Normal blood pressure is now defined as below 120/70 mm Hg. Biofeedback has demonstrated efficacy and cost-effectiveness in cardiovascular disorders like essential hypertension. In essential hypertension, research has shown that effective interventions share common components and that models can be constructed to predict treatment success and the size of blood pressure reductions. For many clients, stress management training, and SEMG and temperature biofeedback are among the best-documented interventions. Based on the results of a psychophysiological profile, HRV and respiratory biofeedback may also be promising.

This unit covers the Pathophysiology, biofeedback modalities, and treatment protocols for specific ANS biofeedback applications (V-D).
Students completing this unit will be able to discuss:

  1. Pathophysiology, biofeedback modalities, and treatment protocols for specific ANS biofeedback
    A. Hypertension
    B. Cardiac arrhythmias

Blood pressure is the product of cardiac output (amount of blood pumped by the heart) and systemic vascular resistance. Systemic vascular resistance represents the total resistance of all systemic blood vessels and is influenced by:

  1. blood viscosity (thickness)
  2. total blood vessel length
  3. blood vessel 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 major role in controlling systemic vascular resistance. A small adjustment in arteriole diameter can significantly change systemic vascular resistance and, consequently, blood pressure and tissue perfusion (Tortora & Derrickson, 2006).

Hypertension (elevated blood pressure) is defined when systolic blood pressure is 140 mm Hg or higher and diastolic blood pressure is 90 mm Hg or higher. A blood pressure classification system for adults revised in 2003 is shown below.

The National Heart, Lung, and Blood Institute (2003) defined blood pressures between 120-139 mmHg systolic and 80-89 mmHg diastolic as prehypertensive. The NHLBI advised that for adults over 50, systolic blood pressure is considerably greater risk factor for cardiovascular disease (CVD) than diastolic blood pressure.

About 90-95% of all cases of hypertension are primary hypertension, which is chronically elevated blood pressure not due to an identifiable cause. The remaining 5-10% are classified as secondary hypertension, which has an identifiable cause.

Disorders that produce secondary hypertension include

  1. obstruction of renal (kidney) blood flow or disorders that injure renal tissue
  2. hypersecretion of aldosterone
  3. hypersecretion of epinephrine and norepinephrine by an adrenal medulla tumor called a pheochromocytoma (Tortora & Derrickson, 2006).

Wang and Wang (2004) estimate that almost 60% of American adults can be classified with prehypertension or hypertension. Groups at highest risk include African Americans, the elderly, individuals with low socioeconomic status, and those who are overweight. While the prevalence of hypertension has increased 10% in the past decade, patient control of hypertension remains low. Thirty-one percent were unaware that they were hypertensive, only 66% were instructed by health professionals to modify lifestyle and take drugs to control their blood pressure, and only 31% achieved satisfactory control.

While blood pressure rises as Americans age, a study in the Journal of the American Medical Association (May, 2004) reported that Americans are developing hypertension at increasingly earlier ages and that blood pressure is increasing in children (Medline Plus, August 23, 2004).

"High blood pressure is a major risk factor for coronary heart disease, kidney failure, heart failure, stroke and other conditions," said Dr. Larry Fields of the Department of Health and Human Services, who led a major study reported in Hypertension: Journal of the American Heart Association, August, 2004.

Essential hypertension is a heterogeneous disorder produced by diverse genetic and environmental factors. Estimates of the genetic contribution vary from 30% (Weiner, 1979) to 60% (Feinleib, 1977). A positive family history of hypertension raises the risk of elevated blood pressure. Twenty-five percent of the children will be hypertensive if one parent is hypertensive; 50%, if both parents are hypertensive (Olson & Kroon, 1987).

Factors that may produce essential hypertension are shown below in a diagram adapted from McGrady (1996). Hyperinsulinemia means an abnormally high level of insulin in the blood. Insulin resistance is a complication of diabetes mellitus where more than 200 units of insulin are required daily to regulate hypoglycemia and ketosis. Dyslipidemia involves abnormal accumulation of fat deposits. Volume expansion means increased blood volume.


  1. Lose weight. This is the most effective lifestyle change
  2. Limit alcohol intake. Consume less than 2 ounces of 100-proof alcohol per day.
  3. Exercise. Moderate activity for 30-45 minutes several times a week can lower systolic pressure 10 mm Hg.
  4. Reduce salt intake. About 50% of hypertensives are "salt-sensitive.
  5. Maintain recommended dietary intake of potassium, calcium, and magnesium.
  6. Don't smoke.
  7. Manage stress.

Small blood pressure reductions can significantly reduce premature heart attack deaths. A 2-mm Hg decrease reduces the risk of premature death 8-10% (Raloff, 1990).

The main drugs used to treat hypertension include diuretics, ACE inhibitors, beta blockers, and calcium channel blockers. The National Heart, Lung, and Blood Institute (2003) advises control of hypertension with two agents, including a thiazide-type diuretic, when blood pressure is greater than 20/10 mmHg over the patients' goal blood pressure.

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 blood pressure reductions. Patients should monitor their blood pressure on a daily basis and discuss medication adjustment with their physician before making changes on their own.

Evidence-Based practice in biofeedback and neurofeedback (2004) rates biofeedback for essential hypertension at level 4 efficacy, efficacious. The criteria for level 4 efficacy include:"

  1. In a comparison with a no-treatment control group, alternative treatment group, or sham (placebo) control utilizing randomized assignment, the investigational treatment is shown to be statistically significantly superior to the control condition or the investigational treatment is equivalent to a treatment of established efficacy in a study with sufficient power to detect moderate differences, and
  2. The studies have been conducted with a population treated for a specific problem, for whom inclusion criteria are delineated in a reliable, operationally defined manner, and
  3. The study used valid and clearly specified outcome measures related to the problem being treated, and
  4. The data are subjected to appropriate data analysis, and
  5. The diagnostic and treatment variables and procedures are clearly defined in a manner that permits replication of the study by independent researchers, and
  6. The superiority or equivalence of the investigational treatment has been shown in at least two independent research settings" (pp. 24-25).

Biofeedback has been shown to be 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).


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 (95 degree F goal) and then the feet (93 degree F goal), and frontal SEMG training in 18-26, 1-hour sessions. These researchers stressed home practice twice a day using autogenic biofeedback, daily blood pressure monitoring, and diaries of relaxation practice.

Results at the end of training were impressive in this uncontrolled series of patients as reported by 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 one month following treatment and one year following treatment:

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 waiting list control. The stress management protocol included D’Zurilla’s problem solving training (PST) to improve the patients’ ability to cope with everyday problems.

PST has been shown to reduce stress and anxiety, and help patients control anger. The researchers included it to reduce stress due to deficient coping skills and change defensive cognitive appraisals that might contribute to hypertension.

At the end of two months of stress management training or waiting list, the authors reported:

Jacob et al. (1991) reported a meta-analysis over 75 treatment groups and 41 control groups. The treatment groups produced markedly greater blood pressure reductions than control groups.

The treatments that produced the greatest blood pressure reductions were ranked as follows:

  1. stress management
  2. SEMG biofeedback
  3. temperature biofeedback

Relaxation and blood pressure biofeedback produced the smallest reductions in systolic blood pressure, and meditation produced the smallest reductions in diastolic blood pressure. Patient expectations concerning treatment efficacy and their perception of relaxation depth during treatment discriminated between treatment success and failure.

Yucha, Clark, 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 blood pressure measurement. Both biofeedback and active treatments produced significant, but equivalent, reductions in systolic and diastolic blood pressure. Biofeedback produced greater systolic (6.7 mmHg) and diastolic (3.8 mmHg) blood pressure reductions than the inactive treatments.


Rau, Bührer, and Weitkunat (2003) studied the effects of R-wave-to-pulse interval (RPI) biofeedback on 12 participants with high blood pressure and 10 with low blood pressure. 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 blood pressure decreases (high blood pressure) or blood pressure increases (low blood pressure) were rewarded. The high blood pressure group decreased systolic blood pressure 15.3 mmHg and diastolic blood pressure 17.8 mmHg from the start of training session 1 to the end of training session 3. The low blood pressure group increased systolic blood pressure 12.3 mmHg and diastolic blood pressure 8.4 mmHg from the start of training session 1 to the end of training session 3.

McGrady (1996) identified six factors in efficacy studies reporting the largest and most consistent blood pressure reductions.

First, patients received sufficient training to master the technique. Second, home relaxation or biofeedback practice was required. Third, biofeedback was combined with relaxation. Passive exercises like autogenics were more effective than active exercises like Progressive Relaxation. Fourth, patients monitored their own blood pressures throughout treatment. Fifth, multiple blood pressure measurements were recorded (home, clinic, and ambulatory halter), starting at least three weeks before treatment and after treatment ended. Sixth, patient adherence to responsibilities for keeping appointments, practice, and record keeping.


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 blood pressure monitoring.

The most responsive patients showed a high heart rate, cool hands, high SEMG, and high plasma renin activity. The best predictors of how much blood pressure decreased were high heart rate, cool hands, high anxiety, and high-normal cortisol.

Patients can lower blood pressure through multiple mechanisms, by reducing cardiac output, cortisol and norepinephrine levels, skeletal muscle contraction, systemic vascular resistance, and by stimulating the baroreflex.

Different hypertension treatments may operate through different 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 both 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) observes that when individuals breathe at their resonant frequency, heart rate and blood pressure are 180o out of phase, which implies that breathing about 6 times per minute stimulates the baroreflex. He proposes that 0.1 Hz biofeedback may lower blood pressure by stimulating the baroreflex.


Prescription medications and social drugs can affect biofeedback measurements. Inderal, which produces peripheral vasodilation, can raise hand temperature so that patient measurements appear healthy (92 degrees F instead of 88 degrees F). When medication artificially raises hand temperature, the clinician should train the patient to achieve a higher value (95 instead of 92 degrees F).

Medications (Cafergot and Fiorinal) or beverages that contain caffeine can increase heart rate and constrict peripheral blood vessels. Since these effects could interfere with blood pressure 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 blood pressure since it raises heart rate and is a potent vasoconstrictor. Smoking cessation treatment should be considered in these cases.

McGrady's (1996) six factors for successful hypertension interventions should be the foundation of any treatment program. Essential hypertension treatment should be tailored to your individual patient 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 medical evaluation, a biofeedback therapist 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 the systems that are malfunctioning, promotes relevant lifestyle changes, and teaches stress management when needed shows the greatest clinical promise.

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 an important independent risk factor for cardiac patient morbidity and mortality, so increasing 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 increased 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 can increase HRV using cardiorespiratory biofeedback.

The cardiac cycle consists of systole (heart muscle contraction), and diastole (relaxation). During systole, blood pressure peaks as contraction by the left ventricular ejects blood from the heart. Systolic blood pressure is measured here.

During diastole, blood pressure is lowest as the left ventricle relaxes. Diastolic blood pressure is measured at this time. The heart contains internal pacemakers, the sinoatrial (SA) and atrioventricular (AV) nodes, which are primarily responsible for the heart rhythm.

The electrocardiogram (ECG) records the action of this electrical conduction system. In a normal heart, the SA node initiates each cardiac cycle through its spontaneous depolarization. The SA node’s rapid and frequent generation of action potentials usually prevents other parts of the conduction system and myocardium (heart muscle) from generating competing potentials.


In a healthy heart, the SA node initiates each cardiac cycle through spontaneous depolarization of its autorhythmic fibers. The SA node’s firing of about 100 action potentials per minute usually prevents other parts of the conduction system and myocardium (heart muscle) from generating competing potentials. The SA node fires an impulse that travels through the atria (upper heart chambers) to the AV node in about 0.03 s and causes the AV node to fire. The P wave of the ECG is produced as contractile fibers in the atria depolarize and culminates in contraction of the atria (atrial systole).

The AV node can replace an injured or diseased SA node as pacemaker and spontaneously depolarizes 40-60 times per minute. The signal rapidly spreads through the atrioventricular (AV) bundle reaching the top of the septum. These fibers descend down both sides of the septum as the right and left bundle branches and conduct the action potential over the ventricles about 0.2 s after the appearance of the P wave, Conduction myofibers, which extend from the bundle branches into the myocardium, depolarize contractile fibers in the ventricles (lower chambers), resulting in the QRS complex. The ventricles contract (ventricular systole) soon after the emergence of the QRS complex and this continues through the S-T segment. The repolarization of ventricular contractile fibers generates the T wave about 0.4 s following the P wave. The ventricles relax (ventricular diastole) 0.6 s after the P wave begins.

While the SA node generates the fundamental cardiac rhythm, autonomic motor neurons and circulating hormones influence the interbeat interval and force of myocardial contraction. Sympathetic cardiac accelerator nerves (arising 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. The parasympathetic vagus (X) nerves (also arising from the medulla’s cardiovascular center) decrease the rate of spontaneous depolarization in SA and AV nodes, and slow the heart rate, Heart rate increases often reflect reduced vagal inhibition.

There is a dynamic balance between sympathetic and parasympathetic influences over the heart. Parasympathetic control predominates at rest, resulting in an average heart rate of 75 beats per minute that is significantly slower than the SA node’s intrinsic rate of 100 beats per minute. The parasympathetic branch can slow the heart to 20 or 30 beats per minute, or briefly stop it.

The medulla is not the only structure that controls heart rate. The amygdala, cerebellum, and hypothalamus also help regulate cardiovascular reflexes. 

A normal sinus rhythm is where the sinoatrial node is the pacemaker and heart rate is between 60-100 beats per minute. Below is a BioGraph ® Infiniti EKG display.

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).

A cardiac arrhythmia 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. Researchers have successfully treated patients diagnosed with supraventricular arrhythmias and ventricular ectopic beats.

A supraventricular tachycardia (SVT) is a regular and rapid (160-200 beats-per-minute) heart rate that originates in heart tissue (atria) located above the ventricles. 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 may be triggered during strenuous exercise (Merk manual of medical information, 2003).

Engel and Bleecker (1974)
successfully trained two paroxysmal atrial tachycardia patients to slow their heart rates using EKG biofeedback.

Sinus tachycardia is 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 (Huether & McCance, 2004).

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 EKG. 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, which lasts from seconds to several hours, and may cause fainting. Older patients may additionally experience chest pain and shortness of breath (Merk manual of medical information, 2003).

Bleecker and Engel (1973)
also taught one patient with Wolff-Parkinson-White syndrome to control her heart rate and both produce and inhibit normally and pathologically conducted beats (bidirectional control).

Atrial fibrillation is a form of supraventricular arrhythmia with a heart rate above 300 beats per minute. This arrhythmia is more commonly seen in older patients and decreases filling time and mean arterial pressure (Huether & McCance, 2004). Due to the heart's reduced pumping capacity, patients may experience fainting, shortness of breath, and weakness. Older patients may experience chest pain or heart failure (Merk manual of medical information, 2003).

In fixed atrial fibrillation there is a fixed ratio of saw-toothed flutter waves to QRS complexes. Bleecker and Engel (1973) trained six fixed atrial fibrillation patients to increase and decrease their ventricular rates.

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 & McCance, 2004). While PVCs are not dangerous in themselves, frequent PVCs in individuals with heart disease may be followed by ventricular tachycardia or ventricular fibrillation, which can produce sudden death (Merk manual of medical information, 2003).

Two laboratories have successfully trained patients to reduce ventricular ectopic beats using heart rate feedback (Weiss & Engel, 1971; Pickering & Gorham, 1975; Pickering & Miller, 1977).

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 alternately increase and decrease symptoms like premature ventricular contractions.

Relaxation training may be helpful when the clinician teaches the patient to slow the heart rate. As the clinician observes the continuous display of the patient’s heart rate, he or she will 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).

Syncope means fainting. In response to abnormal vagus nerve activity, blood vessels dilate, blood pools in the lower body, the brain receives less blood, and the patient becomes light-headed and may faint.

Triggers for neurocardiogenic syncope include:

Common symptoms include:

Neurocardiogenic syncope is the most common cause of loss of consciousness in otherwise normal individuals and occurs in up to 20% of the population. About 9% will experience recurrent episodes of fainting (Weeks & Sheldon, 2004).

McGrady, Kern-Buell, Bush, Devonshire, Claggett, and Grubb (2003)
examined the effects of biofeedback assisted relaxation therapy (BFRT) on neurocardiogenic syncope.

The authors evaluated subjects during a two-week pretest condition and then randomly assigned them to treatment or a waiting list control condition. Treatment consisted of 10 (50-min) 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 two-week posttest condition. The BFRT group achieved greater reductions in headache index and loss of consciousness than the waiting list control group. Both groups improved on measures of state anxiety and depression.

Now that you have completed this module, describe your protocol for treating essential hypertension. How would you refine your protocol after reviewing the cited hypertension studies?

Blanchard, E. B., McCoy G. C., Musso, A., Gerardi, M. A., Pallmeyer, T. P., Gerardi, R. J., et al. (1986). A controlled comparison of thermal biofeedback and relaxation training in the treatment of essential hypertension: I. Short-term and long-term outcome. Behavior Therapy, 17, 563-579.

Carlson, J. G., Seifert, A. R., & Birbaumer, N. (Eds.). (1994). Clinical applied psychophysiology. New York: Plenum Press.

Del Pozo, J. M., Gevirtz, R. N., Scher, B., & Guarneri, E. (2004). Biofeedback treatment increases heart rate variability in patients with known coronary artery disease. American heart Journal, 147(3), E11.

Engel, B. T., & Baile, W. F. (1989). Behavioral applications in the treatment of patients with cardiovascular disorders. In J. V. Basmajian (Ed.) Biofeedback: Principles and practice for clinicians (3rd ed.). Baltimore: Williams & Wilkins.

Etminan, M. (December 13, 2004). British Medical Journal Online First.

Garcia-Vera, M. P., Labrador, F. J., & Sanz, J. (1997). Stress-management training for essential hypertension: A controlled study. Applied Psychophysiology and Biofeedback, 22(4), 261-283.

Gevirtz, R. N. (2005). Heart rate variability biofeedback in clinical practice. AAPB Fall workshop.

Guyton, A. C., & Hall, J. E. (1997). Human physiology and mechanisms of disease. Philadelphia: W. B. Saunders Company.

Huether, S. E., & McCance, K. L. (2004). Understanding pathophysiology (3rd ed.). St. Louis, MO: Mosby.

McGrady, A., Kern-Buell, C., Bush, E., Devonshire, R., Claggett, A. L., & Grubb, B. P.(2003). Biofeedback-assisted relaxation therapy in neurocardiogenic syncope: A pilot study. Applied Psychophysiology and Biofeedback, 28(3), 183-192.

McGrady, A., Olson, R., & Kroon, J. S. (1995). Biobehavioral treatment of essential hypertension. In Schwartz and associates, Biofeedback: A practitioner's guide. New York: The Guilford Press.

Merk manual of medical information: Second home edition (2003). New York: Pocket Books.

Mitchell, A. R. (2002). Atrial fibrillation in the new millennium-the role of pacemaker and defibrillator therapy. Med Sci Monit, 8, RA233-RA239.

Nakao, M., Nomura, S., Shimosawa, T., Fujita, T., & Kuboki, T. (1999). Blood pressure biofeedback treatment, organ damage and sympathetic activity in mild hypertension. Psychotherapy and Psychosomatics, 68(6), 341-347.

Nakao, M., Nomura, S., Shimosawa, T., Fujita, T., & Kuboki, T. (2000). Blood pressure biofeedback treatment of white coat hypertension. Journal of Psychosomatic Research, 48(2), 161-169.

Nattel, S., Khairy, P., & Roy, D., et al. (2002). New approaches to atrial fibrillation management: a critical review of a rapidly evolving field. Drugs, 62, 2377-2397.

National Institutes of Health,  National Heart, Lung, and Blood Institute (2003). The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure. NIH Publication No. 03-5233.

Patel, C. (1977). Biofeedback-aided relaxation and meditation in the management of hypertension. Biofeedback and Self-regulation, 2, 1-41.

Pickering, T. G., & Miller, N. E. (1977). Learned voluntary control of heart rate and rhythm in two subjects with premature ventricular contractions. British Heart Journal, 39, 152-159.

Rau, H., Bührer, M., & Weitkunat, R. (2003). Biofeedback of R-wave-to-pulse interval normalizes blood pressure. Applied Psychophysiology and Biofeedback, 28(1), 37-46.

Savelieva, I., & Camm, A. J. (2002). Atrial pacing for the prevention and termination of atrial fibrillation. Am J Geriatr Cardiol, 11, 380-398.

Savelieva, I., & Camm, A. J. (2003). The results of pacing trials for the prevention and termination of atrial tachyarrhythmias: is there any evidence of therapeutic breakthrough? J Interv Card Electrophysiol, 8, 103-115.

M. S. Schwartz, & F. Andrasik (Eds.). (2003). Biofeedback: A practitioner's guide (3rd ed.). New York: The Guilford Press.

Sharma, S., & Kortas, C. (2002). Essential hypertension. eMedicine.

Somers, P. J., Gevirtz, R. N., Jasin, S. E., & Chin, H. G. (1989). The efficacy of biobehavioral and compliance interventions in the adjunctive treatment of mild pregnancy-induced hypertension. Biofeedback and Self-Regulation, 14(4), 309-318.

Taub, E., Steiner, S. S., Weingarten, E., & Walton, K. C. (1994). Effectiveness of broad spectrum approaches to relapse prevention in severe alcoholism: A long-term randomized controlled trial of transcendental meditation, EMG biofeedback, and electronic neurotherapy. Alcoholism Treatment Quarterly, 11(1/2), 187-220.

Tortora, G. J., & Derrickson, B. H. (2006). Principles of anatomy and physiology (11th ed.). New York: John Wiley & Sons, Inc.

Wang, Y., & Wang, Q. J. (2004). The prevalence of prehypertension and hypertension among US adults according to the New Joint National Committee Guidelines. Archives of Internal Medicine, 164(19), 2126-2134.

Weeks, S. G., & Sheldon, R. (2004). Neurally mediated syncope and pacemakers: Time to rethink? Cardiovasc Rev Rep, 25(4), 171-174.

Weiss, T., & Engel, B. T. (1971). Operant conditioning of heart rate and rhythm in patients with premature ventricular contractions. Psychosomatic Medicine, 33, 301-321.

Yucha, C. B., Clark, L., Smith, M., Uris, P., Lafleur, B., & Duval, S. (2001). The effect of biofeedback in hypertension. Applied Nursing Research, 14(1), 29-35.

Yucha, C. B., & Gilbert, C. D. (2004). Evidence-based practice in biofeedback and neurofeedback. Wheat Ridge: AAPB.