steps and gradually increase them to 10,000 steps per day, (2) record his alcohol and food intake and weigh himself weekly, (3) log his BP every morning after he woke up, and (4) take a large movement break every hour.
He initiated his Level Two interventions 1 month later since his BP had not yet significantly decreased. These steps included (1) recruiting an exercise partner for 35-minute walks at least five times a week and (2) practicing slow, abdominal breathing using an Institute of HeartMath Inner Balance HRV biofeedback training system. At this time, he added a new Level One intervention, which was listening to classical music at home for at least 30 minutes per day.
After 2 months, his blood pressure had gradually declined, but he had made no progress reducing his weight. He added a new Level One intervention of using an activity tracker to measure and log his sleep and to adjust his work schedule to ensure 8 hours of sleep each night. His single Level Three intervention was to consult twice with a licensed dietician to assess and modify his diet. Dietary counseling guided him to reduce saturated fats and simple carbohydrates by adopting a Mediterranean diet.
At the end of 6 months, Richard's diet, sleep, and energy had significantly improved. His physician encouraged him to eliminate the beta-blocker and halve the dosage of his ACE inhibitor while continuing daily charting of his blood pressure. His BPs declined to the normotensive range, his blood lipids were normal, and he lost 15 pounds. At 1-year follow-up, his BPs remained well controlled on reduced medication. He continued his Mediterranean diet, but regained half of the weight he had lost, and his sleep continued to be excellent.
Richard's case history shows that the success of biofeedback can depend on the foundation provided by Level One and Level Two interventions. Richard's self-monitoring of his BP, diet, physical activity, sleep, and weight, and self-directed HRV biofeedback practice, helped him develop mindfulness. His recruitment of an exercise partner leveraged the power of a social network to motivate him to exercise. He ensured his safety by partnering with his physician to reduce his medication gradually and logging his progress. Finally, while he should celebrate his success in losing weight, he might consider how to get back on the "path" to more consistent weight control.
McGrady's (1996) Analysis of Efficacy Studies with the Best Outcomes
McGrady (1996) identified six factors
in efficacy studies reporting the largest and most consistent BP reductions.
Prediction Models of Clinical Response to Biofeedback
McGrady and Higgins (1989) and Weaver and McGrady (1995) studied
unmedicated white adult males with mild to moderate hypertension. These
patients received SEMG and temperature biofeedback, autogenic training,
home practice, and BP monitoring.
The most responsive patients showed a high heart rate, cool hands, high
SEMG, and elevated plasma renin activity. The best predictors of how much
BP decreased were high heart rate, cool hands, high anxiety,
and high-normal cortisol.
A multi-modal strategy that combines biofeedback, relaxation training, and medical management may be most effective for patients whose BP reacts to stressors (Frank et al., 2010).
Blood Pressure Reduction Mechanisms
Patients can lower BP through multiple mechanisms: by
reducing cardiac output, cortisol and norepinephrine levels, skeletal
muscle contraction, systemic vascular resistance, and stimulating the
baroreflex.
Different hypertension treatments may operate through various
mechanisms. Temperature biofeedback may reduce systemic vascular resistance and plasma norepinephrine levels
(McCoy et al., 1988). Relaxation training may reduce
cardiac output (Gervino & Veazey, 1984), and deep
muscle relaxation may lower cardiac output and plasma
norepinephrine. The multi-modal therapy used by McGrady and colleagues
reduced plasma cortisol levels (McGrady, Woerner, Bernal, & Higgins,
1987).
Gevirtz (2005) observed that when
individuals breathe at their resonance frequency, heart rate and BP are 180o out of phase, which
implies that breathing about six times per minute stimulates the
baroreflex. He proposes that resonance frequency biofeedback may lower BP
by stimulating the baroreflex.
Effects of Prescription Medication
Prescription medications and social drugs can affect biofeedback
measurements.
Inderal, which produces
peripheral vasodilation, can raise hand temperature, so that patient temperature
measurements appear healthy, 92° F (33.3° C) instead of 88° F (31.1° C). When
medication artificially raises hand temperature, the clinician should
train the patient to achieve a higher value.
Medications (Cafergot and Fiorinal) or beverages that contain caffeine
can increase heart rate and constrict peripheral blood vessels. Since
these effects could interfere with BP reduction, the
clinician should consult with the patient’s physician to gradually
eliminate or restrict caffeine intake.
Nicotine can also potentially
interfere with biofeedback treatment to lower BP since it
raises heart rate and is a potent vasoconstrictor. Smoking cessation
treatment should be considered in these cases.
Designing a Treatment Program for Your Client
McGrady's (1996) six factors for
successful hypertension interventions, reviewed earlier, should be the foundation of any
treatment program. Essential hypertension treatment should be tailored to
your client based on detailed medical and behavioral
assessments. Biofeedback for hypertension should not be attempted without
a recent medical workup and continuing communication with your patient's
physician. Medical oversight can be critical throughout treatment and
especially when medication requirements change.
Following the medical evaluation, a biofeedback practitioner should evaluate a
patient diagnosed with essential hypertension with a psychophysiological
profile to identify which response systems require training. A multi-modal strategy that retrains
dysregulated systems, promotes relevant lifestyle changes,
and teaches stress management when needed shows the most clinical
promise.
Biofeedback Studies
Biofeedback is superior to control
treatments for both white coat and essential hypertension (Nakao, Nomura,
Shimosawa, Fujita, & Kuboki, 2000) and for primary and secondary
hypertension (Nakao et al., 1999). Thermal and electrodermal biofeedback appear superior to direct BP biofeedback (Linden & Moseley, 2006).
Click on the Read More button to review research studies supporting the efficacy of biofeedback.
Green, Green, and Norris (1979)
estimated that 75-80% of their hypertensive patients achieved normal
pressures without medication. The Menninger program treated 54 medicated
patients from 1975 to 1983. The protocol included breathing
modification, autogenic biofeedback for the hands to reach 95° F (35° C) and then the feet to achieve
93° F (33.9° C), and
frontal SEMG training in 18-26, 1-hour sessions. These researchers
stressed home practice twice a day using autogenic biofeedback, daily
BP monitoring, and diaries of relaxation practice. Thirty-two of 42 medicated patients reduced pressure 15/10 mmHg at a 33-month follow-up (Fahrion et al., 1987).
Blanchard et al. (1986) compared
temperature biofeedback with autogenic exercises against Progressive
Relaxation. The temperature biofeedback group was superior to the
Progressive Relaxation group 1 month following treatment and 1 year
following treatment. Thirty-five percent of the temperature biofeedback group remained off their 2nd
stage medication for over 12 months. The temperature biofeedback
group had a 50% long-term success rate compared with 37.5% for the
Progressive Relaxation group.
McCoy et al. (1988) compared 16
sessions of temperature biofeedback with 8 sessions of Progressive
Relaxation. The temperature biofeedback group reduced mean arterial
pressure and plasma norepinephrine in supine and standing positions. The
Progressive Relaxation group did not change on either measure. These
results are consistent with the model that temperature biofeedback
reduces hypertension by reducing peripheral sympathetic activity.
Garcia-Vera, Labrador, and Sanz (1997)
examined the effectiveness of stress management training for essential
hypertension. The authors randomly assigned 43 patients diagnosed with
essential hypertension to one of two conditions: seven sessions of
education, relaxation, and problem-solving training or a wait- list
control. After 2 months, the stress management group reduced blood pressure 17/13 mmHg compared to 6.9/47 mmHg for the wait-list condition.
Jacob et al. (1991) reported a
meta-analysis over 75 treatment groups and 41 control groups. The
treatment groups produced markedly greater BP reductions than
control groups. Stress management, SEMG biofeedback, and temperature biofeedback produced the greatest blood pressure reductions, respectively. Relaxation and blood pressure biofeedback produced the smallest systolic reductions whereas meditation produced the smallest diastolic reductions.
Yucha et al. (2001) reported
a meta-analysis of 23 studies between 1975 and 1996 that compared
biofeedback training with active treatments like meditation and inactive
treatments like sham biofeedback controls and BP measurement.
Both biofeedback and active treatments produced significant and equivalent SBP and DBP reductions.
Biofeedback achieved greater SBP (6.7 mmHg) and DBP (3.8 mmHg)
reductions than the inactive treatments. Carolyn Yucha is shown below.
Rau, Bührer, and Weitkunat (2003)
studied the effects of R-wave-to-pulse interval
(RPI) biofeedback on 12 participants with high BP
and 10 with low BP. The R-wave-to-pulse interval is the time
elapsed between the R-wave of the ECG and the maximum amplitude of the
peripheral pulse wave during a single cardiac cycle. Participants
received three sessions over two weeks in which BP decreases
(high BP) or BP increases (low BP)
were rewarded. The high BP group decreased SBP 15.3 mmHg and DBP 17.8 mmHg from the start
of training session 1 to the end of training session 3. The low BP group increased SBP 12.3 mmHg and DBP 8.4 mmHg from the start of training session 1 to the end
of training session 3.
Xu et al. (2007)
compared SEMG biofeedback combined with relaxation training with a control condition. Prehypertensive students who received combined treatment decreased both systolic and DBP compared to the control group.
Wang et al. (2010) conducted a randomized controlled trial with prehypertensive post-menopausal women. They compared the effects of 10 sessions of
slow abdominal breathing with frontal SEMG biofeedback with 10 sessions of slow abdominal breathing on BP in 22 prehypertensive post-menopausal women. The researchers trained subjects to breathe at 6 breaths
per minute. They assigned all participants to daily home practice. The researchers randomly assigned the participants to
the experimental or control conditions. Experimental participants, who received combined SEMG biofeedback and slow
abdominal breathing training, decreased SBP 8.4 mmHg and DBP 3.9 mmHg.
Control participants, who only received slow abdominal breathing training, decreased SBP 4.3
mmHg. The experimental group achieved larger BP reductions than the control group and increased the
RR interval. Both groups increased SDNN.
Zerr, Allen, and Shaffer (2015)
conducted a meta-analysis of 10 randomized controlled studies of device-guided breathing (DGB), which enrolled 573 hypertensive patients. Eight studies used a device known as RESPeRATE, while two used a Breathe with Interactive Music (BIM) instrument (both developed by InterCure Ltd., Israel). Compared with controls, DGB resulted in non-significant reductions with trivial effect sizes for both SBP and DBP measures. Moderator analyses revealed no significant differences in effect size for the type of hypertension (essential, secondary, or mild) or whether or not the authors had a conflict of interest with the device manufacturers. The authors proposed that further research should implement significantly longer training periods and incorporate follow-up assessment at 6 and 12 months to better evaluate DGB’s potential.
Heart rate variability biofeedback studies are summarized below.
Clinical Efficacy
Based on three RCTs for essential hypertension and five for pre-hypertension treatments, Angele McGrady (2023)
rated biofeedback for essential hypertension as level 4 -
efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.).
The biofeedback interventions trained participants to lower electrodermal and SEMG activity, and SBP, and increase HRV.
Participants lowered DBP and SBP, and increased baroreflex sensitivity (BRS). If the baroreflex system reacts strongly to a small BP change, BRS would be high. If it reacts weakly, BRS would be low.
Vasovagal Syncope
Syncope is a temporary loss of consciousness (LOC). Vasovagal syncope (VVS), also called neurocardiogenic syncope, features a brief LOC, frequently while standing.
Neurocardiogenic syncope is the most common cause of loss of consciousness in otherwise normal individuals. About 50% of the United States population may experience an episode of syncope during their lifetime, and it accounts for 1-3% of emergency room visits and 6% of hospital admissions each year (Morag, 2015).
Biofeedback Studies
BART has been used to treat VVS, including SEMG and thermal biofeedback, autogenic and progressive relaxation training.
Click on the Read More button to review research studies evaluating biofeedback's efficacy in treating VVS.
McGrady, Bush, and Grubb (1997) reported a case series of 10 consecutive VVS patients treated with EMG and temperature biofeedback, diaphragmatic breathing, and autogenic training and progressive relaxation. They received an average of 8.5, 50-minute training sessions. By the end of training, 6 of 7 patients diagnosed with syncope reduced these episodes by at least 50%, and 5 of 10 patients reported improvement on each of their symptoms.
McGrady, Kern-Buell, Bush, Devonshire,
Claggett, and Grubb (2003) examined the effects of
biofeedback-assisted relaxation therapy (BART) on VVS. The authors evaluated subjects during a two-week
pretest condition and then randomly assigned them to treatment or a
wait-list control condition. Treatment consisted of 10 (50-minute)
training sessions that incorporated SEMG and thermal biofeedback,
autogenic and progressive relaxation training, and suggestions for
applying techniques like progressive relaxation to specific symptoms.
Patients were instructed to practice with provided scripts and
audiotapes for 10-15 minutes twice a day. The authors evaluated patient
gains during a 2-week post-test condition. The BART group achieved
greater reductions in headache index and loss of consciousness than the
wait-list control group. Both groups improved on measures of state
anxiety and depression.
Clinical Efficacy
Based on one RCT, Fred Shaffer (2023) rated biofeedback for vasovagal syncope as level 2 -
possibly efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (4th ed.). He assigned this rating due to the limited number of studies and patients.
Heart Failure and Coronary Artery Disease
HRV biofeedback shows promise in heart failure (HF) and coronary artery disease (CAD).
Heart failure is caused by cardiac factors, like myocardial damage, valvular disorders, arrhythmias,
conduction defects, ischemia, and systemic factors, like disorders that increase CO2 demand
and increase resistance to cardiac output (Tortora & Derrickson, 2021).
Heart failure affects 2% of the United States population (5.7 million), is responsible for 34% of deaths due to cardiovascular disease (277,000 each year). Heart failure is the leading cause of hospitalization for patients over 65 (Dumitru, 2014).
Medical treatment may involve support with a left ventricular assist device (LVAD) while patients wait for a suitable heart transplant. Graphics courtesy of HeartWare International Inc, Framingham, MA and Africa Studio/ Shutterstock.com.
Biofeedback Studies
There is
increasing evidence that HRVB may improve cardiac function by restoring autonomic balance (Gevirtz, 2013). This
represents a paradigm shift from the earlier model of reducing SNS activation (Moravec & McKee, 2013).
Several studies have demonstrated the promise of HRVB in treating congestive heart failure and coronary
artery disease. Click on the Read More button to review heart failure studies.
Del Pozo, Gevirtz, Scher, and Guarneri (2004)
studied whether cardiorespiratory biofeedback can increase heart rate
variability (HRV) in coronary artery disease (CAD) patients. Decreased
HRV may be a significant independent risk factor for cardiac patient
morbidity and mortality. Training to restore HRV could produce clinical
improvement. The authors randomly assigned 63 patients diagnosed with CAD
to either traditional cardiac rehabilitation or 6 biofeedback sessions
consisting of training to breathe abdominally, cardiorespiratory
biofeedback to increase HRV, and 20-minute daily breathing exercises.
They measured HRV as the standard deviation of normal-to-normal QRS
complexes (SDNN). The
QRS complex of the EKG consists of a
series of waveforms representing the depolarization of the ventricles.
The two groups were equivalent on HRV when measured at baseline.
However, while the cardiorespiratory feedback group increased HRV from
baseline to weeks 6 and 18 (mean SDNN rose from 28 to 42 ms), the
control group deteriorated. Several HRV biofeedback patients changed
their heart attack risk from "unhealthy" to "compromised health." This
study demonstrated that patients with CAD could increase HRV using
cardiorespiratory biofeedback.
Swanson et al. (2009) randomly assigned 29 heart failure patients to an
experimental group that received six weekly sessions of respiratory training, HRVB, and daily
practice or a comparison group that received six weekly sessions of sham alpha-theta biofeedback and daily
practice. The experimental group increased exercise tolerance from baseline to follow-up.
These subjects did not improve on their quality of life or SDNN. The authors concluded that combined training
could enhance exercise tolerance in heart failure patients with a left ventricular ejection fraction (LVEF) of
31% or higher.
Clinical Efficacy
Christine Moravec and Michael McKee (2016) rated biofeedback for heart failure and coronary artery disease as level 2 -
possibly efficacious in Evidence-Based Practice in Biofeedback and Neurofeedback (3rd ed.).
Cardiac Arrhythmia
The cardiac cycle consists of systole
(heart muscle contraction) and diastole (relaxation). During
systole, BP peaks as left ventricle contraction ejects blood from the heart. SBP is
measured here.
During diastole, BP is
lowest as the left ventricle relaxes. Diastolic BP is
measured at this time. The heart contains internal pacemakers, the
sinoatrial (SA) and atrioventricular (AV) nodes, primarily
responsible for the heart rhythm.
Supraventricular tachycardias (SVTs) are the most prevalent arrhythmias. Atrial fibrillation (AF) is the most
frequently diagnosed form of supraventricular arrhythmia and is found in 2% of the United States population
(Mitchell, 2002; Nattel et al., 2002; Savelieva & Camm, 2002; Savelieva & Camm, 2003).
Types of Cardiac Arrhythmia
A cardiac arrhythmia (or dysrhythmia) is a heart
rhythm disturbance along a continuum from "missed" or rapid beats to
impairment of the heart's ability to pump blood, which can be fatal.
Paroxysmal atrial tachycardia is a
form of supraventricular arrhythmia in which an episode of tachycardia
starts and ends suddenly. Paroxysmal supraventricular tachycardia is most commonly diagnosed in young patients,
and maybe triggered during strenuous exercise (Tortora & Derrickson, 2021).
Three research teams have successfully trained sinus tachycardia patients
to slow down their heartbeat, in and outside a laboratory setting, using
several weeks of beat-to-beat heart rate feedback (Scott et al., 1973;
Engel & Bleecker, 1974; Vaitl, 1975).
Wolff-Parkinson-White syndrome is a
form of supraventricular arrhythmia in which there are two AV conduction
pathways, and a delta wave precedes the QRS complex on the ECG.
This is a common cause of paroxysmal
supraventricular tachycardia. When this syndrome first occurs in teenagers and young adults in their early 20s,
they often experience an episode of paroxysmal supraventricular tachycardia during exercise. This episode lasts from
seconds to several hours and may cause fainting. Older patients may additionally experience chest pain and
shortness of breath (Tortora & Derrickson, 2021).
Bleecker and Engel (1973) also taught
one patient with Wolff-Parkinson-White syndrome to control her heart rate
and produce and inhibit normally and pathologically conducted beats
(bidirectional control).
Ventricular ectopic beats, also
called premature ventricular contractions (PVCs),
are heartbeats originating in the ventricles instead of the sinoatrial
node. These extra beats are common and benign in individuals without
heart disease. PVCs result in decreased cardiac output (Huether et al., 2020). While PVCs are not
dangerous in themselves, frequent PVCs in individuals with heart disease may be followed by ventricular
tachycardia or ventricular fibrillation, producing sudden death (Tortora & Derrickson, 2021).
Continuous beat-by-beat heart rate biofeedback is the treatment of choice for
supraventricular arrhythmias and
ventricular ectopic beats. Research by Engel and colleagues supports
training patients to achieve bidirectional control where patients learn
to increase and decrease symptoms like premature ventricular
contractions.
Relaxation training may be helpful when a clinician teaches clients
to slow heart rates. As a clinician observes a continuous display
of the patient's heart rate, they encourage strategies that
slow the heart and discourage those that speed it up.
Engel and Baile (1989) cautioned that
while behavioral methods show promise as adjunctive treatments, "none of
these procedures has been established with sufficient reliability to
justify calling them established treatments" (p. 229).
Clinical Efficacy
Evidence-Based Practicein Biofeedback and Neurofeedback (4th ed.) did not evaluate this application.
Glossary
arterioles: the almost microscopic (8-50 microns in diameter) blood vessels that
deliver blood to capillaries and anastomoses. These vessels may control up to 50% of peripheral resistance through
their narrow diameter, contractility, and massive surface area that follows a fractal pattern.
atrial fibrillation: a form of supraventricular arrhythmia with a heart rate above 300 beats per minute.
This problem is more commonly seen in older patients and is associated with decreased filling time and mean
arterial pressure.
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.
beta-blockers: drugs like Inderal (propranolol) that block the action of epinephrine and norepinephrine
on b-adrenergic receptors, inhibit renin secretion, and decrease heart rate and cardiac contractibility. They are
used to lower blood pressure and prevent cardiac arrhythmia.
blood pressure: the force exerted by blood as it presses against arteries.
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.
calcium channel blockers: drugs like nifedipine (Procardia, Adalat) that slow Ca2+ entry
into myocardial fibers, reducing the heart's workload and contraction force and blood pressure.
cardiac accelerator nerves: sympathetic motoneurons that arise from the medulla's cardiovascular
center increase the rate of spontaneous depolarization in SA and AV nodes and increase stroke volume by
strengthening the contractility of the atria and ventricles.
cardiac arrhythmia: abnormal cardiac conduction, which may result in slow or rapid and regular or
irregular heartbeats.
cardiac cycle: sequence of contraction (systole) and relaxation (diastole) of the ventricles and
atria during one heartbeat.
cardiac output: the amount of blood pumped by the heart in a minute calculated by multiplying
stroke volume times heart rate. Cardiac output is 5.25 liters/minute (70 ml x 75 beats/minute) in a normal, resting
adult.
conduction myofibers: the fibers that extend from the bundle branches into the myocardium, depolarize
contractile fibers in the ventricles (lower chambers), and generate the QRS complex.
continuous beat-by-beat heart rate biofeedback: a treatment of choice for supraventricular arrhythmias
and ventricular ectopic beats in which patients are trained to achieve bidirectional control guided by the display
of each heartbeat. In this approach, clients learn to increase and decrease symptoms like premature
ventricular contractions.
deep muscle relaxation: the voluntary reduction of skeletal muscle contraction, which may lower
cardiac output and plasma norepinephrine.
diastole: the period when the ventricles or atria relax.
diuretics: drugs like Lasix (furosemide) that increase the rate of urination and loss of water and salt
in the urine to reduce blood volume and blood pressure.
dyslipidemia: elevated or abnormal lipid or lipoprotein levels in the blood. This contributes to
atherosclerosis and hypertension.
electrocardiogram (ECG): a recording of the electrical activity of the heart using an electrocardiograph.
fixed atrial fibrillation: supraventricular arrhythmia in which there is a fixed ratio of saw-toothed
flutter waves to QRS
complexes.
hyperinsulinemia: abnormally high blood levels of insulin caused by type 2 diabetes mellitus or insulin resistance. Hyperinsulinemia
contributes to atherosclerosis and hypertension.
hypertension: elevated blood pressure where systolic blood pressure is 130 mmHg or higher and/or diastolic
blood pressure is 80 mmHg or higher.
insulin resistance: a condition in which higher-than-normal insulin levels are required to maintain
normal blood glucose levels. Insulin resistance contributes to atherosclerosis and hypertension.
left ventricular ejection fraction (LVEF): the percentage of the total blood in the heart's left ventricle pumped out with each heartbeat.
Level One interventions: interventions that a client can develop and implement to restore disrupted biological rhythms.
Level Two interventions: interventions that teach basic skills needed for psychological and physical health, which may use educational and community resources
Level Three interventions: interventions that build on the first two levels and are generally managed by professionals.
medulla: the brainstem structure that contains a cardiovascular center that projects sympathetic cardiac
accelerator and parasympathetic vagus (X) nerves.
multi-modal strategy: an intervention thatcontains several
treatment components.
nicotine: a stimulant that binds to nicotinic acetylcholine receptors that can interfere with biofeedback
treatment to lower blood pressure since it raises heart rate and is a potent vasoconstrictor.
normal sinus rhythm: the sinoatrial node is the pacemaker and the heart rate is between 60-100 beats per
minute.
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: the cranial nerves that arise from the medulla's cardiovascular
center, decrease the rate of spontaneous depolarization in SA and AV nodes, and slow heart rate from the SA
node's intrinsic rate of 100 beats per minute.
paroxysmal atrial tachycardia: a form of supraventricular arrhythmia in which an episode of tachycardia
starts and ends suddenly. This is most commonly diagnosed in young patients and maybe triggered during strenuous
exercise.
primary (essential) hypertension: chronically elevated blood pressure, not due to an identifiable cause.
problem solving training (PST): D'Zurilla's intervention to improve clients' ability to
cope with everyday issues. This intervention reduces stress and anxiety, helps patients control anger, and can
help lower blood pressure.
QRS complex: an ECG structure that corresponds to the depolarization of the ventricles.
relaxation training: procedures thatreduce arousal and produce
complex changes in the individual, including blood pressure reduction. Six families of relaxation training include
stretching, progressive muscle relaxation, breathing exercises, autogenic training, imagery/positive self-talk,
and mediation/mindfulness.
R-wave-to-pulse interval (RPI) biofeedback: the display of the elapsed time between the R-wave of the ECG and
the maximum amplitude of the peripheral pulse wave during a single cardiac cycle to a client to reduce blood
pressure.
secondary hypertension: elevated blood pressure with an
identifiable cause, such as obstruction of renal (kidney) blood flow or disorders that injure renal tissue,
hypersecretion of aldosterone, and hypersecretion of epinephrine and norepinephrine by an adrenal medulla tumor
called a pheochromocytoma.
sinoatrial (SA) node: the sinoatrial node of the heart initiates
each cardiac cycle through spontaneous depolarization of its autorhythmic fibers.
sinus tachycardia: a type of supraventricular arrhythmia in which a heart rate of 100-150 beats per
minute is generated by stimulation of the SA node. The effects of this arrhythmia include decreased filling times,
decreased mean arterial pressure, and increased myocardial demand.
S-T segment: an ECG structure that connects the QRS complex and the T wave. Ventricular contraction
continues through the S-T segment.
stroke rate: the number of heartbeats per minute.
stroke volume: the amount of blood ejected by the left ventricle during one contraction.
supraventricular tachycardia (SVT): a regular and rapid (above 100 beats-per-minute) heart rate that
originates in the SA node, atria, or AV junction located above the ventricles.
systemic vascular resistance: the total resistance of all systemic blood vessels influenced
by blood viscosity (thickness), and blood vessel length and radius.
systole: the period when the ventricles or atria contract.
T wave: an ECG structure that represents ventricular repolarization.
temperature biofeedback: the display of a client’s skin temperature information back to the individual to produce desired physiological changes. Temperature biofeedback is a hypertension treatment
component.
thrombus: stationary clot formed in a blood vessel that is usually a
vein.
vasovagal syncope (VVS): in response to abnormal vagus nerve activity during stressful events, blood vessels dilate,
blood pools in the lower body, the brain receives less blood, and the client becomes light-headed and may
faint.
ventricular ectopic beats: premature ventricular contractions (PVCs) are heartbeats originating in
the ventricles instead of the sinoatrial node. These extra beats, which are common and benign in individuals without
heart disease, result in decreased cardiac output.
volume expansion (hypervolemia): increased fluid, mainly containing salt and water, in the blood.
Volume expansion is a hypertension risk factor.
Wolff-Parkinson-White syndrome: a form of supraventricular arrhythmia in which there are two AV
conduction pathways and a delta wave precedes the QRS complex on the ECG. This syndrome is a common cause of paroxysmal
supraventricular tachycardia.
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Assignment
Now that you have completed this module, describe your protocol for
treating essential hypertension. How would you refine your protocol after
reviewing the most recent hypertension studies?
References
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